test #39 4.29 Flashcards Preview

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Flashcards in test #39 4.29 Deck (159)
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1
Q

what does “end-organ” blood supply mean?

A

interruptions in blood flow lead to formation of infarct

renal: small number of collaterals between segmental renal arteries

brain too?

2
Q

recall nephrotic syndrome presents w/ 5 things

A
  1. edema (loss of albumin / oncotic pressure
  2. proteinuria
  3. hyperlipidema
  4. hypercoagulation (loss of antithrombin III & increased coag factors
  5. infection (loss of immunoglobulins)
3
Q

histology of crohn’s vs. ulcerative colitis

A

crohns: noncaseating granulomas & lymphoid aggregates (Th1 mediated)

ulcerative colitis: crypt abscesses (Th2 mediated)

4
Q

blood in crohn’s vs. ulcerative colitis

A

crohn’s: + occult blood

ulcerative colitis: gross bleeding

5
Q

string sign on barium swallow

A

crohn’s disease: narrowing of the intestinal segment due to inflammation of intestinal wall

6
Q

ulcers in crohn’s? gross morphology?

A
  1. linear or serpiginous ulcerations
  2. cobblestone mucosa
  3. transmural inflammatory infiltrate.

“string sign”

7
Q

gross morphology of ulcerative colitis

A
  1. mucosal & submucosal inflammation
  2. friable mucosal pseudopolyps w/ freely hanging mesentary

loss of haustra = lead pipe

8
Q

cells in moles vs. choriocarcinoma

A

mole: only trophoblasts; swelling villi
choriocarcinoma: trophoblasts & syncitiotrophoblasts; NO VILLI

9
Q

clinical presentation of:

complete vs. partial hydatidiform mole

A

both: vaginal bleeding & cramps/pressure

complete:
- SIZE greater than dates &
- extremely HIGH b-hCG

partial:

  • normal size
  • b-hCG high/normal

[hCG can lead to:

  • hyperemesis gravidarum
  • pre-eclampsia
  • hyperthyroidism
  • theca-lutein cysts
10
Q

macroscopic: complete vs. partial hydatidiform mole?

A

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)

11
Q

micropscopic appearance: complete vs. partial hydatidiform mole?

A

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

12
Q

karyotype of complete & partial hydatidiform mole?

A

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
(TRIPLOID)
usu 1 egg w/ 2 sperms

13
Q

risk of malignancy in complete & partial hydatidiform mole?

A

complete: 15-20% risk of malignant trophoblastic disease
partial: low risk of malignancy <5%

14
Q

where is TRH made?

A

paraventricular nucleus of hypothalamus

15
Q

main regulator of TSH section?

A

T3

  • T3 acts on paraventricular nucleus to decrease synthesis/release of TRH.
  • down regulate TSH gene transcription & TRH receptor expression
16
Q

T4 in peripheral tissues

A

converted to T3 or rT3 by specific deiodinases

t3 cannot become T4 or rT3

17
Q

potency, half-life, metabolism of T4, T3, rT3

A

half-life
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]

18
Q

acute acalculous cholecystitis

A

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

19
Q

porcelain gallbladder

A

diagnosed on abdominal radiograph: rim of calcium deposits outline gallbladder

associated w/ gallbladder carcinoma

20
Q

cholechondral cysts

A

congenital dilations of common bile duct

21
Q

chronic cholecystitis results in..

A

thickening of gallbladder wall.

US: shruken, fibrosed gallbladder

22
Q

clornarchis infxn of gallbladder is associated w..

A

brown pigment stones

23
Q

black vs. brown gallstones

A

pigment stones

black: intravascular hemolysis
brown: biliary infxn

24
Q

how does valsalva affect heart?

A

decrease preload.

exhale against closed glottis

25
Q

systemic mastocytosis

A

abnormal proliferation of mast cells & increased histamine secretion

–> increase histamine –> gastric hypersecretion

can see nests of mast cells in bowel mucosa

26
Q

Rokitansky-Aschoff sinus

A

chronic cholecystitis:

chemical irritation from long-standing cholethiasis

herniation of gallbladder mucosa into muscular wall –> Rokitansky-Aschoff sinus: ducts in muscle

late complication: porcelain gallbladder

27
Q

mast cells in GI tract?

A

systemic mastocytosis!

28
Q

systemic mastocytosis

A

mast cell proliferation in bone marrow & other organs

increase histamine

  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
29
Q

H2 receptors increase intracellular

A

cAMP

gastrin/Ach = Ca2+

30
Q

gastrin & Ach increase intracellular..

A

Ca2+

H2 = cAMP

31
Q

most potent action of gastrin

A

most potent: increase histamine synthesis & release by ECL cells

also: stimulates Ca2+ and acid release from parietal cells

32
Q

what intracellular mediators increase H+ efflux from parietal cells

A

cAMP and Ca2+

via H+/K+ ATPase

33
Q

6-mercaptopurine / azathioprine blocks what enzyme?

A

PRPP amidotransferase

inhibit de novo purine synthesis after being converted to active metabolites by HGPRT

34
Q

how is 6-mp / azathioprine degraded?

A

xanthine oxidase

reduce dose when also on allopurinol

35
Q

pentostatin

A

cytotoxic purine that is an irreversible inhibitor of ADA

36
Q

cladribine

A

cytotoxic purine analog that is resistant to degradation by ADA

37
Q

retroperitoneal structures

A

SAD PUCKER

Suprarenal/adrenal
Aorta / IVC
Duodenum (2-4th)

Pancreas (except tail)
Ureters & Bladder
Colon (descending & ascending)
Kidney
Esophagus (lower 2/3rd)
Rectum (partial) 

or:

  1. major vessels:
    - abdominal aorta
    - IVC
    - their branches
  2. solid organs:
    - pancreas (except tail)
    - kidney
    - adrenal glands
  3. hollow organs:
    - parts 2/3 & part of 4 of duodenum
    - ascending & descending colon (secondarily)
    - rectum
    - ureters
    - bladder
  4. vertebral column & pelvic muscles
38
Q

retroperitoneal hematoma (in a stable patient) associated w/

A

abdominal/pelvic trauma

PANCREATIC injury –> retroperitoneal hematoma

39
Q

abdominal blow from malpositioned seat belt / steering wheel –> retroperitoneal hematoma (in a stable patient) bc of damage to

A

PANCREAS

40
Q

transverse colon, spleen, liver..

A

INTRAperitoneal organs

41
Q

testicular malignancy w/ hyperthyroidism

A

must secrete b-hCG

choriocarcinoma; disordered syncitiotrophoblasts & cytotrophoblasts.

hematogenous metastasis to lung, liver, brain.

can produce gynecomastia or hyperthyroidism (B hCG like LH & TSH)

42
Q

95% of all testicular tumors are..

A

germ cell tumors, often malignant, in young men

43
Q

testicular tumor w/ fried-egg appearance, high placental ALP?

A

seminoma! malignant, painless, usu 3rd decade, late mets, excellent prognosis

44
Q

testicular tumor w/ schiller-duval bodies and high AFP

A

yolk-sac (endodermal sinus tumor)

45
Q

presentation of teratoma in male scrotum

A

may be malignant. benign in children though.

50% have both b HCG and AFP elevations

46
Q

malignant hemorrhagic mass w/ necrosis in testes w/ glandular/papillary morphology

A

embryonal carcinoma

worse prognosis than seminoma

usu mixed w/ other types

associated w/ elevated bHCG.
also AFP if mixed

47
Q

testicular nongerm cell tumors

A
  1. Leydig cell
  2. Sertoli cell
  3. testicular lymphoma

mostly benign

48
Q

Reinke crystal in testicular tumor

A

Leydig cell tumor, nongerm cell.

androgen producing, gynecomastia in men, precocious puberty in kids.

golden brown colour

49
Q

Sertoli cell tumor in male

A

androblastoma from sex cord stroma

50
Q

most common testicular malignancy in older men

A

testicular lymphoma

not a primary cancer, usu arises from lymphoma mets to testes

aggressive

51
Q

demographics of squamous cell carcinoma

A

asia, africa, south america

associated w/ HPV and lack of circumcision

52
Q

precursor in situ lesions of squamous cell carcinoma of penis

A
  1. bowen disease
  2. erythroplasia of Queyrat
  3. bowenoid papulosis
53
Q

bowen disease

A

precursor lesion to SCC of penis

on penile shaft
leukoplakia

54
Q

erythroplasia of Queyrat

A

precusor lesion of SCC of penis

on glans
erythroplakia

55
Q

Bowenoid papulosis

A

precursor lesion to SCC of penis

reddish papules

56
Q

priapism associated w/ (3)

A

painful sustained erection

  1. trauma
  2. sickle-cell: trapped RBC
  3. medications: anticoagulants, PDE-5 inhibitors, cocaine, alpha-blockers, trazodone
57
Q

hCG is structurally similar to (3)

A

FSH, LH, TSH

58
Q

which hormones can bind to TSH receptors

A

TSH and HCG (at much lower affinity)

note: FSH cannot! even though structurally similar!

59
Q

cranial n. emerge from..

A

CN III and IV
oculomotor & trochlear (dorsal)
midbrain

CN V
pons

CN VI, CN VII, VIII, IX,
between pons & medulla

CN X
between olive & medulla

CN XI
spinal cord

CN XII
between pyramid and olive

60
Q

which is the only CN to emerge dorsally

A

CN IV trochlear

dorsal midbrain

61
Q

anterior pons lesion

A

dysarthria & ataxic hemiparesis

  • corticopsinal tract (contralateral hemiparesis & babinski)
  • corticobulbar tract (contralateral lower facial palsy & dysarthria

also affect pontine nuclei & pontocerebellar fibers –> contralateral dysmetria & dysdiadochokinesia

62
Q

lesions of cerebellum produce (contralateral/ipsilateral lesion)? lesions of pontocerebellar fibers in basis pontis?

A

cerebellar: ipsilateral

pontocerebellar fibers: contralateral
bc fibers enter cerebellum through contralateral cerebellar peduncle

63
Q

where does facial n arise?

A

pontomedullary junction
level of facial colliculus
below middle cerebellar peduncle

64
Q

middle cerebellar peduncles

A

incoming information from cerebrum to cerebellum, either side of pons

65
Q

where does trigeminal n arise

A

lateral aspect of midpons, at level of middle cerebellar peduncle

66
Q

where does hypoglossal n arise

A

preolivary sulcus at level of rostral medulla

67
Q

where does oculomotor n. arise?

A

at level of superior colliculus & red nucleus (midbrain)

68
Q

where does trochlear n. arise

A

behind midbrain
level of interior colliculus

level of red nucleus.

only cranial n. to decussate before innervate target

69
Q

what is the only CN to decussate?

A

trochlear, CN IV

70
Q

glucocorticoids increase protein synthesis in..

A

LIVER (related to gluconeogenesis & glyocgenesis, proteolysis, lipolysis)

increase synthesis of PEP carboxykinase & glucose 6-phosphatase, glycogen synthetase

71
Q

major effects of glucocorticoids (mnenomic)

A

BIG FIB

increase:

  1. blood pressure a1 receptor (permissive)
  2. insulin resistance
  3. gluconeogenesis, glycogenesis, proteolysis, lipolysis (synthesize more PEP carboxykinase & G 6-phosphatase & glycogen synthetase

decrease:

  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
72
Q

what receptor does glucocorticoids upregulate

A

alpha-1 BLOOD PRESSURE

73
Q

what receptor does T3 upregulate?

A

beta-1 HEART RATE. etc

74
Q

glucocorticoids favor catabolism of which 2 tissues? how?

A

skeletal muscle & adipose tissue

bc block insulin effects

results in proteolysis & lipolysis

75
Q

glucocorticoid induced decrease in fibroblast activity causes (2)

A
  1. skin thinning: purple striae, easy damage

2. CT around capillary thin –> easy bruising

76
Q

positive skew

A

smaller numbers predominant in the data set

long slope / tail extends in positive direction

mean > median > mode

median = better measure of central tendency here

77
Q

negative skew

A

larger numbers predominate in data set

long slope / tail extends in negative direction

mean < median < mode

median is better measure of central tendency here

78
Q

carbon tetrachloride CCl4

A

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

79
Q

symptoms of thyrotoxicosis

A

palpitations, nervousness, easy fatigability, fine tremor, diarrhea, hyperhidrosis, heat intolerance, weight loss, hyperreflexia, dermopathy, opthalmia

80
Q

thyroid opthalmia

A

exopthalmos, conjunctival hyperemia, periorbital edema

81
Q

exopathalmosis due to..

A

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.

82
Q

finely granular eosinophilic granules in hepatocytes?

A

hepatitis B!

hepatocellular cytoplasm becomes filled w/ spheres & tubules of HBsAg

GROUND GLASS APPEARANCE

83
Q

mallory bodies

A

eosinophilic big inclusion in hepatocytes. hepatocytes will also have fatty changes

ubiquinated keratin fibers

in liver of alcoholics

84
Q

describe the PI3K signalling pathway

A

important for cell proliferation

growth factor
RTK
autophosphorylation
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.

85
Q

mTOR activation is usu inhibited by? activated by

A

inhibited by PTEN (phosphatase & tensin homolog), removes phosphate added by PIP3

activated: growth factors & PIP3 (PI3K/Akt/mTOR)

86
Q

what determines fate of pyruvate?

A

oxygen.

low oxygen: lactate dehydorgenase converts pyruvate -> lactic acid (regenerate NAD+)

oxygen: pyruvate dehydrogenase converts pyruvate -> acetyl CoA

87
Q

soleus & paraspinal muscles contain what type of fibers

A

postural

type 1: red, slow twitch. ATP = oxidative metabolism

88
Q

cells involved in granuloma formation (TB formation)

A
  1. Th1 CD4+ cells secrete IFN-y
  2. activates CD8+ cytotoxic T cells and macrophages
  3. macrophages secrete TNF-alpha, important for granuloma formation
89
Q

d-xylulose

A

monosaccharide that can be absorbed w/o action of pancreatic enzymes.

see if malabsorption due to pancreatic or intestinal pathology

90
Q

dobutamine on the heart

A

B-adrenergic agonist
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

  1. increases cardiac conduction velocity (undesirable –> arrythmia)
91
Q

nitroglycerin on HR

A

venous pooling -> reflex tachycardia

92
Q

nitroglycerin on myocardial oxygen consumption

A

reduce preload –> reduce oxygen consumption, used to rx: angina pectoris.

93
Q

what decreases pulmonary capillary wedge pressure

A

aka left atrial pressure?

decreased preload: i.e. nitroglycerin, furosemide

increased contracility: i.e. dobutamine

94
Q

anything that increases perfusion also..

A

increases urine output!

increased renal perfusion.

95
Q

warfarin in pregnancy

A

TERATOGEN. no.

96
Q

where are snRNP synthesized? by which polymrease

A

in the nucleus, RNA pol II

97
Q

how does sleep apnea lead to pulmonary HTN?

A

hypoxemia –> pulmonary vasoconstriction

50% will also develop systemic HTN due to chronic sympathetic cardiovascular stimulation (re: hypoxemia)

98
Q

official diagnosis of narcolepsy

A

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

  1. low CSF hypocretin
  2. shortened REM latency

associated w/ hypnagogic or hynopompic hallucinations and sleep paralysis

99
Q

most common cause of excessive daytime sleepiness

A

obstructive sleep apnea

constantly waking up w/ apnea

100
Q

first generation antihistamines have what common side effects

A

chlorpheniramine and diphenhydramine

antimuscarinic, antialpha-adrenergic, anti-5HT

101
Q

how do H1 receptor blockers work?

A

reverse blockade

decrease receptor activity by increasing proportion of inactive H1 receptors!

102
Q

alcohol induced hepatic steatosis

A

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
103
Q

stain for lipids w/ (2)

A

sudan black or oil red O

104
Q

what is transferrin & total iron binding capacity

A

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

105
Q

normal ferritin states

A

in plasma. usu 1/3rd saturated w/ Fe2+

106
Q

iron panel in iron deficiency anemia (ferritin, transferrin, MCV, folate, neutrophils

A

low ferritin
high transferrin
low MCV (microcytic)

normal folate & neutrophils

107
Q

cyanotic toe discoloration, renal failure following invasive vascular procedure suggests

A

atheroembolic disease of renal arteries (cholesterol lodged)

108
Q

livedo reticularis

A

swelling of venules bc of clogged capillaries

many causes

109
Q

isoniazid resistance (2)

A
  1. stop catalase-peroxidase enzyme expression

2. genetic modification of mycolic acid synthesis enzyme

110
Q

resistance to ethambutol

A

increased production of arabinosyl transferase

111
Q

resistance to rifampin

A

mutation in gene for DNA-dependent RNA polymerase

112
Q

resistance to streptomycin

A

modification of 30S ribosomal protein stxr

113
Q

how does pyrazinamide work?

A

converted to pyrazinoic acid, lowers environmental pH in susceptible strains of TB.

must be converted to active form via pyrazinamidase

114
Q

resistance to pyrazinamide?

A

modified pyrazinamidase (needed to convert pyrazinamide to active form)

115
Q

tryptophan is essential amino acid & precursor for (3)

A

(1) niacin (nicotinic acid)
(2) 5-HT
(3) melatonin

116
Q

Hartnup disease (defect & clinical manifestation)

A

defective intestinal & renal absorption of tryptophan.

clinical: niacin B3 deficiency: pellagra (dermatitis, neuro: ataxia, usu wax & wane,

117
Q

differentiate Hartnup disease from Fanconi syndrome

A

both aminoaciduria.

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

118
Q

seborrheic keratosis

A

flat, greasy, pigmented squamous epithelial proliferation.

keratin-filled cysts.

look “stuck on”
head, trunk, extremities

common benign neoplasm on older people

associated w/ Leser-Trelat sign

119
Q

Leser-Trelat sign

A

sudden appearance of multiple seborrheic keratosis, suggesting underlying malignancy

(GI, lymphoid)

120
Q

riboflavin deficiency (B2)

A

FMN, FAD (needed for enzymes in ETC)

2 C’s of B2

CHEILOSIS, glossitis, keratitis, conjunctivitis, photophobia, lacrimation, CORNEAL VASCULARLIZATION, seborrheic dermatitis

121
Q

decarboxylation & transamination requires what cofactor

A

vitamin B6 (pyridoxine)

122
Q

clinical presentation of pyridoxine B6 deficiency

A

anemia, peripheral neuropathy, dermatitis

123
Q

tocopherol

A

vitamin E
free radical scavenger (antioxidant)

deficiency: myelopathy / neuro dysfunction

124
Q

erythematous papules w/ central scale due to hyperkeratosis. “sandpaper-like” texture

can turn into cutaneous horns

A

actinic keratosis

precursor to squamous cell carcinoma

125
Q

well-circumscribed RAISED papules & plaques covered w/ thick silver scale

A

psoriasis

usu scalp, trunk, extensors (elbow/knee)

126
Q

spongiosis

A

edema of the epidermis

associated w/ atoptic dermatitis (type I HSR)

127
Q

pityriasis rosea presentation

A

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

128
Q

patent PDA associated with..(3)

A
  1. prematurity
  2. congenital rubella
  3. fetal alcohol syndrome
129
Q

ductus arteriosus comes from what aortic arch

A

6th

also proximal pulmonary artery

130
Q

1st aortic arch

A

maxillary artery

1=max

131
Q

2nd aortic arch

A

stapedial / hyoid artery

stapedial is second

132
Q

3rd aortic arch

A

common carotid & proximal internal carotid

C = 3rd letter of alphabet

133
Q

4th aortic arch

A

left: aortic arch
right: right subclavian

4 -> 4 limbs, systemic

134
Q

6th aortic arch

A

PDA & proximal pulmonary artery

135
Q

path of right recurrent laryngeal & left recurrent laryngeal

A

right: under right subclavian
left: under PDA (lower)

136
Q

tissue development of branchial cleft, arch, and pouch

A

cleft: ectoderm
arch: mesoderm (cartilage/muscle)
pouch: endoderm

137
Q

rhomboid major innervation

A

dorsal scapular nerve

138
Q

teres major innervation

A

subscapular nerve

adduct & medially rotate

139
Q

inheritance of hereditary spherocytosis

A

autosomal dominant

140
Q

describe HFE expression and regulation of Fe2+ load

A

autosomal recessive

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

141
Q

two types of amyloid deposits in alzheimer’s disease

A
  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

142
Q

pseudodementia

A

depression in elderly, can cause confusion & declining mental function

143
Q

histology of Pick’s disease?

A

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

144
Q

gross/microscopic features of craniopharyngioma

A
  1. calcified cysts: lined w/ stratified squamous epithlium
  2. keratin pearls
  3. yellow, viscious fluid rich in cholesterol crystals
145
Q

6 complications of crohns

A
  1. intestinal-
    fistula, stricture, perianal disease, risk of adenocarcinoma
  2. skin: pyoderma gangrenosum, erythema nodosum
  3. joint: arthritis, ankylosing spondylitis
  4. eyes: iritis, uveitis, episcleritis
  5. malabsorption:
    oxalate kidney stone, anemia, hypoproteinemia, b12 & folate def, gallstones
  6. liver: cholangiocarcinoma
146
Q

pyoderma gangrenosum

A

deep ulcer w/ violaceous border, usu on leg

associated w/ ulcerative colitis & crohns

147
Q

describe oxalate excretion in gut.

A

Ca2+ binds oxalate –> insoluble Ca2+ oxalate salts –> excretion

148
Q

how does crohn’s disease lead to increased kidney oxalate stones?

A

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

149
Q

oxalate stones in kidney, think (2)

A

(1) ethyelene glycol posioning

(2) crohn’s disease

150
Q

what does window period in HBV infection refer to?

A

time when HBsAg is down, but HBsAb is not yet up.

HbcAb IS detectable in window period –> diagnose HbsAg cleared

151
Q

most specific marker for diagnosis of ACUTE hep B

A

IgM HbcAb (window period)

152
Q

most common appendiceal tumor

A

carcinoid

153
Q

octreotide mechanism

A

analog of somatostatin

inhibit secretion of many hormones

used for carcinoid & VIPoma

154
Q

ondansetron

A

potent anti-emetic

selectively block 5HT-3

155
Q

3 histological features in acute hepatitis

A
  1. diffuse ballooning degeneration: hepatocyte swelling
  2. mononuclear cell infiltrate
  3. councilman bodies (eosinophilic apoptotic hepatocytes
156
Q

aminoglycoside mechanism of resistance

A

bacterial transferase enzymes inactivate drug by acetylation, phosphorylation, adenylation

157
Q

ONLY renal stone that is radiolucent

A

uric acid stone

158
Q

how is Fe2+ absorption regulated (2)

A
  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

159
Q

most common malignancy of SMALL BOWEL

A

carcinoid (esp appendix)