test #29 4.19 Flashcards Preview

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Flashcards in test #29 4.19 Deck (184):
1

what surface marker (cell type) is deficient in Bruton's X-linked agammaglobulimemia?

CD19 (no mature B cells in circulation)

2

B cell markers

CD19, 20, 21

3

CD15

neutrophil marker. also present in reed sternberg cells

4

CD16

NK cells (and others)

5

two types of abnormal ventilation during sleep

(1) apnea (cessation of breathing for >10 seconds)
(2) hypopnea (reduced airflow causing SaO2 to decrease >4%)

6

obstructive sleep apnea

noturnal hypoventilation w/ a transient upper airway obstruction due to poor pharyngeal muscle tone

most common cause of excessive daytime sleepiness

exam: erythrocytosis, obesity, increased soft tissue in oropharynx

arterial blood gas in day: normal

7

obesity hypoventilation syndrome (aka Pickwickian syndrome)

obesity impedes expansion of chest and abdominal wall during breathing.

increased respiratory work & decreased respiratory drive.

underventilation during all hours (chronically elevated PaCO2 and reduced PaO2)

arterial blood gas = abnormal

8

differentiation obesity hypoventilation syndrome from sleep apnea?

sleep apnea: normal arterial blood gas in day time

9

central sleep apnea

patient's central DRIVE to initiate breaths is absent.

neurological problem (not mechanical)

10

tumor w/ fat, smooth muscle, blood vessel

angiomyolipoma (benign tumor)

associated w/ tuberous sclerosis

11

tuberous sclerosis inheritance

autosomal DOMINANT

12

tuberous sclerosis symptoms

HAMARTOMAS

- hamartomas in CNS and skin
- angiofibromas (face, adenoma sebaceum)
- mitral regurgitation
- angiomyolipoma (renal)
- tuberous sclerosis
- autosomal dOminant
- mental retardation
- ash-leaf patch (hypopigmented)
- shagreen patch (thick leathery, dimpled, organge

also: subependymal astrocytoma and ungual fibromas

13

NF2

autosomal DOMINANT. bilateral acoustic neuromas.

also have multiple meningiomas, gliomas, ependymomas of spinal cord.

14

cerebellar hemangiomas, retinal hemangiomas, liver cysts, bilateral renal cell carcinoma, pheochromocytoma

von-hippel-lindau

15

sturge-weber syndrome

STURGE:

Somatic
Tram track Ca2+ opposite gyrus
Unilateral leptomeningeal angioma& port-wine stain
Retardation
GNAQ (activating mutation)
& Glaucoma (episcleral hemangioma)
Epilepsy

port-wine stain -- nonblanching in V1/V2 distribution

developmental anomaly of neural crest derivatives (mesoderm/ectoderm)

16

hereditary hemorrhagic telangiectasia

Osler-Rendu-Weber syndrome

multiple tenangiectasia of skin & mucosa.

presentation is recurrent epistaxis or GI bleed (melena)

17

how does B agonists (increased camp) increase contractility?

cAMP increases conductance of Ca2+ channels in SR.

18

when patient takes exogenous glucocorticoids, worry about..

how is this prevented?

acute adrenal insufficiency (when used for 3+ wks)

prevent by tapering off treatment

19

where does suppression occur when extended exogenous glucocortoids are taken?

the WHOLE axis: hypothalamic, pituitary, and adrenal!

low CRH, low ACTH, low cortisol!

20

mutation in NF1

mutation in NF1, tumor suppressor that regulates Ras

autosomal dominant

21

how does alcohol lead to pancreatitis?

obstruction via ductal concreations & direct parenchymal injury

22

three types of damage in pancreatitis

(1) pancreatic autodigestion - proteases
(2) vascular damage & hemorrhage - elastase
(3) fat necrosis - lipase / phospholipase

23

amylase makes..

hydrolyze starch into maltose (a glucose-glucose dissacharide), trisaccharide maltotriose, limit dextins

24

17 alpha hydroxylase needed for (2)

(1) pregnenolone -> 17 hydroxypregnenolone
(2) progesterone -> 17 hydroxyprogesterone

25

17 alpha hydroxlase deficiency on secondary sex characterestics

prevents in both males & females.

no menarche in females

26

5-alpha reductase deficiency on secondary sex characteristics?

abnormal external genitalia development, but will have normal secondary sex (increased muscle mass and phallus enlargement) bc of testosterone

prostate and hair = DHT

27

urine from umbilicus

persistant allantois remnant

28

allantois becomes..

URACHUS

29

urachus

duct between bladder (urogenital sinus) and yolk sac

30

failure of urachus to obliterate results in..

1. patent urachus: umbilicus to bladder: pee from belly button

31

vesicourachal diverticulum

failure to close part of urachus adjacent to bladder.

outpouching of apex of bladder. commonly asymptomatic.

32

urachal sinus

failure to close distal part of urachus (adjacent to umbilicus)

periumbicilical tenderness & purulent discharge from umilicus due to persistent and recurrent infection.

33

vitelline duct

omphalo-mesenteric duct connect yolksac to midgut lumen.

connect small intestine w/ skin at umbilicus

34

failure of vitelline duct to obliterate

(1) vitelline fistula
(2) meckel diverticulum

35

vitelline fistula

failure of vitillene duct to obliterate

meconium from umbillicus

36

meckel's diverticlum

partial closure of vitilline duct. patent portion attached to ileum (true diverticulum)

ectopic gastric mucosa / pancreatic tissue --> melena, periumbilical pain, ulcers

rule of 2!
2 inches, 2 feet from ileocecal valve, 2% of population, 2 epithelial

37

omphalocele

incomplete closure of anterior abdominal wall.

-- failure of abdominal contents to return to body cavity

presents as ventral opening at the umbilicus, protruding viscera covered by peritoneum

SEALED in peritoneum

38

gastroschisis

inadequate enlargement of peritoneal cavity during fetal life.

viscera PROTRUDE through defect in anterior abdominal wall adjacent to umbilicus

NOT covered by peritoneum.

39

closure of abdominal wall (rostral, lateral, caudal)

rostral fold: sternal defects
lateral: omphalocele, gastroschisis
caudal fold: bladder extrophy

40

duodenal atresia results from..

failure to recanalize

41

jejunal, ileal, colonic atresia results from...

vascular accident -- apple peel atresia

42

midgut development

6th wk: midgut herniates through belly button

10th: return to abdominal cavity, rotates around SMA, 90 degree counter clockwise

43

granules in whipple's disease

diastase-resistant granules in macrophages (lysosomes w/ partially digested bacteria)

44

what medication can decrease formation of adenomatous polyp formation?

aspirin! cox-2 overexpression in colon mucosa help lead to adenocarcinoma in adenoma-to-carcinoma sequence

45

adenoma to carcinoma sequence

AK53 & DCC
1. APC (b-catenin) --> AT RISK
(cox-2 overexpression & methylation increase too)
2. K-ras -->ADENOMA
3. p53 & DCC --> CARCINOMA

46

how does APC mutation lead to at risk colon?

APC keeps beta-catenin low --> maintains intercellular adhesion

47

FAP --> carcinoma always involves..

RECTUM (left, despite being an "exophytic mass'

48

HNPCC --> carcinoma always involves

PROXIMAL COLON (right, despite not being exophytic)

49

febuxostat

like allopurinol, inhibits xanthine oxidase

50

probenicid

blocks reabsorption of uric acid.

so does HIGH dose of salicylates

51

caspase

cysteine protease

52

what two enzymes can act on fructose intracellularly

fructokinase (fructose 1-phosphate) and hexokinase (fructose 6-phosphate)

53

where is fructose absorbed

proximal intestine, facilitative hexose transporter GLUT 5

54

how is fructose metabolised in essential fructosuria?

absent fructokinase, cannot make fructose-1-phosphate. mostly loose in urine.

BUT small amount converted by hexokinase in liver into fructose-6-phosphate --> phosphoglucomutase turns it into --> glucose 6 phosphate.

can be used for glycogenesis, glycolysis, HMP, etc.

55

aldolase B converts..

fructose 6-phosphate --> DHAP (dihydroxyacetone P) and glyceraldehyde

glyceraldehyde --> glyceraldehyde 3-phoshpate via triose kinase

56

galactose metabolism

galactose --> galactose-1-phosphate
(via galactokinase)

galactose 1-phosphate --> glucose 1-phosohate
(via galacose-1-uridyltransferase, which also converts UDP-glucose --> UDP-galactose

UDP glucose is regenerated from UDP galactose with UDP-galactose-4-epimerase

57

aldose reductase

[low affinity for glucose, only relevant when glucose is high]

converts glucose --> sorbitol.
also galactose --> galactitol

will accumulate if there is no sorbitol dehydrogenase to convert sorbitol ---> fructose

58

which tissues (4) lack sorbitol dehydrogenase? what is the manifestations of this?

lens, schwann cells, retina, kidney.

glucose --> sorbitol via aldose reductase. sorbitol accumulates (can't convert to fructose).

has osmotic pull. results in..

cataracts, peripheral neuropathy, retinopathy, nephropathy (as seen in diabetes)

59

acute interstitial pancreatitis vs. acute necrotic pancreatitis

acute interstitial: GROSS EDEMA: microscopic: calcifications. l

ipase digests adipose cells, form fatty acids that bind Ca2+ & ppt calcium salts.

if inflammation continues, trypsin activated, autodigestion of pancreas --

acute necrotic pancreatitis: GROSS CHALKY. destroy vessels --> white chalky fat necrosis. spread onto mesentery, omentum, other parts of abdominal cavity.

60

mesenteric ischemia on gross

bowel is dusky red and congested. see subserosal ecchymoses, edema, defined necrosis

(probably related to arcades, mult sources of blood to bowel)

61

calcification on bowel mesentary, omentum, etc

pancreatitis. lipase release free fatty acids, which bind Ca2+ and ppt calcium salts

62

gastroesophageal mural injury: mallory-weiss vs. boerhaave syndrome?

both caused by forceful vomiting

mallory-weiss: MUCOSAL tear. submucosal arterial or venous plexus bleeding

boerhaave: esophageal TRANSMURAL tear. esophageal air/fluid leakage into mediastinum & pleura

63

ethanol metabolism

in cytosol:
ethanol --> acetaldehyde
(alcohol dehydrogenase, makes NADH)

in mitochondria:
acetaldehyde --> acetate
(acetaldehyde dehydroganse, makes NADH)

overall increase in NADH/NAD+

64

why does alcohol cause lactic acidosis?

high NADH/NAD+
need NAD+ for glycolysis, will regenerate AND+ via lactic acid production

pyruvate -> lactate
consume NADH --> NAD+

65

why does alcohol cause steatosis in liver (2)?

high NADH/NAD+

1. glyceradehyde-3-phosphate --> glycerol-3-phosphate. combine w/ fatty acids --> triglycerides
2. high acetyl-CoA (due to inhibition of TCA) promotes lipogenesis

TCA inhibited bc oxaloacetate is converted to malate (to regenerate NAD+)

66

what 4 metabolic pathways are affected by alcohol?

high NADH/NAD+

1. pyruvate -> lactate
(consumes NADH--> NAD+)
2. oxaloacetate -> malate
(consumes NADH --> NAD+)
3. glyceraldehyde-3-phosphate --> glycerol-3-phosphate
(combines w/ fatty acids to make triglyceride)

4. blocked TCA, build up acetyl-CoA, permits ketogenesis & lipogenesis

67

supine hypotension syndrome

aortocaval compression syndrome

hypotension, pallor, sweating, nausea, dizziness

when preggers lady > 20wks lay on back

68

inheritance of hemochromatosis

autosomal recessive
fairly common among northern europeans

intestinal absorption of iron
usu C282Y mutation on chr 6 in HFE gene

69

symptoms of hemochromatosis (5)

1. micronodular cirrhosis
2. diabetes mellitus
3. skin pigmentation
4. testicular atrophy
6. CHF

increased risk of HCC

all related to DEPOSITS of Fe2+

70

most common source of e. coli bacteremia

URINARY TRACT!

urosepsis risk: BPH, fecal incontinence, neurogenic bladder secondary to diabetes, frequent indwelling catheterization.

71

why does mucor, rhizopus, absidia <3 diabetic ketoacidosis

have ketone reductase.

proliferate in vasculature, causes downstream tissue necrosis --> black eschar

72

differentiate paranasal infxn w. aspergillus and mucor?

histology.
aspergillus: acute angle septate

mucor: broad angle, nonseptate

73

diagnosis of allergic bronchopulmonary aspergillosis

SEROLOGICAL TESTING.

increased IgE and Ab to aspergillus fumigatus = diagnostic

74

quadratus lumborum

muscle of posterior abdominal wall

75

erector spinae

large group of back muscle. longitudinally along spinous processes. contraction = spine extension

76

transversus abdominis (transversalis)

most internal component of anterior abdominal wall musculature. below inferior oblique

77

ligamentum flava

paired elastic ligaments, connect vertebral laminae.

form posterior wall of spinal canal. help hold body erect.

78

psoas major

anterior surface of transverse processes & lateral surface of vertebral bodies of T12-L5

79

long delay between diet change and vitamin deficiency (~4yr) suggests..

cobalamin B12
(hepatic reserves last for up to several years)

80

which vitamins present w/ deficiency rapidly

WATER SOLUBLE, quickly wash out of body (except B12 and folate -- have stores in liver)

81

time frame of B12 and folate deficiency

B12: hepatic reserves last for years

folate: about 1/2 stored in liver, lasts 3-4 months.

folate deficiency faster

82

storage of vitamin D (25-vitD)

in adipose tissue.

deficiency takes a few months

83

vitamin A storage

90% stored in liver, perisinusoisal stellate (Ito cells)

last 6 months

84

vitamin K storage

small amount in liver, lasts 1-3 weeks only.

heavily dependent on that made from large intestinal microbes

85

diagnosis of hashimoto

usu (1)hypothyroidism, (2) high TSH, low T4/T3, and (3) anti-TPO antibody

can do biopsy: see intense mononuclear infiltration w/ lymphocytes and plasma cells. germinal centers.

86

characterestics of papillary thyroid cancer (3)

tall variant?

MOST COMMON. GOOD PROGNOSIS.

(1) branching papillary structure
(2) psamomma bodies
(3) ground glass nucleus w/ intranuclear grooving "orphan annie eyes'

tall variant: follicular hyperplasia, lined by tall epithelial cells. older individuals, worse prognosis compared to well-differentiated papillary thyroid cancer.

87

in thyroid; follicular hyperplasia lined by tall epithelial cells in older individual?

tall variant of papillary thyroid carcinoma. worse prognosis.

88

mixed cellular infiltration w/ occasional multinuclear giant cells in thyroid

subacute thyroiditis or,
de Quervain thyroiditis or,
granulomatous thyroiditis

89

presentation of subacute thyroiditis, de Quervain, granulomatous thyroiditis

painful tender thyroid. first thyroxoticosis, then hypothyroid

usu post-viral illness

90

origin of Riedel's thyroiditis

IgG4-related systemic illness

91

Riedel's thyroiditis vs. anaplastic carcinoma

both are firm, fixed, painless masses, but..

Riedel -- young female. anaplastic -- old people.

92

rapid relief for rheumatoid arthritis

glucocorticoids

NSAIDs woud help too

93

sulfasalazine, hydroxychloroquine, minocycline in rheumatoid arthritis

used to treat mild, early, seronegative rheumatoid arthritis.

do NOT have anti-inflammatory.

effects work as immune modulators (disease modifying)

94

colchicine

NOT used in rheumatoid arthritis.

binds to tubulin and inhibts MT polymerization of neutrophils. reduce inflammatory response to uric acid crystals

95

rx for acute gout:

NSAID, glucocorticoids (short-term only), colchine

96

rx for chronic gout:

allopurinol, febuxostat, probenicid, also colchine

97

mechanism of pain in migraines

(1) trigeminal afferents to meninges activated
(2) release substance P and CGRP (calcitonin gene related peptide)
(3) causes neurogenic inflammation --> vasodilation and plasma protein extravasation

98

sumatriptan for cluster headache and migraines

agonist of 5-HT 1B/1D on post-synaptic vasculature & presynaptic trigeminal neuron. inhibit release of vasoactive peptides. blocks vasodilation.

ABORTIVE.

contraindicated in prinzmetal angina and CAD bc can cause coronary vasospasm

99

buprprion activity

NDRI and nicotine agonist

100

which drugs block presynaptic reuptake of 5-HT and NE?

(1) TCA
(2) SNRI (venlafaxine and duloxetine)

note: TCA also have..
(1) anti-alpha adrenergic
(2) anti-muscarinic
(3) anti-H1 histamine

101

SNRI used for? specific extra use of each>

rx: depression.
venlafaxine also: generalized anxiety disorder & panic
duloxetine: also peripheral diabetic neuropathy

102

drugs used for migraine prophylaxis

b-blockers
antidepressants (TCA and SNRI)
anticonvulsants (valproate and topiramate)b

103

didanosine

nucleoside reverse transcription inhibitor.

side effect: pancreatitis

104

ganciclovir toxicity

interfere w/ human host cell DNA synthesis

105

zidovudine toxicity

inhibit mammalian cellular and mitochondria DNA polymerases

bone marrow suppression (anemia, granulocytopenia)

106

common side effect in non-nucleotide reverse transcriptase inhibitors (nnRTIs: efavirenz, nevirapine, delaviridine)

specific ones?

rash and hepatotoxicity

efavirenz: vivid dreams and CNS

delaviridine and efavirenz contraindicated in pregnancy

107

rx for reducing risk of fetal transmission of HIV?

zidovudine

108

common side effect of nucleotide reverse transcriptase inhibits (nRTIs)

bone marrow suppression (reverse with G-CSF and EPO)

peripheral neuropathy, lactic acidosis (nucleosides)

anemia: zidovidine

didanosine: pancreatitis

109

what is more toxic: acyclovir or gancyclovir?

gancyclovir

110

toxicity with gancyclovir

bone marrow suppression & renal toxicity

111

toxicity with acyclovir

obstructive crystalline nephropathy & acute renal failure

112

foscarnet toxicity

nephropathy, results in electrolyte abnormalities: hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia

113

cidofovir toxicity

nephrotoxic! give w/ probenecid and IV saline to reduce toxicity

114

nonselective beta and alpha blockers

carvedilol and labetalol (modified endings)

115

nebivolol

combines cardioselective B1 blockage w/ stimulation of B3 (activates NO synthase in vasculature)

116

short acting benzo (<10hr)

MOAT

midazolan, oxazepam, alprazolam, triazolam

117

medium acting benzo (10-20)

LET

lorazepam, estazolam, temazepam

118

long acting benzo (days)

chlordiazepoxide, clorazepate, diazepam, flurazepam

119

choosing duration of a benzo?

long-acting: more severe drowsiness, but less addicting/dependent

older people: short acting or they will fall
drug addict: long acting, or they will get addicted!

120

association between risk of dependence and rate of clearance.

directly proportional.

rate of clearance high, more dependence

121

association between duration of action and withdrawal symptoms

shorter duration of action, more likely withdrawal symptoms will occur

122

short acting benzo vs. zolpidem

short acting benzo = addictive.

zolpidem = rapid onset of action & short half-life, but LOW POTENTIAL for tolerance and dependence

123

normal P50 (partial pressure of oxygen at which hemoglobin is 50% saturated)

26mmHg.

shifted to lower numbers in lungs (LEFT = lungs)

shifted to higher numbers in tissue (RIGHT = tissue)

124

oxygen dissociation curve for sickle cell

shifted to RIGHT (easier to release oxygen)

125

subperiosteal thinning w/ cystic degeneration filled with brown fibrous tissue?

hyperparathyroidism! usu cortical bones

126

excessive osteoid matrix accumulation around trabeculae. and widening between osteoid seems

(as measured by bone histomorphometry and double tetracycline labeling)

vitamin D deficiency

127

trabecular thinning w/ few interconnections

osteoperosis

128

lamellar bone structure resembling mosaic?

paget's disease of bone

129

spongiosa filling medullar canal with no mature trabeculae

osteopetrosis

130

after vitamin D is absorbed from GI tract or skin..

must be activated by LIVER and KIDNEY

131

genu varus, rachitic rosary, harrison's sulci, craniotabes, growth retardation

vitamin D deficiency

-genu varus: bowed legs
-rachitic rosary: bony prominence at costochondral junction
-Harrison's sulci: indentations in lower ribs
-craniotabes: softening of skull

132

strong neutrophil chemotactic agents

leukotriene B4, C5a, 5-HETE

133

3 fates of arachodonic acid

(1) cox 1-2: prostacyclin, prostaglandin, thromboxane

(2) 5-lipooxygenase: leukotrienes

(3) 12-lipooxygenase:
lipoxin

134

fxn of lipoxins

made from arachadonic acid via 12-lipooxygenase

lipoxin A4 and B4
1. vasodilate
2. inhibit neutrophil chemotaxis
3. stimulate monocyte adhesion

135

LTC4, LTD4, LTE4

made from arachadonic acid via 5-lipooxygenase

1. increased bronchial tone
2. vasoconstriction
3. increased permeability

think: constrict everything

136

LTB4 & 5-HETE

neutrophil chemotaxis

137

prostacyclin (PGI2)

made from arachadonic acid via cyclooxygenase (PGH2 intermediate)

1. inhibit platelet aggregation
2. vasodilate
3. reduce bronchial tone
4. reduce uterine tone
5. increases permeability

relaxes everything

138

prostaglandins (PGD2, PGE2, PGF2a)

made from arachadonic acid via cyclooxygenase

1. vasodilate
2. increase permeability
3. increase uterine tone
4. reduce bronchial tone

139

main difference between prostacyclin and prostaglandins?

prostaglandin (PGD2, PGE2, PGF2) INCREASE uterine tone

prostacyclin reduces uterine tone and reduces platelet aggregation

140

misoprostol

PGE1 analogue. used to increase production of gastric mucosa & decrease acid production.

also an abortifactant, increases uterine tone

141

thromboxane

made from arachodonic acid via cyclooxygenase

counteracts prostacyclin (PGI2)

(1) increases platelet aggregating
(2) vasoconstriction
(3) increases bronchial tone

'increases everything'

142

important neutrophil chemoattractants (6)

5-HETE
LTB4
C5a
IL-8
PAF
kallikrein

143

bradykinin on vasculature

- vasodilation
- increases vascular permeability
- stimulates muscular contraction
- mediates pain

144

initial concern w/ given ACE inhibitors?

hypotension, esp if using a diuretic, hyponatremic, renal impairment

esp worry if taking a thiazide!

reduce venous return, secondary to decrease in angiotensin II levels

can activate Bezold-Jarisch reflec: vagally mediated hypotension and bradycardia

145

don't combined ACE with.. (2)

1. beta blockers, won't help much

2. thiazides, will give too much hypotension

146

three exposures related to liver angiosarcoma

- arsenic (pesticides)
- thorotrast (radioactive contrast)
- polyvinyl chloride

147

angiosarcoma on stain

CD31+, PECAM, impt for leukocyte extravasation

148

QT interval encompasses

start of QRS and end of T wave

149

inherited long QT? predisposed to

- K+ channel
- predisposed to torsades de pointes

(1) romano-warD
autosomal Dominant
no deafness

(2) lange-jervell-nielsen
autosomal recessive
sensorineural deafness

150

mutations in cardiac cell cytoskeleton & mitochondrial enzymes of oxidative phosphorylation related to..

inherited dilated cardiomyopathy

151

progressive fibrofatty replacement of right ventricular myocardium

arrhythmogenic right ventricular cardiomyopathy -- mutation in calcium-binding sarcoplasmic reticulum protein

152

follicular carcinoma on histology

sheets of follicular cells or large cells w/ eosinophilic cytoplasm (hurthle)

adenoma: no capsular / vascular invasion
carcinoma: capsular / vascular invasion

153

urease test

H. pylori

give isotopic urea.

H. pylori converts urea into CO2 and ammonia. isotpically labelled CO2 absorbed in blood and exhaled. measured 30min later.

154

distinguish ARDS from cardiogenic pulmonary edema?

pulmonary capillary wedge

155

histology: extreme myofiber disarray w/ interstitial fibrosis

hypertrophic cardiomyopathy

156

immunity to hepB indicated by

Anti-Hbs (HbsAb)

157

HbsAg

- detectable during acute infection
- persistence after 6 months -- chronic infection

158

anti-HBc IgM vs IgG

IgM:
- present acute infection & window phase when HbsAg and HbsAb absent

IgG:
- detectable w/ HbsAb & HbeAb after recovery
- present w/o HbsAb in chronic infxn
-not present after vaccination

159

window period in hep B

no HbsAg or HbsAb.
can have HbcAb IgM

160

HBeAg

another component of core
- appears AFTER HBsAg
- marker for viral replication activity
- detetable in chronic infectoin

161

HBeAb

present after recovery from acute infection
- HBeAg/anti-HBe seroconversion indicates transition of chronic infection from high to low viral replication & infectivity

162

hepatitis B infection presentation

- long asymptomatic incubation period (6-8 wks)
- acute disease, lasting several week to months

163

when does HBsAg appear in blood? when does it peak?

appear in blood: before symptom onset

peak: when patient is most ill

undetectable in 3-6 months

164

markers for active viral replication (hep B)? what else rises in this time

HBeAg and HBV DNA in serum. rises shortly after HBsAg comes in.

also increase in anti-HBc IgM and serum transaminases [shortly after symptoms arise]

165

exacerbation of chronic hepatitis B?

abrupt increase in liver enzyme, increased levels of HBV DNA.

exacerbation frequently occurs w/ HbeAg seroconversion & accompanying transition from high infectivity to low infectivity.

166

acute hepatitis that has progressed to chronic hepatitis w/ low infectivity

HbsAg (>6 months), HbeAb, HbcAb

no HbeAg, no HbsAb

167

acute hepatitis that has progressed to chronic hepatitis w/ high infectivity

HbsAg (>6 months), HbeAb, HBV DNA

no HbeAb, no HBsAb

168

vaccinated against Hep B? resolved HepB?

vaccine: HbsAb, no anything else

resolved hepB: HbsAb, HbcAb

169

inguinal hernia vs. direct hernia

inguinal hernia: failure of processus vaginalis to oliterate, travels through indirect inguinal. out of external inguinal canal, scrotum

external hernia: weakness in abdominal wall (hesselbach's triangle, between rectus abominus, inferior epigastric, inguinal ligament). come out near external inguinal ring. NOT in scrotum bc has no passage (no processus vaginalis)

170

hernia in scrotum? hernia above inguinal ligament? hernia below inguinal ligament?

in scrotum: indirect inguinal

above inguinal ligament: direct

below inguinal ligament: femoral

171

hernias relative to inferior epigastrics

indirect: lateral.
direct: medial

172

deep inguinal nodes receives drainage from?

reside under fascia lata, medial side of femoral vein.

glans penis // clitoris & superficial nodes

173

superficial inguinal nodes receives drainage from?

scrotum & all cutaneous structures inferior to umbillicus. including genitalia and anus up to pectinate line

174

testes drain to? scrotum? glans penis?

testes: para-aortic nodes.
scrotum: superficial inguinal nodes --> deep
glans penis --> deep inguinal nodes

175

specific iron deficiency signs (anemia)

dysphagia, spoon nails or koilonychia (disfigured finger nails)

176

filgastrim

G-CSF

177

what help w/ iron absorption

vitamin C, reduces it to Fe2+ state

178

factor V leiden

resistant to cleavage by protein C -- thrombophilia

179

antiphospholipid presents with (3) abnormal lab finding?

1. venous thromboembolism
2. arterial thromboembolism
3. frequent fetal loss

LONG aPTT

180

most common cause of long PTT?

lupus anticoagulant

181

why is folic acid deficiency --> prothrombotic?

hyperhomocysteinemia

182

lipofuscin is composed of..

product of lipid peroxidation.

lipid polymers and protein-complexed phospholipids.

'wear & tear'

seen in heart & liver of aging or cachectic, malnourished patients.

183

mediators of cachexia?

TNF-alpha!!!!

also: IFN-gamma, IL-6

184

chromogranin + lung cancer?

small cell carcinoma!

also: neuron specific enolase, synaptophysin. secretory granules on EM