test #20 4.10 Flashcards
describe alcoholic cirrhosis
form of micronodular cirrhosis, associated w/ hepatocyte death followed by fine fibrosis of liver.
will result in increased portal HTN.
pathogenesis of ascites in patients w/ cirrhosis. rx (2)?
- mechanical compromise of portal vein (fibrotic tissue)
- vasoactive agents cause dilation of splanchnic arterial vasculature & further intrahepatic vasoconstriction.
ascitic fluid formation –> overall, decreases systemic fluid pressure –> kidney’s RAA –> Na+ and H20 retention.
rx: furosemide and spironolactone
male mesonephric ducts form (3)
internal genitalia: epididymis, ductus deferens, seminal vesicles.
urogenital folds form? in male & female?
male: ventral aspect of penis.
female: labia minora
genital swellings form? in male & female?
male: scrotum
female: labia majora
urogenital sinus in males? females?
male: bladder, urethra, prostate, bulbourethral glands.
female: bladder, urethra, lower vagina, bartholin glands.
female paramesonephric ducts form?
internal genitalia: uterine tubes, uterus, cervix, upper vagina
DHT role in embryonic life? adult life?
embryonic life: formation of external male genitalia.
adult: secondary sex characteristics.
why are inferior MI associated w/ bradycardia? rx?
usu result from right coronary artery occlusion, which also feeds sinoatrial node.
rx: atropine. recall side effects though (i.e. myadriasis: acute-angle glaucoma)
risk for closed angle glaucoma?
asian’s and inuits
iridovyclitis
aka uveitis. anticholinergics can help reduce pain & prevent adhesion formation
rx for bradycardia?
atropine!
PTSD criteria
repeatedly reliving traumatic, life-threatening event in form of nightmare / flashbacks. avoid reminders. social detachment. poor sleep/concentration. hypervigilance. LONGER THAN 4 wks.
acute stress disorder
identical symptoms to PTSD, but symptoms from 2 days - 4 weeks.
adjustment disorder
behavioral or emotional symptoms in response to a psychosocial stressed that arose within 3 months. marked distress in EXCESS of that EXPECTED from exposure to stressor. functional expected.
differentiate PTSD from acute stress disorder? from adjustment disorder?
PTSD > 4 wks. acute stress 2 days - 4wks.
adjustment: distress in excess of what you’d expect for a given exposure.
repeated & prolonged kneeling causes..
PREPATELLAR bursitis. “housemaid’s knee”. see in roofers, carpenters, plumbers. pain erythema, swelling, inability to kneel on affected side.
located between patella & the overlying skin & prepatellar tendon. lined by synovium, contains little fluid.
popliteal and gastrocnemius bursitis associated w/
formation of Baker’s cyst
anserine bursitis (pes anserinus bursitis)
pain along medial aspect of knee. overuse in athletes, or chronic trauma in patients w/ heavy body habitus. tenderness to palpation 4xm distal to anteromedial joint margin of knee.
diabetic ketoacidosis
low total K+: low intracellular stores w/ normal-HIGH extracellular levels.
acidosis, lack of insulin = pulls into extracellular environment.
osmotic diuresis = pulls K+ out of body
MUST REPLACE K+ during ketoacidosis.
what drug reduces morbidity and mortality in class III and IV heart failure patients?
spironolactone / epleperone (more selective)
(in addition to standard therapy of ACEIs, digoxin, diuretic)
less about its diuretic effect. more about blockade of aldosterone on heart remodeling.
elastase can be found..
in macrophage lysosomes & large, azurophil (primary) granules of neutrophils.
what does clara cell CCSP do?
inhibit neutrophil recruitment and activation.
where do goblet cells stop
are not in bronchioles downwards.
urge incontinence / overactive bladder syndrome caused by…
uninhibited bladder contractions (detrusor instability) rx: oxybutynin: antagonist muscarinic receptors, esp M3 on smooth muscle of bladder.
b1 receptors are located..
in heart & renal juxtaglomerular cells
a2-agonists? rx?
methyldopa and clonidine. decrease sympathetic outflow and BP.
B2 stimulation causes..
bronchodilation, vasodilation, and tocolysis (baby extrusion)
5-HT, serotonergic neurons are located in brain…
raphe nucleus of brainstrem (midbrain, pons, medulla)
sleep-wake cycle, arousal.
NE-secreting neurons found in brain…
nucleus ceruleus. DORSAL PONS
acetylcholine neuron cell bodies located in..
nucleus basalis of Meynert
red nucleus of midbrain?
motor coordination of upper extremeities.
for blood flow to be continuous..
systemic blood flow / minute = pulmonary blood flow / minute (in both exercise and rest)
continuous circuit!
in all scenarios, arterial resistance is higher in systemic circulation.
normal systemic & pulmonary blood pressure
systemic: 120/80.
pulmonary: 14mmHg
rx for tinea (pityriasis) versicolor
(1) topical antifungals or (2) selenium-containing shampoo.
present as hypopigmented spots on sun-tanned skin. only really a cosmetic problem.
most important factors locally regulating coronary blood flow?
adenosine and NO
formation of NO in coronary endothelial cells? downstream signalling?
arginine + oxygen —> nitric oxide (with eNOS, endothelial nitric oxide synthase).
works on cytosolic guanylate cyclase
a2 receptors are..
CENTRALLY located!
Courvoisier sign
palpable but not tender gallbladder
(5) risk for pancreatic adenocarcinoma (at head)
- age: 65-75
- SMOKING (most impt environment risk factor; DOUBLE risk)
- diabetes mellitus: increases w/ duration of disease
- chronic pancreatitis
- genetic predisposition: hereditary pancreatitis, MEN, HNPCC, FAP
low-fiber diet increases risk of…
colon adenocarcinoma
alcohol consumption increases risk for which malignant tumors?
head, neck, esophagus, liver
strawberry hemangioma
unencapsulated aggregates of closely packed, thin-walled capillaries. benign, common. found in skin, subcut tissue, oral mucous membranes, lips. can occur in liver, spleen, kidney.
initially, grow in proportion to child. ‘regress spontaneously before/at puberty.
cortisol receptor and downstream signal cascade
cytoplasmic, binding causes homodimerization. translocate to nucleus, control gene expression by binding to DNA at hormone-response elements in promoter region of genes.
increase transcription of genes needed for gluconeogenesis (formation of glucose from fat and protein)
growth hormone signal transduction
membrane bound receptor –> dimierzation, conformational chain in JAK, stimulates tyrosine kinase, activates STAT transcription activity.
increases gluconeogenesis by increasing lipoylysis, gluconeogenesis in liver.
catecholamines & glucagon signal transduction
GPCRs coupled to adenylyl cyclase.
epinephrine and glucagon increase glycogenolysis. stimulate glycogen phosphorylase kinase, which activates glycogen phosphorylates & liberates glucose.
abnormal transformation of mullerian ducts can result in
wide range of defects: hypoplasia or agenesis of vagina / uterus, duplication of vagina, cervix, uterus; and unicornate, bicornuate, septate uterus.
2 most common causes of eugonadotropic amenorrhea
imperforate hymen and mullerian duct abnormalities.
distinguish presentation of HUS and TTP
different points on spectrum of disease. both: fever, thrombocytopenia, microangiopathic hemolytic anemia.
TTP: often adult w/ neurological symptom
HUS: often children w/ renal involvement
BOTH life threatening
HUS
endothelial damage, isolated activation of platelets, shearing on RBCs (hemolysis)
autoimmune hemolytic anemia can occur w/ (2)
mycoplasma pneumonia and EBV
leukoerythroblastosis peripheral smear?
nucleated red cells, immature white cells. seen when bone marrow replaced w/ fibrosis or metastatic cancer. dacrocytes on smear
schistocytes suggests..
microangiopathic hemolytic anemia (TTP, HUS, DIC) or mechanical damage (i.e. mechanical valve)
most common inherited blood disorder in US
sickle cell anemia
sicking in sickle cell anemia promoted by..
low oxygen, increased acidity, low blood volume (dehydration)
how does 2,3 DPG increase oxygen delivery?
binds 2 beta chains (ionic), stabilize taut deoxyhemoglobin.
pseudomonas cepacia =
Burkholderia cepacia
heart failure
broadly defined term meaning heart either cannot pump enough blood to meet tissue metabolic requirements or can do so only from an elevated ventricular filling pressure.
systolic vs. diastolic heart failure
diastolic: NORMAL ejection fraction, NORMAL contractility. POOR compliance.
systolic: POOR EF, POOR contractility
long-standing HTN leads to both impaired relaxation & stiffness of heart (diastolic heart problems)
isolated diastolic heart failure on pressure-volume curve
upward and to the left (bc of compliance problems)
increased LVEDP. normal ejection fraction, normal LVEDV.
decompensation when LVEDP is so high we get pulmonary edema, dyspnea. etc
isolated systolic heart failure on pressure-volume curve
poor stroke volume. to counter this and maintain CO –> increase LVEDP and LVEDV (to improve stroke volume)
differentiate rubella (german measles) and measles (rubeola)
both maculopapular rash that begins on face and spreads to trunk & extremities.
rubella spreads faster.
measles darkens / coalesces.
rubella: postauricular & occipital lymphadenopathy (togavirus)
describe appearance of varicella zoster rash
maculopapular rash, begins on trunk and spreads centrifugally to face & extremities.
describe rash of roseola (HHV-6)
exanthem subitum (roseola infantum)
transient maculopapular rash that appears for a few days on chest & trunk, disappears when fever subsides.
differentiate carboxyhemoglobin & methemoglobin.
carboxyhemoglobin: CO bound to hemoglobin at heme binding sites (normally occupied by oxygen)
methemoglobin: when Fe2+ in heme is oxidized to Fe3+. results from drug exposures (dapsone, nitrites) as well as enzyme deficiencies and hemoglobinopathies.
carbon monoxide poisoning causes..
(1) binds to hemoglobin w/ 250x affinity more than O2. reduce number of heme binding sites available for oxygen.
(2) CO causes leftward shift of hemoglobin-oxygen dissociation curve (decrease tendency to unload)
(3) interruption of oxidative phosphorylation
CO + hemoglobin = carboxyhemoglobin
hypoxia seen w/ CO poisoning is similar to that in..
anemia! decreases in oxygen carrying capacity of blood [CO is worse, bc of leftward shift]
most dangerous side effect of amphotericin B
nephrotoxicity.
decrease GFR and direct toxic effects on tubular epithelium.
can lead to anemia & electrolyte abnormalities –> hypokalemia (weakness and arrhythmia) due to increased distal tubular membrane permeability.
ECG findings of hypokalemia
T-wave flattening, ST-degment depression, prominent U waves, premature atrial and ventricular contractions. even ventricular tachycardia / fibrillation.
acetaminophine and halothane toxic effect..
liver necrosis.
chronic rejection of lungs
affects small bronchioli – obstructive lung diesase: BRONCHIOLITIS OBLITERANS
acute rejection of lungs
perivascular mononuclear infiltrates on histology. dry cough, dyspnea, fever
leading cause of death in lung transplant recipients?
infection. CMV, most significant opportunitistic infection.
primadone
antiepileptic that is metabolized to phenobarbital and PEMA (phenylethylmalonamide). all 3 are active anticonvulsants.
acylclovir toxicity. prevent?
crystalline nephropathy. prevent w/ aggressive hydration
1st most common brain tumor in adult? 2nd?
1st: glioblastoma multiforme.
2nd: meningioma.
describe meningioma
benign slow growing tumor arising from arachnoid villi. concentrically-arranged meningothelial cells. psammoma bodies.
commonly parasagital or adjacent to lateral convexity of hemisphere (sphenoid wing & olfactory groove)
dihydrofolate reductase important for..
reducing folic acid –> tetrahydrofolate. needed for transfer of carbon groups.
5-fluorouracil
pyrimidine analog, inhibits thymidylate synthetase (after conversion to floxuridine monophosphate)
binds THF and thymidylate synthetase in a stable rxn intermediate form (decreases amount of thymidylate synthetase available for thymidine synthesis)
requires THF
leucovorin (N5-formyl-tetrahydrofolate) w/ methotrexate? w/ fluoropyrimidines (5-FU)?
THF derivative that does not require reduction by dihydrofolate reductase to act as cofactor for thymidylate synthase. can RESCUE normal cells from toxicity of methotrextate
leucovorin can POTENTIATE toxicity of 5-FU by strengthening the association of drug w/ thymidylate synthase (more THF available)
cytarabine
pyrimidine analogue antimetabolite. incorporate into DNA, strand termination.
gemcitabine
pyrmidine analogue, not S-phase specific. also can inhibit ribonucleotide reductase.
fludarabine
deamination-resistant purine analogue. many mechanisms of action: inhibit DNA pol, DNA primase, DNA ligase, ribonucleotide reductase. rx for CLL.
rx for CLL
fludarabine and alemtuxumab
how long can glycogen stores keep us going
depleted after 12-18 hours
energy source when fasting (between meals)
mostly hepatic glycogenolysis
energy source 1-3 days of starvation
glycogen delete after day 1. hepatic gluconeogenesis.
energy source after 3 days of starvation
adipose stores. then protein degradation.
from what can glucose be generated from in gluconeogenesis. describe pyruvate conversion to glucose (initial steps)
glucose formed from pyruvate, from lactate, glycerol, glucogenic amino acids.
pyruvate cannot be converted to phosphoenolpyruvate directly (pyruvate kinase is unidirectional).
- pyruvate –> oxaloacetate (pyruvate carboxylase, increased activity w/ acetyl-CoA).
- oxaloacetate –> malate (malate dehydrogenase) and shuttled out of mitochondria
- malate —> oxaloacetate (malate dehydrogenase)
- oxaloacetate —> PEP (phosphoenolpyruvate (PEP carboxykinase)
why does acetyl-CoA stimulate gluconeogenesis
pyruvate builds up when converted from lactate, glycerol, glucogenic amino acids. stimulate pyruvate —> oxaloacetate (pyruvate carboxylase)
pyruvate & alanine relationship
(1) muscle converts pyruvate –> alanine (alanine aminotransferase) via transamination.
(2) alanine transported to liver
(3) alanine used in gluconeogenesis
alanine inhibits pyruvate kinase (inhibits glycolysis, but does not promote gluconeogenesis)
fructose 2,6-bisphosphate role in gluconeogenesis / glycolysis
LOW fructose 2,6-bisphosphate promotes GLUCONEOGENESIS (via fructose-2,6-bisphosphatase)
HIGH F2,6BP promotes GLYCOLYSIS. (via phosphofructokinase-2)
how does shiga-like toxin cause pathology?
transmitted to e.coli via bacteriophage. B-subunit allows for internalization.
A-subunit removes a single specific adenine residue in rRNA, preventing binding of tRNA to 60S subunit (inhibit protein synthesis) –> intestinal mucosal death
salmonella infectious path
enters orally, penetrates intestinal mucosa, travels to mesenteric lymph nodes, multiples & phagocytosed by macrophages, where it lives.
oxalate crystals suggest..
ethylene glycol ingestion (automobile antifreeze, engine coolants, hydraulic breaks).
rapidly metabolized into glycolic acid (toxic to renal tubules) and oxalic acid (ppts calcium oxalate crystals)
folded envelope / dumbell crystal in urine
calcium oxalate
coffin-shaped crystal in urine
AMP
rhomboid or rosette crystal in urine
uric acid
hexagonal crystal in urine
cysteine
early death in rheumatic fever due to..
myocarditis (pancarditis) –> cardiac dilation –> DEATH
early valvular disease w/ acute rheumatic fever
mitral valve regurgitation
late valvular disease w/ acute rheumatic fever
mitral valve stenosis
valvular damage in rheumatic fever
vegetation & fibrosis
tubular adenoma vs. villous adenoma in colon
TUBULAR adenoma: tubular-shaped glands, often smaller & pedunculated.
VILLOUS adenoma: long-fingerlike projections. large & more commonly sessile. can have velvety / cauliflower like projections. more likely to progress to adenocarcinoma. can also secrete fluid – SECRETORY DIARRHEA.
peutz-jegher syndrome
(1) multiple hamartomatous polyps in GI tract.
(2) black spots on skin & mucosa.
AUTOSOMAL DOMINANT, but RARE.
intestinal carcinoid location
usu appendeix, ileum, rectum. RARE
signet cell carcinoma locations
stomach, breast, ovary, colorectal area, etc.
symptoms of villous adenoma
bleeding, secretory diarrhea (mucous), partial intestinal obstruction. typically sessile w/ cauliflower / velvety appearance. more likely to progress to adenocarcinoma
appearance of uterus w/ ectopic pregnancy
will see pregnancy-related endometrial changes: decidualization of stroma
(w/o embryonic tissue or chorionic villi)
main risk factor for ectopic pregnancy
PID
capacity-limited (saturable) enzyme kinetics
from first-order (constant proportion metabolized over time) to zero-order (constant-AMOUNT) metabolized over time.
arteries affected in thrombangitis obliterans (buerger’s). caused by? can present w/
radial and tibial. thought to related to direct toxic injury from tobacco or hypersensitivity. often presents w/ raynaud’s
which vasculitis can extend into contiguous veins and nerves?
thrombangitis obliterans
craniopharyngioma on MRI? presentation?
usu 3 components:
- solid: actual tumor cell
- cystic: filled w/ ‘machinery oil’ liquid
- tooth-enamel califications
most common supratentorial tumor in children. present w/ headache, visual field fects, hypopituitarism (but potentially hyperprolactinemia bc of compression of pituitary stalk –> loss of dopaminergic inhibition
which amino acid becomes ESSENTIAL in PKU?
tyrosine, can no longer synthesize from phenylalanine.
clinical presentation of PKU
mutation in phenylalanine hydroxylase. can no longer make tyrosine. autosomal recessive.
fair pigmentation w/ MOUSY odor, mental impairment by 1 year, seizure, hyperactivity, gait abnormalities, problems w/ postural control, eczema.
3 major distinguishing factors between pemphigus vulgaris & bullous pemphigoid
- oral mucosa involvement
PV: affects oral mucosa most commonly.
BP: does not affect oral - rupture
PV: rupture easily
BP: does not rupture easily - immune problem
PV: desmosomes
BP: hemidemosomes
Nikolsky & Asboe-Hansen sign w/ pemphigus vulgaris
Nikolsy: new bullae form w/ gentle traction
Asboe-Hansen sign: bullar spread laterally w/ pressure
autoantibodies to cutaneous basement membrane proteins seen in
epidermylosis bullosa acquista and cicatrical pemphigoid
palmoplantar keratoderma & deafness ichthyosis
related to connexin defects
NAD+ regeneration on glycolysis.
needed for glycolysis, must be regenerated from NADH for glycolysis to continue.
aerobic conditions: NAD+ –> NADH in TCA, and NADH –> NAD+ in oxidative phosphorylation.
anaerobic glycolysis: NADH –> NAD+ in formation of lactate.
when strenuously exercising, can be limited by degree of NAD+ regeneration
when is FADH2 produced
TCA, conversion of sucinate to fumarate (succinate dehydrogenase)
carnitine
amino acid responsible for transport of fatty acids into mitochondria for beta-oxidation. synthesized from lysine and methionine, requires vitamin C
citrate is formed by.. powerfully inhibits..
formed by acetyl-CoA + oxaloacetate. powerfully inhibits phosphofructokinase-1 (rate limiting step in glycolysis)
