High yield review 5 Flashcards
(16 cards)
Hemolytic uremic syndrome
Classic Triad (MUST KNOW):
Microangiopathic hemolytic anemia
Thrombocytopenia
Acute renal failure (↑ BUN/Cr)
Endothelial injury → microthrombi in small vessels → mechanical RBC damage + platelet consumption → renal ischemia
Caused by Shiga toxin from EHEC (O157:H7) → inhibits 60S ribosome
↑ LDH, ↑ indirect bilirubin, ↓ haptoglobin
Schistocytes on blood smear
↑ BUN/Cr, ↓ platelets, normal PT/PTT (non-DIC)
Hemolytic Uremic Syndrome tips
Child + recent bloody diarrhea + renal failure + anemia + low platelets = HUS
Differentiate from TTP:
HUS = more renal
TTP = more neuro, adults, ADAMTS13 deficiency
Schistocytes + thrombocytopenia + renal injury = think HUS/TTP spectrum
If PT/PTT are normal → rules out DIC
Conn Syndrome (Primary Hyperaldosteronism)
Aldosterone-secreting adrenal adenoma → leads to Na⁺ retention, K⁺ loss, and H⁺ loss
Key Clinical Findings:
Hypertension (often resistant)
Hypokalemia → muscle weakness, cramps
Metabolic alkalosis (H⁺ loss from kidneys)
Low renin (negative feedback due to volume expansion)
No edema (due to aldosterone escape via ANP)
USMLE Step 1 Tips:
HTN + hypokalemia + metabolic alkalosis + low renin = Conn syndrome
If renin is high, think secondary hyperaldosteronism (e.g., renal artery stenosis, CHF)
Don’t confuse with Cushing syndrome — Conn has normal cortisol
Know that aldosterone escape prevents edema despite Na⁺ retention
Spironolactone → anti-androgen effects; eplerenone is more selective (fewer side effects)
Hepatitis B Serology Markers
Marker What it Means High-Yield Points
HBsAg
Active infection (acute or chronic)
First marker to appear; if >6 months → chronic
Anti-HBs (HBsAb)
Immunity
From vaccination or recovery (never present with HBsAg)
HBcAb (IgM)
Recent infection
Window period marker
HBcAb (IgG) Past or chronic infection Present for life after exposure
HBeAg
High infectivity
Indicates active viral replication
Anti-HBe
Lower infectivity
Sign of seroconversion toward resolution
HBV DNA
Viral load
Monitors replication and treatment response
Hep B Interpretation Scenarios
Acute Infection
HBsAg+, HBeAg+, Anti-HBc IgM+, Anti-HBs−
High infectivity + active viral replication
🔹 Window Period
HBsAg−, Anti-HBs−, Anti-HBc IgM+
No surface markers detectable; core IgM is key
🔹 Chronic Infection
HBsAg+ >6 months, Anti-HBc IgG+, Anti-HBs−
HBeAg or Anti-HBe depending on replication stage
🔹 Recovery from Infection
HBsAg−, Anti-HBs+, Anti-HBc IgG+
Immune after natural infection
🔹 Vaccination
HBsAg−, Anti-HBs+, Anti-HBc−
No core antibodies (never infected)
Hep B USMLE Step 1 Tips
Only Anti-HBs is protective → appears after vaccination or recovery
Anti-HBc IgM = acute, Anti-HBc IgG = chronic or past infection
In window period, only Anti-HBc IgM may be positive
Vaccinated person: Anti-HBs only
If HBsAg >6 months, it’s chronic HBV
HBeAg = high infectivity, Anti-HBe = lower infectivity
High-Yield Lymphoma Translocations
Lymphoma Translocation Gene Involved Pathway Affected
Burkitt lymphoma t(8;14)
c-MYC (8), IgH (14)
↑ Transcription factor (MYC)
Follicular lymphoma t(14;18)
BCL2 (18), IgH (14)
↓ Apoptosis (BCL2 ↑)
Mantle cell lymphoma t(11;14)
Cyclin D1 (11), IgH (14)
↑ G1→S phase progression
Diffuse large B-cell lymphoma (DLBCL) Variable May have BCL6, BCL2 Often aggressive mutations
Anaplastic large cell lymphoma t(2;5) ALK gene
ALK fusion protein (activating
Lymphoma Translocations tips
USMLE Step 1 Tips
Burkitt = t(8;14), c-MYC, “starry sky”, linked to EBV (especially in endemic/African form)
Follicular = t(14;18), BCL2, inhibits apoptosis → painless waxing/waning lymphadenopathy
Mantle cell = t(11;14), Cyclin D1, older males, CD5+, very aggressive
Know Ig heavy chain = chromosome 14 → common in B-cell lymphomas
Mnemonic to remember translocations:
Burkitt = c-MYC goes wild (8)
Follicular fights apoptosis (BCL2)
Mantle marches cell cycle (Cyclin D1)
CML Translocation
t(9;22)(q34;q11) → Philadelphia chromosome
Creates BCR-ABL fusion gene
BCR (chr 22) + ABL (chr 9) → constitutively active tyrosine kinase
↑ Cell proliferation, ↓ apoptosis
t(9;22) = CML, but also seen in some ALL (bad prognosis in ALL)
If question shows ↑ WBC + basophilia + low LAP → think CML
Imatinib = keyword for targeted therapy
Know the mechanism: BCR-ABL = tyrosine kinase → cell proliferation
Differentiate from leukemoid reaction: in CML → low LAP, basophils present
RR interpretation
Interpretation:
RR Value Meaning
= 1 No association
> 1 Positive association (risk ↑)
< 1 Negative association (protective)
🧠 USMLE Tip:
If RR = 2.0, the exposed group is 2× more likely to develop the disease
If RR = 0.5, the exposure halves the risk
RR is not used in case-control studies (they use odds ratio)
Power in biostatistics
Power (1 − β)
🔹 Definition:
Probability of correctly rejecting the null hypothesis when it is false
Power = 1 − Type II error (β)
🔹 High-Yield Factors That Increase Power:
Larger sample size
Larger effect size
Higher alpha level (e.g., 0.05)
Less variability (lower standard deviation)
🧠 USMLE Tip:
Power increases with sample size → always a correct answer in study design Qs
Low power = higher chance of Type II error (false negative)
A well-powered study is more likely to detect true differences
Most Tested Occupational Exposures & Diseases
Exposure At-Risk Occupation Associated Disease(s)
Asbestos
Shipyard workers, construction, insulation
Mesothelioma, bronchogenic lung cancer, asbestosis
Silica
Sandblasting, mining, quarrying Silicosis, ↑ risk of TB (disrupts macrophages)
Beryllium
Aerospace, electronics
Berylliosis (noncaseating granulomas, like sarcoid)
Benzene
Industrial solvents, rubber, chemical plants
Aplastic anemia, AML
Vinyl chloride
Plastic industry (PVC pipes)
Angiosarcoma of the liver
Arsenic
Pesticides, smelting
Squamous cell skin cancer, liver angiosarcoma
Radon
Underground miners, basements Lung cancer (2nd most common cause after smoking)
Coal dust
Coal miners
Coal workers’ pneumoconiosis (black lung disease)
Nitroglycerin
Munitions workers
Monday disease (reflex tachycardia after weekend off)
Occupational Exposures tips
USMLE Step 1 Tips:
Asbestos = pleural plaques, ferruginous bodies, and mesothelioma with psammoma bodies
Silica = upper lobe nodules, egg-shell calcifications, TB risk ↑
Benzene and vinyl chloride = think blood or liver cancers
If a question includes occupation + lung or hematologic disease, think toxic exposure
Noncaseating granulomas in a worker = berylliosis (mimics sarcoidosis)
Always associate radon with lung cancer, especially in non-smokers
Apolipoproteins
Key Apolipoproteins and Their Functions
Apolipoprotein Location Function
Apo A-I HDL Activates LCAT (cholesterol esterification)
Apo B-48 Chylomicrons Mediates chylomicron secretion from enterocytes
Apo B-100 VLDL, IDL, LDL Binds LDL receptor; required for LDL uptake
Apo C-II Chylomicrons, VLDL Cofactor for lipoprotein lipase (LPL)
Apo E Chylomicron remnants, IDL, HDL Mediates remnant uptake by liver
🧠 USMLE Step 1 Tips
Apo B-48 = chylomicron secretion
Apo B-100 = LDL binding to LDL receptor (think: “B-100 for Bad cholesterol”)
Apo E = involved in remnant clearance → deficiency → Type III dyslipidemia
Apo C-II = activates LPL → necessary for TG breakdown
Apo A-I = activates LCAT → esterifies cholesterol for transport in HDL
Apolipoprotein Clinical Correlations
Familial dysbetalipoproteinemia (Type III):
Defective Apo E → ↑ chylomicron remnants, ↑ IDL
Palmar xanthomas, premature atherosclerosis
Abetalipoproteinemia:
Defective Apo B-48 & B-100 → ↓ chylomicrons, VLDL, LDL
Steatorrhea, acanthocytosis, neurologic defects
