In the early postoperative period (within 6 weeks), the standard approach is surgical debridement of the infected tissue while retaining the hardware if the bone is not stable without it. Intravenous antibiotics are then initiated. Immediate hardware removal is usually avoided at this stage to maintain fracture stability unless necessary.

In managing an infected fibular plate after ORIF (open reduction and internal fixation) within 4 weeks post-op, the treatment approach often depends on the stability of the fracture, the severity of the infection, and the time since the surgery.

Early Postoperative Infections (within 6 weeks):

At 4 weeks post-op, the fracture is still healing, and the hardware plays an important role in maintaining fracture stability.  The primary goals are to:

1. Control the infection without compromising fracture healing.
2. Retain the hardware if possible to ensure that the fracture remains stable.

Standard Approach:

• Surgical Debridement: Removing the infected and necrotic tissue around the incision and hardware is essential. It helps decrease bacterial load and allows for better penetration of antibiotics. Retention of hardware is typically attempted if the fracture is still reliant on it for stability, as removing the hardware too early can result in fracture displacement or nonunion.
• Intravenous Antibiotics: IV antibiotics are used to treat the infection systemically and are culture-directed.

Hardware Retention vs. Removal:

• Retention: If the hardware is necessary for fracture stability (which it often is at 4 weeks), it is usually kept in place while the infection is treated. Removing it too early could lead to instability and poor healing.
• Removal: Hardware removal is generally considered later in the course (usually 6 weeks or later) when the fracture is more stable, or if the infection persists despite debridement and antibiotics.

Why Not Immediate Removal?

At 4 weeks, the fracture hasn't fully healed, so removing the hardware could destabilize the bone and lead to complications such as nonunion, malunion, or even the need for reoperation with new hardware. By debriding and using IV antibiotics, you can often control the infection while keeping the hardware in place until the fracture heals sufficiently for safe removal later.

Reaming the medullary canal during intramedullary nailing increases the diameter of the medullary canal, leading to increased stability at the fracture site due to using a larger diameter nail. Reaming enlarges the canal to match the diameter of the nail, improving the nail's fixation within the bone and promoting better load-sharing. However, reaming can disrupt the endosteal blood supply, increase the risk of fat embolism, and can cause thermal necrosis.

See the cheat sheet on plating techniques

Bridge plating is used in comminuted fractures where direct reduction of each fracture fragment is not necessary. The plate acts as a bridge across the fracture, maintaining length and alignment while allowing for relative stability and indirect healing.

A) Simple transverse fractures

• Explanation: Simple transverse fractures can often be treated with compression plating, which allows for direct apposition and compression of the fracture ends, leading to primary bone healing with absolute stability.

B) Comminuted fractures with minimal soft tissue damage

• Explanation: Bridge plating is ideal for comminuted fractures where direct manipulation of small fragments is avoided to preserve the soft tissue and blood supply. The plate spans across the fracture zone and maintains the overall alignment, allowing for relative stability and indirect bone healing. This technique is beneficial when the fracture has multiple small pieces, making direct reduction of each fragment impractical.

C) Spiral fractures requiring compression

• Explanation: Spiral fractures can benefit from compression with an interfrag screw and neutralization plate, as these fractures are usually longer and involve less comminution, allowing for the application of compression forces to bring the fracture ends together.

D) Intra-articular fractures with joint involvement

• Explanation: Intra-articular fractures require anatomic reduction and absolute stability to prevent joint incongruity and early osteoarthritis. Techniques like compression or buttress plating are often preferred in these scenarios.

Biologic agents like TNF inhibitors (e.g., adalimumab) can increase the risk of perioperative infections. Therefore, it is recommended to stop these agents about 1-2 weeks before surgery and resume them once adequate wound healing has been confirmed. Prednisone should be continued, often with stress dosing, to prevent adrenal insufficiency.

See the cheat sheet on compartment syndrome

Compartment syndrome is diagnosed based on the difference between diastolic blood pressure (DBP) and compartment pressure. A differential pressure (ΔP) of less than 30 mmHg (DBP − compartment pressure) is a critical threshold for diagnosing compartment syndrome and indicates the need for emergent fasciotomy. A compartment pressure of 30 mmHg or higher is also highly suggestive of compartment syndrome. Immediate surgical intervention is required to prevent permanent tissue damage.

See the cheat sheet on the Sanders classification system

The Sanders classification is based on the number of fracture lines involving the posterior facet of the calcaneus seen on a coronal CT scan. Sanders Type III involves three articular fragments and is considered a displaced fracture. Type II involves two articular fragments, and Type IV is a comminuted fracture with more than four fragments.

See the cheat sheet for the Gustilo-Anderson classification system

The correct answer for a Gustilo-Anderson type IIIa is D, a comminuted fracture with an open wound measuring 5 cm in length, with adequate soft tissue coverage of the wound after debridement.  If there was inadequate soft tissue coverage requiring a flap, that would make it a IIIb, and if there was vascular injury requiring a repair, this would then be a IIIc.

See the cheat sheet for the Lauge-Hansen Classification

In the Supination-External Rotation (SER) injury pattern, the fibula typically shows a spiral fracture at the level of the ankle joint (Weber B), and the medial malleolus often has a transverse fracture. The widening of the syndesmosis suggests injury to the interosseous membrane, all characteristic of SER injuries.

See the NEW cheat sheet of the Tscherne Classification 

The Tscherne classification system is designed to assess soft tissue injuries associated with open and closed fractures. It helps to determine the severity of soft tissue damage, which can influence treatment decisions and prognosis. The classification has four grades (0 to 3), ranging from minor to severe soft tissue injuries.  The Tscherne classification is especially useful in evaluating closed fractures, which do not break through the skin but may still have significant internal soft tissue damage. It provides a guide for assessing injury severity and choosing appropriate treatment, especially for cases where soft tissue damage is a critical concern.

A transverse fracture of the distal fibula and a vertical fracture of the medial malleolus are classic findings in a Supination-Adduction (SA) injury. This mechanism typically causes a tension failure in the lateral fibula and compression on the medial side, leading to the vertical fracture of the medial malleolus.

In cases of localized or early-stage pyoderma gangrenosum, potent topical corticosteroids can be an effective first-line treatment to control inflammation and promote healing.  When a topical potent corticosteroid is not effective within 2-4 weeks of treatment, it has been recommended to attempt either oral Dapsone, oral Minocycline, or topical .03/.1% Tacrolimus ointment as a secondary treatment option.

See the cheat sheet on wound VAC therapy 

The wound VAC device promotes wound healing by creating mechanical forces (also known as microdeformation) at the cellular level, which stimulates angiogenesis and encourages granulation tissue formation. The negative pressure also helps remove excess exudate and reduces bacterial load.

Sodium thiosulfate’s mechanism of action in treating calciphylaxis is not fully understood, but its therapeutic effects are attributed to the following key mechanisms:

1. Calcium Chelation: Sodium thiosulfate acts as a calcium chelator, binding to calcium and solubilizing calcium deposits in the affected tissues. This helps to reduce the vascular calcifications seen in calciphylaxis.
2. Antioxidant Properties: It has antioxidant effects, neutralizing reactive oxygen species (ROS) that can contribute to vascular damage and tissue ischemia.
3. Vasodilation: Sodium thiosulfate has mild vasodilatory effects, improving blood flow and tissue perfusion, which may promote healing of the ulcerative skin lesions.

Sodium thiosulfate is typically administered intravenously for the treatment of calciphylaxis. The dosing and administration depend on the severity of the condition and the patient's renal function.

• Route of Administration: Intravenous (IV) infusion.
• Dosing: A typical dose is 25 grams of sodium thiosulfate administered three times a week, often after hemodialysis sessions in patients with end-stage renal disease.
• Duration: Treatment usually continues for several weeks to months, depending on the response to therapy and healing of the ulcers.

See our NEW CHEAT SHEET on the role of collagen dressings on wound healing

Collagen dressings provide a scaffold for fibroblasts and keratinocytes, which are important for the proliferation phase of wound healing. This matrix promotes the deposition of new extracellular matrix and aids in the formation of granulation tissue, which is essential for healing chronic wounds like diabetic foot ulcers.

Santyl (collagenase) is an enzymatic debriding agent used primarily in wound care, particularly for chronic wounds like diabetic foot ulcers, pressure ulcers, and burns. Here's an explanation of the answer to the question:

• Answer: D - Acts by selectively breaking down collagen in necrotic tissue, facilitating wound debridement.

Santyl contains collagenase, which is an enzyme that selectively digests collagen. Collagen is a major structural protein found in the extracellular matrix of tissues. In chronic wounds, necrotic tissue often contains large amounts of denatured collagen. By breaking down this collagen, Santyl helps remove the dead tissue, facilitating debridement and allowing healthy tissue to grow. This enzymatic process is gentler and more targeted compared to surgical or mechanical debridement.

Santyl (collagenase) is derived from the bacterium Clostridium histolyticum. This organism produces collagenase enzymes that are capable of breaking down collagen, which is a key component of necrotic tissue in chronic wounds. By isolating these enzymes from Clostridium histolyticum, Santyl can enzymatically debride wounds, promoting healing by removing dead tissue and allowing the formation of healthy tissue.

Dantrolene is the only specific antidote for malignant hyperthermia. It works by inhibiting calcium release from the sarcoplasmic reticulum in muscle cells, reducing muscle rigidity and hypermetabolism.

In arterial ulcers, surgical debridement of stable eschar is not recommended until sufficient blood flow is restored. Eschar can sometimes act as a protective cover for underlying tissues, and removing it prematurely without improving perfusion can worsen the wound. The other options, such as hyperbaric oxygen therapy, smoking cessation, and pharmacologic management to improve circulation, are more appropriate treatments.

Pentoxifylline is commonly used as an adjunctive therapy in the treatment of venous stasis ulcers due to its ability to improve microcirculation by increasing red blood cell flexibility and reducing blood viscosity. It is often used in combination with appropriate compression therapy for patients with chronic venous insufficiency.

Furosemide is a diuretic and is not directly involved in ulcer healing. Clopidogrel is an antiplatelet agent used to prevent arterial thrombosis but has no direct role in venous stasis ulcer treatment. Doxycycline may be used if there is evidence of infection but is not routinely indicated for venous stasis ulcerations without infection.

Drawtex is a hydroconductive wound dressing designed to manage moderate to heavy exudate by absorbing and wicking away fluid. It helps protect the surrounding skin from maceration by drawing excess moisture away from the wound bed and peri-wound area, promoting a favorable environment for healing.

• Hydrocolloid dressing: Suitable for wounds with low to moderate exudate but not as absorbent as Drawtex for managing larger amounts of drainage.
• Hydrogel: More suitable for dry wounds or wounds with minimal exudate, as it provides moisture rather than absorbing it.
• Silver sulfadiazine: Primarily used for infected or burn wounds due to its antimicrobial properties, but it is not designed for managing heavy exudate or protecting the periwound area from maceration.

Explanation:

• Anti-centromere antibodies are highly specific for limited cutaneous systemic sclerosis (formerly called CREST syndrome), a subtype of scleroderma.
• ANA is positive in most cases of scleroderma but lacks specificity.
• Anti-Smith antibodies are more associated with systemic lupus erythematosus.
• Rheumatoid factor (RF) is typically seen in rheumatoid arthritis and is not specific to scleroderma.

Dystrophic calcification occurs in damaged or necrotic tissue despite normal calcium and phosphate levels, often in association with chronic inflammation or trauma. This is distinct from metastatic calcification, which results from elevated calcium or phosphate levels. The patient’s history of inflammatory arthritis and normal lab values are consistent with dystrophic calcification. Calcinosis cutis is the deposition of calcium in the skin and subcutaneous tissues

This patient has palmoplantar pustulosis that has not responded to topical corticosteroids, indicating the need for systemic therapy. Acitretin, an oral retinoid, is effective in treating cases of palmoplantar pustulosis. Increasing the potency of topical corticosteroids is unlikely to benefit someone who has already failed high-potency topical therapy. Topical calcineurin inhibitors are used for other types of psoriasis but are not first-line for pustular forms. Antibiotics are not indicated as pustules are sterile.

Increase the potency of topical corticosteroids:
While topical corticosteroids are often first-line for mild to moderate localized pustular psoriasis, this patient has not responded to 6 weeks of treatment with high-potency steroids. Increasing potency further is unlikely to be effective and could lead to side effects such as skin thinning, particularly in delicate areas like the feet.

Acitretin:
Acitretin is an oral retinoid and a systemic therapy that is commonly used for refractory forms of pustular psoriasis, including palmoplantar pustulosis. It helps regulate skin cell turnover and can reduce inflammation. Since the patient has not responded to topical therapy, systemic treatment with acitretin is an appropriate next step. It is particularly useful in pustular psoriasis because it targets both the inflammatory and hyperkeratotic aspects of the disease.

Oral antibiotics:
Palmoplantar pustulosis involves sterile pustules, meaning there is no bacterial infection to treat. Antibiotics are not appropriate in this case unless there is clear evidence of a secondary bacterial infection, which is not suggested in this scenario.

Topical calcineurin inhibitors:
These medications (such as tacrolimus or pimecrolimus) are used for inflammatory skin diseases like atopic dermatitis and sometimes for facial or intertriginous psoriasis, where skin is thinner. However, they are not effective for pustular psoriasis, especially in thickened skin areas like the soles of the feet. They are not considered a standard treatment for palmoplantar pustulosis.

Chronic exertional compartment syndrome (CECS) is a condition where increased pressure within a muscle compartment (usually in the lower extremities) during exercise leads to pain, swelling, and sometimes nerve dysfunction. It is typically seen in athletes or individuals who perform repetitive activities, such as runners, soccer players, and skiers.

Pathophysiology:

• Compartments in the leg (like the anterior, lateral, or deep posterior compartments) are enclosed by non-expanding fascia.
• During exercise, muscles swell as blood flow increases, but the fascia does not stretch enough to accommodate the increased volume.
• This leads to increased pressure within the compartment, which restricts blood flow, decreases oxygen delivery, and compresses nerves.
• As a result, pain, tightness, and sometimes tingling occur during activity.

Further Explanation:

• Pain onset with activity: The patient experiences pain that starts after 15-20 minutes of running and resolves with rest, which is classic for CECS.
• Location of pain: The pain is in the anterior compartment of the leg, a common location for CECS.
• Tense compartment on examination: After exercise, the compartment may feel firm or tight, though pulses and other signs of vascular compromise are usually normal.
• Rest provides relief: CECS pain typically subsides once activity stops, distinguishing it from acute conditions like stress fractures or shin splints.

Why not the other options?

• Tibial stress fracture: Typically presents with localized, focal tenderness and pain that persists even with rest, rather than resolving completely.
• Medial tibial stress syndrome (shin splints): Causes pain along the distal two-thirds of the tibia, not usually in the specific compartments. Pain is often continuous with activity and improves with rest but is not associated with a tense compartment after exercise.
• Achilles tendinopathy: Causes pain along the Achilles tendon and at the insertion on the calcaneus, not in the anterior compartment of the leg.

The patient’s acute kidney injury (AKI) is likely caused by acute tubular necrosis (ATN), which can be due to a combination of hypoperfusion and nephrotoxins, such as nonsteroidal anti-inflammatory drugs (NSAIDs). The first step in management is to discontinue the offending agent (ibuprofen) and provide intravenous fluids to restore perfusion and support kidney recovery.

Acute kidney injury (AKI) is a rapid decline in kidney function, characterized by an increase in serum creatinine, a reduction in urine output, or both. The causes of AKI are typically classified into three categories:

1. Prerenal (due to reduced kidney perfusion, like dehydration or hypotension),
2. Intrarenal (due to direct kidney damage, such as acute tubular necrosis), and
3. Postrenal (due to obstruction of urine flow, such as from a kidney stone or enlarged prostate).

Case Discussion:

• Patient History:
  • The patient is a 67-year-old man with a history of hypertension, diabetes, and coronary artery disease—conditions that make him susceptible to AKI.
  • He recently started taking ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), which is nephrotoxic and can impair kidney function.
  • He presents with decreased urine output and leg swelling, common symptoms of AKI.
• Lab Findings:
  • Elevated serum creatinine and BUN suggest impaired kidney filtration.

Pathophysiology:

• NSAID-induced AKI: NSAIDs block the production of prostaglandins, which normally dilate blood vessels in the kidneys to maintain perfusion, especially when blood flow is reduced (e.g., in conditions like dehydration, heart failure, or chronic kidney disease). Without prostaglandin-mediated vasodilation, NSAIDs can cause renal vasoconstriction, reducing blood flow to the kidneys and causing prerenal AKI. If prolonged, this can lead to acute tubular necrosis (ATN), which is an intrarenal cause of AKI, evidenced by the muddy brown casts on urinalysis.

Answer Explanations:

• Administer intravenous fluids and discontinue ibuprofen (Correct Answer):
  This option is correct because the patient’s AKI is likely due to a combination of decreased kidney perfusion (from either dehydration or reduced blood flow) and NSAID-induced nephrotoxicity.
• • The first step in treating prerenal or ATN-induced AKI is removing the offending agent (in this case, ibuprofen).
  • IV fluids help restore blood flow to the kidneys, potentially reversing prerenal causes of AKI and preventing further damage in ATN.
  • This is the most appropriate initial management strategy.
• Start diuretics to manage fluid overload:
  Although the patient has fluid overload (leg swelling), diuretics are not the first-line treatment in AKI unless there is severe fluid overload or pulmonary edema. Diuretics do not treat the underlying cause of AKI and may worsen kidney perfusion if used too early in this context.
• Initiate dialysis due to rising creatinine:
  Dialysis is a treatment for severe or refractory AKI when there are life-threatening complications, such as severe electrolyte imbalances, fluid overload unresponsive to diuretics, or uremic symptoms. This patient does not meet criteria for urgent dialysis yet, as initial conservative management (IV fluids and stopping nephrotoxins) has not been attempted.
• Begin corticosteroids to reduce kidney inflammation:
  Corticosteroids are used for certain inflammatory causes of AKI, like glomerulonephritis or interstitial nephritis, but they are not indicated for ATN or NSAID-induced kidney injury. There is no indication of an inflammatory process in this patient’s presentation.

In patients with systemic lupus erythematosus (SLE) undergoing surgery, several considerations are important to minimize the risk of complications, including managing their medications. Here’s n explanation of the key points relevant to the question:

1. Hydroxychloroquine:
   • Hydroxychloroquine is a disease-modifying antirheumatic drug (DMARD) commonly used in lupus. It helps control the activity of lupus but does not significantly impact infection risk. Therefore, continuing this medication through the perioperative period is generally safe. Stopping it might lead to lupus flare, which could complicate recovery.
2. Prednisone (Corticosteroids):
   • Patients with SLE often take long-term corticosteroids like prednisone to control inflammation and prevent lupus flares. Chronic use of steroids suppresses the hypothalamic-pituitary-adrenal (HPA) axis, which can impair the body’s ability to produce cortisol, particularly in stressful situations like surgery.
   • During surgery, the body requires higher levels of cortisol to handle the stress of the procedure. In patients on long-term steroids, there is a risk of adrenal insufficiency (an inability to mount an adequate cortisol response) if additional steroids are not given.
   • To prevent this, stress-dose steroids (higher doses of corticosteroids) are administered perioperatively. This compensates for the body’s reduced ability to produce cortisol and reduces the risk of adrenal crisis.

Explanation:
The patient’s presentation is consistent with pyoderma gangrenosum (PG), a neutrophilic dermatosis often associated with inflammatory conditions such as ulcerative colitis. PG typically begins as a small pustule or nodule and rapidly evolves into a painful ulcer with a necrotic base and violaceous, undermined borders. The hallmark of treatment is immunosuppression, typically with high-dose corticosteroids or other immunosuppressive agents like cyclosporine, infliximab or azathioprine.

Surgical debridement (A) is contraindicated in PG because it can lead to pathergy, worsening the ulcer. Topical antibiotics (C) would not address the underlying inflammatory nature of PG. Wide local excision (D) is inappropriate for this inflammatory condition.

Doxycycline is the first-line treatment for early-stage Lyme disease in most adult patients. Amoxicillin can be used for pregnant women or children under 8.

For early-stage Lyme disease, Borrelia burgdorferi infection is treated primarily with antibiotics. The treatment choice depends on factors like age, pregnancy status, and allergy history.

• Doxycycline is the first-line therapy for most adults. It is effective against Borrelia burgdorferi  Doxycycline is generally well-tolerated, but it is contraindicated in children under 8 years old and pregnant women due to the risk of tooth discoloration and bone development issues in children.
• Amoxicillin is a good alternative, particularly for children or pregnant women, because it is safe in these populations and still effective for treating Lyme disease.

Here’s a breakdown of the answer choices:

• Oral terbinafine for 4 weeks:
  Oral terbinafine is effective but typically reserved for severe, widespread, or resistant cases of tinea pedis. It is not the first-line therapy in a mild case confined to the interdigital location.
• Topical Nystatin for 2-4 weeks
  • Not effective for dermatophyte infections
• Topical Lotrisone for 2-4 weeks
  • The local immunosuppressive effects of topical corticosteroids can worsen dermatophyte infections and alter the clinical findings, making diagnosis more difficult (ie, tinea incognito).  The immunosuppressive effects can also worsen/deepen the infection leading toMajocchi's granuloma, which requires oral antifungal treatment.
• Topical Econazole for 2-4 weeks
  • Applied once per day for dermatophyte infections
  • The best answer choice listed 

For patients using an insulin pump, the basal rate should generally be reduced by 20-50% during surgery to prevent hypoglycemia, as the patient will not be eating. Close monitoring of blood glucose is critical during this time to avoid hypoglycemia.

Explanation:

Cefazolin (Ancef) is a first-generation cephalosporin that is highly effective against methicillin-susceptible Staphylococcus aureus (MSSA). It is often used as a first-line agent for MSSA infections, particularly in patients without allergies to beta-lactam antibiotics. The other options (vancomycin, clindamycin, and linezolid) are not first-line treatments for MSSA in patients who can tolerate beta-lactams. Vancomycin, in particular, is reserved for methicillin-resistant Staphylococcus aureus (MRSA) infections.

Explanation of the Options:

• Vancomycin
  Vancomycin is typically reserved for treating infections caused by methicillin-resistant Staphylococcus aureus (MRSA). In this case, the bacteria is methicillin-susceptible, so vancomycin is not necessary. Using it here would be unnecessary, and it can cause toxicity if not carefully monitored.
• Cefazolin (Ancef)
  Cefazolin is a first-generation cephalosporin that is highly effective against methicillin-susceptible Staphylococcus aureus (MSSA). It is commonly used for skin and soft tissue infections, as well as surgical prophylaxis. It has excellent coverage for MSSA and streptococci, making it the most appropriate choice for this patient with an MSSA infection.
• Clindamycin
  Clindamycin can be used for skin and soft tissue infections, especially in penicillin-allergic patients. However, it's generally not the first-line treatment for MSSA if beta-lactams can be used. There's also an increased risk of C. difficile infection with clindamycin.
• Linezolid
  Linezolid is an oxazolidinone antibiotic that is usually reserved for MRSA or vancomycin-resistant infections. It would not be appropriate here, as cefazolin is a more specific and effective choice for MSSA.

Acute gout is caused by the deposition of monosodium urate crystals in joints, often due to hyperuricemia. This can occur due to overproduction of uric acid or, more commonly, reduced renal excretion of uric acid. These crystals trigger an intense inflammatory response, leading to the characteristic symptoms of acute gout such as pain, swelling, and erythema. The needle-shaped, negatively birefringent crystals seen on microscopy are diagnostic of gout.

1. Hyperuricemia: The underlying cause of gout is an elevated level of uric acid in the blood (hyperuricemia). Uric acid is the end product of purine metabolism. While hyperuricemia can result from increased production of uric acid, the most common cause is impaired renal excretion. Other factors like high purine intake (meat, seafood), alcohol consumption, obesity, and certain medications (e.g., diuretics) can exacerbate hyperuricemia.
2. Crystal Formation: When uric acid levels exceed its solubility (> 6.8 mg/dL), monosodium urate crystals can form and deposit in the joints. These needle-shaped crystals are recognized by the immune system as foreign.
3. Inflammatory Response: The deposited urate crystals trigger a potent inflammatory response. Immune cells, particularly neutrophils, attempt to phagocytose the crystals, which results in the release of inflammatory cytokines and chemokines. This leads to the recruitment of more immune cells, further amplifying the inflammation.
4. Clinical Presentation: The acute inflammatory response causes the rapid onset of intense pain, swelling, redness, and warmth in the affected joint, which is characteristic of an acute gout attack. These attacks often occur at night, likely due to lower body temperatures favoring crystal formation.

Key Diagnostic Findings:

• Synovial fluid analysis: Needle-shaped, negatively birefringent monosodium urate crystals under polarized light microscopy.
• Serum uric acid levels: Elevated, though during an acute attack, levels may sometimes be normal.

See the cheat sheet on ASA Classification

The ASA II classification is for a patient with mild systemic disease that does not limit their daily activities. In this case, the patient has well-controlled hypertension, hyperlipidemia, and obesity. These conditions are considered mild systemic diseases that are well-managed and do not impair her functional capacity.

• Incorrect Answers:
  • A) is incorrect because ASA I is reserved for a healthy patient with no medical conditions. The patient has hypertension, hyperlipidemia, and obesity, which exclude her from being classified as ASA I.
  • C) is incorrect because ASA III is for patients with severe systemic disease that limits activity, such as uncontrolled hypertension or morbid obesity, neither of which applies to this patient.
  • D) is incorrect because ASA IV is for patients with a severe systemic disease that is a constant threat to life, which is not the case here.
  • E) is incorrect because ASA V is reserved for patients who are moribund and not expected to survive without the operation, which clearly does not apply to this patient.

ASA Classification Summary:

• ASA I: Healthy patient
• ASA II: Mild systemic disease (e.g., controlled hypertension, mild obesity)
• ASA III: Severe systemic disease limiting daily activity (e.g., poorly controlled diabetes)
• ASA IV: Severe systemic disease that is a constant threat to life
• ASA V: Moribund patient not expected to survive without the surgery

See the cheat sheet on SCIP protocol antibiotic selection

SCIP guidelines recommend an alternative antibiotic, such as vancomycin or clindamycin, for patients with a severe penicillin allergy. Vancomycin should be administered within 2 hours before incision due to its longer infusion time if chosen as the prophylactic antibiotic.

In CKD, the kidneys are unable to produce adequate amounts of calcitriol- 1,25-dihydroxycholecalciferol (the active form of vitamin D), which leads to reduced calcium absorption from the intestines. This hypocalcemia triggers secondary hyperparathyroidism, which increases bone resorption, contributing to renal osteodystrophy.

The D-zone test is important in detecting inducible clindamycin resistance. If a Staphylococcus aureus strain shows erythromycin resistance and clindamycin susceptibility, inducible clindamycin resistance may still occur, mediated by the erm gene. The D-zone test involves placing erythromycin and clindamycin discs close to each other. If erythromycin induces clindamycin resistance, the zone of inhibition around the clindamycin disc will be flattened, forming a "D" shape. This would indicate that clindamycin should not be used.

Ciprofloxacin can inhibit the renal tubular secretion of methotrexate, leading to increased levels and enhanced toxicity of methotrexate. Patients on both drugs should be monitored for signs of methotrexate toxicity, such as gastrointestinal symptoms, hematological effects, and liver enzyme abnormalities.

Explanation: The Cockcroft-Gault equation is used to estimate creatinine clearance (CrCl) based on serum creatinine, age, weight, and gender. The equation is:

(140-age) x weight (kg) / 72 x serum creatinine

For women, the result is multiplied by 0.85.

In this male patient:

The estimated creatinine clearance is approximately 42 mL/min. For a patient with this level of renal function, a reduction in the dose of a renally cleared antibiotic like vancomycin, along with an extension of the dosing interval, is necessary to prevent drug accumulation and toxicity.

See the cheat sheet on tetracyclines

Doxycycline is generally avoided in children under 8 because it can cause irreversible yellow, gray, or brown discoloration of teeth. This discoloration occurs due to the drug's deposition in developing dentin and enamel, where it binds to calcium.  The drug does not cause bone fragility by replacing calcium in the bone matrix nor lead to growth plate closure.

See Tetanus Prophylaxis Cheat Sheet

For patients with a clean or minor wound who have received a full series of tetanus vaccinations, a tetanus booster is recommended if the last dose was given more than 10 years ago. However, for more severe or contaminated wounds, a booster is recommended if the last dose was given more than 5 years ago. This patient has a puncture wound (considered more severe), and his last tetanus vaccine was 8 years ago, so a tetanus booster (Tdap or Td) is required. Tetanus immune globulin (TIG) is indicated only if the patient has an uncertain or incomplete vaccination history.

Tension pneumothorax is a life-threatening emergency that can occur during surgery, especially in patients with underlying lung conditions like COPD. It presents with acute respiratory distress, hypotension, hypoxemia, and decreased breath sounds on the affected side. The drop in end-tidal CO₂ is due to decreased cardiac output (decreased venous return to the heart). Immediate intervention, typically with needle decompression followed by chest tube insertion, is required to relieve the tension and stabilize the patient.

A few causes of tension pneumothorax include:

1. Barotrauma: Excessive positive pressure ventilation, particularly in patients with pre-existing lung conditions like chronic obstructive pulmonary disease (COPD) or those undergoing mechanical ventilation, can lead to the rupture of alveoli and the accumulation of air in the pleural space.
2. Pre-existing Lung Conditions: Patients with bullous lung disease, emphysema, or other forms of COPD are at higher risk because the weakened lung parenchyma is more susceptible to rupture during ventilation.
3. Central Venous Catheter Placement: Inadvertent puncture of the pleura during central venous catheter insertion, particularly when accessing the subclavian or internal jugular veins, can introduce air into the pleural space, leading to pneumothorax.
4. Surgical Procedures: Certain surgeries, such as laparoscopic procedures, can increase the risk of tension pneumothorax. For example, increased intra-abdominal pressure during insufflation can compress the lungs and lead to alveolar rupture.

See the cheat sheet on plate fixation techniques 

Key Concepts of Bridge Plating:

• Bridge Plate Technique: The plate spans the fracture site without directly compressing the bone fragments. Instead of achieving absolute stability (where the bone fragments are compressed for primary bone healing), the bridge plate allows for some micro-movement at the fracture site, promoting secondary bone healing through callus formation.
• Relative Stability: This is the main biomechanical principle in this technique. By spanning the fracture, the bridge plate stabilizes the bone segments, while still permitting small movements that encourage the formation of callus—a new bone that gradually remodels to heal the fracture.
• Indirect Bone Healing: Because the bone fragments are not compressed together, the healing occurs through the formation of a soft callus, which later hardens and remodels into mature bone. This process is known as secondary or indirect bone healing.

Gadolinium is contraindicated in patients with an eGFR below 30 mL/min due to the risk of nephrogenic systemic fibrosis (NSF).

Gadolinium is not known to cause pulmonary edema, and this is not a reason to avoid its use in patients with low GFR.

While allergic reactions can occur, gadolinium is less likely to cause allergic reactions compared to iodinated contrast agents, so this is not a primary concern.

Hypertension is a concern, but not the main reason to avoid Gadolinium in a patient with a GFR < 30 ml/min.

Piperacillin-tazobactam is primarily excreted by the kidneys and requires dose adjustment in patients with reduced renal function to avoid toxicity and maintain therapeutic effectiveness. In contrast, clindamycin and linezolid are metabolized by the liver and do not require dose adjustments in renal impairment. Doxycycline also does not require significant renal dosing adjustments. Piperacillin-tazobactam, commonly used in severe diabetic foot infections, must be dosed carefully in CKD.

Pathophysiology of Skin Manifestations in CKD:

1. Uremic Toxins Accumulation:
   • In CKD, the kidneys lose their ability to effectively filter and excrete waste products and toxins. As a result, uremic toxins accumulate in the bloodstream. These toxins can cause systemic inflammation, leading to various skin manifestations, such as pruritus (itchiness) and xerosis (dry skin).
2. Pruritus (Itchiness):
   • The exact cause of pruritus in CKD is multifactorial but is believed to be associated with uremic toxins, systemic inflammation, and secondary hyperparathyroidism. This intense itching is often generalized but can be more pronounced on the back, chest, and limbs. It can lead to scratching and subsequent excoriations or lichenification of the skin.
3. Hyperpigmentation:
   • Hyperpigmentation in CKD is thought to occur due to increased melanin production, which may be triggered by chronic inflammation and the accumulation of uremic toxins. Additionally, the deposition of hemosiderin and other pigments in the skin can contribute to the darkening of the skin.
4. Xerosis (Dry Skin):
   • Xerosis is common in CKD and results from reduced sweat and sebaceous gland activity, leading to a decrease in natural skin moisture. The skin becomes dry, scaly, and prone to cracking, which exacerbates pruritus.
5. Uremic Frost:
   • In advanced CKD, uremic frost can occur, where urea crystals are deposited on the skin surface, especially when sweat evaporates. This is a sign of severe uremia and is more common in patients not receiving dialysis.

These findings are classic for ichthyosis vulgaris, a common inherited disorder of keratinization that results in dry, scaly skin. The condition typically presents in early childhood, with scaling that primarily affects the extensor surfaces (e.g., arms, legs) and spares the flexural areas and face. The skin becomes drier and scalier in cold weather, making symptoms more noticeable in the winter. Palmar hyperlinearity (increased skin markings on the palms) is a characteristic feature.

Why Stress Fracture is the Correct Answer:

Stress fractures occur due to repetitive stress, common in athletes like long-distance runners. The second metatarsal is especially vulnerable due to the increased load it bears during activities such as running. Patients often present with insidious pain that worsens with activity. Initial X-rays are often negative, which may lead to delays in diagnosis. Advanced imaging, like MRI or bone scans, might be needed for confirmation.

Key Takeaways:

• Presentation: Gradual onset of activity-related pain with localized tenderness.
• Common Sites: Second and third metatarsals - especially in runners.
• Imaging: X-rays may be negative early; MRI or bone scans are more sensitive.

Stress fractures require early recognition to prevent worsening and complications, such as complete fractures or chronic pain. Treatment usually involves rest and activity modification.

Explanation:
The Parkland formula is used to calculate fluid requirements in burn patients. It is:

Total fluid (mL)=4×body weight (kg)×%TBSA burned

For this patient:

• Weight:  75 kg.
• TBSA burned: 40%

Applying the formula:

$=12,000\text{mL}$

This total is given over the first 24 hours, with half administered in the first 8 hours and the remainder over the next 16 hours.

The patient's presentation of palpable purpura, recent history of taking amoxicillin, and biopsy findings of leukocytoclastic vasculitis suggest a diagnosis of drug-induced vasculitis. This form of vasculitis often occurs secondary to medication use, with common ones including antibiotics like penicillins. The absence of systemic symptoms, normal laboratory findings, and recent medication history support this diagnosis.

Key Points:

1. Palpable Purpura: This is a hallmark sign of small-vessel vasculitis, which includes conditions like drug-induced vasculitis, Henoch-Schönlein purpura (IgA vasculitis), and cryoglobulinemic vasculitis.
2. Leukocytoclastic Vasculitis: The biopsy findings of leukocytoclastic vasculitis indicate inflammation and necrosis of small blood vessels, often seen in drug-induced vasculitis, Henoch-Schönlein purpura, and other small-vessel vasculitides.
3. Recent Medication Use: The fact that the patient is taking amoxicillin is important. Antibiotics are a common cause of drug-induced vasculitis, which usually presents with palpable purpura and a biopsy showing leukocytoclastic vasculitis.
4. Lack of Systemic Involvement: The absence of systemic symptoms (like fever, joint pain, or kidney involvement) and the normal laboratory tests make it less likely that this is a systemic vasculitis such as microscopic polyangiitis or cryoglobulinemia.

Diagnosis Explanation:

• B. Drug-induced vasculitis is the correct answer because the patient’s clinical history (recent antibiotic use) and biopsy findings strongly suggest that the vasculitis is secondary to her medication.

Choosing an implant with a modulus of elasticity similar to bone reduces the risk of stress shielding. This allows for a more natural distribution of stress, encouraging bone remodeling and maintaining bone density around the implant.

Stress shielding is a phenomenon that occurs when a rigid implant, such as a metal plate, nail, or prosthesis, takes on too much of the load that the bone would normally bear. This reduction in mechanical load on the bone can lead to bone resorption, delay in hearing, and weakening of the bone over time.

Mechanism:

• Bone remodels in response to the loads it experiences, a principle known as Wolff's law. When an implant is too stiff or absorbs too much of the load, the surrounding bone experiences less stress.
• This reduced stress leads to decreased bone density because the bone is no longer stimulated to maintain or increase its strength, which can result in bone atrophy or osteopenia around the implant.

Clinical Implications:

• In surgery, stress shielding is a concern because it can compromise the long-term success of implants, leading to loosening, fractures, or even failure of the implant.

The STOP-Bang questionnaire is a validated screening tool for obstructive sleep apnea. It assesses the following criteria:

• Snoring
• Tiredness
• Observed apnea
• Pressure (Hypertension)
• BMI > 35 kg/m²
• Age > 50 years
• Neck circumference > 16 inches (for women) or > 17 inches (for men)
• Gender (male)

These factors help determine the patient's risk for sleep apnea.

Reperfusion syndrome can occur when a tourniquet is deflated after prolonged use, leading to the release of accumulated metabolic byproducts from ischemic tissues back into circulation. This can cause metabolic acidosis, hyperkalemia, hypotension, and respiratory distress, as seen in this patient. Pulmonary embolism and fat embolism are possible differentials but do not typically cause hyperkalemia. Malignant hyperthermia and acute is less likely in this context.

See the NEW cheat sheet on the Pirani Classification of Clubfoot

The Pirani score evaluates six clinical signs of clubfoot, divided into midfoot and hindfoot parameters. It includes assessments such as:

1. Medial foot create
2. The curvature of the lateral border
3. Position of the talus head
4. Posterior crease
5. Rigidity of equinus
6. Empty heel

Local anesthetics, like lidocaine, work by blocking sodium channels in nerve cells, preventing depolarization and thus inhibiting the transmission of pain signals. In inflamed or infected tissues, the local environment is more acidic, reducing the effectiveness of the anesthetic. The acidic pH increases the ionization of the anesthetic, which limits its ability to penetrate nerve membranes and exert its effect.

• Option B is incorrect because epinephrine causes vasoconstriction, not vasodilation, which helps to prolong the effect of the anesthetic and reduce systemic absorption, thereby decreasing the risk of toxicity.
• Option C is incorrect because lidocaine is not contraindicated in asthma; however, caution is advised in patients with cardiac conditions.
• Option D is incorrect because local anesthetics block sodium channels, not calcium channels.

See the cheat sheet on contraindications to NSAIDS

This patient is at high risk for complications from NSAID use due to a history of coronary artery bypass grafting (CABG) and current dual antiplatelet therapy. NSAIDs are known to increase the risk of cardiovascular events, particularly in patients with a history of heart disease, and can interfere with the effectiveness of antiplatelet therapy. Additionally, NSAIDs can exacerbate the risk of gastrointestinal bleeding, especially in patients on antiplatelet therapy.

Dynamization refers to controlled micromovement at the fracture site. This controlled movement can stimulate callus formation and promote secondary bone healing. Increasing the rigidity or reducing movement would inhibit this process while enhancing blood supply is not directly related to the concept of dynamization.

Examples of dynamization:

• Intramedullary Nails: Nails can be designed to allow for gradual loading of the fracture site by removing interlocking screws or by using nails with telescoping capabilities. This creates controlled micromovement, encouraging callus formation.
• External Fixators: In some cases, external fixators can be loosened or adjusted during the healing process to permit slight motion at the fracture site. This dynamization helps transition from rigid to more flexible fixation, promoting healing.

The clinical presentation and radiographic findings are characteristic of an osteoid osteoma. This benign bone tumor commonly causes nocturnal pain that is relieved by NSAIDs. The typical radiographic appearance is a small, well-demarcated, radiolucent nidus (<1.0 to 1.5 cm) surrounded by reactive bone sclerosis.  Osteoid osteomas are benign bone-forming tumors. The nidus produces high levels of prostaglandins which is why they tend to respond to NSAIDs to manage their symptoms.

Vitamin A has been shown to counteract the inhibitory effects of steroids on wound healing. The correct approach is to administer a moderate dose of Vitamin A (25,000 IU) orally for a short duration (3 days) prior to surgery.

For an unconscious patient with severe hypoglycemia, the immediate treatment is intramuscular or subcutaneous glucagon to rapidly raise blood glucose levels. Oral treatments like juice or glucose gel are not suitable as the patient is unconscious and at risk for aspiration.  The patient is at home without IV access, therefore D50W would not be the best option in this scenario.

Conscious Patient:

• Treatment: The patient should be given 15-20 grams of fast-acting carbohydrates, such as glucose tablets, fruit juice, or regular soda. After ingestion, blood glucose should be rechecked in 15 minutes, and additional carbohydrates should be provided if levels remain low.

Unconscious or Unresponsive Patient:

• Key Concern: Aspiration risk if trying to give oral glucose or food.
• Treatment:
  • Intramuscular Glucagon: The first-line treatment for an unconscious patient. Glucagon stimulates the liver to convert stored glycogen into glucose, raising blood sugar levels. It can be administered by caregivers or medical personnel, and it’s particularly useful in settings where intravenous (IV) access is not readily available.
  • Alternative: If in a hospital setting, and if IV access is available, an intravenous bolus of 25-50 mL of 50% dextrose can be given, which works rapidly.

Statins, such as atorvastatin, are the first-line treatment for lowering LDL cholesterol in patients with cardiovascular risk factors, such as hypertension and diabetes. They work by inhibiting HMG-CoA reductase, leading to a reduction in cholesterol synthesis and an increase in LDL receptor activity. This effectively lowers LDL cholesterol levels and reduces the risk of cardiovascular events.

Wrong answer choices:

Niacin:
Niacin (nicotinic acid) is a lipid-lowering agent that can raise HDL cholesterol and lower triglycerides. It can also modestly reduce LDL cholesterol. However, it is not considered first-line therapy due to its side effect profile, which includes flushing, gastrointestinal discomfort, and potential worsening of glucose control. It is usually reserved for specific cases, such as patients with very high triglycerides or those who cannot tolerate statins.

Ezetimibe:
Ezetimibe inhibits the absorption of cholesterol in the small intestine, leading to a modest reduction in LDL cholesterol. It is often used in combination with statins in patients who do not achieve their LDL target with statin therapy alone. However, it is not recommended as initial monotherapy for lowering LDL cholesterol, particularly in patients with high cardiovascular risk like the one in this case.

Gemfibrozil:
Gemfibrozil is a fibrate, a class of medications that primarily lowers triglycerides and can modestly raise HDL cholesterol. Fibrates are not effective at lowering LDL cholesterol and are therefore not appropriate as initial therapy for a patient with elevated LDL. They are generally reserved for patients with hypertriglyceridemia or in combination with other agents when triglyceride levels are extremely high.

Explanation

• Increasing protein intake is not recommended in CKD, as it can accelerate kidney damage.
• Sodium restriction helps control blood pressure and fluid balance, which is crucial in CKD management.
• High potassium foods are generally avoided in CKD due to the risk of hyperkalemia.
• Fluid intake might need to be limited in more advanced CKD, but this is not typically necessary in stage 3.

The earliest event in the pathogenesis of atherosclerosis is endothelial cell injury. This injury can be caused by factors such as hypertension, hyperlipidemia, smoking, and diabetes. Following endothelial injury, there is increased permeability to lipoproteins, adhesion of leukocytes, and migration of inflammatory cells into the vessel wall. Foam cell formation, fatty streak, smooth muscle cell migration, and the development of a fibrous cap occur later in the process. Plaque rupture is a late event that can lead to acute cardiovascular events such as myocardial infarction or stroke.

Granuloma annulare is a chronic skin condition characterized by the appearance of small, firm, flesh-colored or erythematous papules that typically form a ring or annular pattern. These lesions are often asymptomatic, meaning they don't cause itching or pain, and they tend to develop gradually over time. Granuloma annulare is commonly seen on the dorsal surfaces of the hands and feet, as described in the question.

Why the other options are less likely:

• Erythema multiforme: This condition usually presents with target lesions, which are red, circular patches with a central blister or darker area, often associated with infections or drug reactions. It typically affects the palms, soles, face and mucous membranes, which does not match the presentation in the question.
• Lichen planus: Lichen planus is characterized by purple, polygonal, pruritic (itchy), flat-topped papules that may appear on the wrists, legs, and mucous membranes. The presentation of annular lesions on the feet does not fit lichen planus.
• Erythema chronicum migrans (ECM) is the characteristic skin lesion associated with the early stage of Lyme disease, caused by the bacterium Borrelia burgdorferi. It typically appears as an expanding red rash at the site of a tick bite, often with a central clearing, giving it a "bull's-eye" appearance.

Explanation:

• Unfractionated heparin is often used for DVT prophylaxis in patients with renal impairment, as its effects are more easily monitored and reversed compared to other anticoagulants.
• Fondaparinux is contraindicated in patients with severe renal impairment (creatinine clearance <30 mL/min).
• Direct oral anticoagulants (DOACs) are not typically used in patients with significant renal dysfunction due to the risk of accumulation and bleeding.
• Graduated compression stockings can be used as an adjunct but are not sufficient as sole prophylaxis in high-risk patients.

Dyshidrotic eczema is characterized by the appearance of small, deep-seated vesicles on the palms, sides of the fingers, and occasionally the soles of the feet and toes. These vesicles are often pruritic and can lead to scaling and fissuring. Unlike contact dermatitis, dyshidrotic eczema is not directly related to an external allergen or irritant. It can sometimes be exacerbated by stress, heat, or moisture. Tinea manuum typically presents with different characteristics.

This question emphasizes the standard initial management approach for GERD, particularly in the presence of erosive esophagitis. PPIs are recommended as the first-line therapy due to their effectiveness in reducing gastric acid secretion and healing erosive esophagitis. Lifestyle modifications are also essential, including dietary changes, weight loss, and avoiding factors that can exacerbate symptoms.

1. Lifestyle Modifications: These are often the first step in managing GERD symptoms. They include dietary changes (avoiding foods that trigger symptoms, such as spicy foods, chocolate, and caffeine), eating smaller meals, not lying down immediately after eating, losing weight if overweight, quitting smoking, and elevating the head of the bed. These changes can help reduce the frequency and severity of reflux.
2. Proton Pump Inhibitors (PPIs): PPIs are the most effective medication for reducing stomach acid production and are considered the first-line treatment for GERD, especially in cases with erosive esophagitis. PPIs help heal the esophagus, reduce symptoms, and prevent complications. They are typically more effective than H2 receptor antagonists in this regard.

Other Options Explained:

• H2 receptor antagonists and a high-fiber diet: While H2 receptor antagonists can reduce stomach acid and are useful for mild cases, they are generally less effective than PPIs for treating erosive esophagitis. A high-fiber diet is beneficial for overall digestive health but is not a primary treatment for GERD.
• Prokinetic agents and dietary changes: Prokinetic agents, which help increase the motility of the gastrointestinal tract, can be used in specific situations, particularly when there is evidence of delayed gastric emptying. However, they are not first-line treatments due to limited efficacy and potential side effects. Dietary changes alone are often insufficient without acid suppression.
• Antacids and weight loss counseling: Antacids can provide quick relief for mild, infrequent symptoms but are not suitable for long-term management of erosive esophagitis - also this patient has not responded to OTC antacids. While weight loss can significantly improve symptoms in overweight individuals, it should be part of a comprehensive treatment plan that includes acid suppression.

Unfractionated heparin does not require dose adjustments with kidney disease and because IV unfractionated heparin has a short half-life (3-5 hours) and a known reversal agent (protamine sulfate), it is the preferred anticoagulant when an anticoagulant may need to be discontinued or reversed.

Seborrheic dermatitis is a common inflammatory skin condition characterized by red, scaly, and greasy patches. It commonly affects areas rich in sebaceous (oil) glands, such as the scalp, face, and upper trunk. While the exact cause of seborrheic dermatitis is not fully understood, it is believed to be associated with the overgrowth of a specific yeast found on the skin.

Answer Explanation:

• Malassezia species: This is the correct answer. Malassezia is a genus of yeast that is normally found on the skin. It is thought to play a significant role in the development of seborrheic dermatitis, possibly due to its interaction with skin lipids, leading to inflammation and characteristic symptoms.
• Pityriasis rosea: Pityriasis rosea is a common skin condition characterized by a distinctive, often itchy rash that typically starts with a single, large "herald" patch followed by smaller lesions.
• Candida albicans: This is a yeast that can cause infections such as thrush, but it is not typically implicated in seborrheic dermatitis.
• Trichophyton rubrum: This is a dermatophyte fungus responsible for conditions like tinea pedis, not seborrheic dermatitis.

Therefore, the most likely organism associated with seborrheic dermatitis is Malassezia species.

Methotrexate is considered the first-line disease-modifying antirheumatic drug (DMARD) for the treatment of rheumatoid arthritis due to its efficacy in controlling disease activity and preventing joint damage. NSAIDs may be used for symptom relief, but they do not alter the course of the disease. Prednisone can be used as a short-term measure to control inflammation but is not recommended as monotherapy. Hydroxychloroquine and sulfasalazine can be considered as part of a combination therapy but are generally not as effective as methotrexate when used alone in moderate to severe RA.

Contraindications to using Methotrexate include the following:

Methotrexate is contraindicated in the following scenarios:

1. Women who are contemplating becoming pregnant
2. Pregnancy
3. Patients with liver disease or excessive alcohol use
4. Patients with severe kidney disease [eGFR] less than 30 mL/min

• Metformin: Typically stopped 24-48 hours before surgery due to the risk of lactic acidosis, especially with procedures involving contrast dye.
• Sulfonylureas (e.g., glipizide, glyburide): Usually held on the day of surgery due to the risk of hypoglycemia.
• SGLT2 inhibitors (e.g., canagliflozin, empagliflozin): Often stopped 3 days before surgery due to the risk of ketoacidosis.
• GLP-1 inhibitors - typically held 7 days before surgery due to delayed gastric emptying effect

Gram-negative infections caused by bacteria producing Extended-Spectrum Beta-Lactamase (ESBL) enzymes are challenging to treat because ESBLs confer resistance to many beta-lactam antibiotics, including penicillins and cephalosporins.

Explanation:

Amoxicillin-clavulanate: This combination includes a beta-lactamase inhibitor (clavulanate) to counteract beta-lactamase enzymes, but ESBL-producing bacteria can still resist this treatment.

Meropenem: Carbapenems, such as meropenem, are considered the drugs of choice for treating infections caused by ESBL-producing bacteria. Carbapenems are resistant to hydrolysis by ESBL enzymes and are highly effective against these resistant organisms.

Vancomycin: Only covers Gram + organisms.

Ceftriaxone: While it is a third-generation cephalosporin, ESBL-producing bacteria are resistant to most cephalosporins, including ceftriaxone.

Therefore, Meropenem is the preferred treatment option for infections caused by gram-negative bacteria with ESBL enzymes due to its broad spectrum of activity and resistance to ESBL-mediated hydrolysis.

• Secukinumab (Cosentyx)
  • Mechanism: Secukinumab is a monoclonal antibody that binds directly to IL-17A, inhibiting its interaction with its receptor and preventing its inflammatory effects.
  • Indication: Used for moderate to severe psoriasis, including both plaque psoriasis and psoriatic arthritis.
• Ixekizumab (Taltz)
  • Mechanism: Ixekizumab is a monoclonal antibody that targets IL-17A, blocking its ability to bind to the IL-17 receptor and thereby reducing inflammation.
  • Indication: Approved for moderate to severe plaque psoriasis and psoriatic arthritis.
• Dupixent (dupilumab) is a biologic medication used for the treatment of various inflammatory conditions, including psoriasis. Dupixent targets and inhibits Interleukin-4 (IL-4) and Interleukin-13 (IL-13), both of which are key cytokines involved in the inflammatory process of various diseases. 
• Skyrizi (risankizumab) is a biologic medication used primarily for the treatment of psoriasis. Skyrizi targets Interleukin-23 (IL-23), a cytokine that plays a crucial role in the inflammatory process of psoriasis. By blocking IL-23, it prevents the activation of Th17 cells and the subsequent release of IL-17, which is involved in driving the inflammation and pathology of psoriasis.

The diagnosis of prediabetes is based on specific criteria defined by health organizations such as the American Diabetes Association (ADA). Prediabetes is a condition where blood sugar levels are higher than normal but not high enough to be classified as diabetes. It serves as an early warning sign that a person is at increased risk of developing type 2 diabetes, heart disease, and stroke.

Diagnostic Criteria for Prediabetes:

• Fasting Plasma Glucose (FPG): 100-125 mg/dL
• Hemoglobin A1c: 5.7-6.4%
• 2-hour Plasma Glucose during Oral Glucose Tolerance Test (OGTT): 140-199 mg/dL

Incorrect Options Explained:

Normal glycemic range:

• This is not correct because the patient’s FPG and A1c levels are higher than normal.

Type 2 diabetes:

• Type 2 diabetes is diagnosed when FPG is ≥126 mg/dL or A1c is ≥6.5%. The patient's levels are below these thresholds.

Latent Autoimmune Diabetes In Adults (LADA) - type 1.5 diabetes is a form of diabetes that begins in adults and slowly progresses over time. Similar to type 1 diabetes, LADA occurs when the pancreas stops making insulin due to an autoimmune process damaging cells in the pancreas.

Explanation:

Administer a single dose of long-acting insulin daily

This approach may not adequately control blood glucose levels throughout the day, as it does not address postprandial (after meals) hyperglycemia. Long-acting insulin alone may lead to periods of hypoglycemia or hyperglycemia.

Use a sliding scale insulin regimen with regular insulin - without basal insulin

Sliding scale insulin alone is not recommended because it only reacts to high blood glucose levels after they occur, leading to more significant glucose variability and increased risk of both hyperglycemia and hypoglycemia. It does not provide the steady background insulin needed to maintain baseline glucose control through a long acting insulin.

Initiate a basal-bolus insulin regimen with adjustments based on blood glucose monitoring

This is the recommended approach. A basal-bolus regimen involves a combination of long-acting insulin (basal) to maintain steady blood glucose levels throughout the day and night and short-acting or rapid-acting insulin (bolus) to manage blood glucose spikes related to meals. Adjustments based on frequent blood glucose monitoring allow for individualized and responsive control of blood glucose levels, minimizing the risk of hyperglycemia and hypoglycemia.

Utilize oral antidiabetic medications

Oral antidiabetic medications may not be sufficient in the inpatient setting, especially for patients with significant hyperglycemia, stress-induced hyperglycemia, or those unable to take medications orally due to their medical condition. Inpatient management often requires more immediate and precise control of blood glucose, which insulin can provide.

The most appropriate treatment for erythrasma, which is caused by Corynebacterium minutissimum, includes topical or oral antibiotics. Topical treatments such as clindamycin can be effective, but oral erythromycin is often used for more extensive or resistant cases. The characteristic coral-red fluorescence under a Wood's lamp is a key diagnostic feature. Topical antifungals like clotrimazole and oral antifungals like terbinafine are not effective against this bacterial infection.

See the cheat sheet on renal dosing guidelines 

Here is a list of antibiotics that are the safest in patients with kidney disease:

Link to new cheat sheet!

1. Ceftriaxone
   • Primarily excreted via the biliary system.
   • Does not require dose adjustment in renal impairment.
2. Clindamycin
   • Primarily metabolized by the liver.
   • Minimal renal excretion.
3. Doxycycline
   • Mostly excreted via feces.
   • Minimal renal excretion.
4. Erythromycin
   • Primarily metabolized by the liver.
   • Minimal renal excretion.
5. Azithromycin
   • Metabolized and excreted primarily through the liver.
   • Minimal renal excretion.
6. Metronidazole
   • Metabolized by the liver.
   • Minimal renal excretion.
7. Linezolid
   • Metabolized and excreted primarily through the liver.
   • Minimal renal excretion.

These antibiotics are generally safer options for patients with renal impairment

A positive Buerger's test, characterized by pallor of the foot when elevated and rubor (redness) when the foot is lowered and dependent, indicates poor arterial blood flow. This test is specifically used to assess for peripheral artery disease (PAD), where arterial insufficiency leads to reduced perfusion of the extremities. Prolonged pallor with the leg elevated > 45 degrees for 1 minute is indicative of arterial disease.

Untreated pneumothorax is an absolute contraindication to HBO therapy due to the risk of expansion and further complications under hyperbaric conditions. Upper respiratory infection, history of seizure disorder, and asthma are relative contraindications that may require careful consideration and management but do not absolutely preclude the use of HBO therapy.

A pneumothorax occurs when air leaks into the space between the lung and chest wall, causing the lung to collapse. Under hyperbaric conditions, the increased pressure can cause the trapped air in the pleural space to expand, worsening the pneumothorax and potentially leading to a life-threatening situation. Therefore, HBO therapy is absolutely contraindicated until the pneumothorax is treated.

Asthma can complicate HBO therapy, especially if the patient experiences an acute asthma attack during treatment. However, with proper management and precautions, such as ensuring the patient’s asthma is well-controlled before starting therapy, asthma is not an absolute contraindication.

Explanation:

• Type I: Wound less than 1 cm, minimal soft tissue damage, and minimal contamination. No periosteal stripping. Adequate soft tissue coverage and no vascular injury requiring repair. Managed with cefazolin.
• Type II: Wound 1-10 cm with moderate soft tissue damage and moderate contamination. Managed with cefazolin.  Adequate soft tissue coverage and no vascular injury requiring repair.
• Type IIIA: Wound larger than 10 cm, extensive soft tissue damage, and adequate soft tissue coverage. No vascular injury requiring repair.  Farm injuries are automatically at least a Gustilo-Anderson IIIA.  Managed with cefazolin, gentamicin, and penicillin (if farm injury).
• Type IIIB - Wound larger than 10 cm, extensive soft tissue damage, and periosteal stripping. Requires soft tissue coverage (flap). Managed with cefazolin, gentamicin, and penicillin (if farm injury).
• Type IIIC: Open fractures with arterial injury requiring repair, regardless of wound size and contamination. Managed with cefazolin, gentamicin, and penicillin (if farm injury)

Given the wound size (4 cm) and moderate soft tissue damage without significant contamination, the appropriate classification is Type II, and the recommended initial antibiotic regimen is cefazolin.

Antibiotics are initiated as soon as possible and continued for at least 24-72 hours.

There are newer antibiotics that have widely replaced the use of aminoglycosides, but aminoglycosides are included in the original Gustilo-Anderson open fracture guidelines.

Hyperkalemia: Hyperkalemia is not commonly associated with tetracycline use.

Tendon rupture: This adverse effect is more commonly associated with fluoroquinolone antibiotics (e.g., ciprofloxacin), not tetracyclines.

Tooth discoloration: Tetracyclines are known to cause tooth discoloration, especially when used during tooth development in children (up to the age of 8) and in the developing fetus if taken by pregnant women. The discoloration can be yellow, brown, or gray.

Nephrotoxicity: Although tetracyclines can affect renal function, especially in patients with pre-existing kidney conditions, nephrotoxicity is not the most common adverse effect.

See the cheat sheet for tetanus prophylaxis guidelines 

Explanation:

• Abdominal Pain and Chronic Diarrhea: Both are common symptoms of IBD, which includes Crohn's disease and ulcerative colitis. The lower right quadrant pain is particularly suggestive of Crohn's disease because it often affects the terminal ileum.
• Weight Loss, Fever, and Fatigue: These systemic symptoms are indicative of an inflammatory process, consistent with IBD.
• Elevated Inflammatory Markers and Anemia: Elevated CRP and ESR are signs of inflammation. Anemia can result from chronic inflammation, malabsorption, or gastrointestinal bleeding, all of which are common in Crohn's disease.
• Colonoscopy Findings: The key findings are:
  • Transmural Inflammation: This means inflammation affects the entire thickness of the bowel wall, which is characteristic of Crohn's disease.
  • Skip Lesions: Areas of inflamed tissue interspersed with normal tissue, another hallmark of Crohn's disease.
  • Cobblestoning: The appearance of the mucosa due to deep ulcers and edematous mucosa, typical of Crohn's disease.

Differentiation from Other Conditions:

• Ulcerative Colitis: Typically causes continuous inflammation of the colon and rectum and is limited to the mucosal layer. It does not show transmural inflammation or skip lesions.
• Irritable Bowel Syndrome (IBS): Does not cause inflammation, elevated inflammatory markers, anemia, or the specific colonoscopy findings described.
• Celiac Disease: While it can cause chronic diarrhea and weight loss, it is characterized by villous atrophy in the small intestine, not the described colonoscopy findings.

Thus, the combination of clinical presentation, laboratory results, and colonoscopy findings strongly suggests Crohn's disease.

Raynaud's disease is characterized by episodic vasospasm of the small arteries, usually in the fingers and toes, leading to color changes in the skin. These episodes typically follow a specific sequence: the affected areas first turn white (due to lack of blood flow), then blue (due to prolonged lack of oxygen), and finally red (when blood flow returns).

Explanation of the Answer Choices:

A) Calcium channel blockers: This is the correct answer. Calcium channel blockers, such as nifedipine, are commonly used as the first-line pharmacological treatment for Raynaud's disease. They help to dilate the small blood vessels and reduce the frequency and severity of the vasospastic episodes.

B) Aspirin: While aspirin is used for its antiplatelet effects and can be beneficial in certain vascular conditions, it is not the first-line treatment for Raynaud's disease. Aspirin does not specifically address the vasospasm of small arteries characteristic of Raynaud's.

C) Beta-blockers: These medications are generally contraindicated in Raynaud's disease because they can exacerbate symptoms by promoting vasoconstriction.

D) Antidepressants: Although some antidepressants, particularly those with serotonergic activity, might have a role in managing stress-related triggers, they are not the primary treatment for the vasospasm seen in Raynaud's disease.

Tinea incognito occurs when a fungal infection is masked or altered by the use of topical corticosteroids or immunosuppressive agents, leading to atypical presentations that can mimic other dermatological conditions, such as eczema.  The local immunosuppressive effects of topical steroids can worsen the dermatophyte infections and change the clinical findings. Further, topical corticosteroid use may cause extension of the fungal infection into the hair follicle and dermis, resulting in Majocchi's granuloma - requiring an oral antifungal to treat.

A) 0.45% sodium chloride (half-normal saline): This is a hypotonic solution that contains lower sodium concentration than normal saline (0.9% sodium chloride). It is used in the treatment of mild to moderate hypernatremia.

B) 5% dextrose in water (D5W): This is a hypotonic solution that provides free water once the glucose is metabolized, but it does not contain significant electrolytes. It is generally not used to treat hyponatremia because it can exacerbate the condition by diluting sodium levels.

C) 3% sodium chloride (hypertonic saline): This is a hypertonic solution with a high concentration of sodium chloride. It is the preferred choice for treating severe hyponatremia, especially in acute symptomatic cases where there is a risk of cerebral edema and neurological complications. It helps to rapidly increase serum sodium levels and corrects the imbalance.

D) Lactated Ringer's solution: This is an isotonic solution that contains sodium, potassium, calcium, chloride, and lactate. While it is useful for fluid resuscitation and electrolyte replacement, it is not typically used as the first-line treatment for severe hyponatremia.

The correct answer is C) 3% sodium chloride (hypertonic saline), which is specifically used to treat severe hyponatremia due to its ability to rapidly increase serum sodium levels and correct the imbalance.

Explanations:

Conscious sedation does not lead to complete loss of consciousness. Instead, it keeps the patient awake but relaxed and able to respond to verbal commands. MAC, on the other hand, can vary in the depth of sedation, sometimes keeping the patient awake and responsive, and at other times leading to deeper sedation where the patient might not respond.

MAC requires the oversight of an anesthesiologist or a certified registered nurse anesthetist (CRNA), due to the potential for deeper sedation and the need for continuous monitoring. Conscious sedation, however, can be administered by a wider range of healthcare providers, including dentists, nurses, and physicians, especially in settings where less intensive sedation is appropriate.

During conscious sedation without an anesthesiologist or CRNA, the depth of sedation should not make the patient unable to independently maintain their airway. However, during MAC, an anesthesiologist or CRNA must be prepared and qualified to convert to general anesthesia with management of the patient's airway if needed.

Both conscious sedation and MAC can be used for procedures of varying lengths and complexities. The choice between them depends more on the specific needs of the patient and the type of procedure rather than the duration or complexity alone.

Both conscious sedation and MAC can involve intravenous medications. Conscious sedation might also use oral medications, but MAC is not limited to intravenous methods and can include various routes of administration depending on the situation.

Conscious sedation is designed to keep patients in a state where they are relaxed but can still respond to verbal commands. MAC, however, can range from minimal to deep sedation, where the depth of sedation can vary from a state of slight drowsiness to a level where the patient is less responsive or even unresponsive to verbal commands.

The relative contraindication to the use of an LMA in this patient is Obesity. Obesity increases the risk of difficult airway management, challenging ventilation, and potential aspiration due to increased intra-abdominal pressure. Therefore, while not an absolute contraindication, obesity makes the use of an LMA less ideal compared to endotracheal intubation in ensuring a secure airway.

Diagnosis - lymphedema tarda (lymphedema manifesting later in life - after 35 years of age)

The patient's presentation of unilateral, non-pitting, firm edema is most characteristic of lymphedema. Lymphoscintigraphy, while not often required to confirm the presence of lymphedema), is a diagnostic test to evaluate lymphatic system function and confirm the diagnosis. Other imaging options to diagnose lymphedema include MR lymphangiography and indocyanine green lymphangiography. Chronic venous insufficiency typically presents with pitting edema, varicose veins, and possibly skin changes. Nephrotic syndrome generally causes bilateral edema and is associated with proteinuria and hypoalbuminemia. Congestive heart failure usually leads to bilateral edema and other systemic symptoms. Cellulitis presents with erythema, warmth, and tenderness, along with systemic signs of infection, not chronic, non-pitting edema.

Atherosclerosis is a complex disease process that leads to the formation of plaques in the arterial walls. The key initial event in this process is the oxidation of low-density lipoprotein (LDL) in the subendothelial space. Here’s a step-by-step outline of the pathogenesis of atherosclerosis:

1. Endothelial Dysfunction: The process often begins with damage or dysfunction of the endothelial layer of the blood vessels. This can be due to factors such as high blood pressure, smoking, high cholesterol, or diabetes.
2. LDL Accumulation and Oxidation: LDL particles infiltrate the subendothelial space through the compromised endothelium. Once in the subendothelial space, LDL particles become oxidized. This oxidation is crucial because oxidized LDL (oxLDL) is highly atherogenic and triggers an inflammatory response.
3. Inflammatory Response: Oxidized LDL stimulates the endothelial cells to express adhesion molecules. These molecules attract and bind monocytes from the bloodstream. The monocytes then migrate into the subendothelial space and differentiate into macrophages.
4. Foam Cell Formation: Macrophages engulf oxidized LDL through scavenger receptors. As they take up more and more oxLDL, they transform into foam cells, which are lipid-laden cells that contribute to the fatty streaks visible in early atherosclerosis. (appear like sea foam on a histology slide)
5. Plaque Development: Foam cells release cytokines and growth factors that further propagate the inflammatory response and recruit more immune cells to the site. Smooth muscle cells from the tunica media migrate into the intima, proliferate, and secrete extracellular matrix components, contributing to plaque growth.
6. Fibrous Cap Formation: Over time, a fibrous cap composed of collagen and other extracellular matrix proteins forms over the lipid core, providing some stability to the plaque. However, if the cap is thin or weakened, it can rupture, leading to the formation of a thrombus (blood clot) that can occlude the artery.

Hypertension is not commonly associated with statin use.

Hypoglycemia is also not a typical complication of statin medications.

Myopathy is a condition characterized by muscle pain or weakness and is a known potential complication of statin therapy. In severe cases, it can progress to rhabdomyolysis, a serious condition involving the breakdown of muscle tissue.

Hyperthyroidism is a condition in which the thyroid gland is overactive, which is not commonly linked to the use of statins.

Statins and Their Use

Statins are a class of medications commonly prescribed to lower cholesterol levels in the blood. They work by inhibiting an enzyme called HMG-CoA reductase, which plays a crucial role in the synthesis of cholesterol in the liver. By reducing cholesterol levels, statins help prevent cardiovascular diseases, including heart attacks and strokes.

Potential Complications of Statins

While statins are generally well-tolerated and effective, they can have potential side effects and complications. One of the most significant and well-known complications is myopathy.

Myopathy

Myopathy refers to any disease affecting the muscles, and in the context of statin use, it often manifests as muscle pain, tenderness, or weakness. The severity of myopathy can range from mild discomfort to severe muscle damage. The risk of myopathy increases with higher doses of statins, but it can occur at any dose.

• Symptoms: Common symptoms of myopathy include muscle aches, stiffness, cramps, and fatigue. In severe cases, patients may experience significant muscle weakness, making it difficult to perform everyday tasks.
• Mechanism: The exact mechanism by which statins cause myopathy is not entirely understood, but it is believed that statins may interfere with muscle cell function and energy production. Statins inhibit the synthesis of coenzyme Q10 (CoQ10), a molecule involved in mitochondrial energy production, which might contribute to muscle damage.
• Rhabdomyolysis: In rare and severe cases, statin-induced myopathy can progress to rhabdomyolysis, a serious condition where muscle fibers break down and release their contents into the bloodstream. This can lead to kidney damage, electrolyte imbalances, and, if untreated, can be life-threatening. Symptoms of rhabdomyolysis include severe muscle pain, dark urine, and weakness.

Other Potential Complications

While myopathy is a significant concern, there are other potential side effects associated with statin use:

• Liver Dysfunction: Statins can cause elevations in liver enzymes, indicating liver inflammation or damage. Regular monitoring of liver function tests is recommended during statin therapy.
• Diabetes: Some studies suggest that statin use may slightly increase the risk of developing type 2 diabetes, particularly in individuals already at risk for diabetes.
• Neurological Effects: There have been reports of memory loss and confusion in some statin users, although these effects are generally rare and reversible upon discontinuation of the drug.

Metformin is a widely used oral antihyperglycemic agent primarily prescribed for the management of type 2 diabetes mellitus. Its primary mechanisms of action include:

1. Reducing Hepatic Gluconeogenesis

Metformin decreases the production of glucose in the liver. This is important in diabetes, where the liver often produces excessive glucose, contributing to elevated blood sugar levels. Metformin inhibits gluconeogenesis.

2. Enhancing Peripheral Glucose Uptake

Metformin improves insulin sensitivity, particularly in muscle and adipose tissue. This enhances the uptake and utilization of glucose by these tissues, reducing blood glucose levels. The drug increases the activity of insulin receptors and improves the post-receptor signaling pathways, leading to more efficient glucose uptake.

Additional Effects

• Inhibition of Glucose Absorption: Metformin may also reduce the absorption of glucose from the gastrointestinal tract, although this is a secondary mechanism.
• Effect on Lipid Metabolism: It can also favorably alter lipid metabolism, potentially reducing triglyceride levels and improving lipid profiles, which is beneficial for patients with type 2 diabetes who often have concomitant dyslipidemia.

Common Side Effects

1. Gastrointestinal Disturbances:
   • Nausea
   • Vomiting
   • Diarrhea
   • Abdominal discomfort
   • Bloating
   • Flatulence
2. Taste Disturbance:
   • Metallic taste in the mouth

Serious Side Effects

1. Lactic Acidosis:
   • A rare but serious side effect that can be fatal. Symptoms include malaise, myalgia (muscle pain), respiratory distress, somnolence, and abdominal pain. Risk factors include renal impairment, congestive heart failure, and use of other medications that impair renal function.
2. Vitamin B12 Deficiency:
   • Long-term use of metformin can interfere with vitamin B12 absorption, leading to deficiency. Symptoms of deficiency include anemia, neuropathy, and cognitive changes.

For a patient with diabetes who is NPO for surgery, the goal is to prevent both hyperglycemia and hypoglycemia. Administering half the usual dose of long-acting insulin (Option D) helps maintain basal insulin levels without causing hypoglycemia. The rapid-acting insulin should be held as the patient will not be consuming any meals. Discontinuing all insulin (Option A) can lead to hyperglycemia and ketosis. Administering the usual doses of both insulins (Option B) is not appropriate due to the risk of hypoglycemia while NPO. Giving the full dose of long-acting insulin (Option C) may cause hypoglycemia. Switching to an insulin infusion (Option E) can be considered in certain cases but is more complex and typically reserved for patients with significant glucose management issues or in a critical care setting.

In an NPO patient experiencing a hypoglycemic episode, the quickest and most effective method to raise blood glucose levels is to administer an intravenous (IV) bolus of 50% dextrose. Oral glucose gel is not appropriate because the patient is NPO and cannot take anything by mouth. Subcutaneous glucagon is an alternative if IV access is not available, but it is generally less effective than IV dextrose in rapidly raising blood glucose levels. A continuous infusion of normal saline does not address the hypoglycemia directly.

Prehydration with isotonic saline is the most evidence-based strategy to reduce the risk of contrast-induced nephropathy (CIN). Hydration helps to dilute the contrast agent and promotes diuresis, reducing its nephrotoxic effects. While N-acetylcysteine (NAC) has been studied for this purpose, its efficacy remains somewhat controversial and is not as strongly supported by evidence as hydration. Restricting fluid intake is not advisable as it may increase the risk of CIN. Diuretics (furosemide) would not be used for this purpose.

Antibiotics are effective in reducing the severity and duration of the illness: This statement is incorrect because hand-foot-and-mouth disease is caused by a virus (most commonly Coxsackievirus), and antibiotics are only effective against bacterial infections. Therefore, antibiotics do not help in treating this viral illness.

Antiviral medications are routinely prescribed to manage the infection: This statement is incorrect because, for most cases of hand-foot-and-mouth disease, antiviral medications are not commonly used. The disease is usually self-limiting and mild, resolving on its own without the need for specific antiviral treatment.

Supportive care, including hydration, fever management, and pain relief, is the mainstay of treatment: This statement is correct. The primary approach to managing hand-foot-and-mouth disease involves supportive care to relieve symptoms. This includes keeping the patient hydrated, managing fever with medications like acetaminophen or ibuprofen, and providing pain relief for oral ulcers and skin lesions. Most cases of the disease resolve on their own with supportive care.

Steroids are not used to treat this viral condition.

Beta-blockers should generally be continued throughout the perioperative period in patients who are already on them, as abrupt discontinuation can lead to rebound hypertension and tachycardia, increasing the risk of myocardial ischemia. Discontinuing metoprolol 24 hours before surgery can be harmful. Increasing the dose preoperatively is not recommended, as it may cause bradycardia and hypotension. Switching to a short-acting beta-blocker on the day of surgery is unnecessary and can complicate management. Maintaining the current dose ensures stable heart rate and blood pressure control during the perioperative period, reducing the risk of adverse cardiac events.

See the NEW cheat sheet on antibiotics most likely to cause a C. diff infection.

See the NEW cheat on C. Diff antibiotic risks

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common X-linked enzymatic disorder that leads to hemolytic anemia, particularly after exposure to certain triggers such as fava beans, infections, or certain medications (e.g. Bactrim). G6PD is essential for the pentose phosphate pathway, which helps protect red blood cells from oxidative damage. A deficiency in this enzyme can lead to the buildup of reactive oxygen species, causing hemolysis (low haptoglobin and elevated reticulocyte count - immature RBCs).

• Pyruvate kinase deficiency also causes hemolytic anemia but is not triggered by oxidative stressors like fava beans.
• Hexokinase is involved in the initial steps of glycolysis and its deficiency is not associated with hemolytic anemia.
• Lactate dehydrogenase is involved in the conversion of pyruvate to lactate and its deficiency would not cause hemolytic anemia.

The middle cerebral artery (MCA) is the most commonly affected artery in ischemic strokes and supplies the lateral aspect of the cerebral hemispheres, including areas responsible for motor and sensory functions of the face and upper extremities, as well as language areas in the dominant hemisphere (usually the left). The patient's right-sided weakness and expressive aphasia indicate involvement of the left MCA.

Streptococcus pneumoniae is the most common cause of community-acquired lobar pneumonia, particularly characterized by rust-colored sputum and the presence of Gram-positive, lancet-shaped diplococci. It commonly presents with fever, chills, productive cough, and signs of consolidation on physical examination and imaging.

• Staphylococcus aureus is a common cause of post-viral pneumonia and typically presents with abscess formation rather than lobar consolidation. Gram stain also appears as gram + cocci in clusters.
• Klebsiella pneumoniae is associated with currant jelly sputum and often occurs in individuals with alcoholism or chronic illnesses. Gram stain reveals gram negative rods.
• Mycoplasma pneumoniae causes atypical pneumonia, often referred to as "walking pneumonia," which typically has less severe symptoms.  Mycoplasma pneumoniae lack a cell wall, making them resistant to penicillins and invisible on Gram stain.

This patient's presentation is consistent with macrocytic anemia, indicated by the elevated MCV. The elevated homocysteine levels suggest a deficiency in vitamin B12 (cobalamin). Vitamin B12 is a cofactor for methylmalonyl-CoA mutase, which converts methylmalonyl-CoA to succinyl-CoA in the metabolism of odd-chain fatty acids and certain amino acids. Deficiency in vitamin B12 can lead to elevated methylmalonic acid and homocysteine levels, and it is essential for proper red blood cell formation.

Case Study

• Patient Profile: A 65-year-old male with chronic heart failure.
• Current Medications: Lisinopril (ACE inhibitor), Metoprolol (beta-blocker), Furosemide (loop diuretic), and Spironolactone (potassium-sparing diuretic).
• Vital Signs: Blood pressure 130/85 mmHg, heart rate 70 bpm, mild peripheral edema.
• Lab Results: Sodium 135 mmol/L (normal), Potassium 5.3 mmol/L (elevated), Creatinine 1.4 mg/dL (slightly elevated).

Case Scenario:

1. Blood Pressure and Heart Rate: The patient’s blood pressure and heart rate are within acceptable ranges for someone with chronic heart failure. No immediate concerns here.
2. Edema: Mild peripheral edema is present, which could be managed with diuretics.
3. Laboratory Results:
   • Sodium: Normal.
   • Potassium: Elevated. Normal potassium levels are usually between 3.5 and 5.0 mmol/L.
   • Creatinine: Slightly elevated, indicating some degree of renal impairment, but not critically high.

Pharmacology Review

1. Lisinopril: An ACE inhibitor that helps with heart failure by reducing blood pressure and decreasing the workload on the heart. It can also increase potassium levels.
2. Metoprolol: A beta-blocker that helps reduce heart rate and blood pressure, improving heart function.
3. Furosemide: A loop diuretic that helps remove excess fluid, which can help reduce edema and improve heart function. It can cause potassium loss.
4. Spironolactone: A potassium-sparing diuretic that helps with heart failure by reducing fluid overload while retaining potassium.

Answer Choices

Increase the dose of Furosemide: This could help reduce edema but may further increase the risk of hypokalemia (low potassium), which is not a current problem.

Add Hydrochlorothiazide to his regimen: This would add another diuretic, potentially worsening electrolyte imbalances and causing excessive potassium loss.

Decrease the dose of Spironolactone: This is the most appropriate action given the elevated potassium levels. Spironolactone is a potassium-sparing diuretic, and reducing its dose can help lower potassium levels.

Discontinue Metoprolol: This is not indicated, as Metoprolol is important for managing heart failure and the patient’s heart rate and blood pressure are well-controlled.

The correct answer is to Decrease the dose of Spironolactone. This adjustment is necessary to manage the patient's hyperkalemia (elevated potassium levels), which can be dangerous if left untreated.

Beta-lactam antibiotics, such as penicillins and cephalosporins, work by inhibiting the synthesis of bacterial cell walls, specifically targeting penicillin-binding proteins (PBPs) involved in the formation of the peptidoglycan layer. However, bacteria can develop resistance to these antibiotics through several mechanisms:

1. Modification of the Target Penicillin-Binding Proteins (PBPs): Some bacteria alter the structure of their PBPs, reducing the binding affinity of beta-lactam antibiotics. This mechanism is particularly important in Gram-positive bacteria like methicillin-resistant Staphylococcus aureus (MRSA).
2. Overproduction of Efflux Pumps: Efflux pumps are membrane proteins that actively transport a wide variety of substrates, including antibiotics, out of bacterial cells. While efflux pumps contribute to antibiotic resistance, they are not the most common mechanism for beta-lactam resistance in Gram-negative bacteria.
3. Production of Beta-Lactamase Enzymes: This is the most common mechanism of beta-lactam antibiotic resistance in Gram-negative bacteria. Beta-lactamases are enzymes that hydrolyze the beta-lactam ring of these antibiotics, rendering them ineffective. There are various types of beta-lactamases, including extended-spectrum beta-lactamases (ESBLs), which can hydrolyze a wide range of beta-lactam antibiotics.
4. Alteration of Outer Membrane Porin Channels: Some Gram-negative bacteria can alter their outer membrane porin channels to decrease the uptake of beta-lactam antibiotics. While this can contribute to resistance, it is typically less common compared to beta-lactamase production.

Among these mechanisms, the production of beta-lactamase enzymes (Option C) is the most prevalent cause of beta-lactam antibiotic resistance in Gram-negative bacteria. This enzyme effectively inactivates the antibiotic by breaking the beta-lactam ring, preventing the antibiotic from exerting its antimicrobial effect.

The patient's persistent dry cough is a well-known side effect of ACE inhibitors, such as lisinopril. This side effect is due to the accumulation of bradykinin. None of the other listed medications (amlodipine, losartan, metoprolol, hydralazine) are typically associated with causing a dry cough. Losartan, an angiotensin II receptor blocker (ARB), is often used as an alternative in patients who develop a cough from an ACE inhibitor.

The patient’s presentation, including a non-healing ulcer with purulent exudate, foul odor, crepitus upon palpation, and a history of diabetes mellitus, suggests a severe bacterial infection, potentially involving gas gangrene. The presence of Gram-positive rods is characteristic of Clostridium perfringens, which is known for producing gas and causing tissue necrosis. This organism is commonly associated with gas gangrene and soft tissue infections, particularly in patients with underlying conditions such as diabetes.

Explanation:

The combination of right upper quadrant pain, fever, and jaundice is known as Charcot's triad and is indicative of cholangitis, an infection of the bile ducts. A positive Murphy's sign (pain on palpation of the right upper quadrant during inhalation) is commonly associated with cholecystitis, but the presence of jaundice and fever makes cholangitis more likely in this scenario, especially with the patient's history of gallstones.

Explanation:

• Carvedilol is a medication used primarily in the treatment of heart failure and hypertension. It is unique because it has both beta-adrenergic blocking and alpha-1 adrenergic blocking properties.
• Non-selective beta-adrenergic receptor antagonism: Carvedilol blocks both beta-1 and beta-2 adrenergic receptors. By blocking beta-1 receptors, it reduces the heart rate and myocardial contractility, which lowers myocardial oxygen demand and reduces the workload on the heart. This is crucial in managing heart failure because it helps the heart function more efficiently.
• Alpha-1 adrenergic receptor blockade: Carvedilol also blocks alpha-1 receptors, which causes vasodilation (widening of blood vessels). This reduces systemic vascular resistance and blood pressure, which decreases the afterload (the resistance the heart has to overcome to eject blood). This vasodilatory effect further helps in the management of heart failure by improving cardiac output and reducing symptoms of congestion.
• Option A refers only to selective beta-1 blockade, which does not account for carvedilol's additional alpha-1 blocking effects.
• Option C describes the action of ACE inhibitors, which are a different class of drugs used in heart failure management but do not represent the mechanism of carvedilol.
• Option D describes the action of phosphodiesterase III inhibitors, such as milrinone, which increase cAMP levels leading to positive inotropic effects (increased force of contraction). Carvedilol does not work through this mechanism.

See the cheat sheet on blood cultures.

Repeat blood cultures should be obtained 24-48 hours after starting antibiotics to ensure that the bloodstream infection is clearing. This helps in assessing the effectiveness of the therapy and confirming that the chosen antibiotic regimen is appropriate. If blood cultures remain positive, it may indicate a need to adjust the treatment plan or investigate potential complications such as abscess formation or the presence of resistant organisms.

Tolvaptan is a vasopressin V2 receptor antagonist. Vasopressin, also known as antidiuretic hormone (ADH), plays a crucial role in regulating the body's water balance. It acts on the kidneys to promote water reabsorption, which can dilute the blood sodium levels, potentially leading to hyponatremia (low blood sodium levels).

By inhibiting the V2 receptors, tolvaptan blocks the action of vasopressin in the kidneys. This results in increased excretion of free water (without sodium), thereby concentrating the sodium in the blood and correcting hyponatremia. Essentially, tolvaptan promotes water diuresis, which helps to normalize sodium levels in patients with conditions like Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) and congestive heart failure.

The AHA guidelines recommend that during CPR, chest compressions for adults should be at least 2 inches (5 cm) deep (between 2 inches and 2.4 inches). This depth is critical for creating enough pressure to circulate blood effectively through the heart and to the rest of the body, especially to vital organs such as the brain. Compressing the chest to this depth helps to ensure that each compression adequately pumps blood, thereby increasing the chances of survival and reducing the risk of long-term damage due to lack of oxygen.  The rate of compression should be between 100-120/min.

Patients on methotrexate therapy require regular monitoring to detect potential adverse effects. The following tests are particularly important:

• Complete blood count (CBC): Methotrexate can cause bone marrow suppression, leading to leukopenia, anemia, and thrombocytopenia. Regular CBCs are crucial to detect these conditions early.
• Liver function tests (not listed but important to mention): Methotrexate can cause hepatotoxicity, so liver function tests should be regularly checked.
• Renal function tests (Serum creatinine): Methotrexate is excreted by the kidneys, and renal function should be monitored to prevent toxicity.

Given the answer choices provided, Complete blood count (CBC) is the most appropriate answer, as it directly monitors for the hematologic toxicity associated with methotrexate therapy.

Start an angiotensin-converting enzyme (ACE) inhibitor

ACE inhibitors are commonly used in the management of chronic kidney disease (CKD), especially in patients with hypertension and proteinuria. They help reduce proteinuria and slow the progression of kidney disease by lowering glomerular pressure. This is particularly important in a patient with diabetes and hypertension, as these conditions are major risk factors for the progression of CKD. Starting an ACE inhibitor is the most appropriate next step in managing this patient and is often the first recommended antihypertensive medication used to treat hypertension in diabetic patients with CKD.

Initiate hemodialysis

Hemodialysis is typically reserved for patients with end-stage renal disease (ESRD), which is generally defined by a GFR of less than 15 mL/min/1.73 m² or in the presence of severe symptoms related to kidney failure (such as uremia, refractory hyperkalemia, or fluid overload unresponsive to diuretics). This patient's GFR of 35 mL/min/1.73 m², while indicative of stage 3 CKD, does not warrant immediate initiation of hemodialysis.

Refer for renal biopsy

Renal biopsy is usually indicated for specific conditions where the diagnosis is unclear, or when there is suspicion of glomerular disease that requires histological confirmation. In this case, the patient's presentation with hypertension, diabetes, reduced GFR, and proteinuria fits a common clinical picture of diabetic nephropathy or hypertensive nephrosclerosis, and does not immediately suggest the need for a biopsy.

Prescribe a low-protein diet

While dietary management, including protein restriction, can be part of the overall strategy in managing CKD, it is not the primary next step in this patient's management. The initial focus should be on optimizing pharmacologic treatment to control blood pressure and reduce proteinuria, which has a more significant impact on slowing CKD progression.

Answer explanation:

The patient presents with symptoms of early satiety, nausea, and occasional vomiting, which are indicative of delayed gastric emptying. Given her long-standing history of type 2 diabetes mellitus, these symptoms are suggestive of diabetic gastroparesis.

Diabetic gastroparesis is a disorder characterized by delayed gastric emptying in the absence of any mechanical obstruction. It is most commonly due to autonomic neuropathy, a complication of diabetes that affects the vagus nerve, which is responsible for controlling the movement of food through the digestive tract.

Autoimmune destruction of parietal cells - This is associated with pernicious anemia and chronic atrophic gastritis, which would not typically present with the described symptoms.

Delayed gastric emptying due to autonomic neuropathy - Correct. This is the most common cause of gastroparesis in diabetic patients. Autonomic neuropathy impairs the vagus nerve, leading to slowed gastric motility and the symptoms described.

Increased gastric acid secretion - This is more commonly associated with conditions like Zollinger-Ellison syndrome and does not directly cause delayed gastric emptying.  Zollinger-Ellison syndrome is a rare disorder characterized by the formation of gastrin-secreting tumors (gastrinomas) in the pancreas or duodenum, leading to excessive gastric acid production and recurrent peptic ulcers.

Small bowel bacterial overgrowth - While this can occur in diabetes due to altered gut motility, it is more often associated with bloating and diarrhea rather than the primary symptoms of early satiety, nausea, and vomiting.

Gastric outlet obstruction due to a peptic ulcer - This condition would present with signs of mechanical obstruction, such as a palpable mass, and a different set of symptoms.

See the cheat sheet on preventing post-op nausea and vomiting

An enchondroma is a benign cartilaginous tumor commonly occurring within the small bones of the hands and feet, particularly the metatarsals. Radiographic findings typically show a well-defined, radiolucent lesion with chondroid matrix calcifications. Osteochondromas are usually found on the surface of bones rather than within the bone. Osteosarcomas are malignant and often present with a mixed lytic and sclerotic appearance with aggressive periosteal reactions. Chondrosarcomas are also malignant and typically present in older patients with more aggressive and destructive radiographic features. Giant cell tumors usually occur at the epiphyses of long bones and are characterized by a lytic appearance without chondroid calcifications.

See the cheat sheet on acute kidney injury and hyperkalemia

In a patient with acute kidney injury (AKI) presenting with hyperkalemia (potassium level of 6.2 mEq/L), the immediate management priority is to address the hyperkalemia to prevent life-threatening complications. Restricting potassium intake and using medications such as sodium polystyrene sulfonate, which helps to lower potassium levels, is a critical initial step. Hemodialysis may be considered if the patient does not respond to medical management or if there are other indications such as severe acidosis or fluid overload. Intravenous furosemide may help with fluid overload but is not the first-line treatment for hyperkalemia. Intravenous normal saline is inappropriate as this patient will likely be fluid-overloaded.

Anemia of chronic disease (ACD), also known as anemia of inflammation, is a type of anemia that occurs in patients with chronic infections, inflammatory diseases, or malignancies. The pathophysiology of ACD is primarily related to the body's response to prolonged inflammation. Here’s an explanation of the answer choices:

Iron deficiency due to chronic blood loss

• Explanation: While chronic blood loss can lead to iron deficiency anemia, it is not the primary mechanism behind anemia of chronic disease. In iron deficiency anemia, both serum iron and ferritin levels are typically low, and TIBC is high, which does not match the lab findings in this case.

Chronic inflammation leading to increased hepcidin production

• Explanation: This is the correct answer. In ACD, chronic inflammation leads to increased production of hepcidin, a liver-derived hormone that regulates iron metabolism. Hepcidin inhibits iron absorption from the gut and traps iron in macrophages, reducing its availability for erythropoiesis (red blood cell production). This results in low serum iron levels, low TIBC (reflecting low transferrin levels), and high ferritin (reflecting increased iron stores).

Autoimmune destruction of erythrocytes

• Explanation: Autoimmune destruction of erythrocytes is seen in autoimmune hemolytic anemia, not in anemia of chronic disease. In hemolytic anemia, there is typically evidence of hemolysis (such as elevated bilirubin and LDH levels, decreased haptoglobin) which is not described in the given laboratory results.

Decreased renal production of erythropoietin

• Explanation: There is nothing stated in the stem of this question that points to the patient having renal disease

In summary, the key mechanism behind anemia of chronic disease is the body's inflammatory response, which increases hepcidin production. This results in decreased iron availability for red blood cell production despite adequate or increased iron stores, as evidenced by the laboratory findings of low serum iron, low TIBC, and high ferritin.

Common Causative Organisms:

• The most common causative organisms for cellulitis are Staphylococcus aureus and Streptococcus species.

Antibiotic Choices:

1. Ciprofloxacin:
   • Primarily effective against Gram-negative bacteria.
   • Less effective against the common Gram-positive bacteria causing cellulitis, like Staphylococcus and Streptococcus.
   • Not typically recommended as first-line treatment for cellulitis.
2. Clindamycin:
   • Effective against Staphylococcus aureus (including MRSA) and Streptococcus species.
   • Appropriate for patients with penicillin allergy.
   • Provides good coverage for the common pathogens in cellulitis and is suitable for both mild and severe cases.
3. Trimethoprim-sulfamethoxazole:
   • Effective against MRSA.
   • Not very effective against Streptococcus species, which are also common in cellulitis.
   • Typically used in combination with another antibiotic when Streptococcus coverage is needed.
4. Augmentin:
   • Although effective for cellulitis, Augmentin should be used cautiously in patients with a history of severe penicillin allergy due to potential cross-reactivity.

Explanation:

• Effectiveness: Clindamycin is effective against the most common causative organisms of cellulitis, Staphylococcus aureus (including MRSA) and Streptococcus species.
• Penicillin Allergy: Clindamycin is a safe and effective option for patients with a penicillin allergy.
• Comprehensive Coverage: It provides good coverage for both mild and severe cases of cellulitis and can be used as monotherapy.

Given the patient's diabetic status (a risk factor for more severe infections) and penicillin allergy, clindamycin is an appropriate and effective choice for initial treatment.

• Chronic exertional compartment syndrome (CECS):
  • CECS is characterized by increased pressure within a muscle compartment during exercise, leading to reduced blood flow and ischemia.
  • Symptoms typically include pain, swelling, and sometimes a burning sensation that begins with activity and subsides with rest.
  • The tenderness in the distal third of the tibia and burning sensation in the foot are consistent with this diagnosis, particularly involving the anterior compartment where the deep peroneal nerve can be affected.
• Shin splints (medial tibial stress syndrome):
  • This condition involves pain along the inner edge of the tibia due to inflammation of the muscles, tendons, and bone tissue around the tibia.
  • Pain is usually diffuse and along the medial tibia rather than localized to the distal third, and it doesn’t typically present with a burning sensation in the foot.
• Stress fracture of the tibia:
  • Stress fractures typically cause localized pain that worsens with activity and improves with rest.
  • However, they do not commonly cause swelling and burning sensations as described in the scenario.
• Tarsal tunnel syndrome

  • Tarsal tunnel syndrome is a condition caused by compression of the tibial nerve as it passes through the tarsal tunnel, a narrow space found on the inside of the ankle. This compression can lead to symptoms such as pain, numbness, and tingling in the sole of the foot and toes, often exacerbated by standing or walking for extended periods. The condition is similar to carpal tunnel syndrome in the wrist but occurs in the foot.  The symptoms described in this case do not fit the typical symptoms of tarsal tunnel syndrome.

Methicillin-Resistant Staphylococcus aureus (MRSA) is a type of Staphylococcus aureus bacteria that has developed resistance to methicillin and other beta-lactam antibiotics. The primary mechanism of resistance in MRSA involves the acquisition of the mecA gene.

Mechanism of Methicillin Resistance:

mecA Gene:

• mecA gene: This gene encodes an altered penicillin-binding protein known as PBP2a (or PBP2'). Penicillin-binding proteins (PBPs) are essential for bacterial cell wall synthesis and are the target sites for beta-lactam antibiotics, including methicillin. PBP2a has a low affinity for beta-lactam antibiotics, meaning that these drugs cannot effectively bind to and inhibit this protein, allowing the bacteria to continue synthesizing its cell wall and survive in the presence of methicillin and other related antibiotics.

Incorrect Options Explained:

• Overproduction of beta-lactamase enzymes: While some Staphylococcus aureus strains produce beta-lactamase enzymes that degrade beta-lactam antibiotics, MRSA's primary resistance mechanism is the production of PBP2a due to the mecA gene, not beta-lactamase overproduction.
• Mutation in the bacterial ribosomal RNA: This mechanism is commonly associated with resistance to antibiotics that target the bacterial ribosome, such as aminoglycosides or macrolides, but not beta-lactams like methicillin.
• Efflux pump overexpression: Efflux pumps can contribute to antibiotic resistance by pumping out antibiotics from the bacterial cell. While this mechanism can be important for resistance to several other antibiotics, it is not the primary mechanism for methicillin resistance in Staphylococcus aureus.

Tenderness in the anatomical snuffbox following a fall onto an outstretched hand is highly suggestive of a scaphoid fracture. The scaphoid bone is the most commonly fractured carpal bone, and prompt diagnosis and treatment are important to prevent complications.

• Lachman Test: The knee is flexed at 20-30 degrees, and the examiner pulls the tibia anteriorly while stabilizing the femur. Increased anterior translation of the tibia indicates a positive test.
• Anterior Drawer Test: With the knee flexed at 90 degrees, the examiner pulls the tibia forward. Excessive forward movement suggests an ACL tear.
• Pivot Shift Test: The knee is extended and internally rotated, and a valgus force is applied while flexing the knee. A positive test is indicated by a "clunk" as the tibia reduces on the femur.
• LeSegue test: also known as the Straight Leg Raise (SLR) test, is a clinical maneuver used to evaluate for lumbar nerve root irritation or lumbar disc herniation (Sciatica), where the patient lies supine and the examiner passively raises the patient's straightened leg to assess for pain radiating down the leg.

Answer Explanation:

• The femoral neck is a critical part of the hip joint and is supplied primarily by the medial circumflex femoral artery.

• • This artery provides the majority of the blood supply to the femoral head, an area crucial for the survival of the bone and joint integrity.Risk of Injury:
    • In femoral neck fractures, the medial circumflex femoral artery is at high risk because it wraps around the femur and supplies blood to the femoral head.
      • Injury to this artery can lead to avascular necrosis (AVN) of the femoral head, a serious complication where the bone tissue dies due to lack of blood supply.

• Other Options:
  • • • Sciatic nerve: While important, it is not typically at risk in a femoral neck fracture. It's more associated with hip dislocations or fractures of the pelvis.
      • Obturator nerve: Mainly affects medial thigh sensation and adduction; not commonly injured in femoral neck fractures.
      • Superficial femoral artery - not as frequently injured during femoral neck fracture

Answer explanations:

• Superficial spreading melanoma is the most common type of melanoma. It is characterized by a prolonged radial growth phase, during which the melanoma spreads horizontally within the epidermis and is usually less than 1 mm thick. This phase can last for years before the lesion becomes vertically invasive and penetrates deeper into the skin. The lesion typically presents as a flat or slightly elevated, asymmetrical patch with irregular borders and varying colors (remember the ABCDE's of melanoma)

Other Options:

• Nodular melanoma: This type of melanoma does not have a significant radial growth phase. It tends to grow vertically from the outset, leading to early invasion into deeper skin layers. Nodular melanomas are often more aggressive and present as raised, dome-shaped nodules.
• Lentigo maligna melanoma: This melanoma subtype primarily affects older adults and often arises in chronically sun-exposed areas, such as the face. It has a prolonged radial growth phase, similar to superficial spreading melanoma, but it usually starts as a lentigo maligna (a flat, tan, or brown lesion) that can persist for many years before becoming invasive.
• Acral lentiginous melanoma: This type of melanoma is more common in darker-skinned individuals and occurs on the palms, soles, and under the nails. It also has a radial growth phase but is typically more aggressive and often diagnosed at a later stage.

See the cheat sheet on carbapenems

Extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli are resistant to many beta-lactam antibiotics, including penicillins and cephalosporins. The presence of ESBLs necessitates the use of carbapenems, which are often stable against these enzymes and are considered the treatment of choice for serious infections caused by ESBL-producing organisms.

• Ceftriaxone - ESBL-producing E. coli are resistant to ceftriaxone, making it an inappropriate choice.
• Piperacillin-tazobactam - Though sometimes used in less severe cases, ESBL-producing organisms can exhibit resistance, making it less reliable than carbapenems for serious infections.
• Meropenem - Meropenem is a carbapenem antibiotic effective against ESBL-producing organisms and is the most appropriate choice for treating serious infections caused by these bacteria.
• Ciprofloxacin - While some ESBL-producing E. coli may remain sensitive to fluoroquinolones, resistance is common, making it an unreliable choice without specific sensitivity data.
• Trimethoprim-sulfamethoxazole - Resistance among ESBL-producing organisms to this antibiotic is also common, making it a less appropriate choice for empirical therapy in severe infections.

Charcot-Marie-Tooth (CMT) disease is a hereditary motor and sensory neuropathy characterized by progressive muscle weakness, muscle atrophy, and sensory loss, primarily affecting the distal extremities. The pathophysiology of CMT is related to genetic mutations affecting the peripheral nerves.

In this particular case, the patient's genetic testing reveals a duplication of the PMP22 gene, which is the most common genetic abnormality associated with CMT type 1A (CMT1A). The PMP22 gene encodes peripheral myelin protein 22, a critical component of the myelin sheath in peripheral nerves.

See the cheat sheet on the Seddon's Classification of nerve injuries

Neurapraxia: The mildest form of nerve injury, often due to compression or ischemia, such as from an ankle tourniquet, resulting in a temporary conduction block without loss of axonal continuity. It typically resolves completely over time.

Axonotmesis: Involves damage to the axons with preservation of the myelin sheath; more severe than neurapraxia and requires a longer recovery period.

Neurotmesis: The most severe form of nerve injury with complete transection of the nerve, requiring surgical intervention for recovery.

Neuroma: A benign growth of nerve tissue that can develop after nerve injury but is not a classification of the injury itself.

Explanation Of Answer choices :

• Acute renal failure: This can occur as a complication of rhabdomyolysis but is not the primary diagnosis in this case study.
• Guillain-Barré syndrome: Presents with ascending muscle weakness and areflexia but does not typically involve myalgia, dark urine, or elevated CK levels.
• Rhabdomyolysis: Characterized by muscle pain, weakness, dark urine (due to myoglobinuria), and markedly elevated CK levels following intense physical exertion or trauma.
• Chronic exertional compartment syndrome: Presents with pain during exercise that resolves with rest and is not associated with elevated CK or myoglobinuria.

Pemphigus vulgaris is an autoimmune blistering disorder characterized by flaccid blisters and erosions on the skin and mucous membranes. The key diagnostic features include:

• Clinical presentation: Painful oral ulcers and flaccid blisters on the skin.
• Histology: Suprabasal acantholysis (separation of epidermal cells).
• Direct immunofluorescence: Intercellular deposition of IgG and C3 in the epidermis.

Bullous pemphigoid typically presents with tense blisters and subepidermal separation.

Dermatitis herpetiformis is characterized by pruritic papules and vesicles, often associated with celiac disease.

Epidermolysis bullosa acquisita is a rare, chronic autoimmune blistering disorder characterized by the formation of subepidermal blisters, often resulting in fragile skin, mucosal involvement, and scarring, typically caused by autoantibodies targeting type VII collagen at the dermoepidermal junction.

• Continue all medications without any adjustments: Incorrect. Some adjustments are often necessary to reduce the risk of perioperative complications such as infections.
• Discontinue methotrexate 2 weeks prior to surgery and resume 2 weeks postoperatively: Incorrect. Current guidelines suggest continuing methotrexate perioperatively as discontinuation might lead to a flare of RA.
• Continue methotrexate and prednisone, but discontinue adalimumab 1-2 weeks prior to surgery and resume after wound healing: Correct. Methotrexate is generally continued, but TNF inhibitors like adalimumab should be held 1-2 weeks before surgery and resumed after adequate wound healing to reduce the risk of infections.
• Discontinue prednisone 1 week before surgery and resume after wound healing: Sudden discontinuation of corticosteroids can lead to adrenal insufficiency. Instead, perioperative stress dosing of corticosteroids is usually required.

Intermittent claudication is a classic symptom of peripheral artery disease (PAD) and is characterized by pain in the muscles of the legs that occurs during exercise and is relieved by rest. The initial management of PAD with intermittent claudication typically includes lifestyle modifications and medical therapy aimed at reducing cardiovascular risk factors.

• Supervised exercise programs are considered one the most important initial therapy for intermittent claudication as they have been shown to improve walking distance and symptoms.
• Daily aspirin/clopidogrel and anti-lipid therapy is important for secondary prevention of cardiovascular events
• Cilostazol is a phosphodiesterase inhibitor that can improve symptoms and increase walking distance but is often considered AFTER smoking cessation, exercise program, antihypertensive therapy, anti-lipid therapy, weight reduction, and antiplatelet therapy have failed.  Cilostazol can be used in conjunction with an exercise program.
• Complete smoking cessation is crucial for reducing cardiovascular risk and improving overall outcomes.

The initial management of patients presenting with septic arthritis includes joint drainage AND antibiotic therapy.  Septic arthritis represents a closed abscess and therefore requires some form of joint drainage (needle aspiration, arthroscopic, or open arthrotomy)

The clinical presentation of acute onset pain, swelling, and erythema of the knee joint, along with the synovial fluid analysis showing a high white blood cell count predominantly of neutrophils and gram-positive cocci in chains, is most consistent with septic arthritis caused by Strep species.

See the new cheat sheet on burn injury classification

A superficial partial-thickness burn, also known as a second-degree burn, affects both the epidermis (the outermost layer of the skin) and the upper part of the dermis (the second layer of skin). Here are its key characteristics:

1. Appearance: The skin usually appears red and blistered. The blisters may be filled with clear fluid. The area might also look wet or moist due to the loss of the skin barrier.
2. Pain: These burns are typically very painful due to the exposure of nerve endings in the dermis.
3. Sensation: The affected area is usually sensitive to touch and can be painful when exposed to air or pressure.
4. Blanching: When pressure is applied to the burn, the redness will typically blanch (turn white) and then return to red when the pressure is released. This indicates good blood flow in the area.
5. Healing Time: Superficial partial thickness burns generally heal within 10 to 21 days without significant scarring, though some color changes in the skin may remain.
6. Risk of Infection: Due to the damage to the skin’s protective barrier, there is an increased risk of infection. Proper wound care is essential to prevent complications (topical silvadene).
7. Common Causes: These burns are commonly caused by scalding from hot liquids, brief contact with hot objects, or sunburn.

On the contrary, a deep partial-thickness, also known as a deep second-degree burn, extends deeper into the dermis than a superficial partial-thickness burn. Here are its key characteristics:

1. Appearance: The skin may appear mixed red and white, or it may have a mottled red and white appearance. The burn may look waxy or have a dry texture. Blisters may or may not be present, and if they are, they may be larger and more prone to rupture.
2. Pain: These burns can be less painful than superficial partial thickness burns because nerve endings are more extensively damaged. However, they can still be quite painful, especially around the edges where some nerve endings remain intact.
3. Sensation: Sensation in the burned area may be diminished. The patient might feel pressure but not light touch or pinprick in the center of the burn.
4. Blanching: The burn may not blanch as well upon pressure due to damage to the blood vessels in the deeper layers of the dermis. If blanching occurs, it might be slower to return.
5. Healing Time: Deep partial thickness burns take longer to heal than superficial partial thickness burns, typically between 3 to 8 weeks. These burns are more likely to result in scarring and may require skin grafting to heal properly.
6. Risk of Infection: The risk of infection is higher due to more extensive skin damage. Proper wound care is critical to prevent complications.
7. Common Causes: These burns are often caused by prolonged exposure to hot liquids or objects, flames, chemical burns, or severe sunburn.

Explanation of answer choices:

A) It increases insulin sensitivity by activating peroxisome proliferator-activated receptors (PPARs).

• Explanation: This describes the mechanism of action for a class of drugs known as thiazolidinediones (TZDs), such as pioglitazone and rosiglitazone. These drugs help to increase insulin sensitivity in peripheral tissues, but this is not the mechanism by which Ozempic (semaglutide) works.

B) It inhibits the reabsorption of glucose in the kidneys by blocking sodium-glucose cotransporter 2 (SGLT2).

• Explanation: This mechanism is characteristic of SGLT2 inhibitors, such as canagliflozin, dapagliflozin, and empagliflozin. These drugs work by preventing glucose reabsorption in the kidneys, leading to increased glucose excretion in urine. Again, this is not how Ozempic functions.

C) It mimics the action of glucagon-like peptide-1 (GLP-1), enhancing glucose-dependent insulin secretion and inhibiting glucagon release.

• Explanation: This is the correct mechanism of action for Ozempic (semaglutide). Ozempic is a GLP-1 receptor agonist. It mimics the incretin hormone GLP-1, which increases insulin secretion in response to meals, inhibits glucagon release, slows gastric emptying, and promotes satiety. These actions collectively help to lower blood glucose levels.

D) It delays gastric emptying and reduces appetite by antagonizing the ghrelin receptor.

• Explanation: While Ozempic does delay gastric emptying and reduce appetite, it does not do so by antagonizing the ghrelin receptor. The ghrelin receptor is associated with the hormone ghrelin, which stimulates appetite. Ozempic’s effects on gastric emptying and appetite are mediated through its action on the GLP-1 receptor, not the ghrelin receptor.

The pathophysiology of post-thrombotic syndrome (PTS) primarily involves persistent venous hypertension due to valvular incompetence and residual thrombus. After a DVT, the veins can have damaged valves or remain partially obstructed by thrombus, leading to impaired venous return and increased venous pressure. This chronic venous hypertension results in symptoms such as pain, swelling, skin changes, and venous ulcers.

• Chronic inflammation and fibrosis within the venous wall leading to luminal narrowing can occur but is not the primary mechanism of PTS. The key issue is valvular incompetence and venous hypertension.
• Increased arterial pressure causing backward flow into the venous system is incorrect because arterial pressure and venous insufficiency are distinct entities. PTS is related to venous pressure, not arterial.
• Increased lymphatic permeability leading to protein-rich fluid accumulation refers to the pathophysiology of lymphedema, not PTS.

Correct answer - Thromboangiitis obliterans (Buerger's disease) is common in young male smokers and presents with pain in extremities, diminished pulses, and ulcerations.

• Incorrect - While peripheral artery disease can cause diminished pulses and pain, it typically affects older individuals and those with a history of diabetes, hyperlipidemia, or hypertension.
• Incorrect - Raynaud's phenomenon involves color changes in the extremities (white, blue, red) and is usually not associated with ulcerations or diminished pulses. Secondary Raynaud's (Raynaud's phenomenon) is associated with other diseases, particularly connective tissue disorders such as scleroderma, lupus, and rheumatoid arthritis. It can be more severe and is often associated with digital ulcers and tissue damage.
• Incorrect - Chronic venous insufficiency presents with symptoms like edema, varicose veins, and skin changes, but not typically with diminished pulses or severe pain worsened by cold exposure.

In the evaluation of post-operative fever, it is important to consider the timing and potential sources of infection. The "5 W's" (Wind, Water, Wound, Walking, Wonder drugs) help guide the differential diagnosis of post-operative fever:

• Wind (Atelectasis/Pneumonia): Typically occurs within the first 48 hours.
• Water (Urinary tract infection): Usually occurs between days 1-3.
• Wound (Surgical site infection): Generally occurs after day 3.
• Walking (Deep vein thrombosis): Can occur anytime post-operatively.
• Wonder drugs (Drug fever): Can occur anytime post-operatively.

Given that this patient's fever occurred on postoperative day 2 and there are no signs of respiratory issues or wound infection, a urinary tract infection (UTI) is a common cause at this stage. Therefore, assessing for a UTI with a urinalysis and urine culture is the most appropriate initial step.

A chest X-ray might be appropriate if there were respiratory symptoms or signs, but her lungs are clear. Blood cultures are more appropriate if there is a suspicion of systemic infection or sepsis. Empiric antibiotic therapy should not be started without identifying a specific source of infection.

This patient's presentation is consistent with acute kidney injury (AKI), as evidenced by the recent increase in serum creatinine (see the cheat sheet on AKI). His history of NSAID use, with physical findings and laboratory results, suggests acute tubular necrosis (ATN) as the most likely cause. NSAIDs can lead to kidney injury by reducing renal blood flow, causing ischemia and subsequent tubular damage.

• Prerenal azotemia: Typically caused by decreased renal perfusion. It is less likely here given the presence of granular casts, which are more indicative of intrinsic renal damage.
• Acute tubular necrosis: Commonly caused by ischemia or nephrotoxins. The presence of granular casts and recent NSAID use supports this diagnosis.
• Postrenal obstruction: Often presents with anuria or oliguria and may be associated with distended bladder, kidney stones, prostate issues, etc.
• Chronic kidney disease: Usually presents with a more gradual increase in creatinine and persistent symptoms over months to years, not days. (see the cheat sheet on chronic kidney disease)
• Glomerulonephritis: Typically presents with hematuria, proteinuria, and possibly RBC casts, but less commonly with granular casts and the clinical scenario described here.

Topical corticosteroids are often the first-line treatment for granuloma annulare, especially for localized cases. They help reduce inflammation and may promote lesion resolution. Granuloma annulare is generally a benign and self-limited condition, but treatment can help speed up the resolution of lesions and improve cosmetic appearance.

Incorrect Options:

• Oral antihistamines: These are not effective for granuloma annulare as it is not an allergic condition and does not typically cause itching.
• Systemic corticosteroids: These are generally reserved for more severe or widespread cases of granuloma annulare. They are not considered first-line due to potential side effects.
• Antibiotic therapy: Granuloma annulare is not an infectious condition, so antibiotics are not indicated.

ACE inhibitors like lisinopril can increase the risk of intraoperative hypotension. It is generally recommended to discontinue ACE inhibitors 24 hours before surgery to minimize this risk. Metformin should typically be discontinued 48 hours before surgery in patients with renal impairment due to the risk of lactic acidosis, but it is not mentioned in the answer choices. Instead of switching to insulin, more conservative glycemic control strategies might be considered (especially with an HbA1C of 7.5%), and elective surgeries are not typically delayed for modestly elevated blood pressures such as 145/85 mmHg. The administration of intravenous fluids must be carefully considered in patients with CKD to avoid fluid overload.

Pustular psoriasis, particularly when localized to the palms and soles (also known as palmoplantar pustulosis), can be challenging to treat. While high-potency topical corticosteroids can be used as part of the management, oral retinoids such as acitretin are often considered the initial treatment of choice for moderate to severe cases. Oral retinoids help reduce inflammation and promote normalization of skin cell growth. Topical antifungals and systemic antibiotics are not appropriate as pustular psoriasis is not an infection. Oral prednisone and oral antibiotics are not appropriate for the treatment of psoriasis.

See the cheat sheet on the Sanders Classification!

The Sanders classification system is based on coronal CT imaging and categorizes calcaneal fractures according to the number of fracture lines and the number of fragments in the posterior facet of the calcaneus. Here is a brief overview of the classification:

• Type I: Non-displaced fractures.
• Type II: One fracture line creating two primary fragments.
• Type III: Two fracture lines creating three primary fragments.
• Type IV: Three or more fracture lines creating four or more primary fragments.

In the provided case, the correct description for a Sanders Type II fracture is a displaced intra-articular fracture with one fracture line creating two primary fragments

See the cheat sheet on the Berndt-Hardy classification stages.

The Berndt-Hardy classification is used to describe the severity of osteochondral lesions of the talus:

1. Stage I: Compression fracture of the subchondral bone without displacement.
2. Stage II: Incomplete separation or partially detached osteochondral fragment.
3. Stage III: Completely detached but non-displaced osteochondral fragment.
4. Stage IV: Displaced osteochondral fragment.

See the cheat sheet on chronic gouty arthritis

The patient has recurrent episodes of gouty arthritis, indicated by the history of painful swelling in the joints and elevated serum uric acid levels. Long-term management of gout involves reducing uric acid levels to prevent future attacks. Allopurinol is a xanthine oxidase inhibitor that reduces uric acid production and is indicated for chronic management to prevent recurrent gout attacks. While NSAIDs and colchicine are effective for treating acute attacks, they are not suitable for long-term management alone. Weight loss and dietary modifications are important supportive measures but may not be sufficient as the sole therapy. Intra-articular corticosteroid injections can help manage acute attacks but are not used for long-term management. Initiating allopurinol therapy is the most appropriate long-term strategy in this case.

The patient presents with painful, ulcerated lesions with purplish borders and necrotic centers on her lower extremities, which are characteristic of pyoderma gangrenosum. This condition is often associated with systemic diseases such as inflammatory bowel disease, rheumatoid arthritis, and hepatitis C. The presence of elevated liver enzymes, positive rheumatoid factor, and low complement levels supports an underlying systemic condition, particularly hepatitis C, which is known to be associated with pyoderma gangrenosum. Erythema nodosum usually presents with painful nodules on the anterior lower legs, livedo reticularis with a net-like rash, and porphyria cutanea tarda with blistering lesions, none of which match this patient's presentation.

Anemia of chronic disease is typically normocytic and normochromic, though it can be microcytic. It can be associated with chronic inflammatory conditions such as rheumatoid arthritis. Key laboratory findings include low serum iron, low TIBC, and high ferritin, reflecting iron sequestration within macrophages and decreased iron availability for erythropoiesis despite adequate or increased total body iron stores. With anemia of chronic disease, there is an increased production of hepcidin from the liver which limits the release of stored iron in macrophages and inhibits the absorption of iron through the duodenum.  The transferrin saturation may be low or normal.

Explanation:

• Incorrect. Linezolid therapy requires monitoring for hematologic abnormalities, such as thrombocytopenia and anemia, especially with prolonged use.
• Correct. Linezolid is a weak monoamine oxidase inhibitor, and patients should avoid tyramine-rich foods (e.g., aged cheeses, cured meats) to prevent the risk of hypertensive crisis.
• Incorrect. Linezolid is metabolized by the liver and excreted by both renal and non-renal routes, but does not typically require significant dose adjustment in mild to moderate renal impairment.
• Incorrect. Concurrent administration of linezolid with SNRIs or other serotonergic drugs is contraindicated due to the risk of serotonin syndrome.

A common side effect of gabapentin is sedation. Patients may also experience dizziness and peripheral edema.

Tight glycemic control is crucial in managing diabetic neuropathy to prevent further nerve damage and progression of symptoms.

Gabapentin is one of the first-line treatments for diabetic neuropathy, effective in reducing neuropathic pain. Other first-line options include pregabalin and duloxetine.

The maximum recommended dose of plain lidocaine (without epinephrine) for a healthy adult is generally 4.5 mg/kg of body weight, not to exceed a total dose of 300 mg. This dosage limit is set to minimize the risk of systemic toxicity, which can occur if too much of the drug is absorbed into the bloodstream.

In clinical practice, it is crucial to calculate the dose based on the patient's weight and to monitor for any signs of toxicity, especially in procedures requiring large volumes of the anesthetic.

Lidocaine works by blocking voltage-gated sodium channels, which inhibits the propagation of nerve impulses, leading to a loss of sensation in the targeted area.

See the cheat sheet on the stages of lymphedema

Lymphedema is classified into four stages:

• Stage 0 (Latent or Subclinical Stage): No visible edema despite impaired lymph transport. Patients might experience a feeling of heaviness or discomfort in the affected area.
• Stage I (Early Accumulation of Fluid): Edema is present and is pitting. Swelling reduces with elevation of the limb.
• Stage II (Spontaneously Irreversible): Edema is non-pitting and does not significantly reduce with elevation. The skin begins to thicken, and fibrosis develops. This stage is often described with features such as peau d'orange (orange peel appearance) due to skin changes.
• Stage III (Lymphostatic Elephantiasis): Severe swelling with significant skin changes such as hyperkeratosis, papillomatosis, and deep skin folds. The limb may become large and misshapen.

In this patient, the non-pitting edema, thickened skin with an orange peel appearance, and lack of significant reduction in swelling with limb elevation are characteristics of Stage II lymphedema.

Ichthyosis vulgaris is a common inherited skin disorder characterized by dry, scaly skin. It typically presents in early childhood and is often worse in cold, dry climates. The characteristic features include fine white to gray scales, particularly on the extensor surfaces of the extremities, and prominent palmar creases. The condition is inherited in an autosomal dominant pattern, explaining the family history in this case.  It is often caused by mutations in the filaggrin (FLG) gene, which plays a crucial role in skin barrier function.

• Psoriasis usually presents with well-demarcated, red plaques with silvery scales, and it commonly affects the scalp, elbows, and knees.
• Atopic dermatitis often involves the flexural areas and is associated with intense pruritus, erythema, and oozing.
• Seborrheic dermatitis typically affects areas rich in sebaceous glands, such as the scalp, face, and trunk, and presents with greasy scales over erythematous skin.

Therefore, the clinical presentation of dry, scaly skin that worsens in the winter, along with the family history, is most consistent with ichthyosis vulgaris.

The correct answer is Stevens-Johnson Syndrome; discontinuation of the offending drug and supportive care.

Explanation:

• The patient's symptoms of fever, malaise, painful rash with erythematous macules, and epidermal detachment suggest Stevens-Johnson Syndrome (SJS).
• The involvement of less than 10% of body surface area with central necrosis and blistering is consistent with SJS (as opposed to toxic epidermal necrolysis (TEN), which involves more than 30% of body surface area).
• SJS is often triggered by medications, and in this case, the new antiepileptic drug is likely the offending agent.
• The most appropriate initial management involves immediate discontinuation of the suspected offending drug and providing supportive care, including fluid management, wound care, and pain control. Referral to a burn unit or intensive care unit may be necessary for severe cases.

See the cheat sheet on carbapenems

Ertapenem is a broad-spectrum carbapenem antibiotic that is often used in the treatment of complicated infections, including diabetic foot infections and osteomyelitis. However, unlike other carbapenems, ertapenem does not cover Pseudomonas aeruginosa. This characteristic is important when selecting an appropriate antibiotic, especially in healthcare settings where Pseudomonas infections are a concern. Ertapenem has a relatively long half-life, allowing for once-daily dosing, which is advantageous for outpatient therapy and adherence. It generally has good tissue penetration, including bone, making it a good choice for osteomyelitis. It is not typically associated with a high incidence of nephrotoxicity.

Lymphedema praecox presents during adolescence and fits this patient's presentation and family history.

Primary lymphedema is a congenital or hereditary disorder characterized by the abnormal development of the lymphatic system, leading to impaired lymphatic drainage and chronic lymph fluid accumulation in the interstitial tissues.

See the cheat sheet on reversal agents for anticoagulants

• Vitamin K is used to reverse the effects of warfarin, not Eliquis.
• Protamine sulfate is used to reverse the effects of heparin and low molecular weight heparins like enoxaparin, not Factor Xa inhibitors.
• Fresh frozen plasma can provide clotting factors but is not the primary reversal agent for Factor Xa inhibitors.
• Andexanet alfa is specifically approved to reverse the anticoagulant effects of factor Xa inhibitors, including Eliquis and Xarelto.

The radiographic findings in this case include:

• An oblique fracture of the distal fibula starting at the level of the syndesmosis.
• Medial clear space widening, indicative of a deltoid ligament injury.
• A small posterior malleolus fracture.

These findings are consistent with a Lauge-Hansen Supination-External Rotation (SER) injury, Stage IV. The stages of SER injuries are:

1. Stage I: Injury to the anterior inferior tibiofibular ligament
2. Stage II: Oblique fracture of the distal fibula at the syndesmosis level or rupture of the interosseous membrane
3. Stage III: Rupture of the posterior inferior tibiofibular ligament or fracture of the posterior malleolus
4. Stage IV: Medial malleolus fracture or deltoid ligament rupture

In this scenario, the oblique fracture of the fibula at the syndesmosis level, medial clear space widening due to deltoid ligament injury, and the small posterior malleolus fracture fit the criteria for SER Stage IV.

• Danis-Weber Type C: Fracture above the syndesmosis
• Lauge-Hansen Pronation-Abduction (Stage III): Typically involves a transverse medial malleolus fracture and a higher fibular fracture, often above the tibial plafond transverse or comminuted in orientation.
• Lauge-Hansen Pronation-External Rotation (Stage IV): Involves a high fibular fracture above the syndesmosis, a transverse fracture of the medial malleolus, and potential injury to the posterior structures.

Given the described injury, the Lauge-Hansen Supination-External Rotation (Stage IV) classification is the most appropriate.

Iron deficiency anemia is characterized by low serum iron and ferritin levels, and elevated TIBC due to increased iron-binding capacity as the body attempts to bind more iron.

The patient’s presentation is consistent with rhabdomyolysis, a condition characterized by muscle breakdown leading to the release of muscle contents, including myoglobin, into the bloodstream. Key features include muscle pain, weakness, elevated CK levels, and myoglobinuria (indicated by dark urine and positive myoglobin in urinalysis).

• Intravenous fluid resuscitation is the cornerstone of initial management to prevent acute kidney injury by diluting myoglobin and facilitating its excretion. This helps in preserving renal function and preventing complications associated with rhabdomyolysis.
• Administration of intravenous sodium bicarbonate may be used to alkalinize the urine and prevent myoglobin-induced renal damage, but it is not the first step.
• Oral potassium supplementation is not appropriate as rhabdomyolysis often leads to hyperkalemia due to the release of intracellular potassium from damaged muscles.
• Administration of diuretics is not indicated as the first-line treatment and can potentially worsen renal perfusion.

Myositis ossificans is a condition characterized by the formation of bone tissue inside muscle or other soft tissues following trauma. The history of blunt trauma followed by the development of a firm mass and the presence of a well-demarcated, calcified mass on radiographs are key features that support this diagnosis.

• Osteosarcoma typically presents with pain and swelling but usually affects the metaphyseal region of long bones and may show a "sunburst" pattern on imaging rather than a well-demarcated mass within the muscle.
• Deep vein thrombosis would present with pain, swelling, and possibly erythema, but not with a calcified mass.
• Hematoma can present as a mass following trauma but would not typically show calcification on imaging studies.

• The common fibular (peroneal) nerve is responsible for dorsiflexion and sensation on the dorsum of the foot and the anterior lower leg. Injury to this nerve commonly results in foot drop.
• The common fibular nerve wraps around the fibular head before dividing into the superficial and deep fibular (peroneal) nerves.
• The tibialis anterior muscle, innervated by the deep fibular nerve (a branch of the common fibular nerve), will atrophy if the nerve injury is left untreated, as it is primarily responsible for dorsiflexion of the foot.

Lichen planus is a chronic inflammatory condition that typically presents with itchy, violaceous, flat-topped papules and plaques. These lesions are often found on the wrists, ankles, and lower back, and may exhibit fine white lines known as Wickham striae. Lichen planus can be idiopathic or associated with certain medications, such as those for hypertension.

Psoriasis usually presents with erythematous plaques covered by silvery scales, commonly on the extensor surfaces and scalp. Atopic dermatitis is characterized by pruritic, erythematous, and sometimes vesicular lesions, often in flexural areas. Seborrheic dermatitis presents with erythematous, greasy, scaly patches, typically in areas rich in sebaceous glands like the scalp, face, and upper trunk.

Basal cell carcinoma (BCC) is the most common type of skin cancer and typically presents as a pearly, flesh-colored nodule with telangiectasias. It often occurs in sun-exposed areas of the skin, such as the face, particularly in individuals with extensive sun exposure. The slow growth and occasional bleeding are also characteristic features of BCC.

Actinic keratosis presents as rough, scaly patches on sun-exposed skin and is considered a precursor to squamous cell carcinoma (SCC). Malignant melanoma is characterized by asymmetrical pigmented lesions with irregular borders and color variations. Squamous cell carcinoma typically presents as a firm, red nodule or a flat lesion with a scaly, crusted surface. Seborrheic keratosis presents as well-demarcated, waxy, stuck-on lesions and does not typically resemble BCC.

The patient’s symptoms are consistent with tarsal tunnel syndrome, which involves compression of the tibial nerve as it passes behind the medial malleolus through the tarsal tunnel. The tibial nerve provides sensory innervation to the sole of the foot and motor innervation to the muscles of the foot that control toe flexion. The burning sensation along the inner side of the ankle and sole of the foot, as well as the positive Tinel sign (a tingling sensation upon tapping over the nerve), are characteristic findings.

A posterior hip dislocation commonly results from significant trauma and can lead to the shortening, adduction, and internal rotation of the affected limb. The sciatic nerve, which runs posteriorly to the hip joint, is at high risk of injury in such cases due to its proximity to the dislocation site. This can result in neurological deficits, including weakness or paralysis of the muscles supplied by the sciatic nerve and sensory loss in the posterior aspect of the thigh, leg, and foot. Prompt recognition and reduction of the dislocation are crucial to prevent long-term complications.

Erythema multiforme (EM) is characterized by target-like lesions with a central blister, often precipitated by infections such as herpes simplex virus (HSV). The history of a recent cold sore supports this diagnosis. Urticaria presents with transient wheals or hives and lacks the central blister and target appearance. Stevens-Johnson syndrome (SJS) involves more extensive skin involvement and mucosal surfaces and is often triggered by medications, not just infections. Bullous pemphigoid typically presents with tense blisters on an erythematous base, primarily in older adults.  Erythema chronicum migrans, the hallmark rash of early Lyme disease, presents as an expanding red patch often with central clearing, resembling a bull's-eye, and typically appears within 3-30 days after a tick bite.

The patient's symptoms of pain and tightness in the lower legs that begin with exercise and subside with rest, along with the feeling of fullness and swelling, are characteristic of chronic exertional compartment syndrome (CECS). This condition involves increased pressure within the muscle compartments of the leg during exercise, leading to reduced blood flow and nerve function. The immediate onset of swelling and tenderness after exercise further supports this diagnosis. CECS primarily affects the muscle compartments of the lower leg, causing pain and discomfort during physical activity.

The patient's symptoms of pain radiating from the lower back to the leg, along with numbness and weakness, suggest sciatica, which is often due to compression of a lumbar or sacral nerve root. The loss of the Achilles reflex (ankle jerk) is a key indicator that the S1 nerve root is affected. Intervertebral disc herniation is a common cause of such nerve root compression. Therefore, the S1 nerve root compression due to an intervertebral disc herniation best explains the patient's symptoms.

This patient presents with macrocytic anemia (elevated MCV), neurological symptoms (numbness, unsteady gait, mild memory problems), and a history that increases the risk of vitamin B12 deficiency (chronic gastritis and long-term PPI use). Chronic gastritis and prolonged use of PPIs can lead to decreased gastric acid production, impairing the absorption of vitamin B12. The presence of a positive Romberg sign and decreased vibratory sensation also points towards a neurological deficit due to vitamin B12 deficiency. Elevated homocysteine and methylmalonic acid levels are specific markers for vitamin B12 deficiency, helping to differentiate it from folate deficiency, which would not elevate methylmalonic acid. Iron deficiency anemia typically causes microcytic anemia, not macrocytic. Copper deficiency and vitamin E deficiency could cause neurological symptoms but would not present with macrocytic anemia and specific lab findings like elevated methylmalonic acid.

See the cheat sheet on quinolone antibiotics

Ciprofloxacin, a fluoroquinolone antibiotic, is commonly associated with photosensitivity reactions, making it important to advise patients to avoid excessive sun exposure and use sunscreen. While rare, fluoroquinolones can cause tendinopathy and tendon rupture, but this is not listed as an option here. Hyperkalemia, hypoglycemia, myopathy, and Torsades de Pointes are not commonly associated with ciprofloxacin.

This patient has cellulitis, a common bacterial skin infection often caused by Streptococcus and Staphylococcus species, including MRSA (methicillin-resistant Staphylococcus aureus). Given her history of anaphylaxis to penicillin, clindamycin is a reasonable alternative. Clindamycin is effective against both Streptococcus and Staphylococcus species, including many strains of MRSA. It is also well-tolerated in patients with penicillin allergies.

• Amoxicillin is contraindicated due to the patient’s history of anaphylaxis to penicillin.
• Cephalexin is a first-generation cephalosporin and may have cross-reactivity with penicillin, posing a risk in this patient.
• Trimethoprim-sulfamethoxazole is effective against Staph/MRSA but lacks reliable coverage for Streptococcus species.
• Ciprofloxacin is not the first choice for cellulitis as it does not provide adequate coverage for Gram-positive organisms like Streptococcus.

Thus, clindamycin is the most appropriate choice in this scenario.

Virchow's triad consists of three factors that predispose to thrombus formation: hypercoagulability, vascular damage, and stasis. This patient has a history of cancer and recent chemotherapy, both of which can contribute to a hypercoagulable state. Additionally, if her cancer treatment involved any central venous catheters or surgeries, these could cause vascular damage. Prolonged periods of immobility due to illness or recovery can lead to stasis of blood flow. All these factors together increase the risk of DVT, which is consistent with the components of Virchow's triad.

The patient presents with chronic gastrointestinal symptoms, a positive tissue transglutaminase IgA antibody test, and iron deficiency anemia, all indicative of celiac disease. In celiac disease, damage to the small intestine leads to malabsorption of various nutrients.

Folate (B) deficiency is common in celiac disease due to malabsorption in the proximal small intestine where folate is absorbed. This can contribute to anemia, particularly if the anemia is of a mixed type (microcytic from iron deficiency and macrocytic from folate deficiency).

Vitamin B12 is absorbed in the terminal ileum, which is less commonly affected in celiac disease compared to the proximal small intestine. Vitamin D and calcium deficiencies can occur due to fat malabsorption, but they are less likely to directly cause anemia.

Thus, folate deficiency is the most likely additional nutritional deficiency in this patient with celiac disease and iron deficiency anemia.