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Flashcards in Block I And II Review Deck (117):
1

Where are Nm receptors found

Somatic skeletal muscle

2

Where does succinylcholine work

Nm receptors on skeletal muscle

3

Bethanechol

-bowels and bladder
-used for pts with urinary retention and gastric atony
-M agonist

4

Pyridostigmine

-Tx for MG
-works on No receptor
-doesn’t enter CNS, no convulsions
-Achase inhibitors

5

Autoimmune disease where Ab to the Na receptors are produced; it causes weakness in skeletal muscles especially in the facial area

MG

6

Toxicity of Achase inhibitors

DUMBBEELSS: diarrhea, urination, miosis, bronchoconstriction, bradycardia, excitation (of skeletal muscle and CNS), emesis, lacrimation, salivation, and sweating

Toxicity resembles too much parasympathetic stimulation + sweating + nicotinic effects

7

Treatment for Achase inhibitors

Atropine
-blocks M, doesn’t stop any Nm

Pralidoxime used in extreme cases to keep diaphragm from stoping

8

Atropine

-M blocker
-belladonna alkaloid
-central and PNS
-used for Achase inhibitor poisoning

9

Tropicamide

-shorter half life
-dilated eye exam
-M blocker

10

Succinylcholine

-Nm blocker that persistently stimulates skeletal muscle until it causes paralysis (depolarizing)
-can cause hyperkalemia
-can cause malignant hyperthermia

11

Epi

-a1,a2,B1,B2 agonist
-low dose: beta, decrease BP
-high doses: alpha, increase BP
-used for anaphylaxis

12

Phenylephrine

A1 agonist
-increases BP, reflex Brady
-dilated eye exam
-nasal decongestant

13

Prazosin

-blocks a1a receptors
-used for BPH and HTN
-may cause orthostatic hypotension and reflex tachy

14

No specific B blockers

N-Zolols
-bad for COPD and vasospatic angina

15

B1 specific blockers

A-Molols
-atenolol and metoprolol

16

Alpha 1 and B blockers

Labetolol and carvedolol

17

Sotalol

B blocker, K channel blocker

18

Clinical uses of B blockers

Glaucoma
HTN (2nd line)
CHF (1st line)
SVTs
Stable angina

19

Vasospastic angina and B blockers

Never use!

20

What is the best combo for CHF

ACEI and BBlocker

21

Adverse effects of B blockers

-bronchoconstriction
-hypotension, bradycardia, fatigue, drowsiness
-increased plasma lipids;TGs and LDLs

22

What drugs for HTN increase lipids?

B blockers and Thiazieds

23

Which drugs could cause increased GI motility

Bethanechol
Pyridostigmine

24

Which drugs could decrease GI motility

Atropine
Tropicamide

25

Which drugs lower BP

Prazosin
Atenolol,metoprolol
M agonist (bethanechol)
Epi in low doses

26

What drugs would raise BP

Epi in high doses
Phenylephrine

27

Competitive antagonism

Right shift
-maximal effect is not decreased

28

Non competitive antagonism

Maximal effect is shifted down

29

Potentiation

Curve shifts left
Allosteric agonist

30

Refers to the concentration required to produce 50% of that drugs maximal response (EC50)

Potency
-the graph most left is the most potent

31

Reflects the upper limit response relation on the response axis (Emax)

Efficacy
-height, tallest curve

32

When pH is less than PKA, the protonated forms __________ dominate

HA and BH+

33

When pH is greater than PJa, the deprtonates form ________ predominate

A- and B

34

Increased urine pH

Acid is ionized, gets eliminated

35

Decreased urine pH

Base gets ionized, gets eliminated

36

Weeks acid overdoes

Bicarbonate

37

Weak base overdoes

NH4Cl

38

What do we want to manipulate to correct ph balance

Urine ph

39

Stomach ph

1

40

Small intestine ph

6

41

Blood ph

7.4

42

Urine ph

5-8

43

What does a p450 inducer do to active drug

Enhances metabolism
-decreases drug effect

44

What does a P450 inhibitor do to active drug

Increases drug effects and toxicity, stops metabolism

45

What does a P450 inducer do to a prodrug

Makes it moire active, increase effect

46

What does a p450 inhibitor do to prodrug

Decrease effect, stays inactive

47

CYP inducers

Benzopyrenes
Chronic ethanol
Carbamazepine
Rifampin

48

CYP inhibitors

Cimetidine
Erythromycin
Grapefruit juice

49

A patient is taking warfarin and is later Rxed cimetidine fro peptic ulcers, what happens?

Increased warfarin toxicity=bleeding

50

First order elimination

-most drugs
-constant fraction eliminated
-constant half life

51

Zero order elimination

-phenytoin
-ethanol
-aspirin
-constant amount elimainted
-half life not constant

52

Steady state

4-5 half lives
Function of a drugs half life

53

Half way to steady state

One half life

54

75% to steady state

2 half lives

55

Maintainece dose has to do with: clearance or Vd?

Clearance

56

Loading dose has to do with: clearance or volume of distribution?

Vd

57

Normally, acetaminophen has a Vd=70L and Cl=350mL/min. If acetaminophen was administered to a patient with 50% normal rental function, what parameter would differ from normal

Md would be lower

58

A 55 year old women with HTN is to be started on a thiazides diuretic. Thiazides A in a does of 5 Mg produces the same decrease in BP as 500mg of thiazide B, which two statements are accurate about these drugs

-both drugs have equal efficacy
-A is about 100x more potent than B

59

We start an IV infusion of a drug using a pump that ensures that rate of delivery of drug over time is constant. Which of the following factors determines how long it takes for the drug to reach steady state concentration in the blood

Half life

60

A patient is admitted for treatment of drug overdoes. It is observed that when the urine pH is acidic the renal clearance of the drug is less than the GFR. When the urine pH is alkaline, the clearance is greater than the GFR. The drug is probably a

Weak acid

61

Dopamine via D1 receptors, epinephrine via B2 receptors, and histamine via H2 receptors are important transmitters. When these ligand interact with their cellular receptors, how do they mainly elicit their responses

Activating adenlyl cyclase

62

Initial fluid loss, long term vasodilation via hyperpolarization of smooth muscle

Thiazides
HCTZ

63

What CCBs are good for the heart

Verapamil

64

Which CCB is good for both heart and vessels

Diltiazem

65

Which CCB is good for the vessels

Amlodipine

66

What does amlodipine do

Vasodilator, reflex tachycardia

67

Decreases production of ang II, decreased aldosterone, vasodilation

ACEI
Lisinopril
-blocks ACE

68

ACEI and bradykinin

Causes dry cough

69

What accumulates when you take lisinopril

ANG I

70

Block the action of Ang II, decrease aldosteron, vasodilation

ARBs
Losartan

71

What happens in cardiac failure to compensate?

Increase Blood volume
Increase end diastolic volume (Preload)

Increase HR

Increase arteriolar constriction (AFTERLOAD)

72

What do we want to do to decrease preload in CHF

HCTZ, furosemide, lisinopril, losartan

Lisinopril and losartan act like diuretics because they stop aldosterone so lose Na+ and water, can also dilate veins

73

What do we want to do to decrease heart rate in CHF

Metoprolol
B blocker to control HR

74

What do we want to do to decrease afterload in CHF

Lisinopril, losartan
-dilates arterioles

75

What drug do we give for CHF that is a positive inotrope that will help improve contractility

Digoxin

76

Which drug for CHF has a very low TI

Digoxin

77

Cardiac remodeling in CHF

Fibrosis of the heart, want to stop this

78

What drugs do we use to stop cardiac remodeling via aldosterone in CHF

Lisinopril, losartan, spironolactone

79

Which drug stops aldosteron production and can help fight cardiac remodeling in CHF

Lisinopril and losartan

80

Which drug blocks aldosteron receptors and can help stop cardiac remodeling in CHF

Spironlocatone

81

When is digoxin used

CHRONIC CHF

82

MOA of digoxin

Inhibits Na-K ATPas
Blocks pump= Na increase
Increases Na/Ca exchange
Brings more Ca in and goes to SR=stronger cardiac contractions

83

Fast response AP

Atrial and ventricular muscle, Perkinje fibers

84

What kind of drugs would you want to treat ventricular tachycardia

Drugs that ablock Na, K channels
-amiodarone

85

Slow response AP

SA and AV nodes, supraventricular arryhtmias

86

What kind of drugs to treat SVTs

Drugs that block Ca, beta blockers

87

What CCB would you use for AVTs

Diltiazem

88

What beta blockers would you use to treat SVT

Atenolol and metoprolol
-cause Ca channels to stay closed -decreased phase 4

89

SVTs and digoxin

Has a PNS affect-slow HR down
-decrease phase 4 and 0

90

Patient taking antiarrhymic drug, monitored for thyroid drug, which drug are they probably on

Amiodarone
-iodine
-thyroid problems
-blue skin
-eyes, liver, lungs

91

Three classes of drugs effective for angina either alone or in combination for stable angina

Nitrates (nitroglycerin)
BBlockers
CCB (amlodipine or diltiazem)

92

What kind of drug would you use prophylatcically for angina

BBlocker every day

93

How do nitrates work on angina

Venodilation thereby decreasing preload

94

How do BBlockers work on angina

Decrease the oxygen demands of the heart

95

How do CCB work for angina

Cause vasodilation of smooth muscle or decrease HR

96

Patients with variant angina, what are they preferred classes of drugs

Nitrates
CCB

97

What kind of angina should you only use BBlockers in

Stable (not vasospasm)

98

What is the drug of choice for acute angina attack

Nitroglycerin under the tongue

99

MOA of statins

HmG CoA reductase inhibitors
-rate limiting step in cholesterol synthesis

100

Side effect of statins

Mild muscle pain

101

What is the drug of choice for hyperlipidemia

Atorvastatin

102

Most common antiplatelt drug

Aspirin

103

MOA of aspirin

Inhibits COX to stop TXA2
Stops platelets from aggregating

104

What drug is common to use in mini strokes

Aspirin

105

Anticoagulant drugs

Warfarin
Rivaroxaban

106

Synthesis inhibitor of vit K

Warfarin

107

What coagulation factors are affected by warfarin

Vit K dependent factors
2,7,9,10

108

What do you give someone who has had too much warfarin

Vit K

109

MOA of rivaroxaban

Blocks factor Xa, rapid onset

110

Site of action of acetazolamide

Proximal convuluted tubule

111

Site of action of furosemide

Ascending loop of Henle

112

Site of action of thiazides

Distal convoluted tubule

113

Site of action of sprinolactone

Collecting duct

114

MOA of CAIs (acetazolamide)

PCT
-block CA, cant get bicarbonate
-H from the bicarbonate cant swap with the Na to get in the cell
-blocks Na from getting in

115

MOA of thiazides (HCTZ)

DCT
-block Na/CL transporter
-saves Ca

116

MOA of loops (furosemide)

Block the Na/L/CL pump
-also lose Ca and Mg

117

MOA of spironolactone

Blocks aldosterone receptors
-not affecting Na
-K sparing