HTN Flashcards
(139 cards)
1
Q
Changes in heart rate by an increase in the firing of the SA node
A
chronotropy
2
Q
Pacemaker cells are influenced by the ___________
A
autonomic nervous system
3
Q
Affects permeability of K+, Na+, and Ca2+
A
pacemaker cells
4
Q
______________ increases heart rate (positive chronotropy)
A
sympathetic nervous system
5
Q
______________ decreases heart rate (negative chronotropy)
A
parasympathetic nervous system
6
Q
Changes in the conduction velocity in the pacemaker cells at the AV node resulting in an altered interval
A
dromotropy
7
Q
Force of contraction
A
inotropy
8
Q
Inotropy is influenced by __________
A
- preload
- afterload
- free cytosolic Ca2+
9
Q
Inotropy is commonly influenced by the ________
A
sympathetic nervous system (norepinephrine)
10
Q
This is the end diastolic volume related to right atrial pressure
A
preload
11
Q
An (increase/decrease) in end diastolic volume (increases/decreases) contractility
A
increase, increase
12
Q
An increase in venous return will _________
A
- increase prelaod
- stretches the sarcomere
- increases contractility
13
Q
This is the arterial pressure that must be overcome by the ventricle
A
afterload
14
Q
(Increase/decrease) in work load can worsen ______
A
increase, ischemia
15
Q
Responsible for transitioning blood from a pulsatile flow into a smooth, continuous flow
A
arteries
16
Q
________ of arteries allows greater pressure control
A
elasticity
17
Q
During systole, arteries _______ and store some of the stroke volume (1/3 of the time in healthy arteries)
A
expand
18
Q
What is the greatest pressure exerted on the arteries?
A
systolic blood pressure
19
Q
During diastole, arteries ________ and create a smooth blood flow (2/3 of the time in healthy arteries)
A
recoil
20
Q
What is the lowest arterial blood pressure?
A
diastolic blood pressure
21
Q
DBP is largely affected by the _____________
A
elasticity of the arteries
22
Q
Wide pulse pressure indicates (increased/decreased) elasticity or (increased/decreased) stiffness
A
decreased, increased
23
Q
Average blood pressure over time; typically set at 100 mmHg
A
mean arterial pressure (MAP)
24
Q
What is the formula for MAP?
A
MAP=2/3(DPB) + 1/3(SBP)
25
Name the catecholamines
- norepinephrine (NE)
- dopamine (DA)
- epinephrine (EPI)
26
Which catecholamine is of main importance in HTN?
norepinephrine
27
Name the adrenergic receptors
- alpha 1 adrenoreceptor
- alpha 2 adrenoreceptor
- beta 1 adrenoreceptor
28
Which adrenergic receptor is located on the post synaptic cell of smooth muscle tissue and the heart?
alpha 1
29
Which adrenergic receptor regulates smooth muscle contraction (vascular tone) and myocardial inotropy (force)?
alpha 1
30
In alpha 1 adrenreceptors, NE causes __________
vasoconstriction in smooth muscle and increased contractility in the heart
31
Which adrenergic receptor is located on presynaptic cells and regulates NE?
alpha 2
32
Activation of alpha 2 (increases/decreases) NE release?
decreases
33
Which adrenergic receptor is located in the heart, kidney, and adipose tissue?
beta 1
34
Activation of beta 1 causes _____________
increases in HR and force of contraction, stimulates lipolysis in fat cells, and stimulates renin activity from the kidney
35
What is the rate limiting step in the RAAS?
production of renin
36
What is the function of renin?
angiotensinogen to angiotensin I
37
What is the function of angiotensin converting enzyme (ACE)?
converts angiotensin I to angiotensin II
38
What cleaves peptides such as bradykinin, LH releasing hormone, and substance P?
ACE
39
What receptors does Ang II have?
AT1 receptor and AT2 receptor
40
Which receptor increases vasoconstriction, aldosterone secretion, sodium reabsorption, and release of ADH?
AT1 receptor
41
Which receptor stimulates formation of superoxide?
AT1
42
What is the function of superoxide?
deactivates NO
43
What is the function of NO?
causes vasodilation
44
What is the function of the AT2 receptor?
antagonizes the effects of AT1 (causes vasodilation and natiuresis)
45
Why is HTN more prevalent in AAs?
they have tissues that can produce Ang II independent of the RAAS
46
What does Ang II do?
increases BP
47
Tissue Ang II contributes to __________
blood pressure, inflammation, fibrosis, and remodeling
48
What is the function of the ANS?
monitors and regulates HR, blood flow, and BP
49
What is the function of the medulla?
maintains SNS activity using information from baroreceptors and chemoreceptors
50
What is the function of the hypothalamus?
regulates BP using neurohormonal feedback
51
What is the function of cortical/subcortical areas?
effect CV function based on emotion and stress
52
Name the arterial baroreceptors
- stretch receptors
| - mechanoreceptors or "high pressure" receptors
53
Where are the arterial baroreceptors located?
- aortic arch
- carotid bifurcation
- kidney
54
What does the baroreceptor reflex do?
decreases in MAP result in result in decreased stretch in arteries and decreased baroreceptor stimulation
55
What is the result from decreased baroreceptor stimulation?
decreased nerve signals to the medulla oblongata
56
What is the result of decreased nerve signals to the medulla due to decreased baroreceptor stimulation?
decrease in parasympathetic outflow and an increase in sympathetic outflow
57
What is the function of postganglionic nerve fibers from the baroreceptor reflex?
innervate the heart and blood vessels to release NE
58
What are the "low pressure" receptors?
cardiopulmonary receptors
59
Where are cardiopulmonary receptors located?
- cardiac atria
- ventricles
- lungs
60
What is essential HTN known as and what percentage of people does it effect?
primary HTN; 95%
61
What is the cause of essential HTN?
it is idiopathic or unknown
62
What is the cause of secondary HTN and what percentage of people does it effect?
related to a specific, known cause; 5%
63
What are some disease states that are related to HTN?
CKD, obstructive sleep apnea (OSA), aldosteronism, renal artery stenosis, thyroid disease, and pheochromocytoma
64
What are some common medications related to HTN?
amphetamines, corticosteroids, decongestants, estrogen, NSAIDs
65
What are some other factors that lead to HTN?
nicotine, cocaine, sodium, low potassium diet, and increase BP
66
What is the predominant form of HTN in adolescents and young adults?
isolated systolic HTN (ISH)
67
What is the cause of ISH?
increased stroke volume
68
ISH increases again in PTs >50 years of age due to ___________
vascular stiffness
69
What is the reasoning behind increased ISH in PTs over 50 yo?
rise in SBP, decrease in DBP, thus a rise PP
70
What is the predominant form of HTN in those aged 30-50?
diastolic HTN
71
What causes diastolic HTN?
increased vascular resistance (decreased elastin, increased collagen and calcium deposits in arteries)
72
What is a major predictor of IHD before age 50?
diastolic HTN
73
(Central/Peripheral) obesity is more closely associated with HTN than (central/peripheral) obesity
Central; peripheral
74
What is the function of insulin?
increases sodium and water retention, increases adrenergic activity, and causes smooth muscle hypertrophy
75
What happens with insulin resistance?
diminishes insulin-mediated vasorelaxation
76
What do obese patients have that largely distributes centrally?
higher total body volume
77
What does increases fluid volume cause?
increased ventricular filling and cardiac output
78
Sympathetic activity in the kidneys is likely related to ___________
elevated leptin levels
79
Where is leptin produces and what is its function?
located in adipose tissue and regulates food intake
80
What does leptin do that causes an elevated BP?
increases sympathetic outflow
81
What is the effect of chronic infusion of leptin?
decreases natiuresis and NO production
82
BMI is correlated with ___________
increased plasma angiotensinogen, renin activity, ACE concentration and aldosterone
83
What initiates/maintains the low-grade inflammation present in HTN?
inflammatory cytokines released from adipose tissue
84
What is a common cause of resistant HTN?
sleep apnea
85
What triggers an increase in sympathetic activity?
decreased oxygenation due to apnea
86
What is present during sleep and wakeful periods?
increased sympathetic activity
87
What aspects of the RAAS are associated with OSA?
elevated ang II and aldosterone
88
What impairs endothelin function?
hypoxia (endothelin increases, NO decreases)
89
What kind of vascular remodeling is associated with OSA?
OSA leads to increased carotid intima-media thickness and arterial stiffness
90
True of false: most patients are asymptomatic when it comes to HTN?
true
91
What type of organ damage can occur with the heart with HTN?
- left ventricular hypertrophy and diastolic dysfunction
- chronic HF
- vascular remodeling and microvascular changes
- oxidative stress
- endothelial dysfunction
92
What type of organ damage can occur with the brain in HTN?
- stroke/TIA
- hypertensive encephalopathy
- cognitive impairment and dementia
93
What type of organ damage can occur with the kidney in HTN?
- nephrosclerosis
| - CKD
94
True or false? Diagnosis of HTN requires 3 or more separate readings
False; 2 readings
95
What is resistant HTN?
inability to achieve BP goals with 3 or more antihypertensive agents including a diuretic
96
What should a patient do with their diet if they are hypertensive?
- salt reduction
- increase potassium
- increase fresh fruits and veggies
97
Where do thiazides bind?
bind to receptors on the luminal side of the DCT
98
What is the function of thiazides?
compete for the Cl binding site and thus inhibit the Na, Cl symporter causing increased secretion of Na, Cl, H2O, and K
99
What is the starting/max dose for thiazides and when should they be taken?
12.5-25 mg/day in pm/HS
100
What can decrease the efficacy of thiazides?
CrCl
101
Where do the loop diuretics bind?
bind receptors on the luminal side of the thick ascending limb of the loop of Henle
102
What is the function of the loops?
compete for the Cl binding site of the Na, K, 2Cl symporter causing increased excretion of Na, Cl, H20, K, Ca, and Mg
103
What is the function of Na channel blockers (amiloride, triamterene)?
block Na channels in the late distal tubule and collecting duct; rarely used for HTN alone
104
Where do the aldosterone inhibitors (spironolactone, eplerenone) bind?
bind the mineralocorticoid receptor in the late distal tubule and collecting duct
105
What is the effect of the aldosterone inhibitors?
blockade of Na movement from luminal to interstitial space through Na channels and pumps
106
When should aldosterone antagonists be used?
they are rarely used unless other comorbidities exist such as HF, alcohol liver disease, post-MI, refractory HTN
-can be useful in resistant HTN
107
Which medication can cause gynecomastia?
spironolactone
108
What is the MOA of ACE inhibitors?
- inhibits conversion of ang I to ang II
| - inhibits conversion of active bradykinin to inactive bradykinin
109
What is the function of active bradykinin and what is its result?
stimulates NO and prostaglandin release; result is vasodilation and Na excretion
110
Which class of drugs is most useful for renal protection in patients with DM by decreasing glomerular filtration pressures?
ACE-Is
111
ACE-Is are less effective in _______ due to lower renin release
african americans
112
What are some side effects associated with the ACE-Is?
- cough due to bradykinin build up in lungs
- hyperkalemia
- acute renal failure
- hypotension
- angioedema (more common in AAs)
113
What is the MOA for ARBs?
inhibits the effects of ang II at its various sites of action
- decrease SVR
- increase Na and H20 excretion
114
What is the MOA for direct renin inhibitors?
inhibits the conversion of angiotensinogen to ang I via direct renin inhibition
- decrease SVR
- increase Na and H20 excretion
115
What class of drug is contraindicated with ACE-I or ARB?
direct renin inhibitor
116
What is the MOA for CCBs?
blocks transmembrane influx of calcium into smooth muscle (heart and vascular muscles)
117
Which type of CCB is more selective for vascular smooth muscle?
dihydropyridine (amlodipine/felodipine)
118
Which type of CCB is more likely to have a depressant effect on the heart and can lead to leaky vasculature which will lead to edema?
non-dihydropyridine (verapamil/diltiazem)
119
Which CCB should not be used in heart failure or in conjunction with BBs?
non-dihydropyridine
120
What is the MOA of beta blockers?
- decrease NE binding at beta 1 receptors resulting in decreased HR and CO
- decrease renin release due to beta 1 blockade in kidneys
121
In which type of patient should a beta 1 selective BB such as metoprolol be used in?
patient with asthma/COPD due to potential for beta 2 blockade
122
What is the MOA for the alpha 2 agonist (clonidine)?
- centrally acting
| - decreases CO by decreasing HR and SVR through decreased sympathetic activity
123
What is the MOA for alpha 1 antagonists (doxazosin/terazosin)?
block postsynaptic alpha 1 receptors resulting in vasodilation and decreases SVR
-located postsynaptically in the vasculature
124
Which class of drug can be used to treat BPH in men?
alpha 1 antagonists
125
Which class of drug can be used to help with PTSD?
alpha 1 antagonists
126
What is the MOA for methyldopa?
centrally acting agent that decreases SVR as well as HR and CO to some extent
127
Which drug is preferred for HTN during pregnancy?
methyldopa
128
Which drug(s) is a direct arteriolar vasodilator?
- hydralazine
| - minoxidil
129
Which drug is used more commonly in HR and hypertensive crisis?
hydralazine
130
Is minoxidil or hydralazine more potent of the arteriolar vasodilators?
minoxidil
131
Which arteriolar vasodilator stimulates hair growth?
minoxidil
132
What is the MOA of reserpine?
depletes central and peripheral stores of NE, DA, and 5-HT. BP lowering is accomplished through decreased sympathetic activity
133
Which drug frequently causes sedation, mental depression, and parkinsonian symptoms?
reserpine
134
HOPE
ramipril reduced incidence of CV events and death in high risk patients including patients with diabetes and prior stroke
135
ALLHAT
Patients either give chlorthalidone, amlodipine, or lisinopril. Primary outcome is combined fatal CHD or non-fatal MI
136
ONTARGET
telmisartan and ramipril have similar outcomes with regard to renal protection; combination therapy is not warranted although it may decrease albuminuria
137
RENAAL
ARBs are effective for treating patients with type 2 DM and nephropathy though they have not been shown to reduce mortality
138
PROGRESS
ACE-I with a diuretic for secondary stroke prevention
139
When should aspirin be administered to a patient with DM?
should only be initiated when BP is controlled due to increased risk of hemorrhagic stroke
