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Pharmacology Exam 3 > Pharm General > Flashcards

Pharm General Flashcards

1
Q

How is histamine made?

A

rapidly broken down to inactive metabolites (MAO-B)

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2
Q

Autacoid

A

released and act locally includes histamine, serotonin, prostaglandins, leukotrienes, kinins

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3
Q

Major role of histamine

A

immune response, NT in CNS

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4
Q

Where is histamine found?

A

NT in periphery widespread in skin lung etc and synthesized and stored in mast cells and in CNS

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5
Q

H1 histamine receptor location

A

smooth muscle, endothelium, CNS

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6
Q

H2 histamine receptor location

A

vascular smooth muscle, cardiac muscle, gastric smooth muscle

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7
Q

Post receptor response of H1

A

Inc NO and Inc cGMP

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8
Q

Post receptor response of H2

A

Increase cAMP

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9
Q

What induces histamine release?

A

allergic rxn (type I hypersensitivity), inflammation, mechanical release and drugs (opioids)

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10
Q

What blocks release of histamine?

A

epinephrine and cromolyn (not substitute for epi)

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11
Q

What is the effect of histamine binding to smooth muscle cell?

A

phosphorylates MLCK and causes contraction

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12
Q

What is the effect of histamine binding to endothelial cell?

A

dephosphorylation of MLCP and relaxation

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13
Q

What does histamine regulate in CNS?

A

wakefulness, appetite and body temperature

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14
Q

Histamine toxicity in fish

A

nausea, vomiting, HA

suppressed by H1 receptor blockers

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15
Q

What are antihistamines most effective to treat?

A

urticaria and allergic rhinitis

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16
Q

What is the stimulus for cortisol synthesis?

A

ACTH

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17
Q

What is stimulus for aldosterone synthesis?

A

angiotensin II and K+

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18
Q

What is the pathway of regulation of glucocorticosteroid synthesis?

A

circadian rhythm and stressors
(or immune system) cause CRH to be released from hypothalamic neurons and go to anterior pituitary where ACTH is released which stimulates cortisol release (neg FB loop)

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19
Q

Why doesn’t aldosterone provide feedback inhibition on ACTH secretion?

A

levels are too low

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20
Q

What is the mechanism of ACTH on cortisol secreting cells in adrenal cortex?

A

ACTH binds to receptor and increased cAMP activates PKA which phosphorylates cholesterol ester hydrolase and more free cholesterol is formed

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21
Q

coactivators

A

facilitate steroid response

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22
Q

corepressors

A

inhibit steroid response

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23
Q

How do glucocorticoids suppress inflammation?

A

dec production of prostaglandin/leukotriene products which inhibits A2 and decreased synthesis of COX2

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24
Q

What normal physiological functions are under control of cortisol?

A

mobilizes AA in response to prolonged fast

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25
Q

What is a glucocorticoid response element (GRE)?

A

specific nucleotide sequence that is recognized by steroid hormone receptor hormone complex

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26
Q

How do you inhibit inflammatory events via glucocorticoid receptor?

A

increase Annexin A1 and decrease COX 2 and TNF alpha synthesis

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27
Q

What does annexin A1 do?

A

inhibit PLA2

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28
Q

What is the role of TNF?

A

transmits signals from immune cells for induction of inflammation

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29
Q

Why cant glucocorticoids bind equally to mineralocorticoid receptor?

A

enzyme (11B-HSD2) converts cortisol to cortisone which cannot bind to receptor

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30
Q

Why does eating excessive amounts of licorice cause HTN?

A

glycyrrhizic acid Inhibits 11B-HSD2 so cortisol binds to mineralocordicoid receptor and causes Na uptake

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31
Q

What causes airway increase in asthma?

A

mucus, thickened wall, smooth muscle constriction, narrowed airway

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32
Q

Mast cell effect on airways

A

decreases diameter and increases mucus secretion

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33
Q

Maintenance asthma medications

A

anti-inflammatory-affect airway responsiveness to stimulus

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34
Q

Quick relief medications

A

bronchodilators-affect airway resistance (open up airways)

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35
Q

What is the optimal particle size inhaled with inhaler?

A

2-5 micrometers

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36
Q

What is the most effective treatment in preventing asthma attacks?

A

inhaled corticosteroids (ICS)

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37
Q

Why is fluticasone good to use with β2 agonist?

A

It increases the number of β2 receptors

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38
Q

What is most common pphx for asthma?

A

ICS and β2 agonist

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39
Q

Asthma is NOT adequately controlled if rescue inhaler is used more than how many times/ week?

A

2

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40
Q

What is datura stramonium?

A

atropine bronchodilator plant

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41
Q

COPD

A

presence of airflow limitation that is not fully reversible with or without presence of sx

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42
Q

Sx of COPD

A

cough with mucus production, dyspnea, wheezing

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43
Q

What are the catecholamines?

A

epinephrine (adrenal), NE (post ganglionic), isoproterenol, dopamine (renal and mesentery beds) and dobutamine

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44
Q

Where are B1 receptors?

A

heart

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45
Q

What happens when you activate B1 receptors in the heart?

A

increase HR, conduction and contractility

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46
Q

Where are a1 receptors?

A

blood vessels and sphincters

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47
Q

What happens when a1 receptors are activated?

A

constriction

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48
Q

What happens when B2 receptors are activated?

A

dilation

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49
Q

Where are B2 receptors located?

A

blood vessels and uterus

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50
Q

What is renin release regulated by?

A

B1

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51
Q

What decreases mobility and tone in GI tract?

A

a1B2

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52
Q

What is the function of a2 receptor?

A

sense how much NE is there (if theres a lot BP is high)

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53
Q

Why do you get reflex tachycardia with alpha1 blockers?

A

a2 is trying to counteract the decrease in BP so increases NE output which will increase HR

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54
Q

Why is tachycardia worse in non-selective alpha blocker?

A

alpha 2 is also blocked and can’t regulate the amount of NE so HR is increasing more

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55
Q

What is epi reversal?

A

when you give epi in presence of alpha blocker and there is no “pressor” response (no increase in BP)

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56
Q

What is selectivity issue with beta blockers?

A

want to block B1 not B2 because if you block B2 you will have bronchoconstriction

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57
Q

Low levels of which lipoprotein puts people at risk for coronary artery disease?

A

HDL

58
Q

What are mechanisms for replenishing hepatic cholesterol pool?

A

↑ biosynthesis of cholesterol

↑ LDL receptor expression leading to ↑ LDL clearance from blood

59
Q

What is fiber good for?

A

absorbs cholesterol, slows cholesterol absorption and ↑ GI motility

60
Q

What do statins structurally look like?

A

HMG CoA which is eventually converted to cholesterol

61
Q

What does PCKS9 do?

A

binds to and interacts w/ LDL receptor to degrade it

62
Q

How do statins indirectly lower LDL levels?

A

Increasing hepatic LDL receptor expression

63
Q

What does PCSK9 do?

A

binds to and degrades LDLR

64
Q

What is stable angina?

A

narrowing of epicardial coronary artery, ischemia presents upon exercise at predictable level

65
Q

What is acute coronary syndrome (ACS) AKA variant angina?

A

vasospasm of coronary artery

66
Q

What is unstable angina?

A

plaque ruptures and must be treated quickly

67
Q

How can you increase oxygen supply?

A

Increase oxygen flow

68
Q

What are ways to decrease ischemia?

A

decrease HR, decrease contractility, decrease wall tension

69
Q

Why would you want to use combo therapy with β-Adrenergic blocker for HTN?

A

↑Preload and tension so might want to use with something that ↓preload

70
Q

BP=

A

CO x TPR

71
Q

How do you decrease BP?

A

Decreasing TPR

and CO

72
Q

How do you decrease TPR?

A

by directly vasodilating or decreasing sympathetic activity

73
Q

How do you decrease CO?

A

by decreasing contractility and preload with decrease in venous tone with diuretics

74
Q

How is preload decreased?

A

inhibit Na Cl pump so more will be excreted and they bring water with them which will decrease preload

75
Q

How do Thiazides work?

A

LT treatment to reduce vascular resistance and reduce afterload

76
Q

What is the dominant receptor that angiotension II works on?

A

AT1

77
Q

What is the effect of activation of AT1 receptors?

A

vasoconstriction, aldosterone secretion and Na retention

78
Q

When do you treat HTN?

A

> 140/90

79
Q

What is order of treatment for HTN?

A

lifestyle modifications, then if uncomplicated Diuretics or Beta blockers

80
Q

What anti HTN for diabetics?

A

ACE inhibitors and ARBS

81
Q

What is good tx for pts with arrhythmias and fibrillation?

A

beta blockers and Ca antagonists (not DHP)

82
Q

What should you do if no response or troublesome SE to anti-HTN med?

A

subsutitie to different class

83
Q

What should you do if no response but well tolerated to anti-HTN med?

A

Add second agent from different class (diuretic)

84
Q

For an AA woman 3 mo pregnant with type 1 diabetes w/ BP 160/90 and HR 50 bpm. What is the best tx option?

A

ARB (losartan) or ACE inhibitor (captopril)

85
Q

For white male with hx MI with angina upon exercising and BP 160/90 and HR 75 bpm. What is the best tx option?

A

Beta blockers (propanolol)

86
Q

For white male w/ hx LVH and BP 160/90 and HR 75 bpm. What is the best tx option?

A

ACE inhibitors (Captopril)

87
Q

What tachy needs to be treated?

A

symptomatic or potentially life threatening

88
Q

Whats happening at phase 0 of ventricular AP?

A

opening Na channels moving in

depolarization, affects conduction velocity

89
Q

Whats happening at phase 2 of ventricular AP?

A

Ca going in and K going out
depolarizing
affects AP duration

90
Q

Whats happening at phase 3 of ventricular AP?

A

More K flow out than Ca flow in

repolarizing, affects AP

91
Q

Whats happening at phase 4 of ventricular AP?

A

“pacemaker curent”
K out < Na + Ca in
If channels
affects heart rate (automaticity)

92
Q

Whats does the slope of phase 0 tell you?

A

conduction velocity
if shallower of a slope its slower conduction
affects resting membrane potential

93
Q

What is the time from the Na channel closing from the time it becomes activatable?

A

refractory period duration (usually the same as the refractory period duration)

94
Q

What channels affect pacemaker cells?

A

only Calcium

95
Q

What current affects myocardium cells?

A

Large Na current initiates the AP but not in SA and AV nodes

96
Q

What does the PR interval tell us?

A

conduction time from atrium to apical ventricular myocardium

97
Q

What does QRS duration tell us?

A

time needed for all ventricular myocardium to be activated

98
Q

what is ventricular flutter

A

organized, regular, 180-350

99
Q

What are causes of tachycardias?

A

ectopic pacemaker or reentry circuits, early after depolarization, delayed after depolar

100
Q

What is ventricular fibrillation

A

disorganized, irregular >350

101
Q

What happens in coronary heart disease?

A

Partial vessel occlusion → regional hypoxia (ischmia)

Hypoxia → ↓ATP → ↓ Na+/K+ ATPase activity → ↓ depolarization → ↑refractory period

102
Q

Where are reentry circuits more common?

A

in ventricle

103
Q

What causes reentry circuit?

A

multiple conduction pathways, refractory tissue, conduction time>refractory period

104
Q

What is concern for patients with A fib?

A

risk of blood clot formation in atria which can lead to strokes (but not every patient gets anticoags)

105
Q

What is goal of frug therapy of arrhythmias?

A

dec automaticity, dec conduction velocity, inc QT duration

106
Q

When do you use anticoag for patients with a fib?

A

if CHA2DS2-VASc score > or = 2

107
Q

Which Class I antiarrhythmic drug has longest refractory period? shortest?

A

Longest =IC

Shortest =IB

108
Q

What are schedule I drugs?

A

LSD, heroin, marijuana

high potential for abuse and no acceptable use ad therapeutic

109
Q

What are schedule II drugs?

A

morphine, oxycodone, codeine, amphetamine, cocaine, barbiturates
high potential for abuse but have acceptable medical use

110
Q

What are schedule III drugs?

A

codeine+acetaminophen, anabolic steroids

less potential for abuse

111
Q

What are schedule IV drugs?

A

benzos, tramadol

low potential for abuse

112
Q

What are schedule V drugs?

A

low potential for abuse OTC meds w/ codeine

113
Q

How does tolerance occur?

A

major mech: changes in cell receptors

minor mech: enhanced elimination

114
Q

What do drugs of abuse target?

A

GABAergic interneurons
dopaminergic neurons in VTA
medium sipny GABAergic interneurons in NA
(activate mesolimbin dopamine reward pathway)

115
Q

What are seizures by cocaine due to?

A

local anesthetic effects in CNS

116
Q

What are seizures by amphetamines due to?

A

lowering of seizure threshold

117
Q

What are the catecholamines?

A

epinephrine, NE, dopamine

118
Q

What is isoproterenol?

A

selective B agonist used to stimulate the heart

119
Q

What is DA?

A

transmitter in the CNS precursor for NE in post ganglionic sympathetic nerve terminals

120
Q

What is epinephrine?

A

neuro horomone released from adrenal medulla

121
Q

What is NE?

A

transmitter of postganglionic sympathetic neurons

122
Q

What inhibits NE release?

A

PGE2 and NE feedback at presynaptic alpha 2 receptors

123
Q

What enhances release of NE?

A

angiotensin II

124
Q

What metabolizes catecholamines?

A

MAO and COMT

125
Q

What is heart failure with reduced ejection fraction?

A

systolic dysfunction-problem of volume overload (big chamber) which increased LVEDV and decreased SV

126
Q

What is heart failure with preserved ejection fraction?

A

diastolic dysfunction-pressure overload (thick wall), decreased SV and decreased LVEDV

127
Q

What happens when the heart is under chronic stress signals?

A

changes from alpha MHC to beta MHC and decreased contractility and hypertrophies

128
Q

What does CHF do to the starling curve?

A

pushes it down because it decreases SV and increases EDV to compensate (if too much becomes pulmonary edema)

129
Q

What happens if chronic B1 receptor stimulation and chronic Ang II stimulation?

A

adverse remodeling

130
Q

What is seuqence of tx for systolic CHF?

A

↓weight, ↓activity, stop smoking, ↓preload (and sodium intake)
If doesn’t work then: ARNI or ACEI or ARB to dec BP, preload and afterload
Once stable on RAAS add Beta blocker (in slow fashion because dec contractility and calcium if too fast will get hypotension)
Then give diuretic to decrease preload
More severe-give aldosterone antagonist (protects against fibrosis) or digoxin in worst case

131
Q

What is goal in tc of CHF?

A

decrease preload, decrease afterload and decrease contractility

132
Q

What is neprilysin?

A

degrades vasoactive peptides (ANP, BNP) which decreases renin secretion, increases vasodilation and also targets bardykinin (cough)

133
Q

What does sacubitril get decomposed to?

A

LBQ657 the active compound of neprilysin

134
Q

What are the K+ wasting diuretics?

A

Loop diuretics and Thiazide diuretics

135
Q

When do you use diuretics?

A

edematous states

HTN

136
Q

What diuretic is best for edematous states?

A

loop diuretics

137
Q

What are K+ sparing diuretics?

A

ENaC Inhibitors and Aldosterone antagonists

138
Q

What is first drug of choice for HTN?

A

HCTZ

139
Q

What is the main determinant of extracellular fluid volume?

A

Sodium

140
Q

What are most diuretics aimed at?

A

decrease ECFV by increasing Na excretion

141
Q

What are the compensatory mechanisms that occur as effect of diuretics?

A

increase sympathetic activity, increase renin-angiotensin-aldosterone activity, increase ADH, decrease ANP

142
Q

What does carbonic anhydrase do in the proximal tubule?

A

breaks down carbonic acid into CO2 and water at luminal surface

Pharmacology Exam 3 (6 decks)

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