Pharm Test 3- Cardio 1

Front 1

PreHTN numbers

Back 1

S- 12-139
D- 80-89

should adopt lifestyle changes

Front 2

Stage 1 HTN

Back 2

S- 140-159
D- 90-99

If its Systolic >140 and Diastolic <90, that is isolated systolic HTN (ISH)

Front 3

Stage 2 HTN

Back 3

S->160
D- >100

Always base dx on higher of two numbers

Front 4

Types of HTN

Back 4

Primary-
No known cause
Chronic Progressive

Hint 4

Secondary HTN-
Can usually fix if you fix underlying problem.

Front 5

When is CV dx risk doubled?

Back 5

Risk for CV dz is doubled by an increase in systolic 20 mmHg, and diastolic 10 mmhg (beginning in 115/75 and ending in 185/155)

Front 6

Tx Goal for HTN

Back 6

Maintain systolic < 140
diastolic < 90 mm Hg

For pts with diabetes or chronic kidney dz target BP is 130/80

Front 7

Tx intervention for HTN

Back 7

Weight loss (can dec BP by 60-80%)

Na+ restriction(< 2.4 g/day)
DASH (Dietary Approaches to Stop HTN)
eat fruits, veggies, low-fat dairy products, low in saturated & total fat & cholesterol, whole grain, fish, poultry & nuts
Alcohol & smoking restriction, aerobic exercise

Maintenance of K+ & Cl- intake
K+ can lower BP, so maintain K+ intake (fresh fruits, veggies)

Front 8

What influences BP?

Back 8

Heart rate (HR),

myocardial contractility (force of contraction),

blood volume,

venous return of blood to the heart

*Increase in any of these will cause a rise in CO & therefore an inc in BP*

Front 9

Drugs that affect BP

Back 9

Drugs that dec HR & contractile force: beta blockers, verapamil, diltiazem

Drugs that dec blood vol: diuretics

Venodilators, which reduce venous return

Arteriolar dilation can counteract peripheral vascular resistance

Front 10

Regulation Blood Pressure

Back 10

-Renal regulation of BP: neutralize renal effects on BP with diuretics

-Sympathetic Barorecptor Reflex: Sets BP at normal rate & can cause reflex tachycardia if drugs drop BP too low. After extended period of time using BP lowering agents the baroreceptors are set at a lower level.

-Direct & Indirect drug affects on BP: Different drugs can affect blood pressure in various ways.

-Regulatory systems: Sympathetic Nervous System, Renin-Angiotensin-Aldosterone system (RAAS), the kidney

Front 11

RAAS System

Back 11

kidney released renin in response to reduced renal blood flow, volume or pressure. Renin converts angiotensin to angiotensin I & ACE converts this to angiotensin II which constricts systemic & renal blood vessels. Which inc BP

Hint 11

RAAS also releases aldosterone which further inc retention of Na+ & H2O

Ways to counteract renin release: suppress renin with beta blockers. Prevent conversion of angioten I with ACE inhibitors & angiotensin II rec with ARB’s & block aldosterone with aldosterone antagonist

Front 12

Thiazide Diuretics

Back 12

Thiazide diuretics – reduce blood vol (initial HTNsive effects)& reduce arterial resistance (long term HTNsive effects) (HCTZ, chlorthalidone) 1st line

Adverse effect: hypokalemia so eat K+ rich foods (bananas citrus fruits)or K+ supplements, Dehydration, hyperglycemia & hyperuricemia

Front 13

Loop diuretics

Back 13

Loop diuretics – highest diuresis used for pts that need greater diuresis than with thiazides & pts with low GFR (thiazides will not work if GFR is low). Reduce blood vol & promote vasodilation (furosemide, torsemide)

Front 14

Potassium-Sparing Diuretics –

Back 14

diuresis is small but K+ loss is small also. (spironolactone)

Adverse effect: hyperkalemia (do NOT use with ACE inhibitors, ARB’s or aldosterone antagonist)

Front 15

Antihypertensive Sympatholytic Drugs- Beta Blockers and AE

Back 15

Beta 1 blockers – less effective in blacks than whites. Blockade of beta1 rec dec HR & contractility thus dec CO, suppress reflex. tachycardia caused by vasodilators, reduces release of renin reducing angiotensin II vasoconstriction & suppression of aldosterone-mediated volume expansion, reduce peripheral resistance. (beta blockers: atenolol, propranolol etc…)

Adverse rxn – bradycardia, dec AV conduction, reduced contractility, bronchoconstriction (try to use beta selective), can mask sx of hypoglycemia

Front 16

Antihypertensive Sympatholytic Drugs- Alpha 1 Blockers and AE

Back 16

blockade of alpha1 rec on arterioles & veins thus preventing vasoconstriction which reduces peripheral resistance & venous return to the heart (doxazosin, Prazosin, terazosin, labetalol (beta blocker with alpha blocking activity)

Not 1st line medication
Adverse rxn – orthostatic hypotension

Front 17

Antihypertensive Sympatholytic Alpha/beta blockers and AE

Back 17

Alpha/Beta Blockers – combo of axn. Alpha1 blockade promotes dilation of arterioles & veins.
Beta1 blockade reduce release of renin, HR & contractility (carvedilol, labetalol)

Adverse rxn:
Beta blockers: bradycardia, AV heart block & asthma
Alpha blockers: postural hypotension

Front 18

Antihypertensive sympatholytic- Centrally Acting Alpha2 agonist
and AE

Back 18

Centrally Acting Alpha2 Agonist – Act within the brainstem to suppress sympathetic outflow to the heart & blood vessels thus vasodilation & reduced CO, HR, & myocardial contractility which dec BP (clonidine, methyldopa)

Adverse effects – dry mouth sedation
Clonidine: can cause rebound HTN if abruptly stopped.
Methyldopa: hemolytic anemia & liver disorders

Front 19

Antihypertensive Sympatholytics-Adrenergic Neuron Blockers and AE

Back 19

Adrenergic Neuron Blockers – Guanethidine & quanadrel inhibit release of NE & reserpine causes NE depletion both result in decreased sympathetic stimulation of the heart & blood vessels

Adverse effects:
Guanethidine & guanadrel: orthostatic hypotension
Reserpine: depression

Sympathetic ganglia – ganglionic blockade reduces sympathetic stimulation of the heart & blood vessels (dilation of arterioles & veins) (mecamylamine) so profound dilation only used in HTNisve emergencies

Front 20

Antihypertensive Direct Acting Vasodilators- AE

Back 20

Direct acting vasodilators – dilation of arterioles with very little venous dilation (hydralazine, monoxidil)

Vascular Smooth Muscle – relaxation of vascular smooth muscle (Na+ nitroprusside & diazoxide) Used only in HTNsive emergencies and also in chronic HTN (Hydralazine)

Adverse effect: reflex tachycardia & release of renin (which can be stopped with a beta blocker), fluid retention (stopped with a diuretic)
AE of minoxidil is fluid retention which can cause pericardial effusion (fluid beneath the myocardium) and hypertrichosis (excessive hair growth)

Front 21

Antihypertensive drugs- Calcium Channel Blockers

Back 21

Calcium channel blockers – both groups promote dilation of arterioles & non-dihydropy have direct suppressant effects on the heart

2 groups:
Dihydropyridines (nifedipine, amlodipine)
Adverse effects: reflex tachycardia (mostly dihydropy & can be substantial b/c they do not block cardiac Ca++ channels)

Non-dihydropyridines (verapamil, diltiazem)
Adverse effects: use in caution in pt with bradycardia & heart failure or AV block b/c of their suppression of the heart

Front 22

Antihypertensive Drugs- ACE inhibitors

Back 22

Ace Inhibitors – peripheral & renal vasodilation & suppression of aldosterone mediated volume expansion by preventing formation of angiotensin II. These drug can slow the progress of kidney failure in diabetic pt with renal damage (lisinopril, captopril)
Less effective in African Am. Than whites

AE: persistent cough, 1st dose hypotension, angioedema & hyperkalemia. Can cause fetal harm in 2nd & 3rd trimester and is only antihypertensive that is contraindicated in pregnancy

Front 23

Antihypertensive Drugs- Angiotensin 2 Rec Blockers

Back 23

Angiotensin II rec blockers – same MOA as ACE inhibitors except they block the axns of angiotensin (losartan, ibersartan)

AE: angioedema, do not use in pregnancy
Aldosterone antagonist – blockade of rec in kidney promotes excretion of Na+ & H2O thus reducing blood volume (spironolactone, eplerenone)

AE: hyperkalemia,
do not give with K+ sparing diuretics or K+ supplements

Front 24

Choosing a Drug for HTN

Back 24

Thiazides & beta blockers are most effective at reducing morbidity & mortality

1st line agents: thiazides, beta blockers, ACE inhibitors, ARB’s, CCB’s & alpha/beta blockers
Stage 1 HTN: thiazide diuretic
Stage 2: thiazide diuretic combined with beta blocker, ACE inhibitor, CCB or ARB

Front 25

Starting Therapy

Back 25

Use drug from different classes
Start at low dose and increase
Remember if giving a vasodilator give a beta blocker also to prevent reflex tachycardia
After HTN controlled for 1 year then can begin step down tx

Front 26

Special Considerations

Back 26

Renal dz: nephrosclerosis (hardening of the kidney) causes H2O retention which causes HTN. Target is 130/80. ACE inhibitors & ARB’s work best with a diuretic. thiazides may not work in severe renal dz may have to use loop.
Diabetes: target BP is 130/80 with ACE inhibitors, ARB’s, CCB’s & diuretics.
Beta blockers can be used but may mask the S/Sx of hypoglycemia & can suppress glycogenolysis.
Thiazides & loops can promote hyperglycemia so use with caution

Front 27

Antihypertensive drugs- Calcium Channel Blockers

Back 27

Calcium channel blockers – both groups promote dilation of arterioles & non-dihydropy have direct suppressant effects on the heart

2 groups:
Dihydropyridines (nifedipine, amlodipine)
Adverse effects: reflex tachycardia (mostly dihydropy & can be substantial b/c they do not block cardiac Ca++ channels)

Non-dihydropyridines (verapamil, diltiazem)
Adverse effects: use in caution in pt with bradycardia & heart failure or AV block b/c of their suppression of the heart

Front 28

Antihypertensive Drugs- ACE inhibitors

Back 28

Ace Inhibitors – peripheral & renal vasodilation & suppression of aldosterone mediated volume expansion by preventing formation of angiotensin II. These drug can slow the progress of kidney failure in diabetic pt with renal damage (lisinopril, captopril)
Less effective in African Am. Than whites

AE: persistent cough, 1st dose hypotension, angioedema & hyperkalemia. Can cause fetal harm in 2nd & 3rd trimester and is only antihypertensive that is contraindicated in pregnancy

Front 29

Antihypertensive Drugs- Angiotensin 2 Rec Blockers

Back 29

Angiotensin II rec blockers – same MOA as ACE inhibitors except they block the axns of angiotensin (losartan, ibersartan)

AE: angioedema, do not use in pregnancy
Aldosterone antagonist – blockade of rec in kidney promotes excretion of Na+ & H2O thus reducing blood volume (spironolactone, eplerenone)

AE: hyperkalemia,
do not give with K+ sparing diuretics or K+ supplements

Front 30

Choosing a Drug for HTN

Back 30

Thiazides & beta blockers are most effective at reducing morbidity & mortality

1st line agents: thiazides, beta blockers, ACE inhibitors, ARB’s, CCB’s & alpha/beta blockers
Stage 1 HTN: thiazide diuretic
Stage 2: thiazide diuretic combined with beta blocker, ACE inhibitor, CCB or ARB

Front 31

Starting Therapy

Back 31

Use drug from different classes
Start at low dose and increase
Remember if giving a vasodilator give a beta blocker also to prevent reflex tachycardia
After HTN controlled for 1 year then can begin step down tx

Front 32

Special Considerations

Back 32

Renal dz: nephrosclerosis (hardening of the kidney) causes H2O retention which causes HTN. Target is 130/80. ACE inhibitors & ARB’s work best with a diuretic. thiazides may not work in severe renal dz may have to use loop.
Diabetes: target BP is 130/80 with ACE inhibitors, ARB’s, CCB’s & diuretics.
Beta blockers can be used but may mask the S/Sx of hypoglycemia & can suppress glycogenolysis.
Thiazides & loops can promote hyperglycemia so use with caution

Front 33

Antihypertensive drugs- Calcium Channel Blockers

Back 33

Calcium channel blockers – both groups promote dilation of arterioles & non-dihydropy have direct suppressant effects on the heart

2 groups:
Dihydropyridines (nifedipine, amlodipine)
Adverse effects: reflex tachycardia (mostly dihydropy & can be substantial b/c they do not block cardiac Ca++ channels)

Non-dihydropyridines (verapamil, diltiazem)
Adverse effects: use in caution in pt with bradycardia & heart failure or AV block b/c of their suppression of the heart

Front 34

Antihypertensive Drugs- ACE inhibitors

Back 34

Ace Inhibitors – peripheral & renal vasodilation & suppression of aldosterone mediated volume expansion by preventing formation of angiotensin II. These drug can slow the progress of kidney failure in diabetic pt with renal damage (lisinopril, captopril)
Less effective in African Am. Than whites

AE: persistent cough, 1st dose hypotension, angioedema & hyperkalemia. Can cause fetal harm in 2nd & 3rd trimester and is only antihypertensive that is contraindicated in pregnancy

Front 35

Antihypertensive Drugs- Angiotensin 2 Rec Blockers

Back 35

Angiotensin II rec blockers – same MOA as ACE inhibitors except they block the axns of angiotensin (losartan, ibersartan)

AE: angioedema, do not use in pregnancy
Aldosterone antagonist – blockade of rec in kidney promotes excretion of Na+ & H2O thus reducing blood volume (spironolactone, eplerenone)

AE: hyperkalemia,
do not give with K+ sparing diuretics or K+ supplements

Front 36

Choosing a Drug for HTN

Back 36

Thiazides & beta blockers are most effective at reducing morbidity & mortality

1st line agents: thiazides, beta blockers, ACE inhibitors, ARB’s, CCB’s & alpha/beta blockers
Stage 1 HTN: thiazide diuretic
Stage 2: thiazide diuretic combined with beta blocker, ACE inhibitor, CCB or ARB

Front 37

Starting Therapy

Back 37

Use drug from different classes
Start at low dose and increase
Remember if giving a vasodilator give a beta blocker also to prevent reflex tachycardia
After HTN controlled for 1 year then can begin step down tx

Front 38

Special Considerations

Back 38

Renal dz: nephrosclerosis (hardening of the kidney) causes H2O retention which causes HTN. Target is 130/80. ACE inhibitors & ARB’s work best with a diuretic. thiazides may not work in severe renal dz may have to use loop.
Diabetes: target BP is 130/80 with ACE inhibitors, ARB’s, CCB’s & diuretics.
Beta blockers can be used but may mask the S/Sx of hypoglycemia & can suppress glycogenolysis.
Thiazides & loops can promote hyperglycemia so use with caution

Front 39

Major Applications of Diuretics

Back 39

1.Hypertension (HTN)
2.Dec edema (heart failure, cirrhosis, kidney disease)
3. Prevent renal failure

Front 40

Special Consideration for Nitroprusside

Back 40

Sodium Nitorprusside: Used for acute severe HTN that needs a rapid reduction in BP

Front 41

Special HTN drug considerations in pregnancy

Back 41

Pregnancy: Except for ACE inh & ARB’s drugs that were taken before preg can be taken after. If drug is initiated DURING preg. Methyldopa is drug of choice.

Hint 41

Depending on gestation tx can be bed rest to anticonvulsants DOC is Mg+ sulfate also can give vit C or vit E

Front 42

Special HTN drug considerations in Preeclampsia and Eclampsia

Back 42

Preeclampsia & Eclampsia: elevated BP 140/90 & proteinuria (300 mg in 24 h) that develop after the 20th week of gestation. If seizures develop the condition is called eclampsia

Front 43

DOC for Acute lowering BP?

Back 43

Hydralazine

Front 44

Special HTN Drug Considerations for Renal Dz

Back 44

Renal dz: nephrosclerosis (hardening of the kidney) causes H2O retention which causes HTN. Target is 130/80. ACE inhibitors & ARB’s work best with a diuretic. thiazides may not work in severe renal dz may have to use loop.

Front 45

Special HTN Drug Considerations for Diabetes

Back 45

Diabetes: target BP is 130/80 with ACE inhibitors, ARB’s, CCB’s & diuretics.
-Beta blockers can be used but may mask the S/Sx of hypoglycemia & can suppress glycogenolysis.
-Thiazides & loops can promote hyperglycemia so use with caution

Front 46

Where does Active Transport occur in the kidneys?

Back 46

Proximal Convoluted Tubule

Front 47

What happens in the Proximal Convoluted Tubule (PCT)?

Back 47

Most of filtered Na+ & Cl- (& H2O follows Na+) occurs & almost all of the K+ & bicarb. are reabsrobed at the PCT

Loop of Henle – decsending loop is freely permeable to H2O which causes the urine to become more conc.

The ascending limb of Henle which is not permeable to water filters about 20% of Na+ & Cl-

Hint 47

Early segment PCT – 10% of Na+ & Cl- is reabsorbed & H2O follows
Late segment PCT – Exchanges Na+ for K+ under aldosterone (mineralocorticoid) influence. This is the final conc of the urine & is regulated by antidiuretic hormone (ADH)

Front 48

Where does Na+/K+ exchange occur?

Back 48

Aldosterone stimulates resorption from the distal nephron

Front 49

Drug actions in proximal nephron vs distant nephron

Back 49

Drugs whose site of axn is early in the nephron have the opportunity to block the greatest amt. of solute resorption. Accordingly these agents produce the greatest diuresis

Hint 49

Diuretics that act at the distal sites have very little reabsorption available to block.

Front 50

Classifications of Diuretics

Back 50

1) High ceiling (Loop) diuretics (furosemide)
2) Thiazide diuretics (hydrochlorothiazide HCTZ)
3) Osmotic diuretics (mannitol)
4) Potassium-sparing diuretics
a. Aldosterone antagonist (spirinolactone)
b. Non-aldosterone antagonist (triamterene)
5)Carbonic anhydrase inhibitors (dec. intraocular pressure)

Front 51

High Ceiling Diuretics

Back 51

Furosemide (Lasix),
Bumetanide (Bumex), Torsemide (Demadex), Ethacrynic acid (Edecrin)

Hint 51

Known as “loop diuretics (Henle),” are the most effective diurectics b/c of placement in the nephron. Can produce profound diuresis.

Block reabsorption of Na+ & Cl- (20%)which blocks reabsorption of H2O

Front 52

Pharmacokinetics of High Ceiling Diuretics

Back 52

PO, IV, IM

Hint 52

IV diuresis begins within 5 min, DOA 2h (used for critical pulmonary edema)

Front 53

Therapeutic Uses for High Ceiling Diuretics

Back 53

Try other diuretics 1st & if unresponsive use “loops”
Edema (CHF, hepatic, cardiac, renal), HTN, severe renal impairment b/c can promote diuresis even when renal blood flow & glom. Filtration rate is low.

Front 54

AE of FUROSEMIDE

Back 54

Hyponatremia,
Hypochloremia & Dehydration (b/c loss of NaCl & H2O)
dry mouth, thirst, oliguria, wt. loss,
thrombosis, embolism,
HA,
chest, calve & pelvis pain
Hypotension (get up slowly), Hypokalemia (usually give K+ supplement, take K+ sparing diuretic,
eat K+ rich foods (dried fruits, nuts, spinach, citrus, potatoes, bananas)
Ototoxicity (rare), hyperuricemia, hyperglycemia
Inc LDL & TG & dec HDL
Dec excretion of Ca++ (kidney stones)
Inc excretion of Mg++ (muscle weakness, tremor, dysrhythmias)

Front 55

Furosemide Drug Interactions

Back 55

Digoxin (monitor K+ levels if must give “loop” w/ digoxin)
Ototoxic drugs (aminoglycosides)
Lithium

Front 56

How do Thiazides work?

Back 56

Inc renal excretion of Na+, Cl- & H2O by blocking reabsorption in the early segment of the distal convoluted tubule


thiazides DO NOT work well if kidneys not working well.

Front 57

Pharmacokinetics of Thiazides

Back 57

Diuresis beings within 2h , peak 4-6h, DOA 12h
Therapeutic Uses:
Essential HTN (often 1st choice)
Edema in mild-moderate heart failure
Diabetes insipidus

Front 58

AE and Drug interactions of Thiazides

Back 58

AE-same as loop diuretics

Drug Interactions: Same as Loop, except that thiazides can be mixed with ototoxic drugs

Front 59

Two types of Potassium-Sparing Diuretics

Back 59

1) Aldosterone antagonist: Spironolactone (Aldactone)

2) Non-aldosterone antagonist: Triamterene (Dyrenium), Amiloride (Midamor)

Produce modest inc in urine production & produce substantial dec in K+ excretion (but diuretic effects are limited)

Front 60

K+ Sparing Diuretic- SPIRINOLACTONE

MOA

Back 60

Blocks axn of aldosterone in the distal nephron. Opposite effect of aldosterone retention of K+ & inc excretion of Na+
Scanty diuresis b/c of placement

Front 61

Pharmacokinetics of Spirinolactone

Back 61

Takes up to 48h to work

Front 62

Therapeutic uses for Spirinolactone

Back 62

HTN, edema

Usually used in combo with loop or thiazides to combat K+ wasting effects

Front 63

AE of Spirinolactone

Back 63

Hyperkalemia (possible fatal dysrhythmias & insulin could dec K+ levels by K+ uptake into cells)

Spirinolactone is a steroid derivative (gynecomastia, menstrual irregularities, impotence, hirsutism & deepening of voice

Front 64

Drug interactions of Spirinolactone

Back 64

Agents that inc K+ levels (K+ supplements, salt substitutes that contain KCl, ACE inhibitors

Front 65

K+ Sparing Diuretic- TRIAMTERENE

Back 65

Disrupts Na+/K+ exchange in the distal nephron. Unlike spirinolactone which blocks Na+/K+ exchange through aldosterone triamterene directly blocks Na+/K+ exchange. Na+ excretion is inc while K+ is spared

Front 66

Pharmacokinetics of Triamterene

Back 66

Acts much more quickly than spirinolactone but still only cause scanty diuresis

Front 67

Therapeutic uses for Triamterene

Back 67

Alone or in combo to tx edema or HTN

Front 68

AE of Triamterene

Back 68

Hyperkalemia (esp with other K+ sparing diuretics including ACE inhibitors)
N/V, leg cramps & dizziness
Blood dyscrasias (Rare

Front 69

MOA of Mannitol (osmitrol)

Back 69

Creates an osmotic force in the lumen of the nephron which prevents passive reabsorption of H2O. Amt of diuresis is directly correlated to the amt of mannitol in the filtrate

Has no significant effect on excretion of K+ or electrolytes

Front 70

Pharmacokinetics of Mannitol

Back 70

IV Only!


Drug is not absorbed PO therefore must be given IV to get systemic

Diuresis begins within 30-60 min, DOA 6-8h & excreted intact in the urine.

Front 71

Therapeutic uses for Mannitol

Back 71

Prophylaxis of renal failure when urine production ceases mannitol will stay in nephron pulling H2O with it

Reduction of intracranial pressure b/c of osmotic force it pulls fluid away from brain.

Reduction of intraocular pressure

Front 72

AE of Mannitol

Back 72

Edema except in the brain (use in extreme caution in pts with CHF & pulmonary edema)

HA, N/V

Front 73

What is Angina Pectoris?

Back 73

Sudden pain beneath the sternum often radiating to the left shoulder & arm

Precipitated when O2 demand to heart is not met

Occurs SECONDARY to atherosclerosis of the coronary arteries. So is a secondary dz use anticholesterol & antiplatelet drugs to decrease risk of MI.

Front 74

Drugs used to Tx Angina Pectoris (4)

Back 74

Organic nitrates: Dec O2 demand by dilating veins which dec. preload (for stable angina) or inc. O2 supply by relaxing coronary vasospasm (Variant)

Beta blockers: Dec O2 demand by dec HR & contractility (propranolol)(stable angina). Not used in variant

Hint 74

CCB’s: Dec O2 demand by dilating arterioles, which dec afterload (all CCB’s), & by dec HR & contractility (verapamil & diltiazem) (for stable angina) or by inc O2 supply by relaxing coronary vasospasm (variant)

Aspirin: to reduce risk of MI

Front 75

Three forms of Angina Pectoris

Back 75

1) Chronic Stable (exertional Angina)
2) Variant Angina (prinszmetal's or vasospastic angina)
3) Unstable Angina

Front 76

Chronic Stable Agina

Back 76

triggered by physical activity (exertion), large meals, cold. Cause is plague (coronary artery dz which cause blockage). Need to inc. O2 supply & dec O2 demand

Front 77

Variant Angina

Back 77

which causes pain which can happen ANYTIME.

Front 78

Tx that treat variant Angina

Back 78

INC O2 SUPPLY with vasodilators to prevent or relieve coronary artery spasm.

Drugs used to tx variant angina: CCB’s, organic nitrates. Beta blockers are NOT effective in variant

Drugs are for Sx tx ONLY they do not tx underlying dz.

Front 79

Unstable Angina

Back 79

MEDICAL EMERGANCY. Sx from severe CAD complicated by vasospasm, platelet aggregation & transient coronary thrombi or emboli. Death risk is greater with stable but smaller than risk with MI

Sx- may present: at rest, by exertion, intensification of existing angina

Front 80

Tx of Unstable Angina

Back 80

SL or spray, then IV

-beta blockers then non-dihydropyridine CCB’s (verapamil or diltiazem)

-O2 supply for pt with cyanosis or respiratory distress, IV morphine

-ACE inhibitor (only if persistent HTN or left ventricular dysfxn or CHF.

-SQ low molecular weight heparin (dalteparin [Fragmin]

Hint 80

-Aspirin,
Clopidogrel (Plavix),
Abciximab (ReoPro): use ONLY if angioplasty is planned,

Eptifibatide (Intergrilin or Tirofiban (Aggrastat) Only if high risk pt with ischemia and ONLY if angioplasty is NOT planned

Front 81

Nitrates Pharmacokinetics

Back 81

PO, SL, buccal, IV, transdermal, spray, ointment

Absorption- High lipid Soluble, crosses membranes

VERY IMPORTANT- have at least 8 h drug free period with patches.

Discontinue long acting NTG slowly.

Front 82

Nitrates

Back 82

DOC to tx angina.

Works through Vasodilation (primarily on Veins)

Front 83

AE of Nitrates

Back 83

Ha

Hypotension

Tachycardia

Front 84

Drug Interactions of Nitrates

Back 84

Drug Interactions: use in caution in all drugs that can lower BP, Viagra, Cialis, Levitra which can intensify vasodilation (absolutely CI)

Front 85

Guidelines for using Sublingual Nitrates

Back 85

Sublingual: is best/quickest for terminating ongoing attack & short-term prophylaxis when exertion is anticipated
If pain is not relieved in 5 min call 911.
can take up to 3 SL tabs 5 min apart.
Tightly closed, light resistant container with an easy open cap. Only good for 1 yr or for 3 mo after opening

Sustained release: take ONLY qd-bid. Not used for ongoing attack

Front 86

guidelines for using Transdermal Nitrates

Back 86

Transdermal: qd to hairless area. Need patch free 12 h period. Not used for ongoing attack

Front 87

Guidelines for using Translingual spray

Back 87

same as SL

Front 88

Guidelines for Buccal Nitrates

Back 88

Dossolves over 3-5 H, can be used for acute attack or prophylaxis

Front 89

Guidelines for using Nitrate Ointment

Back 89

Chest, back abdomen, thigh. Used for sustained protection against anginal attack

Front 90

Guidelines for using Nitrate IV infusion

Back 90

Used only to tx angina pectoris and is only used when other NTG methods have failed. Short DOA so continuous infusion is required. Monitor HR & BP

Front 91

What drugs will you use in Acute Tx of Angina?

Back 91

use SL tabs, buccal & spray. Can use it for acute attack or prophylaxis in anticipation of exertion

Front 92

What drugs will you use for sustained prophylaxis of Angina?

Back 92

Patches, ointment, SL, SR caps

Front 93

What drugs will you use for preoperative control of BP?

Back 93

Nitroglycerin IV infusion for surgery, tx of heart failure associated with acute MI & is also used for unstable & chronic angina when Sx cannot be controlled with preferred medications

Front 94

Other Organic Nitrates

Back 94

Isosorbide Mononitrate and Dinitrates : Identical to NTG
-used for Angina. AE: HA, Hypotension and reflex tachcardia
(Difference is route of admin (PO) and time

Hint 94

Amyl Nitrate: Ultra short acting to tx acute episodes if angina pectoris. Same MOA as NTG. Ampule is crushed to be inhaled. Axn begin within 30 sec & last 3-5 min.

Is also used to intensify sexual orgasm.