Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology 2 > TEST 2 > Flashcards

TEST 2 Flashcards

1
Q

In the Loop of Henle, ______% of NaCl gets reabsorbed at the ascending loop.

A

20%

remember that water follows solute.. so 20% of water will be PASSIVELY reabsorbed here

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

Loop Diuretic work in the ________ loop in the Loop of Henle.

A

Ascending

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

_________ diuretics work by preventing the reabsorption of 20% of solute.

A

Loop

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

The Distal Convoluted Tubule is where _____% of NaCl is actively reabsorbed into the ECF.

A

10

remember that water follows solute.. so 10% of water will be PASSIVELY reabsorbed here.

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

Diuretics that work at the distal convoluted tubule are _____ as effective as loop diurectics

A

half

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

In the collecting ducts, you have ________ exchange pumps…

A

Sodium Potassium

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

The collecting ducts are where _____% of NaCl is actively reabsorbed.

A

5

remember that water follows solute.. so 5% of water will be PASSIVELY reabsorbed here.

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

__________ is the hormone that is a stimulant for the production of the sodium-potassium exchange pumps

A

Aldosterone

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

What is ADH?

A

Anti Diuretic Hormone

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

What does ADH do?

A

ADH is a hormone within the body that causes the membranes in the collecting ducts to be more permeable to water.

This allows free water to be pulled into the body and thus concentrates the urine.

This is independent of solute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When you are running a marathon, and your body needs to conserve free water ______ is released and it causes free water to be absorbed which darkens the urine.

A

ADH

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

Diuretic therapy:
MOA- General diuretics prevent active NaCl reabsorption and by doing this, it will limit the _______ reabsorption of water through the concentration gradient.

A

Passive

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

The degree of urine flow is directly proportional to the amount of NaCl reabsorption in line…so the Loop diuretics produce ____ urine than thiazide diuretics that work further down the line at the distal convoluted tubule.

A

more

they produce twice as much urine because 20% gets blocked here vs. 10% at the distal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

True or False

Loop Diuretics are less powerful than Osmotic Diuretics

A

False.

Loops are first in line so they prevent 20% of NaCl reaborption

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

The closer to the glomerulus the ______ powerful the diurectic is.

A

more

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

The closer to the collecting duct the ______ powerful the diuretic is

A

less

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

Name the 2 categories of Potassium Sparing Diuretics.

A

Aldosterone Antagonists and Non-Aldosterone Antagonists

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

Loop Diuretics are the __________ effective Diuretics

A

Most

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

What kind of diuretic is Furosemide?

Must know for test

A

Furosemide is a Loop Diuretic

Other loop diuretics are:
Ethacrynic Acid
Bumetamide
Torsemide

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

What is the method of action of loop diuretics?

A

To prevent the active reabsorption of NaCl by 20% at the ascending loop of henle

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

What are the Pharmacokinetics of loop diuretics?

A

they are available in various dosage forms- orally, IV, IM

Diuresis of a pill starts in about 60 minutes and IV startes in around 5 minutes

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

Name the therapeutic uses for loop diuretics

A 
more severe cases
when greater fluid mobilization is needed such as:
CHF
fluid overload
edema from hepatic and renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name the only Non sulfa loop diuretic

A

Ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Dehydration symptoms (one ADRs of diuretics)

A 
orthostasis
dry mouth
dizzy
skin turger
BUN ratio (normal 10-1) when it gets wider it means dehydrated
thirst
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ADR of loop diuretics

A 
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Loops and Thiazides together can be dangerous

true or false

A

true

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

IV loop diuretics can cause damage to the ears

True or false

A

true

usually transient ototoxicity
can also increase blood suger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hyperuricemia can be caused by loop diuretics. Why is this important

A

because it increases uric acid which can cause gout

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

Where do Thiazide and Thiazide like diuretics work and what percentage of sodium do they block from getting reabsorbed

A

they work at the distal convoluted tubule

they block 10% of sodium and water from being reabsorbed

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

What was the prototype for Thiazide and Thiazide like diuretics

A

used to treat Hypertension and edema

initial drug of choice for HTN

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

ADR’s for Thiazides

A

the same as loop diuretics except for it increased serum CALCIUM

*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is different about potassium sparing diuretics compared to loop or thiazides

A

they are diuretics that reduce potassium loss

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

How do potassium sparing diuretics work

A

Aldosterone Antagonists work by blocking the effects of aldosterone

the net effect is less sodium potassium pump production

they retain k and excrete Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the therapeutic uses for Potassium sparing diuretics (aldosterone antagonists)

A

cirrosis of the liver
CHF
primary hyperaldosteronism

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

Name 2 aldosterone antagonists**

A

spironolactone (more hormonal)

eplerenone (less hormonal)

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

ADR’s of Potassium sparing diuretics (aldosterone antagonists)

A 
hyperkalemia
menstrual irregularities
deepening of the voice
excessive hair growth in girls
gynomastia in men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

name 2 non-aldosterone antagonists

A

triamterene and amiloride

MOA- block sodium potassium pumps

USES- electrolyte benefits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Osmotic Diuretics: Prototype Mannitol

A
  • have to have a filtered needle to administer because it will crystalize as it cools
  1. Four Properties
    A. filtered- small enough
    B. Undergoes minimal reabsorption (stays in Nephron
    C. Not Metabolized
    D. Pharmacology innert (doesnt do anything)
  • Kinetics: has to be IV

Theraputics: prophalaxis of renal failure
intracranial pressure

ADR’s - can make third spacing worse
DEATH

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

beta 1 receptors

A

heart rate increases
contractility increases

sympathetic nervous system

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

alpha 1 receptors

A

CONSTRICTION of the arteries and veins which leads to increased afterload

Sympathetic Nervous system

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

Stimulation of muscarinic receptors

A

is part of the parasympathetic nervous system

Decreases HR and contractility

reduces cardiac output

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

lower the preload

A

lower the cardiac output

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

vasodilater

A

is an afterload reducer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

heart rate

A

increased through the sympathetic nervous system + beta 1 receptors when stimulated -> increase in HR and Contractility

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

Myocardial contractility

A

the force of contraction of the ventricals - beta 1 vs. muscarinic stimulation + more stretch

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

cardiac afterload (arteries):

A

the force that the heart has to overcome to pump blood

the greatest determinant is arteriole vasoconstriction and vasodilation

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

Starlings law

A

force of ventricular contraction is proportional to the stretch

soggy boggy- ends up not pumping as well

the greater the stretch the greater the contraction

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

Cardiac preload (veins)

A

how much volume gets to the heart

reduced preload: over diuresis, dehydrated,vasodilater

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

natriuretic peptides

A

protectors of volume overload

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

Baroreceptors

A

pressure sensor- stimulates the sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

alpha 1 receptors

A

cause constriction of both arteries and veins

decrease contractility HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Atrial Natriuretic Peptide

A

released from stretching in the atria

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

Brain Natriuretic Peptide

A

released from stretching in the ventricals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

C natriuretic Peptide

A

released from stretching in the veins and the arteries

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

Name 2 NON-DHP Calcium channel blockers

A

Verapamil and Diltiazem

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

What is the MOA of NON-DHP Calcium channel blockers

A

block calcuim channels on arterioles and on the heart

works similar to a Beta Blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the effects of Verapamil?

A

dilation of peripheral arteries

dilation of coronary arteries (increases perfusion)

Blockade of CA+ channels at SA Node (reduces HR)

Bockade of CA+ channels at the AV node

Blockade of CA+ channels in the myocardial tissue (decreases contractility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the effect of blocking the SA node

A

the SA node is the pacemaker of the heart so blocking it would reduce Heart Rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the effect of blocking the AV node?

A

calcium influx increases conduction through the AV node, blocking this would cause a decrease in the rate of electrical conduction in the Heart

this is important in regards to arrhythmias such as a-fib or a-flutter.

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

What kind of effect does calcium entry have on the Myocardium?

A

positive inotropic effect (pumping ability)

so blocking it with calcium channel blockers causes a negative inotropic effect

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

calcium channels in general:

A

vascular smooth muscle: calcium channels regulate contraction. So actually when calcium goes down the calcium channels, it causes vasoconstriction.

Vasoconstriction causes BP to increase.

If we block the calcium channels it produces the opposite effect. (vasodilation) which makes BP go down.

This is especially true on the arterial side of our vasculature, which is afterload.

Blocking calcium channels on the heart produces the same effects as beta blockers. Decreased heart rate and decreased contractility.

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

Calcium Channel Blockers =

A

the number one class of BP medication in the country

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Beta Blockers end in

A

LOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

If it ends in SIN, what class of medication is it

A

Alpha 1 Antagonist

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

What is afterload

A

the force that the heart has to overcome to pump blood to the body (systole)

Afterload = Arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is preload

A

Preload is the blood filling the heart on diasole (resting Phase)

Preload = veins

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

What is SVR

A

Systemic Vascular Resistance

same as PVR - Peripheral Vascular Resistance

= Afterload

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

What are the two classes of calcium channel blockers?

A

Nondihydropyridine Calcium Channel Blockers

Dihydropyridine Calcium Channel Blockers

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

What is a couple of differences between Nondihydropyridine Calcium Channel Blockers
and
Dihydropyridine Calcium Channel Blockers

A

NON-DHP=

  • blocks calcium channels on arteries and heart
  • Causes constipation
  • bradycardia
  • Prophylaxis of migranes

DHP-

  • No constipation
  • Reflex tachycardia
  • Immediate release causes MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the formula for Arteriole Blood pressure

A

Arteriole BP= CO x PVR

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

What is the formula for determining Cardiac Output

A

CO= SV x HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the therapeutic uses of Verapamil

A

Angina - Vasospastic and Exertional

HTN- Arterial Vasodilator, will lower BP by dilating arteries to reduce the pressure, and also compromising Cardiac Output

Cardiac Arrhythmias- especiall super ventricular tachycardic arrhythmias

Prophylaxis of migranes

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

What are the ADR’s of Verapamil

A 
*** Constipation
Headache
Edema 
Gingival Hyperplasia
bradycardia
*** Partial or Complete AV Block
*** Exacerbate CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is angina

A

when the supply of oxygen is receeded by the demand of oxygen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is Vasospastic Angina

A

where there is actually a spasm of the blood vessel

76
Q

What is Excertional Angina

A

is where the supply of oxygen is exceeded by the demand.

for example- sprinting and feeling a burning sensation in your legs, if you slow down and walk, the burning goes away.

Same thing with your heart if you reduce the heart rate, the hear doesnt beat as hard, thus reducing your oxygen demand.

It is like pushing a piano without wheels on it, but if you put wheels on it, it is less difficult

77
Q

All pure afterload reducers can cause:

A

Edema

Headache

78
Q

What are the contraindications for NON-DHP Verapamil and Diltiazem

A

2nd or 3rd degree heart block

CHF

79
Q

What are the drug interactions for NON-DHP Verapamil and Diltiazem

A

Digoxin- is a narrow therapeutic index drug that if added to verapamil NON-DHP can exacerbate bradycardia and lower HR way to much. Digoxin might need to be reduced by as much as 50% while taking Verapamil

Beta Blockers- causes profound supressant effects on the heart because NON-DHP verapamil has the same effects as a beta blocker (lowers HR and Contratility)

80
Q

What are the effects of Diltiazem

A

essentially the same as Verapamil except causes less constipation

dilation of peripheral arteries
dilation of coronary arteries (increases perfusion)
Blockade of CA+ channels at SA Node (reduces HR)
Bockade of CA+ channels at the AV node
Blockade of CA+ channels in the myocardial tissue (decreases contractility)

ADR-
*** Constipation
Headache
Edema 
Gingival Hyperplasia
bradycardia
*** Partial or Complete AV Block
*** Exacerbate CHF
81
Q

Verapamil and Diltiazem are both ______ of CP450

A

inhibitors

this can cause other drugs to build up to toxic levels

82
Q

Dihydropyridine Calcium Channel Blockers (DHP)

A

anything that ends in PINE

most common antihypertensive peripheral artery dilating class, not as much effect on the heart as NON-DHP

83
Q

What is the DHP prototype

A

Nifedipine

84
Q

What is the MOA of Nifedipine

A

Profound blockade of calcium channels in the arteries. This is a substantial afterload reducer. Has little to no effect on the heart so not going to use for heart issues such as A-Fib or A-flutter

85
Q

What are the direct hemodynamic effects of Nifedipine

A

vasodilation and thus reduces SVR (PVR-Afterload)

Dilates coronary arteries somewhat, which may help coronary artery perfusion.

Helpful in Angina as well

86
Q

What are the indirect hemodynamic effects of Nifedipine

A

by lowering BP significantly, they can trigger the Barrowreceptor reflex

Barroreceptors are little monitors in our blood vessels that protect us from shock, when BP drops significantly they kick in.

This is a sympathetic response (Norepi) Beta 1 ->alpha 1…stimulated HR and Vasoconstriction.

Primarily occurs with Immediate Relsease DHP only

Immediate relsease calcium channel blockers are now banned due to causes MI

87
Q

What are the therapeutic uses of Nifedipine

A

Angina (vasospastic and excertional) - works by decreasing afterload
HTN (only in extended release forms)

88
Q

What are the ADR’s of Nifedipine

A 
dizziness and Headache
**** Peripheral EDEMA
Gingival Hyperplasia
Reflex Tachycardia (more with immediate rel)
No consipation
Fast acting Linked to MI
89
Q

Nifedipine Toxicity

A

if taken in excessive doses, it loses selectivity

lowers HR and contractility

Presents with heart block and Bradycardia

90
Q

Basic Concepts of Vasodilators

Afterload reducers:

A

drugs that dilate resistance vessesls (Arteries)

cause a decrease in afterload (the force that the heart has to overcome to pump blood)

91
Q

Basic Concepts of Vasodilators

Preload reducers:

A

Drugs that dilate capacitance vessels (veins)

Reduces the drive for blood to return to the heart, lowers BP by reducing Cardiac Output. (reduces ventricular filling)

70% of our blood is on the venous side

92
Q

Side effects of Vasodilators

A

Posterial Hypotension (especiall with venodilators)
Reflex Tachycardia
Volume Expansion
Edema (especially with afterload reducers)

93
Q

What is posterial Hypotension

A

a fall in BP brought on by moving from a sitting or lying postition to standing

Mostly in Elderly population

Referred to as Orthostasis

**First Dose Effect of SIN drugs

94
Q

What is reflex Tachycardia

A

Occurs from dilation of arteries or veins through the barrow receptor reflex.

over time this can lead to volume expansion by reducing the blood flow to the kidneys which triggers the RAAS system resulting in Aldosterone release which causes retention of sodium and water

95
Q

Hydralazine MOA

A

selective arterial vasodilator (pure afterload reducer)

Very Powerful direct acting arteriole vasodilator

96
Q

What is unique about the metabolism of Hydralazine?

A

Metabolism: through acetalation (the ability to acetalate a drug is genetic) idiosyncratic effects (genetic predisposition)

Slow acetalator = low doses

Fast acetalator = high dose

97
Q

What are the primary uses of Hydralazine

A

Hypertensive Crisis (IV)

Drug Resistant Hypertension

Heart Failure if combined with Isosorbide (which is a nitrate

98
Q

What is drug resistant hypertension

A

when on three drugs to the max and blood pressure still sucks

99
Q

What are the ADR’s of Hydralazine

A

reflex tachycardia (barrorecptor reflex) fixed with beta blocker

volume expansion (use diuretic)

Systemic Lupus Erythematosus like syndrome

100
Q

What causes reflex tachycardia

A

barroreceptor reflex

101
Q

What causes volume explansion

A

aldosterone complments of barroreceptor reflex stimulating RAAS

102
Q

Minoxodil MOA

A

more severe vasodilator. Effects Afterload

103
Q

What is Minoxidil used for

A

severe hypertesion

104
Q

What are the adverse effects of Minoxidil

A

volume expansion
reflex tachycardia
**hypertrichosis (hair growth)
Pericardial Effusion (Tamponade)

105
Q

Sodium Nitroprusside MOA

A

Body’s own natural Vasodilator, veno and arterial. Once in the body breaks down into Nitricoxide

This is a preload and afterload reducer

This is purely an IV med, very useful in ICU for HTN Emergency

106
Q

Sodium Nitroprusside Toxcity

A

Thiocynate toxcity presents with hallucinations and psychotic behaviors. Similar to ICu psychosis, treatement is to reduce the medication slowly and discontinue

cannot abruptly discontinue

107
Q

RAAS

A

When blood volume is low, juxtaglomerular cells in the kidneys activate their prorenin and secrete renin directly into circulation.

Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I

Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs.

Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure.

Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex.

Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure.

108
Q

The vast majority of CLINICAL hypertension is cause by clinical ________.

A

Inertia

Clinical inertia is when you have the knowledge about something and choose to ignore it.

In the US, 31-34% of BP patients are controlled

109
Q

What is normal BP

A

< 120/80

110
Q

What is pre-hypertension

A

120/80 to 139/89

111
Q

What is stage 1 hypertension

A

140/90 to 159/99

112
Q

What is stage 2 hypertension

A

greater than or equal to 160/100

113
Q

What is ISH

A

Isolated Systolic Hypertension

When systolic pressure is 140mmHg or higher and diastolic pressure is less than 90 mmHg

classic in the agin population

past the age of 65 diastolic pressure drops and systolic increases due to athlerosclerosis

114
Q

What are the two main types of hypertension?

A

Primary Hypertension
and
Secondary hypertension

115
Q

What is primary hypertension

A

hypertension of aging

Essential Hypertension

Hypertension that has no identifiable cause

116
Q

What is secondary hypertesion

A

elevation of blood pressure induced by an identifiable cause.

Cure is Possible

Caused by things such as:
Smoking
Obesity
Drug Users
SIADH
MAOI
Pheochromocytoma (adrenaline secreting tumor)
Hyperaldosteronism
Renal Artery Stenosis
Hyperthyroidism
Parahyperthyroidism
117
Q

What do you use to persuade patients to control their hypertension?

A

The consequences of Hypertension

Silent Killer

CHF = Reduce by 50%
Stroke= Reduce By 35-40% 
MI = Reduce by 20- 25%

Target end organ damage - kidney diasease and eye disease

118
Q

If a person and 55 and does not have HTN yet, what are their changes of developing it?

A

90%

119
Q

What is the treatment goal for hypertension

A

Goal for most < 140/90

Goal for Diabetes or Chronic Kidney disease <130/80

120
Q

What is TLC

A

Therapeutic Lifestyle Changes

*** Weight loss #1 way to help BP
Sodium Resriction
DASH Diet
Alcohol Restriction
Excercise

Smoking Cessation is a cardiac risk factor

121
Q

Can TLC be as effective as pharmacotherapy?

A

Yes and everyone gets TLC no matter what

122
Q

What are the determinants of Blood Pressure

A

Arterial Pressure = CO x PVR

PVR, SVR, and Afterload are all the same thing

Every blood pressure medication lowers BP some how or some way through this process

123
Q

How do preload reducers work?

A

by reducing cardiac output

124
Q

Cardiac output =HR x SV is influenced (ehanced or reduced) by how hard or how fast the heart beats.

A

So as far as reducing CO,

Beta Blockers- reduce HR and Contractility

NON-DHP (verapamil and diltiazem) decrease HR and contractility too

Blood Volume- the greater the blood volume that gets to the heart, the greater the stretch. The greater the stretch, the greater the contraction. (preload)

Venous return- how much blood gets back to the heart, reducing this lowers BP (venodilators)

All of these things effect cardiac output

125
Q

How is peripheral vascular resistance regulated

A

by arterial constriction

126
Q

What systems regulate blood pressure

A

RAAS
Barroreceptor Reflex - prevents hypoperfusion, shock.
Is a sympathetic response- increases HR, causes vasoconstriction.

Never adjust blood pressure meds within 3-4 weeks because during this time you are fighting the barroreceptor reflex

127
Q

What are the classes of antihypertensive medications

A 
Alpha 2 agonists 
Beta Blockers = LOL
Alpha 1 antagonist = SIN
Afterload Reducers
Diuretics
Ace Inhibitors = PRIL
ARB's = Sartans
Aldosterone Antagonists
128
Q

Name an Alpha 2 Agonist

A

Clonadine

MOA slows Norepi release so norepi builds up

SNS says Whoa

Can cause:
rebound hypertension
drowiness
dry mouth

129
Q

Reserpine moa

A

takes away the precursor molecule that makes norepi

norepi declines

ADR depression

130
Q

What two beta blockers have Alpha 1 and Beta 1 blockade capabilities

A

Carvedilol and Labetalol

131
Q

Name some alpha 1 antagonists

A

Tamsulosin (used in BPH)
Phentolamine (used in Pheo)
Prazosin

SIN DRUGS

MOA- preload and afterload reducers by blockade of Alpha 1

Uses: 
Essential HTN,
Alpha 1 Agonist Toxicity, 
****BPH
****Pheochromocytoma 
Raynauds Disease
ADR's
Orthostasis
Reflex Tachycardia
Nasal Congestion
Inhibition of Ejaculation (retro Ejaculation)
Sodium and Water Retention
132
Q

Beta Blockers (LOL)

A
  • Decrease heart rate
  • Decrease contractility
  • Decrease electrical conduction through your heart

Used for patients who have an elevated HR, have HTN, and have arrithmias

side effects: could have heart failure

133
Q

Vascular system is solely controlled by the

A

Sympathetic nervous system

134
Q

Alpha 1

A

Vaso constriction

Alpha 1 blockade used for bph

135
Q

Whoa receptor

A

Alpha 2

Shuts Down additional release of neurotransmitters

136
Q

Beta 1

A

On heart.

Increases conduction, contraction, rate

137
Q

Beta 2

A

Arteries. Dilation

Sympathetic

Lungs- cause bronchi dilation- albuterol

Liver- glycogen breakdown

Skeletal muscle- enhances contraction

138
Q

Norepinephrine is

A

Recycled in the nerve terminal

Or broken down by monoaminoxydase

139
Q

Name the afterload reducers

A

Minoxadil
Hydralazine
DHP (Arteriole Vasodilators)

ADR=
Pheripheral Edema
Reflex Tachycardia
Volume Expansion

140
Q

What is SVR

A

Systemic Vascular Resistance

How dilated or constricted arteries or arterioles are

141
Q

Name a loop diuretic

A

furosemide

Other loop diuretics are:
Ethacrynic Acid
Bumetamide
Torsemide

ADR  
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
142
Q

What is the most common diuretic used to treat HTN

A

Thiazides

ADR’s-

the same as loop diuretics except for it increased serum CALCIUM

*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
143
Q

What is the main ADR difference between Loop diuretics and Thiazides?

A

Loops decrease serum calcium

Thiazides increase serum calcium

144
Q

What class are PRIL’s?

A

Ace Inhibitors

MOA- Reduces levels of Angiotension 2, Dilates arteries and veins. Preload and afterload reducer.

Lisinopril, Captropril

ADR- 
Hypotension
HYPERKALEMIA
cough
angioedema

DRUG OF Choice for diabetic nephropathy and heart failure.

CONTRAINDICATED- Renal Artery Stenosis

CATEGORY X

145
Q

Name the ARBS (Angiotension 2 Receptor Blockers)

A

SARTANS

Losartan and Telmisartan

MOA- Does not interfere with the production of of angiotension 2 just blocks the receptor site.

Use SARTAN when you have ACE Cough, possibly angioedema

ADR-
Hyperklemia
Can still cause cough
Can Still cause Angioedema

CATEGORY X

CONTRAINDICATED- Renal Artery Stenosis

146
Q

Name the aldoserone antagonists

A

potassium sparing diuretics

Spironolactone and Eplerenone (less Hormonal)

MOA- selectively blocks aldosterone receptors, eliminate volume expansion

Uses-
HTN
HF NYC 3-4 (trophic agent)

ADR’s Hypoklemia, Gynecomastia, Mentral Irregularity, Deep Womans Voice, Hairgrowth

147
Q

True or False

Don’t use Ace Inhibitors and Potassium Sparing diuretic together.

A

True

148
Q

Angiotension 2 + Aldosterone =

A

causes heart to change shape which leads to heart failure

149
Q

Where is renin produced

A

by juxtaglomerular cells (JG apparatus)

150
Q

What triggers the release of renin

A

Decline in BP
Low blood Volume
reduced sodium plasma
reduction in renal perfusion **

151
Q

Aldosterone

A

sodium and water retention
potassium wasting

released dehydration, bleeding, shock

152
Q

anything that lowers preload also lowers

A

cardiac output

153
Q

Vasodilators reduce

A

afterload

154
Q

vasoconstriction

A

increases afterload

155
Q

what is the most important determinant of blood flow?

A

vessel diameter

156
Q

volume expansion

A

increase in total body water. Can also be classified as isotonic, hypertonic, or hypotonic

157
Q

Hypokalemia

A

when serum levels drop less than 3.5 Meq/L

Causes: acidotic state, diuretics, vomiting, diarrhea, laxative use,

Significance- weakness, paralysis, and arrhythmias

treatment give K

158
Q

Hyperkalemia

A

greater than 5 Meq/L

Cuases: renal failure, excessive k administration, spironalactone and eplerinone

significance- arrhythmias, cardiac arrest

treatment: if the heart is irritated infuse calcium salt. insulin with D5W, Kxlate

159
Q

What Class Causes the First Dose Effect?

A

Adrenergic Antagonists- Alpha 1 Blockers

Tamulosin
Phentolamine
Prazosin

SIN drugs

160
Q

Propranolol

A

Non Selective Beta Blocker

Blocks beta 1 and Beta 2

Uses- 
HTN
Angina
dysrhythmias
MI
Hyperthyroidism
Stage fright
Migraines
Pheochromocytoma Glaucoma
ADR's
Bradycardia
Decreased Cardiac Output
Heart Failure
AV Heart Block
Rebound Cardiac Excitation
Bronchoconstriction
Inhibition of Glycogenolysis

NOT GOOD FOR DIABETICS

161
Q

Metroprolol

A

Specific Beta 1 Blocker

Uses- 
HTN
Angina
dysrhythmias
MI
Hyperthyroidism
Stage fright
Migraines
Pheochromocytoma Glaucoma
ADR's
Bradycardia
Decreased Cardiac Output
Heart Failure
AV Heart Block
Rebound Cardiac Excitation
162
Q

Carvedilol / Labetalol

A

Alpha 1 Beta 1 Blockade

preload afterload reducer
reduces HR and Contractility

163
Q

Patients with Newly diagnosed essential hypertension, who do not have compelling indications should get what treatment?

A

TLC

Thiazide Diuretic

164
Q

Patients who have been diagnosed with HTN but have other compelling indications such as:

Stable Angina or arrhythmia
Unstable Angina
S/P MI

A

Beta Blockers

165
Q

Patients who have been diagnosed with HTN but have other compelling indications such as:

BPH
Diabetes
CHF
ISH

A

BPH (alpha 1 antagonists, SINS)

Diabetes (ACE Inhibitor, ARB)

CHF (BETA OR ACE or ARB)

ISH (Thiazide and DHP- PINE)

166
Q

stage 1 HTN = ______ drugs

A

1

167
Q

Stage 2 HTN = ______ drugs

A

2

168
Q

Hypertensive Emergencies: Emergent?

A 
Target end organ damage Present.
Headaches
Visual Changes
Chest Pain
Stroke

Lower asap with Nitroprusside drip IV MEDS ONLY

169
Q

Hypertensive Emergencies: Urgent?

A

No target end organ damage present

lower bp slowly with oral medications within a 24-48 hour period

170
Q

Chronic HTN during pregnancy leads to a

A

placental abruption

give methyldopa alpha 2 agonist

171
Q

What are the two main causes of heart failure

A

Uncontrolled Chronic Hypertension

MI

172
Q

Which Neurohormonal Systems drive the remodeling changes to compensate for loss of heart function?

A

SNS

RAAS

173
Q

Name the Signs and Symptoms of Heart Failure

A 
Orthopnea
SOB
DOE
Fatigued at rest
Tachycardia
Cardiomegaly
Pulmonary Edema
Peripheral Edema
Hepatomegaly
JVD
Weight Gain *****
174
Q

New York Heart Association

A

Class 1- HF no symptoms
Class 2 - Symptoms that worsen with exertion
Class 3- Minimal Exertion to get fatigued
Class 4- Symptoms at rest

flows in and out. Measures the “right now”
so a 3 can go back to a 1

175
Q

American College of Cardiology

A

based on the progression of the disease

Stage A- best- pt is at risk for developing HF No Symptoms or structural disease

Stage B- Structural Damage but no symptoms (remodeling)

Stage C- worst- advanced Structural damage- symptoms even at rest

Never go backwards so once a C never go back to a B ect..

176
Q

Aldosterone Antagonists Spironalactone and Eplerinone

A

increase life expectancy

NYC 3-4 symptoms

177
Q

CARVEDILOL

A

protects against SNS overstimulation, protects against cardiac arrhythmia

has shown to improve Ejection Fraction, increase excercise tolerance, and slow the progression of HF. Reduces hospitalizations, prolong survival

178
Q

Digoxin

A

can improve exercise intolerance, but does not improve their mortality rate or make you live longer. Try everything else then Digoxin

Positive ionitropic efects on the heart. makes the heart more efficient. Improves functional status, Decreases heart rate

179
Q

Digoxin and Potassium relationship

A

If K is even a little bit low, it can cause Digoxin Toxicity. This drug is very sensitive to low K.

It causes Arrhythmias and is a very low therapeutic index drug

180
Q

What would you see with Digoxin Toxicity

A

Bradycardia
Arrhythmias
GI: anorexia, nausea, vomiting
CNS: fatigue and visual disturbances

181
Q

What is Digoxin’s therapeutic Range

A

0.5 - 0.8 ng/ml

182
Q

What are the drugs that interact with Digoxin

A

Diuretics- hypokalemia

ACE I / ARBS - increase potassium levels and decrease therapeutic effects of Digoxin

QUINIDINE / AMIODARONE / VERAPAMIL

183
Q

Stage A drugs

A

Cease high risk behaviors

Treat disease states that compound risks

184
Q

Stage B drugs

A

Cease high risk behaviors
Treat disease states that compound risks
Add ACE I / ARB plus BETA Blocker

185
Q

Stage C Drugs

A

ACE I / ARB
Diuretics
Digoxin
Isosorbide or Hydrolazine (to replace ACE/ARB)

Drugs to avoid stage C- 
Dysrhythmic agents- cause death make worse
NONDHP 
DHP ONLY Amlodipine and Felodipine
NSAIDS-- cause NA  H2o retention

Pharmacology 2 (7 decks)

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