Unit 3 Exam Flashcards
(167 cards)
1
Q
Arterial Vasodilators
A
CCBs
2
Q
Venous Vasodilators
A
Diuretics
Long term use can also affect arterial
3
Q
Arteriovenous Vasodilators
A
ACE/ARBs
BBs
Alpha agonists/blockers
Nitrates
4
Q
Anti-HTN therapy for DM only
A
Goal SBP <140/90
NB = Thiazide, ACE/ARB, or CCB alone
B = Thiazide or CCB
5
Q
Anti-HTN therapy for CKD w/ DM
A
Goal SBP <140/90
All = ACE/ARB
6
Q
Anti-HTN therapy for CKD only
A
Goal SBP <130/80
Albuminuria >300 mg/dl = ACE
Stage 1-2 Albuminuria = ACE/ARB
7
Q
Side Effects of Statins
A
Muscle pain, myopathy, weakness, fatigue, headache, GI distress, increased LFTs.
8
Q
Adverse Reactions of Statins
A
Rhabdomyolysis or AKI
CKMB to r/o rhabdo
Reduce or dc med
Possibly reversible
9
Q
Considerations with Statins
A
Pregnancy Class X - no breastfeeding
Very strong CYP450 inducer - multiple drug interactions.
10
Q
High Dose Statin Indications (4 groups)
A
- <75 yo w/ ASCVD
- LDL >190
- 45-75 yo, DM, no ASCVD, LDL 70-189
- 45-75 yo, no DM or ASCVD, LDL 70-189, Calc risk >7.5% next 10 year serious CV/ASCVD event.
11
Q
Monitoring Statin Therapy
A
Baseline lipid panel + LFTs
Medication history d/t medication interactions.
Estimated risk calculator
Avoid grapefruit juice
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)
13
Q
Fibric Acid Derivatives MOA
A
Reduce triglycerides by enzymatic destruction.
Ex. Gemfibrizol (Lopid), Fenofibrate (Tricor)
14
Q
Cholesterol Absorption Inhibitors MOA
A
Decreases absorption of cholesterol in the small intestines.
Decreased stored cholesterol in the liver.
Ex. Ezetimbide (Zetia)
15
Q
Omega 3 Fatty Acids MOA
A
Lowers triglycerides, increased HDLs (must take at high doses, 3g/day).
Ex. Lovazza
16
Q
Niacin MOA
A
B vitamin that increased HDLs and lowers LDLs and triglycerides.
17
Q
Acute Treatment for Angina (not MI)
A
Short acting nitrate
ASA (if not contraindicated)
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)
19
Q
Beta Blockers MOA
A
Block beta-1 and/or beta-2 receptors centrally and peripherally, leading to decreased CO and sympathetic outflow.
20
Q
Beta Blocker Contraindications
A
Bradycarida
2nd/3rd degree HB
Decompensated HF
Severe bronchospastic disease
Caution in asthma + COPD
21
Q
Beta Blocker Side Effects
A
Fatigue
Drowsiness
Bronchospasm
N/V
Bradycardia
AV conduction abnormalities
CHF
Can mask hypoglycemia symtpoms
22
Q
CCB MOA
A
Inhibit the movement of calcium ions across a cell membrane leading to cardiac muscle relaxation and vasodilation
23
Q
Non-Dihydropyridines vs Dihydropyridines MOA
A
ND = Decreased HR and slows cardiac conduction at the AV node (diltiazem)
D = Potent vasodilators (“-dipines”)
24
Q
CCB Contraindications
A
Heart failure
Can worsen WPW
Check hepatic function before therapy
25
CCB Side Effects
Peripheral edema (d/t vasodilation)
Constipation (effects smooth muscle in gut)
May worsen GERD (decreased sphincter contraction)
26
ACE-I MOA
Prevents the conversion of angiotensin I to angiotensin II
Inhibits the degradation of bradykinin and increase the synthesis of vasodilating prostaglandins.
27
ACE-I Contraindications
Bilateral renal artery stenosis (acute renal failure)
Pregnancy (avoid in childbearing age)
Hx of angioedema
28
ACE-I Side Effects
Dry cough
Hyperkalemia
Angioedema
Laryngeal edema
29
ARB MOA
Blocks the binding of angiotensin II to the angiotensin II receptor, which blocks vasoconstriction and aldosterone secreting effects.
30
ARB Contraindications
Renal artery stenosis
Pregnancy
Caution in renal/hepatic impairment
31
ARB Side Effects
URI
Viral infection
Sinusitis
Pharyngitis
Rhinitis
Diarrhea
32
Loop Diuretics MOA
Inhibit the reabsorption of Na and Cl in the proximal and distal tubules and the loop of Henle.
33
Diuretic Contraindications
No K sparing diuretics in pts with renal impairment (Cr Cl <25-30)
Patients with gout
High risk of falls
Dehydration
34
Diuretic Side Effects
Electrolyte imbalances
Glucose intolerance
Hyperuricemia (d/t decreased Ca + uric acid excretion)
Dehydration/Hypotension/Falls
Muscle cramps, paresthesias, impotence.
Drug interactions
35
Thiazide Diuretics MOA
Inhibits Na, K, Cl reabsorption in the distal tubule of the nephron
36
K-Sparing Diuretics MOA
Alter Na reabsorption in the distal tubule further than where K is reabsorbed.
37
K-Sparing Contraindications (4)
Hyperkalemia
Addison's disease (Decreased aldosterone)
Pts taking ACE-I/ARBs
Pts taking eplerenone (Tx HTN/HF; blocks aldosterone)
38
K-Sparing Side Effects (4)
Gynecomastia
Hirsutism
Gout symptoms
Menstrual irregularities
39
Alpha-2 Receptor Agonists MOA
Inhibits cardiac acceleration and vasocontriction centers in the brain
Stimulates A2 → decrease peripheral outflow of NE → vasodilation, decreased PVR, HR and BP.
40
A2RA Side Effects
Sedation
Xerostomia (dry mouth)
Hypotension
41
A2RA Contraindications
Dry eye syndrome
Antipsychotic meds (TCAs/MAOIs)
Beta Blockers
ETOH, benzos, antihistamines
42
A2RA Cautions
Renal impairment
Recent MI
Severe CAD
43
Class 1 - Antiarrhythmics
Sodium channel blockers:
Procainamide
Lidocaine
Quinidine
44
Causes of procainamide toxicity?
Renal impairment → accumulating levels
45
Causes of lidocaine toxicity?
Reduced hepatic blood flow d/t HFrEF → delays metabolism
46
Class II - Antiarrhythmics
Betablockers:
Esmolol
Metoprolol
Atenolol
47
Class III - Antiarrhythmics
Potassium channel blockers:
Amiodarone
Sotalol
Defetilide
48
Medications to avoid with amio and drondarone?
Azoles
Cyclosporines
Clarithromycin
Ritonavir
Rifampin
Phenobarbital
Phenytoin
Carbamazepine
St. John's Wort
49
Dronedarone Interactions
Increases serum digoxin + dabigatran
Caution with statins - risk of myopathy
Can cause pulm toxicity
50
Causes of sotalol toxicity?
Poor renal function
Concurrent diuretic use increases risk for Torsades
51
What drugs causes dofetilide toxicity?
Cimetidine
Dolutegravir
Ketoconazole
HCTZ
Megestrol
Prochlorperazine
Bactrim
Verapamil
52
Causes of dofetilide toxicity?
Poor renal function
Avoid other meds that prolong QTc.
53
Class IV - Antiarrhythmics
CCB:
Diltiazem
Verapamil
54
Causes of digoxin toxicity?
Poor renal function → excreted by the kidneys
Electrolyte disturbances (hypokalemia → dig toxicity)
Drug interactions (amio, verapamil)
55
Digoxin MOA
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
56
Amiodarone MOA
Reduces automaticity and conduction velocity and prolongs refractoriness.
No inotropic effects.
Potassium channel blocker.
57
Amiodarone Med Interactions
Increases digoxin concentration and potentiates warfarin (increases INR).
58
Indication for Digoxin
Slowing Vent. rate in AF + AFL
HFrEF w/ AF + AFL due to positive inotropic effects
59
Indications for Amio
Management of acute VT/VF and AF
60
Heart Failure Treatment Order (4)
1st line = ACE/ARB + BB
2nd line = Diuretic
3rd line = Digoxin
4th line = ARB, aldosterone antagonist, long-acting nitrates (HYD/ISDN)
61
ACE-I/ARBs use in Heart Failure
Reduce afterload
Prevent cardiac remodeling
62
BB use in Heart Failure
Reduced mortality
Decrease O2 demand and workload
63
Diuretic use in Heart Failure
Reduce preload
64
Nitrate use in Heart Failure
Relax coronary + systemic vasculature to impact O2 supply and demand
65
Medication not appropriate in HF
CCBs
66
Acute MI Treatment
1. ASA
2. Nitrates (SL initial, then IV if needed).
3. O2 (if SpO2 <90% or dyspneic)
4. Morphine (if pain persists despite nitro).
67
Afib/Aflutter Treatment
1. Cardio version if unstable
2. Goal = ventricular rate control (rate control > rhythm control)
68
Afib/Aflutter Treatment for Normal LV
Dilt
Verapamil
Beta-blocker
(All IV)
Can use amio if refractory to other meds.
69
Afib/Aflutter Treatment with HFrEF
IV beta blocker
IV digoxin
70
Indications for EPO
Treats anemia in...
... ESRD
... Zidovudine administration in HIV
... Chemotherapy
Give if hgb <10 to avoid transfusion
71
Administration of EPO
SQ injection 3x per week
Stop if >12 hgb
72
EPO Education
Take multivitamin + iron supplement for EPO to work
73
Contraindications for EPO
Uncontrolled HTN
Sensitivity to mammalian products/albumin
74
Side Effects of EPO (6)
HTN
HA
Seizures
Nausea
Edema
Fatigue
75
Monitoring Labs/VS for EPO (10)
H+H
Ferritin
Transferrin
B12
Folate
BP
Clotting times
Plts
BUN/Cr
76
Indications for Antiplatelet Therapy (4)
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
Antiplatelet Agents
ASA
P2Y12 Inhibitors: Plavix, Effient, Brilinta
78
Indications of ASA
Post ACS
Prevent thrombosis
Add on for AC (dual-platelet therapy)
79
Length of platelet dysfunction with ASA
7-10 days after dc
d/t lifespan of the platelets exposed to irreversible inhibition of COX
80
Contraindications for Antiplatelet Therapy (3)
Active GI bleed
ICH
PUD
81
How long before surgery should plavix be dc'd?
5-7 days
Bleeding time and platelet aggregation returns to baseline
82
Side Effects of ASA (3)
GI upset (nausea, heartburn, epigastric discomfort).
Bleeding
May potentiate PUD
83
Side Effects of Plavix (3)
Diarrhea
Brusing
Bleeding
84
Initiation of Anticoagulation
1. Warfarin + injectable AC
2. D/c LMWH when INR is therapeutic
3. No bridging with DOACs (onset 2-4 hours after admin).
85
Indications of Anticoagulation (4)
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
Contraindications for Anticoagulation (9)
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
Considerations with Anticoagulation
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
Education for Anticoagulation (2)
1. Diet (Vit K can make warfarin sub-therapeutic)
2. Avoid contact sports and intense exercise that could increase bleeding risk.
89
Examples of DOACs
Direct thrombin inhibitors = Dabigatran (Pradaxa)
Factor Xa inhibitors = Savaysa, Eliquis, Xarelto (SEX)
90
Drugs for VTE (3)
Lovenox
Warfarin
DOACs
91
Anticoagulant Drugs for Afib
DOACs (over warfarin, except for prosthetic valve).
Dabigatran (Pradaxa).
Xarelto or Eliquis (ESRD).
Recommended for CHADS score >2 (men) >3 (women).
92
AC Drugs for Prosthetic Heart Valves
Warfarin (some cases dual-antiplatelet therapy = +ASA)
93
AC Drugs for TAVR
Dual antiplatelet therapy (DAPT)
ASA + Plavix for 3-6 months → ASA for life
94
AC Drugs for Ischemic Stroke
ASA
ASA/Dipyridamole
Plavix
95
AC Drugs for MI (2)
S/p MI → ASA, Plavix, Prasugrel (Effient) and Ticagrelor (Brilinta)
ASA + P2Y12 inhibitor
96
Anticoagulant Bridge Therapy
Warfarin + injectable AC
D/c LMWH when INR in therapeutic range (~2-3)
No bridging with DOACs (onset 2-4 hours)
97
Recombinant EPO MOA
Stimulates production of RBCs from the erythroid tissue in the bone marrow.
Serum half-life 8.5 hours.
98
EPO Indications
Anemia d/t chronic renal failure
Zidovudine administration in HIV
Chemo administration
99
EPO Administration/Dosing
Starting dose is 50-100 units/kg SQ x3 per week
2-6 weeks required to evaluate effectiveness
100
Education Regarding Iron Supplementation
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
Examples of DOACs
Dabigatran (Pradaxa) - Direct thrombin inhibitor
Rivaroxaban (Xarelto)
Apixaban (Eliquis)
Edoxaban (Sayvasa)
Binds to Factor Xa = “-xaban”
102
When to prescribe DOACs?
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
Anemias of Increased Destruction (2)
Acute post-hemorrhagic anemia/Chronic blood loss
Sickle Cell Anemia
104
Anemias of Diminished Production (6)
Iron deficiency
Chronic renal failure
Chronic disease
Thalassemia
Vitamin B12 Deficiency
Folate Deficiency
105
Acute post-hemorrhagic anemia/Chronic blood loss
Massive hemorrhage from spontaneous or traumatic rupture or incision of a large blood vessel.
Initial H/H may be high due to vasoconstriction
106
Sickle Cell Anemia
Autosomal recessive disorder where abnormal hemoglobin leads to chronic hemolytic anemia
Hgb S
Sickle cell crisis: occurs due to hypoxia, dehydration or acidosis.
107
Sickle Cell Anemia Population
African-american
108
Iron Deficiency Anemia
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
Iron Deficiency Anemia Population
Vegetarians
Malabsorption
Women (menstrual loss, pregnancy, lactation).
110
Chronic Renal Failure Anemia
Chronic renal failure leads to reduced EPO production by the kidneys.
111
Anemia of Chronic Disease
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
Thalassemia
Hereditary disorder of hgb synthesis - hypo-proliferative anemia
Decreased production of alpha- or beta-globins or a structurally abnormal globin change.
113
Types of Thalassemia
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
Vitamin B12 Anemia (Pernicious Anemia)
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
Vitamin B12/Pernicious Anemia Population
Inadequate intake / malnourished
Malabsorption
Lack of intrinsic factor
116
Folate Deficiency Anemia
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
Folate Deficiency Anemia Population
Women (pregnancy, lactation, infancy)
Malignancy
Dialysis
Phenytoin/phenobarbital use
118
Warfarin Reversal
Vitamin K PO/IV
FFP (not as quick or affective)
119
Heparin Reversal
IV protamine sulfate
May also be used for LMWH and Fondaparinux but no clear evidence of effectiveness.
120
Dabigatran (Pradaxa) Reversal
Idarucizumab (monoclonal antibody)
121
DOACs Reversal
Andexanet Alpha - modified factor Xa decoy protein that binds to factor Xa with higher affinity than factor Xa inhibitors.
122
Antiplatelet (ASA/P2Y12) Reversal
Platelet transfusion - no reversal agent
123
Warfarin and Pregnancy
CONTRAINDICATED
124
DOACs and Pregnancy
No data
125
UFH/LMWH and Pregnancy
SAFE - does not cross placenta
126
ASA and Pregnancy
Prevents preeclampsia
127
Clopidogrel (Plavix) and Pregnancy
Okay if needed
128
Process of Antimicrobial Selection
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
Mechanisms of Resistance (6)
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
3 ways antibiotics work on the bacterial cell?
1. Interfere with CELL WALL synthesis
2. Interfere with NUCLEIC ACID synthesis
3. Interfere with PROTEIN synthesis
131
Antibiotics that interfere with cell wall synthesis (BVBPD)
Beta-lactams (PCCCM)
Vancomycin
Bacitracin
Polymyxins
Daptomycin
132
Antibiotics that interfere with nucleic acid synthesis (STQRSA)
Sulfonamides
Trimethoprim
Quinolones
Rifampin
Streptovaricins
Actinomycin
133
Antibiotics that interfere with protein synthesis (CLMCSTA)
Clindamycin
Linezolid
Macrolides
Chloramphenicol
Streptogramins
Tetracyclines
Aminoglycosides
134
Glycopeptide Adverse Events
Fever, chills, phlebitis
RED-MAN syndrome → histamine-mediated phenomenon affiliated with the rate of infusion
Ex. Vancomycin
135
Cephalosporin Pharmacokinetics (i.e. "Cef-/Ceph-") ADE
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
Fluroquinolone Pharmacokinetics (i.e. "-floxacin") ADE
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
Beta-Lactam Pharmacokinetics (i.e. Penicillins, Cephalosporins, Carbapenems, Monobactams) ADE
Distribution → Diffuse into most body tissues, with exception of the brain and CSF.
Elimination → Glomerular filtration (need to check renal function)
138
MRSA Treatment
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
Common Side Effect/Diagnosis resulting from Antibiotic Treatment
C. Diff
140
C. Diff Treatment
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
Pencillin Side Effects + Half life
SE = Hypersensitivity
1/2 = 30-90mins
142
Beta-Lactam/Beta-Lactamase Inhibitors Side Effects + Half life
SE = Hypersensitivity reactions
1/2 = 1 hour
143
Cephalosporin Side Effects + Half life
SE = Safe
1/2 = 1-2 hours
144
Monobactams Side Effects + Half life
SE = Safer than aminoglycosides
1/2 = 1.5-2 hours
145
Carbapenems Side Effects + Half life
SE = Neurotoxicity (seizure activity)
1/2 = 1 hour
146
FluoroQuinolones Side Effects + Half life
SE = QTC prolongation, GI upset
1/2 = 6-12 hours
147
Macrolides Side Effects + Half life
SE = GI side effects (erythromycin)
1/2:
Erythro - 2 hours
Clarithro - 4-5 hours
Azithro - 50-60 hours
148
Aminoglycosides Side Effects + Half life
SE = Nephro/ototoxicity
1/2 = 1-3 hours
149
Tetracyclines Side Effects + Half life
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
Sulfonamides Side Effects + Half life
SE = Rash, fever, GI side effects
1/2 = hours to days
151
Glycopeptides Side Effects + Half life
SE = Fever, chills, phlebitis, red man syndrome (r/t infusion rate)
1/2 = vanc 5-11 hours
152
Clindamycin Side Effects + Half life
SE = C. Diff
1/2 = 3 hours
153
Metronidazole Side Effects + Half life
SE = Safe/well tolerate
1/2 = 6-9 hours
154
Antibiotics with longest half lives? (MSTFGM)
#1 = Macrolides (up to 60 hours)
#2 = Sulfonamides (up to days)
#3 = Tetracyclines (up to 18 hours)
#4 = Fluoroquinolones (up to 12 hours)
#5 = Glycopeptides (up to 11 hours)
#6 = Metronidazole (up to 9 hours)
155
HIV Diagnosis
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
CD4+ T-Cell Count
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
Viral Load Goal
Goal = undetectable levels (<20-75 copies/mL)
158
Reverse Transcriptase Inhibitors MOA (Ex. Truvada)
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
Protease Inhibitors MOA
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
Fusion Inhibitors MOA (Ex. Fuzeon)
Prevents FUSION of the virus to the cell membrane of the CD4 host cell
Often useful in patients with other drug resistance.
161
Integrase Inhibitors MOA (Ex. Dolutegravir, Elvitegravir, Raltegravir)
Prevents INTEGRATION of the viral DNA into the host cell's genome.
162
CCR5 Antagonist (Ex. Maraviroc)
Blocks the CCR5 receptors on the CD4 cell membrane.
163
Goals of HIV Treatment (5)
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
Initiation of ART Therapy
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
Monitoring ART Therapy
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
Change in ART Therapy
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
Most important aspect of ART?
Adherence → Must crucial factor → stopping medication can increase resistance.
