A way to help remember first-generation versus second-generation antihistamines is that first-generation antihistamines often end with the suffix
A way to help remember first-generation versus second-generation antihistamines is that first-generation antihistamines often end with the suffix “-amine” (eg, diphenhydramine, chlorpheniramine, doxylamine), whereas second-generation antihistamines often end with the suffix “-adine” (eg, fexofenadine, loratadine).
A 31-year-old man comes to the physician because of a 2-day history of nausea, abdominal discomfort, and yellow discoloration of the eyes. Six weeks ago, he had an episode of fever, joint pain, swollen lymph nodes, and an itchy rash on his trunk and extremities that persisted for 1 to 2 days. He returned from a backpacking trip to Colombia two months ago. His temperature is 39°C (101.8°F). Physical examination shows scleral icterus. Infection with which of the following agents is the most likely cause of this patient’s findings?
✅ Hepatitis B virus (HBV)
Key Associations:
Virus type: Enveloped, partially double-stranded circular DNA (Hepadnavirus)
Transmission: Parenteral, sexual, perinatal
Characteristic prodrome: Serum sickness-like reaction — fever, arthralgia, lymphadenopathy, pruritic rash (immune complex mediated)
Later findings: Jaundice, ↑ALT/AST, hepatomegaly
Complications: Chronic hepatitis, cirrhosis, hepatocellular carcinoma
Other serum sickness-like causes: Cefaclor, penicillin, streptococcal infection, vaccines
Key buzzwords:
Serum sickness-like reaction → then jaundice → HBV infection
A 42-year-old woman presents with 6 months of fatigue and exertional dyspnea. She had a gastric bypass 2 years ago and lost 45 kg (100 lb). Vitals are normal except for mild tachycardia. Physical exam shows pallor. A peripheral smear shows microcytic, hypochromic red blood cells.
Which of the following sets of laboratory findings on a CBC and iron panel is most likely?
A. Low MCV; high Fe²⁺; low transferrin
B. Low MCV; low Fe²⁺; high transferrin
C. Low MCV; normal Fe²⁺; normal transferrin
D. Normal MCV; low Fe²⁺; low transferrin
E. Normal MCV; normal Fe²⁺; normal transferrin
B. Low MCV; low Fe²⁺; high transferrin
💡 Key Explanation:
Diagnosis: Iron-deficiency anemia secondary to decreased iron absorption after gastric bypass (iron is absorbed in the duodenum and proximal jejunum, which are bypassed).
Labs:
↓ Serum iron
↑ Transferrin (↑ TIBC)
↓ Ferritin
↓ Transferrin saturation
↓ MCV (microcytic anemia)
Mechanism:
Bypass → loss of duodenal absorption → depleted iron stores → liver increases transferrin synthesis to capture more iron.
🧠 High-Yield Pearls:
Iron absorbed as Fe²⁺ (ferrous) in duodenum → remember “Fe²⁺ goes in through DUO.”
Ferritin ↓ = best indicator of depleted iron stores.
Common post–gastric bypass deficiencies: Iron, Vitamin B₁₂, Folate, Calcium, Vitamin D.
The lower extremities receive sympathetic innervation from spinal cord segments at levels
A. L4–L5
B. T1–T4
C. T5–T7
D. T8–T9
E. T11–L2
E. T11–L2
💡 Key Explanation:
Diagnosis: Complex Regional Pain Syndrome (CRPS) — characterized by chronic pain, allodynia, edema, vasomotor/trophic changes (skin, hair, nails) following trauma or surgery.
Pathophysiology: Thought to involve abnormal sympathetic overactivity → vasoconstriction, edema, pain, trophic changes.
Sympathetic innervation:
Upper extremity: T1–T4
Lower extremity: T11–L2
Therefore, a sympathetic block or treatment directed at T11–L2 would reduce excessive sympathetic tone to the affected leg.
🧠 High-Yield Pearls:
CRPS Type I (Reflex Sympathetic Dystrophy): No confirmed nerve injury
CRPS Type II (Causalgia): Confirmed nerve injury
Symptoms: Pain out of proportion, allodynia, swelling, skin/hair/nail changes, stiffness
Treatment: Physical therapy, pain control, sympathetic nerve block, bisphosphonates, corticosteroids
A 55-year-old man presents for a routine exam. His wife reports personality and behavioral changes, including impulsivity and poor food choices. He has gained 30 lbs in the past year. Mental status exam shows difficulty naming objects (anomia) but intact memory.
Neurologic exam is otherwise normal.
Laboratory results are unremarkable.
Which of the following is the most likely finding on diagnostic workup?
A. Brain biopsy demonstrating prion protein
B. Brain mass composed of glial cells positive for GFAP
C. Diffuse cortical atrophy with senile plaques and neurofibrillary tangles
D. High opening pressure on lumbar puncture
E. Temporal and frontal lobe atrophy with silver-staining tau protein aggregates in brain tissue
E. Temporal and frontal lobe atrophy with silver-staining tau protein aggregates in brain tissue
💡 Key Explanation:
Diagnosis: Frontotemporal dementia (FTD), also called Pick disease
Core features:
Early personality/behavior changes (disinhibition, apathy, hyperorality, impulsivity)
Possible language deficits (aphasia)
Memory relatively spared early
Pathology:
Frontal and temporal lobe atrophy
Pick bodies = round tau protein inclusions (silver staining) inside neurons
Distinguishing features:
Alzheimer → memory loss first
Prion disease → rapidly progressive dementia, myoclonus
Normal pressure hydrocephalus → urinary incontinence, gait disturbance, dementia (triad)
🧩 High-Yield Pearls:
FTD = “Personality before memory.”
Often presents in 50s–60s
Associated with tau or TDP-43 inclusions
May resemble psychiatric illness initially
A 58-year-old man with chronic kidney disease is being evaluated for kidney function. You want to measure the volume of plasma that is filtered by the glomeruli per minute. Which of the following is the most accurate way to measure this?
A. Creatinine clearance
B. Para-aminohippurate (PAH) clearance
C. Inulin clearance
D. Blood urea nitrogen
E. Urine sodium concentration
C. Inulin clearance
A patient is being evaluated for renal perfusion. You want to determine the volume of plasma that actually passes through the kidneys per minute. Which substance is best used to measure this?
A. Creatinine
B. Para-aminohippurate (PAH)
C. Inulin
D. Glucose
E. Sodium
B. Para-aminohippurate (PAH)
Explanation:
RPF = volume of plasma flowing through the kidneys per unit time (~600–700 mL/min)
PAH clearance is used because PAH is freely filtered and completely secreted → nearly all plasma is cleared
Provides a measure of renal blood flow/perfusion, not filtration
Key point: RPF tells you how much plasma reaches the kidneys, while GFR tells you how much is filtered.
A 70-year-old woman with chronic heart failure with reduced ejection fraction (HFrEF, EF 35%) presents with worsening dyspnea and bilateral edema. She is started on a medication designed to increase natriuretic peptide levels.
Which of the following is an additional effect of this medication?
A. Activation of neprilysin
B. Decreased levels of aldosterone
C. Decreased levels of bradykinin
D. Inhibition of angiotensin-converting enzyme
E. Vasoconstriction of systemic vessels
B. Decreased levels of aldosterone
💡 Key Explanation:
Medication: ARNI (angiotensin receptor–neprilysin inhibitor, e.g., sacubitril/valsartan)
Sacubitril → inhibits neprilysin, preventing breakdown of natriuretic peptides → vasodilation, natriuresis, diuresis
Valsartan → blocks angiotensin II type 1 receptor → reduces vasoconstriction, aldosterone, and sympathetic activation
Effects of ARNI:
↑ Natriuretic peptides → vasodilation, natriuresis, diuresis
↓ Aldosterone → decreased sodium/water retention
↓ Blood pressure → afterload reduction
No direct effect on ACE or bradykinin metabolism (unlike ACE inhibitors)
Distractors:
A. Activation of neprilysin → wrong; it’s inhibited
C. Decreased bradykinin → wrong; bradykinin actually increases slightly because neprilysin also breaks it down
D. Inhibition of ACE → wrong; that’s a separate drug class
E. Vasoconstriction → opposite effect; ARNI vasodilates
ARNI = Sacubitril (neprilysin inhibitor) + Valsartan (ARB) → main benefits: ↑ natriuretic peptides + ↓ RAAS activation → improved morbidity/mortality in HFrEF.
When treating the cervical spine with high-velocity low-amplitude, placing the patien ________ should be avoided in order to prevent injury
in hyperextension and excessive rotation
A 77-year-old man presents 4 days after coronary angiography via femoral approach for stable angina. He feels well and has no complaints.
Labs: BUN 30 mg/dL (6–20), creatinine 2.7 mg/dL (0.7–1.3) — baseline creatinine was 1.0 mg/dL prior to procedure.
Renal biopsy shows cholesterol clefts in small renal arteries.
What is the most likely cause of this patient’s acute kidney injury?
A. Atheroembolic disease
B. Contrast-induced nephropathy
C. Diabetic nephropathy
D. Membranous nephropathy
E. Renal vein thrombosis
A. Atheroembolic disease
💡 Key Explanation:
Timing: AKI days to weeks after arterial catheterization → consistent with atheroembolic renal disease.
Pathophysiology: Dislodgement of cholesterol crystals from atherosclerotic plaques → lodge in small renal arteries → ischemic injury.
Biopsy hallmark: Biconvex, needle-shaped cholesterol clefts within small arteries/arterioles.
Clinical clues:
Older patients with extensive atherosclerosis
May have blue toes, livedo reticularis, or other embolic phenomena
Contrast-induced nephropathy occurs within 24–48 hours, usually peaks at 3 days, often reversible, and biopsy does not show cholesterol clefts.
Diabetic nephropathy, membranous nephropathy, renal vein thrombosis → chronic or nephrotic presentations, not acute post-procedure AKI.
🧠 High-Yield Pearl:
Atheroembolic renal disease = AKI days after vascular procedure + biopsy showing cholesterol clefts.
Think “blue toe + AKI after catheterization”.
A 45-year-old woman with a history of asthma presents with progressive dyspnea over 2 days, wheezing, rales, and labored breathing. She does not respond to repeated beta-agonist therapy and requires intubation.
Which of the following would most likely be observed in this patient?
A. Normal 1-second FEV1/FVC ratio
B. Elevated serum hydrogen concentration
C. Compensation by decreasing respiratory rate
D. Decreased FVC and total lung capacity
E. Increased expiratory flow rates
B. Elevated serum hydrogen concentration
💡 Key Points:
Diagnosis: Acute severe asthma (status asthmaticus) → life-threatening, unresponsive to standard beta-agonists
Pathophysiology:
Severe airway narrowing → reduced alveolar ventilation
Despite increased respiratory rate, tidal volume is low → CO₂ retention → respiratory acidosis
Leads to elevated serum hydrogen concentration
Other features of status asthmaticus:
Hypoxemia, hypercapnia
Decreased air entry, prolonged expiration
Risk of respiratory failure
Mnemonic: “Status asthmaticus → stuck bronchi → H⁺ rises”
A patient has daytime asthma symptoms >2 times/week (less than daily), 3–4 nocturnal awakenings/month, and minor interference with activities. Pulmonary function is normal between exacerbations.
What is the preferred management?
A. SABA as needed
B. Low-dose ICS daily + SABA as needed
C. Low-dose ICS + LABA daily + SABA as needed
D. Medium/high-dose ICS + LABA + LAMA daily
B. Low-dose ICS daily + SABA as needed
💡 Key Points:
Mild persistent asthma → more frequent symptoms
ICS = inhaled corticosteroid → reduces airway inflammation
SABA = rescue medication
A patient has daytime asthma symptoms ≤2 days/week, ≤2 nocturnal awakenings/month, and normal pulmonary function tests between exacerbations.
What is the preferred management?
A. Low-dose ICS daily
B. SABA as needed
C. Low-dose ICS + LABA daily
D. Medium/high-dose ICS + LABA + LAMA daily
B. SABA as needed
💡 Key Points:
Intermittent asthma → mild, infrequent symptoms
Pulmonary function normal between exacerbations
SABA = short-acting beta-agonist for symptom relief
A patient has daily asthma symptoms, ≥1 nocturnal awakening/week, and some limitation of normal activity.
What is the preferred management?
A. SABA as needed
B. Low-dose ICS daily
C. Low-dose ICS + LABA daily + SABA as needed
D. Medium/high-dose ICS + LABA + LAMA daily
C. Low-dose ICS + LABA daily + SABA as needed
💡 Key Points:
Moderate persistent asthma → daily symptoms
ICS-LABA combination improves asthma control
SABA still used for acute relief
Which of the following are MAOIs used clinically?
A. Fluoxetine, sertraline
B. Phenelzine, tranylcypromine, isocarboxazid, selegiline
C. Amitriptyline, nortriptyline
D. Bupropion, mirtazapine
B. Phenelzine, tranylcypromine, isocarboxazid, selegiline
A patient takes phenelzine, a monoamine oxidase inhibitor (MAOI), and eats aged cheese. Minutes–hours after the meal, he develops a sudden severe headache, palpitations, and a spike in blood pressure.
Which mechanism explains this reaction, and what is it called?
A. Excess dopamine → serotonin syndrome
B. Tyramine displaces norepinephrine → hypertensive crisis
C. Serotonin reuptake inhibition → serotonin syndrome
D. Alpha-2 blockade → reflex tachycardia
B. Tyramine displaces norepinephrine → hypertensive crisis
💡 Key Points:
Timing: Minutes to hours after tyramine-containing meal
Pathophysiology: Tyramine normally metabolized by MAO-A in the gut → when inhibited, tyramine enters circulation → displaces norepinephrine from sympathetic nerve terminals → sudden hypertension, headache, palpitations
High-yield foods: aged cheese, cured meats, fermented foods, draft beer, soy products
A 47-year-old man has been experiencing persistent low mood, excessive sleep, increased appetite, and significant social withdrawal for the past year. He also reports intense generalized anxiety that has not improved with multiple trials of SSRIs and SNRIs. His psychiatrist considers starting a monoamine oxidase inhibitor (MAOI).
MAOIs are particularly indicated for which of the following conditions?
A. Mild, intermittent depression
B. Bipolar mania
C. Atypical depressive disorders and severe anxiety disorders
D. Acute psychosis
E. ADHD
C. Atypical depressive disorders and severe anxiety disorders
💡 Key Points:
MAOIs (e.g., phenelzine, tranylcypromine) are reserved for treatment-resistant depression and atypical depression.
Also used in severe anxiety disorders when first-line treatments fail.
Avoid in mild depression or other psychiatric conditions due to risk of hypertensive crisis and drug interactions.
The pattern of Weber syndrome in a cerebral vascular accident is characterized
by an ipsilateral third nerve palsy causing “down and out” eye deviation, ptosis, mydriasis, and contralateral limb weakness/hemiparesis.
what can maarfann syndrome do to the eyes
separation of the inner layers of the retina from the underlying retinal pigment epithelium
Which of the following treatments works by increasing aqueous humor outflow through contraction of the ciliary muscle in glaucoma?
A. Beta-adrenergic agonists
B. Muscarinic agonists
C. Alpha-1 agonists
D. Ciliary muscle paralysis (atropine)
E. Carbonic anhydrase activation
B. Muscarinic agonists
Explanation:
Glaucoma (most commonly open-angle) is an optic neuropathy causing progressive peripheral vision loss, eventually affecting central vision.
Elevated intraocular pressure (IOP) occurs due to decreased outflow or increased production of aqueous humor.
Muscarinic agonists (e.g., pilocarpine) contract the ciliary muscle, increasing outflow through the trabecular meshwork/Canal of Schlemm, lowering IOP.
Beta-blockers decrease aqueous humor production, not outflow.
Ophthalmic exam may show optic disc cupping and peripheral visual field defects.
Retinoblastoma RB gene function
Rb inhibits the G1-to-S progression in the cell cycle
Frontal lobe abscess: Usually results from
direct spread of frontal or ethmoid sinusitis
Temporal lobe abscess: Typically arises from
otitis media that spreads to the mastoid air cells
Is congestive heart failure transudative or exudative?
transudative
