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19 Cards in this Set
- Front
- Back
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What chemicals act on NMDA receptors? What Rx's antagonize?
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NMDA Receptors activated by:
- Glutamate - Glycine (co-agonist) NMDA Antagonists: - Ketamine (arylcyclohexylamine) - Dextromethorphan (codeine analog; anti-tussive) |
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What are the causes of SMA syndrome and what part of the gut is affected?
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Causes of SMA syndrome:
1) ↓ mesenteric fat 2) lordosis (profound) 3) scoliosis sx correction Entraps the transverse duodenum → partial obstruction symptoms |
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What are the findings of Tuberous Sclerosis?
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AD, variable presentation (incomplete penetrance)
HAMARDOMAS - H-amartomas (CNS, skin) - A-denoma sebaceum (face) - M-itral regurgitation - A-sh leaf spots - R-habdomyoma (heart) - DO-ominant (AD) - M-ental retardation - A-ngiomyolipoma (renal) - S-eizures |
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What is the cellular effect of morphine and its receptor?
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Morphine activates mu receptor.
GPCR that increases K+ efflux out of cells (phosphorylates to open them and therefore further polarize the cell and prevent excitation) |
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What are the characteristic findings of papillary adenocarcinoma?
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1) Psammoma bodies (concentric calification)
2) "Orphan Annie" nuclei (appear empty) NOTE: papillary carcinoma of thyroid is most common endocrine cancer / thyroid cancer |
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What diseases are associated w/ Psammoma bodies?
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PSaMMoma:
-P = Papillary Thyroid -S = Serous Ca (Ovaries) -M = Meningioma -M = Mesothelioma |
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How do ß-blockers help tx glaucoma? What are some examples?
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Decrease aqueous humor production by the epithelial cells of the ciliary body.
T-arget C-iliary B-ody: -timolol -carteolol -betaxolol |
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What are the chemical effects of Conn's syndrome?
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Conn's = Primary Hyper-Aldosteronism
↑Na+ ↓K+ Metabolic Alkalosis ↓Renin |
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What is the difference between primary and secondary hyperaldosteronism?
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Primary = Too much ADH (d/t tumor or hyperplasia of zona glomerulosa in cortex)
Secondary = Too much RAAS activation (d/t perceived low volume by kidneys) |
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How does diphtheria cause disease?
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Via it's exotoxin = AB Exotoxin:
- B = Binding - A = Active (ADP ribosylates a histidine residue on EF-2 and inhibits ribosomal translation) Toxic to: - Cardiac (cardiomyopathy, heart failure) - Neurons (neuropathy) |
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What are the auto-antibodies found in SLE?
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1) ANA (antinuclear) = sensitive but not specific
2) anti-dsDNA = Specific (only 60% SLE have these) 3) anti-snRNP (anti-Smith) = Specific (20-30% SLE have these) |
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What is a major complication of systemic mycoses treatment?
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Amphotericin B causes nephrotoxicity → increased DT permeability leading to:
- hypokalemia - hypomagnesemia |
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In order, what are the most common metastatic tumors to the brain?
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1) Lung
2) Breast 3) Melanoma |
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What is the most common form of congenital adrenal hyperplasia?
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CAH d/t 21-hydroxylase deficiency (90%)
Causes: - HYPO-TN (↓Na) - HyperK+ - XX Pseudohermaphrodite - Volume depletion (emesis) "Salt wasting" |
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What are the signs of lead poisoning?
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B-ody C-an't H-andle LEAAD
B-asophilic stippling (RBC's) C-onstipation H-eadache L-ines (Burton's; blue; gingiva) E-ncephalopathy A-nemia (microcytic; hypochromic) A-bdominal colic D-rops (wrist/foot) |
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How does ESRF affect bone?
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Causes renal osteodystrophy → subperiosteal thinning
↓VitD3 → ↓Ca (less absorbed) & ↑PO4 (retained - also causes ↓Ca) Low Ca → HyperPTH |
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What syndromes are a/w Renal Cell Carcinoma (RCC)?
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1) Von Hippel-Lindau (gene deletion on chromosome 3)
3) Paraneoplastic syndromes |
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What is a precursor of squamous cell carcinoma?
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Actinic Keratosis
a/w sun exposure (garderner). Small (<1cm), rough, erythematous or brown lesions. Show basal cell layer atypia, hyperkeratosis and parakeratosis. |
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What immune deficiencies lead to infections w/ Candida albicans?
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1) Neutropenia → Disseminated (ACE):
- Abscesses (liver/kidney) - Candidemia - Endocarditis (R-sided) 2) T-Cell → Superficial/Local (e.g. HIV) |
