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CRRAB I Final > PBL 1-3 Pharmacology > Flashcards

PBL 1-3 Pharmacology Flashcards

1
Q

What is the mechanism of Ceftriaxone?

A

Third Gen. Cephalosporin: Binds P. B. P. and blocks transpeptidation of peptidoglycan in bacterial cell walls.

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2
Q

What are the therapeutic uses of Ceftriaxone?

A

MSSA & Strep. with some gram (-) coverage

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3
Q

What is the mechanism of Vancomycin?

A

Binds D-ala-D-alanine to prevent NAM/NAD-peptide subunits from forming peptidoglycan. BLOCKS TRANSGLYCOSYLATION

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4
Q

What are the therapeutic uses of Vancomycin?

A

Broad Gram (+) coverage including MRSA

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5
Q

What is Vancomycin often given in conjunction with?

A

Ceftriaxone for EMPIRIC TREATMENT to PROTECT the patient

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6
Q

What is the mechanism for Penicillin G?

A

Beta-lactam: Binds PBP and blocks transpeptidation of peptidoglycan in bacterial cell walls.

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7
Q

What is the therapeutic use of Penicillin G?

A

Limited to sensitive gram (+) organisms. PRETTY MUCH STREP

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8
Q

What should you know about Penicillin G?

A

FINAL AB FOR PATIENT

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9
Q

What is the mechanism of Amoxicillin?

A

AMINO-Beta-Lactam: Binds PBP and blocks transpeptidation of peptidoglycan in bacterial cell walls.

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10
Q

What is the therapeutic use for Amoxicillin?

A

Strep and some Gram (-)

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11
Q

What is a con of using amoxicillin?

A

It’s still inactivated by beta-lactamases –> need to give in conjunction with Clavulanate

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12
Q

What is the mechanism of Alteplase?

A

t-PA: converts plasminogen to plasmin –> plasmin cleaves fibrin –> FDPs –> Breaks up clot

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13
Q

What is the therapeutic use of alteplase?

A

Non-hemorrhagic stroke or clot (emboli or thrombi)

  • Pulmonary Embolism
  • Myocardial Infarction
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14
Q

What is alteplase contraindicated in?

A

ENDOCARDITIS

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15
Q

What is the mechanism of Morphine?

A

Acts on mu receptors in three locations:

(1) Presynaptic nociception pathway (blocks Ca2+ pump thus blocking vesicle release)
(2) Postsynaptic nociception pathway (Inc. K+ permeability thus blocking depolarization)
(3) Presynaptic descending inhibitory pathway (Blocks GABA release allowing inhibitory neuron firing and blocking nociception pathway)

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16
Q

What is the therapeutic use of morphine?

A

Analgesic

Myocardial Infarction

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17
Q

What is the mechanism of Nitroglycerin?

A

Forms free radical NO –> Activates guanylyl cyclase –> Inc. cGMP –> Inc. MLC phosphatase –> Inc. MLC phosphorylation –> Smooth muscle relaxation –> VEINS vasodilate –> Dec. blood returning to heart –> Dec. preload

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18
Q

What are the therapeutic uses of Nitro?

A

Angina/Myocardial Infarction

  • Decreases myocardial activity and oxygen demand = Decreased Ischemic Damage
  • ACUTE CHF treatment
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19
Q

What is the mechanism of Clopidogrel?

A

Blocks ADP receptors on platelets –> inhibits platelet activation

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20
Q

What is the therapeutic use of Clopidogrel?

A

Post-MI anticoagulation therapy

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21
Q

What is the mechanism of Heparin?

A

Inc. activity of antithrombin III –> Inhibits thrombin (and others in coag. cascade) –> blocks conversion of fibrinogen –> fibrin = no clot

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22
Q

What is the therapeutic use of Heparin?

A

Post-MI anticoagulation therapy

23
Q

What is the mechanism of Eptifibatide?

A

Binds GPIIb/IIIa receptor on activated platelets and inhibits binding of fibrinogen –> blocks initiation of coagulation cascade post-platelet plug

24
Q

What is the therapeutic use of Eptifibatide?

A

Post-MI anticoagulation therapy

25
Q

What is the mechanism of aspirin?

A

Irreversibly inhibits COX1/COX2 –> blocks production of thromboxane A2 –> inhibits platelet aggregation

26
Q

What is the therapeutic use of aspirin?

A

Blocks further occlusion through platelet aggregation and activation

27
Q

When should you use aspirin?

A

Used immediately upon suspected MI, UNLESS patient recently took Aspirin

28
Q

What is the mechanism of Statins?

A

Drugs for dyslipidemia

  • Inhibit cholesterol synthesis
  • HMG-CoA reductase inhibitors
29
Q

What is the therapeutic use of statins?

A

Treats dyslipidemia thus decreasing atherosclerosis risk of CAD

  • Reduces plaque formation in vessels
  • Used for Coronary Artery Disease and high cholesterol
30
Q

What two ACE inhibitors should we know?

A

Lisinopril

Enalapril

31
Q

What is the mechanism for ACE inhibitors?

A

Suppresses RAAS system by inhibiting conversation of Angiotensin I to Angiotensin II
Net effects: Dec. Aldosterone release –> Dec. Na+ reabsorption by kidney —> Dec. blood volume and preload
Dec. vasoconstriction —> Dec. afterload

32
Q

What are the therapeutic uses for ACE inhibitors?

A
  • They dec. preload and afterload (strain on heart)
  • Post-MI management
  • Chronic CHF management
33
Q

What beta blockers should we know?

A

Metoprolol

Propranolol

34
Q

What is the mechanism for Metoprolol?

A

Blocks Beta1 receptors:

  • Main activity on heart –> dec. HR and contractility thus decreasing myocardial oxygen demand
  • Decreases BP
35
Q

What is the mechanism for Propanolol?

A

Non-specifc Beta blocker (Beta 1 & 2)

-Same major effects as Metoprolol but with differences in TPR

36
Q

What are beta blockers used for therapeutically?

A

Post-MI management

  • Chronic CHF management
  • MI to reduce ischemia
37
Q

When are beta-blockers contraindicated?

A

Acute CHF (need to preserve heart function and complete diuresis first)

38
Q

How is nitroglycerin activated?

A

By aldehyde dehydrogenase which is expressed at higher levels in VENOUS TISSUE

39
Q

What is the mechanism for Isosorbide dinitrate?

A

Same as nitro.

40
Q

What is different between nitroglycerin and isosorbide dinitrate?

A

It has a longer half-life (60-90 minutes)

This is why nitro has to be given IV when the patient gets to the hospital.

41
Q

What is the mechanism for Hydralazine?

A

Increases NO synthesis in endothelium. Same as nitro.

42
Q

What are three drugs used for vasodilation in CHF?

A

Nitroglycerin, Isosorbide dinitrate, Hydralazine

43
Q

What is different between nitro and hydralazine?

A

Hydralazine has HIGHER SELECTIVITY FOR ARTERIOLES = DEC. AFTERLOAD

44
Q

What is the mechanism of Furosemide?

A

Loop Diuretic
-Inhibits NKCC2 (the luminal symporter in thick ascending limb of loop of Henle) –> Dec. reabsorption of Na+ and Cl- –> Increased Na+ and water excretion –> Dec. Blood Volume –> Dec. Preload

45
Q

What is the therapeutic use of Furosemide?

A

Diuretic. Dec. edema

-ACUTE CHF treatment

46
Q

What two aldosterone receptor antagonists do you need to know?

A
  • Eplerenone

- Spirinolactone

47
Q

What is the mechanism of action for aldosterone receptor antagonists?

A

Blocks aldosterone action.
Net effects:
-Decreases Na reabsorption in kidney –> decreases blood volume and preload

48
Q

What happens to plasma when using an aldosterone receptor antagonist?

A

Causes an increase in Aldosterone and Renin plasma concentrations = INHIBITION OF NEGATIVE FEEDBACK of aldosterone on renin secretion

49
Q

When should you use an aldosterone receptor antagonist?

A

NYHA class II-IV heart failure (CHF) & Very low left ventricular ejection fraction (

50
Q

What class does digoxin belong to?

A

Cardiac glycoside

51
Q

What is the mechanism for Digoxin?

A

Inhibits Na+/K+ ATPase:
-Increased Na+ intracellular concentration
-Increased Na+/Ca2+ co-transporter activity
-Increased intracellular Ca2+
-Increased contractility (positive ionotrope)
ALSO - prolongs nodal action potentials thus DECREASING HEART RATE
(-) Chromotrope
(+) ionotrope
Dec. HR, Inc. SV

52
Q

What is the therapeutic use for Digoxin?

A

ACUTE CHF management

  • Atrial fibrillation
  • HF (along w/diuretic & ACE inhibitor)
53
Q

When do we REALLY use Digoxin?

A

It has HIGH TOXICITY!

-Used in people with refractory CHF (management with furosemide and enlalapril not controlling symptoms)

CRRAB I Final (21 decks)

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