Pathophysiology Flashcards
Pancreatitis causes
- ERCP
- Drugs (eg azathioprine, sulfasalazine, furosemide, valproic acid)
- infections (eg mumps, coxsackie, mycoplasma pneumoniae)
- hypertriglyceridemia
- structural abnormalities of the pancreatic duct (strictures, cancer, pancreas divisum) or of the ampullary region (choledochal cyst, stenosis of sphincter of Oddi)
- surgery (particularly of stomach, biliary tract, and cardiac surgery)
- hypercalcemia
Crohn’s Disease labs
inc urine oxalate (from intestinal malabsorption) –> calcium oxalate stones
Pheochromocytoma
- arises from neuroendocrine/chromaffin cells in adrenal medulla
- 25% inherited (VHL, RET, NF1)
- inc catecholamine secretion –> headaches, tachycardia/palpitations, sweater, HTN
- Rule of 10s: b/l, extra-adrenal (paragangliomas), malignant
dx = elevated urinary & plasma catecholamines & metanephrines
Thyroiditis
acute, suppurative, subacute, postpartum
- excessive release of preformed thyroid hormone
- symptoms continuous
exam 1 q13
Carcinoid syndrome
excess 5HT and its metabolite 5HIAA from metastatic mid-gut neuroendocrine tumor
sx = flushing, bronchospasm, diarrhea, HoTN
Schwannoma
peripheral nerve tumor located at cerebellopontine angle
sx = tinnitus and unilateral hearing loss
CN III palsy
unilateral ptosis and gaze palsy (“down and out” gaze)
c/b berry aneurysm or uncal herniation or microvascular ischemia (e.g. due to DM)
Wernicke Syndrome triad
ophthalmoplegia, ataxia, confusion
Wernicke Syndrome cause and pathology
chronic thiamine deficiency –> dec glucose utilization esp in CNS
*erythrocyte transketolase levels increased after thiamine infusion
foci of hemorrhage and necrosis in mamillary bodies and periaqueductal gray matter on autopsy
hemolytic anemia cause
decreased G6PD
vitamin B12 deficiency
elevated methylmalonic acid levels
Erythropoietic protoporphyria (EPP)
increased erythrocyte protoporphyrin concentration, i.e. one of the precursors of heme
cholesterol gallstones risk factors
- high TG
- combo of fibric acid derivates and bile acid-binding resins –> inc cholesterol concentration in bile
- etoh
Sickle cell disease
single amino acid substitution: glutamic acid (negatively charged) –> valine (nonpolar, neutral charge) at 6th position in beta-globin chain of Hb molecule
alteration of a region on beta-globin surface that allows hydrophobic interaction among Hb molecules –> aggregation of Hb molecules –> sickling
sickling promoted by hypoxia, inc acidity, dehydration
Hb C disease
glu is replaced by a basic polar (positive charge) lysine
no hydrophobic interactions among Hb molecules as in SCD, hence less severe condition
Saccular (berry) aneurysms
most common cause of SAH (AVM = 2nd most common cause)
usually occur at Circle of Willis
*Anterior communicating artery = most common site
Associated diseases:
- Ehlers-Danlos
- AD polycystic kidney disease
Cerebral amyloid angiopathy
elderly patients
- asx
- or sx from recurrent intracerebral hemorrhages affecting small areas = HA, focal neuro deficits
Charcot-Bouchard aneurysms
- lenticulostriate vessels of basal ganglia 2/2 HTN
bluish neoplasm under nail bed
Possible origin:
- glomus tumor (glomangioma) - thermoregulation function; tumor of modified smooth muscle cells of glomus body whose task is to shunt blood away from skin surface in cold temperature and direct it toward skin surface in hot environments
- subungual melanoma - pigmentation fxn
nephritic syndrome
HTN, hematuria, moderate proteinuria (can see pitting edema)
- Post-streptococcal glomerulonephritis (happens weeks after)
- Anti-GBM disease
- Rapidly progressive glomerulonephritis
- IgA nephropathy
- Alport syndrome
Post-streptococcal glomerulonephritis
Ab against strep Ag cross-react with GBM
Anti-GBM disease
Ab agains type IV collagen GBM –> C3 and IgG deposition in basement membrane
these Ab can cross-react with collagen type IV in alveolar basement membrane –> pulmonary hemorrhage –> renal failure + pulmonary hemorrhage = Goodpasture syndrome
Rapidly progressive glomerulonephritis
severe immune injury (e.g. anti-GBM Ab, immune complex deposition)
glomerular crescents = proliferating parietal cells with infiltration of monocytes and macrophages seen on LM
IgA nephropathy
deposition of IgA-containing complexes