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Pharm Test 2 > 09/30 > Flashcards

09/30 Flashcards

1
Q

What is considered hypertensive urgency?

A

180/110 with out end organ damage

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2
Q

What drug is used for htn emergencies?

A

Sodium nitroprusside

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3
Q

What does sodium nitroprusside do?

A

it increases cyclic GMP= relaxation of smooth muscle = decreased BP

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4
Q

Why is sodium nitroprusside somewhat toxic?

A

It is an iron molecule surrounded by cyanide and 1 molecule of NO. The cyanide can be toxic if it reaches high enough levels

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5
Q

Any NO compound dilates both

A

arteries and veins

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6
Q

Why does sodium nitroprusside have to be protected from light?

A

light will release the NO before it even enters into the body

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7
Q

How is CN normally excreted through the body?

A

kidneys

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8
Q

If you have a build up of cyanide in the body, what can you give to help facilitate metabolism?

A

Sodium thiosulfate or Hyposodium thiosulfate

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9
Q

What are the drugs for HTN emergencies?

A

sodium nitroprusside
fenoldopam

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10
Q

How does fenoldopam work?

A

it works on the dopamine type 1 receptors found in the renal vasculature bed.
it dilates the renal vasculature bed= reduced bp and the dilation also increases blood flow to the kidneys which leads to higher urine excretion. so it kind of works as a diuretic in that sense

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11
Q

What are calcium channel blockers used for?

A

htn
agina
arrhythmias

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12
Q

What are the 3 main groups of CCB?

A

verapamil
diltiazem
dihydropyridine

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13
Q

What do dihydropyridine drugs end in?

A

-ipine

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14
Q

verapamil is more targeted towards the

A

heart with minor peripheral effects

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15
Q

diltiazem targets both the

A

heart and the periphery

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16
Q

dihydropyridine drugs mostly target the

A

periphery

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17
Q

Despite verapamil, diltiazem, and dihydropyridine working in different areas of the heart, they all

A

lower blood pressure equally

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18
Q

When the SNS is stimulated, NE binds to Beta receptors and stimulate what to be released?

A

renin

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19
Q

What is a physiologic factor that will stimulate renin release?

A

low blood pressure in the renal tubules

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20
Q

Why is renin released with low blood pressure in the renal tubules?

A

systemically: increase BP
Locally: kidneys taking care of the kidneys by increasing blood flow to them

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21
Q

Renin activates the angiotensinogen system, then what?

A

angiotensinogen activates
angiotensin 1 which is converted by ACE to
angiotensin 2 which leads to
vasoconstriction and aldosterone secretion which
increases PVR and Na+ and water retention which
increases blood pressure

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22
Q

What is angiotensinogen made by

A

the liver

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23
Q

Where is Angiotensin Converting Enzyme found?

A

in the lungs

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24
Q

What releases aldosterone?

A

adrenal cortex

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25
Q

What is the only renin inhibitor?

A

Aliskiren

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26
Q

What drugs block ACE?

A

ace inhibitors
-prils

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27
Q

what is the prototype ACE inhibitor?

A

captopril

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28
Q

Ace inhibitors block ACE and also block the break down of what?

A

bradykinin

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29
Q

What is the inactive precursor to bradykinin?

A

kininogen

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30
Q

When bradykinin is released, it stimulates what?

A

prostaglandin synthesis

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31
Q

What is prostaglandin synthesis involved in?

A

the inflammatory cascade

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32
Q

why do patients have a nonproductive cough with ace inhibitors?

A

because the increase in bradykinin stimulates the inflammatory cascade in the lungs

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33
Q

What are ARBS?

A

angiotensin receptor blockers

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34
Q

Where in the body does ARB’s work?

A

in the blood vessels and the adrenal cortex, blocking the effect of angiotensin 2

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35
Q

ACE inhibitors are eliminated where?

A

in the kidneys

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36
Q

ACE inhibitors can cross the _____ barrier so should not be used for ________ women

A

placental
pregnant

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37
Q

People who stop ACE inhibitors usually get switched over to

A

ARBS

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38
Q

ARBS end in

A

-artan

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39
Q

why don’t ARBS produce a cough?

A

they have no effect on bradykinin

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40
Q

Which drug has a more complete effect on angiotensin action?

A

ARBS

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41
Q

Why do people with pulmonary htn have poorer outcomes?

A

The smooth muscle builds up and can’t really be reversed

42
Q

What is used to decrease pulmonary htn in the hospital?

A

prostaglandins

43
Q

What is used to decrease pulmonary htn to take home?

A

endothelin receptor antagonists

44
Q

Where are endothelin receptor antagonists found?

A

found in the vasculature that feeds into the lungs

45
Q

Where does preproendothelin come from?

A

Low shear stress
ANG II
inflammatory cytokines
thrombin

46
Q

What causes the vasoconstriction and proliferation of smooth muscle cells in the lungs?

A

endothelin binding to endothelin receptors

47
Q

What inhibits preproendothelin from becoming active?

A

High shear stress
Nitric oxide
prostaglandin I2
Atrial natriuretic peptide

48
Q

Where does ANP come from?

A

the heart

49
Q

What does PGI2 do?

A

lowers blood pressure

50
Q

Endothelin has a negative feedback loop whereby it binds to the endothelial cells themselves and stimulates the production of

A

nitric oxide= vasodilation

51
Q

What does endothelin receptor antagonists end in?

A

-entan

52
Q

endothelin receptor agonists are ____ so should not be given to pregnant women

A

teratogenic

53
Q

Summary: which drug classes decreases vascular tone which decrease blood pressure?

A

alpha-adrenoceptor antagonist
endothelin antagonist
potassium channel openers
calcium channel blockers
Nitrodilators
Direct acting vasodilators
RAA system:
renin inhibitors
ace inhibitors
angiotensin receptor blockers

54
Q

What is vascular tone?

A

the continuous partially contracted state of smooth muscle cells in the walls of the vessels

55
Q

What are the 3 types of vascular tone?

A

arteriolar tone
capillary tone
venous tone

56
Q

What does arteriolar tone consist of?

A

arteries
arterioles
precapillary sphincters

57
Q

Which vascular tone has the most squeeze?

A

arteriolar tone

58
Q

what do precapillary sphincters do?

A

they shut off blood flow from the arteries from going into the capillaries and shunt blood directly to the venous system

59
Q

skeletal muscle contracts by shortening in one direction, smooth muscle contracts by

A

bunches up, squeezing in all directions

60
Q

a vessel that is constricted to half of it’s size will exert a blood flow force _________ greater than that of the relaxed muscle

A

16X

61
Q

blood vessel contraction steps

A

influx of Ca++ from ECF and SR
Ca++ binds to the protein calmodulin
This complex activates MLCK
MLCK phosphorylates MLC
Activated MLC acts with actin and causes contraction

62
Q

increase in cAMP blocks MLCK which leads to _______ in the smooth muscles around the blood vessels

A

relaxation

63
Q

the venous system is important in

A

capacitance

64
Q

Which vessels have valves?

A

veins

65
Q

how much of our blood is in the venous system?

A

70%

66
Q

how much blood is in our sphlanchnic bed

A

20-30%

67
Q

How does venous blood get moved around the body?

A

By the contractions of skeletal muscle squeezing the veins

68
Q

What is the job of the venous system?

A

maintain filling of the heart despite variance in blood volume

69
Q

What is End diastolic volume?

A

the amount of blood left in the heart after diastole

70
Q

What is stretch governed by?

A

starlings law

71
Q

What is starlings law?

A

Increase in stretch=increase in force of contraction

72
Q

What does myoglobin do?

A

stores oxygen in the heart

73
Q

why do we have chest pain in anaerobic metabolism of the heart?

A

Metabolites like lactic acid build up

74
Q

What are the 2 main drugs to prevent angina?

A

calcium channel blockers
beta blockers

75
Q

What is classic angina, or angina of effort?

A

a narrowing of the vessels in the heart. involves plaque
effort increases oxygen demands and the heart goes into anaerobic metabolism
pain goes away when the effort stops

76
Q

What is variant angina?

A

angina that is caused by decreased blood flow from a vasospasm

77
Q

What is unstable angina?

A

A blockage from an embolism.
happens at rest. Plaque is involved

78
Q

treatment for classic angina?

A

rest

79
Q

treatment for variant angina?

A

nitrates
CCB can be used prophylactically

80
Q

coronary blood flow is directly related to

A

prefusion pressure
duration of diastole

81
Q

if we block potassium channels in the heart, we can prevent repolarization and therefore increase

A

blood flow to the heart

82
Q

beta 2 agonists increase

A

cAMP

83
Q

Nitric oxide increases

A

cGMP

84
Q

The short acting nitrates and nitrites last

A

minutes

85
Q

The longer acting nitrates and nitrites last

A

hours

86
Q

what does nitroglycerin release to vasodilate?

A

nitric oxide

87
Q

cGMP leads to the _______ of MLCK

A

dephosphorylation

relaxation response

88
Q

What is the main side effect of nitrates/nitrites

A

headache

89
Q

nitrates/nitrites can bind to hemoglobin and cause it to have

A

less affinity for O2

90
Q

Tolerance to nitrates/nitrites builds up most in the people who

A

work in an environment with high exposure like fertilizer and food processing plants

91
Q

what is methelmoglobin?

A

a hemoglobin with high levels of nitrates/nitrites

92
Q

What is a benefit to methelmoglobin?

A

it helps get rid of CN poisoning

93
Q

epicardial arteries have primarily what receptors?

A

alpha1 beta1

94
Q

microarteries have mostly ____ receptors and some _____ receptors

A

beta 2
alpha 2

95
Q

What are the 3 generations of beta blockers?

A
  1. nonselective beta 1 and beta 2
  2. beta 1 selective
  3. vasodilatory beta 1 very very selective
96
Q

What is fatty acid oxidation?

A

a way the heart can get energy

96
Q

pFOX inhibitors help angina because

A

patients who would normally slip into fatty acid oxidation and then anaerobic metabolism quickly afterwards, are pushed to turn to glycolysis instead= less likely to switch to anaerobic

97
Q

What is the only pFOX inhibitor in the US ?

A

Ranolazine

98
Q

What are the contraindicated vasodilators ?

A

hydralazine
sodium nitroprusside
fenoldepam

99
Q

Angina can be better treated with ______ rather than one drug alone

A

polypharmacy

100
Q
A

Pharm Test 2 (9 decks)

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