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Pharm/Patho > Summexam2 > Flashcards

Summexam2 Flashcards

1
Q

Where does the hearts electrical activity start?

A

SA node through the chambers

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2
Q

What does the p wave represent?
QR?
S?

A

atrial depolarization
ventricle depolarization
ventricle re-polarization

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3
Q

What is CHD also called?

A

called ischemic heart disease and

coronary artery disease (CAD)

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4
Q

What are the problems associated with CHD/CAD?

A 
Angina
MI
Dysrhythmia
Heart failure
Cardiac death
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5
Q

What is the defining characteristic of CAD/CHD?

A

Defining characteristic: ischemia (insufficient delivery of O2 blood) to myocardium

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6
Q

What is the etiology of CHD/CAD?

A

Atherosclerosis**narrowing of the arterial lumen –> ischemia

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7
Q

How does atherosclerosis cause narrowing? 3 processes

A

1-Thrombus
2-Coronary vasospasm
3-Endothelial cell dysfunction – interference with relaxation/contraction of blood vessels

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8
Q

What are the 3 types of risk factors for CHD?

A

non-modifiable
Lipid
non-lipid
other

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9
Q

What are the non-modifiable risk factors of CHD?

A

Age- men over 45, women over 55
Gender- males
Family history
First degree relative with myocardial Infarction or sudden cardiac death

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10
Q

What are the lipid risk factors of CHD?

A

High total lipids (total cholesterol, LDL, triglycerides)

Low HDL

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11
Q

What are the non-lipid risk factors of CHD?

A 
Hypertension
Cigarette smoking
Thrombogenic state
Diabetes
Obesity
Lack of physical activity
Artherogenic diet
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12
Q

What are other risk factors for CHD?

A

Lipoprotein(a)
Homocysteine
C-reactive protein
Elevated fasting glucose levels

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13
Q

What is the role of lipids?

A

Transported via apoproteins

High-density lipoproteins transport cholesterol from peripheral tissue back to the liver, clearing atheromatous plaque

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14
Q

HDLs

A

High density lipoprotein
Our friend; want HDL level HIGH
Takes cholesterol from our tissue and brings it back to the liver to deal with it
HDL decreases atherosclerosis

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15
Q

LDLs

A

Low density lipoprotein
Not our friend
Carry cholesterol to tissues/keep it in circulation, directly contributing to the building of atherosclerotic plaques
Want LDL to be LOW

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16
Q

What are the 4 stages of Atherosclerosis?

A

Normal artery
Fatty Streak
Partially occluded vessel
Totally occluded vessel

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17
Q

How does atherosclerosis start?

A

injury/damage to the endothelium of the coronary artery

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18
Q

What is the connection between HTN and Atherosclerosis?

A

HTN causes chronic stress on the heart and can cause injury, which is how Atherosclerosis starts

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19
Q

What is insudation?

A

Once the endothelium has been damaged- endothelium is permeable and LDLs leak through into the vessel wall

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20
Q

What are foam cells and how are they formed?

A

Foam cells= lipid filled macrophages.

The macrophages follow the LDLs through wall and engulf the lipids.

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21
Q

What do foam cells do?

A

foam cells release inflammatory mediators/ growth factors which attracts more leukocytes and stimulates smooth muscle cells to grow.
results with a bulging of the coronary artery blood vessel wall. Causes a blockage of blood flow.

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22
Q

What causes the lipid core of plaque?

A

Excess lipids/debris accumulation from the damage, macrophages and inflammation

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23
Q

Are large or small cores more dangerous? why?

A

Large, they are more fragile and can rupture more easily, once they rupture, platelets aggregate and then thrombus forms and can block vessel

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24
Q

`Why are smaller plaques more stable?

A

they have collagen and fibrin caps-they tend to settle into the vessel.

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25
Q

Coronary perfusion can be altered in what 3 ways?

A

Atherosclerotic plaques
Blood clot formation
Vasospasm of blood vessels

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26
Q

Cardiac workload depends on what factors?

A

HR
Preload
Afterload
Contractility

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27
Q

What is acute coronary syndrome?

A

blood clots formed or plaque ruptures

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28
Q

What is chronic coronary occlusion ?

A

lots of blood vessels with lots of narrowing with sustained perfusion.
Body can maintain sufficient perfusion is by the development of collateral circulation (body finds different routes to send blood.)

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29
Q

What are the two branches of ischemia ?

A

Stable angina

Acute Coronary Syndromes

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30
Q

What are the two branches of acute coronary syndromes?

A

Unstable angina

MI

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31
Q

What are the two branches of MI?

A

NSTEMI

STEMI

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32
Q

What two groups of people could have abnormal manifestations of angina pectoris?

A

Women and people with diabetes

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33
Q

What is the difference between unstable and stable angina?

A

Stable- they know every time they go up stairs they will get it
Unstable- they will randomly get it

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34
Q

What is an example of acute coronary syndrome? (ACS)

A

plaque ruptures with thrombus development

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35
Q

What are the manifestations of ACS?

A

more severe; severe/excruciating chest pain, more likely to radiate to other parts of the body. Typically always accompanied by other symptoms such as n/v, diaphoresis

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36
Q

What labs would you draw for ACS?

A

labs and serum to check for markers such as myoglobin, troponin, CKMB (creatine kinase)

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37
Q

If someone has ACS, what would you want to note on a EKG?

A

Elevation of ST segment

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38
Q

What biomarkers are released into the blood with myocardial ischemia?

A

myoglobin, CK, CK-MB, Troponin I

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39
Q

When drawing labs, what is the most important aspect to get accurate readings?

A

Take them as soon as possible, don’t wait, levels could be inaccurate

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40
Q

What are three ways to treat ACS?

A

Decreasing myocardial oxygen demand
Increasing myocardial oxygen supply
Monitoring and managing complications
(medications, interventional radiology to open blood vessel or remove clot)

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41
Q

What is thrombolysis?

A

Enzymatic digestion of thrombus to open lumen

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42
Q

What is a Per-cutaneous transluminal coronary angioplasty? (PTCA)

A

Physical disruption of plaque to open lumen

or stent

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43
Q

What is a coronary artery bypass grafting? (CABG)

A

surgical placement of new conduit to bypass occlusion

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44
Q

Why is nitroglycerine considered a prodrug?

A

It is converted into nitric oxide which then causes the vasodilation

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45
Q

What forms does nitroglycerine come in?

A

SL tabs, Spray, topical ointment, transdermal patch, intravenous

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46
Q

How does nitrogycerine work?

A

dilates veins & decrease venous return (preload) which decreases oxygen demand

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47
Q

What two forms of Nitro have longer effects?

A

ointment and patch

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48
Q

What is isosorbide used for?

A

oral, long acting. Back up for angina to help with vasodilation
** do not use for acute

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49
Q

What type of drug interactions would you worry about for someone on vasodilators?

A

other vasodilators- *viagra (sildenafil) Both increase cGMP

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50
Q

How does tolerance of nitrogylcerin happen?

A

depletion of sulfhydryl groups – can’t be converted

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51
Q

If someone is using a nitro patch, what education would you tell them?

A

Take it of at bedtime and apply new one in morning

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52
Q

What is the lifespan of a platelet?

A

8 days

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53
Q

Giving aspirin of heparin to someone who just has a stent placed is important why?

A

The body will want to send platelets to the site and if there are two many, it could cause a MI- anti-platelet agents will help reduce the risk

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54
Q

Clopidogrel targets what, in relation to platelet aggregation?

A

adenosine diphosphate (ADP)

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55
Q

Aspirin targets what aspect of platelet aggregation?

A

thromboxane A2

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56
Q

Blocking what would be the last resort to platelet aggregation?

A

GP 2b 3a

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57
Q

What does thromboxane A2 do?

A

Produced by activated platelets

Stimulates activation of new platelets and platelet aggregation

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58
Q

Why is irreversible inhibition important to know about if someone comes in bleeding and they are on aspirin?

A

They will need to have platelets given back, no med to reverse the effects

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59
Q

What are the adverse effects of aspirin?

A 
GI bleeding
Bleeding
Renal impairment
Tinnitus (associated with high levels)
Salicylate toxicity
Respiratory alkalosis 
Metabolic acidosis
Renal failure
Altered mental status
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60
Q

What are some pediatric contraindications of aspirin?

A

associated with Reye’s syndrome (with viral illness)

encephalopathy and fatty liver degeneration

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61
Q

What are some reasons for taking aspirin?

A 
Ischemic stroke
Transient ischemic attacks
Acute MI
Previous MI
Chronic stable angina
Unstable angina
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62
Q

What is important about clopidogrel metabolism?

A

it is a pro-drug that is metabolized by P450 2C19 and those who have alterations in enzyme may not have success= could get platelet aggregation
may need genomic screening-

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63
Q

What are the adverse effects of clopidogrel?

A

Bleeding!!

Thrombotic thrombocytopenia purpura (TTP) - rare

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64
Q

What is the biggest drug interaction of clopidogrel?

A

Omeprazole because inhibits 2C19 = clopidogrel wont work and they could still get platelet aggregation

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65
Q

What does niacin do?

A

Reduces LDL and TG and raises HDL

It impacts the amount of adipose being filtered by liver and therefore decreases LDL

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66
Q

What is important about the initiation of niacin therapy?

A

Slow titration due to adverse effects

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67
Q

Why would aspirin be use while taking niacin?

A

because aspirin may help with the initial skin flushing and itching in first couple weeks of therapy

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68
Q

What are the adverse effects of niacin?

A

initial skin flushing and itching-3 weeks
Hepatoxicity: severe liver damage reported
Least likely with extended release product
Increased uric acid
Hyperglycemia

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69
Q

What are the outcomes of atrovastatin?

A

Reduction of LDL
Increase in HDL
Reduction of TG

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70
Q

What are the adverse effects of atrovastatin?

A

hepatotoxicity

Myopathy/rhabdomyolysis

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71
Q

What are the clinical uses for alteplase (tPA)?

A

STEMI, ischemic stroke, pulmonary embolism, restore patency to central IV catheters

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72
Q

What does alteplase do?

A

tissue plasminogen activator

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73
Q

How is alteplase administered?

A

IV only

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74
Q

What are the side effects of phenylephrine?

A

Fast, pounding, or uneven heartbeat.
Swelling of your face, lips, tongue, or throat.
Difficulty breathing.
Severe dizziness or anxiety.
Easy bruising or bleeding, unusual weakness, fever, chills, body aches, or flu symptoms.

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75
Q

What does phenylephrine do to the heart?

A

vasoconstriction

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76
Q

What does dubutamine do to the heart?

A

beta1adrenergic receptors in the heart, which causes an increase in the rate and strength. This allows blood to be pumped effectively around the body in conditions such as heart failure,

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77
Q

How does dopamine affect the heart?

A

inotropic effect on the heart muscle (causes more intense contractions) that, in turn, can raise blood pressure.

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78
Q

What two valves belong to the AV?

A

Tricuspid (R)

Mitral (L)

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79
Q

What two valves belong to the semilunar

A

Pulmonary (R)

Aortic (L)

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80
Q

At what point do symptoms of stenosis start?

A

50%

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81
Q

What is regurgitation?

A

valvular insufficiency- not working right, not shutting all the way so blood flow continues
*can happen fast if there is infection

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82
Q

What two valves are most effected by stenosis and regurgitation?

A

aortic and mitral

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83
Q

What are some secondary complications to aortic stenosis?

A

angina, ischemia, heart failure

Syncopy, fatigue, hypotension, angina

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84
Q

What are the treatments for aortic stenosis?

A

Avoid Vasodilators; Digitalis, Diuretics, Nitroglycerin in inoperable; Surgery

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85
Q

What are the treatments for mitral stenosis?

A

Potential Treatment: Mild=diuretics; Anticoagulation if in atrial fibrillation; Digitalis, Beta blockers, Calcium Channel Blockers for rate control; Surgery

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86
Q

What are the treatments for Aortic Regurgitation?

A

Vasodilators

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87
Q

What are the treatments for mitral Regurgitation?

A

Acute: Vasodilators; chronic: No proven Therapy; surgery

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88
Q

What is the definition of heart failure?

A

Inability of heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs

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89
Q

What are the clinical manifestations of heart failure?

A

dyspnea, pulmonary rales, cardiomegaly, pulmonary edema, S3 heart sound, and tachycardia

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90
Q

What are the two categories of heart failure?

A

Systolic or diastolic

91
Q

Systolic heart failure is seen by what manifestations?

A

not pumping right- reduced contractility- not adequate squeezing, common after and MI – low EF ( ejection fraction)

92
Q

Diastolic heart failure is seen by what manifestations?

A

doesn’t fill right- often with coronary artery disease , not so much MI- ventricle is not compliant, edema, potentially normal ejection fraction

93
Q

What is the difference between forward and backwards heart failure?

A

Forward heart failure is when the heart is not pumping right, low output and poor perfusion, activity intolerance
Backwards heart failure is when the heart is having regurgitation and blood backing up

94
Q

Right sided heart failure can be seem through what manifestations?

A

congestion in systemic, distended belly (ascites), enlargement of liver, spleen, JVD, fatigue, GI problems, edema

95
Q

left sided heart failure can be seem through what manifestations?

A

Pulmonary congestion, respiratory symptoms, edema- pulmonary edema can be life threatening, restlessness, confusion, orthopenia, tachycardia, exertional dyspnea, fatigue, cyanosis

96
Q

What are the three compensatory mechanisms?

A

myocyte growth
fluid retention
SNS activation

97
Q

What happens as a result to SNS activation?

A

increased HR

Increased contractility

98
Q

What happens as a result to fulid retention?

A

Increase preload

99
Q

What happens as a result to myocyte growth?

A

hypertrophy

100
Q

What does FACES stand for?

A 
Fatigue
Activity imitation
Congestion
Edema
Shortness of breath
101
Q

What are the goals of treating Heart failure?

A

Improve cardiac output
Minimize congestive symptoms
Reducing preload- diuretics, modify fluid and sodium

102
Q

What are the three types of cardiac dysrhythmias ?

A

Abnormal rates of sinus rhythm
Abnormal sites (ectopic) of impulse initiation
Disturbances in conduction pathways

103
Q

What is Automaticity?

A

Spontaneous generation of an action potential

104
Q

What is Triggered Activity?

A

Occurs when an impulse is generated during or just after repolarization

105
Q

What is Reentry ?

A

Cardiac impulse continues to depolarize in a part of the heart after the main impulse has finished its path and the majority of the fibers have repolarized

106
Q

What does atrial flutter appear as on a strip?

A

Sharp “teeth” before the p wave- no distinct p wave

107
Q

What does atrial fibrillation appear as on a strip?

A

no distinct p wave- many hills

108
Q

What are the theraputic uses of atropine?

A

Symptomatic bradycardia
Decreasing secretions
Mydriasis (pupil dilation)

109
Q

What are some effects of atropine?

A

Tachycardia, constipation, drying (anticholinergic

110
Q

What is adenosine used for?

A

for supraventricular tachycardia - Over 160bpm

IV PUSH

111
Q

What is unique about the half life of adenosine?

A

its VERY short

about 1.5-10 seconds

112
Q

What does adenosine do on the heart?

A

Decreases automaticity in the SA node & slows conduction through the AV node
Prolongs the PR interval
**rebooting- very uncomfortable for patient

113
Q

What do class I anti-arrhythmic drugs do?

A

block Na+ channels

114
Q

What do class II anti-arrhythmic drugs do?

A

beta-adrenoreceptor agonists

115
Q

What do class III anti-arrhythmic drugs do?

A

prolonged action potential and prolonged refractory period

K blockers

116
Q

What do class IV anti-arrhythmic drugs do?

A

Ca+ channel antagonists

117
Q

What does procainamide do?

A

sodium channel Slow impulse conductions in the atria, ventricles, and Hi-Purkinje system
Delays repolarization

118
Q

What is procainamide used for?

A

SVT, VT, A flutter, Afib

119
Q

Procainamide blocks what channel?

120
Q

What are the adverse effects of procainamide?

A

Systemic lupus syndrome: fever, painful & swollen joints, butterfly-like rash on face
Neutropenia and thrombocytopenia
Cardiotoxicity: widening of QRS and prolonged QT and PR intervals
Hypotension

121
Q

What labs would you check with procainamide?

A

CBC WBC & platelets

122
Q

How does lidocaine work?

A

slows cardiac conduction velocity via blockade
Decrease electrical conduction
Decrease automaticity
Increase rate of repolarization

123
Q

What is lidocaine used for?

A

Short term use for ventricular dysrthythmias

124
Q

What channel does lidocaine work on?

A

Sodium channel blocker

125
Q

What are the adverse effects of lidocaine?

A

CNS: drowsiness, altered mental status, paresthesias, seizures, hypotension, drop in BP, CV collapse

126
Q

Why is lidocaine not very effective orally?

A

it’s metabolized by the liver and has a very high first pass effect

127
Q

How does propafenone work?

A

slows cardiac conduction velocity via blockade
Decrease conduction velocisty in atria, ventricles, and Hi-Purkinje system
Delay ventricular repolarization

128
Q

What is propafenone used for?

A

Used for SVT

129
Q

What are the adverse effects of propafenone?

A 
Bardycardia
Heart failure
Dizziness
weakness,
Hypotension
Bronchospasm 
QRS prolongation
130
Q

How does propranolol work?

A

Beta blocker: prevents sympathetic nervous system stimulation of the heart
Decreased HR
Decreased automaticity through SA node, decrease velocity of conduction through the AV node, decrease myocardial contractility
Decrease atrial ectopic stimulation

131
Q

What is propranolol used for?

A

afib, a flutter, paroxysmal SVT, HTN, angina, PVCs

132
Q

What are some adverse effects of propranolol?

A 
Bronchicoonstriction, wheezing, trouble breathing
Brinchioconstriction
Hypotension
Bizare dreams
blah feeling
133
Q

Why can there be respiratory effects when taking propranolol?

A

acts on beta a and b- lungs and heart

134
Q

How does Amiodarone work?

A

prolongs the action potential and refractory period due to K channel blockade

135
Q

What is amiodarone used for?

A

Used for atrial and ventricular dysrhythmias

136
Q

What is unique about the half-life of amiodarone?

A

Very LONG- 25 – 110 days

aggressive loading doses to get pt up to steady state quicker

137
Q

What are the adverse effects of amiodarone?

A

Hypotension, Pulmonary fibrosis (from chronic use), Sinus bradycardia, Decreased contractility, accumulates in thyroid and can cause hypo or hyper thyroidism, can cause hepatotoxicity, Optic neuropathy and optic neuritis,
Photosensitivity, Bluish-gray skin***

138
Q

How does Verapamil work?

A

prolongs cardiac conduction, depresses depolarization and decreases oxygen demand of the heart by blocking Ca channels
Decrease force of contraction
Decrease heart rate
Slow rate of conduction through SA and AV nodes

139
Q

What is verapamil used for?

A

afib, a flutter, SVT, HTN, angina, Used for headache profylaxis

140
Q

What are the adverse effects of verapamil?

A 
Bradycardia
Hypotension
Heart failure
Constipation**
Peripheral edema
141
Q

What is a unique drug interaction for verapamil?

A

grapefruit juice

142
Q

What are the treatment plans for heart failure?

A
  • Preload reduction: Reducing circulating blood volume
  • Afterload reduction: Vasodilation
  • Myocardial protection: Catecholamines & angiotensin 2 have damaging effect on myocardium
  • Inotropic support
143
Q

What are three drugs that inhibit the RAAS system?

A

lisinopril, losartan, spirinolactone

144
Q

What are the advantages of beta blockers?

A 
Improve LVEF
Increase exercise tolerance
Slow progression of HF
Reduce need for hospitalization
Prolong survival
145
Q

What is the MOA of beta blockers?

A

protecting heart from excessive sympathetic stimulation and protecting against dysrhythmia

146
Q

What are the adverse effects of metroprolol?

A

Fluid retention & worsening heart failure, fatigue, hypotension, bradycardia or heart block

147
Q

What are the potential effects of digoxin?

A

Positive inotrope (inhibits Na-K-ATPase pump)
Increase CO
Alter electrical activity of heart
Favorable effect on neurohormonal systems
Reduces HF symptoms
DOES NOT HAVE AN IMPACT ON MORTALITY

148
Q

What are the adverse effects of digoxin?

A
  • Cardiac dysrhythmias (exacerbated by hypokalemia and elevated digoxin levels)
  • Principal non cardiac toxicities are CNS and GI related
  • Anorexia, nausea, vomiting, visual disturbances (halos around objects)
149
Q

What is the hallmark of HIV and AIDS?

A

Defective cell-mediated immunity-Decrease in CD4+ (T-helper/inducer) lymphocytes
Normally mediate between antigen-presenting cells and B cells and other T cells

150
Q

WHat is the core of the HIV virus called and what does it contain?

A

Core=nucleocapsid

  • RNA strands
  • Enzymes including reverse transcriptase and protease
151
Q

How does HIV binding and inception work?

A

1) One stud called gp120- binds to CD4 receptors
2) Second binding to chemokine coreceptor to help invade= fusing with the cell- core injects into cytoplasm of cell and then in produces HIV infection.
HIV RNA goes into DNA of host = frequent mutations which makes the virus more resistant to medications

152
Q

What is the HIV life cycle?

A

Attaches, moves in, integrates to infect and then programs cell to send retrovirus virion out to infect other cells

153
Q

Where is a major site of HIV replication?

A

The GI system

154
Q

What is the progression of HIV to AIDS?

A 
HIV enters body
Seroconversion
Primary HIV infection
Latency period
Chronic symptomatic HIV infection
AIDS diagnosis
155
Q

What happens in the primary HIV stage?

A

HIV count is very high- CD4 count has decreased at this point with decreased WBC, platelets, elevated ESR 1-4 weeks

156
Q

What happened in the latency phase?

A

– HIV still working inside but at a stable state, not rapid increase- mild symptoms 3-12 years

157
Q

What are some characteristics of AIDS?

A

CD4 below 200 AND one or more opportunistic infections OR tumor or cancer

158
Q

What is Seroconversion?

A

when there is enough antibodies to be detected – 3 weeks to 6 months

159
Q

What are the tests for HIV?

A

ELISA-enzyme linked immunosorbent assay- very sensitive for HIV antibodies
Western Blot- confirm HIV
OraQuick- false negatives an positives – 20 mins

160
Q

What 3 things can be tested for the progression of HIV?

A

Absolute CD4+ cell count
CD4+ lymphocyte percentage
Plasma viral load

161
Q

What type of symptoms does someone have during the primary phase of HIV?

A

flul like symptoms

162
Q

What are the symptoms of HIV?

A

Fatigue, low WBC, poor wound healing, night sweats, diarrhea, weightloss, N/V, confusion, vision changes, pain,

163
Q

What is the goal of HIV therapy?

A

Goals are to delay disease progression, minimize manifestations, prolong life, avoid drug resistence

164
Q

Who is at risk for TB?

A

Those who have had it in the past, immune suppressed, incarceration, long term care, homeless camps, malnourishment

165
Q

What are some clinical manifestations of TB?

A

Cough, fever, fatigue, weight loss, night sweats

166
Q

How do you diagnose TB?

A

Sputum culture for acid-fast bacillus (repeat for total 3 specimens to confirm)
CXR
TB skin test (Mantoux, PPD) – does not differentiate between current or past infection, or prior vaccine

167
Q

How do you treat TB?

A
  • Multi-drug therapy
  • Directly observed therapy (DOT)
  • Ensuring adherence to prevent treatment failure and drug resistance
168
Q

What happens during shock?

A

Lack of oxygen will lead to the production of lactate- sodium and water accumulation in cell, free radicals, Inflammatory release, metabolism

169
Q

What is Reperfusion?

A

being oxygenated after not having much can cause free radicals

170
Q

What are the four types of shock?

A

Hypovolemic
Distributive
Obstructive
Cardiogenic

171
Q

What causes Cardiogenic shock?

A 
cardiomyophaty
MI
venticular rupture
congenital heart defects
papillary muscle rupture
172
Q

What causes obstructive shock?

A

PE
Cardiac tempanade
dissecting aortic aneuryusm

173
Q

What causes hypovolemic shock?

A 
burns
overuse of diuretics
dehydration from diarrhea and vomiting
pancreatitis
acute hemorrhage
174
Q

What causes distributive shock?

A 
anaphylaxis
neurotrauma
spinal cord trauma
spinal anesthesia 
Sepsis
175
Q

What is septic shock?

A

*Systemic inflammatory response to infection
Immune mediators released
Clotting cascade, complement system, kinin system activated
Profound peripheral vasodilation occurs, and result in maldistribution of blood flow

176
Q

What is the process from SIRS to septic shock?

A

SIRS= inflammation
Sepsis- inflammation +infection
Severe sepsis- sepsis + organ damage
Septic shock- Severe sepsis + hypotension

177
Q

What is the NEWS assessment?

A

national early warning score- scores vitals and LOC

178
Q

What are the three stages of shock?

A

Compensated
Progressive
Refractory

179
Q

What happens during compensated stage?

A

Homeostasis, sympathetic nervous system

180
Q

What happens during progressive stage?

A
  • Therapeutic intervention is required, body can no longer compensate
  • Hypotension and tissue hypoxia
181
Q

What happens during refractory stage?

A

Therapy not even working

182
Q

What are clinical manifestations of shock?

A 
low blood pressure
low urine output
increased HR
increased RR
Cool clammy, bluish gray colored skin
slow cap refill
restlessness
thirst
decreased consciousness
183
Q

What are some complications of shock?

A

Acute respiratory distress syndrome (ARDS)
Disseminated intravascular coagulation (DIC)
Acute renal failure
Multiple organ dysfunction syndrome (MODS)

184
Q

What is nystatin used for?

A 
for candidiasis (only superficial)
Skin, mouth, esophagus, vagina
185
Q

What is important about the absorption of fluconasole?

A

90% absorbed, distributed to all body fluids (including CSF, eye, urine); more than 80% is excreted unchanged in the urine

186
Q

How does fluconazole work?

A

inhibits fungal cytochrome P450, enzyme responsible for fungal sterol synthesis (cell wall weakness)

187
Q

What is fluconazole used for?

A

treats mouth, throat and esophageal candidiasis and serious systemic infections (including UTIs, peritonitis, and PNA)

188
Q

How does azole work?

A

Primarily fungistatic rather than fungicidal

Work by inhibiting fungal cytochrome P450, decreasing ergosterol production

189
Q

What infection is a sign of immune suppression?

A

oropharangeal candidiasis

190
Q

when giving acyclovir IV, what should you worry about?

A

phlebitis- infuse slowly and hydrate during and for 2 hours after infusion

191
Q

How does Oseltamivir work?

A

Prevents viral particles from budding off from the cytoplasmic membrane of infected host cells = stops viral spread

192
Q

What are the adverse effects of Oseltamivir?

A

nausea, vomiting, rare but significant hypersensitivity reactions, rare neuropsychiatric effects (delirium in younger patients)

193
Q

What is the standard TB regimen?

A

Initial empiric adult regimen:
INH + RIF + PZA + EMB (or SM) x 2 months

*normally minimum of 6 months

194
Q

Whats the MOA of Isoniazid (INH)?

A

Exact MOA unknown but thought to inhibit DNA synthesis of proteins needed for cell wall.
Effects: Treat active and latent TB

195
Q

What are some adverse effects of Isoniazid?

A

Side effects can include peripheral neuropathy (tingling, numbness, burning, pain as a result of pyridoxine deficiency), potentially fatal hepatitis (usually age related/ETOH use), and hyperglycemia

196
Q

How should you give Isoniazid?

A

Daily with vit B6

197
Q

What should you monitor with Isoniazid?

A

S&S of liver impairment: loss of appetite, fatigue, malaise, jaundice, dark urine
Monitor periodic LFTs

198
Q

What is the MOA of Rifampin- RIF?

A

Inhibits DNA-dependent RNA polymerase activity in susceptible bacterial cells.

199
Q

What are the adverse effects of Rifampin?

A

Side effects include flu-like symptoms, N/V/D, anorexia, hepatitis, thrombocytopenia, ↑ risk renal failure, orange discoloration of urine/secretions and tears (stains contact lenses)
Monitor periodic LFTs

200
Q

What is the MOA of Pyrazinamide (PZA)?

A

Unknown; may be bacteriostatic or bactericidal against depending on the concentration of the drug attained at the site of infection.

201
Q

What are some of the adverse effects of Pyrazinamide (PZA)?

A

hepatoxicity, hyperuricemia (avoid in gout), GI distress, rash and arthralgias
Monitor periodic LFTs and BUN/creatinine

202
Q

What stages of TB does Pyrazinamide (PZA) treat?

A

active and latent TB

203
Q

What is the MOA of Ethambutol (EMB)?

A

Not completely understood, evidence suggests bacteriostatic activity by virtue of inhibition of enzymes needed for metabolism and protein synthesis

204
Q

What are the adverse effects of Ethambutol (EMB)?

A

GI distress and possibly optic neuritis
Monitor visual acuity and color testing monthly
If pregnant with active TB, can use EMB only after first trimester

205
Q

What needs to be tested during TB treatment?

A

LFTs, bilirubin, BUN/creatinine, CBC
PZA - baseline serum uric acid
EMB - document visual acuity

206
Q

What are two expert panels that make recommendations for HIV treatments?

A

International AIDS Society-USA Panel Recommendation (IAS-USA)
Department of Health and Human Services (DHHS)(2015)

207
Q

When should you start ART?

A

Symptomatic HIV infection or opportunistic infection
Asymptomatic infection with CD4 < 350 cells/mm3
CD4 = 200-350 cells/mm3
Pregnant women
HIV-associated nephropathy
Hepatitis B co-infection requiring treatment

208
Q

What T-cell count requires drug prophylaxis?

A

T-cell count <200 cells/mm3

209
Q

What does HIV therapy target?

A

Fusion/Entry Inhibitors
CCR5 Antagonists
Nucleoside reverse transcriptase inhibitors [NRTIs]
Nonnucleoside reverse transcriptase inhibitors [NNRTIs]
Integrase Inhibitors [INSTIs]
Protease Inhibitors [PIs]

210
Q

What is the goal of HIV therapy?

A

Goal → Viral load suppression (↓ plasma levels of HIV [HIV-1 RNA levels])
Stops the destruction of the immune response and allows repair
Reduces drug resistance
Goal → ↑ CD4 counts
Prevents opportunistic infections

211
Q

WHat type of drug therapy would someone with HIV be on?

A 
Combination therapy
2 drugs from nucleoside reverse transcriptase inhibitor (NRTI) class plus a 3rd drug from another class
212
Q

What is the MOA of Maraviroc?

A

prevents HIV from entering lymphocytes by binding to CCR5 on cell membranes

213
Q

What are the adverse effects of Maraviroc?

A

skin rash, cough, upper respiratory tract infections, dizziness, paresthesia, orthostatic hypotension, hepatotoxicty, pseudomembranous colitis

214
Q

If someone was taking maraviroc and had TB, what drug would you worry about giving because of drug interactions?

215
Q

What is the MOA for zidovudine ?

A

Prevents replication by providing faulty proteins for replication
inhibiting DNA synthesis/ viral replication

216
Q

What are the adverse effects of zidovudine?

A

Active metabolite is just as toxic to human DNA polymerase as it is for viral reverse transcriptase
Bone marrow toxicity/suppression (within first 4 -6 weeks), macrocytic anemia, neutropenia, GI intolerance, HA, insomnia, asthenia

217
Q

What is MOA of efavirenz?

A

inactivates reverse transcriptase

218
Q

Efavirenz is often used to help with what?

A

often used to prevent medication resistance

219
Q

What are the adverse effects of efavirenz?

A
  • rash, HA, flu-like sx, fatigue, hepatotoxicity, CNS symptoms (dizziness, drowsiness, insomnia/irritability)
  • vivid dreams/nightmares about 2 weeks
220
Q

What is the MOA of raltegravir?

A

inhibits integrase enzyme (catalyzes the process of putting HIV DNA into human DNA)

221
Q

What are the adverse effects of raltegravir?

A

HA, insomnia, skin rash,hepatotoxicity (jaundice, RUQ pain, nausea)

222
Q

What is the MOA of ritonavir?

A

Alter & inactivate the virus inhibiting enzyme needed for HIV replication

223
Q

What are the adverse effects of ritanovir?

A

bone loss/osteoporosis, hyperglycemia/diabetes, hypersensitivity (rash), N/V, elevated serum lipids, thrombocytopenia, leukopenia

224
Q

What are some results of ART toxicity?

A 
* normaly after 3 months
Abnormal lipid profiles
cholesterol and triglycerides
Fat distribution = lipodystrophy
Insulin resistance
Increased cardiac risk

Pharm/Patho (6 decks)

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