To really know 2 Flashcards

Question

Pulmonary strongest risk factors:

Answer 1

Lung Cancer Strongest RF: Smoking Others: Radon, asbestos (especially in nonsmokers), secondhand smoke ✅ COPD Strongest RF: Smoking Alpha-1 antitrypsin deficiency (young, nonsmokers)

Answer 2

✅ Alzheimer Disease Strongest RF: Age ApoE4 = genetic risk (late-onset), Down syndrome (early-onset) ✅ Parkinson Disease Strongest RF: Age Pesticide exposure, family history

Answer 3

✅ Colon Cancer Strongest RF: Age ***** Others: Family history (FAP, Lynch), IBD, red meat, low fiber ✅ Breast Cancer Strongest RF: Age Others: BRCA1/2, early menarche/late menopause, nulliparity ✅ Cervical Cancer Strongest RF: HPV infection (types 16, 18) *** Others: Multiple sexual partners, smoking, immunosuppression ✅ Prostate Cancer Strongest RF: Age African American race, family history

Answer 4

✅ DVT/PE Strongest RF: Immobility (hospitalization, surgery) Virchow triad: stasis, hypercoagulability, endothelial injury ✅ Atrial fibrillation → Stroke Strongest RF: Previous stroke/TIA Use CHA₂DS₂-VASc for scoring

Answer 5

✅ Type 2 Diabetes Mellitus Strongest RF: Obesity Others: Sedentary lifestyle, family history, metabolic syndrome ✅ Type 1 Diabetes Strongest RF: Autoimmunity HLA-DR3/DR4, younger age onset

Answer 6

✅ Hepatocellular Carcinoma Strongest RF: Chronic HBV/HCV Others: Cirrhosis, aflatoxins ✅ Endocarditis Strongest RF: Pre-existing valve abnormality IVDU → tricuspid, prosthetic valve → early infection (S. epidermidis)

Answer 7

Function: Filtration of plasma Key concept: Size & charge selective (filters small, + charged better) Clinical: Loss of negative charge → proteinuria (e.g., minimal change disease)

Answer 8

Reabsorbs ~65–80% of filtrate Na⁺, Cl⁻, glucose, AAs, HCO₃⁻, water Key transporters: Na⁺/glucose cotransporter (SGLT2) Carbonic anhydrase → HCO₃⁻ reabsorption 🧪 Drug targets: Acetazolamide → inhibits carbonic anhydrase SGLT2 inhibitors (e.g., empagliflozin) 🧠 Fanconi syndrome: PCT defect → loss of all solutes (glucosuria, phosphaturia, aminoaciduria) PCT handles bulk reabsorption of everything — defects = Fanconi

Answer 9

Function: Passive water reabsorption Impermeable to solutes ↑ Osmolarity deeper into medulla

Answer 10

Function: Reabsorbs Na⁺, K⁺, 2Cl⁻ (NKCC2 transporter) Impermeable to water → "Diluting segment" 🧪 Drug target: Loop diuretics (furosemide, bumetanide) 🧠 Side effects: Hypokalemia, ototoxicity, hypocalcemia

Answer 11

Reabsorbs Na⁺, Cl⁻ via NCC transporter Also reabsorbs Ca²⁺ (PTH increases this) Dilutes urine further 🧪 Drug target: Thiazide diuretics 🧠 Side effect: Hypercalcemia, hypokalemic metabolic alkalosis Loop = most powerful diuretics (→ loss of Ca²⁺) DCT = fine-tunes Na⁺ and retains Ca²⁺ (opposite of loop)

Answer 12

Principal cells: Reabsorb Na⁺ (via ENaC) Secrete K⁺ Aldosterone ↑ ENaC + Na⁺/K⁺ pump expression ADH → inserts aquaporins Intercalated cells: Type A: Secrete H⁺ (acid removal) Type B: Secrete HCO₃⁻ (base removal) 🧪 Drug targets: K⁺-sparing diuretics (spironolactone, amiloride) ADH analogs/antagonists (desmopressin, tolvaptan) 🧠 Defects: Liddle syndrome: ↑ ENaC → HTN + hypokalemia (Tx: amiloride) Nephrogenic DI: ADH resistance → dilute urine CD = controlled by aldosterone (Na⁺/K⁺) & ADH (water)

Answer 13

Action: Elevates the mandible (closes jaw) Innervation: CN V3 (mandibular branch of trigeminal nerve) Note: Very powerful — think of chewing force

Answer 14

Action: Elevates and retracts mandible Innervation: CN V3 Clinical: Large fan-shaped muscle — helps with biting force

Answer 15

Action: Elevates and protracts mandible; side-to-side (grinding) Innervation: CN V3 Works with masseter — creates a sling for elevation

Answer 16

Action: Depresses, protracts, and moves mandible side-to-side Innervation: CN V3 Key point: Only muscle that OPENS the jaw! 🧠 Mnemonic: "Lateral Lowers, the others Elevate" Only depressor of mandible = Lateral pterygoid Jaw deviates TOWARD side of lesion in CN V3 injury (unopposed pterygoid on opposite side) All muscles of mastication = CN V3

Answer 17

📌 Mylohyoid Elevates floor of mouth, assists in swallowing Innervation: Nerve to mylohyoid (branch of CN V3) 📌 Digastric (Anterior belly) Depresses mandible, opens mouth Innervation: Anterior belly: CN V3 Posterior belly: CN VII

Answer 18

Streptococcus pneumoniae Pneumonia, sepsis Haemophilus influenzae Otitis media, meningitis Neisseria meningitidis Meningitis Giardia lamblia Chronic diarrhea (no IgA) Asplenic patients = High risk for sepsis → vaccinate against encapsulated organisms

Answer 19

Aspergillus Invasive pulmonary infection → nodules, hemoptysis Candida (systemic) Fungemia, endocarditis Pseudomonas Ecthyma gangrenosum, sepsis Staph aureus Skin infections, abscesses 🧠 Fungal infections = Big risk in neutropenic fever

Answer 20

C5–C9 (MAC) Neisseria (esp. meningitidis) infections C3 Encapsulated bacteria C1 esterase inhibitor Hereditary angioedema (not infectious, but tested!)

Answer 21

CD4 <200 = start TMP-SMX for PCP prophylaxis CD4 <100 = add Toxo prophylaxis (TMP-SMX) CD4 <50 = consider azithromycin for MAC prophylaxis Oral thrush + recent weight loss + LAD → think HIV → test with ELISA + Western blot ''When CD4 drops, bugs pop!" <500 → EBV, Candida <200 → PCP, JC virus <100 → Toxo, Crypto <50 → CMV, MAC

Answer 22

Muscle glycogen phosphorylase (myophosphorylase) Painful muscle cramps, myoglobinuria with exercise, arrhythmia from electrolyte imbalance “Second wind” phenomenon; ↑ CK Exercise intolerance + no rise in lactate = McArdle Exercise intolerance + ↑ CK, myoglobinuria → McArdle

Answer 23

Lysosomal acid α-glucosidase Cardiomegaly, hypotonia, muscle weakness Early death from cardiomyopathy; not just muscle Early death, cardiomegaly, hypotonia → Pompe

Answer 24

Debranching enzyme (α-1,6-glucosidase) Milder hypoglycemia, muscle weakness, hepatomegaly Limit dextrin accumulation

Answer 25

Carnitine transporter Muscle weakness, hypoketotic hypoglycemia, cardiomyopathy Can't transport FA into mitochondria

Answer 26

Carnitine palmitoyltransferase II Muscle pain, myoglobinuria after fasting/exercise Common cause of rhabdomyolysis

Answer 27

Medium-chain acyl-CoA dehydrogenase Hypoglycemia, vomiting, lethargy, seizures No ketones, after fasting ****Muscle symptoms + hypoketotic hypoglycemia = Think Fatty Acid Oxidation Disorders (not Glycogen Storage Disorders)**** Exercise intolerance + normal CK, no lactic acidosis → FAOD Hypoketotic hypoglycemia in infant → MCAD deficiency

Answer 28

Mitochondrial tRNA mutation Stroke-like episodes, seizures, lactic acidosis Ragged red fibers on biopsy

Answer 29

tRNA mutation Myoclonus, epilepsy, ataxia, muscle weakness Maternal inheritance, heteroplasmy Ragged red fibers = mitochondrial disease (oxidative phosphorylation problem)

Answer 30

Mitochondrial DNA deletion Ophthalmoplegia, ptosis, heart block Onset before 20 yrs

Answer 31

Effect: ↓ GFR (can cause acute kidney injury in certain patients). Mechanism: Dilate efferent arteriole → ↓ glomerular pressure. Risk: Acute kidney injury in bilateral renal artery stenosis. ↑ Creatinine is expected but should be monitored. Tip: Stop ACEi if creatinine ↑ >30% or hyperkalemia occurs. ↓ efferent arteriolar tone → ↓ GFR Be careful in renal artery stenosis or low renal perfusion states Be careful in renal artery stenosis or low renal perfusion states

Answer 32

Effect: Similar to ACE inhibitors. Mechanism: Block angiotensin II receptors → efferent arteriole dilation. Risk: Hyperkalemia, ↓ GFR, especially with NSAIDs or diuretics. Tip: Use when ACEi causes cough or angioedema. ↓ efferent arteriolar tone → ↓ GFR Be careful in renal artery stenosis or low renal perfusion states Be careful in renal artery stenosis or low renal perfusion states

Answer 33

Effect: Mild volume depletion → ↓ renal perfusion. Risks: Hyponatremia, hypokalemia, hyperuricemia, ↑Ca²⁺. May cause pre-renal azotemia in elderly or dehydrated. Tip: Good for calcium stones & osteoporosis + HTN can reduce volume too much → pre-renal AKI Monitor electrolytes and volume status closely

Answer 34

Effect: Strong volume depletion → ↓ renal perfusion. Risks: Hypokalemia, hypocalcemia, ototoxicity, nephrotoxicity. Tip: Use in edematous states (CHF, nephrotic syndrome

Answer 35

Effect: Risk of hyperkalemia, especially in CKD. Mechanism: Aldosterone antagonism → ↓ K⁺ excretion. Tip: Monitor K⁺ closely if used with ACEi/ARB Spironolactone + ACEi/ARB = ↑ risk of hyperkalemia Classic USMLE setup!

Answer 36

Effect: ↓ Renin release (via β1 blockade in JG cells). Renal Risk: Generally safe; no direct nephrotoxicity. Tip: Good for HTN with MI, CHF, but not great alone for CKD

Answer 37

Effect: Mostly neutral on renal function. Tip: Dihydropyridines (e.g., amlodipine) → vasodilate afferent arteriole

Answer 38

Effect: ↑ renal perfusion (via ↓ afterload). Risk: Can cause reflex tachycardia and fluid retention → not first-line

Answer 39

Thoracic Outlet Syndrome (TOS) Most important consequence for USMLE. Compression of structures between anterior/middle scalene, first rib, and clavicle. A. Neurogenic TOS (most common) Compression of lower trunk of brachial plexus (C8–T1). Symptoms: Hand weakness Paresthesias in ulnar distribution (medial forearm/hand) Atrophy of intrinsic hand muscles B. Vascular TOS Compression of subclavian artery or vein. Symptoms: Arm swelling (venous) Cold, pale hand (arterial) ↓ pulses with arm abduction (Adson test positive)

To really know 2 Flashcards

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