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HTN Flashcards

1
Q

What makes up BP

What makes up CO

A

CO and SVR

HR and SV

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2
Q

What makes up SV

What makes up preload

A

Contractility and preload

Venous tone and intravascular volume

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3
Q

What makes up SVR

A

Direct innerv, circulating and local regulators

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4
Q

What effects venous tone: 4

A

A1 antagonists, ACEI, ARB, NTP

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5
Q

What affects na and h20 retention, upstream effect

A

Diuretics, acei, arb. Intravascular volume, preload, and SV

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6
Q

Direct innervation SVR

A

A1 antagonists, A2 agonists

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7
Q

Circulating BP regulators

A

A1 antag, A2 agonist, ACEI, ARB

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8
Q

Local BP regulators

A

Endothelin antagonist, ntp, acei, arb

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9
Q

DM or renal disease pts do specifically well on which drugs

A

ACEI or ARB, target RAAS and improve vascular flow to kidneys (underlying atherosclerosis)

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10
Q

Renin secreted by what
Results in what
Synergistic with what

A

Juxtaglomerular apparatus
Vasoconstriction and na retention
SNS inc release of noradrenaline

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11
Q

What controls ang I to II conversion

What leads to dry cough and which drugs impact this/dont

A

Renin

Bradykinin, relaxes smooth muscle w ACEI but not ARB

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12
Q

Angitotensin II effects: 4

A

Adrenal cortex- aldosterone- inc nacl reabs
Renal proximal tubule- inc nacl reabs
Renal efferent arterioles vasoconstriction
Hypothalamus- thirst and inc ADH

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13
Q

Acei first line therapy for 3, delays progression in what

A 
Htn, CHF, mitral regurg. 
Renal disease (esp in DM pts)
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14
Q

Ang II vasoconstricts where, inc ___ secretion

Mediated mainly at which receptor

A

Arterial smooth muscle
Aldosterone
AT 1 > AT2

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15
Q

AT 1 receptor effects 4

A

Generalized vasoconstriction (esp afferrent arterioles)
Inc norepi release
Prox tubule reabs of na
Secretes aldosterone renal cortex

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16
Q

ACEI MOA

A

Blocks conversion Ang I to II in vasc endo by interact w zinc ion of ACE (Peptidyl-dipeptidase). Thus prevents vasoconstriction, na retention, and SNS stim

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17
Q

ACE: highly ___, minimal __ __, good patient __

A

Potent, SE, compliance

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18
Q

ACEI:
Pharm fx: fall in 2
Clinical uses: 5

A

Arterial pressure, cardiac work load

Htn, HF, post MI, diabetic neuropathy, CRI

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19
Q

ACEI SE: 6

A

Prolonged hypotension intra op, granulocytopenia, angioedema, proteinuria, persistent cough, hyperkalemia

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20
Q

ACEI contraindications: 2

A

Pregnancy, renal artery stenosis (aCEI causes efferent arteriole constriction)

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21
Q

Captopril
Onset
1/2 life
Decreases __, doesnt affect __ __

A

15 min
2 hrs
SVR, SNS outflow

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22
Q

Captopril
SE: 4
Drug interaction: main 1

A

Rash, loss of taste, hyperkalemia, angioedema

NSAIDs antagonize its effects

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23
Q

Enalapril
Route
What it has that makes it special why

A

IV

No sulfahydryl group, no rash or renal ins caused by it

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24
Q

Lisinopril

Excretion

A

Unchanged in kidney

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25
Q

Ace prodrugs and what it means

A

Enalapril and ramipril, longer onset

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26
Q

Ace effects __ system more than ___ system

A

Arterial, venous

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27
Q

ARBs

Antagonizes which receptor/MOA

A

Ang II AT1 receptor, competitive binding to inhib ang II at receptor. Doesnt affect ACE. Results in Less peripheral vasoconstriction

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28
Q

Contra ARB: 2

A

Renal artery stenosis, pregnancy

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29
Q

Arterial vasodilator: 2

A

Minoxidil, hydralazine

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30
Q

Hydralazine

MOA

A

Activates guanylate cyclase, directly relaxes vascular smooth muscle. Arteries > veins. Alters ca trans into smooth muscle

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31
Q

Hydralazine
Dose
Peak
Duration

A

2.5-10 mg IV
10-20 min peak
6 hrs

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32
Q

Hydralazine
Metabolism
1/2 time
When in kidney

A

Extensive hepatic 1st pass
3 hrs
After IV <15% unchanged in kidney

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33
Q

Hydralazine SE

Many

A

Reflex tachycardia, DBP reduced >SBP, dec SVR, inc HR/SV/CO, tachyphylaxis, na and h20 retention, angina w ekg changes

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34
Q

Hydralazine

Clinically used with __ and __ to limit what

A

BB and diuretic, inc SNS activity

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35
Q

Minoxidil
MOA
Route

A

Directly relaxes arteriolar smooth muscle, little venous effect. PO

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36
Q

Minoxidil
Clinical uses: 3
Used with what

A

Severe htn due to: renovascular disease, renal failure, transplant rejection
BB and diuretic

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37
Q

Minoxidil

MOA cellular level

A

K channel opener leading to hyperpolarization and vasodilation

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38
Q 
Minoxidil 
Absorption 
Peak 
E 1/2 
What in urine
A

90% abs in GI
1 hr
4 hrs
10% unchanged in urine

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39
Q

Minoxidil SE (many)

A

Inc HR and CO, inc NE and renin leads to: na and h20 ret, wt gain, edema, hypertrichosis, pulm htn, pericardial effusion/cardiac tamponade

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40
Q

Minoxidil EKG effects

A

Flat or inverted T wave, inc voltage of QRS- due to altered K conductance in heart

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41
Q

Peripheral vasodilator

Uses: 3

A

Facilitate forward LV flow in AR/MR/CHF, control htn in OR, tx htn crisis

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42
Q

Peripheral vasodilator: 4 main ones we use

A

Ntp, SNP, isorsorbid, adenosine

43
Q

SNP
Action
Lacks effects where

A

Direct, nonselective peripheral vasodilator (art and vein SM). Lacks effect non vascular SM and cardiac muscle

44
Q

SNP

MOA

A

Interact w oxyhemoglobin- dissociation to methemoglobin- releases NO and cyanide. NO activ guanylate cyc- inc cGMP- inhib Ca entry into vasc SM, inc Ca uptake into smooth ER. Vasodilation via NO

45
Q

SNP metab

A

4 leftover cyanide ions metab in liver and kidney to thiocyanate

46
Q

SNP toxicity occurs due to what
Leads to 3
Caution in

A

High conc thiocyanate. Occurs at rates >2 mcg/kg/min. Pt develops resistance at high rates. Can precipitate tissue anoxia, anaerobic metab, lactic acidosis. Caution in preg.

47
Q

SNP toxicity tx

A

D/c med. 100% o2. Na bicarb- acidosis. Na thiosulfate 150mg/kg over 15 min. Na nitrate 5 mg/kg if severe.

48
Q

Na thiosulfate action

Na nitrate action

A

Sulfur donor- converts cyanide to thiocyanate

Converts hgb to methgb which converts cyanide to cyanomethgb

49
Q

Thiocyanate toxicity
Toxicity/occurance compared to cyanide
Symp: 10

A

Rare (to kidney clearance), less toxic

Nv, tinnitus, fatigue, hyperreflexia, confusion, psychosis, miosis, seizure, coma

50
Q

Methemoglobinemia

What it is

A

Rare, differential dx in pts w imp oxygenation despite good CO and arterial oxygenation

51
Q

Phototoxicity of SNP

Why

A

In light SNP converted to aquapentacyanoferrate, released hydrogen cyanide

52
Q

SNP
Dose
When toxic dose risk
Onset, duration, req what

A

0.3 mcg/kg/min-10.
>2. >10 min max dose.
Immediate, short.
Gtt and a line

53
Q

SNP CV effects
Inc:
Dec:

A

Inc: HR, contractility, intracoronary steal and MI damaged areas, venous capacitance
Dec: venous return, SBP, PVR, SVR

54
Q

SNP Fx
CNS
Pulm
Blood

A

Inc CBF and ICP
Attenuates hypoxic vasoconstriction
Inc cGMP- inhibits plt agg

55
Q

SNP clinical uses, dose if applicable

A 
Controlled hypotension (0.3-0.5 mcg/kg/min)
Htn crisis (1-2 mcg/kg bolus then gtt)
Cv disease: dec LV afterload and good for MR, AR, CHF
56
Q

Ntg
What it is
Acts on

A

Organic nitrate

Venous capacitance vessels and large coronary arteries

57
Q

Ntg MOA

E 1/2

A

Generates NO thru glutathione dependent pathway (glut S transferase). Stim cGMP to cause vasodilation. 1.5 min

58
Q

NTG

What tox can lead to/tx

A

Methemoglobinemia. Caution in high doses. Methylene blue 1-2 mg/kg over 5 min, reconverts methgb to hgb

59
Q

NTG cv effects

A

Venodilation, dec: venous return, R/L ventricular end DBP, CO. No change HR or SVR. Inc coronary BF

60
Q

NTG tolerance

A

Limits use, present after 24 hr of sustained tx

61
Q

NTG Fx
CNS
Pulm

A

Vasodilation and inc ICP HA

Dec PVR, bronchial dilation, inhib hypoxic pulm vasoconstriction

62
Q

Ntg fx
Coag
Gi

A

Prolongs bleeding time, inhib plt agg

Relaxes smooth musc of GI tract

63
Q

Ntg clinical uses

A 
Angina (reduces RVEDP and LVEDP, reduces myo 02 reqs) 
Cardiac failure (dec preload, relieves pulm edema, limits MI damage)
64
Q

NTG

Clinical uses: 2 and doses

A

Controlled hypotension: 4-5 mcg/kg/min (not in cranial sx until dura open)
Sphincter of oddi spasm: 200 mcg/1 ml bolus

65
Q

Isosorbid
Indic, route, abs, duration
Works predom where

A

Angina, PO, GI in 6 hrs
SL- 2 hrs
Venous

66
Q

Isosorbid SE

More active form

A 
Orthostatic hypotension, 
active metabolite (isosorbid 5 mononitrate) > than parent compound
67
Q

Trimethaphan

Actions

A

Ganglionic blocker, peripheral vasodilator. Blocks ANS, relaxes vessels. Lowers CO, BP, SVR. Inc HR from PNS block.

68
Q

Trimethaphan
Route
SE

A

IV, need gtt

Mydriasis, dec GI activity, urinary retention

69
Q

Ca ch blockers

3 main and action overall

A

Verapamil- SA/AV/V tissue > vessels
Diltiazem- heart and vascular tissue
Nifedipine- more smooth muscle in vessels

70
Q

Ca ion channels present where

6

A

Cell membrane in skel muscle, vascular smooth musc, cardiac musc, mesenteric musc, neurons, glandular cells

71
Q

Ca ch blockers action cell level

A

Bind to receptor on voltage gated ca ions maintaining channels in inactive or closed state

72
Q

Which ca ch are we targeting w blockers, what it does

A

L type imp in vascular tone and cardiac contractility. Decreased ca keeps intracellular ca low

73
Q

Ca ch blockers

Classifications 3 based on structure

A

Phenyl alyl amines- av node
1,4 dihydropuridines- arterial beds
Benzothiazepines- av node

74
Q

Nifedipine
Verapamil
Dilt
What they do at binding site

A

N- allosteric modulation at site
V- pore blocker at site
D- not sure

75
Q

Ca ch blockers

Cardiac/vascular effects

A

Dec: contractility, activity at sa node, rate of conduction of impulses at AV. Relaxes vasc SM: dec SVR and BP arterial >venous

76
Q

Ca ch blockers SE

4

A

Cancer, cv depression, prolonged bleeding (ca mediated plt func), constipation

77
Q

Ca ch blockers
Drug interactions
W/: IA, NMB, bb, la

A

IA- myocardial dep and vasodilation
Potentiated NMB
Contraindicated w bb (verapamil)
Inc risk LA toxicity (verapamil)

78
Q

Ca ch blockers drug interac
Dantrolene
Dig
H2 antag

A

D: hyperkalemia, slows inward k, cv collapse
Dig: inc conc dig by decreasing its clearance
H2: ranitidine and cimetitine alt hepatic enzymes, could inc Ccb

79
Q

Ca ch blockers

Toxicity rx

A

IV calcium or dopamine

80
Q

Vascular uses ca ch blockers 5

A

Systemic htn, pulm htn, cerebral arterial spasm, raynauds, migraine

81
Q

Non vascular uses ca ch blockers 4

A

Bronchial asthma, esophageal spasm, dysmenorrhea, premature labor

82
Q

Verapamil
Primary sire of action
Cardiac actions

A

AV node

Depresses AV node, negative chronotropic effect SA, negative inotrope, moderate vasodilation coronary/systemic arteries

83
Q

Verapamil
Clinical uses
6

A

SVT, vasospastic angina, htn, hypertrophic cm, maternal/fetal dysrhythmias, premature labor

84
Q

Verapamil

Protein binding, what inc its activity

A

Highly. Lidocaine, diazepam, propranolol

85
Q 
Verapamil 
Metabolism 
Excretion
Peak 
E 1/2
A

Almost entirely thru first pass, almost no drug unchanged in urine
30-45 min, iv 15 min
6-12h

86
Q

Ca ch blockers
Nifedipine
Uses
Primary site of action

A

Angina and htn

Peripheral arterioles

87
Q 
Nifedipine 
Cv effects 
Comp to verapamil 
No effect where
Other: 4
A

Coronary and peripheral vasodilation stronger than verapamil. No effect sa or av. Dec SVR and bp. Reflex tachycardia. Myo dep in LV dysfunc or bb

88
Q

Nifedipine
Routes
Onset and peak oral

A

IV, oral, SL

20 min, 60-90 min

89
Q 
Nifedipine 
Protein binding
Metabolism 
Excretion 
E 1/2
A

90% protein bound, hepatic metab, urine excretion

3-7h

90
Q

Nifedipine SE

8

A

Vertigo, HA, flushing, hypotension, paresthesiass, muscle weakness, can induce renal dysfunc
Coronary vasospasm w abrupt D/C

91
Q 
Dilt 
Primary action where 
Main Indication 
Strength compared to others in class 
Minimal what
A

AV node
SVTs
Intermediate strength b/w verapamil and nifedipine
Cv depressant effects

92
Q

Diltiazem
Clinical uses
Sim to:
3

A

Verapamil

Vasospastic angina, hypertrophic cm, fetal/maternal dysrhythmias.

93
Q

Diltiazem
Routes
Doses
Gtt

A

Po or iv
.25-.35 mg/kg over 2 min, repeat in 15 min
10mg/hr gtt

94
Q

Diltiazem
Po onset, peak
Protein binding

A

15 min, 30 min

70-80% protein bound

95
Q

Diltiazem
Excretion
E 1/2
Decrease dose in who

A

Bile and urine, inactive metab
4-6hr
Liver disease

96
Q

Centrally acting agents

MOA

A

Reduce sns outflow from vasomotor center in brain stem. Selective partial alpha 2 adrenergic agonist

97
Q

Centrally acting agents
Drug name
Clinical uses 5

A

Clonidine

Htn, induce sedation, dec anesthetic reqs, improve periop hemodynamics, analgesia

98
Q

Clonidine
Effects
Warning w abrupt stop

A

BP reduction from decreased CO d/t dec hr and peripheral resistance
Rebound hypertension

99
Q

Centrally acting agents
SE
9

A

Bradycardia, sedation, dry mouth (zerostomia), imp concentration, nightmares, depression, vertigo, EPS, lactation in men

100
Q

Centrally acting agents
Routes
Metab/exc

A

PO or transdermal

50/50 hepatic metab and renal excretion

101
Q 
Centrally acting agents 
Withdrawal syndrome 
Occurs how, when
Duration 
Tx
A

Doses >1.2 mg/day, 18hrs after acute d/c. 24-72 hour length

Tx rectal or transdermal clonidine

102
Q

Preop med continue

Continue which and why

A

Bb (Reduces periop MI risk)
Cc (benefits outweigh risks unless LV dysfunc)
NO: ACE, withhold 1 dose

103
Q

Htn crisis
What it is
Goal
Tx

A

> 120 DBP, end organ failure
Goal dec DBP 100-105 asap
Ntg, ntp, labetolol

Pharmacology (19 decks)

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