Flashcards in test #39 4.29 Deck (159):
what does "end-organ" blood supply mean?
interruptions in blood flow lead to formation of infarct
renal: small number of collaterals between segmental renal arteries
recall nephrotic syndrome presents w/ 5 things
1. edema (loss of albumin / oncotic pressure
4. hypercoagulation (loss of antithrombin III & increased coag factors
5. infection (loss of immunoglobulins)
histology of crohn's vs. ulcerative colitis
crohns: noncaseating granulomas & lymphoid aggregates (Th1 mediated)
ulcerative colitis: crypt abscesses (Th2 mediated)
blood in crohn's vs. ulcerative colitis
crohn's: + occult blood
ulcerative colitis: gross bleeding
string sign on barium swallow
crohn's disease: narrowing of the intestinal segment due to inflammation of intestinal wall
ulcers in crohn's? gross morphology?
1. linear or serpiginous ulcerations
2. cobblestone mucosa
3. transmural inflammatory infiltrate.
gross morphology of ulcerative colitis
1. mucosal & submucosal inflammation
2. friable mucosal pseudopolyps w/ freely hanging mesentary
loss of haustra = lead pipe
cells in moles vs. choriocarcinoma
mole: only trophoblasts; swelling villi
choriocarcinoma: trophoblasts & syncitiotrophoblasts; NO VILLI
clinical presentation of:
complete vs. partial hydatidiform mole
both: vaginal bleeding & cramps/pressure
-SIZE greater than dates &
-extremely HIGH b-hCG
[hCG can lead to:
- hyperemesis gravidarum
- theca-lutein cysts
macroscopic: complete vs. partial hydatidiform mole?
complete: friable mass of cystic, thin-walled, grapelike structures. exclusively TROPHOBLASTIC TISSUE. "bunch of grapes"
partial: mix of normal & gross enlarged chorionic villi; FETAL PARTS (fetus, cord, amniotic membrane)
micropscopic appearance: complete vs. partial hydatidiform mole?
complete: enlarged, EDEMATOUS villi w/ extensive & diffuse trophoblastic HYPERPLASIA
(no fetal tissue)
partial: some enlarged vili w/ more moderate & FOCAL trophoblastic hyperplasia.
- normal villi & fetal tissue also present
karyotype of complete & partial hydatidiform mole?
complete: completely PAPA 46 XX or 46 XY (sperm fertilizes empty egg; sperm chromosomes duplicate usu: 46 XX more common)
partial: 69 XXX or XXY
usu 1 egg w/ 2 sperms
risk of malignancy in complete & partial hydatidiform mole?
complete: 15-20% risk of malignant trophoblastic disease
partial: low risk of malignancy <5%
where is TRH made?
paraventricular nucleus of hypothalamus
main regulator of TSH section?
- T3 acts on paraventricular nucleus to decrease synthesis/release of TRH.
- down regulate TSH gene transcription & TRH receptor expression
T4 in peripheral tissues
converted to T3 or rT3 by specific deiodinases
(t3 cannot become T4 or rT3)
potency, half-life, metabolism of T4, T3, rT3
T4: 7 days
T3: 1 day
rT3: <1 day
cleared via glucuronidation in liver
[t3 not prescribed bc short half-life & rapid GI absorption = wide fluctuations]
acute acalculous cholecystitis
acute inflammation of gallbladder in absence of stones.
stasis & ischemia
PE: jaundice & palpable right upper quadrant mass = NOT SEEN IN calculous cholecystitis
complications: gangrene, perforation, emphysematous cholecystitis -- infxn w/ gas-producing agent: clostridium, e. coli
usu in hospitalized patients & severely ill
diagnosed on abdominal radiograph: rim of calcium deposits outline gallbladder
associated w/ gallbladder carcinoma
congenital dilations of common bile duct
chronic cholecystitis results in..
thickening of gallbladder wall.
US: shruken, fibrosed gallbladder
clornarchis infxn of gallbladder is associated w..
brown pigment stones
black vs. brown gallstones
black: intravascular hemolysis
brown: biliary infxn
how does valsalva affect heart?
exhale against closed glottis
abnormal proliferation of mast cells & increased histamine secretion
--> increase histamine --> gastric hypersecretion
can see nests of mast cells in bowel mucosa
chemical irritation from long-standing cholethiasis
herniation of gallbladder mucosa into muscular wall --> Rokitansky-Aschoff sinus: ducts in muscle
late complication: porcelain gallbladder
mast cells in GI tract?
mast cell proliferation in bone marrow & other organs
1. GI: increased gastric acid
- inactivation of pancreatic & intestinal enzymes --> diarrhea
- also N/V, cramps, ulcer
2. syncope, flushing, hypotension, tachycardia, bronchospasm
3. pruitus, uticaria, dermatographism
H2 receptors increase intracellular
(gastrin/Ach = Ca2+)
gastrin & Ach increase intracellular..
(H2 = cAMP)
most potent action of gastrin
most potent: increase histamine synthesis & release by ECL cells
also: stimulates Ca2+ and acid release from parietal cells
what intracellular mediators increase H+ efflux from parietal cells
cAMP and Ca2+
via H+/K+ ATPase
6-mercaptopurine / azathioprine blocks what enzyme?
inhibit de novo purine synthesis after being converted to active metabolites by HGPRT
how is 6-mp / azathioprine degraded?
reduce dose when also on allopurinol
cytotoxic purine that is an irreversible inhibitor of ADA
cytotoxic purine analog that is resistant to degradation by ADA
Aorta / IVC
Pancreas (except tail)
Ureters & Bladder
Colon (descending & ascending)
Esophagus (lower 2/3rd)
1. major vessels:
- abdominal aorta
- their branches
2. solid organs:
- pancreas (except tail)
- adrenal glands
3. hollow organs:
- parts 2/3 & part of 4 of duodenum
- ascending & descending colon (secondarily)
4. vertebral column & pelvic muscles
retroperitoneal hematoma (in a stable patient) associated w/
PANCREATIC injury --> retroperitoneal hematoma
abdominal blow from malpositioned seat belt / steering wheel --> retroperitoneal hematoma (in a stable patient) bc of damage to
transverse colon, spleen, liver..
testicular malignancy w/ hyperthyroidism
must secrete b-hCG
choriocarcinoma; disordered syncitiotrophoblasts & cytotrophoblasts.
hematogenous metastasis to lung, liver, brain.
can produce gynecomastia or hyperthyroidism (B hCG like LH & TSH)
95% of all testicular tumors are..
germ cell tumors, often malignant, in young men
testicular tumor w/ fried-egg appearance, high placental ALP?
seminoma! malignant, painless, usu 3rd decade, late mets, excellent prognosis
testicular tumor w/ schiller-duval bodies and high AFP
yolk-sac (endodermal sinus tumor)
presentation of teratoma in male scrotum
may be malignant. benign in children though.
50% have both b HCG and AFP elevations
malignant hemorrhagic mass w/ necrosis in testes w/ glandular/papillary morphology
worse prognosis than seminoma
usu mixed w/ other types
associated w/ elevated bHCG.
also AFP if mixed
testicular nongerm cell tumors
1. Leydig cell
2. Sertoli cell
3. testicular lymphoma
Reinke crystal in testicular tumor
Leydig cell tumor, nongerm cell.
androgen producing, gynecomastia in men, precocious puberty in kids.
golden brown colour
Sertoli cell tumor in male
androblastoma from sex cord stroma
most common testicular malignancy in older men
not a primary cancer, usu arises from lymphoma mets to testes
demographics of squamous cell carcinoma
asia, africa, south america
associated w/ HPV and lack of circumcision
precursor in situ lesions of squamous cell carcinoma of penis
1. bowen disease
2. erythroplasia of Queyrat
3. bowenoid papulosis
precursor lesion to SCC of penis
on penile shaft
erythroplasia of Queyrat
precusor lesion of SCC of penis
precursor lesion to SCC of penis
priapism associated w/ (3)
painful sustained erection
2. sickle-cell: trapped RBC
3. medications: anticoagulants, PDE-5 inhibitors, cocaine, alpha-blockers, trazodone
hCG is structurally similar to (3)
FSH, LH, TSH
which hormones can bind to TSH receptors
TSH and HCG (at much lower affinity)
note: FSH cannot! even though structurally similar!
cranial n. emerge from..
CN III and IV
oculomotor & trochlear (dorsal)
CN VI, CN VII, VIII, IX,
between pons & medulla
between olive & medulla
between pyramid and olive
which is the only CN to emerge dorsally
CN IV trochlear
anterior pons lesion
dysarthria & ataxic hemiparesis
-corticopsinal tract (contralateral hemiparesis & babinski)
-corticobulbar tract (contralateral lower facial palsy & dysarthria
also affect pontine nuclei & pontocerebellar fibers --> contralateral dysmetria & dysdiadochokinesia
lesions of cerebellum produce (contralateral/ipsilateral lesion)? lesions of pontocerebellar fibers in basis pontis?
pontocerebellar fibers: contralateral
(bc fibers enter cerebellum through contralateral cerebellar peduncle)
where does facial n arise?
level of facial colliculus
below middle cerebellar peduncle
middle cerebellar peduncles
incoming information from cerebrum to cerebellum, either side of pons
where does trigeminal n arise
lateral aspect of midpons, at level of middle cerebellar peduncle
where does hypoglossal n arise
preolivary sulcus at level of rostral medulla
where does oculomotor n. arise?
at level of superior colliculus & red nucleus (midbrain)
where does trochlear n. arise
level of interior colliculus
level of red nucleus.
only cranial n. to decussate before innervate target
what is the only CN to decussate?
trochlear, CN IV
glucocorticoids increase protein synthesis in..
LIVER (related to gluconeogenesis & glyocgenesis, proteolysis, lipolysis)
increase synthesis of PEP carboxykinase & glucose 6-phosphatase, glycogen synthetase
major effects of glucocorticoids (mnenomic)
1. blood pressure a1 receptor (permissive)
2. insulin resistance
3. gluconeogenesis, glycogenesis, proteolysis, lipolysis (synthesize more PEP carboxykinase & G 6-phosphatase & glycogen synthetase
1. fibroblast production of collagen
2. immune system
- inhibit production of leukotrienes and prostaglandins (block phospholipase A2 cleavage)
- inhibit leukocyte adhesion (neutrophilia)
- block histamine release from mast cells
- reduce eosinophils
-block IL-2 production
3. bone formation
-decrease osteoblast activity
- increase renal Ca2+ wasting
- decrease Ca2+ GI absorption
what receptor does glucocorticoids upregulate
alpha-1 BLOOD PRESSURE
what receptor does T3 upregulate?
beta-1 HEART RATE. etc
glucocorticoids favor catabolism of which 2 tissues? how?
skeletal muscle & adipose tissue
bc block insulin effects
results in proteolysis & lipolysis
glucocorticoid induced decrease in fibroblast activity causes (2)
1. skin thinning: purple striae, easy damage
2. CT around capillary thin --> easy bruising
smaller numbers predominant in the data set
long slope / tail extends in positive direction
mean > median > mode
median = better measure of central tendency here
larger numbers predominate in data set
long slope / tail extends in negative direction
mean < median < mode
median is better measure of central tendency here
carbon tetrachloride CCl4
causes free radical injury
oxidized by P250 system
makes free radical --> reacts w/ structural lipids of cell membranes
lipid peroxidation --> lipid degradation and hydrogen peroxide formation --> vicious cycle
swelling of ER, destruction of mitochondria, increased membrane permeability
--> hepatic necrosis
symptoms of thyrotoxicosis
palpitations, nervousness, easy fatigability, fine tremor, diarrhea, hyperhidrosis, heat intolerance, weight loss, hyperreflexia, dermopathy, opthalmia
exopthalmos, conjunctival hyperemia, periorbital edema
exopathalmosis due to..
increased soft tissue mass in bony orbit
due to enlargement of extraocular muscles from myositis, fibroblast proliferation, and overproduction of ground substance in response to antithyroid antibodies.
finely granular eosinophilic granules in hepatocytes?
hepatocellular cytoplasm becomes filled w/ spheres & tubules of HBsAg
GROUND GLASS APPEARANCE
eosinophilic big inclusion in hepatocytes. hepatocytes will also have fatty changes
ubiquinated keratin fibers
in liver of alcoholics
describe the PI3K signalling pathway
important for cell proliferation
activates PI3K (PIP2 -> PIP3)
PIP3 activates Akt (protein kinase B), a serine/threonine specific protein kinase
Akt activates mTOR, which translocates to nucleus
-- cell survival, anti-apoptosis, angiogenesis.
mTOR activation is usu inhibited by? activated by
inhibited by PTEN (phosphatase & tensin homolog), removes phosphate added by PIP3
activated: growth factors & PIP3 (PI3K/Akt/mTOR)
what determines fate of pyruvate?
low oxygen: lactate dehydorgenase converts pyruvate -> lactic acid (regenerate NAD+)
oxygen: pyruvate dehydrogenase converts pyruvate -> acetyl CoA
soleus & paraspinal muscles contain what type of fibers
type 1: red, slow twitch. ATP = oxidative metabolism
cells involved in granuloma formation (TB formation)
1. Th1 CD4+ cells secrete IFN-y
2. activates CD8+ cytotoxic T cells and macrophages
3. macrophages secrete TNF-alpha, important for granuloma formation
monosaccharide that can be absorbed w/o action of pancreatic enzymes.
see if malabsorption due to pancreatic or intestinal pathology
dobutamine on the heart
predominant B1 > B2
mostly affects myocardium
1. positive ionotropic: increased contractility. increased cardiac output, decreased ventricular filling presure
2. weakly positive chronotropic: increases heart rate. less pronounced than associated w/ dopamine
both increase myocardial oxygen consumption
3. increases cardiac conduction velocity (undesirable --> arrythmia)
nitroglycerin on HR
venous pooling -> reflex tachycardia
nitroglycerin on myocardial oxygen consumption
reduce preload --> reduce oxygen consumption, used to rx: angina pectoris.
what decreases pulmonary capillary wedge pressure
aka left atrial pressure?
decreased preload: i.e. nitroglycerin, furosemide
increased contracility: i.e. dobutamine
anything that increases perfusion also..
increases urine output!
increased renal perfusion.
warfarin in pregnancy
where are snRNP synthesized? by which polymrease
in the nucleus, RNA pol II
how does sleep apnea lead to pulmonary HTN?
hypoxemia --> pulmonary vasoconstriction
50% will also develop systemic HTN due to chronic sympathetic cardiovascular stimulation (re: hypoxemia)
official diagnosis of narcolepsy
excessive daytime sleepiness, cataplexy, REM-sleep related phenomenon (like hallucinations and sleep paralysis)
recurrent lapses into sleep (minimum 3x/wk for 3 months)
atleast one of following:
1. cataplexy (loss of muscle tone w/ strong emotion
2. low CSF hypocretin
3. shortened REM latency
associated w/ hypnagogic or hynopompic hallucinations and sleep paralysis
most common cause of excessive daytime sleepiness
obstructive sleep apnea
constantly waking up w/ apnea
first generation antihistamines have what common side effects
chlorpheniramine and diphenhydramine
antimuscarinic, antialpha-adrenergic, anti-5HT
how do H1 receptor blockers work?
decrease receptor activity by increasing proportion of inactive H1 receptors!
alcohol induced hepatic steatosis
decrease in free fatty acid oxidation
secondary to excess NADH / NAD+ ratio -->
(due to alcohol and acetaldehyde dehydrogenase)
1. promotes glyceraldehyde 3-phosphate -> glycerol 3-phosphate -> triglyceride synthesis
2. blocks TCA production of NADH -> promotes use of acetyl-CoA for ketogenesis and lipogenesis
mostly: decrease in free fatty acid oxidation secondary to excess NADH
also: impaired lipoprotein assembly/secretion, increase in peripheral fat catabolism
stain for lipids w/ (2)
sudan black or oil red O
what is transferrin & total iron binding capacity
hepatic synthesis of transferrin in markedly increased in states of F2+ deficiency.
transferrin always inverse to saturation
same direction as TIBC
high transferrin means increased serum total Fe2+ binding capacity
high transferrin -> low iron
low transferrin -> high iron
normal ferritin states
in plasma. usu 1/3rd saturated w/ Fe2+
iron panel in iron deficiency anemia (ferritin, transferrin, MCV, folate, neutrophils
low MCV (microcytic)
normal folate & neutrophils
cyanotic toe discoloration, renal failure following invasive vascular procedure suggests
atheroembolic disease of renal arteries (cholesterol lodged)
swelling of venules bc of clogged capillaries
isoniazid resistance (2)
1. stop catalase-peroxidase enzyme expression
2. genetic modification of mycolic acid synthesis enzyme
resistance to ethambutol
increased production of arabinosyl transferase
resistance to rifampin
mutation in gene for DNA-dependent RNA polymerase
resistance to streptomycin
modification of 30S ribosomal protein stxr
how does pyrazinamide work?
converted to pyrazinoic acid, lowers environmental pH in susceptible strains of TB.
must be converted to active form via pyrazinamidase
resistance to pyrazinamide?
modified pyrazinamidase (needed to convert pyrazinamide to active form)
tryptophan is essential amino acid & precursor for (3)
(1) niacin (nicotinic acid)
Hartnup disease (defect & clinical manifestation)
defective intestinal & renal absorption of tryptophan.
clinical: niacin B3 deficiency: pellagra (dermatitis, neuro: ataxia, usu wax & wane,
differentiate Hartnup disease from Fanconi syndrome
Hartnup: lose neutral amino acids
- alanine, serine, valine, threonine, leucine, isoleucine, phenylalanine, tyrosine, tryptophan, histidine)
Fanconi: generalized amino aciduria
- will ALSO have proline, hydroxyproline, argigine
flat, greasy, pigmented squamous epithelial proliferation.
look "stuck on"
head, trunk, extremities
common benign neoplasm on older people
associated w/ Leser-Trelat sign
sudden appearance of multiple seborrheic keratosis, suggesting underlying malignancy
riboflavin deficiency (B2)
FMN, FAD (needed for enzymes in ETC)
2 C's of B2
CHEILOSIS, glossitis, keratitis, conjunctivitis, photophobia, lacrimation, CORNEAL VASCULARLIZATION, seborrheic dermatitis
decarboxylation & transamination requires what cofactor
vitamin B6 (pyridoxine)
clinical presentation of pyridoxine B6 deficiency
anemia, peripheral neuropathy, dermatitis
free radical scavenger (antioxidant)
deficiency: myelopathy / neuro dysfunction
erythematous papules w/ central scale due to hyperkeratosis. "sandpaper-like" texture
can turn into cutaneous horns
precursor to squamous cell carcinoma
well-circumscribed RAISED papules & plaques covered w/ thick silver scale
usu scalp, trunk, extensors (elbow/knee)
edema of the epidermis
associated w/ atoptic dermatitis (type I HSR)
pityriasis rosea presentation
herald patch: pink/brown scale plaque w/ central clearing & collarette of scale on trunk, neck, extremities
followed by: maculopapular rash in "christmas tree" pattern along skin tension lines
patent PDA associated with..(3)
2. congenital rubella
3. fetal alcohol syndrome
ductus arteriosus comes from what aortic arch
(also proximal pulmonary artery)
1st aortic arch
2nd aortic arch
stapedial / hyoid artery
stapedial is second
3rd aortic arch
common carotid & proximal internal carotid
C = 3rd letter of alphabet
4th aortic arch
left: aortic arch
right: right subclavian
4 -> 4 limbs, systemic
6th aortic arch
PDA & proximal pulmonary artery
path of right recurrent laryngeal & left recurrent laryngeal
right: under right subclavian
left: under PDA (lower)
tissue development of branchial cleft, arch, and pouch
arch: mesoderm (cartilage/muscle)
rhomboid major innervation
dorsal scapular nerve
teres major innervation
adduct & medially rotate
inheritance of hereditary spherocytosis
describe HFE expression and regulation of Fe2+ load
basolateral surface of epithelial cells in small intestine crypts..
complexes w/ B2 microglobulin, binds to transferrin receptor to regulate endocytosis of transferrin/Fe2+ complex (ferroportin)
iron released into cell: added to iron regulatory pool --> DETERMINES intensity of APICAL Fe2+ UPTAKE
mutation in HFE -> unregulated Fe2+ absorption
--> liver cirrhosis & hepatocellular carcinoma
two types of amyloid deposits in alzheimer's disease
1. brain parenchyma: senile plaques
2. brain vascular walls: amyloid angiopathy. damage media & adventitia, cause thickening of basal membrane, stenosis, and fragmentation of internal elastic lamina
can both be seen in healthy elderly individuals
depression in elderly, can cause confusion & declining mental function
histology of Pick's disease?
atropy of frontotemporal regions.
can see spherical tau protein aggregates (intracellular)
(don't survive neuron, don't serve as marker for disease progression)
social disinhibition, speech abnormalities, and emotional flattening
gross/microscopic features of craniopharyngioma
1. calcified cysts: lined w/ stratified squamous epithlium
2. keratin pearls
3. yellow, viscious fluid rich in cholesterol crystals
6 complications of crohns
fistula, stricture, perianal disease, risk of adenocarcinoma
2. skin: pyoderma gangrenosum, erythema nodosum
3. joint: arthritis, ankylosing spondylitis
4. eyes: iritis, uveitis, episcleritis
oxalate kidney stone, anemia, hypoproteinemia, b12 & folate def, gallstones
6. liver: cholangiocarcinoma
deep ulcer w/ violaceous border, usu on leg
associated w/ ulcerative colitis & crohns
describe oxalate excretion in gut.
Ca2+ binds oxalate --> insoluble Ca2+ oxalate salts --> excretion
how does crohn's disease lead to increased kidney oxalate stones?
impaired bile acid reabsorption. bile acid bind lipid & prevent reabsorption. Ca2+ binds to this too --> soap complexes
less Ca2+ to bind to oxalate --> increased oxalate absorption
oxalate stones in kidney, think (2)
(1) ethyelene glycol posioning
(2) crohn's disease
what does window period in HBV infection refer to?
time when HBsAg is down, but HBsAb is not yet up.
HbcAb IS detectable in window period --> diagnose HbsAg cleared
most specific marker for diagnosis of ACUTE hep B
IgM HbcAb (window period)
most common appendiceal tumor
analog of somatostatin
inhibit secretion of many hormones
used for carcinoid & VIPoma
selectively block 5HT-3
3 histological features in acute hepatitis
1. diffuse ballooning degeneration: hepatocyte swelling
2. mononuclear cell infiltrate
3. councilman bodies (eosinophilic apoptotic hepatocytes
aminoglycoside mechanism of resistance
bacterial transferase enzymes inactivate drug by acetylation, phosphorylation, adenylation
ONLY renal stone that is radiolucent
uric acid stone
how is Fe2+ absorption regulated (2)
1. hepcidin (internalize basolateral ferroportin -> decrease transport across intestinal epithelium & decrease release from macrophages)
2. HFE -> encourages ferroportin to bring in Fe2+ basolaterally, increasing enterocyte Fe2+ store, increasing apical iron absorption via DMT-1
hepcidin: increases iron stores in macrophages
HFE: decreases iron reabsorption in GI