Summexam2 Flashcards
1
Q
Where does the hearts electrical activity start?
A
SA node through the chambers
2
Q
What does the p wave represent?
QR?
S?
A
atrial depolarization
ventricle depolarization
ventricle re-polarization
3
Q
What is CHD also called?
A
called ischemic heart disease and
coronary artery disease (CAD)
4
Q
What are the problems associated with CHD/CAD?
A
Angina MI Dysrhythmia Heart failure Cardiac death
5
Q
What is the defining characteristic of CAD/CHD?
A
Defining characteristic: ischemia (insufficient delivery of O2 blood) to myocardium
6
Q
What is the etiology of CHD/CAD?
A
Atherosclerosis**narrowing of the arterial lumen –> ischemia
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
8
Q
What are the 3 types of risk factors for CHD?
A
non-modifiable
Lipid
non-lipid
other
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
10
Q
What are the lipid risk factors of CHD?
A
High total lipids (total cholesterol, LDL, triglycerides)
Low HDL
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
12
Q
What are other risk factors for CHD?
A
Lipoprotein(a)
Homocysteine
C-reactive protein
Elevated fasting glucose levels
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
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
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
16
Q
What are the 4 stages of Atherosclerosis?
A
Normal artery
Fatty Streak
Partially occluded vessel
Totally occluded vessel
17
Q
How does atherosclerosis start?
A
injury/damage to the endothelium of the coronary artery
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
19
Q
What is insudation?
A
Once the endothelium has been damaged- endothelium is permeable and LDLs leak through into the vessel wall
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.
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.
22
Q
What causes the lipid core of plaque?
A
Excess lipids/debris accumulation from the damage, macrophages and inflammation
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
24
Q
`Why are smaller plaques more stable?
A
they have collagen and fibrin caps-they tend to settle into the vessel.
25
Coronary perfusion can be altered in what 3 ways?
Atherosclerotic plaques
Blood clot formation
Vasospasm of blood vessels
26
Cardiac workload depends on what factors?
HR
Preload
Afterload
Contractility
27
What is acute coronary syndrome?
blood clots formed or plaque ruptures
28
What is chronic coronary occlusion ?
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.)
29
What are the two branches of ischemia ?
Stable angina
| Acute Coronary Syndromes
30
What are the two branches of acute coronary syndromes?
Unstable angina
| MI
31
What are the two branches of MI?
NSTEMI
| STEMI
32
What two groups of people could have abnormal manifestations of angina pectoris?
Women and people with diabetes
33
What is the difference between unstable and stable angina?
Stable- they know every time they go up stairs they will get it
Unstable- they will randomly get it
34
What is an example of acute coronary syndrome? (ACS)
plaque ruptures with thrombus development
35
What are the manifestations of ACS?
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
36
What labs would you draw for ACS?
labs and serum to check for markers such as myoglobin, troponin, CKMB (creatine kinase)
37
If someone has ACS, what would you want to note on a EKG?
Elevation of ST segment
38
What biomarkers are released into the blood with myocardial ischemia?
myoglobin, CK, CK-MB, Troponin I
39
When drawing labs, what is the most important aspect to get accurate readings?
Take them as soon as possible, don't wait, levels could be inaccurate
40
What are three ways to treat ACS?
Decreasing myocardial oxygen demand
Increasing myocardial oxygen supply
Monitoring and managing complications
(medications, interventional radiology to open blood vessel or remove clot)
41
What is thrombolysis?
Enzymatic digestion of thrombus to open lumen
42
What is a Per-cutaneous transluminal coronary angioplasty? (PTCA)
Physical disruption of plaque to open lumen
| or stent
43
What is a coronary artery bypass grafting? (CABG)
surgical placement of new conduit to bypass occlusion
44
Why is nitroglycerine considered a prodrug?
It is converted into nitric oxide which then causes the vasodilation
45
What forms does nitroglycerine come in?
SL tabs, Spray, topical ointment, transdermal patch, intravenous
46
How does nitrogycerine work?
dilates veins & decrease venous return (preload) which decreases oxygen demand
47
What two forms of Nitro have longer effects?
ointment and patch
48
What is isosorbide used for?
oral, long acting. Back up for angina to help with vasodilation
** do not use for acute
49
What type of drug interactions would you worry about for someone on vasodilators?
other vasodilators- *viagra (sildenafil) Both increase cGMP
50
How does tolerance of nitrogylcerin happen?
depletion of sulfhydryl groups – can’t be converted
51
If someone is using a nitro patch, what education would you tell them?
Take it of at bedtime and apply new one in morning
52
What is the lifespan of a platelet?
8 days
53
Giving aspirin of heparin to someone who just has a stent placed is important why?
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
54
Clopidogrel targets what, in relation to platelet aggregation?
adenosine diphosphate (ADP)
55
Aspirin targets what aspect of platelet aggregation?
thromboxane A2
56
Blocking what would be the last resort to platelet aggregation?
GP 2b 3a
57
What does thromboxane A2 do?
Produced by activated platelets
| Stimulates activation of new platelets and platelet aggregation
58
Why is irreversible inhibition important to know about if someone comes in bleeding and they are on aspirin?
They will need to have platelets given back, no med to reverse the effects
59
What are the adverse effects of aspirin?
```
GI bleeding
Bleeding
Renal impairment
Tinnitus (associated with high levels)
Salicylate toxicity
Respiratory alkalosis
Metabolic acidosis
Renal failure
Altered mental status
```
60
What are some pediatric contraindications of aspirin?
associated with Reye's syndrome (with viral illness)
| encephalopathy and fatty liver degeneration
61
What are some reasons for taking aspirin?
```
Ischemic stroke
Transient ischemic attacks
Acute MI
Previous MI
Chronic stable angina
Unstable angina
```
62
What is important about clopidogrel metabolism?
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-
63
What are the adverse effects of clopidogrel?
Bleeding!!
| Thrombotic thrombocytopenia purpura (TTP) - rare
64
What is the biggest drug interaction of clopidogrel?
Omeprazole because inhibits 2C19 = clopidogrel wont work and they could still get platelet aggregation
65
What does niacin do?
Reduces LDL and TG and raises HDL
| It impacts the amount of adipose being filtered by liver and therefore decreases LDL
66
What is important about the initiation of niacin therapy?
Slow titration due to adverse effects
67
Why would aspirin be use while taking niacin?
because aspirin may help with the initial skin flushing and itching in first couple weeks of therapy
68
What are the adverse effects of niacin?
initial skin flushing and itching-3 weeks
Hepatoxicity: severe liver damage reported
Least likely with extended release product
Increased uric acid
Hyperglycemia
69
What are the outcomes of atrovastatin?
Reduction of LDL
Increase in HDL
Reduction of TG
70
What are the adverse effects of atrovastatin?
hepatotoxicity
| Myopathy/rhabdomyolysis
71
What are the clinical uses for alteplase (tPA)?
STEMI, ischemic stroke, pulmonary embolism, restore patency to central IV catheters
72
What does alteplase do?
tissue plasminogen activator
73
How is alteplase administered?
IV only
74
What are the side effects of phenylephrine?
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.
75
What does phenylephrine do to the heart?
vasoconstriction
76
What does dubutamine do to the heart?
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,
77
How does dopamine affect the heart?
inotropic effect on the heart muscle (causes more intense contractions) that, in turn, can raise blood pressure.
78
What two valves belong to the AV?
Tricuspid (R)
| Mitral (L)
79
What two valves belong to the semilunar
Pulmonary (R)
| Aortic (L)
80
At what point do symptoms of stenosis start?
50%
81
What is regurgitation?
valvular insufficiency- not working right, not shutting all the way so blood flow continues
*can happen fast if there is infection
82
What two valves are most effected by stenosis and regurgitation?
aortic and mitral
83
What are some secondary complications to aortic stenosis?
angina, ischemia, heart failure
| Syncopy, fatigue, hypotension, angina
84
What are the treatments for aortic stenosis?
Avoid Vasodilators; Digitalis, Diuretics, Nitroglycerin in inoperable; Surgery
85
What are the treatments for mitral stenosis?
Potential Treatment: Mild=diuretics; Anticoagulation if in atrial fibrillation; Digitalis, Beta blockers, Calcium Channel Blockers for rate control; Surgery
86
What are the treatments for Aortic Regurgitation?
Vasodilators
87
What are the treatments for mitral Regurgitation?
Acute: Vasodilators; chronic: No proven Therapy; surgery
88
What is the definition of heart failure?
Inability of heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs
89
What are the clinical manifestations of heart failure?
dyspnea, pulmonary rales, cardiomegaly, pulmonary edema, S3 heart sound, and tachycardia
90
What are the two categories of heart failure?
Systolic or diastolic
91
Systolic heart failure is seen by what manifestations?
not pumping right- reduced contractility- not adequate squeezing, common after and MI – low EF ( ejection fraction)
92
Diastolic heart failure is seen by what manifestations?
doesn’t fill right- often with coronary artery disease , not so much MI- ventricle is not compliant, edema, potentially normal ejection fraction
93
What is the difference between forward and backwards heart failure?
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
Right sided heart failure can be seem through what manifestations?
congestion in systemic, distended belly (ascites), enlargement of liver, spleen, JVD, fatigue, GI problems, edema
95
left sided heart failure can be seem through what manifestations?
Pulmonary congestion, respiratory symptoms, edema- pulmonary edema can be life threatening, restlessness, confusion, orthopenia, tachycardia, exertional dyspnea, fatigue, cyanosis
96
What are the three compensatory mechanisms?
myocyte growth
fluid retention
SNS activation
97
What happens as a result to SNS activation?
increased HR
| Increased contractility
98
What happens as a result to fulid retention?
Increase preload
99
What happens as a result to myocyte growth?
hypertrophy
100
What does FACES stand for?
```
Fatigue
Activity imitation
Congestion
Edema
Shortness of breath
```
101
What are the goals of treating Heart failure?
Improve cardiac output
Minimize congestive symptoms
Reducing preload- diuretics, modify fluid and sodium
102
What are the three types of cardiac dysrhythmias ?
Abnormal rates of sinus rhythm
Abnormal sites (ectopic) of impulse initiation
Disturbances in conduction pathways
103
What is Automaticity?
Spontaneous generation of an action potential
104
What is Triggered Activity?
Occurs when an impulse is generated during or just after repolarization
105
What is Reentry ?
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
What does atrial flutter appear as on a strip?
Sharp "teeth" before the p wave- no distinct p wave
107
What does atrial fibrillation appear as on a strip?
no distinct p wave- many hills
108
What are the theraputic uses of atropine?
Symptomatic bradycardia
Decreasing secretions
Mydriasis (pupil dilation)
109
What are some effects of atropine?
Tachycardia, constipation, drying (anticholinergic
110
What is adenosine used for?
for supraventricular tachycardia - Over 160bpm
| IV PUSH
111
What is unique about the half life of adenosine?
its VERY short
| about 1.5-10 seconds
112
What does adenosine do on the heart?
Decreases automaticity in the SA node & slows conduction through the AV node
Prolongs the PR interval
**rebooting- very uncomfortable for patient
113
What do class I anti-arrhythmic drugs do?
block Na+ channels
114
What do class II anti-arrhythmic drugs do?
beta-adrenoreceptor agonists
115
What do class III anti-arrhythmic drugs do?
prolonged action potential and prolonged refractory period
| K blockers
116
What do class IV anti-arrhythmic drugs do?
Ca+ channel antagonists
117
What does procainamide do?
sodium channel Slow impulse conductions in the atria, ventricles, and Hi-Purkinje system
Delays repolarization
118
What is procainamide used for?
SVT, VT, A flutter, Afib
119
Procainamide blocks what channel?
sodium
120
What are the adverse effects of procainamide?
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
What labs would you check with procainamide?
CBC WBC & platelets
122
How does lidocaine work?
slows cardiac conduction velocity via blockade
Decrease electrical conduction
Decrease automaticity
Increase rate of repolarization
123
What is lidocaine used for?
Short term use for ventricular dysrthythmias
124
What channel does lidocaine work on?
Sodium channel blocker
125
What are the adverse effects of lidocaine?
CNS: drowsiness, altered mental status, paresthesias, seizures, hypotension, drop in BP, CV collapse
126
Why is lidocaine not very effective orally?
it's metabolized by the liver and has a very high first pass effect
127
How does propafenone work?
slows cardiac conduction velocity via blockade
Decrease conduction velocisty in atria, ventricles, and Hi-Purkinje system
Delay ventricular repolarization
128
What is propafenone used for?
Used for SVT
129
What are the adverse effects of propafenone?
```
Bardycardia
Heart failure
Dizziness
weakness,
Hypotension
Bronchospasm
QRS prolongation
```
130
How does propranolol work?
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
What is propranolol used for?
afib, a flutter, paroxysmal SVT, HTN, angina, PVCs
132
What are some adverse effects of propranolol?
```
Bronchicoonstriction, wheezing, trouble breathing
Brinchioconstriction
Hypotension
Bizare dreams
blah feeling
```
133
Why can there be respiratory effects when taking propranolol?
acts on beta a and b- lungs and heart
134
How does Amiodarone work?
prolongs the action potential and refractory period due to K channel blockade
135
What is amiodarone used for?
Used for atrial and ventricular dysrhythmias
136
What is unique about the half-life of amiodarone?
Very LONG- 25 – 110 days
| aggressive loading doses to get pt up to steady state quicker
137
What are the adverse effects of amiodarone?
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
How does Verapamil work?
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
What is verapamil used for?
afib, a flutter, SVT, HTN, angina, Used for headache profylaxis
140
What are the adverse effects of verapamil?
```
Bradycardia
Hypotension
Heart failure
Constipation**
Peripheral edema
```
141
What is a unique drug interaction for verapamil?
grapefruit juice
142
What are the treatment plans for heart failure?
- Preload reduction: Reducing circulating blood volume
- Afterload reduction: Vasodilation
- Myocardial protection: Catecholamines & angiotensin 2 have damaging effect on myocardium
- Inotropic support
143
What are three drugs that inhibit the RAAS system?
lisinopril, losartan, spirinolactone
144
What are the advantages of beta blockers?
```
Improve LVEF
Increase exercise tolerance
Slow progression of HF
Reduce need for hospitalization
Prolong survival
```
145
What is the MOA of beta blockers?
protecting heart from excessive sympathetic stimulation and protecting against dysrhythmia
146
What are the adverse effects of metroprolol?
Fluid retention & worsening heart failure, fatigue, hypotension, bradycardia or heart block
147
What are the potential effects of digoxin?
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
What are the adverse effects of digoxin?
- 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
What is the hallmark of HIV and AIDS?
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
WHat is the core of the HIV virus called and what does it contain?
Core=nucleocapsid
- RNA strands
- Enzymes including reverse transcriptase and protease
151
How does HIV binding and inception work?
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
What is the HIV life cycle?
Attaches, moves in, integrates to infect and then programs cell to send retrovirus virion out to infect other cells
153
Where is a major site of HIV replication?
The GI system
154
What is the progression of HIV to AIDS?
```
HIV enters body
Seroconversion
Primary HIV infection
Latency period
Chronic symptomatic HIV infection
AIDS diagnosis
```
155
What happens in the primary HIV stage?
HIV count is very high- CD4 count has decreased at this point with decreased WBC, platelets, elevated ESR 1-4 weeks
156
What happened in the latency phase?
– HIV still working inside but at a stable state, not rapid increase- mild symptoms 3-12 years
157
What are some characteristics of AIDS?
CD4 below 200 AND one or more opportunistic infections OR tumor or cancer
158
What is Seroconversion?
when there is enough antibodies to be detected – 3 weeks to 6 months
159
What are the tests for HIV?
ELISA-enzyme linked immunosorbent assay- very sensitive for HIV antibodies
Western Blot- confirm HIV
OraQuick- false negatives an positives – 20 mins
160
What 3 things can be tested for the progression of HIV?
Absolute CD4+ cell count
CD4+ lymphocyte percentage
Plasma viral load
161
What type of symptoms does someone have during the primary phase of HIV?
flul like symptoms
162
What are the symptoms of HIV?
Fatigue, low WBC, poor wound healing, night sweats, diarrhea, weightloss, N/V, confusion, vision changes, pain,
163
What is the goal of HIV therapy?
Goals are to delay disease progression, minimize manifestations, prolong life, avoid drug resistence
164
Who is at risk for TB?
Those who have had it in the past, immune suppressed, incarceration, long term care, homeless camps, malnourishment
165
What are some clinical manifestations of TB?
Cough, fever, fatigue, weight loss, night sweats
166
How do you diagnose TB?
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
How do you treat TB?
- Multi-drug therapy
- Directly observed therapy (DOT)
- Ensuring adherence to prevent treatment failure and drug resistance
168
What happens during shock?
Lack of oxygen will lead to the production of lactate- sodium and water accumulation in cell, free radicals, Inflammatory release, metabolism
169
What is Reperfusion?
being oxygenated after not having much can cause free radicals
170
What are the four types of shock?
Hypovolemic
Distributive
Obstructive
Cardiogenic
171
What causes Cardiogenic shock?
```
cardiomyophaty
MI
venticular rupture
congenital heart defects
papillary muscle rupture
```
172
What causes obstructive shock?
PE
Cardiac tempanade
dissecting aortic aneuryusm
173
What causes hypovolemic shock?
```
burns
overuse of diuretics
dehydration from diarrhea and vomiting
pancreatitis
acute hemorrhage
```
174
What causes distributive shock?
```
anaphylaxis
neurotrauma
spinal cord trauma
spinal anesthesia
Sepsis
```
175
What is septic shock?
*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
What is the process from SIRS to septic shock?
SIRS= inflammation
Sepsis- inflammation +infection
Severe sepsis- sepsis + organ damage
Septic shock- Severe sepsis + hypotension
177
What is the NEWS assessment?
national early warning score- scores vitals and LOC
178
What are the three stages of shock?
Compensated
Progressive
Refractory
179
What happens during compensated stage?
Homeostasis, sympathetic nervous system
180
What happens during progressive stage?
- Therapeutic intervention is required, body can no longer compensate
- Hypotension and tissue hypoxia
181
What happens during refractory stage?
Therapy not even working
182
What are clinical manifestations of shock?
```
low blood pressure
low urine output
increased HR
increased RR
Cool clammy, bluish gray colored skin
slow cap refill
restlessness
thirst
decreased consciousness
```
183
What are some complications of shock?
Acute respiratory distress syndrome (ARDS)
Disseminated intravascular coagulation (DIC)
Acute renal failure
Multiple organ dysfunction syndrome (MODS)
184
What is nystatin used for?
```
for candidiasis (only superficial)
Skin, mouth, esophagus, vagina
```
185
What is important about the absorption of fluconasole?
90% absorbed, distributed to all body fluids (including CSF, eye, urine); more than 80% is excreted unchanged in the urine
186
How does fluconazole work?
inhibits fungal cytochrome P450, enzyme responsible for fungal sterol synthesis (cell wall weakness)
187
What is fluconazole used for?
treats mouth, throat and esophageal candidiasis and serious systemic infections (including UTIs, peritonitis, and PNA)
188
How does azole work?
Primarily fungistatic rather than fungicidal
| Work by inhibiting fungal cytochrome P450, decreasing ergosterol production
189
What infection is a sign of immune suppression?
oropharangeal candidiasis
190
when giving acyclovir IV, what should you worry about?
phlebitis- infuse slowly and hydrate during and for 2 hours after infusion
191
How does Oseltamivir work?
Prevents viral particles from budding off from the cytoplasmic membrane of infected host cells = stops viral spread
192
What are the adverse effects of Oseltamivir?
nausea, vomiting, rare but significant hypersensitivity reactions, rare neuropsychiatric effects (delirium in younger patients)
193
What is the standard TB regimen?
Initial empiric adult regimen:
INH + RIF + PZA + EMB (or SM) x 2 months
*normally minimum of 6 months
194
Whats the MOA of Isoniazid (INH)?
Exact MOA unknown but thought to inhibit DNA synthesis of proteins needed for cell wall.
Effects: Treat active and latent TB
195
What are some adverse effects of Isoniazid?
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
How should you give Isoniazid?
Daily with vit B6
197
What should you monitor with Isoniazid?
S&S of liver impairment: loss of appetite, fatigue, malaise, jaundice, dark urine
Monitor periodic LFTs
198
What is the MOA of Rifampin- RIF?
Inhibits DNA-dependent RNA polymerase activity in susceptible bacterial cells.
199
What are the adverse effects of Rifampin?
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
What is the MOA of Pyrazinamide (PZA)?
Unknown; may be bacteriostatic or bactericidal against depending on the concentration of the drug attained at the site of infection.
201
What are some of the adverse effects of Pyrazinamide (PZA)?
hepatoxicity, hyperuricemia (avoid in gout), GI distress, rash and arthralgias
Monitor periodic LFTs and BUN/creatinine
202
What stages of TB does Pyrazinamide (PZA) treat?
active and latent TB
203
What is the MOA of Ethambutol (EMB)?
Not completely understood, evidence suggests bacteriostatic activity by virtue of inhibition of enzymes needed for metabolism and protein synthesis
204
What are the adverse effects of Ethambutol (EMB)?
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
What needs to be tested during TB treatment?
LFTs, bilirubin, BUN/creatinine, CBC
PZA - baseline serum uric acid
EMB - document visual acuity
206
What are two expert panels that make recommendations for HIV treatments?
International AIDS Society-USA Panel Recommendation (IAS-USA)
Department of Health and Human Services (DHHS)(2015)
207
When should you start ART?
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
What T-cell count requires drug prophylaxis?
T-cell count <200 cells/mm3
209
What does HIV therapy target?
Fusion/Entry Inhibitors
CCR5 Antagonists
Nucleoside reverse transcriptase inhibitors [NRTIs]
Nonnucleoside reverse transcriptase inhibitors [NNRTIs]
Integrase Inhibitors [INSTIs]
Protease Inhibitors [PIs]
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What is the goal of HIV therapy?
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
WHat type of drug therapy would someone with HIV be on?
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Combination therapy
2 drugs from nucleoside reverse transcriptase inhibitor (NRTI) class plus a 3rd drug from another class
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212
What is the MOA of Maraviroc?
prevents HIV from entering lymphocytes by binding to CCR5 on cell membranes
213
What are the adverse effects of Maraviroc?
skin rash, cough, upper respiratory tract infections, dizziness, paresthesia, orthostatic hypotension, hepatotoxicty, pseudomembranous colitis
214
If someone was taking maraviroc and had TB, what drug would you worry about giving because of drug interactions?
Rifampin
215
What is the MOA for zidovudine ?
Prevents replication by providing faulty proteins for replication
inhibiting DNA synthesis/ viral replication
216
What are the adverse effects of zidovudine?
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
What is MOA of efavirenz?
inactivates reverse transcriptase
218
Efavirenz is often used to help with what?
often used to prevent medication resistance
219
What are the adverse effects of efavirenz?
- rash, HA, flu-like sx, fatigue, hepatotoxicity, CNS symptoms (dizziness, drowsiness, insomnia/irritability)
- vivid dreams/nightmares about 2 weeks
220
What is the MOA of raltegravir?
inhibits integrase enzyme (catalyzes the process of putting HIV DNA into human DNA)
221
What are the adverse effects of raltegravir?
HA, insomnia, skin rash,hepatotoxicity (jaundice, RUQ pain, nausea)
222
What is the MOA of ritonavir?
Alter & inactivate the virus inhibiting enzyme needed for HIV replication
223
What are the adverse effects of ritanovir?
bone loss/osteoporosis, hyperglycemia/diabetes, hypersensitivity (rash), N/V, elevated serum lipids, thrombocytopenia, leukopenia
224
What are some results of ART toxicity?
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* normaly after 3 months
Abnormal lipid profiles
cholesterol and triglycerides
Fat distribution = lipodystrophy
Insulin resistance
Increased cardiac risk
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