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Pharmacology III > Block I: HTN > Flashcards

Block I: HTN Flashcards

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1
Q

How is BP determined?

A

CO X PR

where CO= HR xSV

where SV= EDV-ESV

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2
Q

[] is resistance/friction that arterioles have against the flow of blood

A

peripheral resistance

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3
Q

what can increase PR?

A
  1. vasoconstriction

2. athersclerosis

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4
Q

what can decrease PR?

A

vasodilation

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5
Q

vasoconstriction has [] affect on PR and [] effect on BP

A

increases PR, increases BP

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6
Q

vasodilation has [] affect on PR and [] effect on BP

A

decrease, decrease

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7
Q

atherosclerosis has [] affect on PR and [] affect on BP

A

increase, increase

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8
Q

[] is the amount of blood that is pumped out of the heart per minute

A

cardiac output (normal 5L in avg. adult)

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9
Q

how is CO determined?

A

HR X SV

SV=EDV-ESV

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10
Q

what 4 factors affect HR

A
  1. autonomic innervation
  2. hormones
  3. fitness level
  4. age
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11
Q

what factors affect stroke volume

A
  1. heart size
  2. fitness level
  3. gender
  4. contractility
  5. duration contraction
  6. pre-load (EDV)
  7. afterlaod resistance (ESV)
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12
Q

[] is the volume of blood in ventricles at end of diastole

A

EDV

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13
Q

[] is resistance left than the ventricle must overcome to circulate blood

A

ESV

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14
Q

stimulation of [] will cause all factors of BP to rise

A

SNS

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15
Q

SNS stimulation of BP will cause all factors to []

A

rise

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16
Q

what causes SNS stimulation on heart

A
  1. stress
  2. exercise
  3. pheochromocytoma
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17
Q

[] is failure of heart to adequately pump enough blood to meet body’s needs

A

chronic HF

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18
Q

what are some compensatory mechanisms of heart failure?

A
  1. hypertrophy of cardiac muscle & chamber size
  2. neurohumoral reflex (activate SNS)
  3. kidneys & RAAS
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19
Q

describe the goal of hypertrophy to compensate during HF

A

an attempt to increase stroke volume

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20
Q

describe the goal of neuralhumoral reflexes in HF

A

activate sympathetic nervous system

alpha 1 -> vasoconstrict
beta 1 -> increase HR and force myocardial contraction

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21
Q

what happens when SNS activates alpha-1 receptors

A

vasoconstriction

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22
Q

what happens when SNS stimulates beta-1 receptors

A

increase HR and force myocardial contraction

positive inotropic and choriotropic respectively

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23
Q

describe the role of kidneys in HF

A

will activate RAAS –> vasoconstriction and release aldosterone –> increase Na and water retention

increase BP and blood volume

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24
Q

what needs to be reduced to control heart failure?

A

cardiac work load

  1. HR
  2. SV (EDV-ESV)
  3. PR
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25
what drugs interfere with RAAS?
1. ACEI 2. ARBS 3. Renin inhibitors
26
what drug class do the "prils" belong to?
ACEI
27
what is the moa of the "prils"
ACEI (angiotensin converting enzyme inhibitor) block angiotensin 1 from being converted to angiotensin 2 -thereby decreasing vasoconstriction and aldosterone release (inhib. Na and water retention)
28
what are some indications for ACEI?
1. HTN 2. HF 3. post MI (also CKD)
29
what suffix belongs to ARBs?
"artans"
30
what is the MOA of the "artan" drugs
angiotensin receptor blocker block angiotensin 2 from binding target cell and exerting effect
31
indications ARB
1. HTN 2. HF 3. post MI (helpful in CKD)
32
describe some AE affects of ACEI/ARB
1. cough (due to bradykinin) | 2. angioedema (more common in black individuals)
33
ACEI [>/
ACEI
34
what are some drugs that affect the SNS to help with HTN
1. centrally acting sympatholytic 2. neuronal blockers 3. alpha blockers 4. beta blockers
35
what is the role of alpha-1 receptors when stimulated by SNS
contraction of smooth muscle via NE
36
what is the role of beta-1 receptors when stimulated by SNS
cardiac stimulation via NE (increase force & rate contraction)
37
[] is the name of a centrally acting symatholytic
Clonidine
38
what is the MOA clonidine
centrally acting sympatholytic acts on vasomotor centers of medulla oblongata & stimulates inhibitory receptors to reduce activity of sympathetic nerves that control HR and CO (thereby decreasing BP)
39
what are some other uses for clonidine?
centrally acting sympatholytic 1. AHDH off label 2. drug WD 3. menopausal flushing 4. diarrhea
40
Guanthidine is a []
neuronal blocker
41
what drug is a neuronal blocker?
Guanthidine
42
what drug is a centrally acting sympatholytic?
conidine
43
MOA Guanthidine
Neuronal blockers causes significant inhibition of sympathetic activity reserved for HTN that doesn't respond to other drugs
44
what type of drugs are the 'zosins'
alpha blockers
45
what suffix belongs to alpha blockers
zosins
46
what is the moa of alpha-1 blockers
normally alpha-1 - produces contraction and vasoconstriction when stimulated by NE - increases PR - increases BP blockers reverse these effects
47
where are alpha-1 receptors located
smooth muscle of arteries, veins, sphincters & urinary tract
48
where are alpha-2 receptors located what is their role?
adrenergic nerve endings, activated NE and EPI negative feedback mechanism, regulates release of additional NE - inhibits ACH release - inhibits insulin release * would want to agonize to treat HTN
49
what is the MOA of the zosins
alpha-1 blocker block alpha-1 stimulation from NE, thereby blocking vasoconstriction and reducing PR
50
what drug class do the "olols" belong to
beta blockers
51
beta [] receptors are the predominant heart receptors
1
52
what is the role of beta-1 receptors
predominant heart - increase myocardial contractility - increase HR - increase renin release - cause tachycardia *antagonize to treat heart issues
53
what is the role of beta-2 receptors
primarily in lung - cause bronchodilation - vasodilation (decreased PR) - relaxed uterine smooth muscle *caution use non selective BB in asthmatic and COPD patients
54
where are beta-2 receptors most predominately
smooth muscle and tissue
55
MOA 'olols'
beta blockers | -inhibit sustained NE activation from SNS (inhibit cardiac stimlation)
56
indication beta blockers
1. chronic heart failure (carvedilol, b-olol, metoprolol succ) 2. reduced LV systolic function (L sided heart failure)
57
AE BB
1. exacerbate symptoms in acute decompensated HF 2. WD symptoms (ischemic) 3. may affect glucose levels and mask effect hypoglycemia
58
orthostatic hypotension is a risk in [] drug
alpha inhibitor
59
[] should NOT be used in decompenstated HF
BB
60
[] can mask the symptoms of hypoglycemia
BB
61
[] may cause ischemic WD symptoms
BB
62
what is a relative contraiction in BB
COPD/Asthma in non-selective BBs | -if b-2 stimulation is blocked it may cause bronchoconstriction
63
hydralazine is [] type of drug
arterial vasodilation
64
minoxidil is [] drug
arterial vasodilator
65
MOA hydralazine
decrease sympathetic done, cause vasodilation ARTERIAL
66
MOA minoxidil
decrease sympathetic tone, cause vasodilation ARTERIAL
67
what kind of drug is nitroglycerin
vasodilator of veins and arteries
68
what kind of drug is nitroprusside
venous & arterial dilator
69
[] are often used on comnimation with diuretics and BB due to fluid retention and reflex tachycardia
vasodilators (hydralazine, minoxidil, nitroglycerin, nitroprusside)
70
[] is indicated FOR acute decompensated HF
vasodilators (hydralazine, minoxodil, nitroglycerin, nitroprusside)
71
[] is NOT indicated for decompensated HF
BB
72
[] is indicated for 1. HTN 2. post mi 3. decompnensated HF
vasodilators | hydralazine, minoxodil, nitroglycerin, nitroprusside
73
MOA CCB
bind to long acting calcium channels to block influx of calcium in cardiac smooth muscle - block depolarization - block AP
74
nifedipine, amlodipine, and nicardipine belong to [] class
dihydropyridine CCBs
75
MOA of the dipines
dihydropyridine CCB arterial dilation, decreased HR, decreased AV conduction & decreased myocardial contractility due to blocking of long acting calcium channels
76
indications for dipine drugs
1. HTN 2. CAD 3. angina 4. cardiac arrythmias (diff from nonDHP)
77
what is the drug class verapamil
non DHP CCB
78
what is the drug class of diltiazem
non DHP CCB
79
what is the caution of non DHP
bradycardia
80
what is the MOA diltiazem
non DHP CCB atrial dilation
81
what is the MOA verapamil
non DHP CCB eterial dilation
82
indiations for non DHP CCB
1. HTN 2. CAD 3. angina (DHPs inddicatied for arrythmias, but non DHPs NOT indicated)
83
AE of CCB (CV)
1. hypotension 2. palpitations 3. bradycardia 4. peripheral edema
84
GI AE CCB
constipation
85
how can diuretics be helpful in treating HTN
increase excretion of water and salt from body (reverse effects adolosterone)
86
indications diuretcis
1. edema 2. HTN 3. HF
87
[] is the most common cause of cardiovascular disease
HTN
88
stimulation of alpha-1 receptors leads to []
vasoconstrictoin (antagonize to treat HTN)
89
stimulation alpha-2 receptors leads to []
inhibit NE release (block sympathetic stimulation and vasoconstriction) - negative feedback mechanism - would want to agonize to treat HTN
90
beta-1 receptor activation leads to []
increased HR and contractility, increased renin want to antagonize for HTN
91
beta-2 receptors activation leads to []
smooth muscle relaxation, can cause bronchodilation blocking Beta-2 can lead to bronchoconstrction, caution COPD and asthma
92
[] is the most influential contributor to homeostatic regulation of BP
RAAS
93
effects of RAAS
1. regulate NA (aldosterone causes Na and water retentaion, K wasting) 2. blood volume (increases due to aldosterone) 3. SNS activity & vascular tone (increase BP HR CO)
94
how is RAAS stimulated?
1. decreases perfusion kidneys 2. decreased Na and Cl delivered to distal tubule (activate need to alsodterone to absorb NA) 3. direct stimulation beta-1 receptors (release renin)
95
what receptors release renin?
beta-1
96
what are 2nd causes HTN
1. renovascualr dx 2. pheochromocytoma 3. primary aldosteronism 4. cushing's 5. coarctation of aorta 6. sleep apnea 7. head injury 8. brain tumor
97
medications to cause HTN
1. corticosteroids 2. NSAIDS 3. Na/water retention SE 4. estrogen
98
what are ways SNS Can be activated, what effect does this have on BP
can cause HTN 1. amphetamines 2. sympathomimetic agents 3. antidepressants (SNRI< Trycyclics
99
st. john's wort can [] BP
increase
100
alcohol can [] BP
increase
101
according to ACC/AHA guidelines, what is HTN
> 130/80
102
according to JNCP guidelines what is HTN
> 140/90
103
what is ACC/AHA stage 1 HTN
130-39/80-89
104
what is ACC/AHA Stage 2 HTN
>/= 140/90
105
what is the BP threshold for everyone EXCEPT a 1o year ASCVD risk < 10% and stable ischemic heart disease
>/=130/80
106
what is the BP threshold for a patient a ASCVD risk of < 10%
>/= 140/90
107
what is a BP threshold of a patient with stable ischemic heart disease
>/= 140/90
108
normal BP patients should be followed up how requently
annual
109
patients with hx HTN but are at goal/nonpharm how frequently should they fu
1-6 months
110
medication change, when to see pt back?
1 month
111
1 Kg weight reduction can result in [] BP change
1 mmHG for every 1 KG
112
general counseling points DASH
increase fruits, veggies, whole grains, low fat | -decrease saturated adn total fat
113
what is Na intake goal for HTN pt
< 1500 mg/day | aim for at least 1,00 mg/day reduction
114
what ion should increased dietarily to help with HTN
K+ aim for 3,500-5,000 mg/d
115
what drug class blocks aldosterone release, vasoconstriction, and Na retention (ultimately lowering BP)
prils, ACEI
116
name some AE ACEI
1. hypotension (in volume depleted pts. i.e. diuretic, HF, renal impairment) 2. cough, dry persistent (more prevalent AA) due ot bradykinin 3. angioedema (due to bradykinin)
117
[] is an emergency adverse effect of ACEI and is []x more fatal in AA
angioedema, can happen with ARB too 5x
118
[] is asymmetric swelling of face, mouth, and upper airway | could be in absence of urticaria or itching
angioedema ACEI > ARB
119
what electrolyte disturbance may occur wiht ACEI/ARB
increased K+, due to block in aldosterone
120
ACEI/ARBS contraindicated in []
pregnancy - oligohydraminos - hypotension - renal failure - death renal artery stenosis (BRAS) wont be enough perfusion of glomerulus with artery stenosis and dilation efferent arteriole
121
how might ACEI/ARB affect the kidney
block constriction of efferent arteriole, less pressure in glomerulus decreased GFR, increase Scr
122
what should be monitored while one ACEI/ARB
SCr if increases >30% there is too much strain on kidney
123
what kind of dose adjustment is assoc with ACEI/ARB
50% decrease if on diuretics, elderly or with renal impairment
124
[] have been shown to decrease progression of renal disease and are great for CKD
ACEI/ARB | but caution with AKI
125
what drugs can be benificial in in HFeEF
ACEI/ARB
126
can you combine and combo if ACEI, ARB, or renin inhibitor
NOOOOOOO
127
how would you monitor a patient on ACEI/ARB
1. BMP ( K+, SCr) specificially | 2. BP
128
ARBS have {higher/lower] rates of cough and angioedema in comparison to ACEI
lower
129
can you give an ARB To a pregnant patient
no - oligohydramnios - hypotension - renal failure - death
130
if a patient has a cough on an ACEI, what shoul you do next
switch to an ARB
131
how do you monitor an ARB
1. BMP (K+, Scr) | 2. BP
132
what is the primary action of the dipine drugs
DHP CCB | -primarily DILATE blood vessels
133
AE dipine drugs
DHP CCB - peripheral edema (may not be relieved by diuretics because it is not a fluid retention issue) - HA - dizziness - flushing - reflex tachycardia (more likely IR)
134
caution with dipine drugs
DHP CCB - unstable angina - CYP 3A4 interactions - -simvastatin should not excess 20 mg/day
135
how do you monitory a DHP CCB
BP
136
name non DHP CCB
1. diltiazem | 2. verapamil
137
caution non DHP CCB
bradycardia
138
AE NON DHP CCB
1. Constipation 2. gingival hyperplasia 3. bradycardia 4. avoid in hf pt.
139
how would you monitor non DHP CCB
HR, BP
140
a patient has a HR of 56 BPM, what meds should they avoid?
verapamil, diltiazem, BB " olols"
141
interactions with non DHP?
CYP3A4 interactions | -no more than 10 g simvastatin
142
chlorthalidone is what type of drug
thiazide diuretic
143
HCTHZ is what kindof ddrug
Thiazide diuretic
144
MOA chlorthalidone
thiazide diuretic ``` act on early distal tubule to block reabsorption of Na, Cl, water (HCTZ too) -excretion K + increased -decrease, K, Na, Mg -increase uric acid, glucose, Ca2+ ```
145
what drug may increase uric acid
diuretics, thiazides ecp.
146
what drug may increase glucose
thiazide diuretic
147
what may render HCTZ ineffective
CrCl < 30 (kidneys need to be perfused for thiazide to exert effect)
148
what drug may cause photosensitivity
thiazide diuretics
149
chlorthalidone has a [higer/lower] half life than HCTZ
higher, more likley to reduce CV symptoms ACC/AHA rec. over HCTZ
150
how would you monitor a patient on a thiazide diuretic
1. BMP (Na, K Scr, glucose) | 2. BP
151
fursomide belongs wo what class
loop diuretic
152
torsemide belongs to what class
loop diuretic
153
[] diuretics are preferred if there is concomitant renal dysfunction
loop (furosemide, torsemide)
154
triamterene/HCTZ is a [] diuretic
K sparring
155
aldosterone blocker is a [] diuretic
K sparring
156
epleredone is a [] diuretic
K sparing
157
Spironolactone is a [] diuretic
K sparing
158
what diuretic is thought to have the weakest diuresis
K SPARRING
159
what diuretic can be used to offset thiazide induce K+ loss
K sparring - spironolactone - triamterene/HCTZ - aldosterone blocker - elperedone
160
what caution should be made with spironolactone/aldosterone blocker/triamterene/HCTZ/elperedone and ACEI/ARB
hyperkalemia, using K sparing with ACEI/ARB (that already blocks aldosterone and spares K) may lead to too much K
161
is atenolol selective
yes
162
is betaxolol selective
yes
163
is bisoprolol selective
yeS
164
is metorpolol selective
yes, succ. and tart
165
is nadolol selective
NO
166
is propranolol selective
NO
167
is timolol selective
NO
168
is carvedilol selective
NO (also with alpha-1 activity)
169
is labetalol selective
NO (also alpha-1 activity(
170
what kind of drug is pindolol
BB with intrinsic sympathomimetic
171
MOA BB
stop angiotensin II from binding target cells in heart - decreased contractility - decreased cardiac output
172
Caustion non selective bb
COPD, asthma, may cause bronchonstriction by blocking B2 (bronchodilate when bound to NE)
173
what drugs should not be mixed for fear bradycardia
non DHP CCB (verapamil, diltiazem), BB
174
name the selective BB
beta-1 selective ABBA MEN ``` Atenolol Betaxolol Bisoprolol Acebutolol Metoprolol Esmolol Nevivolol ```
175
what drug can cause hypoglycemia, how is this mechanism
BB, epi acts via beta-adrenergic receptors will increase glucose, but BB will block this action and cause hypoglycemia WIHTOUT warning signs (only hypoglycemia symptom that will occur is sweating)
176
what are some AE of BB
1. decreased exercise tolerace 2. exacerbation decomensated HF 3. bronchospasm 4. mask hypoglycemia 5. depression 6. fatigue 7. sexual dysfunction
177
cuation with stopping BB
rebound HTN
178
what are teh more 1st line HTN drugs
1. ACEI/ARB 2. CCB 3. diuretic
179
how would you moitor a BB patient
1. hr | 2. BP
180
What class does clonidine belong to?
Alpha-2 agonist
181
what class does methyldopa belong to?
Alpha-2 agonist
182
what is the MOA of clonidine
alpha-2 agonist block CNS stimulation to BLOCK increase in vasopressin and sympathetic discharge. (SNS speeds up HR, alpga-2 agonsit will block and constriction) - decrease peripheral resistance to decrease BP - VASODILATE **Remember alpha-2 is the inhibiting factor so you want to AGONIZE it
183
what is the MOA of methyldopa
alpha-2 agonist block CNS stimulation to BLOCK increase in vasopressin and sympathetic discharge. (SNS speeds up HR, alpga-2 agonsit will block and constriction) - decrease peripheral resistance to decrease BP - VASODILATE **Remember alpha 2 is the inhibiting factor, so you want to AGONIZE it
184
What kinds of cautions should you educate your patients on before you give them an alpha 2 agonist
1. AVOID with cradycardia or drugs that can cause it ( BB, non DHP) 2. rebound HTN with aprubt d/c (like BB) 3. may cause orthostatic hypertension
185
what 2 patient groups are important to keep in mind with alpha-2 agonists
1. elderly (orthostatic hypotension) | 2. pregnancy (methyldopa PREFFERED)
186
what drug can be used a patch once weekly to treat HTN?
clonidine, alpha-2 agonist
187
what HTN drug is preferred in pregnancy
methyldopa
188
How would you monitor a patient on an alpha-2 agonist
HR, BP
189
what kind of drug is Aliskiren
a renin inhibitor
190
MOA Aliskiren
inhibit renin release from kidney, block entire RAAS system directly block the conversion of angiotensin to angiotensin 1
191
what 3 drug groups are contraindicated in pregnancy
1. ACEI 2. ARB 3. renin inhibitor
192
what 3 drug groups should NOT be combined
1. ACEI 2. ARB 3. renin inhibitor
193
what are some AE of aliskiren
1. angioedema 2. hyperkalemia 3. elevated SCr 4. decreased GFR 5. hypotenson
194
What cautions must you consider when Rxing Aliskiren
1. pregnancy (cont!) 2. BRAS 3. angioedema
195
how would you monitor a patient on aliskiren
1. BP | 2. BMP (K+, SCr)
196
Doxazosin is a [] drug
Alpha-1 blocker remember alpha-1 STIMULATES heart muscle, want to block this
197
MOA Doxazosin
alpha-1 blocker vasodilate veins/arteries by inhibiting alpha-1 receptors (when stimulated to vasoconstrict)
198
AE doxazosin
1. orthostatic hypotenstion (esp. after 1st dose and elderly) 2. priapaism
199
according to beer's criteria [] is NOT Recommended for routine use in HTN due to risk of orthostatic hypotension
doxazosin
200
what needs monitored for a patient on doxazosin
BP
201
[] is NOT recommended fo rinital monothereapy due to increased risk CV events
doxazosin
202
hydralazine belongs to what group
direct vasodilator
203
minoxodil belongs to what group
direct vasodilator
204
MOA minoxidil
direact vasodilation, relexation or arteriolar smooth musle (LITTLE EFFECT ON VEINS)
205
MOA hydralazine
direct vasodilation, relaxation of arteriolar smooth muscle (LITTLE EFFECT ON VEINS)
206
AE direct vasodilators
reflex tachycardia edema hypertrichosis lupus-like syndrome HF (retention water and salt) ischemic heart disease
207
[] can cause lupus-like syndrome
minoxodil, direct vasodilator
208
[] can cause hypertrichosis
direct vasodilaotr (minoxodil and hydralazine)
209
[] should be given with a diuretic to minimize fluid gain
direct vasodilator, hydralazine or minoxodil
210
[] should be given with a BB to prevent tachycardia and increase myocardial workload
direct vasodilator, hydralazine minoxodil
211
what is preffered inital therapy for HTN
Ccb Acei/ARB Thiazide CAT *just never combine ACEI/ARB
212
what can be given to treat ischemic heart disease?
BB +/- ACEI/ARB +/- CCB if goal not met
213
what should be avoided in ischemic heart diseae
atenolol (use any other BB)
214
What can be used to treat HFrEF?
BB +/- ACEI/ARB
215
what BB are prefered to treat HFrEF?
1. bisoprolol 2. carvedilol 3. metoprolol suc.
216
what should be avoided in treatment of HFrEF?
NON-DHP, CCB
217
what is first like for HFpEF
diuretics remember hfPef, diuretics make you P
218
what treatments are best for CKD
ACIE (pref) ARB if cannot tolerate ACEI
219
for acute intracerebral hemorrhage or acute ischemic stroke, what is important to know when treating these pts.
dont lower NP to quicly
220
what should be done for secondary stroke prevention?
1. wait to start HTN thereapt 2. no HX HTN, start only when BP greater than 140/90 3. select therapy based on comorbidities - thiazide, ACEI/ARB
221
in DM all [] med are appropriate
first line (ACEI.ARB, CCB, Thiazide)
222
Describe how treatment should be done in AA patients
1. use CCB or thiazide first 2. Use ACEI/ARB or BB IFFFFFFF HFrEF or CKD (these are greater than risk AE with BB or ACEI/ARB)
223
what are 3 preferred drugs in pregnancy
1. Nifedipine ER 2. Labetalol 3. Methyldopa
224
How should you treat HTN with airway issues like asthma, COPD
1. avoid non-selective BB 2. use ABBA MEN selective BB 3. sympathomimetic agents may raise BB
225
how to treat HTN pts. with gout
1. avoid thiazides (other diuretics may be okay)
226
define orthostatic hypotension
a decrease in SBP of > 20 mmHG decreased in DBP of > 10 mmHG when changing from supine to standing
227
what drugs put a patient at risk for orthostatic hypotension
1. clonidine 2. alpha blockers 3. sometimes ACEI, ARB, diuretics most common in vasodilators start low and titrate up*
228
describe a hypertensive crisis
SBP > 180 mmHG | DBP > 120 mmHG
229
when do hypertensive crises require hospitalization and IV antihypertensives
if end-organ damage is present reduce SBP < 140 mmHG in first hr SBP < 120 mmHG with IV meds dont correct too quick, should take hours
230
name evidences of end organ damage in hypertensive crisis
1. encephalopathy 2. acute MI 3. untable angina 4. strokes 4. AKI 5. aortic anneurysm
231
if hypertensive crisis present with no end organ damage, what is protocol
reinstiture or intensify PO antihypertensives, arrange f/u

Pharmacology III (6 decks)

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