test #44 5.4 Flashcards Preview

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Flashcards in test #44 5.4 Deck (222):
1

kidney is entirely derived from..

metanephros

metanephric diverticulum (ureteric bud -- collecting duct system)

metanephric mesenchyme (glomeruli & tubules)

2

when does the metanephros develop

5-6th week of gestation

3

most common cause of unilateral fetal (antenatal) hydronephrosis

ureteric bud = initially solid cord, then canalizes (done by 10th wk)

metanephros can produce urine before ureteric bud canalizes --> hydronephrosis

last segment to canalize: ureteropelvic junction (between kidney and ureter)

4

cause of antenatal hydronephrosis obstruction

most common:
-ureteropelvic junction (last to recanalize)

other:
-vesicoureteral junction
-posterior urethral valve (membrane in posterior urethra)

5

when is a fetus able to make urine

8-10th wk

6

pilocytic astrocytoma on imaging

usu in cerebellum, but can't be in cerebral hemisphere

cystic component w/ a tumor nodule.

nodule: active part of tumor

7

most common malignant brain tumor in children

medulloblastoma

exclusively cerebellum

8

histology of medulloblastoma

small, blue cells. hyperchromatic nuclei, scant cytoplasm

can see homer-right rosettes

9

histology of ependymoma

perivascular rosettes w/ rod-shaped blepharoplasts (basal ciliary bodies) near nucleus

10

odds ratio vs relative risk

odds ratio: ad/bc

relative risk: [a/(a+b) / c/(c+d) ]

given chart:
a b
c d

11

expressing support in interview

express concern independent of understanding.

express concern & interest for patient by acknowledging what the patient says. does NOT claim to know how the patient feels

12

facilitation in interview

interviewer encourages patient to talk more about experience. asking "and then what happened"

13

empathy in interview

expression of understanding of experience.

try to "walk in the shoes" to vicariously experience feelings, thoughts, actions.

differs from support, bc tries to project into the experience.

"i can imagine how that experience affected your perspective on life"

14

reflection in interview

when physicial repeats what patient tells him, i.e. by summarizing

"so, you're telling me you were molested as a kid"

15

confrontation in interview

interviewer draws attention to discrepancy in response

"although you say you were disturbed, you sound unaffected as you describe it"

16

mitral valve problems in rheumatic fever

early: mitral valve regurgitation
late: mitral valve stenosis

17

death with rheumatic fever

early: myocarditis

late: valvular heart disease --> valvular issues!

18

diffuse fibrous thickening & distortion of mitral valve leaflets.

commissural fusion at leaflet edges

stenotic orifice w/ diastolic murmur

all suggest

rheumatic fever mitral valvular disease

mitral stenosis --> atrial dilation --> atrial mural thrombus --> stroke

19

most common cardiac manifestation of rheumatoid arthritis

fibrinous pericarditis

20

almost all causes of mitral valve STENOSIS are caused by...

chronic rheumatic heart disease

21

infective endocarditis of mitral valve tends to be..

destructive and regurgitant

22

mitral valvular calcinosis

usually does not impair valve function

usu in women > 60w/o w/ myxomatous floppy mitral valve or elevated left ventricular pressure

23

ASD on ausculation

wide fixed S2 splitting.

does not change w/ respiration

24

split S1?

suggests delayed closure of tricuspid valve, due to right bundle branch block

25

mid-systolic crescendo-decrescendo

aortic stenosis

26

early diastolic decrescendo murmur

aortic regurgitation

27

late systolic crescendo murmur w/ mid-systolic click

mitral valve prolapse

click: sudden tensing of chordae tendinae

most frequent valvular lesion

28

holosystolic high pitched blowing murmur

mitral regurgitation

29

holosystolic harsh murmur, loudest in tricuspid area, accentuated w/

VSD

30

presystolic accentuation

intensity of diastolic murmur before louder just before S1

or when diastolic murmur appears just prior to S1

can result from mitral/tricuspid valve stenosis OR physiological increased flow through valves

31

systolic ejection murmur accentuated by standing

decrease preload

hypertrophic obstructive cardiomyopathy

32

early diastolic decrescendo murmur decreased by amyl nitrate

vasodilate --> decrease afterload

aortic regurgitation

33

late diastolic murmur eliminated by atrial fibrillation

mitral and/or tricuspid stenosis

(related to atrial contraction)

34

drug induced lupus

ANA, anti-histone antibody = specific

Q CHIMPPS

quinidine
chlorpromazine
hydralazine
isoniazid
methyl-dopa
procainimide
phenytoin
sulfa drugs

also etanercept & minocycline

high risk: hydralazine & procainamide

35

immediate side effects of adenosine

chest burning, flushing transient hypotension

but has very short half life

vasodilator in chemical cardiac stress tests & stops acute supraventricular tachycardias

36

where are ureas nitrogen dervived from

1. NH3
2. aspartate (sweet pee)

37

biochemical pathways involving aspartate (3)

-urea cycle (contributes one N)
-pyrimidine synthesis
combines w/ carbamoyl phosphate to make orotic acid (temporary base)

38

orotic acid + PRPP makes

UMP

this path is blocked in orotic acidura

39

leflunomide

blocks combination of carbamoyl phosphate + aspartate --> orotic acid

40

urea cycle

ordinarily, careless crappers are also frivulous about uriantion

ornithine + carbamoyl phosphate --> citrulline + aspartate --> arginninosuscinate --> fumarate (released) + arginine --> urea + ornithine

41

rate limiting step in urea cycle

carbamoyl phosphate synthase I

remember: I pee

42

what forms asparagine. relevance?

non essential amino acid.

produced from oxaloacetate in transamination reaction.

oxaloacetate -> aspartate
using glutamate amino group

aspartate -> asparagine
using glutamine amino group
via asparagine synthase

only comes up as site of N-linked modification in golgi

43

alanine formed by

transfer of an amino group onto pyruvate

44

parasympathetic agents on blood vessels

do not have cholinergic innervation, but do have muscarinic receptors on ENDOTHELIAL surface

1. promote release of NO (endothelium-derivived relaxing factor),
2. activates guanylate cyclase,
3. increase cGMP
4. activates Ca2+ pump &
5. causes Ca2+ efflux.

decrease in Ca2+ in vascular smooth wall --> RELAXATION

45

muscarinics on GI system

increase tone of smooth muscle in viscera; increase motility & secretion, opens sphincters

46

tibial n. sensation & motor

can't TIP toe w/ damage

inversion & plantar flex & toe flex
plantar region of foot

47

common peroneal n. sensation & innervation

foot dropPED w/ damage

eversion & dorsiflex
dorsum of foot

48

cutaneous medial leg?

cutaneous branch of saphenous n (branch of femoral)

49

accentuated second heart sound over upper left sternal border suggests..

pulmonary HTN

50

common cardiac features that can be seen in CREST

pulmonary HTN --> leading to cor pulmonale (right heart failure)

51

pathogenesis of CREST and systemic sclerosis

increased proliferation & accumulation of monoclonal T cells in affected tissue

secrete cytokine, esp TGF-b, increase production of collagen & ECM by fibroblasts

any tissue affected

SMALL ARTERIOLES & capillaries FIRST

52

presentation of lichen planus

6 P's
pruitic, purple, polygonal, planar, papules & plaques.

mucosal involvement
Wickham striae: reticular white lines

sawtooth infiltrate of lymphocytes at dermal-epidermal junction

associated w/ hep C

53

most common cause of death in scleroderma

pulmonary!

interstitial fibrosis or
pulmonary HTN --> COR PULMONALE

54

neisseria meningitidis vaccine

capsular polysaccharide vaccine

55

meningitis in young college student w/ purpuric rash

neiseria meningitidis

56

virulence factors in neisseria meningitidis

1. polysacharide capsule
2. IgA protease
3. LPS endotoxin
4. pili (attach on respiratory mucosa)
5.

57

heat-killed bacteria vaccine

bordetella pertusis, vibrio cholera, yersenia pestis vaccine

58

borrelia burgdorferi vaccine

recombinant bacterial outer surface protein

59

corynebacterium diptherium & clostridium tetani vaccine

inactivated toxin (toxoid)

60

BCG vaccine

TB: live attenuated organisms of a different mycobacterium species

61

salmonella typhi & francisella tularensis vaccine

live attenuated

62

protein A

staph aureus

63

IgA protease

SHiN

strep pneumo
haemphilus influenza
neisseria meningitidis

64

where is proinsulin cleaved to insulin + c-peptide?

endoplasmic reticulum of beta-pancreatic cells

65

what is a good marker of total rate of B-cell endogenous insulin secretion

C-peptide

unlike insulin: C-peptide is not significantly extracted on first pass through the liver!

66

what drug stimulates insulin release from pancreas

sulfonyureas
also GLP-analogues

67

GLUT-2 transporter

liver and pancreas

68

how do GLP-1 analogs increase insulin secretion

increase cAMP, which increases insulin secretion

69

99mTc-pertechnetate detects..

gastric mucosa

70

diagnosis of meckel diverticulum

pertechnetate radionucleotide study

accumulates in gastric mucosa &zenker diverticulum often forms gastric / pancreatic tissue

71

how does meckel diverticulum form

failure of complete obliteration of omphalomesenteric duct / vitelline duct

72

most common manifestation of meckel diverticulum?

lower GI bleed & RLQ pain (due to acid secretion by ectopic gastric mucosa)

could also cause intusseception -- colicky abdominal pain, currant jelly stool

73

inflammed meckel diverticulum difficult to differentiate from..

acute appendicitis

74

failure of proper descent of hindgut

different degrees of anal agenesis or imperforate anus

75

abnormal midgut rotation around SMA can lead too..

fibrous adhesive bands that can lead to intestinal obstruction

76

genetics of tuner's

genetically heterogeneous

in cases of monosomy 45 XO: loss of parental X chromosome during mitosis (after fertilization

- 50% complete monosomy (45, XO)
- 30% mosaicism (46 XX / 45 XO)
-remainder have structural abnormalities of X (such that X fragments or isochromosomes) or partial monosomy deletions of X.

77

weight loss despite normal to increased food intake, polyuria, polydypsia, and fatigue in young adult

type 1 DM

78

diagnosis of type 1 DM

fasting blood sugar > 126 mg/dL on 2 occasions
(only need 1 if symptomatic)

79

when is oral glucose tolerance test used?

usually reserve for pregnant women for gestational diabetes. rarely used. fasting glucose is key.

80

helicotrema

far part of cochlea w/o basilar membrane, allows for communication of scala vestibuli (top) and scala tympani (bottom)

81

high frequency sounds on which part of basilar membrane? low frequency?

high frequency: stiff part (base) closer to oval/round window

low frequency: floppy part (apex) near helicotrema

82

what's in the inner ear

fluid filled site encased in bone that houses cochlea, semicircular canals & vestibule

83

fluid in scala vestibuli, scala media, scala tympani

VMT

vestibuli & tympani have perilymph (high Na+ like extracellular fluid)

media (high K+ like intracellular)

84

what separates scala media from scala tympani

basilar membrane

85

what is housed in scala media

tectorial membrane & organ of corti

86

sources of alkaline phosphate. how can it be differentiated (3)?

bone

also: placenta, liver, intestine

can differentiate between liver & bone via..
1. electrophoresis &
2. specific monoclonal antibodies
3. denaturation (bone denatures easy: bone=boil)

87

tartare resistant acid phosphatase

specific to osteoclasts, but not commonly measured bc not stable protein

88

calcitonin

inhibit osteoclasts

doesn't affect osteoblasts much.

89

urinary deoxypyridinoline and hydroxyproline

measures of osteoclast activity

breakdown of collagen material

note: hydroxyproline not good measure, common in meat products.

90

most reliable measure of osteoclast activity

urinary deoxypyridinoline

91

side effects of thiazides

HYPER GLUC
increase in..
1. glucose
2. lipids & cholesterol
3. uric acid: gouty arthritis
4. calcium: useful rx for calcium nephrolithiasis

HYPO:
decrease in
1. potassium
2. BP : decreased blood volume and peripheral vascular resistance

92

which diuretic is helpful rx for renal nephrolithiasis

thiazides, reabsorb calcium, less in tubules

93

which drugs increase HDL

niacin and fibrates (via ppar-a)

94

high HbA2 suggests

thalasemia trait
a2d2 globin

(due to decrease production of a2b2 = HbA1)

95

Hb types in sickle cell

HbS high
HbA1 low

no affect on HbA2

96

most common pediatric malignancy

acute lymphoblastic leukemia

97

distinguishing between pre-B and pre-T cell ALL clinically?

T-ALL present w/ mediastinal mass

can compress..
-great vessels: SVC syndrome
-esophagus: dysphagia
-trachea: stridor, dyspnea

bcell = 80% of cases
tcell = 15%

B cell: fever, malaise, bleeding, bone pain, hepatosplenomegaly

98

black pigment stones

calcium billirubinate
increased unconjugated bilirubin
associated w/ chronic extravascular hemolysis

small, spiculated, crumbly.

radioopaque-- appear on X-ray

99

glucagon's major effect

liver: increased production of glucose
pancreas: insulin secretion

unlike epinephrine, insignificant affects on skeletal muscle & adipocytes

100

epinephrine glucose related effects?

1. liver: increased glycogenolysis / gluconeogenesis
2. skeletal muscle: decrease glucose uptake & increase alanine release (for liver gluconeogenesis)
3. adipose tissue: increased breakdown of triglycerides, increasing free fatty acids & glycerol in circulation

101

kidney's role in hypoglycemia

first 24 hrs of fasting: liver makes glucose

sustained hypoglycemia: gluconeogenesis in kidney can kick in

102

major risk of clozapine

agranulocytosis, look at complete blood count

also seizures

103

clozapine receptor target

D4

unlikely to cause dopaminergic side effects of pseudoparkinsonism, tardive dyskinesia, hyperprolactinemia

(unlike other antipsychotics: D2)

104

ziprasidone side effect

long QT

105

leading cause of end stage renal disease in US

diabetic nephropathy

106

earliest detection of diabetic nephropathy?

microalbuminemia

30-300mg/day in 24hr collection

30-300microgram/mg of creatinine in spot collection

107

patient w/ dry cough & swollen face & dilated vessels?

superior vena cava syndrome, consider mediastinal mass

108

SVC syndrome

-facial edema / plethora
-venous distension distal to obstruction

due to mass compressing SVC like lung tumor

impaired venuos return from upper body

109

where does SVC form

union of right & left brachiocephalic veins behind 1st costal cartilage

110

most common causes of SVC syndrome

(1) lung mass
(2) non-hodgkin's lymphoma (of perihilar, paratracheal lymph nodes)

111

what hormones does small cell lung cancer secrete

ACTH and ADH

112

what hormone does squamous cell carcinoma in lung secrete

PTHrP

113

superior sulcus tumor

i.e. pancost tumor
at lung apex: cause shoulder pain due to compression of bachial plexus & superior cervical ganglion = horner's

can sometimes cause SVC, but less common than mediastinal mass

114

inactivation of hep A

water chlorination, bleach (1:100), formalin, UV irradiation, boiling to 85 C for 1 min

will not die w/ frying, 20%diethy ether (bc naked), acid (recall - survives in stomach)

115

autoclaving

120 degrees for 20 min

116

boiling in celcius

100

117

cholesterol med w/ unbearable pruritus & flushing

niacin

118

mechanism of niacin

decrease synthesis of hepatic TG and VLDL (due to its suppression of free fatty acid release from peripheral tissue)

also increases HDL

119

how do bile acid resins reduce cholesterol

cholesterol is used in synthesis of bile acids

cholesterol 7a-hydroxylase

120

side effects of bile acid resins

GI upset
increased TG!

121

ezetimibe mechanism

reduces reabsorption of cholesterol and bile acids too

122

what is effective against chlamydia

doxycycline
macrolides

123

risperidone side effect

hyperprolactinemnia (due to dopamine antagonist effect):

prolactin inhibits release of GnRH from hypothalamus

can lead to amenorrhea, galactorrhea, breast soreness

124

anytime see amenorrhea

must rule out pregnancy (b-hCG)

125

"lake-like" cavitary brain lesion

lacunar stroke! HTN arteriolar sclerosis

126

brain injury that does not show up in acute CT, but later does as cystic space in basal ganglia / deep white matter

think lacunar stroke, occlusion of distal penetrating arteriole

most commonly: due to hypertensive changes in arterioles (lipohyalinosis and microatheromas)

127

cause of lacunar infarcts

often chronic HTN --> lipohyalinosis, microatheroma --> ARTERIOLAR SCLEROSIS

diabetes & smoking also risk factors

will not present in acute CT, bc small, later show up as lake-like lesion

128

pure motor hemiparesis

infarct to posterior limb of internal capsule

129

pure sensory stroke

infarct to VPL or VPM of thalamus

130

ataxia-hemiplegia syndrome

infarct to base of pons

131

dysarthria-clumsy hand syndrome

infarct to base of pons or genu of internal capsule

132

types of infarcts caused by cardiac thrombosis & carotid atherosclerosis

usu strokes often involve large territories, due to involvement of large / medium sized vessels

CAN cause lacunar strokes if no other pathological cause can be identified, but these are most often by arteriolar sclerosis due to HTN

133

hypoxic encephalopathy defined as

abrupt cessation to CBF, as from cardiac arrest or shock.
more global

pyramidal cells of hippocampus & purkinjee cells & watershed most often affected

134

hypertensive encephalopathy

leads to cerebral edema due to breakthrough hyperperfusion that is not compensated for by cerebral autoregulation.

headache, nausea and vomiting, other non-localizing neuro symptoms

135

sequelae of cerebral amyloid angiopathy

results in hemorrhage within cortex & subcortical white matter. not usu ischemic stroke

136

Charcot-Bouchard aneursyms

microaneursyms < 1mm in diameter. occur in small penetrating arterioles that perfuse basal ganglia, pons, subcortical white matter

due to long standing HTN and prone to rupture

--> hemmorhagic stroke w/ intraparenchyma hyperdensity

137

what goes into calculating reid index

thickness of gland / thickness of wall between epithelium & cartilage

NOT including cartilage

138

severity of bronchitis depends on.

extent to which the luminal diameter of bronchi / bronchioles is decreased = reid index

major contributor to increase : thickness of mucous gland layer

139

normal reid index

40%

in chronic bronchitis > 50%

140

what rxn does sphingomyelinase normally do

absent in nieman pick

sphingomyelin -> ceramide & phosphorylcholine

141

enzyme deficiency in metachromatic leukodystrophy & accumulated substance

arylsulfatase A

accumulate: sulfatides

142

enzyme deficiency in tay sachs & accumulated substance

hexosaminidase A

accumulate GM2 ganglioside

143

Fabry disease enzyme deficiency & accumulated substances

X-linked recessive
alpha-galactosidase A

accumulate ceramide trihexoside

144

Farber disease

ceramidase deficiency

autosomal recessive

ceramide accumulation in neurons & within skin granulomas

145

IV anesthetics (5)

barbituates, benzodiazepines, arylcyclohexylamines (ketamine), opiods, propofol

146

pharmacokinetics of thiopental (bartibituate)

high potency, high lipid solubility (brain fast), but rapidly redistributed to tissue --> skeletal muscle & fat

induction

decreases CBF

antidote: charcoal / bicarb

IV

147

benzodiazepine for anesthetic

IV

midazolam, for endoscopy

can combine w/ gas & narcotics.

associated w/ anterograde amnesia and respiratory depression

antidote: flumazenil

IV

148

arylcyclohexylamine (ketamine) for anesthetic

PCP analogue, dissociated anesthetic. NMDA receptor antagonist.

cardiovascular stimulant, causes disorientation, hallucination, and bad dreams,

increases CBF

IV

149

opiods for anesthetic

morphine, fentanyl.

used w/ other CNS depressants during anesthesia

IV

150

propofol for anesthesia

IV

sedation in ICU
rapid induction, short procedure

less postop nausea than thiopental

potentiates GABAa

151

local anesthetic classes

esters: cocaine, procaine, tetracaine

amides: lidocaine, bupivacaine, mepivacaine

152

mechanism of action for local anesthetics (esters & amides)

enter cell, bind to voltage gated Na+ channels, prevent AP.

[like class I antiarrhythmics]

enter cell uncharged, bind charged

often given w/ vasconstrictors to increase local concentration

note: if acidic tissue, need increased dose, bc charged species cannot enter cell to work.

153

order of nerve blockade w/ local anesthetics

size is most important

1. small myelinated
2. small unmeylinated
3. large myelinated
4. large unmyelinated

154

order of loss of sensation w/ local anesthetic

1. pain
2. temperature
3. touch
4. pressure

155

succinylcholine mechanism of action

nAch strong agonist (insensitive to AchE)
depolarizing muscle relaxant

phase 1: sustained depolarization & inactivation.
- POTENTIATED w/ AchE inhibitors

phase 2: desensitized to succinylcholine, but continued block of nAchR (nondepolarizing phase)
- ANTIDOTE w/ AchE inhibitors

side effects: hyperkalemia, hypercalcemia, malignant hyperthermia

156

important side effects of succinylcholine

increased:
- potassium
- calcium

malignant hyperthermia

157

nondepolarizing muscle relaxants

nAch antagonists
nondepolarizing muscle relaxants

tubocurarine, atracurium, mivacurium, pancurionium, vecuronium,

reversal: AchE inhibitors (+ atropine, to prevent muscarinic effects)

158

AchE inhibitor during phase I of succinylcholine? phase II?

phase I: depolarizing / inactivating. potentiate

phase II: nondepolarizing block: antidote

159

AchE inhibitor w/ nondepolarizing muscle relaxant (tubocurarine, etc)

antidote! give atrophine to block muscarcinic effects

160

dantrolene

prevent release of Ca2+ from sarcoplasmic reticulum

used as rx: for malignant hyperthermia & neuroleptic malignant syndrome

161

time frame of succinylcholine vs. nondepolarizing NMJ blockers

succinylcholine more rapid (60 seconds)

162

train-of-four stimulation response

used during anesthesia to assess degree of muscle relaxation

stimulate presynaptic neuron & increase Ach in cleft. like an AchE inhibitor

163

train-of-four response to phase I succinylcholine

no response initially

then quickly will gave gradually increased equivalent response in subsequent sets of stimulations

(bc normally quickly metabolized by plasma cholinesterases)

164

train-of-four response to phase II succinylcholine

mirrors nondepolarizing NMJ blockers
nAchR insensitive to depolarization by succinylcholine, but will still block the receptor.

fading pattern w/ progressive reduction in each of the 4 responses

fading, bc of blockade of presynaptic nAchR preventing preparation of vesicle fusion.

165

train-of-four response to nondepolarizing NMJ blockers

nAchR antagonists

fading pattern w/ progressive reduction in each of the 4 responses.

occurs bc nAchR antagonists prevent presynaptic neuron from preparing additional vesicles for release

mirror phase II succinylcholine

166

duration of action of succinylcholine? variation?

determined by
1. diffusion out of NMJ &
2. metabolism by plasma cholinesterase
(insensitive to AChE)

usu < 10min

but! 1/3000 pt homozygous for atypical plasma cholinesterase, which breaks succinylcholine SLOWLY over 1-3 hrs.

neostigmine early: potentiate
neostigmine late: antidote

167

explain normal train-of-four response

stimulate presynaptic neuron & measure depolarization in muscle

in sequential twitches, presynaptic nAchR play an important role in preparing additional vessicles for release

*impt when using NMJ blockers that are depolarizing agonists / nondepolarizing antagonists

168

train-of-four response to succinylcholine in phase I

sustained and equal reduction of all 4 twitches

can overcome w/ additional train-of-four bc drug is metabolized by plasma cholinesterase

169

succinylcholine transition from phase I to phase II

occurs w/ continued infusion

1. depolarized & inactivated
2. eventually desensitize to succinylcholine; acts as a nondepolarizing nAchR blocker

will also block / inactivate presynaptic nAchR needed to prepare vesicles for fusion in phase II

normally succinylcholine rapidly degraded via plasma cholinesterase: phase I then gone.

170

how many Ach molecules must bind to nAchR?

2 molecules!

171

whenever have a drug that is dependent on -esterase, worry about? (i.e. drugs metabolized by AchE)

slow and fast metabolizers!

172

atracurium special considerations

1. safe w/ renal & hepatic impairment
2. spontaneous breakdown to: laudonisine, which can cause SEIZURES
3. activates histamine -> BP fall, flushing, bronchoconstriction

173

mivacurium special considerations

1. very short acting
2. metabolized by AchE (therefore: consider slow / fast metabolizers)

174

special considerations with NMJ blockers

paralytics! patient can still sense things! must give anesthetic & analgesics too.

175

impt feature of nAchR

desensitizes quickly! generally, too much Ach --> depolarization --> cholinergic crisis, which can happen w/ overmedicating for myasthenia gravis.

176

why does succinylcholine trigger malignant hyperthermia?

initially depolarizes muscle, lots of Ca2+ release and ATP generation

177

dilated esophagus, microbial cause? congenital?

microbial: esp from central / south america: trypanosomi cruzi

congenital: achalasia

178

neurotoxin in trypanosoma cruzi?

destroys myenteric plexus in esogagus. similar in colon & ureter

--> megaesophagus, megaureter, megacolon

(also dilated cardiomyopathy)

179

babesia divergens infxn

endemic in northeast US.
transmitted by ticks

malaria-like illness w/ predilection for asplenic patients

fever & hemolytic anemia

see blood smear w/ maltese cross or ring

rx: atovaquone & azithromycin

180

brucella melitensis

drinking infected milk / contact w/ infected sheep & goats

fever, malaise, lymphadenopathy, hepatosplenomegaly

"undulating fever"

181

camplyobacter fetus / intestinalis

opportunistic pathogen
infects immunocompromised

septicemia in newborns, women in 3rd trimester of pregnancy, debilitated elderly

182

intial steps of ketogenesis

start from: leucine / lysine
or

acetyl-CoA --> HMG CoA
via HMG CoA synthase

HMG CoA --> acetoacetate
via HMG CoA lyase

acetoacetate --> B-hydroxybutyrate
via NADH -> NAD+

183

where does ketogenesis occur

mitochondria of hepatocytes

184

metabolism of ketones

in mitochondria of: skeletal muscle, cardiac muscle, renal cortex, brain. (not RBC)

b-hydroxybutyrate -> acetoacetate

acetoacetate --> acetoacetate CoA
via thiophorase
(convert succinyl CoA --> succinate)

acetoacetate --> 2 acetyl CoA

185

what is the major stimulus for ketogenesis

increase in acetyl-CoA

due to..
depletion of oxaloacetate.

1. starving: oxaloacetate used in gluconeogenesis

2. alcoholic: NAD+ depletion converts oxaloacetate -> malate (to generate more NAD+)

186

which 2 cells cannot use ketones

1. RBC; no mitochondria

2. hepatocytes (liver): no thiophorase / succinyl-CoA-acetoacetate CoA transferase

can't convert acetoacetate --> acetoacetyl CoA

187

2 mechanisms for removal of cholesterol

1. excretion of free cholesterol in bile
2. conversion to bile salts (cholesterol 7-a-hydroxylase)

188

bile acid synthesis steps

cholesterol -> cholic & chenodeoxycholic acid
via: cholesterol 7-a-hydroxylase
(rate limiting step)

conjugated w/ taurine / glycine
--> bile salt

189

what solubilizes cholesterol in bile?

bile salt & phosphatidylcholine

190

abnormal keratinization of mucus-secreting columnar epithlelium suggests

vitamin A deficiency
epithelial cell metaplasia

can occur w/ cystic fibrosis
fat-soluble vitamin deficiency & damage to glands w/ inspissated mucous

191

most likely outcome of hepatitis B infection

acute hepatitis w/ complete resolution

192

possible outcomes w/ hepatitis B infection

most common: 1. acute hepatitis w/ complete resolution >95%

2. chronic hepatitis
w/ or w/o cirrhosis & increased risk of hepatocellular carcinoma (4-5% chronic hepatitis; of those 20-50% develop cirrhosis; those 10% get HCC)

3. fulminant hepatitis w/ massive liver necrosis (<1%)

193

fate of patients w/ chronic hepatitis B infection

only occurs w/ 4-5% of hep B infxn

20-50% develop cirhhosis
10% HCC

(hep B--> usu acute hepatitis w/ complete resolution)

194

ras

proto-oncogene

cancer of bladder, lung, colon, pancreas, kidney

195

n-myc

proto-oncogene

neuroblastoma
small cell lung cancer

196

erb-b1

proto-oncogene

squamous cell carcinoma of lung

197

TGF-a

proto-oncogene

astrocytoma, hepatocellular carcinoma

198

sis

proto-oncogene

astrocytoma, osteosarcoma

199

abl

proto-oncogene

CML
ALL

200

BRCA-1, BRCA-2

tumor suppressor

DNA repair gene

breast & ovarian cancer

201

NF-1

tumor supressor

neuroblastoma
neurofibromatosis 1
sarcoma

202

APC/B-catenin

tumor supressor

gastric
colonic
pancreatic cancer

FAP

203

DCC

tumor supressor

colon cancer

204

P53

tumor supressor

majority of cancer
Li-fraumeni

205

Rb

tumor supressor

retinoblastoma
osteosarcoma

G1-S

206

WT-1

tumor supressor

wilms tumor
(pediatric kidney, primitive glomeruli)

207

etiology of ARDs

widespread injury to pulmonary microvasculature endothelium and/or alveolar epithelium

--> causes alveolocapillary membrane to be leaky

208

where do atherosclerotic plaques normally form

in large elastic arteries
(aorta, carotid artery, iliac artery)

& larger medium caliber muscular artery
(coronary, popliteal)

usu not pulmonary artery

209

hyperosmotic volume contraction cause (2)

1. diabetes insipidus
2. profuse sweating

210

GI hemorrhage alters what fluid volume

isotonic fluid loss from ECV only

(bc loose both fluid & osmoles, no pull on fluid from intracellular component)

211

most common cause of death in diabetic?

coronary heart disease!
MI (40%)

(even though have ESRD, still die from coronary heart disease)

stroke also happen, but only 10%

212

HIGHEST risk factors for coronary heart disease

1. noncoronary atherosclerotic disease
2. diabetes mellitus
3. chronic kidney disease

these basically = coronary heart disease equivalents

also: HTN, hyperlipidemia, cigarette smoking, advanced age, obesity, physical inactivity

213

leading causes of ESRD

1. diabetes
2. HTN

214

lung: nodular apical densities w/ calcified nodes filled w/ birefringent particles surrounded by fibrous tissue

silicosis

215

silicosis is defined by

upper lobe nodular densities on x-ray

1. eggshell calcifications of hilar nodes
2. birefringent silica particles surrounded by fibrous tissue

216

x-ray of asbestosis

interstitial pattern, more prominent in lower lobes.

calcified pleural plaques

histology: ferruginous bodies, best w/ prussian blue stain

217

berylliosis x-ray & histology

ill-defined nodular or irregular opacity on x-ray

hilar adenopathy 40%

histology: noncaseating granulomas like sarcoidosis

218

inhalation of organic dust on x-ray, histology

hypersensitivity pneumonitis

diffuse nodular interstitial infiltrates

histology: noncaseating granuloma (foreign body response)

219

which 3 lung diseases can have noncaseating granulomas

1. sarcoidosis
2. hypersensitivity pneumonitis w/ organic dust inhalation
3. berylliosis

220

coal worker pneumoconiosis

x-ray: interstitial opacity

nodal / perilymphatic lung tissue coal dust-laden macrophages

221

most common cause of SCD

death within 1 hr of cardiac symptom

usu cardiac arrhythmia --> ventricular fibrillation

222

Caplan syndrome

rheumatoid arthritis & pneumoconioses w/ intrapulmonary nodules