test #11 3.28 Flashcards
compare distal and proximal radial n. lesion (i.e. motor & sensory involvement)
proximal lesion (i.e. midshaft of humerus) will injure radian n. & posterior cutaneous branch (which comes off above spiral groove). distal lesion near radial head / lateral epicondyle will not impair arm sensation, ONLY wrist extension (deep branch). no sensory defects
lateral and medial branches of median n innervates
sensory innervatino of palmar & dorsral surfaces of distal 3 1/2 digits
when an adult attempts to pull a child upward by the arm…
radial head subluxation “nurse-maid elbow”, can damage the deep branch of the radial n (paralysis of forearm extensor w/o affecting any sensory)
boundaries of guyon’s canal? what n. passes through here?
between hook of hamate and pisiform bone (fibroosseus tunnel)
fracture of the surgical neck of the humerus damages.. what will be lost (3)
axillary n. paralyzed (1) deltoid (2) teres minor (2) sensation on lateral upper arm
immune response to Tb..
macrophage phagocytosis & antigen presentation –> CD4+ T cell stimulate macrophages –> activated macrophages form Langerhans giant cells (multiple nuclei organized peripherally in the shape of a horseshoe)
what cell type is primary responsible for Giant cell formation?
CD4+ Th1 cells –> IFN-gamma
Th2 cells activate..
mast cells, basophils, eosinophils
heavy smoker w/ exertional dyspnea and airspace enlargement on CT likely has…
centriacinar emphysema
descirbe pathophhysiology of centriacinar emphysema
oxidative injury to respiratory bronchioles –> activation & recruitment of resident macrophages –> neutrophil release of elastase, proteinase 3, cathepsin G, matrix metalloproteases, proteases, oxygen free-radicals (inhibit a1-antityrpsin). net protease-antiprotease & oxidant-antioxidant imbalance destroy’s acinar walls.
clara cells histologically are.. located.. secrete..
non-ciliated, secretory constituents of terminal respiratory epithelium. secrete clara cell secretory protein (CCSP), which inhibits neutrophil recruitment and activation, as well as neutrophil-dependent mucin production.
what 3 things can reduce pulmonary compliance?
(1) pulmonary fibrosis (2) insufficient surfactant (3) pulmonary edema
coenzymes needed for pyruvate dehydrogenase
thiamine pyrophosphate (TPP), lipoic acid, CoA, FAD, NAD (mnemonic: tender love and care for nancy)
lipoic acid needed for.. (2)
needed for the (1) decarboxylation of alpha ketoacids and (2) transfer of alkyl groups
PDH is needed to.. absence leads to..
converte pyruvate acid to acetyl-CoA in the TCA cycle. w/o PDH or its 5 coenzymes, pyruvate –> lactic acid (lactate dehydrogenase)
lipoic acid is an important coenzyme for..
alpha ketoglutarate dehydrogenase and branched-chain ketoacid dehydrogenase
citrullinemia
urea cycle disorder that results from deficiency of arginosuccinate synthetase. ATP is cofactor required.
homocysteinuria
deficiency in cystathione synthase. characterized by premature atherosclerosis. disposed by 2 pathways: (1) conversion to cysteine by the combined actions of two vitamin B6-requiring enzymes, cystathione synthase and cystathionase and (2) conversion to methionine by a folate & vitamin B12-dependent process.
orotic aciduria
results from a defective pyrimidine synthesis resulting from a deficiency of the enzyme orotate phosphoribosyl transferase (requires glutathione as a coenzyme)
lipoic acid is a cofactor for which mitochondrial enzymes
(1) PDH (deficiency –> lactic acidosis) (2) alpha-ketoglutarate DH (3) branched-chain ketoacid DH (deficiency results in maple syrup urine disease)
karyotype difference between complete vs. partial moles
complete mole: 46XX or XY (of paternal origin).
partial mole: 69XXX or XXY.
evacuated uterine contents of complete vs. partial mole
complete: trophoblasts only, “bunch of grapes”.
partial: fetus, cord, amniotic membrane, some grossly enlarged villi
microscopic appearance of complete vs. partial mole
complete: enlarged edematous villi and trophoblastic proliferation. no fetal tissue.
partial: some enlarged villi w/ trophoblastic proliferation. normal villi and fetal tissue also present.
risk of complications w/ complete vs. partial mole
complete: 15-20% risk of malignant trophoblastic disease.
partial: low risk of malignancy (>5%)
clinical presentation of complete mole
vaginal bleeding, uterus enlarged out of proportion to gestational age, pre-eclampsia, hyperthyroidism, theca-lutein cysts (hCG driven)
clinical presentation of choriocarcinoma
after molar pregnancy, abortion, or normal pregnancy. presents w/ vaginal bleeding & symptoms of metastatic disease (eg cough w/ lung metastases). inappropriately elevated hCG levels
missed abortion is…
embryonic death in utero. signs: vaginal bleeding w/ closed cervical os, small uterus, absence of fetal heart tones, & low hCG levels
presentation of abruptio placentae
premature placental separation. can occur in 3rd trimester of pregnancy. manifests w/ vaginal bleeding, hypertonic uterus, intense painful contractions
ruptured tubal pregnancy presents w/? curretage will reveal?
vaginal bleeding, abdominal pain, signs of hemorrhagic shock. curretage reveals endometrial lining w/ gestational changes. fetus and trophoblast are absent.
phencyclidine (1) mode of action (2) symptoms (3) examination findings
(1) hallucinogen (2) agitation, dissociation, hallucinations, VIOLENT BEHAVIOR, memory loss (3) NYSTAGMUS, ataxia
cocaine (1) mode of action (2) symptoms (3) examination findings
(1) stimulant (2) euphoria, increased arousal, agitation, CHEST PAIN, headaches, SEIZURES (3) tachycardia, hypertension, MYDRIASIS
methamphetamine (1) mode of action (2) symptoms (3) examination findings
(1) stimulant (2) agitation, PSYCHOSIS, diaphoresis, violent behavior (3) tooth decay, HTN, tachycardia, choreiform movt
LSD (1) mode of action (2) symptoms (3) examination findings
(1) hallucinogen (2) VISUAL HALLUCINATIONS, depersonalization, euphoria, occasional dysphoria, panic (3) mild tachycardia, mild HTN, ALERT & ORIENTED
marijuana (1) mode of action (2) symptoms (3) examination findings
(1) psychoactive drug (2) increased appetite, euphoria, slowed reflexes, impaired time perception (3) dry mouth, CONJUNCTIVAL INJECTION, mild tachycardia
heroin (1) mode of action (2) symptoms (3) examination findings
(1) opioid analgesic (2) mild euphoria or lethargy to coma (3) MIOSIS, DECREASED respiratory rate, DECREASED bowel sounds
PCP mechanism
NMDA receptor antagonist. moderate – dissociative symptoms (detachment & withdrawal). higher – agitation, hallucinations, violent behavior. ataxia, nystagmus (both horizontal and vertical) and memory loss
cocaine mechanism
blocks reuptake of dopamine, NE, and 5-HT at CNS synapses. tachycardia, HTN, blurry vision, euphoria, and agitation. ischemic side effects: i.e. MI and stroke can occur due to severe vasoconstriction. acute intoxication lasts for less than an hour.
differentiate methampetamine and PCP intoxication.
BOTH can have violent behavior, but PCP will produce nystagmus and ataxia. methamphetamine intox typically lasts for up to 20 hours (much longer than PCP)
narcolepsy clinical presentation (3).
excessive daytime sleepiness, episodic loss of motor tone triggered by emotion (cataplexy) and inability to move on awakening (sleep paralysis).
narcolepsy is commonly caused by lack of which neuropeptides? where are these produced?
LACK of hypocretin-1 (orexin-A) and hypocretin-2 (orexin-B). promote wakefulness & inhibit REM sleep-related phenomena. produced only in neurons located in the lateral hypothalamus
clinical diagnosis for narcolepsy (definition and inclusion)
recurrent lapsing into sleep or napping mult times within same day, occurring at least 3x/wk for 3 months. w/ at least one of the following: (1) cataplexy: conscious, brief episodes of sudden, bilateral muscle tone loss precipitated by emotions such as laughing or joking. or spontaneous abnormal facial movements w/o emotional triggers (2) hypocretin-1 deficiency by CSF analysis (3) rapid eye movement sleep latency <15min
low CSF HIAA associated w/ what behaviour?
impulsive, destructive behaviors, particularly – aggression, suicide, and violence
elevated amounts of 14-3-3 protein in CSF helps w/ diagnosis of..
Creutzfeldt-Jakob disease
decreases of melatonin in CSF associated w/
progression to alzheimer’s disease
two most frequent causes of eugonadotropic amenorrhea?
(1) incomplete canalization of the vaginal plate (agenesis or imperforate hymen) or (2) mullerian duct anomalies
primary amenorrhea in a pt w/ fully developed secondary sexual characterestics?
anatomic defect in genital tract. most commonly imperforate hymen or mullerian duct anomaly. former presents w/ cyclic abdominal/pelvic pain w/ hematocolpos
hematocolpos:
accumulation of blood in vaginal canal – distend vaginal, vaginal bulge or mass palpated anterior to rectum
filtration fraction formula?
GFR/RPF
mucosal neuromas
unencapsulated, thickened proliferations of neural tissue
NF1 vs NF2
NF2 – the more ‘central’ form w/ bilateral acoustic neuromas, brain meningiomas, schwanommas of dorsal roots in spinal cord. NF1 – cafe au lait spots, cutaneous neurofibromas, axillary or inguinal freckling, optic glioma, iris hamartomas, ossessous lesions
role of dynein
(1) retrograde transport in cells (2) cillary & flagellar movement
ethambutol side effect
optic neuritis (decreased visual acuity, central scotoma, or colour-blindness). may be reversible w/ discontinuiation
mesoderm derived organ that originates from the dorsal mesentary but receives blood supply by an artery of foregut
spleen (from splenic artery, branch of celiac artery). spleen = NOT a foregut derivative
foregut includes?
esophagus through the 2nd part of duodenum (includes liver, gallbladder, and portion of pancreas)
embryology of liver
endoderm-derivived foregut structure, forms from diverticulum of primitive gut tube within ventral mesentary
loss to follow-up (disproportionately in exposed / unexposed groups) results in
attrition bias – type of SELECTION BIAS. results in over/underestimation of association between exposure and outcome
sampling bias results from..
type of SELECTION BIAS; results from nonrandom sampling of target population. characteristics of study population differ from target population: results are not generalizable.
nondisjunction in meiosis I or II can cause…
monosomy or trisomy
differentiating bet meiosis I or II nondisjunction events
nondisjunction in meiosis I: 2 diff alleles inherited from one parent (homologous chromosomes – child has 3 diff bands). nondisjunction in meiosis II: 2 same alleles inherited from one parent (sister chromatid) – child: 2 0bands, 2x normal amt of one
majority of nondisjunction trisomy 21 occurs during
meiosis I (inherit mom’s homologous chromosomes)
classic triad of congenital rubella
(1) sensorineural hearing loss (2) cataracts (3) PDA
IFN-alpha approved for rx of..
hepatitis B and C, hairy cell leukemia, condyloma acuminatum, kaposi sarcoma
naturally competent bacteria that can undergo transformation (3)
(1) streptococcus pneumoniae (2) haemophilus influenza (3) neisseria gonorrhoeae & meningitidis
generalized transduction vs. specialized transduction
Generalized: during lytic infxn, RANDOM bacterial genes accidentally packaged into viral capsid. Specialized: lysogenic ifxn, SELECT bacterial genes near viral insertion site are excised & packaged into viron
normal relationship between LAEDP (left atrium end diastolic pressure) and LVEDP (left ventricle end diastolic pressure)
equivalent! mitral senosis elevates LAEDP and PCWP relative to LVEDP
kartagener’s is related to..
microtubular dynein arm defect (also have sinusitis, bronchiectasis, and situs inversus)
tuberous sclerosis
AD, angiofibromas (adenoma sebaceum) seizures, and mental retardation
main cardiovascular pathology / developmental defect in down’s?
endocardial cushion defect (ostium primum ASD, regurgitant AV valves)
main cardiovascular pathology / developmental defect in di george?
- Conotruncal - truncus arteriosus
- tetrology of fallot
- interrupted aortic arch (atretic or segment is absent)
main cardiovascular pathology / defect in friedrich’s ataxia?
hypertrophic cardiomyopathy
main cardiovascular pathology / defect in Marfan’s?
cystic medial necrosis of aorta –>
- dissection
- Thoracic aneursym
- aortic valve incompetence
main cardiovascular pathology / defect in tuberous scerlosis?
valvular obstruction due to cardiac rhabdomyomas
GI loss of K+ leading to hypokalemia results from..
prolonged diarrhea
early serum marker of thiamine deficiency
erythrocyte transketolase activity (solely uses thiamine as cofactor).
transketolase fxns to..
in hexose monophosphate pathway (HMP).
w/ phosphopentose isomerase
converts ribulose 5-p (derivived from glucose) to
Ribose 5-phosphate
glyceraldehyde 3P (intermediary of glycolysis)
fructose-6 phosphate
if give glucose to alcoholic / malnourished patient, must also..
give thiamine! needed for glucose utilization. w/o thiamine, may cause acute cerebral damage
glucose-6-6 phosphate dehydrogenase is important for..? low levels suggest..?
rate limiting step in pentose phosphate pathway, needed for (1) NADPH production (2) fxn of the erythrocyte antioxidant system. decrease G6PD suggests hemolytic anemia
methylmalonyl CoA mutase
uses B12 as cofactor. converts methylmalonic acid –> succinyl coA. methylmalonic acid is a product of fatty acid oxidation
why is hypernatremia rarely observed w/ mineralcorticoid excess?
aldosterone escape – increase in Na+, increased volume, increase RBF and GFR –> increase Na+ excretion. also increased volume –> increased ANP –> naturesis
snRNPs are needed for
small nuclear ribonucleoproteins –> splicesosome
transcription factor II D
transcription factor that binds to TATA promoter region.
elongation factors
facilitate tRNA binding and translocation step of protein synthesis
releasing factors
recognize stop codon (UGA, UAA, UAG) to terminate protein synthesis.
severe intellectual disability, history of seizures, and abnormal pallor of catecholaminergic brain nuclei, hair, eye, skin. also classic musty / mousy body odor
phenylketonuria – inability to convert phenylalanine to tyrosine (phenylalanine hydroxylase, requires BH4 (tetrahydrobiopterin; tetrahydropteridine reductase)
hypopigmentation of skin, hair, eyes, catecholaminergic brain nuclei in PKU results from..
inhibitory effect of excess phenylalanine on melanin synthesis.
absence of dopamine hydroxylase
results in rare form of dysautonomia, characterized by ptosis, orthostatic hypotension, hypoglycemia, and hypothermia. can’t convert dopamine to NE
alkaptonuria
autosomal recessive disorder of tyrosine degradation – deficiency of homogentisic acid oxidase. accumulation of homogentisic – hyperpigmentation and degenerative joint disease
albinism
autosomal recessive, defects in biosynth/distribution of melanin. most commonly due to depressed/absent TYROSINASE activity. [melanin synth = tyrosine –> DOPA –> dopaquinone by tyrosinase in melanocytes]
deficiency in which two proteins can lead to phenylketonuria?
phenylalanine hydroxylase or cofactor tetrahydrobiopterin (or enzyme dihydropteridine reductase)
first line treatment for isolated systolic hypertension (common in elderly)
thiazide diuretics and dihydropyridine calcium antagonists, like amlodipine and nifedipine (in non-diabetics. diabetics: ACE-I or ARB)
side effect profile of nifedipine
bilateral ankle swelling and flushing
gynecomastic caused by which 2 diuretic?
spironolactone (9%), epeleperone (1%)
adverse effects from verapamil
constipation and gingival hyperplasia
mechanism of thiazolidinediones
decrease insulin resistance. bind to PPAR-gamma (perioxisome proliferator activated receptor gammA) transcriptional regulator of genes involved in glucose and lipid metabolism. CRUCIAL GENE regulated by PPAR-gamma: adiponectin (cytokine released by fat tissue). adiponectin low in type II diabetics. thiazolidinediones increase adiponectin
genes altered by PPAR-gamma (upregulated by thiazolidinediones)
(1) crucial: adiponectin (2) fatty acid transport protein (3) insulin receptor substrate (4) glucose transporter-4 (glut-4)
main side effects of thiazolidinediones?
fluid retention, weight gain, precipitation of CHF
blood/gas partition coefficient
anesthetics w/ higher blood solubility have larger blood/gas partition coefficients. high solubility –> dissolve easily in blood –> larger amounts must be absorbed before blood is saturated –> delayed rise in partial pressure
if partial pressure rises rapidly in blood..
gas is not very soluble in blood –> rapid onset in brain
speed of anesthetic induction determined by…
rate of uptake in brain –> dependent on solubility of anesthetic in blood. very soluble (high blood/gas partition) –> slower onset
example of poorly soluble gas? highly soluble has?
poor solubility –> nitrous oxide N20 (small amt needed to saturate blood, rapid rise in blood partial pressure, rapid equilibration in brain, rapid onset of action.
high solubility –> halothane. large amount needed to saturate blood, slow rise in PP in blood, slow equilibration in brain, slow onset of action.
potency of gas determined by…
minimal alveolar concentration. potent –> lower partial pressure needed to be effective.
nitrates cause reflex..
tachycardia. block w/ beta-blockers
hydralazine
direct-acting arteriolar dilator
phenylephrine
alpha-agonist – vasopressor
2 uses of N-acetylcysteine
(1) antidote in acetaminophen/tylenol overdose (2) renal protective agent prior to IV iodine contrast for radiologicalstudies
in parkinson’s, prescribe L-dopa with…
(1) carbidopa – peripheral dopa decarboxylase inhibitors (2) entacapone – COMT inhibitor. COMT – catechol-O-methyl-transferase impt in methylation of levodopa. entacapone inhibits peripheral COMT. tolcapone inhibits central and peripheral COMT, but is hepatotoxic.
how does amantadine enhance the effect of endogenous dopamine
increase synthesis, release, and reuptake of dopamine
name some dopamine agonists (4)
bromocriptine, pergolide, pramipexole, ropinerole
selegiline
inhibitor of MAO-B. decreases central dopamine degradation.
anticholinergics used for parkinsons (2)
trihexyphenidyl and benztropine
2 causes of peptic ulcer disease
(1) helicobacter pylori infxn (80-90%) (2) NSAID use.
rx for h. pylori
2 antibiotics (metronidazole, tetracycline, amoxicillin, clarithromycin) and PPI and/or bismuth for 14 days
PPI vs. H2 blockers for peptic ulcer disease?
PPI superior
sucralfate
binds to base of mucosal ulcers, protecting against gastric acid. can help duodenal ulcers heal.
metoclopramide? rx?
dopamine antagonist w/ central & peripheral effects. prokinetic & antiemetic. rx: GI motility disorders, gastroparesis. prevent nausea and vomiting.
misoprostol GI rx?
prostaglandin E1 analog. prevent NSAID induced peptic ulcer disease
three main causes of acute urethritis in healthy young?
N. gonorrhea, C. trachomatis, HSV. if engage in anal sex: e. coli
rx for gonococcal urethritis?
ceftriaxone or fluoroquinolone.
rx for chlamydia urethritis?
single dose of azithromycin or multi-day doxycycline.
pentamidine (3 rx)
prophylaxis and treatment of (1) PCP pneumonia. rx: (2) leishmaniasis and (3) African sleeping sickness.
nifurtimox rx:
trypanosoma cruzi Chagas’ disease
mebenzaole rx (4)
ascariasis, truchuriasis, hookworm, pinworm
nitroprusside use? toxicity? sign? antidote?
use: emergent setting where quick onset of action needed to control BP and prevent target organ damage; mixed arterial and venous vasodilation. could cause cyanide toxicity. metabolized into cyanide and nitric oxide –>
cyanide metabolized in liver (by liver rhodanase to thiocynate (excreted in urine).
sign: altered mental status and lactic acidosis. rx: Na2S2O4 (sodium thiosulfate) –> donates sulfur to lier rhodanase –> enhance metabolism and detox of cyanide to thiocyanide.
oxygen also given to prevent cyanide inhibition of cytochrome oxidase (needed for respiration)
bicornuate uterus
partially septate uterus attached to a single cervix and vagina. results from failure of paramesonephric ducts to fuse. total nonfusion: uterus didelphys – two sep vaginas, cervices, and uterine horns
mesonephric ducts in female and male
female: from Gartner duct. male: epididymis, ductus deferens, seminal vesicles, and ejaculatory duct
paramesonephric ducts in female and male
female: uterine tubes, uterus, cervix, and superior 1/3 of vagina.
male: involute, leaving only vestige appendices of the testes
concentric vs. eccentric left ventricular hypertrophy
concentric: pressure overload: aortic stenosis, chronic HTN. thickens wall uniformly, outer dimension of ventricle remaining unchanged (narrowed cavity).
eccentric: volume overload: aortic or mitral regurgitation, myocardial infarction, dilated cardiomyopathy.
structural heart changes w/ aging (after 65)
decreased LV size, predominately through shortening of the apex-to-base dimension, accompanied by leftward bowing or lower interventricular (sigmoid) septum.
ventricular remodeling post-MI
often results in volume overload, poor contractile fxn – eccentric cardiac hypertrophy
lynch syndrome (HNPCC)
autosomal dominant. microsatellite instability –> DNA mismatch repair defect. inherit one allele, acquire one later.
HNPCC-associated colon adenocarcinoma vs. sporadic
HNPCC: younger than 50, usu right sided, mult cancers are common: synchronous (same time w/ primary) and metachronous (occur after resection). arises from macroscopically-normal areas of dysplastic mucosa. mutation: DNA mismatch repair: MLH-1, MSH-2, MSH-6, PMS-2)
sporadic: older than 50, predominantly left, uncommon to have mult cancer, adenomatous polyp is source. “adenoma-to-carcinoma” sequence (mutation in APC, k-ras, p53 and DCC)
Lynch I and II
Lynch I: familial predisposition to colon adenocarcinoma.
Lynch II: predisposition to colon cancer AND increased incidence of extraintestinal cancers (i.e. endometrial, ovarian, stomach, pancreas, urothelial tract
APC gene
intracellular attachment. mutation: formation of adenomatoius polyp from normal mucosa. mutation detected in MOST sporadic colon cancers and ALL familial polyposis
MEN 2b
medullary carinoma of thyroid (calcitonin), pheochromocytoma, mucosal neuromas & marfinoid habitus
pancreatic tumor in Men 1
often gastrinoma –> zollinger-ellison. rarely: insulinoma –> hypoglycemia. vasoactive intestinal polypeptide: massive diarrhea
pathogenesis of typhoid fever
fecal-oral. penetrate gut mucosa via transporters on enterocytes & phagocytosis by M cells in peyer’s patches. phagocytosed by macrophages (specially designed to live there. macrophages carry to liver, spleen, bone marrow , gallbladder –> hepatosplenomegaly.
in gut lumen –> inflammation of peyer’s patches, intestinal hemmorhage, gut performation – polymicrobial peritonitis & sepsis –> death.
can be carrier in gallbladder: typhoid mary (bile –> stool).
presentation: rose spots on abdomen.
hodgkin’s disease age presentation?
usu bimodal, peak in 20-30s and 50’s. B symptoms, reed-sternberg cell surrounded by normal lymphocytes in node.
histology of follicular lymphoma. 2 major cell types.
aggregates of closely packed lymph follicles. 2 major cell types (1) centrocytes: small cleaved cells. centroblasts: large noncleaved cells.
histology of large B-cell lymphoma
diffuse sheets of large lymphocytes w/ nuclei at least 5x size of small lymphocytes.
describe Reed-Sternberg cells
abdundant cytoplasm, bilobed/double nuclei, inclusion-like eosinophilic nucleoli.
