Exam 4 pcol Flashcards

(57 cards)

1
Q

Pitavastatin

livalo

A

Statin -HMG co Reductase inhibitor
Lowers LDL
Lowers triglycerides
Increases HDL

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2
Q

Atorvastatin

lipitor

A

Statin- HMG coa Reductase inhibitor
Lowers LDL
Lowers triglycerides
Increase HDL
Is metabolize by CYP 3A4
High intensity dose is 40-80mg
Moderate intensity dose is 10-20mg

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3
Q

Rosuvastatin

Crestor

A

HMG coa reductase inhibitor
Lowers LDL
Lowers triglycerides
Increases HDL
If use for high intensity the dose is 20-40mg
If use for moderate intensity the dose is 5-10mg

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4
Q

Pravastatin

Pravachol

A

HMG-Coa Reductase inhibitor
Lowers LDL
Increases HDL
Use for moderate intensity and the dose is 40-80mg

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5
Q

Simvastatin

zocor

A

HMG Coa Reductase inhibitor
It will lower LDL
Lower Triglycerides
Increases HDL
Use for moderate intensity dose is 20-40mg

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6
Q

Lovastatin

Mevacor

A

HMG Coa Reductase inhibitor
It will decrease LDL
Increase HDL
For moderate dose is 40mg

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7
Q

Ezetimibe

A

Cholesterol absorption inhibitor it will inhibit NPC1L1

Zetie

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8
Q

Vitamin B3 Nicotinic Acid (Niacin )

Has Pyridine ring is absober by active transport
A

Lowers LDL lower triglycerides increases HDL

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9
Q

Gemfibrozil

is lipophilic and is acidic has strong plasma protein binding bioavailability is high Phenoxy butyric acid
A

Lowers LDL lowers triglycerides
activated PPAR

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10
Q

Fenofibrate

phenyl isubutyric is lipophilic and is well absorb has high bioavailability
A

Activates PPAR Lowers triglycerides lowers LDL

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11
Q

Cholestyramine

Questran

A

Bile acid sequestran it will inhibit the reabsorption of bile acid
Lowers LDL but AE can increase triglycerides so cannot give to pt that triglyceride levels are >300
Will bind to other drugs and decrease the absorption of other drugs
It causes constipation and bloating–> Acts locally in the GIT because of the quaternary ammonium slat is not absorb
It will inhibit the absorption of fat soluble vitamins Vitamin D,E,A,K
The compensatory mechanism of the body is to increase LDL receptors so decreases LDL in the blood because LDL will be taken in to the liver and is needed so is brokendown need cholesterol in order to form billie acid
Another compensatory mechanism of the body is to increase HMG Reductase –> So need to co-administer a statin

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12
Q

Colestipol

Colestid

A

Is a bile acid sequestran
It will react with the lipophilic backbone of bile acid and will prevent the reabsorption of the bilie acid to the liver because it will form non absorbable complex and acts locally om the GIT
The liver will sense the decrease in the bilie acid and as a compensatory mechanism it will increase LDL receptors so more LDL is taken from the blood so lowers the LDL
It will also cause increase in production of HMG coa reductaser so need to co-administer a statin

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13
Q

Colesevalem

A

bilie acid sequestran

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14
Q

Acetazolamide

Diamox

the liver hates the sulfonamide group so it has high bioavailability but give locally for glaucoma
A

Carbonic anhydrase inhibitor

Works in the proximal tubule

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15
Q

Methazolamide

Is lipophilic and acidic the liver hates the sulfonamide group so bioavailability is high
A

Carbonic anhydrase inhibitor

Works in the proximal tubule

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16
Q

Dorzolamide

A

Carbonic anhydrase inhibitor

works in the proximal tubule

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17
Q

Chlorothiazide

C 6 has Cl electron withdrawing C-7 Sulfonamide Is lipophilic acidic has protein binding The liver hates the sulfonamide so it goes to the kidney but is least potent so dose is 500mg -2g PO QD because short duration of action
A

Thiazide diuretic

works in the proximal distal tubule

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18
Q

Hydrochlorothiazide

6-Cl electron withdrawing 7-Sulfonamide group The double bond is saturated so is more potent Dose is 50-100mg QD
A

Thiazide diuretic

works in the proximal distal tubule

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19
Q

Metolazone

has a methyl at C2 Has Sulfonamide group at 6 Is lipophilic and is acidic has protein binding It is more resistant and quinethazone because of the tolune substituent It is more potent so dose is 0.5mg -5mg QD
A

Thiazide like diuretic
quinazoline derivative

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20
Q

Chlorthalidone

Longer acting 10x more potent dose is 15-50mg has monosubstituted unfused ring
A

Thiazide like diuretics
Phathalamide derivative

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21
Q

Indapamide

It is more potent is only given twice weekly 1.25-5mg Is lipophilic and acidic it bind to plasma proteins
A

Thiazides like diuretics
Indoline derivative

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22
Q

Mannitol

A

Osmotic diuretic it draws H2O and Na+ out

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23
Q

Furosemide

Dose is 80mg in two dived doses is short acting because can be conjugated in phase 2 metabolism (amino acid structure Carboxylic + amine) but has high bioavailability
A

Loop diuretic “high ceiling”

Works in the ascending loop of henly

24
Q

Ethacrynic acid

Dose is 50-100mg Short acting because can be conjugated in phase 2 metabolism
A

Loop diuretics

25
Bumetanide
Loop diuretic
26
Torsemide
Loop diuretic
27
Spironolactone
Aldosterone endocrine antagonist - medchem For pcol is non selective aldosterone antagonist
28
Eplerenone
selective aldosterone antagonist
29
Finerenone
Selective aldosterone antagonist
30
Vasopressin
V1 And V2 agonist | Antidiuretic hormone
31
Desmopressin | DDAVP
Selective V2 agonist
32
Conivaptan | also known as aquaretic
Non selective V1 and V2 antagonist | Treat SIADH
33
Tolvaptan
Selective V2 antagonist | Treat SIADH
34
Oxytocin
Oxytocin receptor ligand agonist
35
Atosiban
VOTRA Vassopresin and Oxytocin Receptor antagonist
36
Colchine
Inhibit WBC migration and phagocytosis to the uric acid crystals so reduce the inflammation | dose for accute is 1.2mg then 0.6mg BID Dose for prophylactic is 0.6mg B
37
Allopurinol
Xanthine oxidase inhibitor | For hyperurecemia dose is 100mg QD first then 300mg then 600mg CrCl 90-6
38
Febuxostat | dose initially is 40mg QD If after 2 weeks goal is not achieve --> Dose
Xanthine oxidase inhibitor | Uloric
39
Probenecid | initial dose is 250mg BID for 7 days then 500mg BID then if needed 2g di
uricosuric agent Inhibit URAT-1 in the proximal tubule so no uric acid reabsorbtion
40
Lesinurad | Zurampic
uricosidic agent Inhibit URAT-1 in the proximal tubule
41
Pegloticase | dose is 8mg every 2 weeks IV
Is a enzyme Uricase and breaks down uric acid to allantoin that is more easy excreted
42
Dobutamine
B1 agonist inotropic drug for treatment of HF -Initially there is a decrease in CO and SV and the heart is enlarge so is harder to contract and pump the blood
43
Dopamine
D1 agonist in cardiac myocyte Treat acute heart failure that initially has decrease in CO and in SV and the heart is enlarge so is harder for the heart to contract and pump the blood
44
Glucagon
release from the pancreas it is link to gS and will bind to the cardiac myocyte and increase CO and Sv and increase contractility -Treat acute heart failure because initially there is a decrease in CO and in SV and the heart is enlarge and is harder for the heart to pump blood
45
Milrinone
PDE 3 inhibitor
46
Inamrinone
PDE 3 inhibitor
47
Adenosine
It binds to A1 receptors in the SA node and the AV node The A1 receptors are couple to Gi --> Decrease in Adenylate Cyclase --> Decrease CAMP. It will also directly open K+ Channels so it causes hyperpolarization Gi M2 M4 in the SA node and AV node -Decrease HR --> Decreases SA node firing -Decreases AV nodal conduction--> Treat atrial arrythmia -But adenosine is taken up by the RBC and very little get to the site of action -->so is only given to terminate the arrythmia given for IV for Acute AE: -Assystole--> The patient feels the heart suddenly stops
48
Procainamide
1a class Na+ channel blocker
49
Disopyramide
Class 1a Na+ channel blockers
50
Lidocaine
Class 1B Na+ Channel blockers
51
Mexilitene
Class 1b Na+ channel blocker
52
Flecainide
Class 1C Na+ Channelo blocker | slow dissociation
53
Propafenone
Class 1c Na+ Channel blocker | Slow dissociation
54
Ibutilide
K+ Channel blocker
55
Sotalol
Non selective Beta blocker also K+ Channel blocker
56
Dofetilide
K+ Channel blocker
57
amiodarone
K+ channel blocker