USMLE Q-bank Flashcards
Signs/Sx of Patget disease in terms of:
Skull/bones:
Lab/Imaging findings:
Dx:
Txt:
Skull/bones: hearing loss, dizziness, bone pain, fracture, osteosarcoma or giant cell tumors, nerve impingement causing neuropathy
Lab/Imaging findings: Elevated serum and bone-specific AlkPhos, normal Ca&PO4, plain film shows osteolysis or slerosis
Diagnosis: radiographic findings, elevated AlkPhos
Txt: Bisphosphonates
What is a test to differentiate between elevated AlkPhos from liver vs bone?
Gamma-glutamyl transpeptidase is elevated in liver origin
Migraines:
Sx:
Preventive Txt:
Abortive Txt:
Sx: young females, aura or neurological Sx preceding HAs, unilateral, pulsating, lasting 4-72hrs, associated with photophobia and phonophobia, lack of other Sx such as F, meningeal signs, focal neurological deficits
Preventive txt: Amitriptyline, propranolol
Abortive txt: NSAIDs, triptans (starts early), and antiemetics (chlorpromazine, prochlorperazine, or metoclopramide)
Polymyalgia rheumatica vs rheumatoid arthritis vs viral arthritis vs acute rheumatic fever?
Polymyalgia rheumatica: pain and stiffness of the pelvis and shoulders in older pts; elevated ESR
Rheumatoid arthritis: polyarticular, symmetric arthritis, joint swelling, morning stiffness, systemic symptoms, and present for at least 6 weeks
Viral arthritis: mimic inflammatory arthritis, but morning stiffness lasting less than 30 min, lack of systemic sx
Acute rheumatic fever: recent streptococal infection, with poly-arthritis, carditis, chorea, erythema marginatum and subQ nodules
Mechanism of action of nitroglycerin in angina relief?
Primary effect: Dilation of veins (capacitance vessels) –> decrease preload –> decrease oxygen requirement of heart
Secondary effect: some arterial dilation –> decreases afterload
Minor effect: increase contractility and reflex tachycardia
Note: in healthy subjects it also increase coronary blood flow, but this might not be true in pts with angia
What is Wernicke’s encephalopathy? Triad?
Presentation?
How is it different from Colabamin (B12) deficiency?
Thiamine deficiency in alcoholic patients.
Triad of encephalopathy, oculomotor dysfuction, and gait ataxia
They present with altered mental status, gait instability, nystagmus, and conjugate gaze palsy. There is also reduced ankle reflex.
B12 deficiency causes neurologic deficits including impaired vibratory and position sense, gait abnormalities, and megaloblastic anemia. Occulomotor symptoms are unusual.
What is the severe form of Wernicke’s encephalopathy?
Korsakoff’s syndrome, with irreversible amnesia, confabulation, and apathy
Lewy body dementia:
Presentation:
Pathology:
Txt:
**Presentation: **Alterations in consciousness, disorganized speech, visual hallucination, extrapyramidal symptoms (inc lower ext tone), and compromised executive functions
Pathology: Lewy bodies = eosinophilic intracytoplasmic inclusions representing accumulations of alpha-synuclein protein. Seen in substantia nigra, locus ceruleus, dorsal raphe, and substantia innominata
**Txt: **acetylcholinesterase inhibitors like rivastigmine, or atypical antipsychotics
Side effects of:
Simvastatin:
Angiotensin receptor blocker:
Simvastatin: muscle injury, causing rhabdomyolysi, leading to renal failture. Lab shows elevated creatine phosphokinase. It can also cause elevated transaminases
Antiotensin receptor blocker: hyperkalemia, hypotension, and renal failure
Pheochromocytoma: what are released, presentation, lab finding, and txt
Released substance: catecholamine (epinephrine, norepinephrine, dopamine)
Presentation: paroxysmal Sx of high BP, palpitation, abdominal pain, tremor, excessive sweating
Lab: elevated urinary vanilylmandelic acid level
Txt: alpha blocker first, then followed by beta blockers. Only beta blocker is dangerous because there is unopposed alpha activation, leading to spike in BP
Non-ketotic hyperglycemia:
Cause:
Dx:
Cause: stressor like infection causes elevation of cortisol and catecholamine –> counter insulin
Dx: Serum glulose > 600mg/dL –> serum hyperosmolarity
Sx: Dehydration by osmotic diuresis, altered consciousness, blurry vision (change in lense thickness and intraocular hypotension)
Sx of Creutzfeld-Jakob disease?
Also called Spongiform Encephalopathy
Sx: rapid progressive dementia, myoclonus and sharp, triphsic, synchronous discharges
Pathogenesis of Parkinson’s disease? Sx?
Progressive loss of nigrostriatal dopaminergic neurons
Sx: bradykinesia, resting tremors, cogwheel rigidity, shuffling gaite and masked facies
Pathogenesis and Sx of Huntington’s dementia?
A defect in autosomal dominant gene on chromosome 4 causes striatal neuro-degeneration.
Early onset of dementia between 35-50 years old, progressive choreiform movements of all limbs, grimacing and ataxic gait
Alzheimer’s dementia: histopathological findings
Amyloid plaques, neurofibrillary tangles, and selective loss of cholinergic neurons
Pick’s disease: Presentation, Sx and pathogenesis?
Presentation and Sx: Females in their 50s, changes in personality and language, some in cognitive
Pathogenesis: neurodegenerative disease of the frontal and temporal lobe
What is the antidote for:
- Opiate intoxication
- Benzodiazepine O/D
**Opiate intoxication: **naloxone
**Benzodiapezine O/D: **competitive antagonist of the GABA receptor, such as flumazenil
Presentation of central retinal vein occlusion?
Prediposing conditions?
Acute, painless, monocular loss of vision, with “blood and thunder” appearance on fundoscopic exam, including optic disk swelling, retinal hemorrhage, dilated vein, and cotton wool spots
Associated with coagulopathy, hyperviscosity, chronic glaucoma, and atherosclerotic risk factors
Complications and treatments for increased serum homocysteine?
**Complications: **venous thrombosis, PE, and atherosclerosis due to vacular damage, activation of clotting mechanism, and inhibition of antithrombotic pathways.
**Treatments: **Start pt on heparin and warfarin therapy. Then also add B12, folate and cobalamine because these are co-enzymes for the breakdown pathways of homocysteine. These might lower the level of homocysteine, but might not reserve hypercoagulability.