test #14 4.2 Flashcards
which n. can be affected by an acoustic schwanomma?
CN VII and CV by proximity
parinaud syndrome (dorsal midbrain syndrome)
paralysis of vertical gaze & pupil issues
germ cell tumors in the brain arise…
in pineal and suprasellar regions
meningiomas are commonly found…
over the lateral hemispheric fissure & parasaggital aspect of the brain convexity
prokaryotic ribosome is composed of…
3 types of rRNA and 50+ proteins
30s ribosomal subunit in prokaryote contains..
16s subunit. essential for INITIATION of protein synthesis.
16S rRNA expresses sequence
complementary to Shrine-Dalgarno sequence in all prokaryotic mRNA. [10bp upstream from AUG]
shrine dalgarno sequence
sequence 10bp upstream AUG on mRNA. binds to 16s rRNA in 30s subunit of prokaryotic ribosome. allows mRNA & 30s ribosomal subunit to bind for protein translation.
when does 50s ribosomal subunit associate?
- mRNA and 30s (w/ 16s rRNA and shrine dalgarno seq). (2) initiator tRNA binds to AUG (3) 50s subunit associates
peptidyl transferase activity of 50s subunit conferred by..
23s rRNA on 50s subunit. facilitates peptide bond formation
energy for translation translocation [where ribosome advances to next mRNA codon to be translated] in prokaryotes
facilitated by elongation factor G, energy by GTP
tissues w/ surface ectoderm origins
rathke’s pouch (anterior pituitary), LENS & CORNEA, INNER EAR SENSORY ORGANS, olfactory epithelium, epidermis, salivary, sweat, & mammary glands
tissues w/ neural crest (ectoderm) origins
autonomic, sensory & celiac ganglia. schwann cell, PIA & ARACHNOID MATER, aorticopulmonary septum & endocardial cushions, BRANCHIAL ARCHES (bones & cartilage), skull bones, melanocytes, adrenal mudella
mesoderm
muscle (skeletal, cardiac, smooth), connective tissue, bone & cartilage, serosa linings (peritoneum), cardiovascular system, blood, lymphatic system, SPLEEN, internal genitalia, kidney & ureters, adrenal cortex
endoderm
GI tract, liver, pancreas, lungs, thymus, parathyroids, thyroid follicular cells, middle ear, bladder & urethra
gastrulation (formation of 3 germ layers) occurs.. initiated by..
3rd wk of embryogenesis. initiated by formation of PRIMITIVE STREAK: thickening of epiblast cell layer that appears caudally and extends cranially. epiblast cells undergo epithelial-to-mesenchymal transition, causing loss of cell-cell adhesion properties– allows migration downward through primitive streak to form mesoderm and endoderm layers. remainder of epiblast = surface ectoderm.
notochord formation
2 days into gastrulation, some epiblasts migrate cranially through the primitive node (cephalic end of primitive streak) to form midline structure –> notochord. which induces overlying ectoderm to differentiate into neuroectoderm & form neural plate –> neural tube & neural crest cells (remainder of ectoderm –> surface ectoderm)
notochord becomes…
nucleus pulposus of intervertebrae disk in adults
clinical manifestation of Edwards syndrome (trisomy 18)
- FACE: microstomia, micropthalmia, cataracts, coloboma (hole in eye), low set & malformed ears, prominent occiput.
- CNS: microcephaly, neural tube defects, holoprosencephaly.
- MUSCULOSKELETAL: CLENCHED HANDS w/ overlapping fingers, rocker-bottom feet, short sternum, hypertonia.
- CARDIAC: VSD, patent duct arteriosus
- GI: Meckel’s diverticulum, malrotation
ultrasound findings suggesting edwards syndrome
intrauterine growth restriction, polyhydramnios, fetus w/ abnormal hand arrangement
direct thrombin inhibitors examples (2)? rx?
lepirudin & agratroban. rx: heparin-induced thrombocytopenia
ticlopidine and clopidergel use (3)
percutaneous coronary interventions (PCI), unstable angina, nonQwave MI
folate deficiency inhibits formation of what substrate?
dTMP (deoxythymidine monophosphate). can reduce erythroid precursor cell apoptosis if supplement thymidine
thymidylate synthase catalyzes what rxn?
methylation of dUMP (deoxyuridine monophosphate) to dTMP (deoxythymidine monophosphate) WHILE converting folate derivative 5-10 methylenetetreahydrofolate (methylene -THF) to dihydrofolate (DHF). de NOVO dTMP production. methylene-THF donates 1 carbon group to dUMP –> dTMP
thymidylate synthase is essential in the supply of which nucleotide precursors?
all 4 precursors of DNA replication (directly – thymidine) indirectly (w/ DHF) – purines
diminished dTMP synthesis w/ folate deficiency can be partially compensated w/
thymidine salvage pathway using thymidine kinase (normally accounts for 5-10% of dTMP synthesis). can use this w/ thymidine supplemenentation
major source of nitrogen in synthesis of nucleotides?
glutamine. i.e. contributes nitrogen atom to biosynthesis of dUMP.
withdrawal symptoms for alcohol & benzodiazepines? exam findings?
symptoms: tremors, agitation, anxiety, delirium, psychosis. benzo, also: perceptual disturbances (depersonalization), insomnia. exam: seziure, TACHYCARDIA, palpitations
heroin withdrawal symptoms? exam findings?
symptoms: nausea, vomiting, abdominal cramping, muscle aches.
exam findings: DILATED PUPILS, YAWNING, piloerection, LACRIMATION, hyperactive bowel sounds
stimulants (eg. cocaine & amphetamine) withdrawal symptoms? examination findings?
symptoms: increased appetite, hypersomnia, INTENSE PSYCHOMOTOR RETARDATION, SEVERE DEPRESSION (“crash”). no significant findings on exam.
nicotine withdrawal? examination findings?
dysphoria, irritability, anxiety, INCREASED APPETITITE
when does opiod withdrawal occur
as soon as 6-12 hrs after use, peaks 24-48 hrs. vitals usu normal.
drug withdrawal w/ potentially fatal symptoms
ALCOHOL withdrawal. 12-24 hrs after, autonomic hyperactivity (tachycardia, HTN), also seizures
layers of bone from middle to end
diaphysis, metaphysis, epiphyseal cartilage (growth plate), and epiphysis
two effect of estrogen on bone growth
(1) stimulates rapid linear growth (stimulates osteoblasts, inhibit osteoclast), but also (2) encourage closure of epiphyseal plates (fusion of epiphysis and metaphysis).
somatomedin C
also known as insulin-like growth-factor 1 (IGF-1)
IGF-1 / somatomedin C on bone growth
differentiation and proliferation of chondrocytes in epiphyseal growth plate (increase in linear growth). unlike estrogen, does not accelerate epiphyseal closure.
why does precocious puberty –> short stature but excess GH pre-puberty –> gigantism?
(1) excess sex steroids –> premature closure of epiphyseal growth plate –> short. (2) excess GH –> IGF-1 –> chondrocyte differentiate & proliferate in epiphyseal plate, no closure
smoking can induce what change in hemoglobin
formation of carboxyhemoglobin – via inhalation of CO
which cells in kidney increase EPO production in response to hypoxia?
cortical cells in kidney
HELLP syndrome
hemolytic anemia, elevated liver enzymes, low platelets (thrombocytopenia)
triad of pre-eclampsia
(1) hypertension, (2) proteinuria, (3) edema in pregnancy (diagnosis can be made w/o edema). occurs in <10% of pregnancies. typical onset after 20th wk of gestation.
gestational diabetes associated w/ increased rates of
(1) still birth and (2) macrosomia (large baby)
eclampsia vs. pre-eclampsia?
PRE-eclampsia: HTN, proteinuria, edema. ECLAMPSIA: w/ seizures.
pre-eclampsia can progress to..
HELLP syndrome. hemolytic anemia, elevated liver enzymes, and low platelets.
(1) older patient w/ (2) bone pain and (3) increase alkaline phosphatase level
Paget’s disease of the bone
microscopic analysis of bone in Paget’s disease of the bone
increased osteoclastic activity —> increased osteoblastic activity. net result: mosaic pattern of lamellar bone w/ irregular sections linked by cement lines (representing previous areas of bone resorption)
describe areas of bone affected by Paget’s disease
increased fibrous tissue deposition & vascularity (induced by proliferation of fibroblasts & endothelial cells)
increased vascularity in Paget’s bone disease can result in..
arteriovenous shunting that can result in high-output heart failure.
oil/water parition
used to describe pharmacokinetic properties of general anesthetics (relative solubility in oil vs. water)
rx for narcolepsy? 2
1st line: modafinil – non-ampetamine stimulate. unclear mech, increase dopamine signaling.
2nd line: amphetamines
carbamazepine rx (2)
trigeminal neuralgia and seizures
zolpidem
non-benzodiazepine hypnotic used for insomnia
melatonin rx (2)
jet-lag and age-related insomnia
CEA (carcinoembryonic antigen)
inreased in 60-90% of patients w/ colorectal cancer. glycoprotein involved w/ cell adhesion. produced in embryonic pancreas, liver, and intestine. can be detected in healthy people.
why can’t CEA be used to diagnose colon cancer? what can it be used for?
increased in pancreatic, gastric, and breast malignancies. also, benign diseases like inflammatory bowel disease, cirrhosis, and pancreatitis. smokers. sensitive indicator of colorectal cancer recurrence (measure pre-op and during surgery).
tumor grade looks at
degree of tumor differentiation
tumor stage reflects..
extent of spread
most important factor determining survival of patients w/ colon cancer?
STAGE: lymph node involvement & distant mets.
metabolic acidosis in diabetes caused by which 2 substrates?
ketones: (1) beta-hydroxybutyrate and (2) acetoacetate
where can meningococci be isolated from in asymptomatic carriers?
oropharynx and nasopharynx (transmission w/ respiratory droplets)
how does meningococci enter blood from pharynx?
pilus-mediated adherence and penetration of mucosal epithelium (to gain access to circulation). recall n. meningitidis makes IgA protease.
recurrent lobar hemorrhages in elderly patient most likely results from..
cerebral amyloid angiopathy. (beta-amyloid deposited into arterial wall, weakining it, predispose to rupture). related to advanced age (not systemic amyloidosis)
most common presentation of cerebral amyloid angiopathy?
recurrent HEMORRHAGIC strokes.
HTN hemorrhagic strokes vs. amyloid-associated strokes
HTN: LARGE and involve basal ganglia. AMYLOID: cerebral hemisphere, involving smaller areas– lower mortality rate, more benign course
carotid artery atherosclerosis & cardiac embolism are common causes of..
ISCHEMIC strokes
great lakes, mississippi, ohio river valley
blastomycosis
lung granulomatous inflammation w/ fungal infxn?
think blastomycoses. can cause illness in immunocompetent too.
histology of blastomycoses
round yeast w/ thick, doubly refractive walls. each yeast –> single broad based bug.
rx for blastomycoses?
itraconozole
typical ECG of atrial fibrillation
absent P waves, chaotic fibrillatory (f) waves, irregularly irregular R-R intervals, narrow QRS complexes (narrow –> tachycardia)
pathophysiology of atrial fibrillation
normally. SA node –> right atrium –> interatrial pathway –> left atrium.
AFIB: atrial excitability is heightened, mult impulses generated in areas other than SA node. some regions = shortened refractory period. other = decreased conductivity. all in all, multiple re-entrant impulses travel.
some abnormal atrial impulses reach AV nodes –> ventricles. majority do not go through bc AV node refractory period.
refractory period in AV node prevents then average atrial rate of 300-500 in afib from transmitting to ventricles
note: SA node and AV node abnormal in atrial fibrillation?
NO! the atria are hyperexcitable and have multiple impulses generated in regions other than SA node. but SA node is fine, so will NOT have new site of impulse generation
effect of competitive & noncompetitive antagonists on ED50 and Emax
competitive = change ED 50 = shift right. noncompetitive = change Emax = shift down (on a effect v. dose curve)
granulosa-theca tumors commonly present in
postmenopausal women
describe histology of granulosa cell tumor
small, cuboidal cells that grows in cords/sheets. can see gland-like structures w/ acidophillic materia: call-exner bodies –> immature follicles
what 2 tissues normally produce AFP?
fetal liver and yolk-sac
AFP is a tumor marker for..
hepatocellular carinoma, nonseminomatous testicular carcinoma, ovarian carcinoma
CA-125 is found in elevated amounts on the surface of which 3 tumors
malignanct ovarian epithelial cells in (1) serous (2) endometroid (3) clear cell carcinomas
Bohr effect (hemoglobin)? how does this happen? Haldane effect?
BOHR: peripheral tissue, release of O2 from hemoglobin facilitated by increase PCO2 and resultant decreased pH (H2CO3 = HCO3- and H+). due to histidine side chains on alpha and beta hemoglobin side chains. HALDANE: in lungs, rise in pO2 increases binding of oxygen to hemoglobin and release of H+ and CO2 from hemoglobin (H + HCO3- back into RBC, to be converted to CO2)
where is the chloride concentration of RBCs highest?
in venous blood (exchanged bicarb into plasma or Cl-)
combined cardiac and vascular fxn curves
cardiac: as cardiac muscle is stretched, cardiac output increases [frank-staring effect]. venous return curve: describes how venous return changes w/ variations in right atrial pressure
when venous return curve intersects w/ x-axis..
means no more venous return. venous pressure = right atrial pressure. the mean systemic filling pressure (measure of the degree of FILLING of the circulatory system relative to the circulatory CAPACITY.
on cardiac - vascular fxn curves, what shifts venous return x-intercept to right? left?
right: increased blood volume i.e. excessive hydration. left: acute hemorrhage
how does increased TPR affect cardiac/vascular fxn curve? decrease?
increased TPR –> decrease slope of both curve, bc higher vascular resistance restricts venous return, and increases afterload.
CREST syndrome symptoms
Calcinosis, Raynaud syndrome, Esophageal dysmotility, Sclerodactyly, Telangiectasia
crest syndrome is.. pathogenesis?
a systemic sclerosis variant that mostly involves SKIN of the FACE & fingers. pathogenesis unclear: unknown antigen stimulates accumulation of CD4+ lymphocytes in skin and other tissues. CD4+ cells stimulate fibroblasts to product collagen
hallmark of systemic sclerosis
excessive tissue fibrosis
GI issues in CREST syndrome
esophageal dysmotility, result of atrophy & fibrous replacement of esophageal muscles (muscularis). esophageal body and LES become atonic & dilated – REFLUX: heartburn, regurgitation, dysphagia. dilated esophagus w/ absent peristalisis.
what disorder results in an increase resting lower esophageal sphincter tone & diminished LES relaxation during meals?
achalasia. barium swallow –> distended esophageal body w/ narrow LES “bird beak”
abnormal location of gastroesophageal junction
sliding hiatal hernia. prone to GERD
periodic non-peristaltic esophageal muscle contractions are seen in..
diffuse esophageal spasm. clinical manifestation = dysphagia and chest pain. barium esophagus = “corkscrew esophagus”
bird-beak esophagus –> stomach in barium swallow
achalasia
corkscrew esophagus on barium swallow
diffuse esophageal spasm
earliest visceral manifestation of systemic sclerosis
esophageal hypomotility & incompetence of LES (due to atrophy and fibrous replacement of esophageal muscles). esophageal dilation –> reflux.
caspofungin is most active against which 2 fungi? not active/limited against which 2?
most active against: candida and aspergillus. not active: cryptococcus neoformas. limited: mucor / rhizopus
normal QRS duration
0.08-0.12 seconds ( 2-3 little boxes)
how does QRS change w/ exercise
normally, QRS interval shortens during exercise (normal = 80-120msec)
antiarrhythmic that exhibits strong use dependence?
normal QRS interval at baseline, prolonged when exercise i.e. FLECAINIDE (class IC antiarhythmic)
explain use dependence of Class IC antiarrhythmics
IC bind to fast Na+ channels; responsible for phase 0 depolarization (block inward Na+ current, prolong QRS). IC are SLOWEST to dissociate from Na+ channel –> so Na+ blocking effects INTENSIFY as HR increases (bc less time between AP for mediation to dissociate from receptor)
which antiarrhythmic drugs do NOT affect QRS interval:
selective B1 blockers (lower HR), digoxin (lower HR), dofetilide, verapamil (slow SA and AV node conduction)
which drug can cause false ST segment depression during exercise?
digoxin
which antiarrythmic drug displays reverse use-dependence?
class III (i.e. dofetilide), block outward K+ currents during repolarization. prolongs QTc interval. the slower the heart rate, the more QT interval is prolonged.
2 toxins w/ clostridium difficile
enterotoxin A: watery diarrhea. cytotoxin B: colonic epithelial cell necrosis & fibrin deposition
clinical presentation of c. diff
(1) range from watery diarrhea to fulminant colitis (toxic megacolon (2) sigmoidoscopy shows characterestic white/yellow pseudomembranes
best method of diagnosis C. diff colitis?
PCR detection of toxin A and B genes in stool
ingestion of undercooked shellfish is associated w/ (3)
(1) vibrio cholerae (2) norwalk virus (3) hepatitis A infxn
vaccine preventable causes of diarrhea (2)
(1) hepatitis A (2) typhoid fever
white/yellow membrane-like plaques on colonoscopy are virtually pathognomonic for…
clostridium difficile colitis
histopatholgoy of acute rejection (usu 1-4 wks following transplant)
dense infiltrate of mononuclear cells usu composed primarily of T-lymphocytes.
histopathological presentation of hypersensitivity myocarditis
perivascular infiltrate w/ abundant eosinophils. often due to initiation of new drug therapy, against which body mounts an atopic response
presentation of chronic rejection
scant inflammatory cells w/ interstitial fibrosis
ulcer found in distal duodenum suggests..
Zollinger-Ellison
suggests of Zollinger-Ellison induced duodenal ulcers?
(1) distal duodenum (2) multiple (3) refractory to therapy (4) recurrence of ulcer after acid-reducing surgery
where are Zollinger-Ellison tumors located. malignant?
majority in pancreas, but some in duodenum, stomach, etc. 2/3 of tumors are malignant.
clinical presentation of zollinger-ellison?
(1) duodenal / gastric ulcers (2) diarrhea (bc pancreatic / intestinal enzymes inactivated by gastric acid, cannot digest nutrients
stress-related mucosal erosions (acute erosive gastritis)
after surgery, head trauma, burns, or heavy NSAID use. multiple shallow mucosal defects seen in the stomach. EROSIONS, by definition, DO NOT PENETRATE MUSCULARIS MUCOSA
chronic gastritis w/ antral sparing…
autoimmune gastritis
chronic antral-predominant gastritis
h. pylori infxn
gastric ulcers are commonly found..
on lesser curvature.
peptic ulcer disease duodenal ulcer…
usu located 3cm from pylorus
ipratropium / tiotropium
blocks action of acetylcholine at muscarinic receptors in lungs (less effective at bronchodilation compared to B2-agonist)
methylxanthines, like theophylline and aminophylline…
bronchial dilitation by (1) decreasing phosphodiesterase activity (increase cAMP) and (2) block adenosine receptors
zileuton
inhibits 5-lipoxygenase. prevents leukotriene formation. prophylatic. use in (1) allergic rhinitis (2) bronchial asthma
flunisolide
inhaled glucorticoid, prophylactic rx
most preferred prophylatic rx: of bronchial asthma?
inhaled glucocorticoids like flunisolide
1st line treatment for most patients w/ acute gouty arthritis? 1st line in elderly? overall 2nd line?
1st line most: NSAID (cox inhibitors). avoid in elderly, pts w/ hepatic and renal fxn [GI bleed risks, fluid retention, aggravation of hypertension, precipitation of CHF). 1st line elderly: systemic or intra-articular glucocorticoids. overall 2nd line: colchicine (bc side effects of nausea and diarrhea)
when are uricosuric agents contrainidicated?
during acute gouty attacks
most important factor in diagnosis tetanus?
strong clinical suspicion! history & physical exam: HISTORY: (1) immunization status (2) length of time since las tetanus vaccine / booster (3) history of penetrating trauma (piercing wound, burn, illicit drug use, contaminated soil, MVA) PHYSICAL EXAM: (1) trismus (2) risus sardonicus (3) opisthotonos – extension of truncal muscles.
note: NO SERUM TOXIN ASSAY AVAILABLE for TETANOSPASM. blood cultures are of little use – local infxn. also, takes long to identify even when it does grow. no Ab test
3 unidirectional enzymes in glycolysis
(1) hexokinase (2) phosphofructokinase (3) pyruvate kinase
4 enzymes needed to ‘reverse’ glycolysis (gluconeogenesis)
(1) pyruvate carboxylase (2) PEP carboxykinase (3) fructose 1,6 bisphophosphatase (4) glucose-6-phosphatase
role of fructose 2,6-bisphosphate
control balance between gluconeogenesis and glycolysis. allosterically inhibits fructose-1,6-bisphosphatase. allosterically activates PFK-1.
conversion of glucose to alanine begins w..
transamination of alanine to pyruvate
how does glucagon & insulin affect gluconeogenesis vs. glycolysis
via interconversion of fructose-6-phosphate and fructose-2,6-bisphosphate. BIFUNCTIONAL enzyme. GLUCAGON PHOSPHORYLATES it: activating the fructose-2,6-bisphosphatase.
INSULIN DEPHOSPHORYLATES, activating phosphofructokinase-2
fatty acid synthesis is upregulated by increased… (2)
(1) insulin (2) citrate – which is increased when acetyl-CoA is abdundant, as w/ active glycolysis.
foramen ovale is patent in..
20-30% of normal adults. usu remains fxnally closed due to pressure. consider when pt w/ DVT has STROKE
in patients w/ persistent truncus arteriosus, always see associated…
ventricular septal defect
persistent ductus arteriosus usu closes..
by 3rd month of life, due to high O2 from left to right.
attributable risk percent
ARP = (relative risk - 1)/RR or..
ARP = risk in exposed - risk in unexposed / risk in exposed
which branch of MCA supplies Broca (inferior frontal)? Wernicke (posterior superior temporal)>
broca –> superior division. wernicke –> inferior division
power (1-B)? depends on.. (2)?
probability of rejecting null when its truly false. depends on sample size & diffference in outcome between two groups
sheehan’s syndrome
high estrogen in pregnancy –> growth of pituitary –> larger & more vascular. hypotension w/ postpartum hemorrhage –> ISCHEMIC NECROSIS of pituitary –> hypopituitary. present w/ inability to lactate, also hypothyroid, hypocortisol
autoimmune hypophysitis: when does it occur? presentation?
sometimes seen late preg / early postpartum – anterior & posterior inflammation. presentation: (1) ACUTE headaches, (2) visual defects, (3) cortisol deficiency (unknown why, but cortisol deficiency before others)
pituitary apoplexy? presentation?
HEMORRHAGE into a preexisting pituitary adenoma. MEDICAL EMERGENCY. present: acute, severe headache, opthalmoplegia, altered sensorium. give steroids.
how would infiltration (i.e. sarcoid, histiocytosis X, mets) into the pituitary present?
compress stalk, decrease hypothalamic dopamine –> loss of inhibition of lactotrophs –> elevated prolactin
most common location for intussusception? presentation
ileocolic junction (small ileum into larger cecum). in pts < 2 = no structural cause, viral infxn. in pts >2 = look for cause i.e. meckle diverticulum, foreign body, tumor. presentation = colicky, intermittent abdominal pain, nausea, vomiting, “currant jelly” stools – blood & mucous
inspiration on cardiac parameter. increase murmur? decrease?
increase R venous return. decrease L venous return. increase right sided murmurs, decrease left sided.
valsalva strain / rapidly standing on cardiac parameter? increase murmur? decrease?
decrease preload and afterload(?). INCREASE HCM and MVP murmurs (due to decrease LV volume) *. decrease most others (i.e. flow through stenotic valve or regurg)
squatting on cardiac parameter? increase murmur? decrease?
increase preload & afterload. increase most murmurs (stenosis / regurg). decrease MVP and HCM.
passive leg raise on cardiac parameter? increase murmur? decrease?
increase preload. like squating, increases most murmurs (regurg/stenosis). decrease HCM and MVP.
handgrip on cardiac parameter? increase murmur? decrease?
increase afterload. increase AR, MR, VSD. decrease HCM and AS
what is valsalva
forced exhalation against a closed glottis, increase intrathoracic pressure
why does MVP murmur decrease w/ increase preload / afterload?
increased LV volume brings valve leaflets into more normal anatomic arrangement (facilitating proper closure)
defect in MVP
mitral incompetency resulting from elongation & redundancy of valve leaflets and chordae tendineae. click –> chordae tendinae as they are pulled taut by ballooning leaflets. murmur – impaired coaptation of valve margins during systole
most common cause of MVP in developed countries? what else can?
most common: sporadic myxomatous degeneration of mitral valve. could also be Marfan or Ehler-Danlos
histology of sporadic myxomatous degeneration of mitral valve?
attenuation of fibrosa (collagen) layer of valve. thickening of spongiosa layer (deposition of mucoid/myxomatous material). also, thinning of collagenous core of chordae tendinae
AIDs patients have risk of which malignant proliferation
EBV associated –> non-Hodgkin’s lymphoma (including aggressive diffuse large B-cell lymphomas and Burkitt’s)
what 2 diseases does BK virus cause?
(1) nephropathy (typically post-transplant when latent virus is reactivated (2) hemorrhagic cystitis
potential causes of dilated cardiomyopathy (4)
viral myocarditis, alcohol toxicity, diptheritic myocarditis, chemo (doxorubicin / daunorubicin)
