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NU 560 - Adv. Pharmacotherapeutics > Unit 3 Exam > Flashcards

Unit 3 Exam Flashcards

1
Q

Arterial Vasodilators

A

CCBs

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2
Q

Venous Vasodilators

A

Diuretics

Long term use can also affect arterial

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3
Q

Arteriovenous Vasodilators

A

ACE/ARBs
BBs
Alpha agonists/blockers
Nitrates

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4
Q

Anti-HTN therapy for DM only

A

Goal SBP <140/90

NB = Thiazide, ACE/ARB, or CCB alone
B = Thiazide or CCB

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5
Q

Anti-HTN therapy for CKD w/ DM

A

Goal SBP <140/90

All = ACE/ARB

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6
Q

Anti-HTN therapy for CKD only

A

Goal SBP <130/80

Albuminuria >300 mg/dl = ACE
Stage 1-2 Albuminuria = ACE/ARB

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7
Q

Side Effects of Statins

A

Muscle pain, myopathy, weakness, fatigue, headache, GI distress, increased LFTs.

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8
Q

Adverse Reactions of Statins

A

Rhabdomyolysis or AKI

CKMB to r/o rhabdo
Reduce or dc med
Possibly reversible

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9
Q

Considerations with Statins

A

Pregnancy Class X - no breastfeeding

Very strong CYP450 inducer - multiple drug interactions.

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10
Q

High Dose Statin Indications (4 groups)

A
  1. <75 yo w/ ASCVD
  2. LDL >190
  3. 45-75 yo, DM, no ASCVD, LDL 70-189
  4. 45-75 yo, no DM or ASCVD, LDL 70-189, Calc risk >7.5% next 10 year serious CV/ASCVD event.
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11
Q

Monitoring Statin Therapy

A

Baseline lipid panel + LFTs

Medication history d/t medication interactions.

Estimated risk calculator

Avoid grapefruit juice

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12
Q

Bile Acid Resins MOA

A

Bind with bile acids and cholesterol in the intestines and excrete them.

Liver increased LDL receptor sites and more LDL is taken up.

Ex. Welchol (Colesevelam), Questran (Cholestyramine)

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13
Q

Fibric Acid Derivatives MOA

A

Reduce triglycerides by enzymatic destruction.

Ex. Gemfibrizol (Lopid), Fenofibrate (Tricor)

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14
Q

Cholesterol Absorption Inhibitors MOA

A

Decreases absorption of cholesterol in the small intestines.

Decreased stored cholesterol in the liver.

Ex. Ezetimbide (Zetia)

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15
Q

Omega 3 Fatty Acids MOA

A

Lowers triglycerides, increased HDLs (must take at high doses, 3g/day).

Ex. Lovazza

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16
Q

Niacin MOA

A

B vitamin that increased HDLs and lowers LDLs and triglycerides.

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17
Q

Acute Treatment for Angina (not MI)

A

Short acting nitrate

ASA (if not contraindicated)

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18
Q

Chronic Prevention of Angina

A

First line = Beta blockers/CCB

Second line = Combo therapy (Add another class - i.e. beta blocker + long acting nitrate)

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19
Q

Beta Blockers MOA

A

Block beta-1 and/or beta-2 receptors centrally and peripherally, leading to decreased CO and sympathetic outflow.

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20
Q

Beta Blocker Contraindications

A

Bradycarida
2nd/3rd degree HB
Decompensated HF
Severe bronchospastic disease
Caution in asthma + COPD

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21
Q

Beta Blocker Side Effects

A

Fatigue
Drowsiness
Bronchospasm
N/V
Bradycardia
AV conduction abnormalities
CHF
Can mask hypoglycemia symtpoms

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22
Q

CCB MOA

A

Inhibit the movement of calcium ions across a cell membrane leading to cardiac muscle relaxation and vasodilation

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23
Q

Non-Dihydropyridines vs Dihydropyridines MOA

A

ND = Decreased HR and slows cardiac conduction at the AV node (diltiazem)

D = Potent vasodilators (“-dipines”)

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24
Q

CCB Contraindications

A

Heart failure
Can worsen WPW
Check hepatic function before therapy

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25
Q

CCB Side Effects

A

Peripheral edema (d/t vasodilation)

Constipation (effects smooth muscle in gut)

May worsen GERD (decreased sphincter contraction)

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26
Q

ACE-I MOA

A

Prevents the conversion of angiotensin I to angiotensin II

Inhibits the degradation of bradykinin and increase the synthesis of vasodilating prostaglandins.

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27
Q

ACE-I Contraindications

A

Bilateral renal artery stenosis (acute renal failure)

Pregnancy (avoid in childbearing age)

Hx of angioedema

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28
Q

ACE-I Side Effects

A

Dry cough
Hyperkalemia
Angioedema
Laryngeal edema

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29
Q

ARB MOA

A

Blocks the binding of angiotensin II to the angiotensin II receptor, which blocks vasoconstriction and aldosterone secreting effects.

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30
Q

ARB Contraindications

A

Renal artery stenosis

Pregnancy

Caution in renal/hepatic impairment

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31
Q

ARB Side Effects

A

URI
Viral infection
Sinusitis
Pharyngitis
Rhinitis
Diarrhea

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32
Q

Loop Diuretics MOA

A

Inhibit the reabsorption of Na and Cl in the proximal and distal tubules and the loop of Henle.

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33
Q

Diuretic Contraindications

A

No K sparing diuretics in pts with renal impairment (Cr Cl <25-30)

Patients with gout

High risk of falls

Dehydration

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34
Q

Diuretic Side Effects

A

Electrolyte imbalances

Glucose intolerance

Hyperuricemia (d/t decreased Ca + uric acid excretion)

Dehydration/Hypotension/Falls

Muscle cramps, paresthesias, impotence.

Drug interactions

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35
Q

Thiazide Diuretics MOA

A

Inhibits Na, K, Cl reabsorption in the distal tubule of the nephron

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36
Q

K-Sparing Diuretics MOA

A

Alter Na reabsorption in the distal tubule further than where K is reabsorbed.

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37
Q

K-Sparing Contraindications (4)

A

Hyperkalemia

Addison’s disease (Decreased aldosterone)

Pts taking ACE-I/ARBs

Pts taking eplerenone (Tx HTN/HF; blocks aldosterone)

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38
Q

K-Sparing Side Effects (4)

A

Gynecomastia

Hirsutism

Gout symptoms

Menstrual irregularities

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39
Q

Alpha-2 Receptor Agonists MOA

A

Inhibits cardiac acceleration and vasocontriction centers in the brain

Stimulates A2 → decrease peripheral outflow of NE → vasodilation, decreased PVR, HR and BP.

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40
Q

A2RA Side Effects

A

Sedation

Xerostomia (dry mouth)

Hypotension

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41
Q

A2RA Contraindications

A

Dry eye syndrome

Antipsychotic meds (TCAs/MAOIs)

Beta Blockers

ETOH, benzos, antihistamines

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42
Q

A2RA Cautions

A

Renal impairment

Recent MI

Severe CAD

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43
Q

Class 1 - Antiarrhythmics

A

Sodium channel blockers:

Procainamide
Lidocaine
Quinidine

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44
Q

Causes of procainamide toxicity?

A

Renal impairment → accumulating levels

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45
Q

Causes of lidocaine toxicity?

A

Reduced hepatic blood flow d/t HFrEF → delays metabolism

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46
Q

Class II - Antiarrhythmics

A

Betablockers:

Esmolol
Metoprolol
Atenolol

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47
Q

Class III - Antiarrhythmics

A

Potassium channel blockers:

Amiodarone
Sotalol
Defetilide

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48
Q

Medications to avoid with amio and drondarone?

A

Azoles
Cyclosporines
Clarithromycin
Ritonavir
Rifampin
Phenobarbital
Phenytoin
Carbamazepine
St. John’s Wort

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49
Q

Dronedarone Interactions

A

Increases serum digoxin + dabigatran

Caution with statins - risk of myopathy

Can cause pulm toxicity

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50
Q

Causes of sotalol toxicity?

A

Poor renal function

Concurrent diuretic use increases risk for Torsades

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51
Q

What drugs causes dofetilide toxicity?

A

Cimetidine
Dolutegravir
Ketoconazole
HCTZ
Megestrol
Prochlorperazine
Bactrim
Verapamil

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52
Q

Causes of dofetilide toxicity?

A

Poor renal function

Avoid other meds that prolong QTc.

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53
Q

Class IV - Antiarrhythmics

A

CCB:

Diltiazem
Verapamil

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54
Q

Causes of digoxin toxicity?

A

Poor renal function → excreted by the kidneys

Electrolyte disturbances (hypokalemia → dig toxicity)

Drug interactions (amio, verapamil)

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55
Q

Digoxin MOA

A

Affects the ANS by stimulating the parasympathetic division, increasing vagal tone.

Slows conduction through the AV node and prolongs the AV nodal refractory period.

Positive inotropic effects → HFrEF

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56
Q

Amiodarone MOA

A

Reduces automaticity and conduction velocity and prolongs refractoriness.

No inotropic effects.

Potassium channel blocker.

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57
Q

Amiodarone Med Interactions

A

Increases digoxin concentration and potentiates warfarin (increases INR).

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58
Q

Indication for Digoxin

A

Slowing Vent. rate in AF + AFL

HFrEF w/ AF + AFL due to positive inotropic effects

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59
Q

Indications for Amio

A

Management of acute VT/VF and AF

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60
Q

Heart Failure Treatment Order (4)

A

1st line = ACE/ARB + BB

2nd line = Diuretic

3rd line = Digoxin

4th line = ARB, aldosterone antagonist, long-acting nitrates (HYD/ISDN)

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61
Q

ACE-I/ARBs use in Heart Failure

A

Reduce afterload

Prevent cardiac remodeling

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62
Q

BB use in Heart Failure

A

Reduced mortality
Decrease O2 demand and workload

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63
Q

Diuretic use in Heart Failure

A

Reduce preload

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64
Q

Nitrate use in Heart Failure

A

Relax coronary + systemic vasculature to impact O2 supply and demand

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65
Q

Medication not appropriate in HF

A

CCBs

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66
Q

Acute MI Treatment

A
  1. ASA
  2. Nitrates (SL initial, then IV if needed).
  3. O2 (if SpO2 <90% or dyspneic)
  4. Morphine (if pain persists despite nitro).
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67
Q

Afib/Aflutter Treatment

A
  1. Cardio version if unstable
  2. Goal = ventricular rate control (rate control > rhythm control)
68
Q

Afib/Aflutter Treatment for Normal LV

A

Dilt
Verapamil
Beta-blocker

(All IV)

Can use amio if refractory to other meds.

69
Q

Afib/Aflutter Treatment with HFrEF

A

IV beta blocker
IV digoxin

70
Q

Indications for EPO

A

Treats anemia in…
… ESRD
… Zidovudine administration in HIV
… Chemotherapy

Give if hgb <10 to avoid transfusion

71
Q

Administration of EPO

A

SQ injection 3x per week

Stop if >12 hgb

72
Q

EPO Education

A

Take multivitamin + iron supplement for EPO to work

73
Q

Contraindications for EPO

A

Uncontrolled HTN

Sensitivity to mammalian products/albumin

74
Q

Side Effects of EPO (6)

A

HTN
HA
Seizures
Nausea
Edema
Fatigue

75
Q

Monitoring Labs/VS for EPO (10)

A

H+H
Ferritin
Transferrin
B12
Folate
BP
Clotting times
Plts
BUN/Cr

76
Q

Indications for Antiplatelet Therapy (4)

A
  1. Ischemic stroke prevention/treatment
  2. Additional AC for Mech Valves
  3. Post-ACS to prevent CV death, MI, and stroke.
  4. Prevent stent thrombosis s/p PCI
77
Q

Antiplatelet Agents

A

ASA

P2Y12 Inhibitors: Plavix, Effient, Brilinta

78
Q

Indications of ASA

A

Post ACS
Prevent thrombosis
Add on for AC (dual-platelet therapy)

79
Q

Length of platelet dysfunction with ASA

A

7-10 days after dc

d/t lifespan of the platelets exposed to irreversible inhibition of COX

80
Q

Contraindications for Antiplatelet Therapy (3)

A

Active GI bleed
ICH
PUD

81
Q

How long before surgery should plavix be dc’d?

A

5-7 days

Bleeding time and platelet aggregation returns to baseline

82
Q

Side Effects of ASA (3)

A

GI upset (nausea, heartburn, epigastric discomfort).

Bleeding

May potentiate PUD

83
Q

Side Effects of Plavix (3)

A

Diarrhea
Brusing
Bleeding

84
Q

Initiation of Anticoagulation

A
  1. Warfarin + injectable AC
  2. D/c LMWH when INR is therapeutic
  3. No bridging with DOACs (onset 2-4 hours after admin).
85
Q

Indications of Anticoagulation (4)

A
  1. Prevention of ischemic stroke
  2. Afib or mech valve
  3. Prevention of extension of existing thrombus (DVT or PE).
  4. Prevent DVT in at-risk patients (post-op).
86
Q

Contraindications for Anticoagulation (9)

A

Active bleed
Recent ICH
Intracranial mass with high risk of bleeding
End-stage liver disease
Severe thrombocytopenia
Recent trauma/trauma surgery
Immediate post op ocular or CNS surgery
Spinal catheters
Aneurysms

87
Q

Considerations with Anticoagulation

A

Baseline PT, INR, aPTT, UA, CBC, LFT, pregnancy test.

R/o bleeds

Med rec: OTC or dietary supplements

For LMWH or DOAC: body weight, serum creatinine, estimation of renal function, creatinine clearance.

For UFH: body weight

88
Q

Education for Anticoagulation (2)

A
  1. Diet (Vit K can make warfarin sub-therapeutic)
  2. Avoid contact sports and intense exercise that could increase bleeding risk.
89
Q

Examples of DOACs

A

Direct thrombin inhibitors = Dabigatran (Pradaxa)

Factor Xa inhibitors = Savaysa, Eliquis, Xarelto (SEX)

90
Q

Drugs for VTE (3)

A

Lovenox
Warfarin
DOACs

91
Q

Anticoagulant Drugs for Afib

A

DOACs (over warfarin, except for prosthetic valve).

Dabigatran (Pradaxa).

Xarelto or Eliquis (ESRD).

Recommended for CHADS score >2 (men) >3 (women).

92
Q

AC Drugs for Prosthetic Heart Valves

A

Warfarin (some cases dual-antiplatelet therapy = +ASA)

93
Q

AC Drugs for TAVR

A

Dual antiplatelet therapy (DAPT)

ASA + Plavix for 3-6 months → ASA for life

94
Q

AC Drugs for Ischemic Stroke

A

ASA
ASA/Dipyridamole
Plavix

95
Q

AC Drugs for MI (2)

A

S/p MI → ASA, Plavix, Prasugrel (Effient) and Ticagrelor (Brilinta)

ASA + P2Y12 inhibitor

96
Q

Anticoagulant Bridge Therapy

A

Warfarin + injectable AC

D/c LMWH when INR in therapeutic range (~2-3)

No bridging with DOACs (onset 2-4 hours)

97
Q

Recombinant EPO MOA

A

Stimulates production of RBCs from the erythroid tissue in the bone marrow.

Serum half-life 8.5 hours.

98
Q

EPO Indications

A

Anemia d/t chronic renal failure

Zidovudine administration in HIV

Chemo administration

99
Q

EPO Administration/Dosing

A

Starting dose is 50-100 units/kg SQ x3 per week

2-6 weeks required to evaluate effectiveness

100
Q

Education Regarding Iron Supplementation

A

Iron rich foods - red meat, fish, poultry, whole-grains or iron-fortified cereals, breads and pastas.

Take supplements on empty stomach with OJ d/t need for acidic environment to absorb it.

Therapy lasts 3-6 months

Can cause constipation.

101
Q

Examples of DOACs

A

Dabigatran (Pradaxa) - Direct thrombin inhibitor

Rivaroxaban (Xarelto)
Apixaban (Eliquis)
Edoxaban (Sayvasa)

Binds to Factor Xa = “-xaban”

102
Q

When to prescribe DOACs?

A

VTE or Afib → stroke prevention (CHADS >2 M; >3 F)

NOT for MI, ischemic stroke, or prothetic heart valves (these require warfarin, P2Y12, ASA)

103
Q

Anemias of Increased Destruction (2)

A

Acute post-hemorrhagic anemia/Chronic blood loss

Sickle Cell Anemia

104
Q

Anemias of Diminished Production (6)

A

Iron deficiency

Chronic renal failure

Chronic disease

Thalassemia

Vitamin B12 Deficiency

Folate Deficiency

105
Q

Acute post-hemorrhagic anemia/Chronic blood loss

A

Massive hemorrhage from spontaneous or traumatic rupture or incision of a large blood vessel.

Initial H/H may be high due to vasoconstriction

106
Q

Sickle Cell Anemia

A

Autosomal recessive disorder where abnormal hemoglobin leads to chronic hemolytic anemia

Hgb S

Sickle cell crisis: occurs due to hypoxia, dehydration or acidosis.

107
Q

Sickle Cell Anemia Population

A

African-american

108
Q

Iron Deficiency Anemia

A

Iron is needed for the creation of heme groups.

Inadequate intake - VEGANS
Inadequate absorption - celiac disease
Post surgical - gastrectomy or gastric bypass
Foods/medications - reduce absorption
Increased iron demands - menstrual blood loss, pregnancy, lactation

109
Q

Iron Deficiency Anemia Population

A

Vegetarians
Malabsorption
Women (menstrual loss, pregnancy, lactation).

110
Q

Chronic Renal Failure Anemia

A

Chronic renal failure leads to reduced EPO production by the kidneys.

111
Q

Anemia of Chronic Disease

A

Hypo-proliferative anemia that is associated with infection, organ failure, trauma, inflammation, and neoplasia.

Characterized by reduced concentrations of serum iron, transferrin, and TIBC, normal or raise ferritin levels and high erythrocyte sedimentation rate.

112
Q

Thalassemia

A

Hereditary disorder of hgb synthesis - hypo-proliferative anemia

Decreased production of alpha- or beta-globins or a structurally abnormal globin change.

113
Q

Types of Thalassemia

A

Alpha-Thalassemia Trait = Mutation in 2-4 genes

Hemoglobin-H = Mutation of 3 of 4 alpha genes → excess beta genes form tetramers.

Beta-Thalassemia Minor = Mutation in 1 of 2 beta genes. No treatment needed.

Beta-Thalassemia Major = Mutation in both beta genes → Hgb F → blood transfusions for LIFE

114
Q

Vitamin B12 Anemia (Pernicious Anemia)

A

Disorder of impaired DNA synthesis → macrocytic anemia

Causes lack of intrinsic factor, inadequate intake, decreased absorption, and inadequate utilization of Vit B12.

If not malabsorption, may need dietary supplementation.

115
Q

Vitamin B12/Pernicious Anemia Population

A

Inadequate intake / malnourished
Malabsorption
Lack of intrinsic factor

116
Q

Folate Deficiency Anemia

A

Development of large functionally immature erythrocytes know as megablasts.

Caused by inadequate intake, absorption or utilization, and increased requirement (pregnancy/lactation) or excretion (dialysis).

117
Q

Folate Deficiency Anemia Population

A

Women (pregnancy, lactation, infancy)
Malignancy
Dialysis
Phenytoin/phenobarbital use

118
Q

Warfarin Reversal

A

Vitamin K PO/IV
FFP (not as quick or affective)

119
Q

Heparin Reversal

A

IV protamine sulfate

May also be used for LMWH and Fondaparinux but no clear evidence of effectiveness.

120
Q

Dabigatran (Pradaxa) Reversal

A

Idarucizumab (monoclonal antibody)

121
Q

DOACs Reversal

A

Andexanet Alpha - modified factor Xa decoy protein that binds to factor Xa with higher affinity than factor Xa inhibitors.

122
Q

Antiplatelet (ASA/P2Y12) Reversal

A

Platelet transfusion - no reversal agent

123
Q

Warfarin and Pregnancy

A

CONTRAINDICATED

124
Q

DOACs and Pregnancy

A

No data

125
Q

UFH/LMWH and Pregnancy

A

SAFE - does not cross placenta

126
Q

ASA and Pregnancy

A

Prevents preeclampsia

127
Q

Clopidogrel (Plavix) and Pregnancy

A

Okay if needed

128
Q

Process of Antimicrobial Selection

A

Identify the source and site of infection → physical exam, underlying medical conditions, where pathogen was acquired?

Identify the causative pathogen → Gold standard = Grow causative organism in culture and perform abx susceptibility.

129
Q

Mechanisms of Resistance (6)

A

Bacterial enzyme production (i.e. beta lactamase)

Alterations of bacterial wall membranes (i.e. lost of porins)

Activation of efflux pumps (expels antibiotics)

Alterations of antibiotic target site of action (ribosomal binding site)

Alteration of target enzymes

Over production of target enzymes leading to resistance

130
Q

3 ways antibiotics work on the bacterial cell?

A
  1. Interfere with CELL WALL synthesis
  2. Interfere with NUCLEIC ACID synthesis
  3. Interfere with PROTEIN synthesis
131
Q

Antibiotics that interfere with cell wall synthesis (BVBPD)

A

Beta-lactams (PCCCM)

Vancomycin

Bacitracin

Polymyxins

Daptomycin

132
Q

Antibiotics that interfere with nucleic acid synthesis (STQRSA)

A

Sulfonamides
Trimethoprim
Quinolones
Rifampin
Streptovaricins
Actinomycin

133
Q

Antibiotics that interfere with protein synthesis (CLMCSTA)

A

Clindamycin
Linezolid
Macrolides
Chloramphenicol
Streptogramins
Tetracyclines
Aminoglycosides

134
Q

Glycopeptide Adverse Events

A

Fever, chills, phlebitis

RED-MAN syndrome → histamine-mediated phenomenon affiliated with the rate of infusion

Ex. Vancomycin

135
Q

Cephalosporin Pharmacokinetics (i.e. “Cef-/Ceph-“) ADE

A

Absorption → Well absorbed from the GI tract, some are still parenteral

Distribution → Penetrate well into tissues and body fluids. Achieve high concentrations in the urinary tract. 3rd/4th gens penetrate CSF.

Elimination → Most excreted by kidneys (Ceftriaxone → liver).

136
Q

Fluroquinolone Pharmacokinetics (i.e. “-floxacin”) ADE

A

Absorption → Well absorbed from GI tract, so highly bioavailable. Administered both enterally and parenterally.

Distribution → Distributes well into most tissues and body fluids, but NOT CNS.

Elimination → Most excreted by kidneys

137
Q

Beta-Lactam Pharmacokinetics (i.e. Penicillins, Cephalosporins, Carbapenems, Monobactams) ADE

A

Distribution → Diffuse into most body tissues, with exception of the brain and CSF.

Elimination → Glomerular filtration (need to check renal function)

138
Q

MRSA Treatment

A

Vancomycin - BEST

Gemifloxacin/moxifloxacin have poor to moderate coverage

Tetracyclines have poor to good coverage, minocycline has the best coverage.

Bactrim has good coverage

Others → tigecycline, linezolid, tedizolid, daptomycin, and quinipristin-dalfopristin

139
Q

Common Side Effect/Diagnosis resulting from Antibiotic Treatment

A

C. Diff

140
Q

C. Diff Treatment

A

PO Vancomycin → does not absorb well, stays in gut

Flagyl is no longer first-line treatment, only used if patient cannot tolerate PO vanc.

141
Q

Pencillin Side Effects + Half life

A

SE = Hypersensitivity

1/2 = 30-90mins

142
Q

Beta-Lactam/Beta-Lactamase Inhibitors Side Effects + Half life

A

SE = Hypersensitivity reactions

1/2 = 1 hour

143
Q

Cephalosporin Side Effects + Half life

A

SE = Safe

1/2 = 1-2 hours

144
Q

Monobactams Side Effects + Half life

A

SE = Safer than aminoglycosides

1/2 = 1.5-2 hours

145
Q

Carbapenems Side Effects + Half life

A

SE = Neurotoxicity (seizure activity)

1/2 = 1 hour

146
Q

FluoroQuinolones Side Effects + Half life

A

SE = QTC prolongation, GI upset

1/2 = 6-12 hours

147
Q

Macrolides Side Effects + Half life

A

SE = GI side effects (erythromycin)

1/2:
Erythro - 2 hours
Clarithro - 4-5 hours
Azithro - 50-60 hours

148
Q

Aminoglycosides Side Effects + Half life

A

SE = Nephro/ototoxicity

1/2 = 1-3 hours

149
Q

Tetracyclines Side Effects + Half life

A

SE = Anorexia, N/V, epigastric distress. Hepatotoxicity if given w/ other hepatotoxic agents.

1/2:
Short acting = 8 hours
Long acting = 16-18 hours

150
Q

Sulfonamides Side Effects + Half life

A

SE = Rash, fever, GI side effects

1/2 = hours to days

151
Q

Glycopeptides Side Effects + Half life

A

SE = Fever, chills, phlebitis, red man syndrome (r/t infusion rate)

1/2 = vanc 5-11 hours

152
Q

Clindamycin Side Effects + Half life

A

SE = C. Diff

1/2 = 3 hours

153
Q

Metronidazole Side Effects + Half life

A

SE = Safe/well tolerate

1/2 = 6-9 hours

154
Q

Antibiotics with longest half lives? (MSTFGM)

A

1 = Macrolides (up to 60 hours)

155
Q

HIV Diagnosis

A

Occurs 2-3 weeks post exposure

CD4+ will rapidly decline and HIV RNA (viral load) will increase greatly

Dx = presence of HIV RNA or p24 antigen w/ negative or indeterminate HIV antibody test

156
Q

CD4+ T-Cell Count

A

Indicates to what extent HIV has damaged the immune system.

Normal = 500-1600

<200 = increased risk of AIDS malignancies

Must get level before starting treatment therapy.

157
Q

Viral Load Goal

A

Goal = undetectable levels (<20-75 copies/mL)

158
Q

Reverse Transcriptase Inhibitors MOA (Ex. Truvada)

A

Nucleoside = work in the target cells to interfere with transcription of RNA to DNA

Non-nucleoside = By binding to reverse transcriptase, NNRTIs also interfere

Monitor renal status

159
Q

Protease Inhibitors MOA

A

Inhibits ability of POLYPROTEIN chains to break apart and create new chains of the virus late in the reproduction phase.

Decreases the production of viral RNA

160
Q

Fusion Inhibitors MOA (Ex. Fuzeon)

A

Prevents FUSION of the virus to the cell membrane of the CD4 host cell

Often useful in patients with other drug resistance.

161
Q

Integrase Inhibitors MOA (Ex. Dolutegravir, Elvitegravir, Raltegravir)

A

Prevents INTEGRATION of the viral DNA into the host cell’s genome.

162
Q

CCR5 Antagonist (Ex. Maraviroc)

A

Blocks the CCR5 receptors on the CD4 cell membrane.

163
Q

Goals of HIV Treatment (5)

A
  1. Maximal suppression of viral load to undetectable levels (diminishes spread of virus).
  2. Restoration and preservation of immune system function (increase CD4).
  3. Enhanced QOL and duration of life.
  4. Reduced M/M from HIV related complications.
  5. Prevent HIV transmission.
164
Q

Initiation of ART Therapy

A

Regardless of CD4 count, offer treatment with ART

H&P, CBC, BMP, LFTs, fasting lipid profile and glucose, urinalysis, CD4+, T-cell count viral load before starting treatment

Rec starting therapy: 2 NRTIs + 3rd drug (boosted PI or INSTI)

Education on adherence is very important.

165
Q

Monitoring ART Therapy

A

CD4 count and viral load.

CD4 baseline, after ART started check CD4 after 3 months.

Check CD4 count every 3-6 months for first 2 years.

Start yearly CD4 counts when ranging between 300-500 cells/mL.

CD4 optional after 2 years on suppressive ART.

166
Q

Change in ART Therapy

A

Viral load should be immediately assess and again 2-8 weeks later.

Repeat q4-8 weeks until less than 200 copies/mL.

Undetectable viral load by 8-12 weeks.

Repeat every 3-4 months.

167
Q

Most important aspect of ART?

A

Adherence → Must crucial factor → stopping medication can increase resistance.

NU 560 - Adv. Pharmacotherapeutics (5 decks)

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