test #40 4.29 Flashcards Preview

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Flashcards in test #40 4.29 Deck (204)
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1
Q

membranous nephropathy is associated w. underlying..

A
  1. systemic disease: DM, solid tumor, immunologic disorders (i.e. SLE)
  2. drugs: gold, penicllamine, NSAID
  3. infection: hep B, hep C, malaria, syphillis
2
Q

focal sclerosing glomerular sclerosis

A

HIV
obesity
sickle cell
heroin abuse

3
Q

spike & dome in membranous glomerulonephropathy

A

immune complex deposition
subepithelial

IgG & C3

no increase in cellularity

4
Q

intoxication, slurred speech, impaired decision making at what alcohol level?

marked motor impairment, loss of consciousness, memory blackouts at what level?

A
  1. 0.10% (100mg/dl)

2. 0.2% (200mg/dl)

5
Q

alveolar-arterial oxygen gradient helps determine

A

CAUSE of hypoxemia

6
Q

normal alveolar PaO2

A

assumed to be partial pressure of oxygen in alveolar air.

healthy person at sea level, usu around 100mmHg

7
Q

alveolar gas equation

to determine A-a gradient

A

PAO2 = 150 - PaCO2/0.8

8
Q

ratio of carbon dioxide production to oxygen consumption

A

0.8 (important in calculating alveolar gas)

9
Q

normal A-a gradient?

A

no more than 10-15mmHg

10
Q

hypoxemia w/ normal A-a gradient? (2)

A
  1. high altitude (FiO2 down)

2. hypoventilation

11
Q

hypoxemia w/ increased A-a gradient? (3)

A
  1. V/Q mismatch
  2. diffusion limitation (pulmonary edema, intersitital fibrosis
  3. right-to-left shunt
12
Q

what values are needed to calculate A-a gradient

A

PaCO2! will assume normal FiO2, etc

PAO2 = 150 - PaCO2 / 0.8

13
Q

when is diffusion capacity of lungs decreased (2)

A

alveolar walls thickened
- pulmonary fibrosis / hyaline membrane / edema

alveolar walls destroyed
- emphysema

14
Q

when is mixed venous blood oxygen increased (2)

A

(1) abnormal hemoglobin binds w/ greater affinity to oxygen, preventing unloading
(2) oxidative metabolism inhibited (i.e. cyanide or CO toxicity)

15
Q

thiazolidinediones (-glitazones) bind..

A

intracellular nuclear receptor

PPAR-gamma

16
Q

pioglitazone, rosiglitazone increase expression of..

A

most importantly, ADIPONECTIN

(a cytokine released by fat cells, what is decreased in type 2 DM

17
Q

exenatide, liraglutide are..

A

GLP-1 analogs, related to incretin effect

increase insulin, decrease glucagon release

18
Q

linagliptin, saxagliptin, sitagliptin are..

A

DPP-4 inhibitors, related to incretin effect

normally cleave GLP-1

also increase insulin, decrease glucagon

19
Q

repaglinide is..

A

meglitinide
like sulfonylurea but does not release insulin when blood glucose is low

weaker binding affinity & faster depolarization

20
Q

GLP-1 is secreted by..

A

intestinal L cells in response to food

‘incretin effect’

21
Q

GLP-1 works on what receptor

A

Gprotein - adenyl cyclase

22
Q

which diabetes drugs work via enzyme inhibition (2)

A

metformin (block enzymes related to liver gluconeogenesis, etc)

alpha-glucosidase inhibitors (acarbose, miglitol)

23
Q

miglitol

A

like acarbose, alpha-glucosidase-inhibitor,

diabetes med.

24
Q

hyperestrinism state of cirrhosis due to (2)

A
  1. decrease metabolism of androstenidione, results in excess estrogen.
  2. increase in sex-hormone binding globulin (SHB) -> binds testosterone, decreases free testosterone

results in: gynecomastia, testicular atrophy, spider angiomata, less hair

25
Q

edema in cirrhosis due to..

A

hypoalbuminemia (liver synthetic processes diminshed)

26
Q

fetor hepaticus (musty breath) and encephalopathy are signs of..

A

hyperammonia (liver failure)

27
Q

4 signs of portal HTN

A
  1. esophageal varices
  2. caput medusa
  3. hemmorhoids
  4. splenomegaly
28
Q

what is major determinant for rate of bone mass decline post menopause

A

RACE. black have higher bone density than caucasians

29
Q

BMI on bone density

A

higher BMI = higher bone density

30
Q

smoking on bone density?

A

overall, anti-estrogenic

–> risk for osteopersosis

31
Q

what does smoking actually decrease risk of?

A

fibrocystic breast disease & uterine cancer

bc anti-estrogenic

overall bad for you though!

32
Q

3 ways glucocorticoids decrease bone formation

A
  1. decrease osteoblast activity
  2. decrease GI absorption of Ca2+
  3. increased renal loss of Ca2+
33
Q

how does estrogen build bone (2)

A
  1. increase osteblast activity

2. decrease osteoclast activity

34
Q

what is the main indicator of ventillation

A

PaCO2 (inversely related)

bc CO2 -> perfusion limited, equilibrates FAST
(high conc gradient)
O2 is also perfusion limited, but does not equilibrate as fast as CO2

35
Q

when see low CO2, think..

A

hyperventilation

36
Q

determinant of PaCO2 =

A

basal metabolic rate / alveolar ventillation

normal BMR: 0.8 CO2 produced for every O2

37
Q

decreased PaO2 & PaCO2

A

PaCO2 = indicator of ventilation.

likely hyperventilation (blowing off CO2) but not sufficient to oxygenate blood

due to PE or pneumonia

38
Q

blood oxygen state after PE or pneumonia

A

hypoxemia causes peripheral arterial chemoreceptors to send neural impulses to CNS respiratory centers, to increase respiratory drive

—> hypocapnia

but, hypoxemia continues –> have increased alveolar-arterial oxygen gradient.

(can correct w/ more oxygen)

39
Q

significant upper airway obstruction on blood gases

A

increase PaCO2, decrease PaO2

hyperventilation does not correct this

40
Q

significant respiratory muscle fatigue on blood gases

// decreased chest wall compliance

A

increase PaCO2

41
Q

blood CO2 determined by (2)

A
  1. respiratory rate

2. tidal volume

42
Q

blood O2 determined by (1)

A

available alveoli

43
Q

alveolar ventilation status determined by..

A

arterial PaCO2

44
Q

“floating” ribs vs “false” ribs

A

floating ribs: 11 & 12, not bound anteriorly to rib cage by cartilage

false ribs: bound to anterior rib cage by cartilage 8, 9, 10

45
Q

which ribs overlie spleen?

A

ribs 9, 10, 11

46
Q

which ribs overlie kidney?

A

rib 12

47
Q

rib 12 can lacerate..

A

displace into retroperitoneum * lacterate kidney

48
Q

which posterior ribs overlie liver?

A

8, 9, 10, 11

49
Q

at rest: inferior margin of left lung along midscap line?

during max inhalation

A

rest: 10th rib

max inhalation: 12th rib

50
Q

what vertebral level does pancreas overlie?

A

L2

51
Q

describe important structures at

T12, L1, L2, L3, L4

A

T12: esophagus enters, celiac branch

L1: SMA

L2: pancreas

L3: IMA

L4: bifurcation of abdominal. aorta

52
Q

perfusion limited gases

A

CO2, N2O

equilibrates FAST (early along capillary).

ventilation determines PaCO2
(when have poor perfusion i.e. w/ PE, hyperventillation can still blow off CO2

53
Q

diffusion limited gases

A

CO

gas does not equilibrate by the end of capillary

54
Q

oxygen in normal health is.. (perfusion/diffusion limited)

in fibrosis, emphysema? exercise

A

normal health: perfusion limited (will equilibrate by end of capillary, though not as fast as CO2

exercise: blood flows fast, but will still equilibrate by end
fibrosis: diffusion limited now (never diffusion limited for CO2)

55
Q

thyroid arterial supply

A
  1. superior thyroid artery (branch of external carotid)

2. inferior thyroid artery (branch of subclavian)

56
Q

ligation of inferior thyroid artery can…

A

injury recurrent laryngeal n (CNX)

–> hoarseness

57
Q

unilateral damage to recurrent laryngeal n. causes?

bilateral damage?

A

recurrent laryngeal n (CN X) feeds all muscles of larynx (except cricothyroid) & sensory below vocal folds

unilateral: hoarseness
bilateral: airway obstruction by immobile vocal folds

58
Q

ligation of superior thyroid artery can..

A

injury to external branch of superior laryngeal n (CNX)

paralysis of cricothyroid m.

impaired ability to produce pitch –> monotone

59
Q

branches of superior laryngeal n.

A

external: supplies cricothyroid (muscle of larynx)
internal: sensory from epiglottis to vocal folds

(below vocal folds -> recurrent laryngeal)

60
Q

ansa cervicalis

A

C1, C2, C3 cervical plexus

courses deep to CNS, loop around IJV

feeds: sternohyoid, sternothyroid, omohyoid
“strap muscles”

61
Q

hypoglossal n (CNXII)

A

exists cranium via hypoglossal canal

innervates all intrinsic muscles of tongue, except palatoglossus

62
Q

spinal accessory N (CNXI)

A

exists via jugular foramen, courses atop levator scapsular –> SCM and trapezius

63
Q

recurrent laryngeal n (CN X)

A

feeds all muscle of larynx (except cricothyroid) & sensory below vocal folds

(above vocal folds: internal branch of superior laryngeal n.)

64
Q

where does a horseshoe kidney get stuck

A

inferior pole by IMA

risk for urinary tract obstruction & development of hydronephrosis

fetal metanephros initially in sacral region, ascent to T12-L3

65
Q

what vertebral levels are kidneys?

A

T12-L3

right is slightly lower

66
Q

4 fates of vitelline duct abnormalities?

A
  1. persistent vitelline duct (full connection from midgut -> umbillicus
  2. meckel diverticulum: outpouch of midgut (umbillicus part -> fibrosis
  3. vitelline sinus: outpouch of umbillicus (midgut part -> fibrosis
  4. vitelline duct cyst (enterocyst) -> pouch between the two, fibrosed on either side.
67
Q

pronephros

A

develops in week 4, then degenerates

68
Q

mesonephros

A

serves as interim kidney in 1st trimester, later contributes to male genital system

(female) paramesonephros

69
Q

metanephros

A

permanent. appears week 5, nephrogenesis from 32-36 wks of gestation

70
Q

origin of the collecting system of kidney (ureter, pelvises, calyces, collecting ducts

A

ureteric bud, from caudal end of mesonephros

71
Q

origin of glomerulus to collecting duct of kidney

A

metanephros

72
Q

describe renal development

A

ureteric bud (from caudal end of mesonephros)
forms ureter, pelvises, calyces, collecting ducts
canalize by week 10

induces differentiation & formation of glomerulus through DCT (metanephros)

73
Q

what is the last region of the kidney to canalize?

A

uteropelvic junction.

most common side of obstruction in fetus (hydronephrosis)

74
Q

blood flow through kidney

A

renal artery -> segmental artery -> interlobular artery -> arcuate artery -> radial artery -> afferent arteriole -> glomerular capillaries -> efferent arteriole -> peritubular capillaries -> interlobar vein.

75
Q

on RPF & FF.

moderate efferent constriction causes? severe?

A

FF = GFR/RPF

moderate efferent arteriole constriction increases GFR & reduces plasma flow –> increases FF

severe efferent constriction will increase capillary oncotic pressure (due to filtration of plasma & increased concentration of non-filterable plasma proteins), which will cause an OVERAL DECREASE in GFR (though filtration fraction will still be up)

76
Q

afferent arteriole constriction on FF and GFR?

A

reduce RPF, will equally decrease GFR, so no net change in FF. /

77
Q

asked for the probabililty that at least 1 false positive test will result in 8 negs (given 95% specificity)?

A
  1. caculate probability that all independently correctly false (0.95^8)
  2. at least 1 means..
    1-probabilty all negative (1-0.95^8)

(accounts for situation where all are false + or at least 1 is)

if events are independent, probability that all events turn out same is product of separate probabilities for each event.

probability of at least 1 event turning out differently is 1-probability all same.

78
Q

linkage disequilibrium

A

pair of alleles from two loci are inherited together in the same gamete (haplotype) more or less often would be expected by random change alone given corresponding allele frequency

79
Q

what can cause linkage disequilibrium?

A

physical proximity of allelic loci, but not always!

can be due to mutations, genetic drift, migration, selection pressure, and non-random mating

80
Q

Hardy-Weinberg principle

A

if p & q are frequency of separate alleles (SAME LOCI)

p^2 + 2pq + q^2 = 1
and p+q = 1

p^2 = frequency of homozygosity for allele p

2pq = carrier frequency / frequency of heterozygosity

q^2 = frequency of heterozygosity for allele q

81
Q

Hardy-weinberg assumptions (4)

A
  1. no mutation in locus
  2. natural selection not occurring
  3. completely random mating
  4. no net migration
82
Q

Hardy-weinberg: frequency of X-linked recessive disease in male? in females?

A
male = q
female = q^2
83
Q

how do we estimate the probability of two alleles appearing together if distinct loci? same loci (in hardy-weinberg)

A

distinct loci: multiple occurance rate –> ‘haplotype freq’

same loci: 2pq

84
Q

antibodies to PRP (polyribitol ribose phosphate) suggests..

A

h. influenza type B capsule

85
Q

presentation of epiglottitis

A

abrupt onset of obstructive laryngeal edema

acute fever, inspiratory stridor, drooling, osynophagia, positive “thumb” sign on lateral cervical x-ray (edematous epiglottis)

86
Q

positive “thumb” sign on lateral cervical x-ray?

A

edematous epiglottis

epiglottitis, prob H. flu type B

87
Q

malignant pustule (painless ulcer w/ black eschar & local edema)

A

b. anthracis

capsule of D-glutamate

88
Q

what can we expect after replenishing Fe2+ after Fe2+ deficient anemia?

A

increased hgb 2g/dl per week for 1st 3 weeks

enhanced erythropoesis & accelerated release of both mature RBC and reticulocytes

89
Q

reticulocyte is..

A

immature RBC. slightly larger & bluer.

lacks nucleus but retains basophillic, reticular, mesh-like network of residual ribosomal RNA.

after wright-giemsa stain

90
Q

rate of reticulocyte in blood stream

A

will mature into RBC, which will live for 120 days

91
Q

adenomyosis

A

presence of endometrial glands in the myometrium

present: menorrhagia & dysmenorrhea

92
Q

why is uterus enlarged w/ adenomyosis?

A

endometrial glands in myometrium

mostly: uterine smooth muscle hypertrophy & hyperplasia in response to ectopic endometrial gland tissue.

93
Q

physical exam of adenomyosis vs. leiomyoma

A

adenomyosis: uniformly enlarged
leiomyoma: IRREGULARLY enlarged uterus or mass

94
Q

most common gynecological malignancy?

A

endometrial (adenocarcinoma)

95
Q

size of uterus w/ ectopic pregnancy?

A

uterus is NOT enlarged, but will

(on biopsy: uterine wall will have decidualized stroma bc hormona changes still occur!

96
Q

a unique tRNA exists for every..

A

mRNA codon sequence

though mult diff codon seq might get the same amino acid

97
Q

t arm of tRNA (thymine, pseudouridine, cytosine)

A

only RNA sequence w/ thymine

binds to ribosome

‘touch’ ribosome

98
Q

D arm of tRNA

A

dihydrouracil residue

helps tRNA recognition by correct aminoacyl tRNA synthetase

‘determine’ synthetase

99
Q

what codon sequence is on tRNA 3’ end

A

3’ -> CCA

‘can catch amino acid’

site for amino acid binding

100
Q

carnitine deficiency will result in…

A

acetoacetate

101
Q

what is carnitine important for..

A

B-oxidation of fatty acids

take fatty acyl-CoA from cytoplasm into mitochondrial matrix

102
Q

describe fatty acid metabolism

A

fatty acid –> acyl-CoA
-via acyl-CoA synthetase

carnitine + aceyl-CoA –> acyl-carnitine CoA
-via CAT1

go through mitochondrial membrane

acyl-carnitine CoA –> carnitine + acyl-CoA
-via CAT 2

then B-oxidation w/
FADH2 + acyl-CoA dehydrogenase

103
Q

what are CAT 1 and CAT 2

A

carnitine-acyl transferase 1:
combines carnitine + acyl-CoA to enter mitochondrial membrane

carnitine-acyl transferase 2:
inside mitochondria, releases carnitine + aceyl-CoA

104
Q

describe process of beta-oxidation

A

like ETC, takes off some e- and moves from FAD/FADH2 and NAD/NADH w/ an ATP synthetase

105
Q

carnitine deficiency

or: myopathic CAT deficiency

A

unable to bring fatty acid from cell into mitochondria to break down

in skeletal muscle

myoglobinemia
weakness following exercise
hypoketonia

106
Q

MCAD deficiency (medium chain acyl-CoA dehydrogenase

A

medium chain = 8-10

present:
- fasting hypoglycemia (no energy from b-ox to fuel gluconeogenesis)
- no ketone in blood, see c8-c10 in blood (not enough acetyl-CoA)
- vomitting

peroxisomes will do w-oxidation, will see

  • dicarboxylic acids
  • & C8-10 in blood
107
Q

link between gluconeogenesis & b-oxidation

A

need beta-oxidation energy to FUEL gluconeopgenesis!

108
Q

differentiate McArdle from carnitine deficiency?

A

McArdle: increased glycogen in muscle

carnitine deficiency: increased fatty acid / triglycerides

bc: when play -> epinephrine increase hormone sensitive lipase, increase FA, enter muscle for energy, but can’t bind to carnitine –> accumulate!

109
Q

ketogenic amino acids

A

leucine & lysine

110
Q

major stimulus for ketogenesis in prolonged starvation & diabetic ketoacidosis? in alcoholics?

A

prolonged starvation: oxaloacetate consumed in gluconeogenesis

alcoholics: oxaloacetate -> malate

both build up acetyl-CoA, which shunts glucose & fatty acids to ketogenesis

111
Q

hexokinase vs. glucokinase

A

hexokinase all tissue

glucokinase in liver

glucokinase only kicks in when glucose is HIGH

112
Q

2 general pathways for apoptosis

A
  1. intrinsic mitochondrial

2. extrinsic death receptor

113
Q

intrinsic path for apoptosis

A
  • cessation of survival signals/ stress

anti-apoptotic Bcl-2 & Bcl-x in mitochondrial membrane replaced w/ Bak, Bax, Bim

allow for increased mitochondrial permeability

release caspase-activating substances (like cytochrome c)

114
Q

release of cytochrome c from mitochondria..

A

pro-apoptotic protein, activate caspase for apoptosis

115
Q

2 types of extrinsic apoptosis

A
  1. death receptor on cell surface [TNF-R1 and Fas]

2. immune cell: perforin/granzyme release

116
Q

2 major death receptors

A

TNF-R1 and Fas (CD95)

117
Q

how does Bcl-2 block apoptosis

A

Bcl-2 prevents cytochrome c release from mitochondria.

Bcl-2 inhibits Apaf-1. Apaf-1 usu activates caspases.

118
Q

receptor-mediated extrinsic apoptosis

A

death receptor: [TNF-R1 and Fas]

  • receptor cross-link w/ ligand
  • form a binding site for FADD (death domain containing adapter protein)
  • caspases flock to FADD & activation is induced
119
Q

physiologic example of intrinsic apoptosis

A

loss of IL-2 stimulation of T cells –> apoptosis

120
Q

physiologic example of extrinsic apoptosis

A

Fas/Fas-L in thymic medullary negative selection

121
Q

what type of physiologic apoptosis is impt for autoimmunity

A

Fas/Fas-L

important for negative selection in thymus medulla

122
Q

succinate dehydrogenase

A

mitochondrial enzyme in ETC.

oxidizing succinate to fumarate & reducing FAD to FADH2.

123
Q

superoxide dismutase

A

reduce superoxide to hydrogen peroxide

124
Q

TTP vs. HUS

A

on a spectrum

both have pentad:
- fever, neuro manifestation, acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia.

TTP:
usu adults, more neuro

HUS:
more kids, mostly renal

isolated activation of platelets (usu don’t bleed) normal PT, PTT, fibrinogen)

125
Q

syrup of ipecac

A

emetic treatment.

used immediately after injection of toxin

126
Q

cryoprecipitant contains

A

factor VIII, factor XIII, vWF, fibrinogen

good for hemophilia A, vwd, hypofibrinoginemia

127
Q

side effects of SNRIs (duloxetine and venlafaxine)

A

high BP

also: stimulant effects, sedation, naseua

128
Q

major side effects of TCA? one’s impt for drug intxn?

A

serious 3 C’s: cardiotoxicity, coma, convulsions

consider:
- a1-blocking effects: postural hypotension
- anticholingeric: tachycardia, urinary retention, dry mouth, hyperthermia
- block NE & 5-HT reuptake: tremor, insomnia
- block fast-acting Na+ channels: conduction defect, arrythmia, hypotension
- H1 antaognist: sedation

129
Q

which TCA has most anticholinergic effects?

A

amitryptyline

130
Q

list TCA’s

A

amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

131
Q

use for diabetic neuropathy? (2)

A

TCA: amityrptyline (also very anticholinergic!)
SNRI: duloxetine

132
Q

TCA (esp amitryptyline) in patient w/ BPH

A

worry about urinary retention bc of anticholinergic effects

133
Q

mechanism of neuroleptic malignant syndrome

A

specific to anti-D2 effects

block central dopaminergic systems involved in thermoregulation & regulation of muscle tone and movt

134
Q

distinguish serotonin syndrome from neuroleptic malignant syndrome

A

serotonin syndrome: myoclonus

neuroleptic malignant syndrome: rigidity

135
Q

rx for neuroleptic malignant syndrome?

A
  • bromocriptine: Dopamine agonist
  • amantidine: increase Dopine efflux
  • dantrolene, stop rigidity
136
Q

vision problems, dry skin, generalized pruitis

A

suggests prolonged biliary obstruction resulting in..

  1. vit A deficiency : vision & dry skin!
137
Q

most common cause of night blindness

A

hereditary retinitis pigmentosa

138
Q

5 signs of vitamin A deficiency

A
  1. nyctalopia: night blindness
  2. xerosis cutis: dry, scaly skin
  3. keratomalacia: corneal degeneration
  4. alopecia
  5. immunosuppression
139
Q

4 differential diagnosis for acquired nyctalopia

A
  1. toxic retinopathy (phenothiazine & chloroquine
  2. vitamin A deficiency
  3. congenital rubella, syph..
  4. diabetic retinopathy
140
Q

light tapping on chin induces masseter muscle spasm..

A

variant of chvostek sign; hyperactive jaw jerk

sign of hypoparathyroidism

141
Q

Chvostek sign

A

facial muscle contraction elicited by tapping on the facial n. just anterior to ear

sign of hypoparathyroidism

(neuromuscular hyperexicitability)

142
Q

Trousseau sign

A

occlusion of brachial artery w/ BP cuff –> carpal spasm

sign of hypoparathyroidism

(neuromuscular hyperexcitability)

143
Q

2 exam signs of hypoparathyroidism

A

Chvostek sign
-tap on cheek, near ear -> facial muscle spasm

Trousseau sign
-BP cuff –> carpal spasm

(neuromuscular hyperexcitability)

144
Q

at what Ca2+ levels do neuromuscular excitability manifest?

A

<7mg/dl

145
Q

complication of thyroid surgery –> neuromuscular hyperexcitability

A

accidentally take out parathyroid!

146
Q

improper fusion of maxillary prominence w/ medial nasal prominence results in..

A

cleft lip (primary palate)

147
Q

improper fusion of lateral palatine process

or

improper fusion of lateral palatine process w/ nasal septum / median palatine process

A

cleft palate (secondary palate

148
Q

inheritance of cleft lip/cleft palate

A

distinct etiology, but often occur together

MULTIFACTORIAL inheritance

[not associated w/ digeorge!]

149
Q

when do lip / palate form

A

6th wk of embryonic development

150
Q

midline intermaxillary segment forms..

A

philtrum of upper lip, four medial maxillary teeth, primary palate

151
Q

choanal atresia

A

bone maldevelopment in fetus, causes obstruction of one or both nasal passage –> respiratory distress & cyanosis

152
Q

how is ammonium from muscle disposed of?

A
alanine shuttle
all transamination, req B6
in MUSCLE: 
-amino acids  a-ketoacids
-alpha-ketoglutatate  glutamate

amino group from amino acids transferred to make glutamate

  • glutamate a-ketoglutarate
  • alanine pyruvate

amino group from glutamate passed to pyruvate to make alanine

alanine can travel in blood to LIVER

  • alanine pyruvate
  • alpha-ketoglutarate glutamate

NH3 released from glutamate via glutamate dehydrogenase, converted to urea & excreted

153
Q

how is ammonia excreted from most other tissues (not muscle / liver?)

A

glutamine is released into blood

in kidney:

glutamine —> glutamate
via glutaminase

which releases NH3, converted to NH4+ and released in urine.

154
Q

alanine cycle

A

alanine form muscle brought to liver, converted into pyruvate (NH3 transferred to make glutamate), pyruvate-> glucose, which goes back to muscle.

in muscle, glucose –> pyruvate –> alanine, all over again

155
Q

cori cycle

A

pyruvate -> lactate, which goes to liver and is converted to pyruvate -> glucose, which goes back to muscle, makes pyruvate, etc

156
Q

important nitrogen transporters in body

A

alanine & glutamine

157
Q

pathogenesis of porcelain gallbladder

A

Ca2+ salts deposit intramurally secondary to chronic irritation // component of natural progression of chronic inflammation

usu asymptomatic, can comlpain of RUQ pain w/ firm nontender mass

158
Q

prognosis of porcelain gallbladder

A

11-33% will develop gallbladder carcinoma

159
Q

clearance of digoxin

A

primarily renal exretion

half-life 2.5 days (40hrs)

160
Q

elderly pt w/ digoxin toxicity..

A

likely related to age-related renal insufficiency!

161
Q

consideration w/ meds for all elderly?

A

reduce doses of renally-cleared medications to prevent toxicity

162
Q

enzyme deficiency in von gierke’s

A

glucose-6-phosphatase

163
Q

2 roles of debranching enzyme

A
  1. cleave 3 of the 4 limit dextrans (1,4 glucosidase) and put them to the main alpha 1,4 chain
  2. cleaves the last alpha-1,6-glycosidic bond to release free glucose
164
Q

liver findings in Cori disease

A

lack of debranching enzyme
hypoglycemia, ketoacidosis, hepatomegaly

accumulation of dextrin-like structures in cytosol of hepatocytes in abscence of histopathlogical fatty liver infiltration

affects both muscle and liver cells

165
Q

organ affected in von girke’s

A

only liver, bc enzyme glucose 6-phosphatase not in muscles

manifestation: hypoglycemia, lactic acidosis, hyperlipidemia, hyperuricemia

hepatic steatosis –> CARDINAL MANIFESTATION

166
Q

why can muscle fxn without glucose 6-phosphatase?

A

bc uses glucose 6-phosphate for gluconeogenesis! isn’t trying to release glucose into circulation

167
Q

cause of tabes dorsalis in tertiary syphillis. presentation

A

damage DORSAL ROOTS, leading to secondary demyelination & loss of axons in DORSAL COLUMN

present w/ lancinating pain, paresthesia, and loss of vibratory & position sense

can also have (1) areflexia & (2) loss of bladder fxn

168
Q

maternal presentation of measles

A

postauricular lymphadenopathy, rash, arthralgia

169
Q

malformed teeth: hutchinson’s incisors & mulberry molars think..

A

congenital syphillis

170
Q

NF-kB is important for..

A

transcription factor for cytokine production

171
Q

possible pathogenesis of crohn’s

A

increased activity of nf-kb (impt for cyotkine production)

appropriate response to intracellular microbes is blunted, microbe persist and produce chronic inflammation in GI tract

172
Q

main CSF difference in viral / bacterial meningitis

A
  1. cell differential
    bacterial: neutrophil
    viral: lymphocyte
  2. glucose & protein
    bacterial:
    glucose < 150mg/dl
  3. gram stain/culture
    bacteria: often +, not always

viral: no organism identified

173
Q

most common viral cause of meningitis

A

echovirus

usu enteroviruses (coxsackie, echo, polio, enterovirus)

174
Q

most common cause of bacterial meningitis

A

s. pneumo

175
Q

2nd most common cause of bacterial meningitis

A

n. meningitidis

176
Q

most common causes of common cold

A

coronavirus, rhinovirus, adenovirus

177
Q

graves vs. hyperthyroidism

A

graves = hyperthyroidism AND..

  1. infiltrative opthalmopathy
    - exopathalmos (GAG deposit)
    - myositis of extraocular musc.
  2. pretibial myxedema

[last 2 caused NOT by hyperthyroidism, but by autoimmune response to anti-TSH receptor, which is located also on fibroblasts & adipocytes]

178
Q

causes of hyperthyroidism (4)

A
  • graves disease (most common)
  • toxic adenoma
  • toxic multinodular goiter
  • thyroiditis
179
Q

describe pretibial myxedema

A

late manifestation of grave’s

NON-PITTING edema that is sometimes scaly in appearance (classically resembling an orange peel)

lower leg skin thickening & induration

180
Q

which is the first factor to go in alcoholic cirrhosis of liver?

A

the one w/ shortest half-life, factor VII

181
Q

why does thrombocytopenia develop in alcoholic cirrhosis of liver

A

hypersplenism – sequestered

182
Q

what is barret’s esophagus a risk factor for

A

esophageal adenocarcinoma

will be clinically silent until it obstructs esophageal lumen

183
Q

achalasia is caused by

A

loss of myenteric ganglion cells of the LES –> can’t relax

leads to high LES opening pressure & uncoordinated peristalisis

184
Q

major risk factors for squamous carcinoma of the esophagus

A
  1. smoking

2. alcohol use

185
Q

squamous vs. adenocarcinoma of the esophagus location? lymph spread?

A

squamous: upper 2/3
adeno: lower 1/3

upper 1/3: cervical nodes
middle 1/3: mediastinal/tracheobrachial
lower 1/3: celiac & gastric

186
Q

most common risk factors squamous carcinoma

A

anything that causes irritation

alcohol & cigarette smoking (both)

187
Q

important side effects of carbamazepine

A
  1. bone marrow suppression: anemia, agranulocytosis, thrombocytopenia
  2. hepatoxotic: monitor LFT
  3. SIADH
188
Q

simple vs. complex seizure

A

simple: no impairment of consciousness during or after
complex: loss of memory during event / post-ictal state

189
Q

important prognosticfactor in poststreptococcal glomerulonephritis

A

AGE

95% of children recover completely w/ conservative therapy

only 60% of cases in adults will result, rest become RPGN or chronic glomerulonephritis

190
Q

pathogenesis of peripheral neuropathy in diabetes

A
  1. diabetic microangiopathy of endoneural arterioles:

nonenzymatic glycosylation of proteins leading to increased thickness, hyalinization, and narrowing of artery walls

  1. intracellular hyperglycemia in periphreal nerves, converted to sorbitol via aldose reductase. osmotic damage to axons & schwann cells
191
Q

diabetic neuropathy sensation

A

paresthesia (tingling, numbness)

intense BURNING pain

192
Q

types of neuropathy in diabetes

A
  1. distal symmetric polyneuropathy: “stocking and glove” distribution
  2. autonomic polyneuropathy: constipation, orthostatic hypotension, incontinence, erectile abnormalities
  3. mononeuropathy: cranial n (i.e. oculomotor, facial, optic), median n, etc
193
Q

histology of cystic medial degeneration

A

fragmentation of elastic fibers in media –> “basket-weave” appearance.

space filled in by amorphous matrix

–> see MYXOMATOUS changes

194
Q

myxomatous changes in media of large artery

A

cystic medial degeneration, related to aortic aneursym

195
Q

which collagen disorder is associated w/ berry aneursym

A

type IV ehlers danlos

196
Q

false aneursym

A

result of a breach in the continuity of all three layers of blood vessel (or heart)

leading to blood leakage / hematoma formation OUTSIDE vascular wall –> in connective tissue surrounding point of arterial wall rupture.

often: leaks at anastamosis sites of vascular grafts, postinfarction myocardial rupture contained by pericardial adhesions

197
Q

where does mycobacterium leprae like to act

A

likes cool temperatures, so infects skin & superficial nerves.
“glove & stocking” loss of sensation

198
Q

leprosy resevoir in US

A

armadillos

199
Q

2 forms of Hansen’s disease

A
  1. lepromatous: diffusely over skin, lion like face, communicable.

low cell-mediated immunity w/ a humoral Th2 response

  1. tuberculoid (milder): limited to a few hypoesthetic, hairless skin plaques.

HIGH cell mediated immunity; largely Th1 type immune mediated

200
Q

immune response to lepromatous vs. tuberculoid forms of hansen (leprosy)

A
  1. lepromatous: weak cell-mediated immunity w/ a humoral Th2 response
  2. tuberculoid: strong cell-mediated immunity. CD4+ Th1 immune response.
201
Q

locally anesthesized hypopigmented spots

A

consider tuberculoid leprosy

202
Q

lepromin skin test

A

m. leprae antigen injected intradermally.

+ test -> indurated nodule at site.

POSITIVE in patients w/ TUBERCULOID leprosy bc strong CD4+ Th1 cell-mediated immune response. –> activates macrophages to kill organism.

NEGATIVE in patients w/ LEPROMATOUS form. weak cell-mediated immunity.

203
Q

which has a strong cell mediated component: tuberculoid or lepromatous form of leprosy?

A

tuberculoid has strong cell-mediated. [think: TB]

lepromatous: look like lepers w/ lion-face, loss of fingers / toes bc can’t feel anymore –> weak cell mediated.

204
Q

skin biopsy of tuberculoid leprosy patient?

A

dominance of CD4+ T lymphocytes in skin lesions