Cardiovascular Pharmacology I Flashcards
(150 cards)
1
Q
What is considered high BP?
A
140/90
Either one of these can be high, doesn’t have to be both
-repeated high measurements
2
Q
What causes hypertension
A
- 10% of patients are the only ones that have a specific cause, and they are secondary to another disease, causing secondary HTN
- 90% of patients we dont know the cause of it
3
Q
How do we cure HTN in the people with secondary HTN (due to another disease/10%)
A
Treat the other disease
4
Q
How do we treat primary HTN? (90% of patients, dont know what it causes)
A
HTN drugs
5
Q
Patients that exhibit no specific causes of HTN are said to have
A
Primary or essential HTN
6
Q
What is blood pressured maintained by
A
Arterioles
Postcapillary venules
Heart
Kidneys
7
Q
How do the kidneys regulate BP
A
Regulating the intravascualr fluid
8
Q
How do the arterioles, venules, heart, and kidney work to regular blood pressure?
A
Baroreflexes
9
Q
What is cardiac performance influenced by
A
- Parasympathetic innervation (vagus)
- sympathetic innervation
10
Q
Heart rate is decreased by
A
Parasympathetic activity at the SA node
11
Q
Heart rate is increased by
A
Sympathetic activity at the SA node
12
Q
Is parasympathetic or sympathetic dominant on HR
A
Parasympathetic
13
Q
Contractile force of heart is reduce by
A
Parasympathetic activity to atrial and ventricular muscles
14
Q
Contractile force of the heart is increased by
A
Sympathetic activity to atrial and ventricular muscles
15
Q
Vascular smooth muscle constricts when
A
In response to sympathetic stimulation
16
Q
Parasympathetic and vascular smooth muscle
A
Doesn’t affected it much
17
Q
Constriction of veins in vascular smooth muscle
A
Increases CO
18
Q
Constriction of arteries in vascular smooth muscle
A
Reduces CO by increases after load
19
Q
Sympathetic actions on the kidney
A
Renin release
20
Q
Causes sodium and water retention (increased fluid volume, increased CO, increased BP)
A
Renin
21
Q
Helps achieve minute to minute control of blood pressure
A
Baroreceptor reflex
22
Q
How do the baroreceptors work
A
The nerve endings detect stretch due to arterial pressure, the reflex is to increase parasympathetic and decrease sympathetic (efferent via vagus)
23
Q
If arterial pressure declines, what does the baroreceptor do
A
Causes an increase in sympathetic and a decrease in parasympathetic activation
24
Q
What happens when changes in blood pressure persist beyond a few minutes?
A
Reflex autonomic responses diminish
- this is called barorefelx adaptation
- increased BP, increased HR in exercise instead of anticipated reflex bradycardia
25
What does the renin-angiotensin-aldosterone system (RAAS) do
Maintains BP
- decreased BP: decreased renal blood flow:renin release which activates the RAAS to increase BP
- sympathetic also causes renin release as well
26
What kind of receptors causes the release of renin
B1
27
What are the important target areas for controlling BP with drugs in the RAAS
Targeting B1 receptors and targeting the RAAS system
28
Decreased arterial pressure and the baroreceptor reflex
Increases sympathetic nervous system activity
29
Increased sympathetic nervous system on the heart
- Increased force and rate of contraction=increased CO
| - renin release: renal retention of Na and water (increased blood volume)
30
What does ADH do
Decreases arterial pressure causes a baroreflex-mediated release of this.
-acts on the renal collecting duct to enhance water retention
31
What areas do we target to decreased blood pressure with drugs?
Blood vessels
Heart
Kidney
Some brain
32
First line treatment for HTN
Thiazides
ACEI
CCB
33
Of the first line medications (thiazides, ACEI, and CCBs), which one is more effective
They are all equally effective
34
Patients requiring combination therapy, the most popular choice is
ACEI with a long lasting CCB
35
Of the first line HTN drugs, which one is most often given because it is cheap
Thiazides
36
Which do you use first, ACEI or ARB?
ACEI
37
What drugs do you want to use or combination therapy?
Pick a combination of 2 of the first line drugs
38
Long term benefit of diuretics
Hyperpolarization, decrease vascular effect, decreased BP
39
MOA of diuretics
Reduce fluid volume, reusults in water and electrolyte excretion, which decreases CO
40
What happens after several days of treatment with diuretics
Urinary excretion returns to normal, and later CO and blood volume return to pretreatment values, but blood pressure remains reduced
- decreased vascular reactivity to NE and decreased structural vascular resistance
- decreases vascular activity
- hyperpolarization of smooth muscle, basically in vessels, maybe due to decreased Na
41
Why is that after taking a diuretic for a few days, urine excretion and blood volume return to pretreatment levels, but BP stays low?
Hyperpolarization: decreased vascular effect, decreased BP
42
Therapeutic use of thiazides (diuretics)
HTN, particularly in black or elderly patients
43
Adverse effects of thiazides (diuretic)
Potassium depletion which could affect:
- chronic arrhythmia
- acute MI
44
Are thiazides potassium wasting or sparing
Wasting
45
What are the 2 most common thiazides (diuretics)
```
Chlorthalidone
Hydrochlorothiazide (HCTZ)
```
46
What do calcium channel blockers work on
Heart and blood vessels
- Slow conduction=decreased CO=decreased BP
- thiazides on BV=vasodilation=decreased TPR=decreased BP
47
What kind of calcium channel do calcium channel blockers work on
L-type in heart and BV
48
Therapeutic use for calcium channel blockers (CCB)
HTN
| -works well in co-morbid conditions. Popular in patients with multiple conditions
49
Adverse effects to CCBs
- Consitpation (block Gi tract Ca2+ channels)
| - gingival hyperplasia (red, bleeding gums)
50
What HTN medication can cause red, bleeding gums?
CCBs (dipines)
51
What is a common name for CCBs
“-dipine”
52
What are the two CCBs for cardiac calcium channels
Verapamil and diltiazem
53
What drug works on vascular calcium channels
Amlodipine
54
Which CCB is most cardiodepressant
Verapamil
55
Which CCBs is good vasodilator
Dipines (amlodipine)
56
Which CCBs most likely to cause reflex tachycardia?
Dipines
- decreased BP=reflex tachy
- verapamil works directly on the heart, so it doesn’t have that reflex
57
Which CCB works on the heart and on the vacualtrue
Diltiazem
58
Which CCB consistently slows heart rate and vasodilates?
Diltiazem
59
MOA of ACEI
Block the enzyme ACE
60
What does the enzyme ACE do
- Converts angiotensin I to angiotensin II
| - acts on bradykinin to make it inactive
61
What does angiotensin II do
- Causes vasoconstriction, increases peripheral vascular resistance, which increases BP
- also causes release of aldosterone, which increases Na and water retention, which increases BP
62
What receptor does angiotensin II bind to
AT-1
63
ACEI effect on bradykinin
Causes increased levels of bradykinin, this promotes vasodilation, which decreases blood pressure.
64
Bradykinin in the presence of ACE enzyme
ACE inactivates bradykinin, but bradykinin’s actions are to vasodilation, decrease peripheral vascular resistance,and decrease BP
65
What does Renin do
It’s an enzyme that converts angiotensinogen into angiotensin I
66
What does aliskiren work on
It is a renin inhibtor
67
What substance accumulates when you take aliskiren?
Angiotensinogen
68
The production of what is immediately inhibited when taking aliskiren
Angiotensin I
69
What does ACEI prevent
The conversion of angiotensin I to angiotensin II
70
What receptor does angiotensin II bind
AT-1
| -vasocontricts
71
Where are AT-1 receptors found
Blood vessels and adrenal cortex
72
What kind of G protein coupled receptor is AT-1 receptor
Go
73
What does aldosterone do
Increases water and Na retention, which increases BP
74
What does ARB2 do
Blocks AT-1 receptors
75
Which drug that targets the RAAS system does not affect Bradykinin?
ARB2
| -works on lower part of the pathway
76
Which drug that works on the RAAS will not cause a cough as a side effect
ARB2 because it does not work on Bradykinin
77
If a patient is on an ACEI and complains of a cough, what is something that can be done
Switch to ARB2
| -we don’t initially start people on these because they are more expensive
78
No matter what drug you use to target the RAAS pathway and no matter what part of the pathway is being targeted, the same things happen:
Same net effect
- deceased aldosterone
- decrease vasoconstriction
- decrease Na and water retention
- decreased BP
79
What does the RAAS pathway normally do?
Increases BP
80
Is bradykinin a vasodilator or vasoconstrictor
Vasodilator
81
What does ACE do it bradykinin and why do we want to stop it
ACE inactivates Bradykinin
-ACE inhibitor will allow more bradykinin to be active, and since bradykinin is a vasodilator, it will decrease BP on its own
82
Therapeutic use for ACEI
- HTN in young, white patients
- CHF given 24 hours after MI
- diabetic nephropathy (delay renal disease)
83
What drug can you give to a diabetic to help with diabetic nephroapthy?
ACEI
84
Adverse effects of ACEI
Dry cough in 30% of patients
-most people can live with it, they dont discontinue
-mediated by bradykinin
Angioedema
Teratogenic
Acute renal failure in bilateral renal artery stenosis
85
What is the most common side effect of ACEI
Dry cough
86
What is the most severe side effect of ACEI
Angioedema
87
What is the one exception to giving ACEI to someone for renal problems
Normal its good for renal problems such as diabetic nephropathy, but in the case of bilateral renal artery stenosis, it could cause renal failure
88
What are the names of ACEI
End in “pril”
Captopril
Lisinopril
89
What does angiotensin II do at the level of the glomerulus
Constricts the efferent arterioles
90
What do prostaglandins do at the level of the glomerulus
Dilated the afferent arterioles
91
How does ACEI help diabetics
- saves kidneys
- stops production of Ang II, efferent side dilates, decreases filtration, decreases GFR, reducing work of kidneys, will decreased amount of protein in urine
92
Why is ACEI bad in someone with bilateral renal stenosis
- pt already has low GFR
- kidneys are already struggling
- very low GFR can cause renal failure
93
MOA of ARBs
Inhibit angiotensin type I receptor (AT-1)
| -blocks actions of angiotensin II, but does not affect bradykinin metabolism
94
Use of ARBs
HTN, CHF, diabetic nephropathy
95
Adverse effects of ARBs
Better than ACEI, teratogenic, acute renal failure in those with bilateral renal stenosis
96
ARB drugs
“Artan”
| Losartan
97
Patients age 18 and older regardless of race with chronic kidney disease and HTN should receive _______ to improve kidney outcomes
ACEI or ARB
| -check GFR first to make sure its not too low though
98
What is the name of the renin inhibitor
Aliskiren
99
MOA of aliskiren
Direct renin inhibitor preventing the conversion of angiotensinogen to angiotensin I
100
Therapeutic use of aliskiren
HTN as a single agent or in combination
101
Adverse affects of aliskiren
Teratogenic
| -very slight chance of angioedema and slight cough, but you would suspect ACEI before this as the culprit)
102
How do B blockers work for HTN
- B1 activation of adrenoreceptors on heart=decreased CO
- decreases renin, which decreases angiotensin II, which decreases aldosterone, which decreases dosing and water retention, which decreases blood volume
These all decrease BP
103
Therapeutic use of B1 blockers
HTN but not first line unless patient has comorbid condition.
104
Who benefits greater from B blockers
Younger white patients.
105
Why are B1 blockers not the best choice for elderly or black patients
They have low-renin HTN
| -use CCB or thiazides
106
General rule for B blockers and cardiac conditions
Use B1 selective drugs for cardiac conditions
107
Adverse effects of B blockers
Nonspecific B clockers can block B2 receptors in the lungs (bronchoconstriction) and disrupt glucose control
-contraindicated in asthmatics and diabetics
108
When are B blockers contraindicated
In asthmatics and diabetics
109
What drugs are B blockers
Atenolol and metoprolol
| B1 selective
110
MOA of alpha 1 blockers
Block a1 receptors in a arterioles and venules
111
Therapeutic use of alpha 1 blockers
HTN, benign prostatic hyperplasia
112
Adverse effects of alpha 1 blockers
Postural hypotension, dizziness
113
What drug is an alpha 1 blocker
Prazosin
114
What drug do we use for HTN and BPH?
Prazosin
115
What drugs for HTN work in the CNS
Central A2 agonists
116
MOA of central A2 agonists
Act on a2 receptors to reduce sympathetic outflow
117
What is the reason that central a2 agonists are not first line, even though they are very powerful
Because they work in the CNS and can cause fatigue
118
Therapeutic use of central a2 agonist
Drug of choice for HTN during pregnancy
119
What is the drug of choice for HTN during pregnancy
Methyldopa, a central a2 agonists
120
What is the only HTN drug that is safe during pregnancy
Methyldopa, a central a2 agonist prodrug
121
Adverse effects of methyldopa (central a2 agonist)
- Sedation
- Sudden discontinued use causes rebound HTN which may be severe
- hemolytic anemia if positive Coombs test
122
What test tells you if you are likely to be at risk for hemolytic anemia
Positive Coombs test
123
Multiple action drugs
Labetolol
Carvedilol
Nebivolol
124
How are labetolol and carvedilol multiple action drugs
Block a1, b1, and b2 receptors
| -decrease BP
125
How is nebivolol a multiple action drug
Blocks B1 and vasodilates via nitric oxide release, lower BP
Even though it starts with N and ends in olol, it is not a nonspecific B blocker. Works on B1 and uses NO
126
Therapeutic use for multiple action drugs
HTN
127
This occurs when HTN is severe enough to cause end-organ damage
HTN emergencies
128
What drug is used as IV therapy for HTN emergencies
Labetolol
129
Stage 1 HTN gets what kind of drugs
Single drug
130
Stage 2 HTN gets what kind of drugs
Combo drugs
131
Highly lethal condition with pulmonary congestion and and peripheral edema
Congestive heart failure
132
Left heart failure
Pulmonary congestion
133
Right heart failure
Peripheral edema
134
What are the first targets you want to hit to treat CHF
BV and kidney
135
What all happens in CHF
- decreased contractility;
- cardiac failure;
- increased symp activity (compensation), which leads to increased arterial constriction (afterload), increased blood volume, increased preload, and increased HR
136
What is the main thing causing the heart to fail in CHF
Decreased contractility
137
What does the compensatory increased sympathetic firing in CHF affect?
Too much of a good thing
- increased HR
- constricts arterioles (increased afterload)
- increased blood volume
138
How can we fix the increased HR in CHF?
Low dose B blocker
139
How do we fix the constricted arterioles and the increased afterload
We want to dilate the arterioles and decrease afterload
140
How do we fix the increased blood volume in CHF
Decrease preload with diuretics or ACEI
| -or can decrease preload with venodilators
141
What is the compensation for the cardiac failure in CHF
Increases sympathetic activity
142
What dose of B blocker is essential when treating CHF and getting the HR to lower
Low dose. If you give high dose, you could make the CHF worse
143
What is cardiac remodeling
Excess fibrosis after cardiac failure (CHF) causing a decrease in function from over stimulating the heart
144
What are the causes of cardiac remodeling?
1. Aldosterone
- 20x the normal level
- heart has receptors for aldosterone so we need to target them
2. NE and epi
- too much sympathetic compensation
145
What drugs do we used to treat cardiac remodeling
ACEI and ARBs for the aldosterone levels and B blockers to stop the epi and NE
146
What is the number one benefit of ACEI and ARBs in CHF
Decreased cardiac remodeling
147
If you inhibit remodeling, what do you do to survivial
Increase it
148
If you increase survival, what do you do to remodeling
Inhibitit
149
What is the main thing you want to do to stop remodeling
Stop aldosterone!
150
Myocardial hypertrophy in CHF
Left ventricle gets large, leads to cardiac remodeling
