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Cardiac > NBME > Flashcards

NBME Flashcards

1
Q

What is apoptosis characterized by

A

cell shrinkage, nuclear shrinkage, (pyknosis) and basophilia, and membrane blebbing, nuclear fragmentation (karyorrhexis) and formation of apoptotic bodies which are then phagocytosed

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2
Q

pyknosis

A

nuclear shrinkage

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3
Q

karyorrhexis

A

nuclear fragmentation

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4
Q

basophilia

A

a dye (basic or positive) that stains DNA/RNA in the nucleus, RNA in ribosomes, which are acidic and negatively charged

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5
Q

what is the intrinsic pathway?

A

involved in tissue remodeling in embryogenesis

occurs when a growth factor is withdrawn from a proliferating cell population,

occurs after exposure to injurious stimuli radiation, toxins hypoxia

changes in proportions of anti and pro apoptotic factors lead to increased mitochondria permeability and cytochrome C release

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6
Q

extrinsic pathway

A

FAS ligand binding to FAS

immune cell 9perforin and granzyme B

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7
Q

necrosis

A

enzymatic degradation and protein denaturation resulting from irreversible injury
intracellular components extravasate
inflammatory process

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8
Q

coagulative necrosis characteristics

A 
eosinophilia, 
loss of cytoplasmic and nuclear detail, 
blurring of cytoplasmic membranes, 
cell otherwise intact 
preservation of tissue architecture
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9
Q

reversible with O2

A

decreased ATP synthesis
cellular swelling ( no ATP —> impaired Na+/K+ pump)
nuclear chromatin clumping
decreased glycogen
fatty change
ribosomal detachment (decrease protein synthesis)

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10
Q

irreversible cell injury

A

nuclear pyknosis, karolysis, karyorrhexis, Ca2+ influx, –> Capsase activation
Plasma membrane damage
lysosomal rupture
mitochondrial permeabillity

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11
Q

red infarcts

A

red infarcts occur in tissues with collateral circulation,

liver lungs, intestine

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12
Q

pale infarcts

A

sold tissues with single blood supply

heart kidney and spleen,

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13
Q

Clinical presentation of hypovolemic and cardiogenic shock

A

low output failure
increase TPR
low cardiac output
cold clammy patient, vasoconstriction

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14
Q

Clinical presentation of septic shock

A

high-output failure
decreased TPR
dilated arterioles, high venous return,
hot patient (vasodilation)

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15
Q

atrophy

A 
decrease hormones (uterus/vagina)
decrease innervation (motor neuron damage)
decrease blood flow 
decrease nutrients 
increase pressure (nephrolithiasis)
occlusion of secretory ducts
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16
Q

Clinical Presentation of Inflammation

A

redness, dolor, calor, tumor, loss of function

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17
Q

vascular component of inflammation

A

increase vascular permeability, vasodilation, endothelial injury

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18
Q

cellular components of inflammation,

A

neutrophils extravasate and participate in inflammation, phagocytosis, degranulation and inflammatory mediator release

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19
Q

acute inflammation

A

rapid onset

lasts minutes to days

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20
Q

key players in acute inflammation

A

neutrophils

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21
Q

chronic inflammation

A

lymphocytes and macrophages
characterized by persistent destruction and repair
blood vesel proliferation and fbirosis

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22
Q

granuloma

A

nodular connections of epithiliods and giant cells, outcomes include scarring and amyloidosis,

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23
Q

outcomes of acute inflammation

A

complete resolution abscess, or progression to chronic inflammation

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24
Q

causes of acute inflammation

A

infection
necrosis
physical injury

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25
Q

causes of chronic inflammation

A

autoimmune disease
chronic irritation
viral infecton

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26
Q

systemic inflammation of acute inflammation

A

chills,
fever,
myalgias

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27
Q

From blood to sites of tissue injury, neutrophils via 4 steps

A

rolling,
adhering,
diapedsis,
migration

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28
Q

which protein allows neutrophils to roll?

A

selectins

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29
Q

which protein allows neutrophils to adhere

A

integrins

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30
Q

what do leukocytes use to travel through interstitium

A

chemotatic signals`

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31
Q

free radicals damage ]

A

membrane lipid peroxidation,
protein damage
and DNA breakage

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32
Q

where do free radicals come from?

A 
gamma rays and x rays, 
metabolism of drugs
redox reactions
NO 
transition metals, 
leukocyte oxidative burst
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33
Q

Elimination of free radicals

A 
catalase
superoxide dismutase,
glutathione peroxidase 
spontaneous decay 
antioxidants
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34
Q

retinopathy of prematurity

A

abnormal blood vessels grow in the retina, retinal detachment –>causing blindness

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35
Q

bronchopulmonary dysplasia

A

in premature infants, chronic lung disease caused by mechanical ventilation and oxygen supply.

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36
Q

wound healing

three stages

A

inflammatory
proliferative
remodeling

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37
Q

inflammatory key mediators

A

platelets, neutrophils, and macrophages

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38
Q

proliferative key mediators

A

fibroblasts, myofibroblasts, endothelial cells, keratinocytes, and macrophages.

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39
Q

remodeling key players

A

fibroblasts

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40
Q

what occurs during inflammation

A

increased vascular permeability, clot formation, neutrophil migration, macrophage clean up debris 2 days later

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41
Q

what occurs during proliferation

A

deposition of granulation tissue and collagen, angiongenesis, epithelial cell proliferation, dossolution of clot and wound contraction mediated by myofibroblasts.

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42
Q

what occurs during remodeling

A

type III collagen replaced by type I collagen

increase tensile strength of tissue

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43
Q

transudate

A

hypocellular
protein poor
specific gravity < 1.012

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44
Q

exudate

A

cellular
protein rich
specific gravity >1.020

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45
Q

cause of exudate

A

lymphatic obstruction

inflammation

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46
Q

causes of transudate

A

increased hydrostatic pressure
decreased oncotic pressure
Na+ retention

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47
Q

caseating granuloma

Dx

A

TB

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48
Q

noncaseating granuloma

A 
Tb 
sarcodoisis 
other infections
foreign material 
fungal infections
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49
Q

Increase erythrocyte sedimentation rate

is an indicator of?

A 
infections, 
inflammation
cancer
pregnancy
SLE
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50
Q

decrease erythrocyte sedimentation rate

A

sickle cell
polycythemia
CHF

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51
Q

Symptoms of iron poisoning

A

acute, gastric bleeding

chronic metabolic acidosis, scarring leading to GI obstruction

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52
Q

metaplasia often the result

A

secondary to irritation and/or environmental exposure

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53
Q

dysplasia

A

abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue, maturation; commonly preneoplastic.

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54
Q

which plasia’s are reversible

A

hyperplasia,
metaplasia,
dysplasia

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55
Q

anaplasia

A

abnormal cells lacking differentiation, resemble primitive cells of same tissue, often equated with undifferentiated malignant neoplasms, little or no resemblance to tissue of origin.

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56
Q

neoplasia

A

a clonal proliferation of cells that is uncontrolled and excessive.
may be benign or malignant

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57
Q

Barret’s esophagus,

A

change from squamous cell adenocarcinoma to esophageal adenocarcinoma.

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58
Q

BCL2

A

follicular lymphoma and undifferentiated lymphoma,
anti apoptotic molecule,
BCL2 sensors,
BCL2 inhibit the sensors, which prevents mitochondria from releasing cytochrome C and activates capsases.

59
Q

aflatoxins are associated

with what cancer

A

hepatocellular carcinoma

60
Q

Asbestos

A

mesothelioma

61
Q

how is volume of distribution impacted with kidney or renal disease

A

Vd is increased

62
Q

describe the characteristics of a drug with high Vd

A

lipid soluble, low protein binding, low rates of ionization

63
Q

equation for half life

A

.7x Vd/Cl

64
Q

Bioavailability

A

fraction of drug that reaches systemic circulation unchanged

65
Q

Equation for the volume of distribution

A

total amount of drug/ plasma drug concentration

66
Q

Acetaminophen toxicisity

classical presentation

A

hepatoxicisity

67
Q

hepatoxicisty what lab value would indicate liver damage

A

ALT

68
Q

What is the cause of acetaminophen toxicisity

A

N-Acetyl Para Benzoquinoneimine

69
Q

acetaminophen overdose situation

A

more drug is available for CYP metabolism to a toxic metabolite.NAPQI

70
Q

what metabolizes the toxic metabolite of acetaminophen

A

glutathione,

71
Q

glutathione is a combination of

A

glutamate, cysteine, and glycine

72
Q

what enzyme catalyze formation of glutathione conjugates?

A

glutathione S transferase

73
Q

what increases

the risk of acetaminophen hepatotoxicity?

A

alcohol inducible CYP2E1 which rapidly forms NAPQI’

malnutrition decreases GSH and UDP glucoronic acid levels

high acute doses, >10grams in adults

74
Q

Stages of Acetaminophen toxicisity

stage 1

A

stage 1 (0-24 hours)
patients are often asymptomatic,
nonspecific symptoms,
nausea vomiting, lethargy, drowsiness, diaphoresis,

75
Q

Stages of Acetaminophen toxicisity

stage 2

A

patients are often asymptomatic,
mild increases AST
and some right upper quadrant pain

76
Q

Stages of Acetaminophen toxicisity

stage 3

A 
AST, ALT levels > 10,000IU/ml
fulminant hepatic failure
encepholapthy, coma
hemorrhage,
jaundice
liver transplantation may be needed renal changes usually less prominent.
77
Q

Stages of Acetaminophen toxicisity

stage 4

A

liver regernates, near normal laboratory values often observed within a week.
complete recovery may take months

78
Q

what’s the treatment of acetaminophen toxicisity

A

NAC

79
Q

acute management

of acetaminophen

A

activated charcoal, if you know its toxic
get blood samples, >4 hours and less than 24 hours after dose,

give it if its above treatment line in the Rumack matthew noomogram

80
Q

Why NAC works

A

it’s a source of systeine to form glutathione
some binds directly to NAPQI
source of sulfate for sulfate conjugation

81
Q

list the following G proteins and what’s it linked to

A

alpha 1—> Gq
alpha 2 —> Gi and Go
B1 B2 B3, D1—> Gs

82
Q

D1

A

produce dialtion of renal arteries

83
Q

LOCATION OF B1 RECEPTORS

A

heart and kidneys

84
Q

B2

A

heart and produce inhibitory effects of sympathetic stimulation

85
Q

B3

A

lipolysis

86
Q

competitive antagonists

on efficcacy grraphs

A

shifts curve to the right, decrease potency, no change in efficacy

87
Q

noncompetitive antagonist

A

shifts curve down, decreases efficacy.

can’t be overcome by increasign agonist substrate concentration,

88
Q

what is a great example of noncompetitive antagonists

A

phenoxybenzamine on alpha receptors

89
Q

partial agonsits,

A

decreases efficacy

90
Q

therapeutic index

A

a comaprison of hte amount of therapeutic agent that causes the therapeutic effect to the amount that causes toxicisity

91
Q

analogy to remember the equation for TI

A

TILE
Therapuetic index= LD50/ ED50
lethal dose/ effective dose

92
Q

therapeutic window

A

refers to range of doses which optimize between eficacy and toxicisity

93
Q

what does higher TI values?

A

SAFER DRUGS

94
Q

which receptor causes mydriasis

A

alpha 1

95
Q

what causes vascular smooth muscle contraction

A

alpha 1

96
Q

what causes intestinal and bladder sphincter muscle contraction

A

alpha 1

97
Q

what works in the CNS and decreases sympathetic outflow

A

alpha 2

98
Q

what causes increase in platelet aggregation

A

alpha 2

99
Q

what causes bronchodilation

A

Beta 2

100
Q

what causes vasodilation

A

beta 2

101
Q

phenelyphrien is use to treat

A

mydriatic agent and decongest agent

102
Q

albertorl terbutaline metaproterenol, salmeterol
formoterol
act on what receptor and are used for what?

A

Beta 2,!!!!!!

bronchodiltion, in asthma and COPD

103
Q

Norepinephrine treats

A

acute hypotension HYPO

104
Q

adverse side effects of alpha agonists

A

hypertension and cerebral hemorrhage

105
Q

adverse side effects of beta agonists

A

tremor and nervousness, tachycardia, and palpitations

106
Q

main use of reserpine

A

blocks VMAT, ultimately depleting NE from terminals,

main use is to treat hyperkinetic movement disorders,

107
Q

main use of ephedrine

A

releases NE and is a direct agonist

treats hypotension and nasal congestion

108
Q

pseudophedrine

A

nasal decongestant

109
Q

phenoybenzame

A

only noncompetitive blocker

110
Q

phentolamine

A

prototype

111
Q

alpha 1 selective

A

prazosin, doxazosin, terazosin

112
Q

to manage pheochomocytoma

A

phenozybenzamin

113
Q

to treat BPH,

A

urinary obstruction BPH!!!

114
Q

why with alpha antagonists do you get tachycardia

A

excess norepinephrine release

but mainly, you lose the control found on alpha 2 receptors which are autoreceptors.

115
Q

what increases outflow of aqueous humor

A

alpha agonist

116
Q

what decreases secretion of aqueous humor?

A

beta blockers

117
Q

beta blockers that reduce the production of aqueous humor

A

timolol betaxolol

118
Q

What’s used to reduce the myocardial infarction?

A

propanolol
metaprolol
timolol.

119
Q

what’s used to treat congestive heart failure

A

metoprolol carvedilol

120
Q

adveser effects of beta blockers

A

heart failure
arrythmias
don’t use with patients iwth asthma

121
Q

ganglionic blockers

A

blocks nicotinic receptors in ANS ganglia,

Destroys ANS,

122
Q

choline esters

A

ACh, methacholine, carbachol, bethanechol

123
Q

characteristics of choline esters

A

poorly absorbed from GIT and doesn’t cross BBB

124
Q

which ones excite nicotinic receptors

A

ACh, and carbachol

125
Q

which drugs have a longer duration of AChE?

A

carbachol and bethanechol

126
Q

what are alkaloids?

A

pilocarpine,

127
Q

alkaloids are better than cholines

A

because they are well absorbed from GIt, and they do cross BBB

128
Q

Pilocarpine,

A

selective for muscarinic receptors.

129
Q

two mechanisms of muscarinic agonists

A

direct stimulation of muscarinic receptor

stimulation of muscarinic receptors on presynaptic terminal to reduce release of neurotransmitter

130
Q

direct acting cholinometics on the vasculature

A

dilation via nitric oxide

131
Q

methacholine

A

diagnosis of asthma

132
Q

pilocarpine

A

xerostomia and glaucoma

133
Q

Bethanecol

A

postoperative ileus and urinary retention

134
Q

carbachol

A

glaucoma

135
Q

contraindications of muscarinic directing acting drugs

A

asthma or cOPD
obstruction in GIT or urinary system
bradycardia hypotension
hyperthyroidism

136
Q

what’s the good thing about edrophonium

A

lasts only 2-10 minutes

137
Q

what’s good about carbamic acid esters?

A

neostigmine, physostigmine pyridostigmine, block up to 6 hours of ACHE

138
Q

organophosphates?

A

echothiopate and malathion

139
Q

echthiopate

A

glaucoma

140
Q

physostigmine

A

glaucoma, antimucarinic drug intoxication

141
Q

edrophonium

A

diagnosis of MG , reversal of neuromucular blockade

142
Q

pyrdistigmine and ambenonium

A

treatment of MG

143
Q

neostigmine

A

postoperative ileus and urinary retention, MG, reversal of neuromuscular blockade

144
Q

muscarinic adverse effects

A 
weakness or paralysis
increased sweating
diarrhea
vomiting 
miosis
bronchial constriction?

Cardiac (3 decks)

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