Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

UWorld mixed > test #40 4.29 > Flashcards

test #40 4.29 Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

focal sclerosing glomerular sclerosis

A

HIV
obesity
sickle cell
heroin abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

spike & dome in membranous glomerulonephropathy

A

immune complex deposition
subepithelial

IgG & C3

no increase in cellularity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

alveolar-arterial oxygen gradient helps determine

A

CAUSE of hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

normal alveolar PaO2

A

assumed to be partial pressure of oxygen in alveolar air.

healthy person at sea level, usu around 100mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

alveolar gas equation

to determine A-a gradient

A

PAO2 = 150 - PaCO2/0.8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ratio of carbon dioxide production to oxygen consumption

A

0.8 (important in calculating alveolar gas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

normal A-a gradient?

A

no more than 10-15mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A
  1. high altitude (FiO2 down)

2. hypoventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what values are needed to calculate A-a gradient

A

PaCO2! will assume normal FiO2, etc

PAO2 = 150 - PaCO2 / 0.8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when is diffusion capacity of lungs decreased (2)

A

alveolar walls thickened
- pulmonary fibrosis / hyaline membrane / edema

alveolar walls destroyed
- emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

thiazolidinediones (-glitazones) bind..

A

intracellular nuclear receptor

PPAR-gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pioglitazone, rosiglitazone increase expression of..

A

most importantly, ADIPONECTIN

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

exenatide, liraglutide are..

A

GLP-1 analogs, related to incretin effect

increase insulin, decrease glucagon release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

linagliptin, saxagliptin, sitagliptin are..

A

DPP-4 inhibitors, related to incretin effect

normally cleave GLP-1

also increase insulin, decrease glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

repaglinide is..

A

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

weaker binding affinity & faster depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

GLP-1 is secreted by..

A

intestinal L cells in response to food

‘incretin effect’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GLP-1 works on what receptor

A

Gprotein - adenyl cyclase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which diabetes drugs work via enzyme inhibition (2)

A

metformin (block enzymes related to liver gluconeogenesis, etc)

alpha-glucosidase inhibitors (acarbose, miglitol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

miglitol

A

like acarbose, alpha-glucosidase-inhibitor,

diabetes med.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

edema in cirrhosis due to..

A

hypoalbuminemia (liver synthetic processes diminshed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A

hyperammonia (liver failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

4 signs of portal HTN

A
  1. esophageal varices
  2. caput medusa
  3. hemmorhoids
  4. splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

RACE. black have higher bone density than caucasians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

BMI on bone density

A

higher BMI = higher bone density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

smoking on bone density?

A

overall, anti-estrogenic

–> risk for osteopersosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does smoking actually decrease risk of?

A

fibrocystic breast disease & uterine cancer

bc anti-estrogenic

overall bad for you though!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how does estrogen build bone (2)

A
  1. increase osteblast activity

2. decrease osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

when see low CO2, think..

A

hyperventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

determinant of PaCO2 =

A

basal metabolic rate / alveolar ventillation

normal BMR: 0.8 CO2 produced for every O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

significant upper airway obstruction on blood gases

A

increase PaCO2, decrease PaO2

hyperventilation does not correct this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

significant respiratory muscle fatigue on blood gases

// decreased chest wall compliance

A

increase PaCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

blood CO2 determined by (2)

A
  1. respiratory rate

2. tidal volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

blood O2 determined by (1)

A

available alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

alveolar ventilation status determined by..

A

arterial PaCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

which ribs overlie spleen?

A

ribs 9, 10, 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

which ribs overlie kidney?

A

rib 12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

rib 12 can lacerate..

A

displace into retroperitoneum * lacterate kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

which posterior ribs overlie liver?

A

8, 9, 10, 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

during max inhalation

A

rest: 10th rib

max inhalation: 12th rib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what vertebral level does pancreas overlie?

A

L2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

diffusion limited gases

A

CO

gas does not equilibrate by the end of capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

thyroid arterial supply

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

2. inferior thyroid artery (branch of subclavian)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

ligation of inferior thyroid artery can…

A

injury recurrent laryngeal n (CNX)

–> hoarseness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

ansa cervicalis

A

C1, C2, C3 cervical plexus

courses deep to CNS, loop around IJV

feeds: sternohyoid, sternothyroid, omohyoid
“strap muscles”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

hypoglossal n (CNXII)

A

exists cranium via hypoglossal canal

innervates all intrinsic muscles of tongue, except palatoglossus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

spinal accessory N (CNXI)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what vertebral levels are kidneys?

A

T12-L3

right is slightly lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

pronephros

A

develops in week 4, then degenerates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

mesonephros

A

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

(female) paramesonephros

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

metanephros

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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

A

ureteric bud, from caudal end of mesonephros

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

origin of glomerulus to collecting duct of kidney

A

metanephros

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what is the last region of the kidney to canalize?

A

uteropelvic junction.

most common side of obstruction in fetus (hydronephrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

afferent arteriole constriction on FF and GFR?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

UWorld mixed (60 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions