High yield review 2 Flashcards

Question

Mesoderm – “Meat, Muscle, Movement, and Middle Stuff”

Answer 1

Muscles (skeletal, smooth, cardiac) Bones Connective tissue Dermis Blood vessels & blood cells Heart Kidneys & adrenal cortex Reproductive organs (ovaries, testes, uterus) Lymphatics Spleen Peritoneum, pleura, pericardium ✅ USMLE Tip: "Mesoderm = the core and transport systems: muscle, blood, bone, heart, kidney, and reproductive organs." For anything involving movement or pumping (heart, muscle, vessels), it’s mesoderm.

Answer 2

Surface Ectoderm: Epidermis, hair, nails Lens of the eye Enamel of teeth Anterior pituitary (Rathke pouch) Inner ear (sensory epithelium) Anal canal below pectinate line ✅ Tip: "Surface = skin stuff + some specialized coverings (lens, enamel)." 2. Neural Tube (Neuroectoderm): CNS (brain, spinal cord) Retina Pineal gland Posterior pituitary ✅ Tip: "Neural tube = CNS and eye stuff." 3. Neural Crest: PNS (cranial nerves, DRG, autonomic ganglia) Adrenal medulla Schwann cells Melanocytes Arachnoid & pia mater Pharyngeal arch bones (face/skull) Odontoblasts Endocardial cushions ✅ Tip: “Neural Crest = MAGIC CREST” Melanocytes Adrenal medulla Ganglia (PNS) Iris stroma Cranial nerves Conotruncal heart Retina (peripheral structures) Enteric nervous system Schwann cells Teeth (odontoblasts) Neural crest pops up in syndromes: DiGeorge, Hirschsprung, neuroblastoma, melanoma Surface ectoderm vs neuroectoderm vs neural crest is a classic distractor trap. Know their differences cold

Answer 3

Most often due to deficiency in pyruvate dehydrogenase complex (PDH) or complex I, II, IV, or V of the electron transport chain. Leads to failure of oxidative phosphorylation → lactic acidosis + energy failure in high-demand tissues (brainstem, basal ganglia). Key Buzzwords: "Previously developing normally, now regressing" "Elevated lactate in serum and CSF" "Symmetric lesions in basal ganglia and brainstem on MRI" Diagnosis MRI: Symmetric necrotic lesions in basal ganglia, midbrain, brainstem. Elevated lactate and pyruvate Genetic testing: mtDNA or nuclear gene mutations (e.g., SURF1 gene)

Answer 4

1. Mitochondrial inheritance clues: If mom has mild symptoms and multiple children affected, think mtDNA. Look for systemic findings + neurology + lactic acidosis. ✅ 2. Think energy failure: Leigh = central nervous system + lactic acidosis = mitochondrial disease. ✅ 3. "Symmetric lesions in basal ganglia" on MRI is classic and heavily tested. ✅ 4. Don't confuse with Tay-Sachs or Krabbe: Leigh = lactic acidosis + mitochondrial inheritance Tay-Sachs = no hepatomegaly + cherry-red macula Krabbe = globoid cells + peripheral neuropathy

Answer 5

disorder of iron overload due to: Primary (hereditary): Mutation in HFE gene (usually C282Y homozygous) Secondary: Chronic transfusions (e.g., in β-thalassemia major) Defective HFE gene → ↓ hepcidin → ↑ intestinal iron absorption Excess iron deposits in organs → free radical damage via Fenton reaction (iron generates ROS) “Bronze diabetes” “MCP joint pain” “Cirrhosis + diabetes + hyperpigmentation” “Elevated ferritin, low TIBC” “Mutation in HFE gene”

Answer 6

A defect in NADPH oxidase, an enzyme used by neutrophils to generate reactive oxygen species (ROS) for killing pathogens. Leads to impaired oxidative burst → inability to destroy certain pathogens inside phagolysosomes ↓ production of superoxide → ↓ hydrogen peroxide → defective killing of catalase-positive organisms (they degrade their own H₂O₂, so neutrophils can't use it). “Recurrent infections with catalase-positive organisms” “Negative nitroblue tetrazolium (NBT) test” “Abnormal dihydrorhodamine (DHR) flow cytometry test”

Answer 7

Catalase-Positive Organisms (High-Yield!) 🔺 “You Need PLACESS for your cats” Nocardia Pseudomonas Listeria Aspergillus Candida E. coli Staphylococcus aureus Serratia ✅ These organisms neutralize their own H₂O₂ — making it harder for neutrophils to kill them.

Answer 8

Chromosome 16 (4 α-globin genes) Cis deletion (Asian) vs trans deletion (African) 🔹 Types: Deleted Genes Condition Features 1 Silent carrier Asymptomatic 2 α-thalassemia trait Mild anemia 3 HbH disease Moderate to severe anemia; excess β-chains form HbH (β₄) 4 Hydrops fetalis Incompatible with life; Hb Barts (γ₄) ✅ USMLE Tip: Hydrops fetalis + Hb Barts (γ₄) = alpha-thalassemia major, especially in Asian ancestry. mjn

Answer 9

Chromosome 11 Mutations (not deletions) in β-globin gene 🔹 Types: Type Description Features β⁺ (minor) ↓β-chain Usually asymptomatic; ↑HbA₂ (diagnostic) β⁰ (major) Absent β-chain Severe anemia, transfusion-dependent 🔹 Beta-Thalassemia Major (Cooley’s Anemia): Presents at 6 months (after HbF declines) Crew-cut skull on X-ray (marrow expansion) Chipmunk facies Hepatosplenomegaly Risk of iron overload from transfusions ✅ USMLE Tip: Think Mediterranean descent + severe microcytic anemia + ↑HbF + skeletal deformities.

Answer 10

Chromosome 11 Mutations (not deletions) in β-globin gene 🔹 Types: Type Description Features β⁺ (minor) ↓β-chain Usually asymptomatic; ↑HbA₂ (diagnostic) β⁰ (major) Absent β-chain Severe anemia, transfusion-dependent 🔹 Beta-Thalassemia Major (Cooley’s Anemia): Presents at 6 months (after HbF declines) Crew-cut skull on X-ray (marrow expansion) Chipmunk facies Hepatosplenomegaly Risk of iron overload from transfusions ✅ USMLE Tip: Think Mediterranean descent + severe microcytic anemia + ↑HbF + skeletal deformities.

Answer 11

Function: Breaks down hydrogen peroxide (H₂O₂) → water + oxygen Prevents oxidative damage in cells 🧠 USMLE Tips: Catalase-positive organisms (e.g. S. aureus, Aspergillus) can neutralize their own H₂O₂. This makes them harder to kill in CGD (NADPH oxidase deficiency) because they eliminate the little H₂O₂ that neutrophils could use. ✅ Key organisms: S. aureus, Pseudomonas, Candida, E. coli, Aspergillus, Serratia, Nocardia 📌 Step 1 Buzzword: “Recurrent infections with catalase-positive organisms” → think CGD.

Answer 12

Function: Breaks down elastin, a key component in lung and blood vessel tissue. Secreted by neutrophils and macrophages Normally inhibited by α1-antitrypsin 🧠 USMLE Tips: Uninhibited elastase → lung tissue destruction → panacinar emphysema, especially in α1-antitrypsin deficiency Elastase is a major contributor to alveolar wall breakdown in smokers and inherited disease ✅ Think: “Unopposed elastase = lung destruction = emphysema (lower lobes in A1AT)” 📌 Step 1 Buzzword: “Young non-smoker with emphysema” → test for α1-antitrypsin deficiency.

Answer 13

Function: Found in azurophilic granules of neutrophils Uses H₂O₂ + Cl⁻ → makes hypochlorous acid (HOCl) = potent antimicrobial 🧠 USMLE Tips: MPO deficiency = ↓ microbial killing, but milder than CGD Patients may have recurrent Candida infections, but often asymptomatic MPO-positive granules help identify AML (especially M3 subtype) ✅ Diagnostic Clue: MPO stain positive in myeloid cells, negative in lymphoid leukemia 📌 Step 1 Buzzword: “Recurrent Candida + normal NBT test” → suspect MPO deficiency

Answer 14

Function: Converts superoxide (O₂*⁻) → H₂O₂ Protects cells from ROS damage Found in mitochondria (SOD1 in cytosol, SOD2 in mitochondria) 🧠 USMLE Tips: SOD1 mutations associated with familial ALS (Amyotrophic Lateral Sclerosis) Leads to motor neuron death via oxidative stress ✅ Think: Antioxidant defense gone wrong → neuron degeneration 📌 Step 1 Buzzword: “SOD1 mutation → progressive motor weakness → ALS”

Answer 15

Sudden, severe epigastric pain → radiates to back Nausea, vomiting Worse after meals, improves with leaning forward Most Common Causes: 🔑 “GET SMASHED” mnemonic (first 2 are the most tested): Gallstones ✅ Ethanol (alcohol) ✅ Trauma (especially kids) Steroids Mumps Autoimmune Scorpion sting Hypercalcemia, Hypertriglyceridemia (>1000 mg/dL) ✅ ERCP Drugs (azathioprine, diuretics, valproate)

Answer 16

Amylase ↑ (nonspecific) Lipase ↑↑ (more specific) ✅ ALT/AST May be ↑ if biliary cause Hypocalcemia Due to fat saponification ✅

Answer 17

Definition: Fully differentiated B cells that produce antibodies (immunoglobulins). Do not express surface immunoglobulin or CD20 once mature. Secrete large amounts of IgG, IgA, IgM, IgE, or IgD (class-switched) Important in humoral immunity 🔬 Morphology (Path buzzwords): "Clock-face" chromatin pattern (eccentric nucleus) Basophilic cytoplasm (due to rER) Perinuclear clearing (Golgi apparatus) 🧠 USMLE Tips: ✅ Seen in chronic inflammation and autoimmune diseases ✅ Multiple myeloma = malignant plasma cells Look for: M-spike, CRAB (hyperCalcemia, Renal failure, Anemia, Bone lesions) ✅ Plasma cells are not typically found in circulating blood 📌 Buzzword: “Clock-face chromatin in bone marrow” = plasma cell

Answer 18

Innate lymphoid cells (type of lymphocyte) Kill virus-infected and tumor cells without prior sensitization 🔑 Mechanism: Use perforin + granzymes to induce apoptosis Recognize cells with: ↓ or absent MHC I (major clue!) Antibody-coated cells (ADCC via CD16) 🧪 Surface Markers: CD16 (binds Fc of IgG) CD56 (NK-specific marker) No TCR or BCR! 🧠 USMLE Tips: ✅ NK cells are part of the innate immune system but are lymphoid in origin ✅ Test questions often mention “cells lacking MHC I are targeted by…” → NK cells ✅ IL-2, IL-12, IFN-α, IFN-β activate NK cells 📌 Buzzword: “Lymphocyte that kills cells without MHC I” = NK cell

Answer 19

Presents endogenous antigens (e.g., viral proteins, tumor antigens) Presents to CD8+ cytotoxic T cells 🧱 Structure: Composed of heavy α chain + β2-microglobulin Encoded by HLA-A, HLA-B, HLA-C 📍 Expressed On: All nucleated cells (except RBCs) 🔁 Processing Pathway: Antigen degraded by proteasome Transported via TAP into RER Loaded onto MHC I → surface expression ✅ USMLE Tips: Virally infected cells → activate CD8+ T cells via MHC I NK cells kill cells missing MHC I MHC I expression is downregulated by viruses → NK cells step in 📌 Buzzwords: "Endogenous antigen" → "MHC I" "CD8+ T cell activation" → "MHC I" "TAP transporter defect" = Bare Lymphocyte Syndrome Type I

Answer 20

Function: Presents exogenous antigens (e.g., bacterial proteins) Presents to CD4+ helper T cells 🧱 Structure: Composed of α and β chains Encoded by HLA-DP, HLA-DQ, HLA-DR 📍 Expressed On: APCs only: Dendritic cells, macrophages, B cells 🔁 Processing Pathway: Antigen phagocytosed → loaded in acidified endosome MHC II synthesized in RER with invariant chain Invariant chain guides MHC II → endosome → gets degraded → allows peptide binding ✅ USMLE Tips: Invariant chain blocks peptide binding in ER Defect in MHC II expression → Bare Lymphocyte Syndrome Type II (↓ CD4+ T cell activation) Superantigens (e.g., TSST-1) cross-link MHC II + TCR → massive cytokine release 📌 Buzzwords: "Exogenous antigen" → "MHC II" "CD4+ T cell activation" → "MHC II" "Invariant chain" → MHC II trafficking

Answer 21

Types of Diverticula (Very Testable) Type Example Description USMLE Key True Meckel’s diverticulum Contains all layers of bowel wall Rule of 2’s False (pseudodiverticulum) Colonic diverticula Only mucosa and submucosa herniate through muscle Most common

Answer 22

Common in elderly (usually >60) Caused by increased intraluminal pressure Found mostly in sigmoid colon Often asymptomatic 📛 Diverticulitis = Inflammation of diverticula LLQ pain, fever, leukocytosis Can lead to abscess, fistula, perforation, or obstruction 📌 Buzzwords: "LLQ pain + fever + leukocytosis" = Diverticulitis "Air in urine" = Colovesical fistula

Answer 23

Rule of 2’s (Step 1 favorite!): 2% of population 2 feet from ileocecal valve 2 inches long Presents before age 2 May have 2 types of ectopic tissue: gastric & pancreatic 🔬 Cause: Failure of vitelline (omphalomesenteric) duct to involute 🧪 Presentation: Painless rectal bleeding in a child Can mimic appendicitis if inflamed 🧪 Diagnosis: 99mTc pertechnetate scan (detects gastric mucosa) 📌 Buzzwords: “Child with painless rectal bleeding” → Meckel “Ectopic gastric mucosa” → ulceration, bleeding Meckel's = painless bleeding in child; think gastric acid in wrong place 5. 99mTc scan detects gastric mucosa — classic for Meckel

Answer 24

✅ 1. Dysphagia to both solids and liquids = think motility disorder → achalasia ✅ 2. Bird beak on barium swallow = classic buzzword ✅ 3. Confirm with manometry (best test!) ✅ 4. Always rule out cancer (pseudoachalasia) with endoscopy, especially in older patients ✅ 5. Chagas disease is the most common secondary cause (Trypanosoma cruzi destroys myenteric plexus) 📌 Mnemonic to remember: Achalasia = Absent peristalsis + Absent LES relaxation

Answer 25

Think microdeletion = loss of multiple genes = syndromic presentation Use FISH to detect small deletions (e.g., DiGeorge) 📌 Buzzword: “Elfin face + friendliness” = Williams 📌 “Absent thymic shadow + hypocalcemia” = DiGeorge Classic USMLE Examples: Cri-du-chat syndrome: 5p deletion → microcephaly, high-pitched crying, epicanthal folds Williams syndrome: 7q11.23 deletion → elfin facies, hypercalcemia, extreme friendliness DiGeorge syndrome (22q11 deletion) → thymic aplasia, cardiac defects, hypocalcemia

Answer 26

Nondisjunction during meiosis I → both homologs go to one gamete Nondisjunction during meiosis II → sister chromatids fail to separate Increased maternal age = higher risk 📌 Buzzword: “AMA (Advanced maternal age) + flat facial profile + hypotonia” = Trisomy 21 Classic USMLE Examples: Trisomy 21 (Down syndrome): mostly from maternal meiosis I nondisjunction Turner syndrome (45,X): monosomy X Klinefelter syndrome (47,XXY)

Answer 27

Inversion of a chromosome segment that does NOT include the centromere. 🧠 USMLE Focus: Usually less harmful, but crossing over in meiosis can cause dicentric or acentric chromatids → miscarriage or abnormal gametes ✅ USMLE Tip: Paracentric = “para”llel to the centromere (does not include it) 📌 Remember: More likely to produce nonviable gametes due to acentric fragments

Answer 28

Inversion of a chromosome segment that includes the centromere. 🧠 USMLE Focus: Can lead to duplications/deletions during meiosis due to misalignment ✅ USMLE Tip: Pericentric = includes the “peri”-meter of the centromere 📌 Buzzword: Structural chromosomal rearrangement involving centromere = pericentric

Answer 29

Exchange of genetic material between two non-homologous chromosomes. Usually balanced (no loss/gain of genetic material), so carriers are often asymptomatic. 🧠 Clinical Relevance: May become unbalanced during meiosis → miscarriage, infertility, or abnormal offspring. Seen in some cancers (e.g., Philadelphia chromosome: t(9;22) in CML) ✅ USMLE Tips: Balanced → normal phenotype Unbalanced → congenital abnormalities or miscarriage Think cancer when you see specific translocations 📌 Buzzwords: “Balanced translocation, normal parent, child with birth defects” → unbalanced segregation “t(9;22)” → Philadelphia chromosome, CML

Answer 30

Fusion of two acrocentric chromosomes (13, 14, 15, 21, 22) at the centromere → loss of short arms (usually nonfunctional rRNA genes) 🧠 Clinical Relevance: Most common chromosomal translocation in humans Can lead to familial Down syndrome (46 chromosomes, but one chromosome 21 translocated onto 14 or 21) ✅ USMLE Tips: Parent with balanced Robertsonian translocation can have a child with trisomy 21 Check karyotype in recurring Down syndrome cases or young mother 📌 Buzzwords: “Child with Down syndrome, mother has normal phenotype” → check for Robertsonian translocation

Answer 31

Microsatellite DNA (3-nucleotide sequence) abnormally expanded → gene silencing or toxic proteins 🧠 Classic Diseases (and repeats): Disease Repeat Inheritance Clue Huntington CAG AD Chorea, caudate atrophy Fragile X CGG X-linked Big jaw, ears, testes Friedreich ataxia GAA AR Ataxia, hypertrophic cardiomyopathy Myotonic dystrophy CTG AD Cataracts, toupee, gonadal atrophy ✅ USMLE Tips: Anticipation = worsening symptoms in successive generations Repeats often occur in noncoding (Fragile X, Friedreich) or coding regions (Huntington) 📌 Buzzwords: “Symptoms start earlier in each generation” → anticipation “Chorea + dementia + CAG” → Huntington

Answer 32

Both copies of a chromosome (or part) are from one parent, none from the other 🧠 Types: Heterodisomy (meiosis I error) → 2 different homologs from one parent Isodisomy (meiosis II error or postzygotic duplication) → 2 identical copies 🧠 Diseases: Prader-Willi syndrome (maternal UPD of chromosome 15) → no paternal expression Angelman syndrome (paternal UPD of 15) → no maternal expression ✅ USMLE Tips: Think of imprinting disorders when UPD is mentioned UPD + imprinting = parent-of-origin effect 📌 Buzzwords: “Child has deletion on maternal 15, father is carrier, child is unaffected” → Angelman via UPD “Imprinting + uniparental disomy” → Step 1 loves this combo!

Answer 33

Occurs in tall, thin young males (usually during rest) Caused by rupture of apical subpleural blebs ✅ USMLE Tip: Think sudden chest pain + dyspnea in young healthy male

Answer 34

Occurs in people with underlying lung disease (e.g., COPD, cystic fibrosis, TB) Air enters pleural space from damaged alveoli ✅ USMLE Tip: COPD + sudden worsening = secondary pneumothorax

Answer 35

Life-threatening Air enters pleural space but cannot escape → tracheal deviation away from affected side Leads to compression of great vessels → ↓ venous return → hypotension, JVD ✅ USMLE Tip: Hypotension + unilateral absent breath sounds + tracheal shift = Tension pneumothorax Immediate needle decompression (2nd ICS, midclavicular

Answer 36

Due to chest trauma, rib fracture, stab wound, or during procedures (e.g., central line) ✅ USMLE Tip: Trauma + dyspnea + absent breath sounds = rule out pneumothorax ✅ USMLE Tip: "No lung markings peripherally" = buzz phrase for pneumothorax

Answer 37

⬆️ INCREASED: Cardiac output (CO): via ↑ heart rate and stroke volume Heart rate (HR) Venous return Systolic blood pressure (due to increased CO) Muscle blood flow (vasodilation from local metabolites like lactate, K⁺, adenosine) ⬇️ DECREASED: Total peripheral resistance (TPR): due to skeletal muscle vasodilation, despite ↑ SNS tone Diastolic blood pressure: usually no change or slight decrease ✅ USMLE Tip: “During exercise, systolic BP ↑, diastolic BP ↓ or unchanged” is a classic question setup.

Answer 38

⬆️ INCREASED: O₂ consumption CO₂ production Minute ventilation (↑ tidal volume early, then ↑ respiratory rate) O₂ diffusion capacity ✅ USMLE Tip: PaO₂ and PaCO₂ remain constant in healthy individuals during exercise due to compensatory ventilation

Answer 39

Parameter Arterial Venous pO₂ ~unchanged ↓ (more O₂ extracted) pCO₂ ~unchanged ↑ (more CO₂ released) pH ~unchanged ↓ (lactic acidosis in intense exercise) ✅ USMLE Tip: If you see ↓ pH, ↑ CO₂ in venous blood, that's normal during exercise But arterial pH only drops in very intense exercise (lactic acid buildup)

Answer 40

Early (first few minutes): ATP from stored ATP and creatine phosphate Anaerobic glycolysis → lactic acid Later: Aerobic metabolism kicks in (glucose, free fatty acids, muscle glycogen) ✅ USMLE Tip: Creatine phosphate = first-line ATP source Lactic acid = main source of acidosis in strenuous activity

Answer 41

Hormone Effect Catecholamines ↑ HR, ↑ BP, ↑ lipolysis Glucagon ↑ gluconeogenesis, ↑ glycogenolysis Cortisol Maintains blood glucose Growth hormone ↑ lipolysis, protein synthesis ✅ USMLE Tip: These hormones work together to maintain glucose levels during exercise.

Answer 42

Etiology – Primary (Idiopathic or Heritable) Often due to **inactivating mutation in the BMPR2 gene → ↓ apoptosis of vascular smooth muscle cells → excess proliferation → narrowed pulmonary arteries Pulmonary vascular remodeling → ↑ pulmonary vascular resistance Leads to RV hypertrophy → cor pulmonale → right heart failure

Answer 43

Autosomal dominant with incomplete penetrance BMPR2 = bone morphogenetic protein receptor type 2 → normally inhibits vascular smooth muscle proliferation ✅ USMLE Tip: “Young woman + progressive dyspnea + loud P2” = think primary PAH, especially with BMPR2 mutation. ✅ USMLE Tip: Use right heart cath to confirm diagnosis Echo is initial test, not confirmatory

Answer 44

Treatment Drug Class Mechanism Endothelin receptor antagonists (e.g., bosentan) ↓ vasoconstriction and proliferation PDE-5 inhibitors (e.g., sildenafil) ↑ cGMP → vasodilation Prostacyclin analogs (e.g., epoprostenol) Vasodilation, ↓ platelet aggregation ✅ USMLE Tip: Bosentan = blocks endothelin → ↓ vascular smooth muscle proliferation

Answer 45

Cerebellar Part Function Mnemonic Lateral hemispheres Coordinate voluntary movement of limbs (extremities) Lateral = Limbs Intermediate zone (paravermis) Controls proximal limb and trunk coordination Vermis Controls axial/trunk muscles, posture, balance Vermis = Vertical Flocculonodular lobe Maintains balance and eye movements (vestibular input) Flocc = Falling (balance)

Answer 46

Cerebellar output is inhibitory (GABA) from Purkinje cells Dentate = lateral hemisphere → planning movement Fastigial = vermis → posture and balance Cerebellar lesions = ipsilateral symptoms (due to double decussation) Lesion of vermis = truncal ataxia (drunken gait) Lesion of lateral hemisphere = limb dyscoordination

Answer 47

Lesion Location Findings Side Lateral hemisphere Limb ataxia, intention tremor, dysmetria, dysdiadochokinesia Ipsilateral Vermis Truncal ataxia, wide-based gait, postural instability Midline Flocculonodular lobe Balance issues, nystagmus, vertigo Midline Cerebellar tonsil herniation Life-threatening—compresses brainstem Alcoholic cerebellar degeneration: atrophy of anterior vermis → truncal ataxia Medulloblastoma in kids: often in vermis → gait instability Stroke: PICA (posterior inferior cerebellar artery) → lateral medullary syndrome ± cerebellar signs

Answer 48

Sudden drop in school performance Changes in friends or isolation Mood swings, irritability Poor hygiene or odd sleep patterns Paranoia or hallucinations (e.g., synthetic drugs) ✅ USMLE Tip: "Teen with declining grades, new impulsivity, withdrawn behavior" → think screen for substance use

Answer 49

Most common in adolescents Signs: red eyes, increased appetite, dry mouth, slow reflexes Can impair memory and motivation ("amotivational syndrome") ✅ USMLE Tip: "Teen with red eyes, poor focus, low motivation" = classic for marijuana use

Answer 50

Often used by younger adolescents (10–14 years) Signs: rash around mouth (glue sniffers rash), dizziness, slurred speech Can cause sudden cardiac death ("sudden sniffing death") ✅ USMLE Tip: Young teen + perioral rash + disorientation = inhalant abuse

Answer 51

CNS stimulants → euphoria, hyperactivity, mydriasis (dilated pupils) Cocaine: vasospasm → MI or stroke in young people Amphetamines: also used for ADHD → potential misuse ✅ USMLE Tip: "Teen with chest pain, anxiety, dilated pupils" → think cocaine

Answer 52

LSD: hallucinations, visual distortions, euphoria PCP: violent behavior, nystagmus, hallucinations, psychosis ✅ USMLE Tip: Teen + violent outbursts + vertical nystagmus = PCP intoxication

Answer 53

Less common in teens than THC or alcohol, but rising Signs: miosis (pinpoint pupils), respiratory depression, track marks ✅ USMLE Tip: Teen with pinpoint pupils + altered consciousness → opioid overdose

Answer 54

✅ Most common: Marijuana ✅ Red flags: behavioral + academic changes ✅ Inhalants = perioral rash, early teen use ✅ PCP = violent + vertical nystagmus ✅ Opioids = pinpoint pupils + sedation ✅ Always use nonjudgmental, confidential screening ✅ Know motivational interviewing as first-line approach

Answer 55

Type Main Problem EF Cause Systolic HF (HFrEF) ↓ Contractility < 40% Ischemia, MI, dilated cardiomyopathy Diastolic HF (HFpEF) ↓ Relaxation (stiff ventricle) ≥ 50% HTN, aging, restrictive/hypertrophic cardiomyopathy ✅ USMLE Tip: HFrEF = reduced EF = eccentric hypertrophy HFpEF = preserved EF = concentric hypertrophy

Answer 56

Pulmonary edema, dyspnea, orthopnea, paroxysmal nocturnal dyspnea S3 gallop (systolic) or S4 (diastolic) ✅ Tip: Orthopnea = fluid backs up when lying down → think left-sided failure

Answer 57

Peripheral edema, JVD, hepatomegaly, ascites Often secondary to left-sided HF or cor pulmonale (from lung disease) ✅ Tip: JVD + leg edema + clear lungs = pure right-sided HF ✅ USMLE Tip: BNP = differentiates dyspnea from HF vs. COPD/asthma

Answer 58

↑ SNS → ↑ HR, contractility → short-term help, long-term harm RAAS activation → vasoconstriction + Na⁺/H₂O retention ↑ ADH → water retention Natriuretic peptides → counteract RAAS ✅ Tip: These all increase afterload and preload, worsening HF over time

Answer 59

Drug Class Use Notes ACE inhibitors / ARBs 1st line for HFrEF ↓ mortality Beta-blockers Carvedilol, metoprolol, bisoprolol Use in stable HFrEF Diuretics Symptom relief Furosemide = ↓ volume overload Spironolactone ↓ mortality in HFrEF Aldosterone blocker Hydralazine + nitrates African American patients Mortality benefit in HFrEF Sacubitril/valsartan ARNI Newer combo that ↑ natriuretic peptides ✅ Tip: ACE inhibitors, beta-blockers, spironolactone = mortality reducers ✅ Loop diuretics = symptom relief only, not survival benefits Heart failure cells = hemosiderin-laden macrophages in lungs → from chronic pulmonary congestion ✅ Tip: “Brownish cytoplasmic granules in alveoli” = chronic left HF

Answer 60

1. Distinguish NF1 vs NF2: • NF1: Chromosome 17 (1 and 7 = 17), skin tumors, optic gliomas. • NF2: Chromosome 22 (think “2” in NF2 → 22), bilateral vestibular schwannomas (hearing loss). 2. Café-au-lait spots appear early (even in infancy). • So if a young child has café-au-lait spots → think NF1. 3. Genetics questions: • Even if the parents are unaffected, new (de novo) mutations occur in about 50% of NF1 cases. 4. NF1 is a RASopathy: • Questions may associate it with overactive Ras signaling and MAPK pathway overactivation. 5. Lisch nodules = pathognomonic for NF1. • If you see a Step 1 question mentioning iris hamartomas → immediately think NF1. 6. Pheochromocytoma association: • Always check blood pressure! (Hypertension clue in NF1 can hint pheochromocytoma). 7. Plexiform neurofibroma = pathognomonic (large, “bag of worms” feeling on palpation). 8. Malignancy risk: • Malignant peripheral nerve sheath tumors (MPNST) are a feared complication. 9. Autosomal Dominant rule of thumb: • One affected parent can transmit it to ~50% of offspring. 10. Chromosome memory trick: • “17 letters” in “von Recklinghausen” → Chromosome 17.

High yield review 2 Flashcards

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