Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Block 2 > Block 2 drugs > Flashcards

Block 2 drugs Flashcards

1
Q

<p>Phylloquinone</p>

A

<p>counteracts effects of excess warfarin or genetic vitamin K deficiency</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

<p>Lyophilized factor VIII</p>

A

<p>Concentrates are prepared from large pools of plasma

| Treatment for Hemophilia A</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

<p>Desmopressin acetate</p>

A

<p>Increases factor VIII activity</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

<p>Factor IX concentrate</p>

A

<p>Contains activated clotting factors

| Treatment for Hemophilia B</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

<p>Cryoprecipitate</p>

A

<p>Plasma protein fraction obtainable from whole blood containing fibrinogen
Treatment for Fibrinogen deficiency</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

<p>Ferrous sulfate, Ferrous gluconate, Ferrous fumarate</p>

A

<p>effective, inexpensive and recommended treatment of most patients</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

<p>Deferoxamine</p>

A

<p>iron-chelating compound given systemically

| binds absorbed iron and promotes its excretion in urine and feces</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q 
<p>Sodium ferric gluconate (Ferrlecit)
Iron sucrose (Saccharate)</p>
A

<p>preferred agents for parenteral iron therapy

| IV</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

<p>Iron Dextran (INFED, DEXFERRUM)</p>

A

<p>Parenteral Iron therapy
IM injection
Greater risk of anaphylactic shock</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

<p>Cyanocobalamin</p>

A

<p>Parenteral B12 therapy- IM injection (NEVER IV)

| Every 4 wks (DOSE 1 microgram to 1 milligram)</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

<p>Hydroxocobalamin</p>

A

<p>Parenteral B12 therapy IM injection

| single dose can last months</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

<p>Folic acid (oral tablets)</p>

A

<p>1 mg per day used for anemia associated with folate deficiency</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

<p>Folinic acid (leucovorin calcium)</p>

A

<p>5-formyl derivative of tetrahydrofolic acid that occurs downstream of antifolate cancer drug targets: effective to counter adverse effects of antifolate theray in cancer</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

<p>Recombinant erythropoietin</p>

A

<p>treatment of the anemia associated with renal failure by increasing RED Blood Cell production (Subcutaneous injection)</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

<p>Iron chelation therapy (Deferoxamine)</p>

A

<p>Thalessemia treatment-is often required to avoid end-organ damage in the heart, endocrine organs, and liver</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

<p>Folate supplementation</p>

A

<p>Lifelong supplementation for Sickle Cell therapy</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

<p>Hydroxyurea</p>

A

<p>reactivates production of fetal hemoglobin (SS treatment)</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

<p>Antiplateletdrugs</p>

A

<p>Prevent primary hemostatic plug formation</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

<p>Anticoagulant drugs</p>

A

<p>Inhibit clotting cascade to prevent fibrin clot formation</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

<p>Thrombolytics</p>

A

<p>digest fibrin to break up existing clot</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

<p>Aspirin (ASA)</p>

A

<p>Antiplatelet---Selectively inhibits thromboxane A2 synthesis by irreversible acetylation of enzyme COX-1 (cyclooxygenase)
Higher dose--leads to inhibition of prostacyclin production and reduced efficacy of ASA therapy
The effect of ASA therapy persists for platelet lifespan (7-10 d)
Antiplatelt drug of choice unless allergy or resistance
30% resistance in population</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

<p>Clopidrogrel (Plavix)</p>

A

<p>Irreversible inhibitor of the P2Y12 receptor
Duration of antiplatelet effect is 7-10 days
Is a prodrug metabolized by CYP2C19
Reduction of the rate of stroke, MI, unstable angina and death in patients with recent MI or Stroke, peripheral arterial disease, or acute coronary syndrome.
Can have reduced effectiveness in patients who are poor metabolizers of Plavix due to CYP2C19 status
</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ticlopidine (Ticlid)

A

Irreversible inhibitor of the P2Y12 receptor
Is a prodrug that is activated by a liver CYP enzyme
Maximal inhibition of platelet aggregation in 8-11 days, and steady state plasma concentration peaks after 14-21 days, due to non-linear pharmacokinetics
Should be discontinued 10-14 days prior to surgery
Used as standard practice combination with ASA to prevent stent thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Prasugrel (Effient)

A

More potent inhibitor of P2Y12 receptor than older drugs
Treat thrombosis in at risk patients, eg accompanying angioplasty
Adverse: hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Ticagrelor (Brilinta)

A

Reversible P2Y12 blocker
Metabolized by CYP3A4
Reduce risk of stroke, heart attack and death in patients with previous MI or angina
Adverse: hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Abciximab (REOPRO)

A

GP IIb/IIIa receptor inhibitor
Fab fragment of antibody targeting the GPIIb/IIIa
Used with ASA and heparin to treat acute coronary thrombosis or during coronary angioplasty, reduces restenosis, recurrent MI
Continuous infusion used in the perioperative setting
Adverse: Major hemorrhagic event 10% of patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Eptifibatide (Integrillin)

A

Peptide inhibitor of fibrinogen binding site of GPIIb/IIIa receptor
Used with ASA and heparin to treat acute coronary thrombosis or during coronary angioplasty, reduces restenosis, recurrent MI
Continuous infusion used in the perioperative setting
Adverse: Major hemorrhagic event 10% of patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Dipyridamole

A

Inhibits thrombus formation due to inhibition of PDE (phosphodiesterase)
Inhibits adenosine uptake
Short duration of action, and is also a vasodilator
Primary therapeutic use in combinatino with aspirin to prevent stroke: cerebrovascular ischemia
Adverse: Not indicated for coronary disease due to “coronary steal”: vasodilation redueces blood circulation to the heart
Hypotension
Increased bleeding risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Anitcoagulants

A

Act on clotting cascade to either inhibit pro-clotting factors or activate anti-clotting factors:
-Direct thrombin inhibitors
-HMW-Heparin
-LMW-Heparin
Prevent synthhesis of coagulation factors via vitamin K-Warfarin
Rivaroxaban (Xarelto): factor Xa inhibitor
Anticoagulant drugs typically reduce global clotting factor activity by 30-50% at therapeutic doses
Cannot dissolve a thrombus that has already formed

30
Q

Dabigatran Etexilate (Pradaxa)

A

Direct thrombin inhibitor
standard oral twice daily
Low molecular weight pro-drug, rapidly (approx 1 hr) converted to active form Dabigatran: competative inhibitor-binds to exosite 1 on thrombin preventing fibrinogen cleavage to mature fibrin
Use: stroke prevention in patients with atrial fibrillation, equal efficacy to warfarin, less patient monitoring and adverse effects. Also for DVT and pulmonary embolism.
Benefits: no patient monitoring/titration as with warfarin, rapid onset of action, less adverse drug reactions.
Adeverse: Hemorrhage, heartburn, stomach upset, increase in risk of MI

31
Q

Hirudin: Irreversible thrombin inhibitor (isolated from leeches)

A

Used in patients with thrombosis related to heparin-induced thrombocytopenia
Derivatives: Lepirudin (Refludan): Single amino acid change

32
Q

Argatroban

A

Reversible thrombin inhibitor

Used in patients with or at risk of heparin-induced thrombocytopenia

33
Q

Bivalirubin

A

Reversible thrombin inhibitor
Used in coronary angioplasty
Adverse: increased bleeding risk

34
Q

HMW Heparin

A

Inhibits clotting factors IXa, Xa, and thrombin bby greatly enhancing Antithrombin III activity (1000 fold)
Not absorbed by GI tract due to large molecular weight therefore use IV and SC injection, im injection can cause hematomas
Short half-life (approx 1 hr) means frequent injections or continuous infusion: not suitable in outpatient setting
Adverse: heparin induced thrombocytopenia
testing required to determine dose effect on coagulation
overdose can be countered with protamin sulfate

35
Q

Protamine sulfate

A

Counteracts a HMW heparin overdose

36
Q

LMW Heparin

A

Fractioned forms of HMW heparin: Dalteparin
Inhibit Factor Xa by antithrombin, but not thrombin
Use: Treat venous thromboembolism, thrombosis, pulmonary embolism, and unstable angina
Neutralization of LMW heparin by protamine is incomplete
Advantages over unfractionated heparin:
Longer halflife (4 hrs) and faster absortion time
Once daily SC injections administered in outpatient setting
Lower risk of thrombocytopenia and osteoporosis
less frequent monitoring required due to more predictable pharmacokinetic response

37
Q

Fondaparinux (ARIXTRA)

A

Penta-saccharide region of heparin
Inhibit Factor Xa by antithrombin, but not thrombin
Use: Treat venous thromboembolism, thrombosis, pulmonary embolism.
Renal excretion, so not used accompanying renal disease
Neutralizationof LMW heparin by protamine is incomplete
Advantages over HMW and LMW heparin:
Longer half life (20 hrs) and afster absortion time
Once daily SC injections administered in outpatient setting
Lower risk for thrombocytopenia

38
Q

Rivaroxaban (Xarelto)

A

Blocks factor Xa
Factor Xa is a component of the coagulation cascade, where the intrinsic and extrinsic pathways meet
Indirectly, prevents the maturation of Thrombin
Advantage over Warfarin: no titration prior to dosing
Use:Preventing venous thromboembolism in patients following knee or hip replacement, and DVT
Adverse:Increased bleeding risk

39
Q

Warfarin (Coumadin)

A

Most widely used oral antcoagulant with predictable pharmacokinetics, bioavailability and anticoagulant response: 1st used as rat poison from 1948.
Indirect inhibition of clotting cascade: Blocks vitamin K epoxide reductase, lowering Vitamin K recycling and slowing maturation of prothrombin and clotting factors VII, IX, and X.
Slow onset of action (8-12 hrs): existing mature clotting factors must be depleted; maximal effect 3-5 days after administration
Use: Acute DVT, pulmonary embolism, venous thromboembolism, following acute MI, prothetic heart valve placement.
Adverse: hemorrhage risk increases with intensity and duration of therapy
Warfarin readily crosses the placenta, can cause hemorrhage at any time and developmental defects during 1st trimester
Phytonadione (Vitamin K1) used to reverse warfarin associated bleeding ‘
Drug interactions: Patient history is crucial
Increased potency: aspirin, Vitamin K deficiency, anabolic steroids, antibiotics, tamoxifen, oral hypoglycemics.
Decreased potency: chronic alcohol abuse, oral contraceptives, corticosteroids, barbituates, increased hepatic synthesis of clotting factors, increased vitamin K intake, Cholestyramine
metabolized by CYP2C9
induction eg barbituate, rifampicin
inhibition-cimetidine

40
Q

Thrombolytics

A

Effective only if used rapidly after onset of thrombosis
Therapeutic uses in hospital: Acute ischemic stroke, MI, pulmonary embolism, severe deep venous thrombosis, ascending thrombophlebitis
Inhibitors: aminocaproic acid: inhibits the conversion of plasminogen to plasmin (to treat thrombolytic overdose)
Side effects: Hemorrhage, especially intracranial hemorrhage is the most serious
Contraindications: Brain tumor or aneurysm, hemmorrhagic stroke, recent major surgery, active bleeding in GI or urinary tract, severe platelet shortage or coagulation disorder, severe uncontrolled hypertension

41
Q

Streptokinase (Streptase)

A

Catalyzes the conversion of inactive plasminogen to active plasmin for fibrin breakdown
Acts throughout the circulation, not just at the clot
Given iv asap after a heart attack to dissolve clots in the ateries of the heart wall
Can cause allergic reaction or develop tolerance: typically only used for patients 1st heart attack, later heart attacks use tPA treament
Associated with increased bleeding risk in acute ischemic stroke therefore not used in this setting

42
Q

Tissue Plasminogen activator (tPA, Altepase, Activase)

A

Endogenous thrombolytic: human gene cloned, expresses and purified using bacteria
Preferentially activates plasminogen bound to fibrin, to target finbrinolysis to the formed thrombus and spare systemic activation
tPA is effective in lysing thrombi during treatment of acute myocardial infarction. also for acute stroke accompanying low bleeding risk
Derivatives: Reteplase (Retavase), Tenecteplase (TNKase)

43
Q

Reteplase (Retavase) tPA derivative

A

Fragment of human tPA gene cloned and expressed in bacteria
Increased plasma half-life allows convenient bolus dosing
Acts on plasminogen only at the site of the clot (like tPA)
Retepase lacks the major fibrin-binding domain, and less fibrin-specific than tPA

44
Q

Tenecteplase (TNKase)

A

Second-generation thrombolytic; fragment of human tPA gene cloned, genetically expressed
More clot-specific than tPA and has some resistance to plasminogen inhibitors

45
Q

Identifiable causes of secondary hypertension

A

Sleep apnea, drug induced, chronic kidney disease, primary aldosteronism, renovascular disease, renovascular disease, chronic steroid therapy, Cushing’s syndrome, pheochromocytoma, coarctation of the aorta, thyroid and parathyroid disease

46
Q

Hypertension goals

A
47
Q

Mortality risk

A

Risk doubles with each 20 of SBP or 10 DBP

48
Q

Measurement techniques

A

In office-Two readings, 5 minutes apart, sitting in chair, confirm elevated reading in contralateral arm
Ambuatory BP monitoring- Indicated for elevation of “white-coat” HTN. Absence of 10-20% BP decrease during sleep may indicate increased CVD risk
Self-measurement- Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN

49
Q

Contributing factors leading to hypertension

A

Obesity, Diet, Stress, lack of exercise, alcohol intake, cigarette smoking

50
Q

Lifestyle modifications

A

normal BMI

51
Q

Dash (Dietary approaches to Stop Hypertension

A

Emphasizes: Fruits, vegetables, low fat dairy foods, and reduced sodium intake
Includes whole grains, poultry, fish, nuts
Reduced amounts of red meat, sugar, total and saturated fat, and cholesterol

52
Q

Components of Mean Arterial Blood Pressure (MAP)

A

CARDIAC OUTPUT-Stroke volume and heart rate

TOTAL PERIPHERAL RESISTANCE- vascular structure, vascular tone, blood volume

53
Q

General antihypertensive drugs

A

diuretics, agents affecting adrenergic function (sympatholytics), vasodilators, agents affecting the Renin Angiotensis Aldosterone System (RAAS)

54
Q

Diuretics

A

THIAZIDES-Chlorothiazide, Hydrochlorothiazide
LOOP DIURETICS-Furosemide, Bumetanide, Ethacrynic acid, Torsemide
K+SPARING-Spironolactone, Triamterene, Amiloride

55
Q

diuretics

A

FIrst line treatment for uncomplicated hypertension
Diuretics have been virtually unsurpassed in preventing the cardiovascular complications of hypertension
Diuretics enhance the antihypertensive efficacy of multidrug regimens, can be useful in achieving BP control, and are more affordable than other anti-hypertensive agents

56
Q

Low dose thiazide

A

Initial therapy for isolated systolic hypertension

57
Q

Adverse effects of diuretics

A

Elevation of plasma renin, angiotensin II, and aldosterone levels due to volume and sodium depletion

58
Q

Considerations

A

Potential drug interactions with thiazide and loop diuretics:
Cardiac glycosides (ie, cardiotoxicity enhanced by hypokalemia)
Acid drugs that compete for renal tubular secretion (penicilin)
Loop diuretics-use for removal of edema (pulmonary edema)
K+ sparing-often combined with K+wasting diuretics

59
Q

Agents that affect Adrenergic Function (Sympatholytics)

A

Non-selective B1/2 antagonist (Propanolol)
Selective B1 antagonist (Atenolol, Metoprolol)
Neuronal Blockers (Reserpine, Guanethedine)
CNS Alpha 2 agonist-(Clonidine)
Slective alpha 1 andrenoceptor antagonists (Prazosin, Terazosin)

60
Q

Actions of Beta-Blockers

A

Block cardiac Beta 1 receptors==>decreases HR, CF and cardiac output
Block renal Beta 1 receptors==>decreases plasma renin, ANG II and TPR (afterload)
Use Beta blockers if MI; Benefits: Antiarrythmic, Anti-ischemic, Antiatherogenic, reverses cardiac remodeling

61
Q

CNS Alpha 2 Agonist actions

A

Decrease in sympathetic outflow==>decreases HR, TPR and MAP while producing diuresis and natriuresis
Not routinely used for treatment of hypertension in elderly dude to marked CNS effects (sedation, confusion) and orthostatic hypertension

62
Q

Selective Alpha 1 adrenoceptor antagonists

A

Block vascular Alpha 1 receptors==> vasodilation, decreased TPR and MAP
Adeverse: Reflex tachycardia, orthostatic hypotension

63
Q

Neuronal blockers

A

Block neural synthesis/release of NE from sympathetic nerve terminals=> vasodilation, decreased TPR and MAP

64
Q

Vasodilator agents

A

Calcium channel blockers (CCBs)
Nifedipine (Procardia; a dihydropyridine)
Diltiazem
Verapamil

65
Q

Calcium channel blocker actions

A

Arterial smooth muscle-CCBs block L-type voltage gated calcium channels and therefore prevent calcium entry into arterial VSM==> vasodilation, decrease in TPR (afterload) and MAP
Adverse: reflex tachycardia; ankle edema due to selective aterial vasodilation
Cardiac tissue: “non-dihydropyridine” CCBs block calcium entry into monocytes ==>decrease in HR, CF and cardiac output
Drug interaction: may precipitate AV block with other drugs that decrease AV node conduction (eg Beta blockers)
Adverse:ankle edema
CCBs do not affect plasma renin activity, GFR, salt and water excretion or body fluid composition

66
Q

Vasodilator Agents

A

Direct acting vasodilator agents
Hydralazine
Minoxidil
Sodium Nitroprusside (iv formulation only)

67
Q

Direct acting vasodilator agents actions

A

Arterial smooth muscle: Hydralazine and Minoidil have a direct, but unknown mechanism (potentially opeing ATP-sensive potassium channels in VSM cells) to cause selective relaxation of arterial smooth muscle==> therefore causing vasodilation, decrease in TPR (afterload) and MAP
Sodium Nitroprusside is a nitrovasodilator. Metabolism of nitroprusside to nitric oxide leads to formation of cGMP and vasodilation.
Uses: Hypertension, CHF
Adverse: Reflex tachycardia
Monoxidil-hirsutism (hair growth), ankle edema
Sodium Nitroprusside-cyanide toxicity with increased dose/duration of use

68
Q

Inhibitors of the RAAS

A 
Angiotensin Converting Enzyme inhibitors (ACEIs)
captopril
enalapril
lisinopril
ramipril
Angiotensin AT1 Receptor Blockers (ARBs)
Iosartan
valsartan
irbesartan
candesartan
azilsartan
69
Q

ACEI and ARBS actions

A

ACEI and ARBS prevent formation of angiotensin II and activation of angiotensin AT1 receptors, respectively, thereby producing beneficial cardiorenal effects that include:
Vasodilation (arterial and venous)
Reduction in ventricular afterload and preload
Natriuretic and diuretic efects
Decrease in sympathetic activity
Inhibition of cardiac and vascular hypertrophy
Adverse: concurrent use of two of the following drugs together may result in hyperkalemia: ACEI, ARB, renin inhibitor, K+sparing diuretic
Contraindicated in pregnant women: Use of ACEI and ARBS during the 2nd or 3rd trimester can cause injury and even death in the developing fetus.
Adverse effects: ACE inhibitor-induced coughing and angioedema due to elevated plasma bradykinin levels

70
Q

Aliskiren: An orally active renin inhibitor

A

Adverse: Concurrent use of two of the following drugs together may result in hyperkalemia: ACEI, ARB, renin inhibitor, K+sparing diuretic

Pharmacology Block 2 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions