HTN - VanRijn Flashcards
1
Q
HTN is: \_\_\_\_ measurements of Bp with a diastolic pressure >\_\_\_\_\_ or Systolic > \_\_\_\_\_ or Resting Pulse Pressure (SBP-DBP) > \_\_\_\_
A
2 or more
D: > 90 mmHg
S: > 140 mmHg
RBP: > 65 mmHg
2
Q
Primary Or Secondary HTN?
Lifestyle
A
Primary
3
Q
Examples of Lifestyle that can affect HTN
A
Excess body weight; Smoking alcohol; excess sodium/too little K+
lack of exercise/sedentary lifestyle
4
Q
Primary Or Secondary HTN?
Hyperlipidemia
A
Primary
5
Q
Primary Or Secondary HTN?
Depression
A
primary
6
Q
Primary Or Secondary HTN?
Age
A
primary
7
Q
HTN (decreases or increases) with age
A
increases
8
Q
If someone is over ____ years old and has a SBP > _____ then they are at a high CVD risk
A
50; 140
9
Q
Primary Or Secondary HTN?
Sex
A
Primary
10
Q
Men are more likely to have HTN in what age range
A
< 55
11
Q
Women are more likely to have HTN in what age range
A
> 55
12
Q
Primary Or Secondary HTN?
genes (family hx)
A
primary
13
Q
Primary Or Secondary HTN?
Race (African Americans more common to have HTN)
A
Primary
14
Q
Primary Or Secondary HTN?
Kidney Disease
A
Secondary
15
Q
Primary Or Secondary HTN?
Renal Artery Constriction
A
Secondary
16
Q
What are some examples of kidney issues that can cause SECONDARY HTN
A
Stenosis; Cysts; Glomerulonephritis
17
Q
Primary Or Secondary HTN?
Tumors
A
Secondary
18
Q
Primary Or Secondary HTN?
Pheochromocytoma
A
Seconary
19
Q
what is Pheochromocytoma?
A
tumor on adrenal gland/ will cause increase in adrenanline
20
Q
Primary Or Secondary HTN?
Endocrine disease
A
secondary
21
Q
what are some endocrine diseases that lead to secondary HTN
A
Cushings Syndrome; Conn’s Syndrome
22
Q
Why does cushing syndrome lead to HTN
A
excessive secretion of gluocorticoids –> increase in BP
23
Q
why does Conn’s syndrome lead to HTN
A
Excessive production of aldosterone (aka hyperaldosteronism)
24
Q
Primary Or Secondary HTN?
Coarctation of the aorta
A
Secondary
25
Primary Or Secondary HTN?
| Pregnancy
Secondary
26
Primary Or Secondary HTN?
| Medication Side Effects
Secondary
27
what are some common meds/side effects that will lead to secondary HTN
High estrogen oral contraceptives; Antidepressants (Clozapine, venlafaxine); Rebound HTN!
28
Diabetes and HTN:
| _____ and _____ lead to vascular damages
Glucose; Fat
29
Diabetes & HTN:
| ___________ can lead to orthostatic HTN
autonomic neuropathy
30
Diabetes & HTN:
| Diabetic Nephropathy can lead to HTN - what is the proposed idea to explain this?
- RAAS system is affected; there is increased oxidative stress; SNS (sodium retention sympathetic nervous system is affected)
31
Chronic HTN is damaging to ______ organs
end
32
"End Organs" are heavily enervated by _______
small vessels
33
What are some end organs that can be affected/damaged by Chronic HTN
Heart, Kidney, Brain, Eyes
34
Blood Pressure = ____ x _____
CO (cardiac Output); PVR (Peripheral Vascular Resistnace)
35
Goals of Pharmacotherapy of HTN:
| Reduce what 3 things
- SYSTOLIC BP (diastolic not as predictive of mortality)
- Cardiac OUtput
- Vascular Resistance
36
The Baroreceptor Reflex:
| Vascular resistance is primarily controlled by ______
SANS (Sympathetic autonomic .....)
37
Cardiac Output = what symbol?
Q
38
Cardiac output is also known as blood ______
flow
39
Cardiac output (or blood flow Q) is made up of what two things?
SV (stroke volume) x HR (heart rate)
40
Baroreceptors located by ________ are important in sensing BP by the _____ in the arteries to keep homeostasis
aortic arch; stretch
41
Chemoreceptors sense changes in what things?
pH; CO(2); O(2)
42
How does the body compensate when chemoreceptors notice low O2
it stimulates SNS/increase HR/cause vasoconstriction
43
How does the body compensate when chemoreceptors notice high O2
decrease HR
44
How does the body compensate when chemoreceptors notice low CO2
decrease HR (Low CO2 = High O2)
45
How does the body compensate when chemoreceptors notice high CO2
this means low O2 and then it stimulates SNS/increase HR/cause vasoconstriction
46
4 main targets for antihypertensive
- Heart
- Resistant arterioles
- Veins (SANS)
- Kidney
47
How does the body compensate when chemoreceptors notice low pH
stimulates SNS/increase HR/cause vasoconstriction
48
ANS:
| Notable signalers of parasympathetic system
Muscarine and Nicotine
(Ach too)
aka
Cholinergic
49
ANS:
| Notable signalers of Sympathetic system
Norepinephrine
Epinephrine
(Adrenergic Receptors)
50
ANS:
| All ______ nerves release ______ onto _______ that are expressing ______ receptors
PREGANG neurons; release Ach; postgang; nicotinic receptors
| this is for BOTH parasympathetic and sympathetic
51
Parasympathetic or Sympathetic ?
| Postganglionic nerves release Ach onto muscarinic receptors
PARASYM
52
Parasympathetic or Sympathetic ?
| Postganglionic nerves primarily release NE that will bind to adrenergic receptors
Sympathetic
53
There are postganglionic nerves in the kidney that release ______ to ______ receptors that will cause _________
release dopamine; to bind to dopamine (D1) receptors; which will cause vasodilation
54
Receptors/Signal Transduction in the ANS:
| What are the possible options
Gs; Gi; Gq
55
Beta receptors use which pathway?
| Gs or Gi or Gq
Gs
56
Alpha1 receptors use which pathway?
| Gs or Gi or Gq
Gq
57
Activation of sympathetic nerves causes release of _________ from adrenals
epi/norepi
58
Activation of sympathetic nerves causes release of epi/norepi from ________
adrenals
59
Does the receptor do relaxation or contraction?
| Alpha1
contraction (vasoconstriction)
60
Does the receptor do relaxation or contraction?
| Beta2
relaxation (vasodilation)
61
Signal transduction through M3 receptor - causes vaso______ and is done via _____
vasoDILATION; via NO
62
Chronotropic Effects:
______ of contraction
and
________
Rate; SA Node cells
63
Ionotropic Effects:
_____ of contraction
and
__________
force; cardiomyocytes
64
What are the two primary ANS receptors that work in the heart?
M2 and B1
65
G__ coupled beta receptors cause an increase in _____ and ______
Gs; heart rate; force of contraction
66
B1 Receptor in Kidney:
| Sympathetic activation causes secretion of _____ which will ______
renin; increase blood pressure
67
B1 receptors are found in _______ cells in the kidney
Juxtaglomerular
68
Renal/Dopamine System:
| Dopamine is made in the ________
Proximal tubules
69
_______ causes natriusesis
Dopamine
70
Dopamine acts on the ____ exchanger in the _________ - which is a transporter that plays an important role in the entry of filtered sodium into the cell
Na-H; luminal membrane
71
Sympathomimetics or Sympatholytics cause a decrease in Blood Pressure...
Sympatholytics
72
What are the options/classes of Sympatholytics that can be used to decrease blood pressure
- Alpha 1 antagonist
- alpha 2 agonists
- catecholamine depleters
- beat-blockers
73
T or F: Sympatholytic drugs are not used as 1st line treatment
TRUE (used as like 3rd or 4th line)
74
Primary use for sympatholytic drugs?
used for rescue hypertensives/"in patient" setting
75
Sympatholytics: short or long acting
short acting
76
Sympatholytics: will reduce sudden _____ in BP
spikes (they are short acting/used for rescues)
77
Why are Sympatholytic drugs not too effective as monotherapy?
due to homeostatic nature of ANS on BP via baroreceptor reflex
78
Avoid sympatholytics drug sin what patients?
pregnant/breast feeding
79
Monitor what types of patients that are using Sympatholytic Drugs
Angina; Parkinsons
80
What drugs are alpha 1 antagonists?
-Osins
| Prazosin; Terazosin; Doxazosin
81
Primary use for alpha 1 antagonists?
BPH! (bc it relaxes urinary sphincter muscles)
82
alpha 1 antagonists are good for BPH; it can also be good for patients with _________
phaechromocytoma
83
Alpha 1 antagonists may reduce _______ levels
cholesterol
84
Side Effects of alpha 1 antagonists?
- slight tachycardia
- first dose orthostatic hypotension
(this is due to increase blood volume)
85
alpha 1 receptors are found around the _____ which leads to one of their common uses
urethra (aka a med for BPH)
86
Non-Selective alpha blockers
- phentolamine
| - phenoxybenzamine
87
Which non-seletctive alpha blocker is REVERSIBLE
phentolamine
88
Which non-seletctive alpha blocker is IRREVERSIBLE
phenoxybenzamine
89
a nonselective alpha blocker will also block alpha 2 receptor which leads to the prevention of ________
prevents alpha 2 receptor negative feedback of NE (blocking a2 = causes more release of NE)
90
a nonselective alpha blocker will also block alpha 2 receptor which leads to what two side effects?
reflex tachycardia; arrhtymias
91
what drugs will work on the a2 receptors in the CNS to inhibit NE release
- Methyldopa
- Clonidine
- Guanabenz
- Guanfacine
92
why do a2 receptor agonist drugs work to decrease BP
they prevent the release of NE (NE will lead to an increase in BP)
93
which sympatholytic drugs can be used in pregnant women?
methyldopa; labetalol
94
what drug is known as a catecholamine depleter
Reserpine (Serpasil)
95
Reserpine's MOA ?
Irreversibly blocks VMAT (vesicular monoamine transporter)
it depletes Neurotransmitter vesicles of Dopamine (DA) & NE
96
Side effects of Reserpine?
GI & CNS
GI: Diarrhea; Cramps; Acid Secretion
CNS: Sedation; nightmares; depression
97
1st generation beta blockers block ______
B1 & B2
98
Propranolol:
| Reduces _______ & ______ & _______
reduces HR; Stroke volume; Renin release via B1 in kidney!
99
What are the partial agonist/1st generation/beta blockers
pindolol; acebutalol
100
What are 1st generation beta blockers primarily used for now?
angina
cardiac arrhythmia
reduce tremors
101
Side Effects of 1st generation beta blockers
- bradycardia
- AV block
- Hypotension
- bronchospasms(B2 effect)
- sedation
- rebound tachycardia
102
Which drug is contraindicated in pts with Asthma, COPD & CHF
1st gen beta blockers (ex: Propranolol)
103
which drug can increase risk for diabetes?
1st gen beta block (propranolol) because it blocks insulin release from pancrease and glucose release from liver
104
T or F: Partial agonist beta blockers have LESS bradycardia response than propranolol
TRUE! (b/c only a partial agonist)
105
what is nifty about 2nd gen beta blockers?
they are CARDIOSELECTIVE aka no beta 2 blocking
106
what are the 2nd gen beta blockers
metoprolol tartrate
metoprolol succinate
Atenolol
107
Metoprolol tartrate or Succinate?
| Which one is long acting
succinate (brand is Toprol XL)
108
what are the 3rd gen of beta blockers?
Nebivolol; Betaxolol
109
what is Nebivolol (Bystolic) "special" property other than being cardioselective
it will also induce vasodilation via Nitric Oxide
110
what is Betaxolol (Betoptic) "special" property other than being cardioselective
induces vasodilation via calcium channel blocking
111
which drugs are non-selective beta blockers but also block alpha 1
carvedilol; labetalol
112
what is max dose of carvedilol
25 mg
113
why is it useful for carvediolol and labetalol to be non-selective beta blockers &block alpha 1
beta blocking activity prevents reflex receptor antagonist tachycardia which is seen in alpha 1 receptor antagonists
114
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one does vasoconstriction?
```
alpha1
115
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
does mydriasis
```
alpha 1
116
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
causes vasodilation?
```
b2
117
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
causes an increase in blood pressure
```
alpha 1 (b1 indirectly via renin)
118
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
inhibits release of NE
```
alpha 2
119
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
increases release of renin
```
beta1
120
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
cause increased closure of internal sphincter of the bladder
```
alpha 1
121
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
causes relaxation of uterine smooth muscle
```
Beta2
122
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
inhibits Ach release
```
alpha 2
123
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one increase lipolysis
```
beta 1
124
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one increases myocardial contractility
```
beta 1
125
what "things" does alpha 2 adrenoreceptor do upon activation
- - inhibit NE release
- inhibit Ach release
- inhibit of insulin release
126
what "things" does beta 1 adrenoreceptor do upon activation
- tachycardia
- increased lipolysis
- increased myocardial contractility
- increased renin release
127
what "things" does alpha 1 adrenoreceptor do upon activation
- vasoconstriction
- increased peripheral resistance
- increased BP
- mydriasis
- increase closure of internal sphincter of the bladder
128
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
increases muscle and liver glycogenolysis
```
beta 2
129
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one increases release of glucagon
```
beta 2
130
```
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
relaxes uterine smooth muscle
```
beta 2
131
3 main types of diuretics used for blood pressure
loop diuretics; thiazide; K+ sparing
132
where (in the kidney) is the largest bulk of sodium reabsorbed?
proximal tubule
133
where (in the kidney) is the second largest bulk of sodium reabsorbed?
loop of henle
134
where do K+ sparing diuretics work?
collecting tubule
135
where do thiazide drugs work?
distal convoluted tubule
136
ascending limb in the loop of henle is permeable to ________
ions/solutes (Na+, Cl-)
137
descending limb in the loop of henle is permeable to ________
water
138
Renin is released from ________ cells in the _____
juxtaglomerular cells in the kidney
139
what are possible reasons that renin would be released?
- due to drop in blood pressure
- due to low NaCl
- due to activation of specific receptors
140
Where are juxtaglomerular cells found? (not in kidney but b/w what things)
b/w glomerulus and macula densa
141
Renin is released into blood stream and it will metabolize _________ into ______
angiotensinogen; angiotensin 1
142
Angiotensin 1 gets converted to _________ by the ______ enzyme
converted to angiotensin 2; by ACE enzyme!
143
where does the ACE enzyme come from?
from pulmonary endothelial cells
144
Angiotensin will cause vaso________ and release of ________ from _____ medulla
vasoconstriction; release aldosterone from adrenal medulla
145
To inhibit release of renin, ______ can be released from _____ gland - it will lead to water absorption in collecting duct
antidiuretic hormone; pituitary
146
Aldosterone increases ______ levels and _____ in the kidney
plasma salt levels; volume
147
```
Angiotensin II - why does it increase BP?
1 - stimulates _______ to release ______
2- causes vaso______ in smooth muscle
3- activates ______ center (_____ gland)
4 - can modulate the _________
5 - causes CV __________
```
stimulates adrenal cortex to release aldosterone
vasoCONSTRICTION
activates thirst center (pituitary glad)
module baroreceptor reflex
causes CV hypertrophy
148
which drug class prevents the making of angiotensin II
ACE Inhibitors (ACE will make angiotensin II)
149
2 ways to indirectly inhibit renin release
- loop diuretics (prevent low Na+ induced release)
| - B1 blockers
150
Which ACE inhibitor is very short acting (< 3 hrs)
Captopril
151
Is lisinopril or enalapril a prodrug?
enalapril
152
what type of drug is Aliskiren?
Renin Inhibitor
153
Can you use ACEIs in pregnant women?
No!
154
ACEIs are typically not used in patients with a _________ value > _____
serum creatinine > 2.5
155
What are some drug interactions for ACEIs?
- food/antacids may reduce bioavailability
- NSAIDs reduce effectiveness
- K+ supplements - hyperkalemia risk
- increase plasma levels of digoxin/lithium
156
NSAIDs make ACEIs less effective because?
NSAIDs inhibit production of prostaglandins which can act as vasodilators
157
There are _____ subtypes of Angiotensin receptors
2
158
What are the 2 subtypes of Angiotensin receptors
AT1 and AT2
159
AT1 and AT2 are ______ receptors
G protein coupled
160
```
Effects of AT1
activating _______ channels
Reduce ____ synthesis
Vaso_______ of smooth muscle
Increase in _________ production
```
activates Ca2+; reduce NO; vasoCONSTRICTION; aldosterone
| all above are why we want to block Ang II to work on AT1
161
which drug class blocks Angiotensin from working on AT1
ARB's (-sartans) aka Angiotensin Receptor Type 1 blockers
162
which drug class will reduce gout risk? and how?
ARBs; by blocking urate transporter
