test #13 4.1 Flashcards
pleuritic pain 2-4 days post-MI
pleuritic (changes w/ cough & swallowing, radiating to neck). fibrinous or serofibrinous early-onset pericarditis. 10-20% fever. rxn to transmural necrosis. short-lived, rx: aspirin
pericarditis vs. myocardial ischemia pain
pericarditis: pleuritic & sharp, changes w/ cough. MI: constant, substernal, crushing
dressler’s syndrome
diffuse pericardial inflammation (& lung pleura) due to autoimmune reaction to necrotic tissue. 1 wk-months post MI (fewer than 4%). fever, pleuritis, leukocytosis, pericardial friction rub, chest radiograph evidence of new pericardial / pleural effusions. autoimmune polyserositis. rx: aspirin, NSAID, glucocorticoids
viral pericarditis usu follows..
upper respiratory infection.
3 major symptoms of klinefelter 47 XXY
(1) primary testicular failure: (hyalinization and fibrosis of seminiferous tubules) —> subsequent lack of testosterone.
(2) eunuchoid body habitus: due to testosterone deficiency: tall w/ gynecomastia. lack body hair.
(3) cognitive symptoms: mild retardation, but mostly normal.
arachnodactyl, scoliosis, and aortic root dilation
Marfan. inherited defect of extracellular matrix protein: fibrillin
short stature, hypotonia, obesity.
prader-willi. microdeletion on chromosome 15 (inherited from fatheR). mental retardation.
exact direction of translocation in CML. karyotype.
t(9,22). fusion gene on shortened 22. BCR gene on 22 to ABL gene on 9. karyotype: long 9
kartagener syndrome
autosomal recessive mutation in gene coding for dynein. male infertility, recurrent sinusitis, bronchiectasis. situs inversus.
karyotype analysis of fragile X syndrome
karyotype of cells cultured in folate-deficient medium, discontinuity of staining on the long-arm of X chromosome.
chromosome of sickle cell anemia
chromosome 11
1 gram of hemoglobin holds how much oxygen?
1.34ml oxygen / 100ml blood
PaO2 100 = how much oxygen dissolved?
0.3ml oxygen dissolved / 100ml blood
cyanide intoxication leads to what blood gas finding
inhibition of cytochrome C, failure of electron transport chain & aerobic metabolism. SaO2 of venous blood INCREASES (oxygen cannot unload)
what 3 factors affect total oxygen content of blood
(1) hemoglobin concentration (2) oxygen saturation of hemoglobin (SaO2) (3) partial pressure of xygen dissolved in blood (PaO2)
SCID presentation
bacterial (i.e. recurrent otitis media), viral (bronchiolitis), and fungal (candidiasis) w/ poor growth & thymic hypoplasia (absent thymic shadow).
absent thymic shadow can mean.. (2)
SCID or DiGeorge (very uncommon)
Bruton’s agammaglobulinemia
X-linked, boys, 6 months after passive immunity passes. BTK gene. insufficient production of mature B cells
common variable immunodeficiency
defect in B cell maturation. many causes.
Ab abnormalities w/ Wiskot-Aldrich
low to normal IgG and IgM. increased IgE and IgA
4 basic payment methods (most contracts between health insurance plans & physicians)
capitation, fee-for-service, discounted fee-for-service, salary
capitation
paid fixed amount per enrollee (not per service). fixed budget aloocated: incentives to contain costs. motivated to catch illness early (preventative care) so less tests needed as patient ages.
fee-for-service
paid fixed amount for every service & diagnostic test. face little financial risk, enticed to increase visits per patient and services per visit.
discounted fee-for-service
similar to FFS, but are reimbursed a discounted price. physician will be more conservative when ordering tests / providing services
salary
fixed amount, pay not tied to service or enrollee. no financial risk. no financial incentive to change treatment patterns.
HMO (health maintenance organization insurance plans) tend to use… Preferred provider organization insurance plans tend to use.. (payment plans)
HMO: capacitation. PPO: FFS or discounted FFS
latency in epidemiological studies
time elapsed from exposure to clinically apparent disease. short: infectious disease. long: heart disease/cancer.
or, exposure to risk modifiers occur significant time before effect on disease process. or must occur continuously over extended period before disease outcome is affected.
idiopathic hirsuitism. rx: (3)
(1) increased conversion of testosterone to DHT (5-alpha-reductase) or (2) increased sensitivity of hair follicles to DHT. rx: spironolactone, flutamide (testosterone receptor antagonist), finasteride (5-alpha-reductase inhibitor)
spironolactone on hirtsuitism
anti-adrogenic properties. block androgen receptors at hair follicles & decreases testosterone production.
flutamide
testosterone receptor antagonist
clomiphene? rx?
antiestrogen. inteferes w/ negative feedback of estrogens on hypothalamus and pituitary. increases GnRH. rx: infertility w/ anovulation
mitotaine? rx?
adrenocortiolytic. rx: adrenocortical carcinoma.
medroxyprogesterone? rx?
Depo Provera. progesterone only contraceptive (intramuscular injection once every 12 wks)
mifepristone? rx?
RU-486. synthetic steroid w/ anti-progestin & anti-glucocorticoid effect. abortifacient.
danazol? rx?
synthetic androgen used to treat endometriosis & hereditary andioedema.
where is vitamin E obtained from? deficiency? results in?
widely available in regular diet. deficiency is unusual: fat malabsorption, abetalipoproteinemia. low birth weight infants. deficiency – subacute combined degeneration of dorsal column & spinocerebellar tract
vitamin E deficiency mimics..
freidrich’s ataxia (ataxia, dysarthria, loss of position & vibration sense)
clinical presentation of acute intermittent porphyria
acute abdominal pain, peripheral neuropathy, hyponatremia
PSGN on light microscope? lab findings? EM?
hypercellular (leukocyte, endothelial, mesangian cell proliferation) glomerular.
lab: elevated titers of anti-streptococcal antibodies (anti-streptolysin O, anti-DNase B, anti-cationic proteinase). low C3. cryoglobulins.
EM: subepithelial humps
lab finding w/ drug-induced interstitial nephritis (tubulointerstitial nephritis)
high serum EOSINOPHILIA. offenders: beta-lactam antibiotics, NSAIDs, diuretics, anticonvulsants. nephritis. hypersensitivity.
early embryonic development, body veins divided into 3 main groups.. what is the fate of these groups?
(1) vitelline – become veins of portal system (2) umbilical – degenerate (3) cardinal – veins of systemic circulation
site of superior vena cava
right, posterolateral to ascending aorta. anterior to right pulmonary artery. below level of carina.
truncus arteriosus gives rise to..
aorta and pulmonary artery
embryological origin of descending aorta
fusion of embryonic left and right dorsal aortas
pupillary light reflex pathway
SENSORY: retina –> optic nerve –> bilateral pretectal nucleus in superior colliculus –> ipsilateral & contralateral edingerwestphal nuclei (decussating fibers traverse posterior commissure)
MOTOR: parasympathetic preganglionic fibers in Edinger-Westphal –> travel w/ oculomotor n. to ciliary ganglion –> synapse onto postganglionic neurons –> project fibers to sphincter of iris.
main contributor to nitrate effect in patients w/ stable angina?
reduced preload –> reduced left ventricular volume.
also have modest dilatory effect on coronary arterioles & decrease afterload, but less impt.
5 major symptoms caused by invasion of pancoast tumors
(1) invasion of parietal pleura, vertebrae, superior ribs: SHOULDER PAIN. (2) invasion of brachial plexus: weakness & paraesthesia of ARM , particular inferior trunk. (3) HORNER (superior cervical ganglion sympathetics) (4) SVC syndrome (5) invasion of recurrent laryngeal n (HOARSENESS
isoniazid mechanism
decrease synthesis of mycolic acid in cell wall. bacterial catalase-peroxidase needed (encoded by KatG) to convert to active metabolite.
ethambutol mechanism
decrease carbohydrate polymerization of cell wall (block arabinosyltransferase)
pyrazinamide mechanism
unknown, acidify intracellular environment (pyrazinoic acid) effective in acidic lysosomes
what feature of mycobacteria makes them acid fast?
mycolic acids in cell wall
mycolic acids are essential for what 2 things in mycobacterium?
(1) proper cell wall structure (2) synthesis of mycobacterial virulence factors (sulfatides, wax D, and cord factor)
streptomycin is indicated in the treatment of… (3)
(1) mycobacteria: TB (2) plague: Yersenia pestis (3) tularemia: Francisella tularensis
skin findings in sarcoidosis (3)
variety: 1. subcutaneous nodules (erythema nodosum), 2. erythemtous plaques 3. macules that are slightly reddened / scaling
liver pathology in sarcoidosis
scattered noncaseating granulomas (75% of cases). affect portal triad far more than lobular parenchyma.
fatty (steatosis) change in liver occurs in.. (3)
reversible (1) hypoxic (2) toxic (3) metabolic injury (i.e. protein malnutrition, diabetes, obesity)
hepatic centrilobular necrosis can be caused by..
death of hepatocytes immediately surrounding terminal hepatic vein. cause: ischemic injury (right heart failure), drugs, toxins, fulminant hepatitis
portal inflammation can be found in
VERY NONSPECIFIC: alcoholic heptatitis, acute/chronic viral hepatitis, secondary biliary cirrhosis due to biliary tract obstruction, primary biliary cirrhosis, sclerosing cholangitis, chronic graft vs. host disease, acute cellular rejection of liver transplant, idiopathic neonatal hepatitis.
periportal fibrosis is a common pathologic finding in..
chronic viral hepatitis
prolactinomas in men v. women? why?
female: < 10mm (micro). male: >10mm (macro). bc men don’t present until it is very large (i.e. no menstrual abnormalities)
renal failure and calcium problems…
VITAMIN D synthesis occurs in kidney. low vitamin D, low Ca2++, high PTH
which bacteria are capable of producing dextrans using sucrose as a substrate?
s. viridans
what is the most likely adherence site for S. viridans?
fibrin & platelets (think: subacute endocarditis, valvular vegetation)
role of subendothelial collagen and subendothelial glycosaminoglycans
subendothelial GAGs form subendothelial fibrous cap over the central core of atherosclerotic plaque. can activate platelets