test #40 4.29 Flashcards Preview

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

membranous nephropathy is associated w. underlying..

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

focal sclerosing glomerular sclerosis

HIV
obesity
sickle cell
heroin abuse

3

spike & dome in membranous glomerulonephropathy

immune complex deposition
subepithelial

IgG & C3

no increase in cellularity

4

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

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

1. 0.10% (100mg/dl)

2. 0.2% (200mg/dl)

5

alveolar-arterial oxygen gradient helps determine

CAUSE of hypoxemia

6

normal alveolar PaO2

assumed to be partial pressure of oxygen in alveolar air.

healthy person at sea level, usu around 100mmHg

7

alveolar gas equation
(to determine A-a gradient)

PAO2 = 150 - PaCO2/0.8

8

ratio of carbon dioxide production to oxygen consumption

0.8 (important in calculating alveolar gas)

9

normal A-a gradient?

no more than 10-15mmHg

10

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

1. high altitude (FiO2 down)
2. hypoventilation

11

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

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

12

what values are needed to calculate A-a gradient

PaCO2! will assume normal FiO2, etc

PAO2 = 150 - PaCO2 / 0.8

13

when is diffusion capacity of lungs decreased (2)

alveolar walls thickened
- pulmonary fibrosis / hyaline membrane / edema

alveolar walls destroyed
- emphysema

14

when is mixed venous blood oxygen increased (2)

(1) abnormal hemoglobin binds w/ greater affinity to oxygen, preventing unloading

(2) oxidative metabolism inhibited (i.e. cyanide or CO toxicity)

15

thiazolidinediones (-glitazones) bind..

intracellular nuclear receptor

PPAR-gamma

16

pioglitazone, rosiglitazone increase expression of..

most importantly, ADIPONECTIN

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

17

exenatide, liraglutide are..

GLP-1 analogs, related to incretin effect

increase insulin, decrease glucagon release

18

linagliptin, saxagliptin, sitagliptin are..

DPP-4 inhibitors, related to incretin effect

normally cleave GLP-1

also increase insulin, decrease glucagon

19

repaglinide is..

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

weaker binding affinity & faster depolarization

20

GLP-1 is secreted by..

intestinal L cells in response to food

'incretin effect'

21

GLP-1 works on what receptor

Gprotein - adenyl cyclase

22

which diabetes drugs work via enzyme inhibition (2)

metformin (block enzymes related to liver gluconeogenesis, etc)

alpha-glucosidase inhibitors (acarbose, miglitol)

23

miglitol

like acarbose, alpha-glucosidase-inhibitor,

diabetes med.

24

hyperestrinism state of cirrhosis due to (2)

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

edema in cirrhosis due to..

hypoalbuminemia (liver synthetic processes diminshed)

26

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

hyperammonia (liver failure)

27

4 signs of portal HTN

1. esophageal varices
2. caput medusa
3. hemmorhoids
4. splenomegaly

28

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

RACE. black have higher bone density than caucasians

29

BMI on bone density

higher BMI = higher bone density

30

smoking on bone density?

overall, anti-estrogenic
--> risk for osteopersosis

31

what does smoking actually decrease risk of?

fibrocystic breast disease & uterine cancer

bc anti-estrogenic

overall bad for you though!

32

3 ways glucocorticoids decrease bone formation

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

33

how does estrogen build bone (2)

1. increase osteblast activity
2. decrease osteoclast activity

34

what is the main indicator of ventillation

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

when see low CO2, think..

hyperventilation

36

determinant of PaCO2 =

basal metabolic rate / alveolar ventillation

normal BMR: 0.8 CO2 produced for every O2

37

decreased PaO2 & PaCO2

PaCO2 = indicator of ventilation.

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

due to PE or pneumonia

38

blood oxygen state after PE or pneumonia

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

significant upper airway obstruction on blood gases

increase PaCO2, decrease PaO2

(hyperventilation does not correct this)

40

significant respiratory muscle fatigue on blood gases

// decreased chest wall compliance

increase PaCO2

41

blood CO2 determined by (2)

1. respiratory rate
2. tidal volume

42

blood O2 determined by (1)

available alveoli

43

alveolar ventilation status determined by..

arterial PaCO2

44

"floating" ribs vs "false" ribs

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

which ribs overlie spleen?

ribs 9, 10, 11

46

which ribs overlie kidney?

rib 12

47

rib 12 can lacerate..

displace into retroperitoneum * lacterate kidney

48

which posterior ribs overlie liver?

8, 9, 10, 11

49

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

rest: 10th rib
max inhalation: 12th rib

50

what vertebral level does pancreas overlie?

L2

51

describe important structures at
T12, L1, L2, L3, L4

T12: esophagus enters, celiac branch

L1: SMA

L2: pancreas

L3: IMA

L4: bifurcation of abdominal. aorta

52

perfusion limited gases

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

diffusion limited gases

CO

gas does not equilibrate by the end of capillary

54

oxygen in normal health is.. (perfusion/diffusion limited)
in fibrosis, emphysema? exercise

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

thyroid arterial supply

1. superior thyroid artery (branch of external carotid)
2. inferior thyroid artery (branch of subclavian)

56

ligation of inferior thyroid artery can...

injury recurrent laryngeal n (CNX)

--> hoarseness

57

unilateral damage to recurrent laryngeal n. causes?

bilateral damage?

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

ligation of superior thyroid artery can..

injury to external branch of superior laryngeal n (CNX)

paralysis of cricothyroid m.

impaired ability to produce pitch --> monotone

59

branches of superior laryngeal n.

external: supplies cricothyroid (muscle of larynx)

internal: sensory from epiglottis to vocal folds

(below vocal folds -> recurrent laryngeal)

60

ansa cervicalis

C1, C2, C3 cervical plexus

courses deep to CNS, loop around IJV

feeds: sternohyoid, sternothyroid, omohyoid
"strap muscles"

61

hypoglossal n (CNXII)

exists cranium via hypoglossal canal

innervates all intrinsic muscles of tongue, except palatoglossus

62

spinal accessory N (CNXI)

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

63

recurrent laryngeal n (CN X)

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

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

64

where does a horseshoe kidney get stuck

inferior pole by IMA

risk for urinary tract obstruction & development of hydronephrosis

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

65

what vertebral levels are kidneys?

T12-L3
right is slightly lower

66

4 fates of vitelline duct abnormalities?

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

pronephros

develops in week 4, then degenerates

68

mesonephros

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

(female) paramesonephros

69

metanephros

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

70

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

ureteric bud, from caudal end of mesonephros

71

origin of glomerulus to collecting duct of kidney

metanephros

72

describe renal development

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

what is the last region of the kidney to canalize?

uteropelvic junction.

most common side of obstruction in fetus (hydronephrosis)

74

blood flow through kidney

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

75

on RPF & FF.

moderate efferent constriction causes? severe?

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

afferent arteriole constriction on FF and GFR?

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

77

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

1. caculate probability that all independently correctly false (0.95^8)

1. 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

linkage disequilibrium

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

what can cause linkage disequilibrium?

physical proximity of allelic loci, but not always!

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

80

Hardy-Weinberg principle

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

Hardy-weinberg assumptions (4)

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

82

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

male = q
female = q^2

83

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

distinct loci: multiple occurance rate --> 'haplotype freq'

same loci: 2pq

84

antibodies to PRP (polyribitol ribose phosphate) suggests..

h. influenza type B capsule

85

presentation of epiglottitis

abrupt onset of obstructive laryngeal edema

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

86

positive "thumb" sign on lateral cervical x-ray?

edematous epiglottis

epiglottitis, prob H. flu type B

87

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

b. anthracis

capsule of D-glutamate

88

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

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

enhanced erythropoesis & accelerated release of both mature RBC and reticulocytes

89

reticulocyte is..

immature RBC. slightly larger & bluer.

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

after wright-giemsa stain

90

rate of reticulocyte in blood stream

will mature into RBC, which will live for 120 days

91

adenomyosis

presence of endometrial glands in the myometrium

present: menorrhagia & dysmenorrhea

92

why is uterus enlarged w/ adenomyosis?

endometrial glands in myometrium

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

93

physical exam of adenomyosis vs. leiomyoma

adenomyosis: uniformly enlarged

leiomyoma: IRREGULARLY enlarged uterus or mass

94

most common gynecological malignancy?

endometrial (adenocarcinoma)

95

size of uterus w/ ectopic pregnancy?

uterus is NOT enlarged, but will

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

96

a unique tRNA exists for every..

mRNA codon sequence

(though mult diff codon seq might get the same amino acid)

97

t arm of tRNA (thymine, pseudouridine, cytosine)

only RNA sequence w/ thymine

binds to ribosome

'touch' ribosome

98

D arm of tRNA

dihydrouracil residue

helps tRNA recognition by correct aminoacyl tRNA synthetase

'determine' synthetase

99

what codon sequence is on tRNA 3' end

3' -> CCA

'can catch amino acid'

site for amino acid binding

100

carnitine deficiency will result in...

acetoacetate

101

what is carnitine important for..

B-oxidation of fatty acids

take fatty acyl-CoA from cytoplasm into mitochondrial matrix

102

describe fatty acid metabolism

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

what are CAT 1 and CAT 2

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

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

104

describe process of beta-oxidation

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

105

carnitine deficiency
or: myopathic CAT deficiency

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

in skeletal muscle

myoglobinemia
weakness following exercise
hypoketonia

106

MCAD deficiency (medium chain acyl-CoA dehydrogenase

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

link between gluconeogenesis & b-oxidation

need beta-oxidation energy to FUEL gluconeopgenesis!

108

differentiate McArdle from carnitine deficiency?

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

ketogenic amino acids

leucine & lysine

110

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

prolonged starvation: oxaloacetate consumed in gluconeogenesis

alcoholics: oxaloacetate -> malate

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

111

hexokinase vs. glucokinase

hexokinase all tissue

glucokinase in liver

glucokinase only kicks in when glucose is HIGH

112

2 general pathways for apoptosis

1. intrinsic mitochondrial
2. extrinsic death receptor

113

intrinsic path for apoptosis

- 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

release of cytochrome c from mitochondria..

pro-apoptotic protein, activate caspase for apoptosis

115

2 types of extrinsic apoptosis

1. death receptor on cell surface [TNF-R1 and Fas]
2. immune cell: perforin/granzyme release

116

2 major death receptors

TNF-R1 and Fas (CD95)

117

how does Bcl-2 block apoptosis

Bcl-2 prevents cytochrome c release from mitochondria.

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

118

receptor-mediated extrinsic apoptosis

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

physiologic example of intrinsic apoptosis

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

120

physiologic example of extrinsic apoptosis

Fas/Fas-L in thymic medullary negative selection

121

what type of physiologic apoptosis is impt for autoimmunity

Fas/Fas-L

important for negative selection in thymus medulla

122

succinate dehydrogenase

mitochondrial enzyme in ETC.

oxidizing succinate to fumarate & reducing FAD to FADH2.

123

superoxide dismutase

reduce superoxide to hydrogen peroxide

124

TTP vs. HUS

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

syrup of ipecac

emetic treatment.

used immediately after injection of toxin

126

cryoprecipitant contains

factor VIII, factor XIII, vWF, fibrinogen

(good for hemophilia A, vwd, hypofibrinoginemia)

127

side effects of SNRIs (duloxetine and venlafaxine)

high BP

also: stimulant effects, sedation, naseua

128

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

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

which TCA has most anticholinergic effects?

amitryptyline

130

list TCA's

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

131

use for diabetic neuropathy? (2)

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

132

TCA (esp amitryptyline) in patient w/ BPH

worry about urinary retention bc of anticholinergic effects

133

mechanism of neuroleptic malignant syndrome

specific to anti-D2 effects

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

134

distinguish serotonin syndrome from neuroleptic malignant syndrome

serotonin syndrome: myoclonus

neuroleptic malignant syndrome: rigidity

135

rx for neuroleptic malignant syndrome?

-bromocriptine: Dopamine agonist
-amantidine: increase Dopine efflux

- dantrolene, stop rigidity

136

vision problems, dry skin, generalized pruitis

suggests prolonged biliary obstruction resulting in..

1. vit A deficiency : vision & dry skin!

137

most common cause of night blindness

hereditary retinitis pigmentosa

138

5 signs of vitamin A deficiency

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

139

4 differential diagnosis for acquired nyctalopia

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

140

light tapping on chin induces masseter muscle spasm..

variant of chvostek sign; hyperactive jaw jerk

sign of hypoparathyroidism

141

Chvostek sign

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

sign of hypoparathyroidism

(neuromuscular hyperexicitability)

142

Trousseau sign

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

sign of hypoparathyroidism

(neuromuscular hyperexcitability)

143

2 exam signs of hypoparathyroidism

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

Trousseau sign
-BP cuff --> carpal spasm

(neuromuscular hyperexcitability)

144

at what Ca2+ levels do neuromuscular excitability manifest?

<7mg/dl

145

complication of thyroid surgery --> neuromuscular hyperexcitability

accidentally take out parathyroid!

146

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

cleft lip (primary palate)

147

improper fusion of lateral palatine process

or

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

cleft palate (secondary palate

148

inheritance of cleft lip/cleft palate

distinct etiology, but often occur together

MULTIFACTORIAL inheritance

[not associated w/ digeorge!]

149

when do lip / palate form

6th wk of embryonic development

150

midline intermaxillary segment forms..

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

151

choanal atresia

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

152

how is ammonium from muscle disposed of?

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

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

glutamine is released into blood

in kidney:

glutamine ---> glutamate
via glutaminase

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

154

alanine cycle

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

cori cycle

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

156

important nitrogen transporters in body

alanine & glutamine

157

pathogenesis of porcelain gallbladder

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

prognosis of porcelain gallbladder

11-33% will develop gallbladder carcinoma

159

clearance of digoxin

primarily renal exretion

half-life 2.5 days (40hrs)

160

elderly pt w/ digoxin toxicity..

likely related to age-related renal insufficiency!

161

consideration w/ meds for all elderly?

reduce doses of renally-cleared medications to prevent toxicity

162

enzyme deficiency in von gierke's

glucose-6-phosphatase

163

2 roles of debranching enzyme

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

liver findings in Cori disease

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

organ affected in von girke's

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

manifestation: hypoglycemia, lactic acidosis, hyperlipidemia, hyperuricemia

hepatic steatosis --> CARDINAL MANIFESTATION

166

why can muscle fxn without glucose 6-phosphatase?

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

167

cause of tabes dorsalis in tertiary syphillis. presentation

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

maternal presentation of measles

postauricular lymphadenopathy, rash, arthralgia

169

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

congenital syphillis

170

NF-kB is important for..

transcription factor for cytokine production

171

possible pathogenesis of crohn's

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

main CSF difference in viral / bacterial meningitis

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

most common viral cause of meningitis

echovirus

usu enteroviruses (coxsackie, echo, polio, enterovirus)

174

most common cause of bacterial meningitis

s. pneumo

175

2nd most common cause of bacterial meningitis

n. meningitidis

176

most common causes of common cold

coronavirus, rhinovirus, adenovirus

177

graves vs. hyperthyroidism

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

causes of hyperthyroidism (4)

-graves disease (most common)
- toxic adenoma
- toxic multinodular goiter
- thyroiditis

179

describe pretibial myxedema

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

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

the one w/ shortest half-life, factor VII

181

why does thrombocytopenia develop in alcoholic cirrhosis of liver

hypersplenism -- sequestered

182

what is barret's esophagus a risk factor for

esophageal adenocarcinoma

will be clinically silent until it obstructs esophageal lumen

183

achalasia is caused by

loss of myenteric ganglion cells of the LES --> can't relax

leads to high LES opening pressure & uncoordinated peristalisis

184

major risk factors for squamous carcinoma of the esophagus

1. smoking
2. alcohol use

185

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

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

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

186

most common risk factors squamous carcinoma

anything that causes irritation

alcohol & cigarette smoking (both)

187

important side effects of carbamazepine

1. bone marrow suppression: anemia, agranulocytosis, thrombocytopenia

2. hepatoxotic: monitor LFT

2. SIADH

188

simple vs. complex seizure

simple: no impairment of consciousness during or after

complex: loss of memory during event / post-ictal state

189

important prognosticfactor in poststreptococcal glomerulonephritis

AGE

95% of children recover completely w/ conservative therapy

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

190

pathogenesis of peripheral neuropathy in diabetes

1. diabetic microangiopathy of endoneural arterioles:

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

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

191

diabetic neuropathy sensation

paresthesia (tingling, numbness)

intense BURNING pain

192

types of neuropathy in diabetes

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

histology of cystic medial degeneration

fragmentation of elastic fibers in media --> "basket-weave" appearance.

space filled in by amorphous matrix

--> see MYXOMATOUS changes

194

myxomatous changes in media of large artery

cystic medial degeneration, related to aortic aneursym

195

which collagen disorder is associated w/ berry aneursym

type IV ehlers danlos

196

false aneursym

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

where does mycobacterium leprae like to act

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

198

leprosy resevoir in US

armadillos

199

2 forms of Hansen's disease

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

low cell-mediated immunity w/ a humoral Th2 response

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

HIGH cell mediated immunity; largely Th1 type immune mediated

200

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

1. lepromatous: weak cell-mediated immunity w/ a humoral Th2 response

2. tuberculoid: strong cell-mediated immunity. CD4+ Th1 immune response.

201

locally anesthesized hypopigmented spots

consider tuberculoid leprosy

202

lepromin skin test

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

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

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

skin biopsy of tuberculoid leprosy patient?

dominance of CD4+ T lymphocytes in skin lesions