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Pharmacology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

__% of hypertension is uncontrolled

A

>61%

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2
Q

___% are unaware they have high BP

A

33%

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3
Q

hypertension= ____BP

A

>140/90 mmHg

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4
Q

secondary hypertension=

A

secondary to a specific disorder

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5
Q

essential hypertesion=

and accounts for __% of all cases

A

no clear identifiable cause

=95% of all cases

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6
Q

RAAS system

A
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7
Q

RAAS is stimulated by

A

SNS… B1 receptors

and barroreceptors

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8
Q

aldosterone is synthesised in the___

and fxn is___

A

adrenal cortex

-increases Na+ re-absorption in collecting duct

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9
Q

vasopressin action=

A

increases TPR and water retention

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10
Q

Big 4 hypertensive agents

A
  1. Diuretics
  2. Direct vasodialtors
  3. Sympatholytic agents
  4. Angiotensin related agents
    (5. Combination therapy - most common)
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11
Q

Diuretics used for__

actions____

A

**first choice for MILD hypertension

  • low cost but effective

initially=increase urine volume

delayed= decrease peripheral resistance by increaseing Na+ excretion

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12
Q

Loop diuretics action

A

=high efficacy

-blocks lots of Na+ readbsorption

= deplete K+ = HYPOKALEMIA

=retain uric acid = gout

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13
Q

loop diuretics list

A

furosemide

ethacrynic acid

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14
Q

thiazides action

A

=moderate efficacy

=stop Na+ reabsorption in distal convoluted tubule

=deplete K+ =HYPOKALEMIA

=retain uric acid= gout

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15
Q

thiazides list

A

hydrochlorothiazide

chlorthalidone

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16
Q

potassium sparing agents action

A

-reduce Na+/K+ exchange in DCT and CD

= Na+ excretion

= K+ retention

-COUNTERACTS HYPOKALEMIA

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17
Q

diuretic that is first line of treatment =

A

thiazides

bc they have moderate efficacy

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18
Q

all diuretics have ___ as a side effect

A

dehydration

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19
Q

Mechanism of Loop Diuretics (draw schematic)

A
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20
Q

Thiazide mechanism (draw schematic)

A
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21
Q

____ is the most effective diuretic and is longer acting

A

chlorthalidone

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22
Q

spironolactone mechanism schematic

A

=a K+ sparing diuretic

-inhibits Muscarinic Receptor ∴ decreases expresion of Na+/K+ ATPase

=big K+ effects

=small Na+ effects

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23
Q

thiameterine and amiloride mechanism (schematic)

A

=K+ sparing diuretics

= inhibit K+ channel on apical membrane

=HUGE K+ resprption

=small Na+ excretion

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24
Q

direct acting sympatholytic agetnts lower blood pressure by

A
  1. beta blockers
    - reduce HR and Force = decreased CO
    - reduce renin production
  2. alpha 1 antagonists
    - vasodilate (block contraction) = decreased TPR
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25
Q

beta blockers for decreasing BP drugs

A

propanolol (non-selective)

atenolol (cardioselectve)

nadolol (long-acting)

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26
Q

don’t use ___ in asthmatics

A

atenolol

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27
Q

indirect acting sympatholytic agents to reduce BP types=

A
  1. alpha 2 agonists
    - trick nerve into thinking theres lots of NT and stop SNS activity
  2. catecholamine release inhibitors
    - inhibit vesiculare release
    - can cause CNS side effects (reduced DA)
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28
Q

alpa 1 adrenergic receptor antagonists to control BP drug list

A

prazosin

terazosin

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29
Q

alpha 2 agonists drug list

A

clonidine

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30
Q

catecholamine release inhibiors drug list

A

reseprine

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31
Q

hydralazine

A

direct vasodilator

oral drug

=selective arterial dilator

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32
Q

Calcium Channel Blockers

A

vasodilator

oral drug

block Ca+ dependent channels on vascular smooth muscle

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33
Q

CCB mechanism schematic

A
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34
Q

minoxidil

A

vasodilator

oral drug

higly effective!

lots of side effects! (excessive hair)

last resort

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35
Q

alpha 1 receptor antagonists will mimic ___ effects

A

CCBs bc they also block the V-G Na+ channels

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36
Q

sodium nitroprusside

A

parenteral drug

vasodilator

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37
Q

diazoxide

A

vasodilator

parenteral drug

highly effective and long acting ∴ not a first choice drug

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38
Q

Nitrates mechanism of action schematic

A
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39
Q

hydralazine, diaxodine, monoxidil mech. of action schematic

A
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40
Q

CCB’s can target____ channels

A

L-type Voltage Dependent Ca2+ channels on cardiac or vascular smooth muscle

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41
Q

Non-cardioactive CCB’s action

A

-more selective for Ca2+ channels on smooth muscle than in heart ∴ don’t have an effect on heart

= dihydropyridines

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42
Q

non-cardioactive CCB’s drug list

A

all =dihydropyridines

  1. amlodipine - long half life
  2. nifedipine - short half life
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43
Q

short acting dihydropyridines

A

= increased risk for acute MI

=AVOID

=nifedipine

-only use extended release version if nifedipine

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44
Q

long acting dihydropyridines

A
  • use these for hypertension or angina pectoris

=amlodipine

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45
Q

cardioactive CCB’s action

A

=equally selective for ca2+ channels on vascular smooth muscle AND in heart

∴ relaxe sm. muscle AND reduce CO

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46
Q

verapamil

diltiazem

A

cardioactive CCB’s drugs

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47
Q

vasodialtor side effects

A
  1. postural (orthostatic) hypotension
  2. flushing/sweating headache
  3. reflex tachycardia
    - body’s reflex is to set at high BP so barroreceptors (+) increased HR
  4. reflex fluid retention
    - juxtaglom. retain Na+ to increase volume
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48
Q

to prevent reflex tachycardia we coadminister ___

A

beta blocker

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49
Q

to prevent reflex fluid retention with vasodilation we coadminister ___

A

diuretic drug

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50
Q

beta blockers tha are also vasodilators drug list

A

=decreas CO AND TPR

carvendilol

nebivolol

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51
Q

carvendilol

A

mixed beta 1/2 and alpha 1 antagonist

∴decreases CO AND TPR

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52
Q

nebivolol

A

beta 1 blocker that promotes NO production

∴decreases CO AND TPR

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53
Q

Angiotensin related agents types and general action

A
  1. ACE inhibitors
  2. Angiotensin Recptor Blockers
  3. Renin Inhibitors

=vasodilate and decrease aldosterone and vasopression ∴ decrease blood volume

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54
Q

ACE Inhibitors action and drug list

A

= (-) angiotension I to II

captopril

enalapril

ramipril

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55
Q

Angiotensin Receptor Blockers action and list

A

=inhibit binding of angiotnesin II to AT1

losartan

valsartan

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56
Q

Renin inhibitors action and list

A

= (-) conversion of angiotensinogen to angiotensin I

aliskiren

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57
Q

captopril

A

ACE Inhibitor

  • not a prodrug
  • associated with higher side effect risk
  • short half life
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58
Q

enalapril

A

=ACE Inhibitor

-pro-drug

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59
Q

ramipril

A

=ACE Inhibitor

-prodrug

*greater cardioprotective

*greater efficacy

∴

**most commonly used**

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60
Q

ACE Inhibitor side effects

A

=BIG DEAL

  1. dry cough- inhibit the breakdown of bradykinins by ACE ∴ they accumulate in lungs
  2. Angioedema - rapid non allergic swelling of skin and mucos -from bradykiin
  3. Hyperkalemia - reduced Na+/K+ exchange in kidney form reduced aldosterone
    - also, TERATOGENIC
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61
Q

Angiotensin Receptor Blockers effects and side effects

A

=competitive antagonist at AT1 Receptors

=some AT2 receptor antagonist

=avoid side effects mediated by interactions with other receptors

side effects = hyperkalemia and are teratogenic

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62
Q

ARBs drug list

A

losartan

valsartan

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63
Q

Renin Inhibitor action, side effects, and normal usage

A

=(-) conversion of angiotensin 1 -> 2

  • same side effects as ARBs (hyperkalemia and teratogenicity)
  • idea is to reduce compensatory increase in renin caused by ARB and ACE inhibitors
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64
Q

AVOID Renin Inhibitors in

A

patients with type 2 diabetes and kidney disease

  • increases incidence of cardiovascular and renal events
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65
Q

Phase 1 hypertension use ___

if phase 2 use__-

A

phase 1= one drug

phase 2= two drugs

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66
Q

for most hypertensive patients first prescribe

A

thiazide diuretics

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67
Q

for diabetic patients first prescrib

______ for hypertension

A

ACE Inhibitors

=protects kideys

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68
Q

for pts with Coronary Heart Disease first prescribe______ for hypertension

A

Beta Blockers

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69
Q

in African American patients __ = first line

A

CCBs or thiazides

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70
Q

NIH Sprint Study

A
  • under 60yrs start tx with BP of 140/90
  • older than 60 start tx with BP of 150/90
  • adults 50yrs or older should maintain systolic <120 mmHg
71
Q

classic angina

A

occlusion of coronary artery resulting form an anthrosclerotic plaque

  • most common
  • symptoms occur during exercise/stress
72
Q

antherosclerosis formation

A
  1. LDL penetrates arterial wall
  2. foam cells
  3. foam cells shear off and expose tissue
  4. clotting
  5. plaque formation

=cholesterol center with platelet/fibrin cap

73
Q

variant (Printzmetal’s) angina

A

=spontaneous vasoconstriction of coronary arteries

  • genetic origin
  • symptoms at rest
  • less common
74
Q

Liproprotiens

A

HDL= good -small amt of cholesterol

-takes cholesterol back to liver

LDL=bad -lots of cholesterol

VLDL=BAD triglycerides

75
Q

Lipid metabolism steps

A
  1. chylomicrons transport cholesterol and TGY from GI into circulation
  2. Lipoprotien lipase cleaves TGYs from chylomicrons and realeases ffa, leaving cholesterol to go to liver
  3. liver makes VLDL
  4. Lipoprotien lipase breaks down VLDL which go back to liver and are turned into LDL
  5. LDL binds to LDL recptors on cells =internalization
  6. HDL is also made in liver = (+) lipoprotien lipase and brings cholesterol back to liver
76
Q

liver makes its own cholesterol via

A

HMG Co-A reductase

77
Q

hypertryiglyceridemas

A

=increased VLDL

=some risk for CHD adn pacreatitis

78
Q

hypercholesterolemias

A

= increased LDL

=high risk for CHD

* most common is = “multifactorial”

-genetic, lifestyle, diet

79
Q

two basic strategies for treating hyperlipidemia

A
  1. decrease lipid entering blood
    - low fat diet
    - reduce lipoprotien synthesis
    - reduce dietary cholesterol absorption
  2. improve clearance of lipid from the blood
    - for VLDL - affect lipoprotien lipse
    - for LDL - increase LDL receptors
80
Q

drugs for hypertriglyceridemia

A

niacin

fibric acid derivatives

81
Q

drugs for hypercholestrolemia

A
  • bile acid binding sequestrants
  • statins
  • ezetimibe
  • nacin
  • combination therapy
82
Q

Niacin

A

treats hypertriglyceridemia

  • decreases circulating VLDL
    1. inhibits VLDL synthesis in liver
    2. stimulates breakdown of VLDL by lipoptotien lipase

=net decrease in LDL

=most effective at increasing HDl

-side effects = tachyfalaxis and flushing

83
Q

gemfibrozil

A

treats hypertriglyceridemia

=fibric acid derivative

  • most effective at reducing VLDL , but minimal effects on LDL and HDL
    1. inhibits VLDL synthesis
    2. stimulates breakdown of VLDL to LDL via lipoprotien lipase - (offsets the reduction of LDL)
84
Q

colesevelam

A

=bile acid sequestrant

=treates hypercholestrealemia

-reduces LDL and increases HDL

*second line of tx after statins

  • take orally, and bind to bile acids in stomach ∴ we need to make more
  • lower cholestrol= upregulation of LDL-R in liver

side effects - reduced folic acid absorption and GI probs

85
Q

Statins action

A

HMG-Co A Reductase Inhibitors

  • treat hypercholestrolemia
  • inhibit cholestrol synthes = upregulation of LDL-R

∴ increast removal of LDL fro blood

  • 60% decrease in cardiovascular events
  • 17% decrease in strokes
86
Q

statins drug list

A

low efficacy=:

pravastatin

lovastatin

medium efficacy:

simvastatin

pitavastatin

high efficacy:

atorvastatin (big one)

rosuvastatin

87
Q

statins side effects

A

los incidence liver toxicity

momory loss

diabetes risk (not enough to avoid tx.)

myopathy

88
Q

statin drug interactions

A

grapefruit juic inhibits metabolism and increases risk for rhabdomyolysis

89
Q

rhabdomyolysis

A

-induced by statins

=skeletal muscle cell lysis and dumping contents onto kidney causeing kidey failure and death

90
Q

ezetimibe

A
  • anticholesterol drug
  • inhibits fxn of protien in brush border of GI that would absorb cholesterol in small intestine

∴reduces LDL

91
Q

enhance study

A
  • reducing LDL may not be affecting coronayr antherosclerotic plaque formation …

maybe statins do other stuff too…

92
Q

AIM High Study

A
  • added niaspan to a statin
  • affected lipid profile as expected BUT didn decrease risk for heart atack

AND increased stroke risk…

93
Q

PCSK9

A

Proprotein convertase subtilisin/kexin type 9

-protien that metabolizes LDL-R insead of recycling them

94
Q

alirocumab

A

=mooclonal antibody

  • inhibits PCSK9
  • injected subcutaneously
95
Q

statin treatment guidelinse from American Heart Association

A
  1. pts with CHD
  2. pts with LDL > 190mg/dL
  3. diabetics 40-75 with out CHD and LDL < 190mg/dL
  4. pts w/out diabetes or LDL > 190 mg/dL who have estimated CHD risk >7.5% and 40-75 yrs old
96
Q

clot formation steps

A
  1. adhesion of platelets
  2. aggregation
  3. clotting vactors activated by endothelium

= (+) prothrombin -> thrombin

= (+) fibrinogen -> fibrin

  1. via PAR-1 receptor, thrombin (+) rlease of ADP nd TXA2
  2. prostacyclin (PGI2) opposes this
  3. fibrin mesh
97
Q
A
98
Q

antithrombin III

A

proteas inhibitor in blood that limits coagualtion

-all heparins area verison of this

99
Q

tissue plasminogen activator (T-PA)

A

fibrinolytic

limits coagutlaition

-all clot-busters are a version of this

100
Q

white thromubs

A

forms in high pressure arteries

  • small amounts of fibrin
  • mostly platelets

∴want to use an antiplatelet drug

  • causes local ischemia from artery occlusion
  • if in coronary arteries =MI PECTORIS!
101
Q

red thrombus

A
  • form in low pressure veins and in the heart
  • have platelets AND buly fibrin tails

∴want to use an anti-coagulant drug

  • DVT fibrin cap breaks off =PULMONARY EMBOLI
  • or cardiogenic emboli = EMBOLIC STROKE
102
Q

anti-coagulant basic function

A

regulate the fuction and sythesis of clotting factors

  • use with RED THROMBI
  • prevent clots form forming in venous system and heart
103
Q

antithrombotics/antiplatelets general fxn

A

inhibit platelet fuction

  • used for WHITE CLOTS
  • dont break down clots, just prevent clots form forming in arteries
104
Q

thrombolytics/fibrinolytics general fxn

A

destroy clots after they are formed

-break down fibrin!!

105
Q

parenteral anti coagulent types

A
  1. heparins
    - indirectly inhibit thrombin via anti-thrombin III
  2. parenteral direct thrombin inhibitors
    - directly inhibit thrombin
106
Q

oral anti-coagulant types

A
  1. warfarin
  2. oral nonpeptide DTI
  3. factor Xa inhibitor
107
Q

heparins

A

=parenteral anticoagulents

-stimulates ANTITHROMBIN III

= inhibits clotting factor synthesis

types:

  1. unfractionated heparin
  2. low molecular weight heparin
    - side effect =bleeding and heparin induce thrombocytopenia (immune rxn cuases clots)
108
Q

unfractionated heparin

A

combination of low and high molecular weights

=more activity

109
Q

low molecular weight heparin

A

less activity

=enoxaparin

110
Q

warfarin

A

=oral anticoagulant

  • delayed effects, need to use up already exixtant clotting factors
  • side effects =bleeding

antidote=vitamin K

111
Q

warfarin fxn schematic

A
112
Q

variation in warfarin enzymes and risks schematic

A
113
Q

dabigatran etixilate

A

=direct thrombin inhibitor

=anticoagulant

=less bleeding risk than warfarin

-no antidote yet

114
Q

rivaroxaban and apixaban

A

=factor Xa inhibitors (anticoagulant)

  • less bleeding risk than warfarin
  • no antidote yet
115
Q

alteplase

A

t-PA activator

-often used for strokes

116
Q

urokinase

A
  • recombinant form of a non t-PA human proteas
  • used for acute MI
117
Q

treating embolic/thrombotic/hemorrhagic stroke

A

80% of occlusions from

  1. ebolic = from red thrombi
  2. thrombotic= from white thrombi
    - treat with ALTEPLASE

20% of occlusions from

  • hemorrhagic stroke
  • DONT GIVE ANTICOAGULANT
118
Q

anti thrombotic drugs inhibit platelet fxn by interfering with…

A
  1. Thromboxane A2
  2. Adensosine diphosphate (ADP)
  3. thrombin
119
Q

thromboxane A2 fxn

A

=released formplatelets and promotes aggregation and vasocosntriction locally

120
Q

ADP fxn

A

released from platelets

binds purinergic receptors on other platelets = (+) aggregation

121
Q

thrombin fxn

A
  • increases fibirn production
  • activates PAR-1 receptor which promotes platelet activation
122
Q

antiplatelet drugs used for=

A
  1. preventing heart attacks/acute MI
    - if signs of unstable angina pectoris/during or after heart attack
  2. preventing arterial thrombus of limbs
  3. preventing thrombotic/ischemic stroke
  4. preventing percutaneous coronar interventions
123
Q

schematic of antiplatelet drugs

A
124
Q

aspin functionn

A

inhibits COX 1> COX 2

∴decreased TXA2 production

∴inhibits platelet aggregation

HAS THESE EFFECTS AT LOW DOSES (because of covalent acetylation of COX)

do not exceede 325mg

125
Q

clopridogrel

A

ADP R eceptor blocker

=a prodrug metabolized by CY2C19

-lots of variation in this enzyme (14%)

126
Q

plasugrel

A

ADP (adenosine diphosphate) Receptor Blocker

  • a prodrug but metabolized by a less variable CYP enzyme
  • stops platelet aggregation
127
Q

vorapaxar

A

PAR-1 antagonist

-long half life and no antidote= bleeding concerns ∴ dont use in pt with stroke history

128
Q

abciximab

tirofiban

A

=platelet recptor antagonists

=a GPIIb/IIIa antagonist

  • parenteral, highly effective drugs
  • prevent platelet-fibrin bond
129
Q

antiplatelet drugs protect against____ as a prophylactic….

A

heart attack

thrombotic stroke

also at time of heart attack (325mg) to prevent further clotting

130
Q

aspirin vs. ADP-R blockers

A

aspirin ADP Blockers

inexpensive expensive

effective more effective

bleeding risk less bleeding risk

more variable effect

131
Q

asprin, vorapaxar, ADP blockers, and GPIIb/IIIa inhibitors produce _________ effects

A

ADDITIVE

-maybe more effective but also more dangerous

132
Q

COX 1

A

produces TXA2

with inhibition by aspirin=

prevents platelet activation

133
Q

COX 2

A

produces prostacyclin (PGI2)

with inhibition by rofecoxib=

platelet activation… CLOT

134
Q

bleeding risk assessment tests

A
  1. APTT (activated partial thromboplastin time ):

for heparin

  1. PT (prothrombin time)

for warfarin

135
Q

for surgeries you may ned to induce clotting ∴ we use______

A
  1. antifibrinolytic drugs (prevent plasmin)
  2. hemostatic aids
  3. anticoagulant antidotes
136
Q

anticoagulant antidotes

A

vitamin K- reverses warfarin

protamine sulfates-binds and reverses heparins

137
Q

angina = imbalance btw__

A

imbalance between O2 demand and O2 supply

-drugs usually treat oxygen demand

138
Q

reucing O2 demand of heart by

A
  1. decrease HR
  2. decrease F of contraction
  3. decrease preload
139
Q

types of drugs for treating stable angina pectoris

A
  1. organic nigrates
  2. beta blockers
  3. CCB’s
  4. Combination therapy
140
Q

vasodilators for angina pectoris

A
  • targeting venous system= reducing preload
  • targeting coronary a. = increasing delivery of blood to myocardium

(dilating arteries is NOT beneficial bc it diverts blood away from coronary arteries)

∴ we use CCB’s and Nitrates

141
Q

CCB’s and variant vs classic angina

A

CCB’s work better agains variant angina

-in classic angina plaques make vessels unresponsive to relaxation

142
Q

organic nitrates are used to treat ____ pectoris

A

classic and variant

143
Q

nitroglycerine

isosorbide di- and mono- nitrate

A

=organic nitrates

=dlate veins and coronary arteries

nitroglycerine -give sublingually or transdermally

isosorbidine di-/mono-nitrate - give orally

TOLERANCE

144
Q

reflexes reactions to nitrates

A
  • reflex tachycardia
  • barroreceptors sense vasodialtion and (+) SNS

∴ coadminister with a BETA BLOCKER

145
Q

toxic effects of nitrates

A
  • 30% get bad headache (but tolerance develops)
  • flushing sweating
  • hypotension
146
Q

NO mechanism schematic

A
147
Q

viagra effects schematic

A
148
Q

beta blockers and angina pectoris use

A

ONLY FOR CLASSIC ANGINA PECTORIS WITH CCB or NITRATE!!

  • for CCB’s ONLY use amlodipin or nifedipine (only relax vascular sm. muscle)
  • NOT verapamil bc they also relax coronary vessels
    1. decreases HR
    2. decreases F of contraction
  • good for stress/exercise tolerance

-may cause vasopsam in prinzmetal’s angina

149
Q

rapid termination of ____ can ppt angin pectoris/heart attack

A

beta blockers

150
Q

CCBs types and effects towards angina pectoris

A
  1. cardioactive and non-cardioactive CCBs
    - dilates coronary arteries
  2. cardioactive CCBs only
    - decreases HR and F of contraction
151
Q

CCB uses for angina

A
  1. are effective against STABLE CLASSIC angina pectoris

monotherapy= cardioactive CCB

combination with a B-blocker= NON-cardioactie CCB

  1. FIRST CHOICE for variant (prinzmetal’s) angina
    - typically a cardioactive CCB
152
Q

use ___ for acute MI

A

urokinase - most effective

-breaks down fibrin

153
Q

surgical correction of coronary artery disease

A
  • drug-eluting oronayr stents
154
Q

overview:

drugs to treat stable angina:

drugs to treat unstable angina:

drugs to treat acute MI:

A

stable angina

beta blockers

nitrates

CCBs

unstable angina

anti-platelet drugs

acute MI

fibrinolytics

155
Q

cardiogenic shock =

A

acute heart failure

frominability of heart to pumb blood

-from MI, arrhythmia valve issues or end stage CHF

156
Q

drug types to treat cardiogenic shock

A
  1. Beta - Receptor agonists (increase HR)

dobutamine

  1. Phosphodiesterase 3 (PDE3)

milrinone

  1. Muscarinic receptor antagonists

atropine

157
Q

chronic congestive heart failure #1 and #2 causes

A

1=coronary artery disease/MI

158
Q

left ventricular systolic HF symtoms

A

pulmonary edema

enlarged heart

fatigue

159
Q

right ventricular symptoms

A

pitting edema

fatigue

160
Q

frank starling mechanism

A

as preload increses CO decreases

161
Q

specific therapeutic goals for treating chronic heart failure

A
  1. improve contractilit with out increasing HR
  2. reduce afterload
  3. reduce preload
162
Q

drugs for CHF

A
  1. ACE inhibitors/Angiotensin-R blockers
  2. Beta blockers (work but we dont know why)
  3. diuretics
  4. vasodialtors (NOT CCBs)
  5. Cardiac Glycosides (only historical use)
163
Q

ACE inhibitors and CHF

A

treat CHF

*** FIRST LINE DRUG FOR CHF with diuretics

  1. relax arterial sm muscle
  2. reduce aldosterone producton release
  3. dilate vens
  4. reduce trophic changes in myocardium
164
Q

ACE inhibitors list

A

(treat CHF)

captopril

enalopril

ramipril

165
Q

Angiotensin Receptor Blockers

A
  • used for CHF were ACE inhibitors are poorly tolerated
  • reduce symptoms AND mortality
166
Q

ARBs used for CHF list

A

valsartan

candesartan

167
Q

Beta Blockers and CHR

A
  • actually reduce cardiac output but improve survival
  • in combinaton with ACE inhibitor and ARB!
  • we dont kno why

only use bisoprolol, carvedilol and metoprolol

-initiate at slow doses

168
Q

bisoprolol and metoprolol

A

cardioselective B-blockers

used for CHR

-weirdly reduce CO

169
Q

carvedilol

A

=beta blocker with alph-1 antagonist effects (vasodilator)

-mechanism not clear but it reduces CO, so use with CHF

170
Q

diuretics and CHD

A

** FIRST LINE OF TX for CHD (with ACE inhibitors)

-actions: reduce Na+ reabsorption in nephron =decreased blood volume

includes thiazides, loob diuretics and K+ sparing drugs

∴reduce edema and preload

171
Q

vasodilators and CHF

A

NOT a first line of treatment

venous dilators =nitrates

∴decrease preload

arteriole dilators = hydralazine

∴ decrease afterload

DO NOT USE CCBS FOR CHF PATIENTS!!

it will reduce CO

172
Q

cardiac glycosides

A
  • used to be a first line of treatment for CHF
  • increase CO by increasing mycoardial contractility
  • can’t switch to ACE inhibitors without deteriorating condition
  • can cause more arrythmias bc it messes with membrane electronics
  • very small therepeutic window

=digoxin and digitoxin

173
Q

digoxin and digitoxin mechanism schematic

A

-used to treat CHF

174
Q

digitalis glycosides and K+ interactions

A

-both compete for same spot on Na+/K+ tansporter

∴

hyperkalemia (spironolactone)= LESS digitalis glycoside effects

hypokalemia (hydrochlorothiazide and furosemide)= MORE digitalis glycoside effects

Pharmacology (11 decks)

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