Antihypertensives Part I Flashcards
(127 cards)
1
Q
What is normal blood pressure range
A
< 120/80
2
Q
What is the range for elevated blood pressure, but not yet stage 1 HTN?
A
120-129 / <80
3
Q
Stage 1 HTN parameters
A
130-139 systolic
OR
80-89 diastolic
4
Q
Stage II HTN parameters
A
> =140 systolic
OR
> =90 diastolic
5
Q
HTN crisis parameters
A
> =180 systolic
OR
> =120 diastolic
6
Q
(t/f) Mild HTN (130/80) will not cause end-organ damage
A
False,
*Starting at 115/75 CV disease risk doubles every increment of 20/10 increase
7
Q
Starting at ___/___ CV disease risk doubles every increment of ___/___ increase
A
115/75
20/10
8
Q
(t/f) Isolated systolic HTN alone is associated with end-organ damage
A
True
*Both systolic and diastolic HTN are associated with end-organ damage
9
Q
The risk of end-organ damage d/t HTN is increased in what population?
A
African Americans
10
Q
The risk of end-organ damage d/t HTN is decreased in what population?
A
Premenopausal women
*(when compared to men)
11
Q
(t/f) HTN is usually asymptomatic until end-organ damage has already occured
A
True
12
Q
(t/f) You have HTN
A
If you don’t know this you should probably check
13
Q
Pts who no specific cause can be found for their HTN have what type of HTN?
A
Essential or Primary HTN
14
Q
Pts who a specific cause can be indentified for their HTN have what type of HTN?
A
Secondary HTN
15
Q
(t/f) In most cases of HTN, CO is decreased
A
False
*CO remains normal despite increases in SVR (systemic vascular resistance, AKA arterial resistance, AKA afterload)
16
Q
What is more common, secondary or essential HTN?
A
Essential HTN
*Secondary HTN only accounts for 10-15% of cases
17
Q
Although we can’t pinpoint what causes essential/primary HTN via studies, what are 3 factors that we think cause it?
A
-Genetics
-Stress
-Diet (increased Na & decreased K or Ca)
18
Q
What 2 hemodynamic factors make up blood pressure?
A
CO & PVR
*the hydraulic equation of BP is BP = CO x PVR
19
Q
(t/f) SVR (systemic vascular resistance) is the same as PVR (peripheral vascular resistance)
*not to be confused w/ PVR (pulmonary vascular resistance)
A
True
*whoever labeled it as peripheral vascular resistance should be imprisoned
20
Q
What is sensing site of BP regulation (MAP specifically) via autonomic/CNS control?
A
Baroreceptors found in the aortic arch & carotid sinus
21
Q
Increase baroreceptor firing d/t HTN causes what baroreflex response?
A
Inhibition of sympathetic action on BP
*Can also cause parasympathetic stimulation that can only decrease HR to combat the increase in MAP/vessel wall stretch
22
Q
Decreased baroreceptor firing d/t HoTN causes what baroreflex response?
A
Sympathetic stimulation (increase in PVR, venous tone, and contractility of heart) to increase BP
23
Q
The endogenous, local release of _____________ from the vascular endothelium causes vasoconstriction
A
Endothelin-1
24
Q
The endogenous, local release of _____________ from the vascular endothelium causes vasodilation
A
NO (nitric oxide)
25
With baroreflexive and renal autoregulation of BP, why do pts remain hypertensive chronically?
Their baroreceptors and the renal blood volume-pressure control systems are "set" at a higher level of BP
*this is straight from the book in Chpt 11 pg. 3 directly beneath the diagram
26
What mechanism of BP autoregulation controls BP during postural changes?
Baroreflexes
27
What mechanism of BP autoregulation controls BP over the long term?
Renal system
28
What two actions does the kidney do when it senses an decrease in renal perfusion pressure?
-increased reabsorption of Na & H2O
-increased production of renin
29
How does the kidney increase production of renin without sensing a decrease in renal perfusion pressure?
Stimulation of B1 receptors in the JGA
30
What things does angiotensin II do?
-Systemic vasoconstriction (increase SVR, efferent arteriole of kidney)
-stimulation of aldosterone production in the adrenal cortex (reabsorption of Na)
-SNS stimulation
-increases the breakdown bradykinin
-Na+ reabsorption in the PCT
-Increased ADH/Aldosterone
31
____________ released from the posterior pituitary gland also plays a role in maintainance of blood pressure through its ability to regulate water reabsorption by the kidney.
Vasopressin (ADH)
32
What are the 4 categories of antihypertensive agents?
(think about the different mechanisms of autoregulation and what drugs need to do to lower blood pressure)
-Diuretics
-Blocking production or action of angiotensin
-Direct vasodilators
-Sympathoplegic agents (AKA sympatholytics, AKA antisympathetics)
33
You give hydralazine to a pt (think long term therapy) and their BP is not responding like it should. What other 2 drugs could you give in conjunction with hydralazine?
Beta-blocker & Diuretic
*hydralazine dilates arteries, reducing SVR. Compensatory mechanisms, via the baroreceptors & kidneys evoke tachycardia & Na/H2O retention. The BB drops the HR and diuretic prevents Na/H2O reabsorption
34
If ACEIs only lower BP less than 10mmHg, why do we give them even in severe HTN?
-They prevent/reduce renal disease in DM pts
-They reduce chance of HF
35
Say you have a pt on ACEI, BB, & Diuretic and you need to add another drug. What drug is particularly useful?
Spironolactone
36
What type of drug is spironolactone?
Mineralocorticoid antagonist
37
What are the 3 main actions of glucocorticoids?
-converting sugar, fat, and protein stores to useable energy
-inhibiting swelling and inflammation
-suppressing immune responses.
(think stress hormones/steroids. Glucocorticoids increase muscle and fat metabolism to increase serum glucose to fuel the fight or flight response)
38
What do mineralcorticoids do?
-Na absorption
-K+ excretion
*Aldosterone is the only endogenous mineralocorticoid
39
What is aldosterone?
A mineralocorticoid
40
What does spironolactone block?
Aldosterone
41
Diuretics lower blood pressure primarily by depleting body _______ stores
Na
42
How does increased serum Na cause vessel stiffness?
(this is a minor/newly found effect)
Altered Na/Ca exchange leading to increase intracellular Ca. This can lead to vessel stiffness and increased neural reactivity.
43
Whats another name for aldosterone receptor antagonists?
Potassium-sparing diuretics
44
_________ diuretics are appropriate for most patients w/ mild or moderate HTN & normal renal & cardiac function
Thiazide diuretics
45
_______ diuretics are indicated in severe HTN. Also when multiple drugs that retain ____ are used, in _______ insufficiency (GFR < __-__) and in _______ failure or _________ when there is increase Na retention
-Loop diuretics
-retain Na
-renal insufficiency
-GFR < 30-40
-cardiac failure or cirrhosis
46
Is the antihypertensive effects of thiazide diuretics dose dependent?
No
*lower doses of thiazide diuretics exert as much anti-HTN effects as larger doses even though the larger doses are more natriuretic (depletes Na). These diuretics work on the DCT so they can only achieve a certain level of anti-HTN as compared to their stronger colleagues, loop-diuretics.
47
Are the anti-HTN effects of loop diuretics dose dependent?
Yes
*high doses produce more anti-HTN effects
48
Renin release is stimulated by what 3 things?
-low renal artery BP
-sympathetic stimulation (B1 receptors)
-low Na delivery or high Na concentration @ DCT
49
What converts angiotensin I to angiotensin II?
ACE (angiotensin converting enzyme)
50
Angiotensin II & III stimulate ___________ release
Aldosterone
51
ACEIs help prevent cardiac __________
remodeling
*cardiac remodeling happens through a angiotensin cascade in the heart
52
What 4 classes of drugs act on RAAS
-ACEI
-ARBs
-Renin blockers (aliskiren)
-Aldosterone antagonists
53
What class of drug is aliskiren?
Renin blocker
54
(t/f) BBs can reduce renin secretion
True
*we went over this already bro
55
Bradykinin is a potent vaso________ and stimulates the release of _______ & _________
-vasodilator
-NO (nitric oxide)
-Prostacyclins
56
Baroreceptor is __________ as the RAAS system is __________
Short-term/immediate
Long-term
57
Why are ARBs more effective in blocking RAAS?
They block the ACE independent pathway to get from angiotensin I to II, unlike ACEIs
58
Aldosterone cause _______ re-absorption where as ADH (vasopressin) causes ______ reabsorption
-Na
-H2O
59
NO (nitric oxide) causes smooth muscle _________ by binding to ________ _________ to convert GTP to ________
-diation
-guanylyl cyclase
-cGMP
60
cGMP does what to smooth muscle?
Relaxes
61
Which one is a direct vasodilator?
Sodium nitroprusside
or
Nitroglycerin
Sodium nitroprusside
*Na nitroprusside converts straight to NO while nitroglycerin has to undergo a few metabolic processes to become NO
62
What is the primary humoral mechanism responsible for BP control?
RAAS
63
What vascular substances are involved in the regulation SVR?
-Endothelin-1
-NO
64
2 main comphensatory mechanisms after giving vasodilator (hydralazine)
-tachycardia
-Na/H2O retention
65
Diuretics can increase your ________ ______ _______ & impair ________ tolerance
-serum lipid profile
-glucose tolerance
66
B2 stimulation cause smooth muscle _________ in vasculature and airway
Dilation
67
Renin & _____________ combine to make angiotensin I
-angiotensinogen
68
What 2 organs can convert angiotensin II to III?
Brain
adrenal gland
69
ACEIs will ________ renin levels
Increase
70
Aliskiren (renin blocker) reduces plasma renin activity but increases plasma renin levels by up to ___x
10x
71
Ending of ACEIs drug names
"pril"
72
Endings of ARBs drug names
"sartan"
73
Endings of Anti-lipid drug names
"statin"
74
Do ACEIs cause reflex SNS activation?
No
*they are long-term and act on the long term system (RAAS). The baroreceptors are a reflex and for short-term control and won't counteract the RAAS inhibition
75
All ACEIs are prodrugs except __________
Lisinopril
76
Lisinopril __________ muscle relaxant effects of depolarizing NMBs (succs)
increases
77
In what 2 ways do ACEIs lower BP?
-blocking angiotensin II formation
-blocking bradykinin metabolism
*bradykinin is a vasodilator so if you stop its metabolism then you have more of it, duh
78
ACEIs have no reflex sypathetic activation so they are safe in pts with _________ _________ disease
*type of cardiac disease
Ischemic heart disease
79
3 main adverse effects of ACEIs
-dry cough
-angioedema
-hyperkalemia
80
__________ block bradykinin-mediated vasodilation, therefore impair the effect of ACEIs
NSAIDs
81
ACEIs/ARBs are contraindicated in _____________ and pts with bilateral ________ artery stenosis
-pregnancy
-bilateral renal artery stenosis
82
Why are ACEIs/ARBs contraindicated in bilateral renal artery stenosis?
Angiotensin II constricts the efferent arteriole more than the afferent. The efferent (exit) arteriole being constricted helps maintain pressure in the glomerulus to increase GFR. By inhibiting efferent constriction in the case of renal artery stenosis, which will result in decreased afferent blood flow, you will have an extremely reduced GFR. Bilateral knocks out GFR in both kidneys so not good bro.
83
Big take-away differences that ARBs have from ACEIs?
-don't interfere with bradykinin metabolism (no dry cough)
-block RAAS more effecitively cause they also block the ACE independent pathway
84
(t/f) you can give ACEI/ARB in unilateral renal artery stenosis
Yep
*you got another kidney
85
Hydralazine dilates _______ more than ________
Arteries more than veins
86
Hydralazine doesn't dilate ________ arteries
epicardial arteries
87
Calcium combines with _________ to activate myosin light chain kinase, which induces smooth muscle contraction in the vasculature
Calmodulin
88
What does IP3 do mainly?
Releases Ca++ from the sarcoplasmic reticulum of smooth muscle (then Ca++ combines with calmodulin to activate myosin light chain kinase to cause contraction)
89
What are the 3 mechanisms of action for hydralazine?
-hyperpolarizes smooth muscle by opening K+ channels
-Inhibits IP3 (decreasing Ca++ release)
-Stimulates formation of NO
90
Given hydralazine's stimulation of the sympathetic nervous system (baroreceptor mediated reflex), it consequently leas to ____________ and _____________
-Tachyphylaxis
-Tachycardia
91
A major side effect of hydralazine is a reversible ______-like syndrome at higher doses
-lupus-like syndrome
*don't ask me why
92
Hydralazine onset is ___-___ minutes and peak effect is __-__ mins and duration is __-__ hrs so it may be difficult to titrate
-Onset = 10-20mins
-peak = 10-80mins
-duration = 1-4hrs
93
Nitroglycerin dilate _______ more than ________ at low doses
Veins more than arteries
94
Minoxidil is similar to ________
hydralazine
95
Minoxidil dilates _________
arteries
96
Mechanism of action of minoxidil
-hyperpolarization by opening K+ channels
97
Is minoxidil stronger than hydralazine?
Yes
98
Minoxidil must be given with a ________ and ________ because it is such a strong arterial vasodilator
-Beta-blocker
-Diuretic
99
Fenoldopam is a ______ agonsist
D1 agonist
100
What 2 things does fenoldopam do?
-arterial dilator
-natriuresis/diuresis
101
Beware of fenoldopam in ___________ because it __________ IOP
-glaucoma
-increases IOP
102
cGMP _________ platlet aggregation
decreases
103
What 4 things does NO do?
-vascular smooth muscle dilation
-inhibits plt aggregation
-inhibits leukocyte-endothelial interactions (WBC inflammatory response)
-prevents reabsorption of Na+ & H2O
104
(t/f) SNP (sodium nitroprusside) and nitrate dilate arteries and veins
True
105
NTG (administered sublingually) can be administered orally via the drugs _________ __________ & ___________
-Isosorbide dinitrate & mononitrate
106
Do you get relfex tachycardia w/ nitrates?
Yep
107
__________ is a metabolite of nitroprusside
*nitroprusside get broken down into NO and this compound
Cyanide
108
Nitroprusside leads to ________ toxicity
Cyanide toxicity
109
To tx cyanide toxicity, you will give ________ __________
Sodium thiosulfate
110
What 3 steps to treat cyanide toxicity?
1 - stop NTP
2 - 100% O2
3 - sodium thiosulfate
111
Cyanide toxicity leads to ______________ which impairs oxygenation
Methemoglobinemia
112
CCBs only work on __-type Ca++ channels
L-type
113
Which type of CCBs don't affect the heart that much?
*aka don't cause decrease in HR, contractility, conduction velocity, etc.
Dihydropyridines
114
Nifedipine, amlodipine, & nicardipine & clevidipine are what kind of CCB?
Dihydropyridines
115
Verapamil is what type of CCB?
Phenylalkylamine
116
What 2 types of CCBs affect the heart?
*aka decrease HR, contractility, conduction velocity, etc.
Phenylalkylamines & Benzothiazepines
117
Diltiazem is what kind of CCB?
Benzothiazepines
118
What 2 common CCB drugs affect the heart?
-verapamil
-diltiazem
119
What type of CCB affects the heart and vasculature?
Benzothiazepines
(diltiazem)
120
What type of CCB only acts mainly on the heart?
Phenylaklylamines (verapamil)
121
Dihydropyridine CCBs dilate ________ more than _______
arteries more than veins
122
With CCBs, avoid concominant use with ________
BBs
123
CCBs are most effective prophylactic tx of _______ angina
-variant (prinzmetals) angina
*aka coronary vasospasms
124
Verapamil should be cautioned in pts taking ________
Digoxin
125
Which CCB can lead to digoxin toxicity
Verapamil
126
(t/f) CCBs are more for rate control because they affect the cardia nodal cells moreso than the myocardial cells
True fact bro
127
What CCB has a greater affinity for the cerebral vascular bed?
Nicardipine
