Unit 3 Flashcards
Do ACEs and ARBs affect arterial vasculature, venous vasculature, or both?
Both
Do CCBs affect arterial vasculature, venous vasculature, or both?
Arterial
Do diuretics affect arterial vasculature, venous vasculature, or both?
venous
long term use can affect arterial
Do BBs affect arterial vasculature, venous vasculature, or both?
both
Do alpha agonists/blockers affect arterial vasculature, venous vasculature, or both?
both
Do nitrates affect arterial vasculature, venous vasculature, or both?
Both
Goal SBP and DBP for Age>60
<150
<90
Goal SBP and DBP for Age<60
<140
<90
Goal SBP and DBP for DM and CKD
<140
<90
Goal SBP and DBP for CKD only
<130
<80
ALL patients with DM and/or CKD with albuminuria >300 should receive what
ACE or ARB
How to treat HTN in non-black with no cormorbidities or just DM
thiazide
ACE/ARB
CCB
How to treat HTN in a black patient with no comorbidities or just DM
thiazide
CCB
statins MOA
inhibit HMG CoA reductase which inhibits LDL production in the liver
2 examples of high dose statins
atorvastatin 80mg
rosuvastatin 40mg
when to prescribe a high dose statin
> 75 with ASCVD
LDL>190
DM 40-75 no ASCVD and LDL 70-189 and estimated risk >7.5% for serious CV event in 10 years
monitoring for statins
baseline lipid panel and LFTs
recheck in 3 mo
if at goal, monitor lipids q3-12 months
education for statins
avoid grapefruit juice
Many med interactions due to CYP3A involvement
SE of statins (4)
myalgia– rhabdo/renal failure
headache
fatigue
GI distress
elevated LFTs
how to manage SE of statins
d/c statin, if symptoms resolve, r/s at lower dose, if tolerated, dose can be gradually increased. If unable to achieve recommended dose, consider non-statins
6 medications for angina
ACEs/ARBs
Spironolactone
Nitrates
BB
CCB
AP- aspirin
2 short acting medications for angina
nitro SL
isordil SL
2 long acting medications for angina
nitro topical/transdermal patch
isosorbide IR/ER
MOA BB
block beta 1 and/or beta 2 receptors centrally and peripherally, leading to decreased cardiac output and sympathetic outflow
BB contraindications (6)
bradycardia
2nd and 3rd degree HB
decompensated heart failure
severe bronchospastic disease
caution in asthma and COPD
SE of BB (8)
fatigue
drowsiness
bronchospasm
N/V
bradycardia
AV conduction abnormalities
CHF
mask hypoglycemia
MOA CCB
inhibit the movement of calcium ions across a cell membrane leading to cardiac muscle relaxation and vasodilation. Non-dihydropyridines decrease HR and slow cardiac conduction at the AV node. Dihydropyridines are potent vasodilators.
Dihydropyridines- nifedipine, amlodipine
Non dihydropyridine- verapamil, diltiazem
CCB non-dihydropyridines contraindications (2)
heart block and sick sinus syndrome (avoid in LV failure)
nifedipine contraindications (2)
essential HTN or HTN emergency (inconsistent fluctuations in BP and reflex tachycardia)
SE non-dihydropyridines (3)
GI upset
peripheral edema
hypotension
SE dihydropyridine (4)
headache
flushing
palpitations
peripheral edema
MOA ACEIs
prevent the conversion of angiotensin I to angiotensin II. Inhibit the degradation of bradykinin and increase the synthesis of vasodilating prostaglandins
ACEI contraindications (3)
b/l renal artery stenosis (acute renal failure)
pregnancy (avoid in women childbearing age)
hx of angioedema
SE ACEIs (6)
cough
rashes
dizziness
hyperkalemia
angioedema
laryngeal edema
MOA ARBs
block the binding of angiotensin II to the angiotensin II receptor which blocks the vasoconstriction and aldosterone-secreting effects
ARB contraindications (3)
b/l renal artery stenosis
pregnancy
caution in renal/hepatic impairment
SE ARBs (8)
dizziness
URI
viral infection
fatigue
diarrhea
sinusitis
pharyngitis
rhinitis
Loop diuretics MOA
inhibit the reabsorption of sodium and chloride in the proximal and distal tubules and the loop of Henle
Loop diuretics contraindications (5)
anuria
hepatic coma
severe electrolyte depletion
hypersensitivity to sulfas
ethacrynic acid contraindicated in infants
Loop diuretics SE (6)
hypokalemia
hypomagnesemia
hypercalcemia
hyperuricemia
hyperglycemia and hyperlipidemia in high doses
Thiazide diuretics MOA
inhibits Na, K, and Cl reabsorption in the distal tubule
Thiazide diuretics contraindications (2)
anuria
hypersensitivity to sulfas
Thiazide diuretics SE (6)
hypokalemia
hypomagnesemia
hypercalcemia
hyperuricemia
hyperglycemia
hyperlipidemia
potassium sparing diuretics MOA
interfere with sodium reabsorption at the distal tubule, decreasing potassium secretion
aldosterone receptor antagonists MOA
inhibit the effect of aldosterone by competitively binding to aldosterone receptors in the cortical collecting duct. Leads to decreased reabsorption of sodium and water and decrease potassium secretion
Potassium-Sparing Diuretics/Aldosterone Receptor Antagonists contraindications (4)
hyperkalemia, Addison disease, anuria, patients taking eplerenone
Potassium-Sparing Diuretics/Aldosterone Receptor Antagonists SE (4)
gynecomastia, hirsutism, menstrual irregularities, gout symptoms
Central Alpha-2 Receptor Agonists MOA
inhibit action of adrenaline on smooth muscle in blood vessel walls, dilating both arterioles and veins and cause relaxation of smooth muscle
Clonidine
Central Alpha-2 Receptor Agonists contraindications
use with tadalafil, sildenafil, and vardenafil (increased risk of symptomatic hypotension)
Central Alpha-2 Receptor Agonists SE (5)
first-dose phenomenon:
dizziness
faintness
palpitations
syncope
ortho hypotension
class 1 antiarrhythmics
sodium channel blockers:
procainamide
lidocaine
quinidine
what leads to quinidine toxicity
substrate of CYP3A4 (interacts with ketoconazole, erythromycin, amio, verapamil, diltiazem, rifampin, phenobarbital, phenytoin)
inhibitor of CYP2D6 (interacts with BB)
what leads to procainamide toxicity
renal impairment leads to accumulating levels
what leads to lidocaine toxicity
reduced hepatic blood flow d/t HFrEF delays metabolism
Class II antiarrhythmics
beta blockers
Class III antiarrhythmics
potassium channel blockers:
amiodarone
dronedarone
sotalol
dofetilide
what leads to amio and dronedarone toxicity
substrate of CYP3A4
inhibitor of CYO3A4, 2C9, 2D6
what not to give with amio and drondarone (9)
azoles
cyclosporine
clarithromycin
ritonavir
rifampin
phenobarbital
phenytoin
carbamazepine
St. John’s Wort
what leads to sotalol toxicity
poor renal function
what drugs lead to dofetilide toxicity (7)
cimetidine
dolutegravir
ketoconazole
HCTZ
megestrol
prochlorperazine bactrim
verapamil
what leads to dofetilide toxicity
poor renal function
class IV antiarrhythmics
CCB
what leads to diltiazem and verapamil toxicity
substrate and inhibitor of CYP3A4 do use cautiously with other meds that are metabolized by that isozyme
what leads to digoxin toxicity
poor renal function
electrolyte disturbance predispose the myocardium to the toxic effects of dig
3 drug interactions of dig
amio
dronedarone
verapamil
MOA of digoxin
predominant antiarrhythmic effect on the AV node of conduction system.
affects the ANS by stimulating the parasympathetic division increasing vagal tone which slows conduction through AV node
indication of digoxin
slow electrical impulse conduction through the AV node, slowing ventricular rate in AF and AFL
great for HFrEF with concomitant AF/AFL d/t to its positive inotropic effect
onset and peak of digoxin
6-8 hours
MOA amio
reduces automaticity and conduction velocity and prolongs refractoriness
blocks the rapid and slow components of the delayed rectifier potassium current
blocks sodium channels
non-selective beta blocking activity
weak CCB properties
minimal to no negative inotropic effects- safe for HFrEF
amio indications
management of acute VT/VF and AF
amio pharacodynamics (4)
poor oral bioavailability
large vol of distribution
long half life
loading dose needed
amio SE (10)
pulmonary toxicity
corneal microdeposits
thyroid abnormalities
N/V
hepatotoxicity
prolonged QT
photosensitivity
blue/gray skin
heart block
tremors
How do ACE/ARBs help with heart failure
reduce afterload
prevent cardiac remodeling
How do BB help with heart failure
reduce mortality, decrease O2 demand and workload
How do diuretics help with heart failure
reduce preload
how do nitrates help with heart failure
relax vasculature (coronary and systemic) to impact O2 supply and demand
Textbook treatment order for heart failure
- ACE (ARB if not tolerated) and BB
- Diuretic
- Digoxin
- ARB, aldosterone agonist, hydral/isosorbide
How to treat AF/AFL with normal LV function
IV diltiazem, IV verapamil, IV BB
dig too slow onset
How to treat AF/AFL with reduced LV function
IV BB or IV digoxin
indication of EPO
treats anemia in ESRD who can’t produce enough EPO due to renal damage
if hgb <10 to avoid transfusion
How is EPO given
SQ 3x/week
Education for patients on EPO
take multivitamin d/t renal restrictive diet and iron supplement
contraindications of EPO
uncontrolled HTN or sensitivity to mammalian products/albumin
SE of EPO (6)
HTN
HA
seizure
nausea
edema
fatigue
monitoring for patients on EPO (10)
H&H
ferritin
transferrin
B12
folate
BP
clotting times
plts
BUN and Cr
4 indications for AP therapy
ischemic stroke prevention and treatment
add on to AC for mechanical valve
post-ACS to prevent CV death, MI, stroke
prevent thrombosis s/p PCI
indications of ASA
post ACS
prevent thrombosis
add-on AC
ASA platelet dysfunction
lasts for 7-10 days after day of d/c
d/t lifespan of the platelets exposed to ASA
irreversible
onset of ASA
5 minutes
onset of plavix
2 hours
how long to d/c plavix before surgery
5-7 days
SE of ASA (3)
GI upset
bleeding
potentiate PUD
SE of plavix (3)
diarrhea
bruising
bleeding
3 contraindications for AP
active GI bleed
ICH
PUD
how to manage a patient with initiation of warfarin
start with warfarin + injectable AC
d/c LMWH when INR therapeutic
don’t bridge with direct thrombin inhibitor (dabigatran)
Contraindications for ACs (10)
active bleed
recen ICH
intracranial mass (at high risk bleeding)
end stage liver disease
severe thrombocytopenia
recent trauma
immediate post-op ocular or CNS surgery
spinal catheters
aneurysms
7 labs to consider before initiating ACs
PT
INR
aPTT
UA
CBC
LFT
pregnancy test
3 considerations for LMWH or DOAC
body wt
Cr
CrCl
3 ACs/APs to prevent VTE
Lovenox
warfarin
DOACs
3 ACs/APs to prevent stroke in AF
DOACs
ESRD: xarelto or eliquis
AC/AP for prosthetic valve
warfarin (and sometimes ASA)
2 ACs/APs for TAVR
ASA+plavix for 3-6 months then ASA for life
3 ACs/APs for ischemic stroke
ASA
ASA/dipyridamole
plavix
4 ACs/APs for MI s/p PCI
ASA
plavix
prasugrel
ticagrelor
recombinant EPO indication
treatment of anemia in chronic renal failure, zidovudine admin (HIV med) and chemo admin
(Darbepoetin - long acting version) not indicated for zidovudine
is warfarin safe in pregnancy
no
is heparin safe in pregnancy
yes
is ASA/plavix safe in pregnancy
only if there is a dire need
indication for DOACs
fast onset
VTE treatment and AF
MOA of recombinant EPO
stimulates production of RBCs in erythroid tissues in bone marrow
why is iron supplementation for anemia important
iron is needed for the creation of heme groups needed for hgb and myoglobin
where is excess iron stored
liver
spleen
bone marrow
when are DOACs inappropriate to prescribe
MI
ischemic stroke
prosthetic heart valves
education regarding taking iron supplements
empty stomach or with OJ because an acidic environment is needed for absorption
DOAC monitoring
renal and hepatic function
prodrug and excreted by kidney
may need to renally dose
reversal for warfarin
vit K
FFP
reversal for dabigatran and pradaxa
idarucizumab
Xa inhibitors (-aban) reversal agent
andexanet
7 medications that worsen HF
flecainide
disopyramide
sotalol
dronedarone
a-blockers (-zosins)
CCBs
moxonidine
mechanisms of antibiotic resistance (6)
-bacterial enzyme production
-alteration of bacterial cell membranes (inhibiting abx from entering the cell)
-activation of efflux pumps expels abx out of the intracellular space back across the cell membrane
-alteration of abx target site of action, mutations alter the ribosomal binding site
-alteration of target enzymes
-overproduction of target enzymes leading to resistance
3 ways abx work
interference with cell wall synthesis
interference with nucleic acid synthesis
interference with protein synthesis
PCN MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
Cephalosporins MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
Monobactams MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
Carbapenems MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
Beta-Lactam/Beta-Lactamase inhibitors MOA
inhibition of cell wall synthesis, binds to PCN-binding proteins
Fluroquinolones MOA
Inhibits DNA gyrase and topoisomerase IV enzymes which are needed to coil the bacteria DNA
Macrolides MOA
inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit
Amioglycosides and tetracyclines MOA
inhibit bacterial protein synthesis by binding to the smaller 30S ribosomal subunit
Sulfa MOA
inhibit the incorporation of para-amiobenzoic acid, the basic building block bacteria use to synthesize dihydrofolic acid which is required for bacterial cell growth
glycopeptide MOA
cell wall active agent
clindamycin MOA
binds to 50S subunit of bacterial ribosome and inhibits protein synthesis
flagyl MOA
interacts with bacterial DNA causing strand breakage and results in protein synthesis inhibition
Glycopeptide SE (2)
Red-man syndrome
nephrotoxicity
red man syndrome
histamine mediated phenomenon affiliated with infusion rate
pruritus
flushing of head, neck, face
hypotension
fluoroquinolones bioavailability
highly bioavailable
fluoroquinolones distribution
most tissues and body fluids except CNS
fluoroquinolones half life
4-12 hours
fluoroquinolones excretion
renal
what type of organism does PCN treat
gram positive
what type of organism do cephalosporins treat
gram positive ad negative
what type of organism does clinda treat
gram positive and MRSA
what type of organism does vanco treat
MRSA and gram positive
what type of organism do carbapenems treat
gram positive and negative
what type of organism do tetracyclines treat
gram positive and some gram negatives
what type of organism do fluoroquinolones treat
gram negative and some gram positive
what type of organism do aminoglycosides treat
gram negative
what type of organism do macrolides treat
gram positive and some negatives
cephalosporins absorption
well absorbed in GI tract
cephalosporins distribution
penetrates well into tissues and body fluids with high concentrations in urinary tract. 3rd and 4th gen penerate CSF
cephalosporin excretion
kidney except ceftriaxone which is excreted by the liver
beta lactams distribution
most body tissues except CSF
beta lactams excretion
glomerular filtration so check renal function
how to treat MRSA (2)
vancomycin
bactrim
most common SE of antibiotic treatment
c diff
treatment of c diff
PO vanco
most common SE of PCN
hypersensitivity
most common SE of beta-lactam and BLI
GI effects
hypersensitivity
most common SE of cephalosporins and monobactams
safe class with favorable toxicity profile
most common SE of carbapenems
neurotoxicity (seizure)
most common SE of quinolones
hepatotoxicity
QTC prolongation
GI upset
most common SE of macrolides
GI upset
most common SE of aminoglycosides
nephrotoxicity
ototoxicity
most common SE of tetracycline
GI side effects
hepatotoxicity
most common SE of sulfas
rash
fever
GI effects
SJS
most common SE(4) glycopeptides
fever, chills, phlebitis, red man syndrome
most common SE of clinda
c diff
azithromycin half life
50-60 hours
sulfa half life
hours to days
tetracyclines half life
short acting- 8
long acting- 16-18
vanco half life
5-11 hours
HIV lab values post exposure
CD4+ will rapidly decline 2-3 weeks post exposure and HIV RNA with increase greatly
Diagnosis of HIV labs
presence of HIV RNA or p24 antigen
negative or indeterminate HIV antibody test
CD4 and plasma HIV RNA viral load
normal CD4+ T-cell count
500-1600
what does a CD+ T-cell count of less than 200 indicate
AIDS malignancies
undetectable viral load number
<20-75 copies/ml
Reverse transcriptase inhibitors MOA
work in target cells to interfere with the transcription of RNA or DNA
proteases inhibiors MOA
activity late in the reproduction phase of the HIV virus inhibiting the ability of the polyprotein chains to break apart and create new chains of the virus
what is the outcome of protease inhibitor
decrease the production of viral RNA
fusion inhibitor MOA
Prevents fusion of the virus to the cell membrane of the CD4 host cell
integrase inhibitor MOA
prevents integration of viral DNA into the host cell’s genome
CCR5 antagonist MOA
Blocks the CCR5 receptor on the CD4 cell membrane. Not all viruses use this receptor for cell entry
5 goals of HIV treatment
maximal suppression of viral load to undetectable levels
restoration and preservation of immune system function
enhance QOL and duration of life
reduce M&M from HIV-related complications
prevent HIV transmission
who is eligible for ART therapy
all patients regardless of CD4+ count should be offered treatment as soon as possible with ART
10 labs before initiating ART
H&P
CBC
BMP
LFTs
fasting lipid profile and glucose
urinalysis
CD4+
T-cell count
viral load
recommended starting ART
2 reverse transcriptase inhibitors and a third drug (either protease or integrase inhibitor)
how often or check CD4+ count after ART initiation and why
3-6 months to assess response for first 2 years of treatment and to determine the necessity of opportunistic infection prophylaxis
how often or check CD4+ count when consistently above the threshold for risk of opportunistic infection
300-500
yearly
how often or check CD4+ count when consistently above 500 after 2 years of ART
optional
how often to check viral load after therapy initiated or changed
immediately before treatment
2-8 weeks later
q4-8 weeks until less than 200
q3-4 months (6 months if immunologically stable and fully suppressed viral load for at least 2 years)
education for HIV
Adherence is the most crucial factor to success-stopping a medication can increase resistance
create a med plan
discuss how to take meds properly
lifesyle changes
SE to monitor for
develop a support system
