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Pharm 1 > exam 4 > Flashcards

exam 4 Flashcards

1
Q

causes of dysrhythmias

A

automaticity (spontaneous depolarziations)
re-entry (propogation of more than one pathway)

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2
Q

Pacemaker/Nodal = “slow” = dependent on ___________ for phase 0

A

calcium

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3
Q

nodal
phase 0: ______ in
phase 3: ___________ out
phase 4:

A

calcium IN
potassium OUT
phase 4: LEAKY

no phase 1 or 2!

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4
Q

blocking K is ____________

A

refractory

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5
Q

blocking Na is ___________

A

velocity

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6
Q

blocking Ca is ___________

A

nodal

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7
Q

increase in heart rate = increase in _______

A

slope

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8
Q

sodium blockers/membrane stabilizers

Blocking sodium moves the threshold potential farther away from the resting potential*

A

Class 1

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9
Q

example of Class I

A

lidocaine

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10
Q

beta blockers

A

Class 2

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11
Q

It is BETTER to use a beta-1 selective blocker (____________), instead of beta-1 and beta-2 (labetalol), which can cause a bronchospasm*

A

metoprolol is better!!!

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12
Q

beta ___ can cause bronchospasm

A

beta 2 (labetalol)

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13
Q

which classes reduce mortality risk

A

CLass 2 (beta blockers)
Class 3 (potassium blockers-amio)

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14
Q

refractory prolongers

A

Class III
potassium blockers

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15
Q

example of a class III drug

A

amio

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16
Q
  • MOA
    o Dilates coronary arteries (anti-angina)
    o Blocks sodium and reduces currents of potassium and calcium
    o Prolongs AP, refractory, and conduction
    o Alpha + beta antagonist = vasodilation
A

class 3

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17
Q

adverse effects of amio (class III)

A

o Hypotension r/t vasodilation
o Pulmonary toxicity (lipophilic, slow elimination)
o Marked QT prolongation
o Resistant to catecholamines
o Reduces oxygen concentrations
bradycardia, AV block
o Altered thyroid function
o LV depression

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18
Q

calcium channel blockers

A

class 4

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19
Q

indicated for Afib, aflutter, paroxysmal SVT (supraventricular/atrial issues)

A

class 4

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20
Q

which classes decrease nodal depolarization

A

class 2 and 4

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21
Q

Effective if rapid bolus though central line only

A

adenosine

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22
Q

o Treats supraventricular/atrial issues

A

digoxin

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23
Q

Useful in ventricular dysrhythmias + digitalis toxicity induced ventricular dysrhythmias*

A

phenytoin

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24
Q

o Useful in
Torsades de Pointes
digitalis-induced dysrhythmias
ventricular ectopy

A

magnesium

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25
Q

Produces decreased lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction

A

vasopressin

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26
Q

What is the negative issue with many antidysrhythmic?

A

cardiac depressant effects

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27
Q

what ultimately propels GFR

A

pressure

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28
Q

↑ Increase in arterial pressure stretches afferent arteriolar wall, reflex constriction occurs

↓ Arterial pressure leads to arteriolar dilation

A

myogenic

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29
Q

↓ Decrease in RBF  ↓ GFR  afferent arteriolar dilation  ↑ increased GFR and RBF  restored filtration

Renin released  AT II  ↑ GFR

A

tubuloglomerular

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30
Q

Inhibit reabsorption of NaCl in LOOP, PROXIMAL + DISTAL tubules

↓ SNS in peripheral smooth muscle due to ↓ total body Na+ stores
o Resulting in vasodilation

A

thiazide diuretics

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31
Q

good for elderly

can cause Gout/hyperuricemia

A

thiazide diuretics

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32
Q

example of thiazide diuretic

A

diuril

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33
Q
  • Most effective, fastest class
  • Stimulates production of prostaglandins
    o Resulting in vasodilation
    o Increases RBF
A

loop diuretics

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34
Q

Inhibit reabsorption of NaCl in ASCENDING loop

A

loop diuretics

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35
Q

BP drop in ________

A

(due to SNS) prostaglandins and vasodilation

LASIX

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36
Q

massive lasix doses ___________ to NMBs

A

resistant

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37
Q

examples of loop diuretics

A
  • Lasix, Bumex, Demadex, Ethacrynic Acid
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38
Q
  • Large molecular weight molecule increases plasma osmolarity
  • Exerts a “pull”
A

osmotic diuretics

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39
Q

works in the LOOP + PROXIMAL tubule

A

osmotic diuretics

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40
Q

used for neurosx
can cause rebound HTN + pulm edema

A

osmotic diuretics

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41
Q
  • Mannitol
  • Urea
A

osmotic diuretics

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42
Q
  • Used in combination with loop diuretics
  • Weak
  • Works in the DISTAL tubules and COLLECTING ducts
A

potassium-sparing

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43
Q

CONTRAINDICATORS
ACE inhibitors and NSAIDs

A

potassium-sparing diuretics

+ aldosterone antagonists?

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44
Q
  • Spironolactone
A

aldosterone antagonists
(can lead to HYPERkalemia)

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45
Q
  • Blocks reabsorption of both Na + HCO3
  • Sodium then pulls water into the proximal tubule as an osmotic diuretic
A

carbonic anhydrase inhibitors

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46
Q
  • Acidosis (Hyperchloremic metabolic acidosis)
  • Drowsiness
  • Paresthesia
  • Renal calculi
A

carbonic anhydrase inhibitors

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47
Q
  • Blocks ADH
A

Vasopression ANTAGONISTS

(Tolvaptan)

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48
Q

D1 receptors in PROXIMAL tubule + LOOP

A

Dopamine

(LOW dose only!)

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49
Q

Causes increased BNP and ANP
“indirectly” cause diuresis

A

neprilysin inhibitors

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50
Q

What category is mannitol?

A

osmotic diuretic

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51
Q

What diuretics can aggravate a diabetic condition/cause hyperglycemia, can also cause hypokalemia (digoxin toxicity)?

A
  • Thiazide and loop diuretics
  • Thiazide diuretics are used in combination with other drugs to control BP
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52
Q

Which diuretics can reduce the cerebral spinal fluid?

A
  • Mannitol and lasix
    (osmotic and loop diuretics)
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53
Q

What diuretic must be used with caution when taking NSAID or ACE inhibitor (which raises potassium)?

A

Potassium sparing diuretics (Triamaterene, Amiloride)

  • Aldosterone antagonists (spironolactone)?
54
Q

What 2 conditions increase aldosterone?

A

Liver Cirrhosis + CHF

so, give aldosterone antagonist (spironolactone)

55
Q

histamine is in mast cells or ___________

A

basophils

56
Q
  • Immunologic mechanism
  • Cells have an Ig__ antibody attached to the membrane
  • When the antigen is exposed to the cell, degranulation (breakdown) of the cell occurs causing release of histamine and other mediators
  • Negative feedback from H2 receptors found in skin and basophils (NOT found in lungs) limits reaction in the skin and blood
A

HISTAMINE MOA
IgE

no positive feedback in the lungs

57
Q

where is histamine found

A

mast cell
brain (non mast cell)
enterochromaffin cells (stomach)

58
Q

what type of reaction is anaphylaxis, antigen-antibody

A

type 1

59
Q

re-exposure to histamine = ___________

A

bridging of IgE

60
Q

re-exposure/bridging causes cascade of __________ INTO the cell

A

calcium

61
Q

Increase vascular permeability, contract smooth muscle, wheal

A

platelet-activating factor

62
Q

Located in brain (nerve endings), endothelium, smooth muscle, cardiac

BronchoCONSTRICTION
slowed HR
coronary artery vasoconstriction (vasospasm)

A

H1

63
Q

RAPID (transient)

A

H1

64
Q

SUSTAINED (slow)

A

H2

65
Q

BronchoDILATION (not as much as H1 though)

Increase in HR

Increase in H ions (acid) from stomach

CNS stimulation

A

H2

66
Q

Decreases norepi release

Decreases histamine (negative feedback)

A

H3 and H4

67
Q

Located in the heart

A

H3

68
Q

Located in the bone marrow
and blood (eosinophils, neutrophils)

A

H4

69
Q

If you are concerned someone is going to have an allergic reaction

A

Pretreat with H1 blocker Benadryl and H2 blocker is Pepcid

Make sure you do not only give H2/Pepcid (since H3 will be blocked)

70
Q

hives =

A

urticaria

71
Q

true allergic reaction causes
pulm HTN and increased inotropy

A

true

72
Q

reactive airways are _____ greater sensitivity

A

100-1000x

73
Q

o Not IgE mediated
o Can be fatal
o Resembles anaphylaxis!

A

anaphylacTOID

74
Q

risk factors for anaphylaxis

A
  • IV drugs
  • Allergies
  • History of reaction
  • Asthma or COPD
  • Women (2.5x more likely)
  • History of previous anesthetic
75
Q

Do NOT inhibit the release of histamine; instead, they BLOCK the receptors
o Benadryl, Dramamine, Bonine, Phenergen

A

H1 blockers

76
Q
  • Tagamet, Pepcid
A

H2 blockers

77
Q

anaphylaxis:

Physiologic antagonist = ______

A

epi

78
Q

anaphylaxis:

Prevent RELEASE of histamine

A

Beta 2 agonists (Cromolyn)

79
Q

anaphylaxis:

Receptor blockers

A

antihistamines

80
Q

top 3 drugs that cause anaphylaxis

A

NMBs
abx (b lactam, cephalosporins + penicillins)
latex

  • Morphine, Demerol, codeine (histamine)
  • Induction agents
  • Local anesthetics (preservatives)
  • Blood products (preservatives in the blood)
  • Protamine
81
Q

Assessment of Type 1 Reaction

Erythema (flushing) Urticaria (hives), with or without angioedema
Mild

A

grade 1

82
Q

Assessment of Type 1 Reaction

Moderate severity Cutaneous signs
Hypotension and tachycardia
Difficult to ventilate

A

Grade 2

83
Q

Assessment of Type 1 Reaction

Life-threatening
Hypotension, tachy or brady
Dysrhythmias
Bronchospasm

A

grade 3

84
Q

Assessment of Type 1 Reaction

Cardiac/resp arrest
PEA

A

grade 4

85
Q

treatment for anaphylaxis

A

remove agent
trendelenburg
intubate
epi + albuterol
fluids
vaso
beta blockade
antihistamines

86
Q

what 2 drugs can be used with pretreatment for histamine

A

ephedrine
decadron

87
Q

mineralocorticoid

A

aldosterone

88
Q

o Function
Maintain extracellular fluid volume, plasma concentrations of ions, conservation of sodium (to attract water)

A

mineralcorticoids

89
Q

what are stimulators of mineralcorticoids

A

 Hyperkalemia
 Hyponatremia
 ACTH (adrenocorticotrophic hormone)
 AT II

90
Q

Glucocorticoids

A

cortisol

91
Q

Essential for life, not stored in the body

A

Glucocorticoids

92
Q

anti-emetic
Increase the number + sensitivity of beta-adrenergic receptors
Decrease immune response
Anti-inflammatory effects
Affects carbs, proteins, and fats

A

cortisol

93
Q

cortisol insufficiency cause of death

A

Unexplained hypovolemic shock
UNRESPONSIVE to catecholamines

94
Q

drug interactions with glucocorticoids

A

 Etomidate suppresses cortisol synthesis
 Opioids (large doses)
 Volatile agents

95
Q

cortisol is also known as

A

hydrocortisone

96
Q

Items that come in contact with mucous membranes or non-intact skin
Items that are soiled by blood, body fluids, or pathogens

HIGH-level disinfection

A

semi-critical risk

97
Q

Items that touch intact skin or do not come in contact with skin

Intermediate or Low-Level Disinfection

A

Non-Critical Risk

98
Q

what is not killed by disinfection

A

spores
prions

99
Q

Decreasing the number of microorganisms on an inanimate surface to acceptable for public health purposes

A

sanitization

100
Q

The process of killing microorganisms, not spores, with hot water or steam

A

pasteurization

101
Q

An agent applied to living tissue to kill or prevent growth of microorganisms

A

Antiseptic

102
Q

Target=only bacteria

A

alcohol

103
Q

Target=bacteria (gram+ and gram-), fungi, viruses
(no effect on TB)

A

Quaternary ammonium compounds

104
Q

If bottles are open, it supports growth of pseudomonas

A

Quaternary ammonium compounds

105
Q

Target=bacteria (gram+ and gram-),
moderate effect on fungi and viruses,
spores’ activity is DECREASED (inhibited, not killed)

A

chlorhexidine

106
Q

Neural toxicity (do not use with epidural catheter)
Sensorineural deafness (do not use with middle ear surgery)

A

chlorhexidine

107
Q

Preferred/best choice for CVL placement over betadine

Residual/persistent effect: keeps working after it is placed

A

chlorhexidine

108
Q

Most active antiseptic for intact skin*

A

iodine

109
Q

Target=bacteria, viruses, and after 15 minutes spores

A

iodine

110
Q

Target=bacteria, mycobacteria, fungi, lipid containing viruses, spores (with prolonged exposure)

A

iodophors

111
Q

Target=bacteria (especially gram+)

Decreased bacteria by only 30-50% initially, but continued to decrease down to 4% (96% elimination)!

A

hexachlorophene

112
Q
  • Caused brain damage in neonates after daily bathing
  • Neurotoxic effects, cerebral irritability if absorbed
  • Do not use routinely while pregnant
A

hexachlorophene

113
Q

An agent or treatment applied to an inanimate surface to destroy most microorganisms or viruses, but NOT spores

A

disinfectant

114
Q

what temp for pasteurization
NOT SPORES
Target=bacteria, gram- rods, mycobacteria TB, fungi, viruses

A

68 C for 30 minutes

115
Q

The process that kills or removes all types of microorganisms, including spores, fungi, and viruses

A

sterilization

116
Q

what is only chemical used for sterilization

A

ethylene oxide

(all organisms at room temp)

117
Q

 Can be absorbed* irritation and allergic reactions
 Associated with latex allergy, spina bifida
 May fail in the presence of organic debris or biofilm

A

ethylene oxide

118
Q

Target=bacteria, fungi, viruses, 2-4 days for spores

A

formaldehyde

119
Q

Target=bacteria, mycobacteria TB, fungi, viruses, spores

A

Cidex

120
Q

Alternative to autoclaves

Target=bacteria (gram+ and gram-), fungi, spores

A

insta pot

121
Q

Target=bacteria (gonococci- eye drops in neonates at risk)

wounds, burns

A

silver nitrate

122
Q

which drugs kill spores

A

sterilization
insta pot
ethylene oxide
cidex

iodine (after 15 minutes)
formaldehyde (after 2-4 days)
iodophors (with prolonged exposure)
chlorhexidine (spores activity is decreased)

123
Q

limitations to depressant medications

A
  • Infants
  • Elderly
  • Decreased LOC
  • Intracranial pathology
  • Severe pulm dx
  • Hypovolemia
  • Full stomachs
124
Q

Implicated as teratogenic (do not use in FIRST trimester pregnancies

A

benzos

125
Q

Prostaglandin INHIBITION may decrease platelet aggregation

A

nsaids

126
Q

o Blocks calcium channels
o Decreases norepi
o Decreases glutamate
 Decreases excitability of dorsal horn neurons

elderly can become more sedated

A

gabapentin

127
Q

vagolytic

A

PREVENTS bradycardia (causes tachycardia)

128
Q

treatment for central anticholinergic syndrome

A

physostigmine

129
Q

o Decreasing the amount of H ions
o Leading to a gradual, slow increase in pH

A

H2 blockers

130
Q

Enhances the effects of Ach on the intestinal smooth muscle to speed gastric emptying, increase LES tone, relax the pylorus and duodenum, and lower gastric VOLUME

A

reglan

131
Q

Increase the gastric pH by neutralizing the H ions with a base
increases gastric volume slightly (negative)

A

antacids

132
Q

MOST effective in controlling both gastric pH and gastric volume

Limits the last step in secretion of H ions (hydrogen-potassium ATPase)

Membrane enzyme proton pump on gastric parietal cells

A

PPIs

Pharm 1 (9 decks)

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