Internal Medicine COMAT Clinical Hub Internal Medicine Shelf Exam Clinical Hub

Single S1 and S2

• Represents normal closure of the atrioventricular (mitral and tricuspid) valves followed by the semilunar (aortic and pulmonic) valves.
• No additional gallops, rubs, or murmurs should be appreciated in a normal exam.

Left ventricular hypertrophy

• Corresponds to an S4 gallop, caused by atrial contraction against a stiff, non-compliant left ventricle.
• Frequently associated with chronic hypertension, aortic stenosis, or hypertrophic cardiomyopathy.

Normal or Cardiomyopathy

• Represents an S3 gallop, which can be a normal physiologic variant in healthy young individuals and pregnant patients.
• In older adults, it signifies pathological volume overload or systolic heart failure due to ventricular dilation.

Barrel chest with increased anterior-posterior diameter

• Caused by chronic air trapping and hyperinflation leading to flattened diaphragms.
• Results from decreased elastic recoil of the alveoli.

High fever, sore throat, drooling, and dysphagia

• Rapidly progressive airway obstruction requiring careful management and securing the airway in a controlled setting.
• Often caused by Haemophilus influenzae type b (Hib) in unvaccinated populations.

Muffled voice and inspiratory stridor

• Stridor indicates critical upper airway narrowing.
• Avoid stressful interventions (like tongue depressors or crying in children) until the airway is secured to prevent complete obstruction.

≥ 70% (Normal or increased)

• Both FEV1 and FVC decrease proportionally, or FVC decreases slightly more than FEV1.
• Total lung capacity (TLC) is reduced below the 5th percentile or < 80% predicted.

Increased alveolar-capillary permeability

• Triggered by pro-inflammatory cytokine release and neutrophil accumulation that damage the capillary endothelium.
• Results in non-cardiogenic pulmonary edema and normal pulmonary capillary wedge pressure (PCWP ≤ 18 mmHg).

Glycoprotein Ib (GPIb) deficiency

• Results in impaired platelet adhesion to von Willebrand factor.
• Characterized by giant platelets ("Big Suckers") and thrombocytopenia with prolonged bleeding time.

Shifts toward the higher volume side with a blunted, scooped-out expiratory downslope

• Peak expiratory flow (PEF) is markedly reduced due to expiratory airflow limitation.
• Air trapping causes an increase in residual volume and total lung capacity.

Shifts toward the lower volume side (witch's hat appearance)

• Retains a normal shape but is miniaturized along the volume axis due to decreased lung volumes.
• Expiratory flow rates are preserved relative to the small lung volume.

Dullness to percussion

• Decreased air within the collapsed lung tissue prevents the normal resonance heard over air-filled parenchyma.
• Associated with decreased breath sounds and decreased tactile fremitus over the affected area.

Towards the side of the lesion (rightward deviation)

• Volume loss and decreased pressure within the affected hemithorax pull mediastinal structures toward the pathology.
• Contrast with tension pneumothorax or large pleural effusion, which push mediastinal structures away.

[Na+] - ([HCO3-] + [Cl-])

• Represents unmeasured serum anions (e.g., albumin, phosphates, sulfates, organic acids).
• Normal reference range is approximately 8–12 mEq/L.

Hyaline casts

• Composed primarily of Tamm-Horsfall mucoprotein secreted by renal tubular epithelial cells.
• Can be seen after strenuous exercise, dehydration, or diuretic therapy without underlying renal disease.

Triad of Hypotension, Clear lung fields, and Jugular Venous Distention (JVD) in the setting of inferior STEMI; Nitrates, Morphine, and Diuretics are strictly contraindicated

• Caused by proximal occlusion of the Right Coronary Artery (RCA); confirmed by ST-segment elevation ≥ 1 mm in right-sided precordial lead V4R.
• The ischemic RV is highly preload-dependent; venodilators precipitate profound cardiovascular collapse. Immediate treatment requires aggressive IV isotonic saline fluid boluses.

1) ARNI (Sacubitril/Valsartan preferred over ACEi/ARB); 2) Beta-blocker (Carvedilol, Metoprolol succinate, Bisoprolol); 3) MRA (Spironolactone, Eplerenone); 4) SGLT2 inhibitor (Dapagliflozin, Empagliflozin)

• When switching from an ACE inhibitor to an ARNI, a mandatory 36-hour washout period is required to prevent life-threatening angioedema.
• Loop diuretics (Furosemide) provide critical symptomatic fluid relief, but DO NOT reduce long-term cardiovascular mortality.

Type A involves the ascending aorta (requires emergent surgical repair); Type B involves only the descending aorta distal to left subclavian (managed medically)

• Presents with sudden-onset tearing or ripping chest/back pain and asymmetric blood pressure (> 20 mmHg differential between arms).
• Medical therapy for Type B: IV Beta-blockers (Esmolol, Labetalol) to achieve heart rate < 60 bpm and SBP < 120 mmHg BEFORE initiating vasodilators (Nitroprusside) to avoid reflex tachycardia.

Men aged 65 to 75 who have ever smoked (≥ 100 lifetime cigarettes)

• Screening is not recommended in women who have never smoked.
• Repair is indicated when the aneurysm reaches ≥ 5.5 cm in men or ≥ 5.0 cm in women.

Clostridioides difficile

• Associated with a 2- to 3-fold increased risk of C. difficile infection due to the suppression of gastric acid barrier defenses.
• Should be used cautiously in hospitalized patients and discontinued promptly when no longer clinically indicated.

Increased production/secretion of the gastric mucous barrier and decreased acid production

• Acts as a prostaglandin E1 analog that replaces endogenous prostaglandins depleted by NSAID therapy.
• Highly effective for preventing NSAID-induced gastroduodenal ulcers, though limited by uterine-contracting adverse effects.

Alcoholic hepatitis: AST > ALT in a > 2:1 ratio ("Scotch > Tonic"), with AST rarely exceeding 500 U/L; Viral hepatitis: ALT > AST with transaminases elevated into the thousands (> 1,000–5,000 U/L)

• In alcoholic hepatitis, AST elevation reflects alcohol-induced pyridoxal 5'-phosphate (vitamin B6) deficiency, which impairs ALT synthesis relative to AST.
• Transaminases exceeding 5,000 U/L suggest ischemic hepatitis ("shock liver") or acetaminophen toxicity.

Ascitic fluid absolute polymorphonuclear neutrophil (PMN) count ≥ 250 cells/mm³; Treat with IV 3rd-generation cephalosporin (Ceftriaxone or Cefotaxime) PLUS IV 25% Albumin

• IV Albumin dosing (1.5 g/kg on day 1 and 1.0 g/kg on day 3) reduces renal impairment and hospital mortality from hepatorenal syndrome by over 50%.
• Diagnostic paracentesis is mandatory before starting antibiotics in any patient with cirrhosis and ascites presenting with fever, abdominal pain, or unexplained clinical deterioration.

1) Hemodynamic stabilization (two large-bore IVs, restrictive transfusion target Hb 7–8 g/dL); 2) IV Octreotide bolus + continuous infusion; 3) Prophylactic IV Ceftriaxone; 4) Emergent EGD with band ligation within 12 hours

• Octreotide inhibits glucagon release and produces splanchnic vasoconstriction, reducing portal venous inflow.
• Prophylactic ceftriaxone for 7 days reduces bacterial infections, recurrent bleeding episodes, and overall hospital mortality.

Diagnosis requires ≥ 2 of 3: 1) Characteristic epigastric pain radiating to the back; 2) Serum lipase or amylase ≥ 3x upper limit of normal; 3) Imaging evidence of pancreatitis

• Serum lipase is more sensitive and remains elevated longer than amylase.
• Abdominal CT with IV contrast is NOT required at admission if criteria 1 and 2 are met; indicated only if diagnostic uncertainty exists or after 48 to 72 hours if the patient fails to improve to evaluate for necrotizing pancreatitis.

Conivaptan, tolvaptan, and demeclocycline

• These medications block the action of vasopressin at the renal collecting duct, promoting free water excretion to correct hyponatremia.

Decreased

• High pH causes hydrogen ions to dissociate from plasma proteins (such as albumin), freeing up binding sites that are subsequently occupied by calcium ions, leading to clinical hypocalcemia.

Renal osteodystrophy

• Caused by secondary hyperparathyroidism, resulting in increased bone resorption, osteomalacia, bone pain, and potential progression to tertiary hyperparathyroidism.

Renal cell carcinoma

• Tumor invasion into the left renal vein increases venous pressure and obstructs drainage from the left gonadal vein.
• Look for associated hematuria, flank pain, and fever.

Prerenal: FENa < 1% and FEUrea < 35%; ATN: FENa > 2% and FEUrea > 50%

• Critical loop diuretic caveat: In patients taking loop diuretics (e.g. Furosemide), FENa is falsely elevated due to pharmacologic natriuresis; FEUrea (< 35%) is the reliable test of choice for prerenal azotemia.
• Prerenal also features BUN/Creatinine ratio > 20:1 and concentrated urine (Urine Osmolality > 500 mOsm/kg) with hyaline casts; ATN shows muddy brown granular casts.

Correct sodium by NO MORE than 8 mEq/L in a 24-hour period (or 4–6 mEq/L in high-risk patients); Exceeding this rate precipitates Osmotic Demyelination Syndrome (ODS / Central Pontine Myelinolysis)

• Rapid hypertonic correction dehydrates brain cells, causing demyelination of pontine white matter tracts.
• Clinical manifestation: Spastic quadriparesis, pseudobulbar palsy, dysarthria, and classic "locked-in" syndrome (awake and conscious but quadriplegic with only vertical eye movements preserved).

Immediate IV Calcium Gluconate (or Calcium Chloride) to stabilize the cardiac myocyte resting membrane potential

• Calcium directly antagonizes the membrane depolarizing effects of hyperkalemia, narrowing the QRS and preventing fatal ventricular arrhythmias; it DOES NOT lower serum potassium.
• Step 2: Shift potassium intracellularly with IV Regular Insulin + 50% Dextrose and nebulized Albuterol; Step 3: Remove potassium with Loop Diuretics (Furosemide), Sodium Zirconium Cyclosilicate (Lokelma), or emergent Hemodialysis.

Hypotonic, euvolemic hyponatremia with inappropriately concentrated urine (Urine Osm > 100 mOsm/kg) and high urine sodium (Urine Na > 40 mEq/L); First-line is fluid restriction (< 800–1000 mL/day)

• Causes: Small cell lung carcinoma, CNS disorders (stroke, trauma), pulmonary infections, and medications (SSRIs, carbamazepine).
• If severe symptomatic hyponatremia (seizures, coma) occurs, treat with a hypertonic (3%) saline bolus to raise serum sodium by 4–6 mEq/L acutely.

Capacity is a clinical assessment made by physicians, whereas competence is a legal determination decided by a judge

• Capacity evaluates a patient's specific ability to understand and communicate a healthcare choice.
• Competence is a global legal status applying to all decisions.

Ensure the patient has a safe place to go during an emergency

• The USPSTF recommends universal screening for IPV in women of reproductive age.
• Always validate the patient's safety plan and provide domestic violence resource contacts.

Talk to the patient directly > Subjective standard > Substituted judgment > Best-interest standard

• Subjective standard relies on the patient's prior explicit statements.
• Substituted judgment uses a surrogate to decide what the patient would have wanted; best-interest applies a rational person standard if preferences are unknown.

Waiver, Legally Incompetent, Therapeutic Privilege, and Emergency

• Waiver occurs when the patient explicitly declines information.
• Therapeutic privilege applies rarely when disclosure poses severe, immediate harm to the patient's psychological or physical well-being.

Decreased synthesis and release of GnRH

• Prolactin indirectly inhibits FSH and LH production by suppressing the hypothalamic pulsatile release of GnRH.

Graves disease

• Caused by thyroid-stimulating immunoglobulin (TSI) antibodies directed against the TSH receptor, resulting in diffuse toxic goiter, exophthalmos, and pretibial myxedema.

Levothyroxine and liothyronine

• Levothyroxine is a synthetic analog of thyroxine (T4), while liothyronine is the synthetic analog of triiodothyronine (T3).

Hyperkalemia

• Also known as Addison disease, primary adrenal insufficiency involves aldosterone deficiency, which normally promotes renal sodium reabsorption and potassium excretion.

Parathyroidectomy

• Indicated in patients under 50, those with symptomatic disease, or specific end-organ complications; asymptomatic patients are monitored with serial calcium, creatinine, and bone density testing.

Decreased serum calcium and increased serum phosphate

• Patients also exhibit decreased urinary phosphate excretion due to the absence of PTH action on the proximal tubules; treatment involves oral calcium and active vitamin D.

Zoledronic acid

• Preferred over pamidronate due to superior clinical efficacy, longer duration of action, and significantly shorter infusion duration (15 minutes vs 2 hours).

Calcium-sensing receptors (CaSR)

• These Gq-coupled receptors regulate PTH secretion in response to extracellular calcium; their mutation leads to a higher set-point for calcium, resulting in mild hypercalcemia and inappropriately normal or elevated PTH with low urinary calcium excretion.

Primary hyperparathyroidism

• Symptoms arise from hypercalcemia causing nephrolithiasis (stones), bone resorption (bones), constipation (groans), polyuria (thrones), and depression or altered mental status (psychiatric overtones).

Hypothyroidism

• Decreased basal metabolic rate results from reduced Na+-K+ ATPase activity.
• Leads to diminished calorigenesis and cold intolerance.

No

• Distinction requires histological evaluation of capsular or vascular invasion.
• A fibrous capsule cannot be adequately assessed via cytology alone on FNA.

Insulin resistance

• Target tissues fail to respond adequately to circulating insulin.
• Contrasts with type 1 diabetes mellitus, which is characterized by absolute insulin deficiency.

HbA1c

• HbA1c represents the glycated form of hemoglobin.
• Serves as a reliable estimate due to the 120-day lifespan of red blood cells.

≥ 200 mg/dL

• Measured two hours following the ingestion of a 75 g anhydrous glucose load in water.
• Equivalent to 11.1 mmol/L.

Postprandial glucose spike

• Rapid onset and short duration closely mimic physiological prandial insulin secretion.

Sulfonylureas and meglitinides

• Mechanism involves increased insulin release, which promotes triglyceride synthesis and fat storage.

GLP-1 receptor agonists

• Glucagon-like peptide-1 receptor agonists enhance glucose-dependent insulin secretion and slow gastric emptying.

Upper respiratory and urinary tract infections

• Commonly manifests as nasopharyngitis or sinusitis due to immunomodulatory effects.

At least 2 of 3 features (hyperandrogenism, oligo/anovulation, and polycystic ovaries)

• Includes clinical or biochemical signs of hyperandrogenism, menstrual irregularity, and ultrasonographic findings.
• If the first two criteria are met, an ultrasound is not strictly required for diagnosis.

Decreased

• Due to decreased TBG synthesis by the liver or increased protein loss
• Decreased TBG is detected via increased resin uptake (T3 resin uptake test)

Decreased

• TBG is primarily produced by the liver; decreased synthesis lowers total T4 levels while free T4 remains normal

No

• Treatment should focus exclusively on managing the primary underlying critical illness
• Thyroid function tests typically normalize spontaneously after resolution of the acute illness

Oral agents carry high risks of acute lactic acidosis (Metformin), euglycemic DKA (SGLT2i), or prolonged hypoglycemia (Sulfonylureas) during acute illness; Standard therapy is structured subcutaneous Basal-Bolus Insulin

• Target in-hospital blood glucose range for most non-critically ill medical inpatients is 140 to 180 mg/dL.
• Sliding-scale regular insulin alone without basal insulin coverage is ineffective and condemned by clinical guidelines.

Step 1: Check serum TSH and obtain thyroid ultrasound. If TSH is suppressed: Radionuclide iodine uptake scan (hot nodule = treat hyperthyroidism; cold nodule = biopsy); If TSH is normal/elevated: Fine-Needle Aspiration (FNA) biopsy for suspicious sonographic features

• Sonographic high-risk features: Microcalcifications, hypoechogenicity, irregular infiltrative margins, taller-than-wide shape, and extrathyroidal extension.
• Papillary thyroid carcinoma is the most common histology (> 80%), featuring ground-glass nuclei (Orphan Annie eyes) and psammoma bodies.

Immediate high-dose IV Hydrocortisone (100 mg bolus q8h) PLUS rapid IV isotonic saline volume resuscitation; DO NOT delay treatment to perform diagnostic testing

• If diagnostic confirmation via cosyntropin (ACTH) stimulation test is urgently desired, administer IV Dexamethasone instead, as dexamethasone does not cross-react with serum cortisol assays.
• Hydrocortisone provides both glucocorticoid and mineralocorticoid activity, rapidly restoring vascular tone and electrolyte balance.

Bone marrow monocytes

• Function as specialized epidermal antigen-presenting dendritic cells containing Birbeck granules

Bone marrow aspiration and core biopsy is the definitive next step to evaluate cellularity, architecture, and marrow infiltration; Flow cytometry rapidly identifies clonal immunophenotypes

• Differentiates aplastic anemia (hypocellular fat-filled marrow), myelodysplastic syndrome (dysplastic hypercellular marrow), and acute leukemias (blasts ≥ 20%).
• Flow cytometry distinguishes acute lymphoblastic leukemia (B-ALL: CD19, CD20; T-ALL: CD3) from acute myeloid leukemia (AML: CD33, CD34, myeloperoxidase positive).

Pentad of "FAT RN": Fever, Anemia (microangiopathic hemolytic with schistocytes), Thrombocytopenia, Renal dysfunction, and Neurologic deficits; Platelet transfusions are contraindicated because they fuel further microvascular thrombosis

• Etiology: Autoantibody deficiency or inhibition of ADAMTS13 metalloprotease, preventing cleavage of ultra-large von Willebrand factor multimers.
• Emergency treatment: Immediate Plasma Exchange (plasmapheresis / PEX) and systemic Corticosteroids; never delay therapy while awaiting ADAMTS13 assay results.

A ≥ 50% drop in platelet count occurring 5 to 10 days following heparin exposure, associated with high risk of venous and arterial thrombosis; Immediately STOP ALL heparin and initiate a Direct Thrombin Inhibitor (Argatroban, Bivalirudin) or Fondaparinux

• Caused by IgG autoantibodies targeting platelet factor 4 (PF4)-heparin complexes, causing platelet activation and hypercoagulability.
• Warfarin is strictly contraindicated until platelets have recovered to > 150,000/µL, as acute protein C depletion precipitates venous limb gangrene and skin necrosis.

Porphobilinogen (PBG) deaminase (also known as hydroxymethylbilane synthase) deficiency; Acute Intermittent Porphyria (AIP); treat immediately with intravenous hemin and high-dose intravenous glucose.

• Deficiency & Accumulation: Autosomal dominant deficiency of porphobilinogen deaminase, causing toxic accumulation of delta-aminolevulinic acid (ALA) and porphobilinogen (PBG) in serum and urine.
• Triggers: CYP450-inducing drugs (sulfa drugs, antiepileptics), alcohol, starvation/low-carbohydrate fasting, and progesterone/luteal phase of menses, all of which upregulate ALA synthase-1.
• The '5 Ps' Clinical Pentad:

1. *Painful abdomen* (severe visceral neuropathic colic without peritonitis)

2. *Port-wine colored urine* (PBG oxidizes to dark porphobilin in light)

3. *Polyneuropathy* (motor-predominant neuropathy, wrist/foot drop)

4. *Psychological disturbances* (delirium, paranoia, hallucinations)

5. *Precipitated by drugs/fasting*

• Targeted Therapy: Intravenous hemin and high-dose dextrose/glucose directly downregulate ALA synthase-1 via negative feedback, shutting down precursor accumulation.

Assess optimal dosing, treatment efficacy, and adverse effects

• Conducted on a moderate number of affected patients.
• Helps determine the dosing parameters utilized in subsequent large-scale randomized studies.

Azithromycin or Doxycycline

• Dual therapy covers concurrent Chlamydia trachomatis infection.
• Ceftriaxone remains the primary treatment for gonorrhea.

Threat of harm (Tarasoff duty to protect)

• Other mandatory breaches include reporting gunshot wounds, suspected child/elder abuse, and specific dangerous communicable public health threats.
• Must notify law enforcement and the intended victim.

No

• Psychotherapeutic notes are maintained separately from the rest of the medical record and are legally excluded from standard patient access requests.
• Information gathered in reasonable anticipation of a civil, criminal, or administrative proceeding is also exempt from disclosure.

Enterococci (Enterococcus faecalis and Enterococcus faecium)

• Suspect enterococcal endocarditis when a patient develops subacute endocarditis symptoms following procedures such as cystoscopy or colonoscopy.
• Enterococci are normal commensal flora of the human colon and urogenital tract with high affinity for damaged heart valves.

Trimethoprim-sulfamethoxazole (TMP-SMX)

• For patients with severe sulfa allergies, alternative regimens for treatment or prophylaxis include dapsone or atovaquone.
• Indicated for prophylaxis in immunocompromised hosts such as patients with HIV when CD4 counts drop below 200/uL.

Toxoplasmosis

• Presents with multiple ring-enhancing lesions, differentiating it from primary CNS lymphoma, which typically presents as a solitary lesion.
• Both toxoplasmosis and primary CNS lymphoma are the leading causes of ring-enhancing intracranial masses in advanced AIDS.

White, creamy purulent discharge

• Commonly presents with dysuria, urethritis, cervicitis, and prostatitis.
• Distinguished from Chlamydia trachomatis, which typically causes a scant, watery discharge.

Ceftriaxone plus either doxycycline or azithromycin

• Ceftriaxone provides targeted coverage for gonorrhea, while the second agent covers potential concurrent Chlamydia trachomatis infection.
• If gonorrhea is confirmed but Chlamydia is ruled out by negative NAAT testing, treatment consists solely of ceftriaxone monotherapy.

Bone conduction greater than air conduction (bone > air)

• Indicates abnormal sound transmission through the external or middle ear

Air conduction greater than bone conduction (air > bone)

• Normal ratio is preserved despite reduced overall hearing perception in the affected ear

Destruction of hair cells at the cochlear base

• Results in progressive, symmetric high-frequency hearing loss

Relative afferent pupillary defect (RAPD / Marcus Gunn pupil)

• Indicates an afferent pathway problem in picking up light, most commonly due to optic nerve damage (e.g., optic neuritis) or severe retinal injury

Pronator teres and flexor carpi radialis

• Characterized by point tenderness near the medial epicondyle.
• Pain is characteristically exacerbated by resisted wrist flexion.

Extensor carpi radialis brevis (ECRB)

• Microtrauma results in excess fibroblast activity and neovascularization at the lateral epicondyle.
• Pain is reproduced with resisted wrist extension and resisted middle finger extension.

Physical therapy (quadriceps and hip strengthening) and activity modification

• Acute phase management relies on the POLICE principle and NSAIDs, whereas recovery focuses on rehabilitative exercise.
• Physical therapy targets stretching and strengthening of the quadriceps and hip abductors to correct lower extremity dynamic malalignment.

Bisphosphonates (first-line) and calcitonin (second-line)

• Paget disease features uncontrolled osteoclast resorption and secondary disorganized bone formation.
• Bisphosphonates induce osteoclast apoptosis, while calcitonin directly inhibits osteoclast activity.

Syringomyelia

• The widened bubble or cavitation first damages neural fibers passing near the center of the spine
• Can be secondary to tumor, trauma (whiplash), or congenital malformations (associated with Chiari malformations)

Bilateral loss of pain and temperature sensation in a 'cape-like' distribution

• Pain loss may present as unrecognized cuts on the arms and upper torso
• Temperature loss may present as unrecognized burns

Chiari I malformation

• Also frequently arises secondary to spinal cord trauma or intramedullary tumors

Sway with both eyes open and eyes closed (negative Romberg sign)

• Important distinguishing feature from dorsal column lesions, which only cause swaying when the eyes are closed (positive Romberg sign)

Gout: Monosodium urate crystals, needle-shaped, strongly NEGATIVE birefringence (yellow when parallel to polarized axis); Pseudogout: Calcium pyrophosphate, rhomboid-shaped, weakly POSITIVE birefringence (blue when parallel)

• Acute gout treatment: NSAIDs (indomethacin), Colchicine (inhibits microtubule polymerization), or intra-articular/oral corticosteroids.
• Long-term urate-lowering therapy: Allopurinol (xanthine oxidase inhibitor) indicated for recurrent flares, tophi, or CKD; target serum urate < 6.0 mg/dL.

Immediately administer high-dose systemic Corticosteroids (IV Methylprednisolone or oral Prednisone 60 mg/day) BEFORE obtaining a temporal artery biopsy

• Delaying steroid therapy to wait for biopsy or specialty consultation risks catastrophic, irreversible bilateral blindness from anterior ischemic optic neuropathy.
• Temporal artery biopsy remains the definitive diagnostic standard and remains histopathologically diagnostic even several weeks after initiating steroid therapy.

Benign: Central, concentric/laminated (granuloma), or popcorn calcification (hamartoma); Malignant: Eccentric, stippled, or ground-glass calcification with spiculation and size > 8 mm

• Hamartomas are the most common benign lung neoplasms and contain fat, cartilage, and smooth muscle.
• If intermediate or high risk for malignancy in an older smoker, obtain contrast CT chest followed by PET/CT or image-guided transthoracic/bronchoscopic biopsy.

1) Inhaled short-acting bronchodilators (Albuterol + Ipratropium); 2) Systemic oral corticosteroids (Prednisone 40 mg x 5 days); 3) Controlled supplemental O2 (target SpO2 88–92%); 4) Antibiotics (Azithromycin or Augmentin)

• Antibiotics are indicated if patient exhibits all 3 cardinal symptoms (increased dyspnea, sputum volume, sputum purulence) or requires non-invasive ventilation.
• Over-oxygenation (SpO2 > 93%) can worsen hypercapnia due to ventilation-perfusion mismatch and loss of hypoxic vasoconstriction (Haldane effect).

Confusion (1), Urea/BUN > 19 mg/dL (1), Respiratory rate ≥ 30 (1), Blood pressure < 90/60 mmHg (1), Age ≥ 65 years (1)

• Score 0–1: Low risk; outpatient management appropriate (Amoxicillin, Doxycycline, or Augmentin + Macrolide).
• Score 2: Moderate risk; short inpatient stay or close supervised outpatient monitoring.
• Score ≥ 3: High risk; inpatient hospital admission indicated; score 4–5 warrants ICU evaluation.

Group 1 (PAH) has normal PCWP (≤ 15 mmHg) with elevated PVR; Group 2 (LHD) has elevated PCWP (> 15 mmHg) reflecting elevated left atrial pressure

• Group 1: Treat with targeted pulmonary vasodilators: Endothelin receptor antagonists (Bosentan), PDE-5 inhibitors (Sildenafil), or prostacyclins (Epoprostenol).
• Group 2: Targeted pulmonary vasodilators are strictly CONTRAINDICATED (causes pulmonary edema); management focuses on optimizing left heart failure GDMT and diuresis.

Sustained hypotension (Systolic BP < 90 mmHg for > 15 minutes or vasopressor requirement); Treat with emergent systemic IV Thrombolytic therapy (Alteplase)

• In patients with absolute contraindications to thrombolysis (recent hemorrhagic stroke, active bleeding), catheter-directed thrombectomy or surgical embolectomy is performed.
• For submassive (intermediate-risk) PE (normal BP with RV strain on echo/CT or elevated troponin/BNP), anticoagulation with therapeutic LMWH or unfractionated heparin is first-line.

'Wet, Wobbly, and Wacky' (Urinary incontinence, Magnetic gait apraxia, and Subcortical dementia); Gait apraxia appears earliest and responds best to VP shunting

• Caused by impaired CSF resorption at arachnoid villi, with normal opening pressure on lumbar puncture.
• Neuroimaging demonstrates ventriculomegaly disproportionate to cortical sulcal enlargement (Evans index > 0.3).

Multicomponent non-pharmacologic interventions (frequent reorientation, natural window daylight, uninterrupted sleep at night, early mobilization, sensory aids like glasses and hearing aids, and avoiding physical restraints)

• Antipsychotics (haloperidol) do not reduce delirium duration or mortality and are reserved strictly for severe agitation threatening immediate patient or staff safety.

Intravenous Calcium Gluconate (10% solution, 10 mL IV over 2–3 minutes); stabilizes the cardiac myocardial cell membrane without lowering serum potassium.

• Mechanism: Severe hyperkalemia partially depolarizes the resting myocardial membrane potential toward threshold, inactivating voltage-gated sodium channels and causing conduction slowing (QRS widening, sine wave, arrest). IV calcium increases the threshold potential, restoring the normal electrical difference and stabilizing the myocardium against ventricular fibrillation.
• Subsequent Steps: After membrane stabilization with calcium, administer agents to shift potassium intracellularly (IV Regular Insulin + 50% Dextrose, nebulized Albuterol), followed by potassium excretion therapies (IV Furosemide, Patiromer, or emergent Hemodialysis).

Acute Tubular Necrosis (ATN) due to ischemic renal injury; contrasted by lost tubular concentrating ability (FENa > 2%, urine Na > 40 mEq/L) compared to intact tubular resorption in prerenal azotemia (FENa < 1%, urine Na < 20 mEq/L, BUN/Cr > 20:1).

• Pathophysiology of ATN: Severe sustained renal hypoperfusion leads to ischemic death and sloughing of renal tubular epithelial cells (particularly in the metabolically active straight portion of proximal tubules and thick ascending limb).
• Diagnostic Hallmarks: Damaged tubular cells cannot reabsorb sodium (FENa > 2%, urine Na > 40 mEq/L) or concentrate urine (urine osmolality < 350 mOsm/kg). Sloughed cells aggregate with Tamm-Horsfall protein to form muddy brown granular casts.
• Management: Discontinue nephrotoxins, optimize hemodynamics and renal perfusion; dialysis if refractory acidosis, hyperkalemia, or volume overload occur.

Type 1 (Distal) Renal Tubular Acidosis; failure of alpha-intercalated cells in the collecting tubule to secrete H+ ions; calcium phosphate stones form due to persistent urinary alkalization and hypercalciuria.

• Cellular Mechanism: Defect in the apical H+-ATPase or basolateral HCO3-/Cl- exchanger in distal collecting duct alpha-intercalated cells impairs net proton excretion into the lumen.
• Diagnostic Hallmarks:
• *Normal anion gap metabolic acidosis* with hypokalemia (distal delivery of non-reabsorbed Na+ drives potassium excretion via principal cells).
• *Urine pH > 5.5*: Hallmark finding; the urine cannot be acidified despite profound systemic acidemia!
• *Positive urine net charge*: Indicates inability to excrete ammonium (NH4+).
• Nephrocalcinosis & Stones: Systemic acidemia causes skeletal buffering (bone resorption), releasing calcium and phosphate. In an alkaline urine environment (pH > 5.5) with low urinary citrate, calcium phosphate precipitates, causing recurrent nephrolithiasis and medullary nephrocalcinosis.

Type 4 (Hyperkalemic) Renal Tubular Acidosis secondary to diabetic hyporeninemic hypoaldosteronism; aldosterone deficiency impairs collecting duct sodium reabsorption and potassium excretion, and hyperkalemia directly suppresses renal ammonium (NH4+) synthesis.

• Etiology: Diabetic nephropathy causes hyalinization of the juxtaglomerular apparatus, leading to hyporeninemic hypoaldosteronism. Lisinopril further blunts aldosterone production.
• Pathophysiology:
• Aldosterone deficiency reduces the activity of apical epithelial sodium channels (ENaC) and the H+-ATPase in collecting tubule principal and intercalated cells.
• This impairs potassium and hydrogen ion excretion, leading to hyperkalemia and mild normal anion gap metabolic acidosis.
• Critical Physiological Mechanism: High extracellular potassium directly enters proximal renal tubular cells and inhibits glutaminase, severely suppressing the synthesis of ammonium (NH4+). Without ammonium buffer, net acid excretion drops.
• Urine pH: Remains < 5.5 (acidic) because distal H+ secretion is not completely blocked, but total net acid excretion is severely blunted due to lack of NH4+ buffer.

Minimal Change Disease; light microscopy and immunofluorescence are completely normal; electron microscopy shows diffuse effacement of podocyte foot processes; treated with oral corticosteroids (prednisone).

• Pathophysiology: Cytokine-mediated T-cell dysfunction leads to loss of the polyanionic charge barrier on the glomerular basement membrane (loss of heparan sulfate), allowing selective albuminuria.
• Biopsy Triad:
• *Light Microscopy*: Normal-appearing glomeruli (hence 'minimal change').
• *Immunofluorescence*: Negative (no immune complex or complement deposition).
• *Electron Microscopy*: Pathognomonic diffuse effacement (flattening) of podocyte foot processes.
• Treatment & Prognosis: Highly responsive to a course of oral corticosteroids (prednisone); complete remission occurs in > 90% of pediatric patients.

S4 gallop (atrial gallop); generated by the contraction of the atria ('atrial kick') forcing blood into a stiff, noncompliant, hypertrophied left ventricle.

• Timing: Late diastole, immediately before the first heart sound (S1).
• Mechanism: Chronic hypertension induces concentric left ventricular hypertrophy. During active atrial systole, blood strikes the noncompliant LV wall, generating low-frequency vibrations audible as S4.
• Clinical Trap: An S4 sound requires active atrial contraction and is therefore absent in atrial fibrillation!
• Contrasting S3: S3 occurs in early diastole during rapid passive ventricular filling into a volume-overloaded, dilated ventricle (systolic heart failure).

Discontinue cervical cancer screening permanently.

• USPSTF & ACOG Guidelines: Cervical cancer screening should be permanently discontinued in women who have undergone a total hysterectomy (cervix removed) for benign disease and who have no prior history of cervical intraepithelial neoplasia (CIN 2 or 3) or cervical cancer.
• Exceptions: Supracervical hysterectomy (cervix intact) or history of CIN 2/3 requires continued routine screening.

Annual Low-Dose Computed Tomography (LDCT) of the chest; discontinue once he has been smoke-free for 15 consecutive years (at age 73) or turns 81.

• USPSTF Criteria: Ages 50–80 + ≥ 20 pack-year history + currently smoke or quit within past 15 years.
• Discontinuation: Discontinue when patient turns 81, has been smoke-free for ≥ 15 consecutive years, or develops comorbidity precluding curative surgery.

Administer the 2-dose series of Recombinant Zoster Vaccine (Shingrix), with the second dose given 2 to 6 months after the first.

• ACIP Recommendations for Shingrix (RZV): Recommended for all adults aged ≥ 50 years, regardless of prior shingles infection or prior receipt of live Zostavax vaccine.
• Efficacy: Provides > 90% protection against herpes zoster and postherpetic neuralgia.

Cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA) targeting Proteinase 3 (PR3-ANCA); Granulomatosis with Polyangiitis (GPA / formerly Wegener's Granulomatosis).

• Diagnostic Triad:

1. *Upper respiratory tract*: Chronic sinusitis, epistaxis, nasal septal perforation, saddle-nose deformity, otitis media, subglottic stenosis.

2. *Lower respiratory tract*: Cough, hemoptysis, bilateral cavitary lung nodules or infiltrates.

3. *Renal*: Pauci-immune necrotizing crescentic glomerulonephritis (rapidly progressive glomerulonephritis, RPGN) with RBC casts.

• Serologic Marker: Antibodies against Proteinase 3 (PR3-ANCA / c-ANCA) with cytoplasmic immunofluorescence pattern (> 90% sensitivity in active systemic disease).
• Biopsy Findings: Necrotizing granulomatous inflammation with geographic necrosis and pauci-immune vasculitis. Treatment: Glucocorticoids + Rituximab or Cyclophosphamide.

Polyarteritis Nodosa (PAN); characteristically spares the pulmonary vasculature (the lungs are NOT involved).

• Pathology: Systemic necrotizing vasculitis of medium-sized and small muscular arteries, leading to transmural inflammation, fibrinoid necrosis, and secondary microaneurysm formation.
• Strong Association: Up to 30% of cases are associated with Hepatitis B virus (HBV) surface antigenemia.
• Hallmark Features: Renal ischemia and secondary renovascular hypertension (due to microaneurysms of renal arteries; note lack of glomerulonephritis), mesenteric ischemia ('abdominal angina'), mononeuritis multiplex (asymmetric peripheral neuropathy), and dermatologic lesions (livedo reticularis, subcutaneous nodules).
• The Definitive Rule: PAN SPARES the pulmonary circulation (contrasting GPA, MPA, and EGPA, which heavily involve the lungs!).