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Therapeutics 2 - Fall 2017 > HTN - VanRijn > Flashcards

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

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2
Q

Primary Or Secondary HTN?

Lifestyle

A

Primary

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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

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4
Q

Primary Or Secondary HTN?

Hyperlipidemia

A

Primary

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5
Q

Primary Or Secondary HTN?

Depression

A

primary

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6
Q

Primary Or Secondary HTN?

Age

A

primary

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7
Q

HTN (decreases or increases) with age

A

increases

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8
Q

If someone is over ____ years old and has a SBP > _____ then they are at a high CVD risk

A

50; 140

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9
Q

Primary Or Secondary HTN?

Sex

A

Primary

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10
Q

Men are more likely to have HTN in what age range

A

< 55

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11
Q

Women are more likely to have HTN in what age range

A

> 55

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12
Q

Primary Or Secondary HTN?

genes (family hx)

A

primary

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13
Q

Primary Or Secondary HTN?

Race (African Americans more common to have HTN)

A

Primary

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14
Q

Primary Or Secondary HTN?

Kidney Disease

A

Secondary

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15
Q

Primary Or Secondary HTN?

Renal Artery Constriction

A

Secondary

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16
Q

What are some examples of kidney issues that can cause SECONDARY HTN

A

Stenosis; Cysts; Glomerulonephritis

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17
Q

Primary Or Secondary HTN?

Tumors

A

Secondary

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18
Q

Primary Or Secondary HTN?

Pheochromocytoma

A

Seconary

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19
Q

what is Pheochromocytoma?

A

tumor on adrenal gland/ will cause increase in adrenanline

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20
Q

Primary Or Secondary HTN?

Endocrine disease

A

secondary

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21
Q

what are some endocrine diseases that lead to secondary HTN

A

Cushings Syndrome; Conn’s Syndrome

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22
Q

Why does cushing syndrome lead to HTN

A

excessive secretion of gluocorticoids –> increase in BP

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23
Q

why does Conn’s syndrome lead to HTN

A

Excessive production of aldosterone (aka hyperaldosteronism)

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24
Q

Primary Or Secondary HTN?

Coarctation of the aorta

A

Secondary

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25
Q

Primary Or Secondary HTN?

Pregnancy

A

Secondary

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26
Q

Primary Or Secondary HTN?

Medication Side Effects

A

Secondary

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27
Q

what are some common meds/side effects that will lead to secondary HTN

A

High estrogen oral contraceptives; Antidepressants (Clozapine, venlafaxine); Rebound HTN!

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28
Q

Diabetes and HTN:

_____ and _____ lead to vascular damages

A

Glucose; Fat

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29
Q

Diabetes & HTN:

___________ can lead to orthostatic HTN

A

autonomic neuropathy

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30
Q

Diabetes & HTN:

Diabetic Nephropathy can lead to HTN - what is the proposed idea to explain this?

A
  • RAAS system is affected; there is increased oxidative stress; SNS (sodium retention sympathetic nervous system is affected)
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31
Q

Chronic HTN is damaging to ______ organs

A

end

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32
Q

“End Organs” are heavily enervated by _______

A

small vessels

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33
Q

What are some end organs that can be affected/damaged by Chronic HTN

A

Heart, Kidney, Brain, Eyes

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34
Q

Blood Pressure = ____ x _____

A

CO (cardiac Output); PVR (Peripheral Vascular Resistnace)

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35
Q

Goals of Pharmacotherapy of HTN:

Reduce what 3 things

A
  • SYSTOLIC BP (diastolic not as predictive of mortality)
  • Cardiac OUtput
  • Vascular Resistance
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36
Q

The Baroreceptor Reflex:

Vascular resistance is primarily controlled by ______

A

SANS (Sympathetic autonomic …..)

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37
Q

Cardiac Output = what symbol?

A

Q

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38
Q

Cardiac output is also known as blood ______

A

flow

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39
Q

Cardiac output (or blood flow Q) is made up of what two things?

A

SV (stroke volume) x HR (heart rate)

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40
Q

Baroreceptors located by ________ are important in sensing BP by the _____ in the arteries to keep homeostasis

A

aortic arch; stretch

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41
Q

Chemoreceptors sense changes in what things?

A

pH; CO(2); O(2)

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42
Q

How does the body compensate when chemoreceptors notice low O2

A

it stimulates SNS/increase HR/cause vasoconstriction

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43
Q

How does the body compensate when chemoreceptors notice high O2

A

decrease HR

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44
Q

How does the body compensate when chemoreceptors notice low CO2

A

decrease HR (Low CO2 = High O2)

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45
Q

How does the body compensate when chemoreceptors notice high CO2

A

this means low O2 and then it stimulates SNS/increase HR/cause vasoconstriction

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46
Q

4 main targets for antihypertensive

A
  • Heart
  • Resistant arterioles
  • Veins (SANS)
  • Kidney
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47
Q

How does the body compensate when chemoreceptors notice low pH

A

stimulates SNS/increase HR/cause vasoconstriction

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48
Q

ANS:

Notable signalers of parasympathetic system

A

Muscarine and Nicotine
(Ach too)
aka
Cholinergic

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49
Q

ANS:

Notable signalers of Sympathetic system

A

Norepinephrine
Epinephrine
(Adrenergic Receptors)

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50
Q

ANS:

All ______ nerves release ______ onto _______ that are expressing ______ receptors

A

PREGANG neurons; release Ach; postgang; nicotinic receptors

this is for BOTH parasympathetic and sympathetic

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51
Q

Parasympathetic or Sympathetic ?

Postganglionic nerves release Ach onto muscarinic receptors

A

PARASYM

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52
Q

Parasympathetic or Sympathetic ?

Postganglionic nerves primarily release NE that will bind to adrenergic receptors

A

Sympathetic

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53
Q

There are postganglionic nerves in the kidney that release ______ to ______ receptors that will cause _________

A

release dopamine; to bind to dopamine (D1) receptors; which will cause vasodilation

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54
Q

Receptors/Signal Transduction in the ANS:

What are the possible options

A

Gs; Gi; Gq

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55
Q

Beta receptors use which pathway?

Gs or Gi or Gq

A

Gs

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56
Q

Alpha1 receptors use which pathway?

Gs or Gi or Gq

A

Gq

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57
Q

Activation of sympathetic nerves causes release of _________ from adrenals

A

epi/norepi

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58
Q

Activation of sympathetic nerves causes release of epi/norepi from ________

A

adrenals

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59
Q

Does the receptor do relaxation or contraction?

Alpha1

A

contraction (vasoconstriction)

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60
Q

Does the receptor do relaxation or contraction?

Beta2

A

relaxation (vasodilation)

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61
Q

Signal transduction through M3 receptor - causes vaso______ and is done via _____

A

vasoDILATION; via NO

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62
Q

Chronotropic Effects:
______ of contraction
and
________

A

Rate; SA Node cells

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63
Q

Ionotropic Effects:
_____ of contraction
and
__________

A

force; cardiomyocytes

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64
Q

What are the two primary ANS receptors that work in the heart?

A

M2 and B1

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65
Q

G__ coupled beta receptors cause an increase in _____ and ______

A

Gs; heart rate; force of contraction

66
Q

B1 Receptor in Kidney:

Sympathetic activation causes secretion of _____ which will ______

A

renin; increase blood pressure

67
Q

B1 receptors are found in _______ cells in the kidney

A

Juxtaglomerular

68
Q

Renal/Dopamine System:

Dopamine is made in the ________

A

Proximal tubules

69
Q

_______ causes natriusesis

70
Q

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

A

Na-H; luminal membrane

71
Q

Sympathomimetics or Sympatholytics cause a decrease in Blood Pressure…

A

Sympatholytics

72
Q

What are the options/classes of Sympatholytics that can be used to decrease blood pressure

A
  • Alpha 1 antagonist
  • alpha 2 agonists
  • catecholamine depleters
  • beat-blockers
73
Q

T or F: Sympatholytic drugs are not used as 1st line treatment

A

TRUE (used as like 3rd or 4th line)

74
Q

Primary use for sympatholytic drugs?

A

used for rescue hypertensives/”in patient” setting

75
Q

Sympatholytics: short or long acting

A

short acting

76
Q

Sympatholytics: will reduce sudden _____ in BP

A

spikes (they are short acting/used for rescues)

77
Q

Why are Sympatholytic drugs not too effective as monotherapy?

A

due to homeostatic nature of ANS on BP via baroreceptor reflex

78
Q

Avoid sympatholytics drug sin what patients?

A

pregnant/breast feeding

79
Q

Monitor what types of patients that are using Sympatholytic Drugs

A

Angina; Parkinsons

80
Q

What drugs are alpha 1 antagonists?

A

-Osins

Prazosin; Terazosin; Doxazosin

81
Q

Primary use for alpha 1 antagonists?

A

BPH! (bc it relaxes urinary sphincter muscles)

82
Q

alpha 1 antagonists are good for BPH; it can also be good for patients with _________

A

phaechromocytoma

83
Q

Alpha 1 antagonists may reduce _______ levels

A

cholesterol

84
Q

Side Effects of alpha 1 antagonists?

A
  • slight tachycardia
  • first dose orthostatic hypotension
    (this is due to increase blood volume)
85
Q

alpha 1 receptors are found around the _____ which leads to one of their common uses

A

urethra (aka a med for BPH)

86
Q

Non-Selective alpha blockers

A
  • phentolamine

- phenoxybenzamine

87
Q

Which non-seletctive alpha blocker is REVERSIBLE

A

phentolamine

88
Q

Which non-seletctive alpha blocker is IRREVERSIBLE

A

phenoxybenzamine

89
Q

a nonselective alpha blocker will also block alpha 2 receptor which leads to the prevention of ________

A

prevents alpha 2 receptor negative feedback of NE (blocking a2 = causes more release of NE)

90
Q

a nonselective alpha blocker will also block alpha 2 receptor which leads to what two side effects?

A

reflex tachycardia; arrhtymias

91
Q

what drugs will work on the a2 receptors in the CNS to inhibit NE release

A
  • Methyldopa
  • Clonidine
  • Guanabenz
  • Guanfacine
92
Q

why do a2 receptor agonist drugs work to decrease BP

A

they prevent the release of NE (NE will lead to an increase in BP)

93
Q

which sympatholytic drugs can be used in pregnant women?

A

methyldopa; labetalol

94
Q

what drug is known as a catecholamine depleter

A

Reserpine (Serpasil)

95
Q

Reserpine’s MOA ?

A

Irreversibly blocks VMAT (vesicular monoamine transporter)

it depletes Neurotransmitter vesicles of Dopamine (DA) & NE

96
Q

Side effects of Reserpine?

A

GI & CNS
GI: Diarrhea; Cramps; Acid Secretion
CNS: Sedation; nightmares; depression

97
Q

1st generation beta blockers block ______

98
Q

Propranolol:

Reduces _______ & ______ & _______

A

reduces HR; Stroke volume; Renin release via B1 in kidney!

99
Q

What are the partial agonist/1st generation/beta blockers

A

pindolol; acebutalol

100
Q

What are 1st generation beta blockers primarily used for now?

A

angina
cardiac arrhythmia
reduce tremors

101
Q

Side Effects of 1st generation beta blockers

A
  • bradycardia
  • AV block
  • Hypotension
  • bronchospasms(B2 effect)
  • sedation
  • rebound tachycardia
102
Q

Which drug is contraindicated in pts with Asthma, COPD & CHF

A

1st gen beta blockers (ex: Propranolol)

103
Q

which drug can increase risk for diabetes?

A

1st gen beta block (propranolol) because it blocks insulin release from pancrease and glucose release from liver

104
Q

T or F: Partial agonist beta blockers have LESS bradycardia response than propranolol

A

TRUE! (b/c only a partial agonist)

105
Q

what is nifty about 2nd gen beta blockers?

A

they are CARDIOSELECTIVE aka no beta 2 blocking

106
Q

what are the 2nd gen beta blockers

A

metoprolol tartrate
metoprolol succinate
Atenolol

107
Q

Metoprolol tartrate or Succinate?

Which one is long acting

A

succinate (brand is Toprol XL)

108
Q

what are the 3rd gen of beta blockers?

A

Nebivolol; Betaxolol

109
Q

what is Nebivolol (Bystolic) “special” property other than being cardioselective

A

it will also induce vasodilation via Nitric Oxide

110
Q

what is Betaxolol (Betoptic) “special” property other than being cardioselective

A

induces vasodilation via calcium channel blocking

111
Q

which drugs are non-selective beta blockers but also block alpha 1

A

carvedilol; labetalol

112
Q

what is max dose of carvedilol

113
Q

why is it useful for carvediolol and labetalol to be non-selective beta blockers &block alpha 1

A

beta blocking activity prevents reflex receptor antagonist tachycardia which is seen in alpha 1 receptor antagonists

114
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one does vasoconstriction?
115
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
does mydriasis
116
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
causes vasodilation?
117
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
causes an increase in blood pressure
A

alpha 1 (b1 indirectly via renin)

118
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
inhibits release of NE
119
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
increases release of renin
120
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
cause increased closure of internal sphincter of the bladder
121
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
causes relaxation of uterine smooth muscle
122
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
inhibits Ach release
123
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one increase lipolysis
124
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one increases myocardial contractility
125
Q

what “things” does alpha 2 adrenoreceptor do upon activation

A
    • inhibit NE release
  • inhibit Ach release
  • inhibit of insulin release
126
Q

what “things” does beta 1 adrenoreceptor do upon activation

A
  • tachycardia
  • increased lipolysis
  • increased myocardial contractility
  • increased renin release
127
Q

what “things” does alpha 1 adrenoreceptor do upon activation

A
  • vasoconstriction
  • increased peripheral resistance
  • increased BP
  • mydriasis
  • increase closure of internal sphincter of the bladder
128
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
increases muscle and liver glycogenolysis
129
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
which one increases release of glucagon
130
Q 
which adrenoreceptor (a1, a2, b1, b2 - or a any combination)? (AGONIST used)
relaxes uterine smooth muscle
131
Q

3 main types of diuretics used for blood pressure

A

loop diuretics; thiazide; K+ sparing

132
Q

where (in the kidney) is the largest bulk of sodium reabsorbed?

A

proximal tubule

133
Q

where (in the kidney) is the second largest bulk of sodium reabsorbed?

A

loop of henle

134
Q

where do K+ sparing diuretics work?

A

collecting tubule

135
Q

where do thiazide drugs work?

A

distal convoluted tubule

136
Q

ascending limb in the loop of henle is permeable to ________

A

ions/solutes (Na+, Cl-)

137
Q

descending limb in the loop of henle is permeable to ________

138
Q

Renin is released from ________ cells in the _____

A

juxtaglomerular cells in the kidney

139
Q

what are possible reasons that renin would be released?

A
  • due to drop in blood pressure
  • due to low NaCl
  • due to activation of specific receptors
140
Q

Where are juxtaglomerular cells found? (not in kidney but b/w what things)

A

b/w glomerulus and macula densa

141
Q

Renin is released into blood stream and it will metabolize _________ into ______

A

angiotensinogen; angiotensin 1

142
Q

Angiotensin 1 gets converted to _________ by the ______ enzyme

A

converted to angiotensin 2; by ACE enzyme!

143
Q

where does the ACE enzyme come from?

A

from pulmonary endothelial cells

144
Q

Angiotensin will cause vaso________ and release of ________ from _____ medulla

A

vasoconstriction; release aldosterone from adrenal medulla

145
Q

To inhibit release of renin, ______ can be released from _____ gland - it will lead to water absorption in collecting duct

A

antidiuretic hormone; pituitary

146
Q

Aldosterone increases ______ levels and _____ in the kidney

A

plasma salt levels; volume

147
Q 
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 \_\_\_\_\_\_\_\_\_\_
A

stimulates adrenal cortex to release aldosterone

vasoCONSTRICTION
activates thirst center (pituitary glad)
module baroreceptor reflex
causes CV hypertrophy

148
Q

which drug class prevents the making of angiotensin II

A

ACE Inhibitors (ACE will make angiotensin II)

149
Q

2 ways to indirectly inhibit renin release

A
  • loop diuretics (prevent low Na+ induced release)

- B1 blockers

150
Q

Which ACE inhibitor is very short acting (< 3 hrs)

151
Q

Is lisinopril or enalapril a prodrug?

152
Q

what type of drug is Aliskiren?

A

Renin Inhibitor

153
Q

Can you use ACEIs in pregnant women?

154
Q

ACEIs are typically not used in patients with a _________ value > _____

A

serum creatinine > 2.5

155
Q

What are some drug interactions for ACEIs?

A
  • food/antacids may reduce bioavailability
  • NSAIDs reduce effectiveness
  • K+ supplements - hyperkalemia risk
  • increase plasma levels of digoxin/lithium
156
Q

NSAIDs make ACEIs less effective because?

A

NSAIDs inhibit production of prostaglandins which can act as vasodilators

157
Q

There are _____ subtypes of Angiotensin receptors

158
Q

What are the 2 subtypes of Angiotensin receptors

A

AT1 and AT2

159
Q

AT1 and AT2 are ______ receptors

A

G protein coupled

160
Q 
Effects of AT1
activating \_\_\_\_\_\_\_ channels
Reduce \_\_\_\_ synthesis
Vaso\_\_\_\_\_\_\_ of smooth muscle
Increase in \_\_\_\_\_\_\_\_\_ production
A

activates Ca2+; reduce NO; vasoCONSTRICTION; aldosterone

all above are why we want to block Ang II to work on AT1

161
Q

which drug class blocks Angiotensin from working on AT1

A

ARB’s (-sartans) aka Angiotensin Receptor Type 1 blockers

162
Q

which drug class will reduce gout risk? and how?

A

ARBs; by blocking urate transporter

Therapeutics 2 - Fall 2017 (22 decks)

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