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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
What is the only renin inhibitor?
Aliskiren
26
What drugs block ACE?
ace inhibitors -prils
27
what is the prototype ACE inhibitor?
captopril
28
Ace inhibitors block ACE and also block the break down of what?
bradykinin
29
What is the inactive precursor to bradykinin?
kininogen
30
When bradykinin is released, it stimulates what?
prostaglandin synthesis
31
What is prostaglandin synthesis involved in?
the inflammatory cascade
32
why do patients have a nonproductive cough with ace inhibitors?
because the increase in bradykinin stimulates the inflammatory cascade in the lungs
33
What are ARBS?
angiotensin receptor blockers
34
Where in the body does ARB's work?
in the blood vessels and the adrenal cortex, blocking the **effect** of angiotensin 2
35
ACE inhibitors are eliminated where?
in the kidneys
36
ACE inhibitors can cross the _____ barrier so should not be used for ________ women
placental pregnant
37
People who stop ACE inhibitors usually get switched over to
ARBS
38
ARBS end in
-artan
39
why don't ARBS produce a cough?
they have no effect on bradykinin
40
Which drug has a more complete effect on angiotensin action?
ARBS
41
Why do people with pulmonary htn have poorer outcomes?
The smooth muscle builds up and can't really be reversed
42
What is used to decrease pulmonary htn in the hospital?
prostaglandins
43
What is used to decrease pulmonary htn to take home?
endothelin receptor antagonists
44
Where are endothelin receptor antagonists found?
found in the vasculature that feeds into the lungs
45
Where does preproendothelin come from?
Low shear stress ANG II inflammatory cytokines thrombin
46
What causes the vasoconstriction and proliferation of smooth muscle cells in the lungs?
endothelin binding to endothelin receptors
47
What inhibits preproendothelin from becoming active?
High shear stress Nitric oxide prostaglandin I2 Atrial natriuretic peptide
48
Where does ANP come from?
the heart
49
What does PGI2 do?
lowers blood pressure
50
Endothelin has a negative feedback loop whereby it binds to the endothelial cells themselves and stimulates the production of
nitric oxide= vasodilation
51
What does endothelin receptor antagonists end in?
-entan
52
endothelin receptor agonists are ____ so should not be given to pregnant women
teratogenic
53
Summary: which drug classes decreases vascular tone which decrease blood pressure?
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
What is vascular tone?
the continuous partially contracted state of smooth muscle cells in the walls of the vessels
55
What are the 3 types of vascular tone?
arteriolar tone capillary tone venous tone
56
What does arteriolar tone consist of?
arteries arterioles precapillary sphincters
57
Which vascular tone has the most squeeze?
arteriolar tone
58
what do precapillary sphincters do?
they shut off blood flow from the arteries from going into the capillaries and shunt blood directly to the venous system
59
skeletal muscle contracts by shortening in one direction, smooth muscle contracts by
bunches up, squeezing in all directions
60
a vessel that is constricted to half of it's size will exert a blood flow force _________ greater than that of the relaxed muscle
16X
61
blood vessel contraction steps
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
increase in cAMP blocks MLCK which leads to _______ in the smooth muscles around the blood vessels
relaxation
63
the venous system is important in
capacitance
64
Which vessels have valves?
veins
65
how much of our blood is in the venous system?
70%
66
how much blood is in our sphlanchnic bed
20-30%
67
How does venous blood get moved around the body?
By the contractions of skeletal muscle squeezing the veins
68
What is the job of the venous system?
maintain filling of the heart despite variance in blood volume
69
What is End diastolic volume?
the amount of blood left in the heart after diastole
70
What is stretch governed by?
starlings law
71
What is starlings law?
Increase in stretch=increase in force of contraction
72
What does myoglobin do?
stores oxygen in the heart
73
why do we have chest pain in anaerobic metabolism of the heart?
Metabolites like lactic acid build up
74
What are the 2 main drugs to prevent angina?
calcium channel blockers beta blockers
75
What is classic angina, or angina of effort?
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
What is variant angina?
angina that is caused by decreased blood flow from a vasospasm
77
What is unstable angina?
A blockage from an embolism. happens at rest. Plaque is involved
78
treatment for classic angina?
rest
79
treatment for variant angina?
nitrates CCB can be used prophylactically
80
coronary blood flow is directly related to
prefusion pressure duration of diastole
81
if we block potassium channels in the heart, we can prevent repolarization and therefore increase
blood flow to the heart
82
beta 2 agonists increase
cAMP
83
Nitric oxide increases
cGMP
84
The short acting nitrates and nitrites last
minutes
85
The longer acting nitrates and nitrites last
hours
86
what does nitroglycerin release to vasodilate?
nitric oxide
87
cGMP leads to the _______ of MLCK
dephosphorylation relaxation response
88
What is the main side effect of nitrates/nitrites
headache
89
nitrates/nitrites can bind to hemoglobin and cause it to have
less affinity for O2
90
Tolerance to nitrates/nitrites builds up most in the people who
work in an environment with high exposure like fertilizer and food processing plants
91
what is methelmoglobin?
a hemoglobin with high levels of nitrates/nitrites
92
What is a benefit to methelmoglobin?
it helps get rid of CN poisoning
93
epicardial arteries have primarily what receptors?
alpha1 beta1
94
microarteries have mostly ____ receptors and some _____ receptors
beta 2 alpha 2
95
What are the 3 generations of beta blockers?
1. nonselective beta 1 and beta 2 2. beta 1 selective 3. vasodilatory beta 1 very very selective
96
What is fatty acid oxidation?
a way the heart can get energy
96
pFOX inhibitors help angina because
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
What is the only pFOX inhibitor in the US ?
Ranolazine
98
What are the contraindicated vasodilators ?
hydralazine sodium nitroprusside fenoldepam
99
Angina can be better treated with ______ rather than one drug alone
polypharmacy
100

Pharm Test 2 (9 decks)

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