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Pathophysiology & Pharmacology > Test 2 > Flashcards

Test 2 Flashcards

0
Q

Warfarin lavender (light purple)

A

2 mg

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1
Q

Warfarin Pink

A

1 mg

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2
Q

Warfarin Green

A

2.5 mg

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3
Q

Warfarin Tan

A

3 mg

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4
Q

Warfarin Blue

A

4 mg

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5
Q

Warfarin Peach (light orange)

A

5 mg

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6
Q

Warfarin teal (blue-green)

A

6 mg

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7
Q

Warfarin Yellow

A

7.5 mg

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8
Q

Warfarin White

A

10 mg

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9
Q

What are the broad adverse effects of anticoagulants?

A

Bleeding! and hypersensitivity

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10
Q

What clotting factors (Vitamin K dependent factors) does Warfarin decrease?

A 
Factor II (prothrombin)
Factor XII
Factor IX
Factor X
Protein C & S
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11
Q

Warfarin’s mechanism of action

A

Inhibits VKORC1 (Vitamin K epioxide reductase complex 1)

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12
Q

What is VKORC1 and what does it do?

A

Vitamin K epoxide reductase complex 1

VKORC1 converts Vitamin K from inactive to active

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13
Q

Warfarin is a(n)…

A

Vitamin K antagonist!

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14
Q

How is Warfarin metabolized?

A

Several CYP (cytachrome P) pathways

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15
Q

How is Warfarin monitored?

A

INR/PT

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16
Q

Factors that affect INR value

A

herbal drugs (G’s and St. John’s wart), ETOH, smoking, fever, diarrhea, malnutrition, Vitamin K rich foods, drugs

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17
Q

Drugs that affect INR value & how INR is affected

A

Azoles (increase INR b/c CYP inhibitor)
Amiodarone (increase INR b/c CYP inhibitor)
Bactrim (increase INR b/c CYP inhibitor)
Metronidzole (unknown)

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18
Q

Drugs for anticoagulation

A 
Warfarin
Rivaroxaban
Dabigatran
Heparin
Low Molecular Weight Heparin (LMWH)
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19
Q

Rivaroxaban mechanism of action

A

Factor XA inhibitor

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20
Q

Dabigatran mechanism of action

A

Direct thrombin inhibitor

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21
Q

2 examples NOACs (new oral anticoagulants)

A

1) Rivaroxaban

2) Dabigatran

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22
Q

NOAC that is superior to Warfarin

A

apixiban

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23
Q

What anticoagulant is preferred in pregnancy?

A

Heparin! (only one)

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24
Q

LMWH’s mechanism of action

A

Factor XA inhibitor

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25
Q

How can heparin be administered?

A

subq or drip

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26
Q

Inpatient drugs for acute MI (without stent placement)

A

morphine, oxygen, nitroglycerin, aspirin

think MONA

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27
Q

What does MONA stand for?

A

morphine
oxygen
nitroglycerin
aspirin

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28
Q

What is MONA used for?

A

inpatient drug scheme for acute myocardial infarction

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29
Q

Outpatient drugs for acute MI

A 
aspirin
statin
ACE inhibitor
beta blocker
clopidogrel (if patient received stent)
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30
Q

What are nitrates used for?

A

chest pain

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31
Q

What are the adverse effects of nitrates?

A

hypotension

orthostatic hypotension

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32
Q

With what drugs are nitrates contraindicated?

A

“fils”: sildenafil, vardenafil, tadalafil (viagra drugs of world)

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33
Q

How long should patients have a nitrate free window?

A

8-18 hours per day

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34
Q

Why do patients need a nitrate-free window?

A

to prevent tolerance to nitrates from building

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35
Q

Equation for cardiac output

A

CO = HR (heart rate) x SV (stroke volume)

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36
Q

Equation for arterial pressure

A

AP = PR (peripheral resistance) x CO (cardiac output)

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37
Q

definition primary hypertension

A

hypertension without a known cause

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38
Q

primary hypertension is also known as

A

essential hypertension

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39
Q

definition of secondary hypertension

A

hypertension with a known cause

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40
Q

RAAS stands for

A

renin-angiotensin-aldosterone system

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41
Q

3 important players of the RAAS

A

1) angiotensin (I & II)
2) angiotensin-converting enzyme (ACE) aka Kinase II
3) aldosterone

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42
Q

Lisinopril mechanism of action

A

ACE enzyme inhibitor

blocks conversion angiotensin I to angiotensin II

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43
Q

What does Lisinopril have mortality data for?

A

heart failure

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44
Q

ACE inhibitors decrease levels of _____ and increase levels of ______

A

decrease levels of ANGIOTENSIN II

increase levels of BRADYKININ

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45
Q

What causes the cough some people experience with ACE inhibitors?

A

increased levels of bradykinin due to block action of ACE inhibitors in converting bradykinin to an inactive product

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46
Q

Decreased levels of angiotensin result in…

A

vasodilation
decreased blood volume
decreased cardiac and vascular remodeling
potassium retention

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47
Q

Drugs with side effect of hyperkelemia

A

Lisinopril
Losartan
Spironlactone
Eplerenone

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48
Q

Drugs with side effects hypokelemia

A

hydrocorothiazide (HCTZ)
furosemide
digoxin (arrythmias secondary to hypokelemia)

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49
Q

The only active ACE inhibitor is…

A

Lisinopril

50
Q

Losartan mechanism of action

A

angiotensin II receptors blockers (ARBs)

51
Q

Spironlactone mechanism of action

A

aldosterone receptor antagonist

potassium sparing diuretic

52
Q

Eplerenone mechanism of action

A

aldosterone receptor antagonist

53
Q

Example first generation beta blocker

A

Propranolol

54
Q

Example second generation beta blocker

A

Metoprolol

55
Q

Third generation beta blocker

A

Carvedilol

56
Q

Ending for beta blocker medications

A

“lol”

57
Q

Ending ACE inhibitors

A

“pril”

58
Q

Important beta blocker side effect

A

Mask all hypoglycemia symptoms except sweating

59
Q

Verapamil mechanism of action

A

Calcium channel blocker w/ calcium channels mainly in cardiac tissue

60
Q

Nifedeipine mechanism of action

A

calcium channel inhibition less localized in heart, more peripheral

61
Q

Where does hydrochorothiazide (HCTZ) works in the nephron?

A

early distal convoluted tubule

62
Q

Where furosemide works in the nephron?

A

thick segment–ascending limb Henle’s Loop

63
Q

NYHA functional classification categories

A

I - Asymptomatic
II - Symptomatic w/ moderate exertion
III - Symptomatic w/ minimal exertion
IV - Symptomatic at rest

64
Q

ACC/AHA stages heart failure

A

A - high risk HF; no structural heart disease; no symptoms HF
B - structural heart disease; no symptoms HF
C - structural heart disease; prior or current symptoms HF
D - advanced structural heart disease; marked symptoms HF at rest despite max medical therapy

65
Q

Digoxin mechanism of action

A

blocks Na-K ATPase pump

66
Q

When is digoxin used?

A

late stage heart failure (stage C)

67
Q

INR range with high risk of clotting

A

less than 2

68
Q

INR range high risk bleeding

A

greater than 3

69
Q

INR ranges 2-3

A

A. Fib
VTE
heart valve
hypercoagulable state

70
Q

INR ranges 2.5-3.5

A

mitral heart valve

71
Q

Is a loading dose of Warfarin good or bad practice?

A

poor practice & weakly supported by evidence!

72
Q

RAAS suppressants subsets include:

A

ACE inhibitors
Angiotensin II receptor blockers (ARBs)
Aldosterone antagonists

73
Q

Diuretic subsets include:

A

thiazides (and related diuretics)
loop diuretics
potassium-sparing diuretics

74
Q

Intermediate Acting Insulins

A

NPH

Detemir

75
Q

Short-acting Insulins

A

Regular

76
Q

Rapid-acting Insulins

A

aspart
lispro
glulisine

77
Q

Long-acting Insulins

A

Detemir

Glargine

78
Q

Onset Aspart

A

10-20 mins

79
Q

Onset Glulisine

A

10-15 minutes

80
Q

Onset lispro

A

15-30 mins

81
Q

Onset regular insulin

A

30-60 mins

82
Q

Onset NPH

A

1-2 hours

83
Q

Onset detemir

A

1-2 hours

84
Q

Onset glargine

A

70 mins (approx.)

85
Q

Peak regular insulin

A

1-5 hours

86
Q

Peak NPH

A

6-14 hours

87
Q

Peak detemir

A 
12-24 hours (if intermediate)
no peak (if long-acting)
88
Q

Peak lispro

A

30 mins-2.5 hours

89
Q

Peak glargine

A

NO PEAK

90
Q

Peak aspart

A

1-3 hours

91
Q

Peak glulisine

A

1-1.5 hours

92
Q

Duration NPH

A

16-24 hours

93
Q

duration detemir

A

varies (long or intermediate)

94
Q

Duration glargine

A

24 hours (approx.)

95
Q

Duration aspart

A

3-5 hours

96
Q

Duration glulisine

A

3-5 hours

97
Q

Duration lispro

A

3-6 hours

98
Q

Duration regular insulin

A

6-10 hours

99
Q

ergocalciferol & cholecalciferol are…

A

vitamin D replacements

100
Q

epoetin alfa works by…

A

mimicking endogenous erythropoietin made in kidneys

101
Q

Iron dextran is…

A

used in patients that can’t take iron supplements PO (ex, if they are on dialysis)

102
Q

Major risk of iron dextran:

A

FATAL ANAPHYLACTIC REACTIONS (why must do a test dose in a controlled setting!)

103
Q

Canagliflozin mechanism of action:

A

inhibition Na-glucose co-transporter-2 in kidney (prevents kidney re-uptake of glucose, glucose excreted through urine)

104
Q

Major side effect canagliflozin:

A

yeast infections (think CAN-dida when see CAN-agliflozin)

105
Q

Repaglinide is a…

A

secretagogue (increases insulin release)

106
Q

Secretagogue drugs:

A

repaglinide

glipizide

107
Q

Major risk of secretagogues & the secretagogue drugs:

A

Major risk of hypoglycemia!

repaglinide & glipizide

108
Q

Pioglitazone mechanism of action:

A

Insulin sensitizer! (increases insulin sensitivity & decreases hepatic glucose production)

109
Q

Pioglitazone metabolism:

A

CYP2C8 pathway

110
Q

2 DM drugs that increase insulin sensitivity and decrease hepatic gluconeogenesis:

A

pioglitazone

metformin

111
Q

Ferrous sulfate is…

A

iron supplement used to transport oxygen on hemoglobin!

112
Q

Major side effects ferrous sulfate:

A

GI effects & HEARTBURN

113
Q

Glipizide is a(n)…

A

sulfonylurea secretagogue (stimulates the secretion insulin)

114
Q

Secretagogue mechanism of action…

A

close potassium channel, open calcium channel which stimulates the release of insulin.

115
Q

These 2 drugs shouldn’t be taken with beta blockers for risk of severe hypoglycemia…

A

1) glipizide
2) repaglinide
(both secretagogues)

116
Q

Exenatide mechanism of action…

A

increases glucose-dependent insulin secretion by mimicking incretin.

117
Q

Sitagliptin mechanism of action…

A

DPP-4 inhibitor (allows incretin to stimulate insulin and inhibit glucagon)
3rd line drug!

118
Q

Acarbose mechanism of action…

A

inhibits carbohydrate absorption through inhibiting the alpha-glucosidase enzyme at the GI brush border.

119
Q

Metformin as therapy…

A

1st line of therapy DM-II

120
Q

Metformin mechanism of action…

A

increases insulin receptor sensitivity & decreases liver gluconeogenesis!

121
Q

Metformin belongs to what class drugs…

A

biguanide!

122
Q

Major risk metformin:

A

stop before and after procedures with iodated IV contrast dyes due to lactic acidosis!

123
Q

Pramlintide mechanism of action…

A

mimics amylin and therefore prevents postprandial hyperglycemia!

Pathophysiology & Pharmacology (2 decks)

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