test #7 3/16 Flashcards
initiation of translation in prokaryotes requires..
N-formylated methionine-tRNA. initiation codon AUG (methionine) is 6-10 bases downstream Shine-Dalgarno element.
Shine-dalgarno element (prokaryotic translation)
6-10 bases upstream intiation codon AUG. recognizes complementary sequences in 16S rRNA and 30S small ribosomal subunit.
how do aminoglycosides affected prokaryotic translation?
bind to 30S, inhibit formation of initiation complex and protein synthesis.
which antibiotic blocks peptidyltransferase activity of prokaryotic ribosome (1)
chloramphenicol
which antibiotics block the translocation of ribosome along mRNA (2)
clindamycin and erythromycin
difference in p-values between studies suggests..
difference in sample size (i.e. underpowered)
Berkson’s bias
selection bias created by selecting hospitalized patients as the control group
congenital torticollis
noted 2-4 wks of age, child prefers to hold head tilted to one side. usu result of malposition of head in utero (due to fetal macrosomia or oligohydramnios) or birth trauma (breech). sternocledomastoid injury and fibrosis. other musculoskeletal abnormalities: hip dysplasia, metatarsus adductus, talipes equinovarus (club foot)
resolve w/ conservative therapy / stretching
chin pointed away from contracted SCM. head tilted towards muscle.
maternal hypertension on intrauterine growth
intrauterine growth restriction w/ normal-almost normal headaize and reduced abdominal circumference
fragile X-syndrome characterestics
main: MR, facial dysmorphism, macroorchidsm. mild-severe mental retardation, long-thin face w/ prominent forehead and jaw, post-pubertal macroorchidism, large protruding ears, tooth crowding, arched palate
gene abnormality in fragile X syndrome
mutation in FMR1 gene, on long arm of chromosome X. normally has 5-55 CGG trinucleotide repeats. >200 repeats –> transcriptional instability. leads to hypermethylation –> gene inactivation.
chromosomal instability disorders (4)
related to mutations in DNA repair: xeroderma pigmentosum, ataxia-telangiectasia, fanconi’s anemia, bloom syndrome
defective mismatch repair genes result in..
Lynch syndrome (increased risk of heriditary non-polyposis colorectal cancer) and extraintestinal malignancy
tay sach’s deficiency & metabolite build-up
lysosomal storage disease. commonly seen in ashkenazi jews. deficiency in beta-hexosaminidase A. accumulation of cell membrane glycolipid GM2 ganglioside in lysosomes.
tay sach’s clinical presentation
2-6 months – progressive weakness, hypotonia, loss of motor skills, abnormal startle w/ acoustic stimuli, CHERRY-RED MACULA w/ NO hepatosplenomegaly. macrocephaly (accumulation of glycolipid in brain). eventually–> seizure, blindness, spasticity. life expectancy of 2-5 years.
histology of tay sach’s (EM)
neurons w/ cytoplasmic distension and lysosomes w/ onion skin lamellar lipid rings
tay sach’s vs. niemann-pick disease
both have cherry-red macular spot. niemann-pick has hepatosplenomegaly.
formula for NNH (number needed to harm)?
1/attributable risk.
attributable risk = adverse event rate in treatment group - adverse event rate in placebo group.
formula for NNT (number needed to treat)?
1/absolute risk reduction
combined OCP primary mode of action. secondary?
estrogen/progesterone suppress synthesis of FSH and LH (gonadotropins) in anterior pituitary (block LH spike needed for ovulation). also cause thickening of cervical mucus (prevent sperm from entering). also, prevents growth of endometrium, making it difficult for embryo implantation.
what is seen in periventricular plaques of MS? what is in CSF? on visual evoked potentials?
loss of myelin sheaths, depletion of oligodendrocytes, lipid-laden macrophages w/ myelin breakdown products. oligoclonal band on protein electrophoresis. slowed conduction velocity on visual evoked potentials.
PT and PTT and bleeding time in vWF deficiency?
both coagulopathy (factor VIII) and platelet deficiency. PTT and bleeding time elevated.
hemophilia C
very rare autosomal recessive, deficiency in factor XI
factor VIII deficiency
classic X-linked hemophilia. PTT prolonged.
which organ is least vulnerable to infarction? exception?
liver, has dual blood supply. portal vein and hepatic artery. also, retrograde arterial flow from accessory vessels (inferior phrenic, adrenal, intercostal). exception: transplanted liver –> hepatic artery thrombosis (collateral circulation severed during transplantation)
is the spleen vulnerable to infarction? why?
yes, bc perfusion via splenic artery = end-arterial. occurs in sickle-cell anemia, infective endocarditis, cardiac mural thrombosis
how long can the myocardium endure complete arterial ischemia
20-30min w/o severe consequence. briefer periods –> myocardial stunning.
organ susceptibility to infarction after occlusion of a feeding artery (greatest to least)
CNS, myocardium, kidney, spleen, liver.
what ions are responsible for -70mV resting potential?
high K+ conductance, low Na+ conductance (Cl- plays little if any role)
what role do the L-type Ca++ channels in myocyte T-tubules play in excitation-contraction.
NO significant flux of Ca++ from L-type Ca++ channels. Instead, they are triggered by depolarization and TETHERED to RyR1 channels in sarcoplasmic reticulum to release Ca++. skeletal muscles do NOT need extracellular Ca++ to contract!
why don’t calcium channel blockers (i.e. Verapamil, Diltiazem) affected skeletal muscles
these block extracellular Ca++ channels. skeletal muscles do NOT need extracellular Ca++ to contract. instead, L-type Ca++ are tethered to RyR1 on sarcoplasmic reticulum –> source of Ca++
describe cardiac muscle & smooth muscle excitation-contraction. how do they differ?
Ca++ through L-type channels stimulate sarcoplasmic RyR2 channels (calcium-induced calcium release). no mechanical coupling of L-type Ca++ channels and RyR. cardiac muscle = troponin. smooth muscle = calmodulin.
which muscle types have T-tubule system (plasma membrane near sarcoplasmic reticulum)?
cardiac and skeletal muscle (NOT smooth muscle)
describe biofilm formation (foreign body via staph epidermidis)
coated w/ fibrinogen & fibronectin –> serve as binding sites for S. epidermidis. bacteria induce ynthesis of extracellular polysaccharide matrix (encase bacteria). barrier to antibiotic penetration & interferes w/ host defenses (opsonization, neutrophil migration, T-lymphocyte activation). can later disperse pathogen seeds from biofilm.
HSV-1 presentation in children
gingivostomatitis, fever, and lymphadenopathy. intranuclear inclusions.
three endocrine effects of prolactinoma
- inappropriate milk production (galactorrhea) 2. suppression of gonadotrophin-releasing hormone (GnRH form hypothal) –> decreased libido, amenorrhea, infertility. 3. can compress normal pituitary cells (hypopitiutarism)
gonadotroph adenomas..
usu do not produce intact FSH or LH. instead, overproduce alpha subunit of glycoprotein hormones (mass effect & hypogonadism).
most non-secretory adenomas arise from…
gonadotrophs
normal distribution of cell types in anterior pituitary
50% somatotrophs, 20% lactotrophs, 15% corticotrophs, 10% gonadotrophs, 5% thyrotrophs
most common pituitary adenoma? most common cell type in normal pituary?
pituitary adenoma = prolactinoma. major pituitary cell type: somatotrophs.
what is contained in the posterior limb of the internal capsule? genu?
posterior limb: runs between globus pallidus/putamen and thalamus; corticospinal motor and somatic sensory fibers, as well as visual and auditory fibers. genu: corticobulbar fibers. anterior limb: separates caudate from globus pallidus, contains thalamocortical fibers.
insular cortex
limbic system, coordination of some autonomic fxn (cardicac)
25% of patients w/ subarachnoid hemorrhage following ruptured berry aneurysm experience… why? when? Rx?
vasospasm leading to clinical symptoms – altered mental status, focal neurological deficits. result of substances generated after degradation of aubarachnoid blood clots. NO EARLIER than 3 days. usu 7-8 days. rx: calcium channel blockers (decrease morbidity / mortality. nimodipine –> cerebral selective drug.
direct dilation of arteries and inhibition of platelet aggregation?
cilostazol (approved for treatment of intermittent claudication –> peripheral arterial disease. superior to aspirin)
cilostazol (2 effects)
(1) decrease platelet phosphodiesterase (high cAMP) –> inhibits platelet aggregation. (2) direct arterial vasodilator.
Rx: heparin-induced thrombocytopenia
argatroban (DTI)
what enzyme does warfarin block?
vitamin K epoxide reductase (decreases available vitamin K)
3 clinical indications for tPA (altepase)
MI, PE, acute ischemic stroke
Rx: peripheral arterial disease
cilastozol, better than aspirin.
stab above clavicle & lateral to manubrium will cause…
tension pneumothorax
symptoms of tension pneumothorax? tx?
decreased systemic venous return, reduced cardiac output –> tachycardia, hypotension, hypoxia, absence of breath sounds, hyperresonance to percussion on the affected side. tx: emergent needle thoracostomy
ansa cervicalis? how can it be injured?
arises from C1, C2, C3 nerve roots. innervates sternohyoid, sternothyroid, omohyoid muscles of anterior neck. injured if penetrating trauma to the neck superior to cricoid cartilage.
how can CN XI be injured?
surgery involving posterior triangle (sternocleidomastoid, clavicle, trapezius)
inferior thyroid artery course
thyrocervical trunk off subclavian artery. courses posterior to carotid artery and supplies inferior pole of thyroid gland.
