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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
What is the mechanism of aspirin?
Irreversibly inhibits COX1/COX2 --> blocks production of thromboxane A2 --> inhibits platelet aggregation
26
What is the therapeutic use of aspirin?
Blocks further occlusion through platelet aggregation and activation
27
When should you use aspirin?
Used immediately upon suspected MI, UNLESS patient recently took Aspirin
28
What is the mechanism of Statins?
Drugs for dyslipidemia - Inhibit cholesterol synthesis - HMG-CoA reductase inhibitors
29
What is the therapeutic use of statins?
Treats dyslipidemia thus decreasing atherosclerosis risk of CAD - Reduces plaque formation in vessels - Used for Coronary Artery Disease and high cholesterol
30
What two ACE inhibitors should we know?
Lisinopril | Enalapril
31
What is the mechanism for ACE inhibitors?
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
What are the therapeutic uses for ACE inhibitors?
- They dec. preload and afterload (strain on heart) - Post-MI management - Chronic CHF management
33
What beta blockers should we know?
Metoprolol | Propranolol
34
What is the mechanism for Metoprolol?
Blocks Beta1 receptors: - Main activity on heart --> dec. HR and contractility thus decreasing myocardial oxygen demand - Decreases BP
35
What is the mechanism for Propanolol?
Non-specifc Beta blocker (Beta 1 & 2) | -Same major effects as Metoprolol but with differences in TPR
36
What are beta blockers used for therapeutically?
Post-MI management - Chronic CHF management - MI to reduce ischemia
37
When are beta-blockers contraindicated?
Acute CHF (need to preserve heart function and complete diuresis first)
38
How is nitroglycerin activated?
By aldehyde dehydrogenase which is expressed at higher levels in VENOUS TISSUE
39
What is the mechanism for Isosorbide dinitrate?
Same as nitro.
40
What is different between nitroglycerin and isosorbide dinitrate?
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
What is the mechanism for Hydralazine?
Increases NO synthesis in endothelium. Same as nitro.
42
What are three drugs used for vasodilation in CHF?
Nitroglycerin, Isosorbide dinitrate, Hydralazine
43
What is different between nitro and hydralazine?
Hydralazine has HIGHER SELECTIVITY FOR ARTERIOLES = DEC. AFTERLOAD
44
What is the mechanism of Furosemide?
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
What is the therapeutic use of Furosemide?
Diuretic. Dec. edema | -ACUTE CHF treatment
46
What two aldosterone receptor antagonists do you need to know?
- Eplerenone | - Spirinolactone
47
What is the mechanism of action for aldosterone receptor antagonists?
Blocks aldosterone action. Net effects: -Decreases Na reabsorption in kidney --> decreases blood volume and preload
48
What happens to plasma when using an aldosterone receptor antagonist?
Causes an increase in Aldosterone and Renin plasma concentrations = INHIBITION OF NEGATIVE FEEDBACK of aldosterone on renin secretion
49
When should you use an aldosterone receptor antagonist?
NYHA class II-IV heart failure (CHF) & Very low left ventricular ejection fraction (
50
What class does digoxin belong to?
Cardiac glycoside
51
What is the mechanism for Digoxin?
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
What is the therapeutic use for Digoxin?
ACUTE CHF management - Atrial fibrillation - HF (along w/diuretic & ACE inhibitor)
53
When do we REALLY use Digoxin?
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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