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Pharmacology- Keiser > Misc. Pharm > Flashcards

Misc. Pharm Flashcards

1
Q

What does DAW stand for?

A

Dispense as Written

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2
Q

What are S&S of Antimalarias?

A

Related to destruction of RBCs & liver toxicity

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3
Q

What is the aimed treatment of Antimalarias?

A

Aims to attack parasite at any stage of development in & out of the human body.

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4
Q

What drug is the best drug to treat Malaria?

A

Quinine

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5
Q

What are Antimalarias?

A

Combo drugs/cocktails designed to attack plasmodium @ various state of its cycle.

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6
Q

What are the 2 most common Helminths?

A

Nematodes/Roundworms

Platyhelminths/Flatworms

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7
Q

What is the definition of a tumor?

A

Neoplasm

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8
Q

How do malignant tumors develop?

A

From one cell w/ somatic mutations occurring during division as tumor grows.

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9
Q

What feeds a tumor?

A

Glucose

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10
Q

What are somatic cells?

A

Any cells that are not sex cells

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11
Q

What are Gamma cells?

A

Sex cells

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12
Q

The nurse is caring for a patient with a fungal infection. Which of the following would be considered an adverse effect of an antifungal medication?

A

Burning or irritation in the sexual partner

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13
Q

What is primary action?

A

Side effects that are extensions of desired effects

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14
Q

What is secondary actions?

A

Effects IN ADDITION to desired effects

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15
Q

What is hypersensitivity?

A

Excessive response to primary/secondary effects

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16
Q

What are the 4 main classifications of drug allergy?

A

Anaphylactic
Cytotoxic
Serum sickness
Delayed

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17
Q

What are the signs of anaphylaxis?

A

Hives/rash
Difficulty breathing
Increased BP
Dilated pupils
Diaphoresis
Panic feeling
Increased HR
Increased RR

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18
Q

What are the interventions for anaphylaxis?

A

Epinephrine
Prevention

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19
Q

What is the symptoms of cytotoxic reaction?

A

CBC: decreased hematocrit, WBCs, platelets
Liver function test: elevated enzymes
Renal function test: decreased renal function

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20
Q

What are cytotoxic reaction interventions?

A

Notify & discontinue
Support to prevent infection
Conserve pt energy until response complete

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21
Q

What are symptoms of serum sickness?

A

Itchy rash
High fever
Swollen lymph nodes
Swollen/painful joints
Edema of face/limbs

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22
Q

What are the interventions for serum sickness?

A

Notify & discontinue
Provide comfort measures to S&S

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23
Q

What are the symptoms of delayed allergic reaction?

A

Rash
Hives
Swollen joints- similar to poison ivy

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24
Q

What are the interventions of delayed allergic reaction?

A

Notify & discontinue
Provide skin comfort measures

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25
Q

What is a superinfection?

A

Infection caused by destrution of normal flora

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26
Q

What are the early symptoms of hypoglycemia?

A

Sweating
Blurry vision
Dizzy
Anxiety
Hungry
Irritable
Shaky
Headache
Weakness/ fatigue

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27
Q

What are symptoms of hyperglycemia?

A

Fatigue
Polyuria (frequent urination)
Polydipsia (frequent thirst)
Deep RR
Restlessness
Polyphagia (increased hunger)
Nausea
Hot/ flushed skin
Fruity breath

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28
Q

What are S&S of hyperkalemia?

A

Serum K+ = 5+ mEq/L
Weakness
Muscle cramps
Diarrhea
Numbness/tingling
Bradycardia
Low BP
Decreased urine output
Difficulty breathing

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29
Q

What is an agonist?

A

Drugs that interacts directly w/ receptor sites
Example: INSULIN

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30
Q

What is an antagonist?

A

Drugs block receptor site activity

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31
Q

What does First-Pass effect do?

A

Destroys large portion of portion of oral drug potency

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32
Q

What is a prototype?

A

Original drug in its class

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33
Q

What are pre-clinical trials?

A

Testing in lab w/ animals.

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34
Q

What is Phase 1 studies?

A

Studies introducing human volunteers

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35
Q

What are Phase ll studies?

A

Studies allowing patients w/ disease

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36
Q

What are scheduled l drugs?

A

Street drugs, highly abusive
Example: Meth

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37
Q

What are schedule ll drugs?

A

Pharmaceuticals w/ high abuse potential
Example: amphetamines

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38
Q

What are scheduled lll drugs?

A

Moderately dependent

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39
Q

What are schedule lV drugs?

A

Less abusive potential, limited dependence

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40
Q

What are scheduled V drugs?

A

Limited abuse, 18+ to get

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41
Q

What are orphan drugs?

A

Drugs discovered but not financially viable; unadapted by drug company

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42
Q

What are sources of drug info?

A

Drug labels
Package inserts
Reference books
Journals
Internet info

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43
Q

What are the comments of the heart?

A

Heart
Arteries
Veins
Venoules
Arterials

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44
Q

What is the cardiovascular systems function?

A

Deliver O2 & nutrients to all cells
Removes waste

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45
Q

What is the flow of deoxygenated blood?

A

Right atrium,
through tricuspid valve,
to right ventricle,
though pulmonary valve
to lungs

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46
Q

What is the flow of oxygenated blood?

A

Through pulmonary veins,
To left atrium
Through mitral valve
To left ventricle
Through aortic valve
To aorta

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47
Q

What is automaticity?

A

Generates action potential (electrical impulses) w/out external stimulant

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48
Q

What is conductivity?

A

Special cells conducting rapid impulse to stimulant at the same time

Example: lub, dub, dub, lub

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49
Q

What are the components of the conduction system?

A

SA node= pace maker
Atrial bundles
AV node
Bundle of His= Bachmann’s bundle
Bundle branches
Purkinje fibers

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50
Q

What is the Starling’s Law of the Heart?

A

= stroke volume of left ventricle; increases LV volume

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51
Q

What is the Diastole of the BP?

A

Rest period
Blood returned to heart by veins

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52
Q

What is the Systole of BP?

A

Contraction period
Blood is pumped from the heart

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53
Q

What does Starling’s law of the heart address?
A. Automatic properties of the heart
B. Conductive properties of the heart
C. Contractile properties of the heart
D. Pressure properties of the heart

A

D.

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54
Q

What are the type of arrhythmias(no rhythm)?

A

Sinus arrhythmias= caused by normal breathing
Supraventricular arrhythmias= Afib, atrial flutter, PAT, PACs
Atrioventricular block
Ventricular arrhythmias= originates BELOW AV node, PVCs, Vfib

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55
Q

Where does the pulmonary circulation take place?

A

Right side if the heart, sending blood to lungs
CO2/wastes are removed
O2 is picked up by RBCs

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56
Q

Where does systemic circulation?

A

Left side of the heart sends oxygenated blood out

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57
Q

What are the forces determining O2 consumption?

A

HR= harder the work, the more O2 needed
Preload= amount of blood return
After load= resistance against heartbeat
Ventricle stretch

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58
Q

Wha this paroxysmal mean?

A

Sudden reoccurrence/attack; sudden worsening symptoms

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59
Q

What happens when you get a high diastolic?

A

Venous pressure increases
Can result in backup if congestion

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60
Q

What happens in heart failure?

A

Blood back ups
Results in edema

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61
Q

What is BP determined by?

A

HR
Stroke volume
Total peripheral resistance
Baroreceptors= relays BP info w/in ANS
Renin-angiotensin-aldosterone system

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62
Q

What is the Risks for CAD related to hypertension?

A

Thickening of heart muscle
Increased pressure by muscle contraction
Increased cardiac workload

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63
Q

What are conditions related to HTN?

A

CAD
Stroke
Renal failure
Loss of vision

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64
Q

What are known factors that increase BP?

A

High levels of psychological stress
Exposure high-frequency noise
High salt diet
Lack of rest
Genetic predisposition

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65
Q

What happens in hypotension?

A

BP too low
Heart muscle is damaged, unable to pump effectively
Severe blood/fluid loss drops, dramatically
NE is depleted is severe stress; body is unable to respond to stimuli

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66
Q

What is the care management steps of HTN?

A
  1. Lifestyle modification
  2. Drug therapy
  3. Drug dose/class, or combo drug therapy
  4. 2nd/3rd agent/diuretic is added
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67
Q

What are the antihypertensive agents?

A

ACE inhibitors
Angiotensin ll receptor blockers
Renin inhibitors
Calcium channel blockers
Vasodilators
Diuretics
Sympathetic nervous system blockers

68
Q

What is the common drug ending for ACE inhibitors?

69
Q

What is the action of ACE inhibitors?

A

Blocks ACE from conversion into angiotensin ll
Decreases BP
Decreases aldosterone production
Slightly increases serum K+ levels
Slightly increases NA+/fluid loss

70
Q

What is the indication for use of an ACE inhibitor?

A

HTN
CHF
Diabetic nephropathy
Left ventricular dysfunction- following MI

71
Q

What is the contraindications for ACE inhibitors?

A

Allergies
Impaired renal function
Pregnancy/lactation
CAUTION: CHF

72
Q

What are the adverse effects of ACE inhibitors?

A

Related to vasodilation effects & blood flow alterations
GI irritation
Renal insufficiency
Cough

73
Q

What is a drug that interacts with ACE inhibitors?

A

Allopurinol

74
Q

What are nursing considerations for ACE inhibitors?

A

HX & physical
Allergy
Impaired kidney function
Pregnancy/lactation
Salt/volume depletion & HF
Baseline status before therapy starts
VS, LS, BS, weight, skin, ECG, CBC w/ diff & electrolytes

75
Q

What is the prototype for ACE inhibitors?

76
Q

What is the action of captopril?

A

Blocks angiotensin l from converting angiotensin ll, leads to decreased BP, aldosterone production, & small increase of serum K+ & Na+/fluid loss

77
Q

What is the onset for captopril?
What is the half life?

A

15 minutes & 2 hrs.

78
Q

What is the adverse effects of captopril?

A

Tachy
MI
Rash
Pruritus
Gastric irritation
Aphthous ulcers
Peptic ulcers
Dysgeusia
Proteinuria
Bone marrow suppression
Cough

79
Q

What is the common drug ending for angiotensin ll receptor blockers?

80
Q

What is the action of angiotensin ll receptor blockers?

A

Blocks vasoconstriction & aldosterone release by selectively binding to angiotensin ll receptors in vascular smooth muscle/adrenal cortex

81
Q

T/F: angiotensin ll receptor blockers doesn’t use the P450 system in the liver.

82
Q

What are the contraindications for angiotensin ll receptor blockers?

A

Allergy, pregnancy, lactation

CAUTION: hepatic/renal dysfunction & hypovolemia

83
Q

What are the adverse effects of angiotensin ll receptor blockers?

A

Headache
Dizzy
Syncope
Weakness
GI complaints
Skin rash/dry skin

84
Q

What drug interacts w/ angiotensin ll receptor blockers?

A

Phenobarbital

85
Q

What are the nursing considerations for angiotensin ll receptor blockers?

A

Assess:
Hx/physical
Allergy
Impaired renal/hepatic function
Pregnancy/lactation
Hypovolemia
Baseline: VS, LS, ECG, renal/function tests

86
Q

What is the prototype for angiotensin ll receptor blockers?

87
Q

What is the indication for use of losartan?

A

HTN
Diabetic neuropathy
Elevated serum creatine
Elevated proteinuria w/ type ll diabetes/HTN

88
Q

What is the action of losartan?

A

Blocks vasoconstriction & release aldosterone associated w/ RAAS

89
Q

What is the onset, peak, and duration for losartan?
What is the half life?

A

Varies, 1-3 hrs, 24 hrs
2 hrs

90
Q

What is the adverse effects of losartan?

A

Dizziness
Headache
Diarrhea
Abdominal pain
Upper respiratory tract infection symptoms
Cough
Back pain
Fever
Muscle weakness
Hypotension

91
Q

What does calcium channel blockers do?

A

Decrease BP
Decrease cardiac workload
Decrease myocardial O2 consumption

92
Q

What is the action of calcium channel blockers?

A

Stops calcium ion movement across cardiac/arterial membrane, leading to slowed conduction, decreased myocardial contractility, arterioles.

Lowering BP & myocardial O2 consumption.

93
Q

What are the contraindications for calcium channel blockers?

A

Allergy
Heart block
Sick sinus syndrome
Renal/hepatic dysfunction
Pregnancy/lactation

94
Q

What are the adverse effects for calcium channel blockers?

A

Effects related to cardiac output
Gi symptoms
Cardiovascular symptoms

95
Q

What is the drug that interacts with calcium channel blockers?

A

Cyclosporine

96
Q

What is the food interactions for calcium channel blockers?

A

Grapefruit juice

97
Q

What should the nurse consider for calcium channel blocker?

A

Hx/physical
Allergy

98
Q

What is the main use for calcium channel blockers?

99
Q

What is the prototype for calcium channel blockers?

100
Q

What is the onset, peak, and duration of diltiazem?
What is the half life?

A

30-60 min
6-11 hrs
12 hrs

5-7hrs= T1/2

101
Q

What is the most powerful natural vasoconstrictor in the human body?

A

Angiotensin ll

102
Q

What does aldosterone play a big part of?

A

Regulating BP

103
Q

What are the adverse effects of diltiazem?

A

Dizzy
Light headed
Headache
Peripheral edema
Bradycardia
Atrioventricular block
Flushing
Nausea

104
Q

What does diuretics do?

A

Increase NA+/water excretion from kidneys to lower BP

105
Q

What is the common drug ending for diuretics?

106
Q

What is the common drug ending for beta blockers? (Sympathetic nervous system blockers)

107
Q

The nurse is caring for a 27-year-old woman who was just prescribed an ACE inhibitor for management of her hypertension. What should be advised related to contraception?
A. The use of spermicidal jellies is recommended.
B. The mini pill is the contraception method of choice.
C. Use barrier contraceptives to prevent pregnancy while taking these drugs.
D. No special precautions need to be taken.

108
Q

What is the CYP-450 system?

A

System of enzymes needed to metabolize in the liver.

109
Q

What does the sympathetic nervous do?
What does the parasympathetic do?

A

Sympathetic= Fight/flight
Parasympathetic= body calmer

110
Q

What is the most important ventricle in the heart?

A

Left ventricle

111
Q

What does the aortic do?

A

Take un-oxygenated blood through heart

112
Q

What does the mitral valve do?

A

Send blood to be pumped though body

113
Q

What is the action potential?

A

Electrical conduction of heart; biogenetic theory depression

114
Q

What are the causes of cardiac arrhythmias?

A

Electrolyte disturbance
Decrease O2 delivery
Structural damage
Acidosis (waste accumulation)
Drugs

115
Q

What tends to be blocked?
What tends to be clogged?

A

Arteries= blocked
Veins= clot

116
Q

What are the types of cardiac arrhythmias?

A

Tachycardia= fast
Bradycardia= slow
PACs (premature atrial contractions)=
PVCs (premature ventricular contractions)=
Atrial flutter=
A-fib=
V-fib=
Alterations in conduction through the muscle (heart blocks & bundle branch blocks)

117
Q

What are the classifications of antiarrhythmics?

A

Class l= blocks NA+ channels in cell membrane
Class ll= blocks beta-receptors; causes phase 4 depression
Class lll= blocks K+ channels; prolongs phase 3
Class lV= blocks CA+ (calcium) channels in cell membrane

118
Q

What are class l anti-arrhythmias?

A

Ia= Disopyramide (Norpace), Procainamide (generic), quinidine (generic)

Ib= Lidocaine (Xylocaine), mexiletine (generic)

Ic= flecainide (generic), propafenone

119
Q

What is the action of class l anti-arrhythmias?

A

Decreases polarization & automaticity of ventricular cells

Increases ventricular fib threshold

120
Q

What is the indication for class l anti-arrhythmias?

A

Management of acute ventricular arrhythmias during cardiac surgery

Or

MI

121
Q

What is class l anti-arrhythmias mostly absorbed through?

122
Q

What are contraindications for class l antiarrhythmics?

A

Allergy
Bradycardia
Heart block
CHF
Hypotension
Shock
Electrolyte disturbance

123
Q

When should you use caution when giving a class 1 anti-arrhythmic?

A

Renal/hepatic dysfunction
Pregnancy

124
Q

What are the adverse affects of class 1 anti-arrhythmias?

A

CNS= dizzy, fatigue, slurred speech
GI= nausea/vomiting
CV= arrhythmias
Respiratory depression
Misc= rash, hair loss, potential bone marrow suppression

125
Q

What drugs interact with class 1 anti-arrhythmias?

A

Quinidine
Oral anticoagulants
Digoxin
Beta blockers

126
Q

What does class ll antiarrhythmics?

A

Blocks beta-receptors, causing a depression of phase 4 action potential

127
Q

What are class ll antiarrhythmics?

A

Acebutolol (Sectral)
Esmolol (Brevibloc)
Propranolol (Inderal)

128
Q

What is the actions of class ll antiarrhythmics?

A

Competitively blocks beta receptor sites in heart/kidneys

Decrease HR, cardiac excitability, cardiac output

Clot AV node conduction

129
Q

What are the indications for use for class ll antiarrhythmics?

A

Supraventricular tachycardia & PVCs treatment

130
Q

What are the pharmacokinetics of class ll antiarrhythmics?

A

Absorbs in GI
Liver metabolized
Urine excreted

131
Q

What are the adverse effects of antiarrhythmics?

A

CNS= dizzy, insomnia, dreams, fatigue
CV= hypotension, bradycardia, AV block, arrhythmias
Respiratory- bronchospasm, Dyspnea
GI= nausea, vomiting, anorexia
Misc= libido loss, decreased exercise tolerance, alterations in blood sugar

132
Q

What does class 2 antiarrhythmics interact w/ drug wise?

A

Verapamil
Insulin

133
Q

What are the class IV antiarrhythmics drugs?

A

Diltiazem (generic)
Verapamil (generic)

134
Q

What are the indications for use for class IV antiarrhythmics?

A

Supraventricular tachycardia
Controls ventricular response to rapid atrial rates

135
Q

What are the pharmacokinetics of class IV antiarrhythmics?

A

Well absorbed
Protein bound
Liver metabolized
Urine excreted

136
Q

What are the contraindications for use in class IV antiarrhythmics?

A

Allergy
Sick sinus syndrome
Heart block
Pregnancy
Lactation
CHF hypotension

137
Q

When you should you use caution when using class lV antiarrhythmics?

A

Idiopathic hypertrophic subaortic Stenosis

138
Q

What are the adverse effects of class IV antiarrhythmics?

A

Dizzy
Weak
Fatigue
Depression
GI upset
Hypotension
CHF
Shock

139
Q

How does the blood flow through the heart?

A

Enters at top right atrium

Blood flows downward through tricuspid into right ventricle

Right ventricle pushes blood up to the pulmonary valve of the heart

Blood goes into lungs and re-enters through top left ventricle

Blood flows down through mitral and into left ventricle

Left ventricle pushes blood up through aortic into body

140
Q

What are the definitions of coronary artery disease?

A

Atheromas- fatty tumor in intima of heart vessels
Artherosclerosis- narrowing heart vessels
Angina pectoris- chest suffocation
MI- myocardial cells die

141
Q

Angina is specific to what part of the heart

A

Coronary artery

142
Q

What is the inner most part of the artery?

A

Tunica intima

143
Q

What is the second layer of an artery?

A

Tunica media

144
Q

What is the outer layer of an artery?

A

Tunica exsterna
Or Tunica Adventia

145
Q

What are the types of angina?

A

Stable angina- no damage to muscle; reflexes restore blood flow

Unstable angina- episodes of ischemia; happens even at rest

Prinzmetal’s angina- caused by blood vessel spams; not just narrowing

146
Q

What is an acute myocardial infarction?

A

Completely occluded & unable to deliver blood to heart muscle resulting in extreme pain, nausea, and severe sympathetic stress reaction (tachy, dilated pupils, increase RR/BP).

147
Q

What is the action of antianginal?

A

Improve blood delivery by dilation of blood vessels to heart

Increases o2 supply

Decreases cardiac workload

Decreases o2 demand

148
Q

What are the factors affecting MI o2 demand & antianginal effects?

A

Increased:
HR
Preload (blood volume)
Afterload (BP)
Left ventricular muscle size
Muscle contractility

149
Q

What are the types of antianginal drugs?

A

Nitrates
Beta-adrenergic blockers
Calcium channel blockers

150
Q

What does Nitrates do?

A

Helps restore supply & demand ratios in O2 delivery to heart muscle when resting isn’t enough

151
Q

What are the nitrate drugs?

A

Amyl nitrate (generic)
Isosorbide dinitrate (Isordil)
Isosorbide mononitrate (Moneket)
Nitroglycerin

152
Q

What are the contraindications for Nitrates?

A

Allergy
Sever anemia
Head trauma/ cerebral hemorrhage
Pregnancy/lactation

153
Q

When should you use caution when using Nitrates?

A

Hepatic/renal disease
Hypotension
Hypovolemia
Conditions limiting cardiac output

154
Q

What are the adverse effects of nitrates?

A

Related to vasodilation & decreased blood flow
CNS= headache, dizzy, weakness
GI= nausea, vomiting
CV= hypotension
Misc= flushing, pallor, increased sweating

155
Q

What drugs interact w/ nitrates?

A

HEPARIN
Ergot derivatives

156
Q

What are the nursing considerations for nitrates?

A

Assess:
Hx/physical exam
Allergy
Early MI
Head trauma
Cerebral hemorrhage
Hypotension
Hypovolemia
Anemia
Low-cardiac output
Pregnancy/ lactation
Skin
Pain- onset, duration, intensity, location, relief measures
RR
LS
Cardiac status
BP
Baseline ECG
Lab values

157
Q

What is the definition of CHF /HF?

A

Heart fails to effectively pump blood throughout body

158
Q

What is the primary treatment?

A

Allowing more efficient contraction of the heart to bring back balance

159
Q

What are the types of CHF?

A

CAD (coronary artery disease)
Cardiomyopathy
HTN
Valvular heart disease

160
Q

What are the S&S of right sided CHF?

A

Elevated jugular venous pressure
Splenomegaly
Hepatomegaly
Decreased renal perfusion when upright
Increased renal perfusion when supine (nocturia)
Pitting edema
Weakness/fatigue

161
Q

What are the S&S of left sided CHF?

A

Anxiety
Tachycardia
Dyspnea
Orthopnea
Hemoptysis
Rales
Cardiomegaly
S3
Increased HR
GI upset
Nausea
Abdominal pain
Decreased peripheral pulses
Hypoxia

162
Q

What are the underlying problems in HF involving muscle function?

A

Muscle damage: atherosclerosis, cardiomyopathy

Increased workload to maintain efficient output: HTN, valvular disease

Structural abnormality: congenital cardiac defects

163
Q

What are the CHF drug treatments?

A

Cardiotonic (inotropic) drugs:
Cardiac Glycosides
Phosphodiesterase inhibitors
HCN blocker

164
Q

What does cardiac glycosides do?

A

Increases force of heart muscle contraction/ renal perfusion and output, decreases blood volume to slow HR, conduction velocity through AV

165
Q

What does a phosphodiesterase inhibitors do?

A

Short term management of HF in pts receiving digoxin/diuretics

166
Q

What does HCN stand for in HCN blockers?

A

Hyperpolarization-activated cyclic nucleotide- gated channel blockers

167
Q

What does HCN blockers do?

A

Slows hearts pacemaker (SA node) in re-polarization (diastole phase) phase of action potential

Pharmacology- Keiser (5 decks)

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