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Pharmacology Exam 2 > Autonomic Hypertension > Flashcards

Autonomic Hypertension Flashcards

1
Q

Review of ANS

A

ANS divided into:

  • Sympathetic
  • Parasympathetic

Sympathetic divided into:

  • Adrenergic agonist (fight)
  • Adrenergic antagonist (rest)

Parasympathetic divided into:

  • cholinergic agonist
  • anticholinergics
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2
Q

What are the neurotransmitters of parasympathetic?

What are the neurotransmitters of sympathetic?

A
  • ACh

- Epinephrine and Norepinephrine

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3
Q

Where does parasympathetic come from in the spinal cord?

Where does sympathetic come from?

A
  • Brain and Lower vertebrae

- Lumbar and Thoracic

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4
Q

What is sympathomimetic?

What drugs are involved with this?

A
  • Promoting the stimulation of sympathetic nerves

- Adrenergic agonists

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5
Q

What is sympatholytic?

What drugs are involved with this?

A
  • Inhibiting the transmission of sympathetic nerve impulses

- Adrenergic antagonists

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6
Q

What are adrenergic drugs used to treat?

A
  • Cardiovascular conditions
  • Respiratory conditions
  • Common cold
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7
Q

How do most adrenergic drugs exert their effect?

A

Binding to postsynaptic receptor

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8
Q

What are the subtypes of adrenergic drugs?

What are each of their actions?

A

Alpha:
1- mainly vascular smooth muscle (vasoconstriction or dilation)
2- presynaptic junctions to influence NE release

Beta:
1- heart, kidney
2- lungs
3-adipose tissue

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9
Q

Is there a clinical use of B3?

A

No

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10
Q

What are the three catecholamines?

A

Catecholamines:

  • Epinephrine
  • Norepinephrine
  • Dopamine
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11
Q

What are catecholamines?

A
  • Hormones produced by adrenal glands.
  • Usually released in response to physical or emotional stress.
  • Released by sympathetic nervous system.
  • Sympathomimetic
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12
Q 
Catecholamines:
Cardiac effects?
Vascular effects?
CNS effects?
Nonvascular Smooth Muscle effects?
Metabolic effects?
A

Cardiac effects: CO=SV*HR

  • Positive inotropic effect (↑SV)
  • Positive chronotropic effect (↑HR)

Vascular Effects:

  • Epinephrine reduced peripheral vascular resistance at low dose, opposite at high dose
  • NE elevates BP

CNS Effects:
-large doses can produce anxiety, tremors, HA

Nonvascular smooth muscle effects:

  • relax smooth muscle of GI tract
  • urinary retention
  • dilation of bronchiole smooth muscle

Metabolic effects:

  • increases blood glucose and fatty acid levels
  • inhibits insulin secretion
  • enhance glycogenolysis and gluconeogenesis
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13
Q

Does epinephrine effect all alpha and beta receptors?

A

Yes

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14
Q

What effect does it have on each receptor?

What is the net effect of all of this?

A
  • B1- increases strength/ rate of cardiac contraction
  • B2- relaxes bronchiole smooth muscle, activates glycogenolysis
  • B3- activate lipolysis in fat cells
  • A1- constricts vascular smooth muscle
  • A2- (presynaptically)

Net effect= potent vasoconstrictor and cardiac stimulant

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15
Q

What can epinephrine be used for?

A
  • Anaphylactic shock (epipen)

- Cardiogenic shock (cardiac arrest)

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16
Q

What receptors does norepinephrine act on?

A
  • Acts on A1 receptors to a greater extent than A2 and B1.

- It has little effect on B2

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17
Q

What does norepinephrine mainly do?

A

Increase BP

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18
Q

What is norepinephrine used to treat?

A
  • Severe hypotension

- Septic shock

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19
Q

What is septic shock?

A

When an organ is injured or damaged in response to an infection, leading to dangerously low BP

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20
Q

What is the precursor to norepinephrine?

What receptors does it activate?

A
  • Dopamine

- Activates A1 and B1 receptors

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21
Q

What is dopamine used to treat?

A
  • Shock in renal failure

- Cardiac decompensation

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22
Q

What are vasopressor drugs?

A

Cause vasoconstriction leading to increased BP and MAP

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23
Q

What are some examples of vasopressors?

A
  • Norepinephrine
  • Epinephrine
  • Dopamine
  • Vasopressin
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24
Q

Difference between Direct and Indirect Acting Adrenergic Drugs?

A
  • Direct- directly stimulate alpha or beta receptors
  • Indirect- Enhance effects of NE or Epi by inhibiting their reuptake or inhibiting their degredation, or increasing release of NE
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25
Q

What are some examples of direct acting adrenergic drugs?

A
  • Pseudophedrine

- Phenylephrine

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26
Q

Are indirect acting adrenergic drugs sympatholytic or sympathomimetic?

A

Sympathomimetic- they mimic the SNS

-Release stored NE, inhibit reuptake, and block degradation

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27
Q

What are some examples of indirect acting adrenergic drugs?

A
  • Cocaine
  • Amphetamine
  • Ephedrine
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28
Q

What is the effect of these adrenergic drugs such as Amphetamine?

A

Amphetamine

  • Taken up by NE transporters (blocks path) which leaves more NE available to have effect
  • inrease alertness, decrease fatigue= used for ADHD, narcolepsy
  • AE related to increased BP and HR, and decreased apetite
  • Enters CNS, stimulating dopamine receptors= euphoria= abuse potential
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29
Q

What are the effects of cocaine, another indirect adrenergic drug?

A
  • Also inhibits the reuptake of NE

- Significant vasoconstriction= hypertensive crisis, MI, stroke

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30
Q

S24-27

A

S24-27

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31
Q

What are mixed adrenergic agonists?

A

Work on both direct and indirect pathways

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32
Q

What are the rehab concerns with sympathomimetics?

A
  • May induce: HTN, cardiac arrhythmias, angina

- Ephedra (weight loss products): cerebral hemorrhage, seizures, and death

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33
Q

Hypertension affects 1 in every _ adults worldwide and is the leading cause of cardiovascular morbitity and mortality. It can be “______”

A
  • 6

- silent

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34
Q

What is the difference between primary hypertension and secondary hypertension?

A

Primary HTN
-multifactorial, accounts for 90% of cases
Secondary HTN
-produced by underlying disease process

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35
Q

What is the Frank-Sterling Law? What does this mean?

A
  • Says that stroke volume increases as left ventricular volume increases
  • Means that preload can be adversely affected by heart disease
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36
Q

What is MAP?

What is Ohm’s law?

A
  • Cardiac output*peripheral resistance
  • V=IR
    • V= vascular pressure
    • I= blood flow
    • R= resistance
  • If peripheral resistance is increased, so is BP
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37
Q

Drugs can affect variables in these equations to alter BP in what ways?

A
  • Reduced HR→ decreased CO and arterial pressure
  • Decrease contractility→ decrease SV→ decrease BP
  • Increase vasodilation→ lower peripheral vascular resistance→ decrease BP
  • Reduce plasma volume→ decrease SV→ decrease BP
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38
Q

What are factors producing HTN?

A
  • Genetics
  • Kidney function
  • Potassium and calcium affects vasodilation
  • Changes in myocardial tissue and vessels
  • Relationship between HTN and hyperinsulinism/ insulin resistance
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39
Q

Renin-angiotensin system + sympathetic nervous system = _____________

A

potent vasoconstriction

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40
Q

What is renin?

A

Renal enzyme that promotes the production of angiotensin

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41
Q

What does renin lead to?

A
  • Gets secreted when 1) decreased renal profusion or 2) decreased Na+
  • Angiotensinogen→ angiotensin I + ACE → angiotensin II
  • Angiotensin II is a VERY powerful vasoconstrictor
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42
Q

Go through the order in depth.

A
  • Low fluid flow or Na+ is sensed
  • Renin is secreted
  • Kidney releases renin into blood, and liver releases angiotensinogen into blood
  • This renin acts on the angiotensinogen to form Angiotensin I
  • Angiotensin-converting enzyme (ACE) in pulmonary blood converts Angiotensin I into Angiotensin II
  • This then stimulates widespread vasoconstriction
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43
Q

What do PGE2 and PGl2 counteract?

A

counteract vasoconstriction effect on kidneys

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44
Q

What does taking NSAIDs do to prostoglandin synthesis?

What can this cause?

A
  • Inhibits prostoglandin synthesis
  • Can cause renal failure and exacerbate HTN with individuals who have cirrhosis, heart failure, nephrotic syndrome, or HTN
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45
Q

What are 2 other things that control BP?

A

Baroreceptors:
-mechanoreceptors located in carotid sinus and aortic arch

Chemoreceptors:
-located in carotid body and aortic bodies

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46
Q

Baroreceptors help to do what?

A

Help blood vessels constrict and dilate as needed

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47
Q

What is the recommended initial therapy for HTN?

A

Diuretics

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48
Q

How do diuretics work?

A

Act directly on the nephron to limit water and sodium reabsorption, thus increasing excretion of Na+ and water by kidneys

  • Increases amount of urine formed
  • Decreases blood volume
  • Inexpensive
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49
Q

What are the three major classifications of diuretics and what are they based on?

A

They are based on location

Loop Diuretics

  • moderate antihypertensive/ strong diuretic
  • descending loop on Henle

Thiazide diuretics

  • powerful antihypertensive, moderate diuretics
  • distal (early) tubules

Potassium-sparing diuretics
-distal (late) tubules

50
Q

What is the MOA of loop diuretics?

A

Acts on ascending Loop of Henle and inhibits reabsorption of Na+/K+/2Cl- which prevents reabsorption of water follows these electrolytes

51
Q

What is the most common side effect of loop diuretics?

A

-Dehydration

Other side effects include:

  • hypokalemia (low potassium)
  • hyponatremia (low sodium)
  • hypocalcemia (low calcium)
  • ototoxicity
  • hyperglycemia
  • increased LDLs
52
Q

K+ supplements or K+ sparing diuretics may be given to reduce risk of what?

A

hypokalemia

53
Q

Where do thiazide diuretics act?

What is their MOA?

A
  • Acts on the early part of the distal convoluted tubes

- Inhibits mechanisms that favor Na+ reabsorption. Results in Na+ and K+ excretion and reabsorption of Ca+.

54
Q

Thiazide diuretics _____ __________ __ more than any other classes of antihypertensive drugs.

Thiazide diuretics are the most ___________ diuretics.

A
  • lower systolic BP
  • frequently used
    • prime choice for HTN
    • may be given along with loop diuretics in cases of CHF and severe edema
    • better choice for individuals prone to renal calculi
    • favored for older adults to reduce to reduce Ca+ loss and maintain bone mass
55
Q

What is the overall importance of thiazide diuretics?

A

Same function as loop diuretics but helps keep calcium in the body. This is important in the elderly who have issues with bone density or kidney stones

56
Q

What are the AE of thiazide diuretics?

A

Similar to loop diuretics except possibly causing hypercalcemia and significant K+ loss (hypokalemia)

57
Q

Where do potassium sparing diuretics act?

What is their MOA?

A
  • Acts on the late distal convoluted tubules,

- Inhibits the sodium-potassium exchange mechanism, limiting the reabsorption of Na+ and excretion of K+

58
Q

Potassium-sparing diuretics are less effective at producing _______ but are _______ _______.

A
  • diuresis

- potassium-sparing

59
Q

What are the AE of potassium sparing diuretics?

A
  • hyperkalemia
  • nausea
  • lethargy
  • mental confusion
60
Q

_________ blocks aldosterone receptor, which produces gynocomastia in males and menstrual irregularities in females

A

-spiranolactone

61
Q

What are the therapeutic concerns with diuretics?

A
  • Be alert for signs of hypokalemia or hyperkalemia
  • Hypokalemia- abonrmal ECG (flattened T waves)
  • Hyperkalemia- abnormal ECG (elevated T waves)
  • Both can trigger arrhythmias
  • Syncope (fainting) may also be present
  • Cardiac arrest can occur
  • Frequently monitor K+ levels
62
Q

What are the therapeutic concerns with diuretics?

A
  • Risk for hyperglycemia and abnormal lipid levels
    • Of concern for individuals with diabetes and high cholesterol/triglyceride levels
    • Reduced plasma volume has issues with hyperglycemia because we are reducing the plasma volume which in return increases concentration
63
Q

What are the therapeutic concerns with diuretics?

A
  • Fluid depletion

- Dehydration may increase BP, which is counter productive

64
Q

What is a normal blood glucose level?

A

70-130 mg/dL

65
Q

What are the main concerns with diuretics?

A
  • Be aware of sings of hypo and hyperkalcemia
  • Fluid depletion
  • Risk for hyperglycemia and abnormal lipid levels
66
Q

Do NSAIDs make diuretics more or less effective?

A

Less, NSAIDs cause Na+ retention and decrease in renal profusion

67
Q

Direct vasodilators MOA?

A

Act to directly vasodilate the peripheral vasculature by inhibiting smooth muscle contraction in the arterioles

68
Q

Vasodilators: Calcium Channel Blockers MOA?

A

Blok Ca2+ entrance into vascular smooth muscle, reducing smooth muscle tone allowing for vasodilation
-This reduced Ca2+ influx results in decreased contractility and CO, and decreased cardiac function and energy demands on the heart

69
Q

What was the original purpose of vasodilator: calcium channel blockers?

A

Originally developed for treating cardia disease

  • HTN
  • angina
  • arrhythmia
70
Q

When are calcium channel blockers useful?

A

When betablockers are contraindicated (asthma, DM, PVD)

71
Q

What are the AE of calcium channel blockers?

A
  • HA
  • dizziness
  • hypotension
  • bradycardia
  • reflex tachycardia
  • sweating
  • tremor
  • flushing
  • constipation
72
Q

What are the three classes of Ca+ channel blockers and the drugs in these classes?

(Just know that these medications are Ca+ channel blockers)

A

Dihydropyridines: reduce arteriolar tone

  • nifedipine
  • nicardipine
  • amlodipine

Phenylalkylamines: affect the heart
-verapamil

Benzothiazepines: affect heart and vasculature
-diltiazem

73
Q

What are B-adrenoceptor blockers (beta blockers) and what are they used to treat?

A

They are adrenoreceptor antagonists used to treat cardiovascular dysfunction

  • HTN
  • angina
  • arrhythmia
  • post-MI survival
74
Q

Beta blockers act as a _________ _________ of B-adrenoceptors.

A

competitive antagonist

results in:

  • negative inotropic effects (reduced contractility)
  • negative chronotropic effects (reduced HR)
  • inhibitory effect on sympathetic nervous system (reduced peripheral vascular resistance)
75
Q

Difference between betablockers that are nonselective or selective for B-adrenoreceptors?

A
  • nonselective- blocks B1 and B2 adrenoreceptors

- selective- blocks B1 receptors only, but this selectivity is lost at high doses

76
Q

What is beta blockers MOA?

A
  • Normal sympathetic function is for NE to bind to B1 and B2 receptors causing an increase in HR, contractility, and conduction
  • Beta blockers reduce the sympathetic influence by competing for the site causing decreased HR, contractility, and conduction
77
Q

Primary location of beta receptors

A

B1- heart

B2- lungs (bronchiole smooth muscle

78
Q

What is the response when these receptors are stimulated?

A 
B1= increase in HR and contractility
B2= smooth muscle relaxation resulting in bronchodilation
79
Q

These beta blockers act to reduce the ________ of the heart

A

workload

HTN and angina are conditions where a decrease in the workload of the heart is very beneficial

80
Q

What leads to the reduced workload on the heart?

A
  • negative chronotropic (decreased HR)

- negative inotropic (decreased SV)

81
Q

What do beta blockers typically end in?

A

-lol

82
Q

What are the adverse effects of inhibiting the SNS via beta blockers?

A
  • may contribute to peripheral vasoconstriction
  • bronchoconstriction
  • bradycardia
  • reduced HR
83
Q

What are cardioselective beta blockers?

A

Selectively block B1 receptors without causing bronchoconstriction

84
Q

What are the AE of cardioselective beta blockers?

A

Same as nonselective minus pulmonary effects

85
Q

What are the therapeutic concerns with beta blockers?

A
  • Depressed HR and CO during exercise
  • May contribute to orthostatic hypotension
  • Watch for signs of CHF
  • Masks symptoms of hypoglycemia in individuals with diabetes
86
Q

Can we use HR as an indicator of patient response to exercise while they are on beta blockers?

A

NO

87
Q

What is destention?

A

sticks out from backload of fluid

88
Q

Where do A1 blocker medications work?

A

Post synaptic

89
Q

What do A1 adrenoreceptor blockers end in?

What is their MOA?

A
  • End in -azosin

- reduce sympathetic tone of blood vessels→ vasodilation→ decreased peripheral vascular resistance

90
Q

How do A1 receptor blockers lower BP?

Are they typically used as a first drug option?

A
  • Decreasing PVR (peripheral vascular resistance)

- No, they are generally used as an “add-on” drug to reduce BP

91
Q

A1 receptor blockers have also been shown to lower ______ and ______

A

-LDL and triglyceride levels

92
Q

What are the AE of these A1 adrenoreceptor blockers?

A
  • orthostatic hypotension
  • nasal stuffiness
  • reflex tachycardia
  • arrhythmia
93
Q

What are the therapeutic concerns with A1 adrenoreceptor blockers?

A
  • first-dose syncope
    • take BP and watch for signs of OH
    • FALLS precaution
  • angina
  • increased incidence of CHF with this class of drugs
94
Q

When are dual alpha and beta blockers useful?

A

Beneficial for individuals who have increased PVR with pure beta blockers

95
Q

Central-acting alpha 2 agonists for HTN MOA?

A

A2 receptor are primarily on presynaptic neurons→ stimulate in CNS→ decrease NE production→ decrease sympathetic outlflow→ decreased peripheral resistance, HR, and BP

96
Q

Common AE of central acting alpha 2 agonists?

A
  • Dizziness (15%)
  • Drowsiness (38%)
  • Fatigue (15%)
  • HA (up to 30% chonidine, 10% methyldopa)
97
Q

__ agonist and __ antagonist treat HTN

A
  • A2

- A1

98
Q

What drug is reserved for resistant HTN?
What type of drug is this?
What is it also used for?

A
  • Clonidine
  • Central-Acting A2 agonist
  • Also used for ADHD
99
Q

What is the 1st line for HTN in pregnancy?

A

Methyldopa

100
Q

What are some concerns with central acting A2 agonists for HTN?

A
  • Orthostatic hypotension
  • Rebound hypertension
    • Critical to not abruptly stop!
101
Q

S77

A

S77

102
Q

What does an ACEi drug end with?

What is its MOA?

A
  • ends with -pril
  • blocks the conversion of angiotensin I to angiotensin II→ increase blood vessel dilation, increase bradykinin which increases vasodilation
103
Q

What patients would be on an ACEi drug for a long amount of time?

A

stroke patients

104
Q

Common AE of ACEi drugs?

A
  • Dry cough
  • Hypotension
  • Hyperkalemia
105
Q

What are the rare, serious side effects of ACEi drugs?

A
  • Acute renal failure

- Angioedema (face swelling)

106
Q

Angioedema is more common with ____ than any other RAAS drugs.

A

ACEi

107
Q

What is ARB (angiotensin II receptor blockers) MOA?
When should these be used?
What do ARBs end in?

A
  • blocks binding of angiotensin II resulting in decreased blood vessel vasoconstriction
  • Use when ACEi intolerant
  • “-sartan”
108
Q

When should you switch from an ACEi to an ARB?

A

Switch if cough is present while on ACEi

109
Q

What is the best tolerated anti HTN?

What are the AE of ARBs?

A
  • ARBs

- Same as ACEi except no dry cough

110
Q

What are the therapeutic concerns for ACEi?

A
  • Cough

- NSAIDs

111
Q

What is the triple whammy?

A

ACEi, Diuretic, and NSAID

112
Q

Direct renin inhibitor use?

MOA?

A
  • HTN (but very uncommon)

- blocks conversion of angiotensinogen to angiotensin I

113
Q

What are the AE of a direct renin inhibitor?

A

Similar to ACEi/ARB

114
Q

Should you use RAAS inhibitors in combination?

A

No, due to increase in AE

115
Q

Hypertension Guidelines

A

S85

116
Q

1st line treatments for Hypertension

A
  • Thiazide diuretic or CCB (or ACEi/ARB if not African American)
  • If CKD- ACEi or ARB first
117
Q

What are other agents to treat hypertension?

A
  • loop diuretics
  • K+ sparing diuretic
  • beta blockers
  • aldosterone antagonists
  • A1 blocker
  • centrally acting A2 agents
  • direct vasodilator
118
Q

What is the last line to treatment of hypertension?

A

centrally acting A2 agents due to effect on CNS

119
Q

Additional therapeutic concerns about hypertensive agents.

A
  • Orthostatic hypotension→ low Bp→ syncope→ FALLS
  • Dehydration
  • Caution with heat modalities
120
Q

HTN Drugs Review

A

S89

Pharmacology Exam 2 (7 decks)

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