Exam 2 Flashcards
Penicillin’s
- MOA
- SE
- Coverage
Bactericidal–interfere with cell wall synthesis
SE: hypersensitivity, GI distress, seizures, encephalopathy
Mostly G+ coverage
Some G- coverage
Cephalosporins
- Method of action
- SE
- Coverage
Bactericidal–interfere with cell wall synthesis
SE: hypersensitivity, GI distress
As you progress from 1st to 4th generation, has more G- and less G+ coverage
Aminopenicillins
- Method of action
- SE
- Coverage
Amoxicillin (oral) and ampicillin (IV)
Bactericidal-interfere with cell wall synthesis
Good for G+ but also can treat some G-
Good for sinusitis, OM, lyme disease, H. Pylori, listeria meningitis
Monobactams
- Method of action
- SE
- Coverage
Aztreonam
Bactericidal–interfere with cell wall synthesis
SE: GI distress, usually no cross-sensitivity with penicillin or cephalosporin
Primarily against G-
Carbapenems
- Method of action
- SE
- Coverage
Imipenem, meropenum, doripenum most broad spectrum agents available Bactericidal--interfere with cell wall synthesis SE: neurotoxicity, GI distress G+ , G-,
Fluoroquinolones
- Method of action
- SE
- Coverage
-Floxacin
Bactericidal–Inhibit DNA gyrase and topoisomerase IV
SE: GI distress, dizziness, confusion, tendon rupture, QT prolongation
G+ and G-
Macrolides
- Method of action
- SE
- Coverage
Erythromycin, azithromycin, clarithromycin
Bacteriostatic–binds to 50S
SE: GI distress, hepatotoxicity, ototoxicity
May cause QT prolongation
DOC for atypical pneumonia/CAP and chlamydia
Broad spectrum: G+, G-, Atypical
Aminoglycosides
- Method of action
- SE
- Coverage
entamicin, Neomycin, Streptomycin, Tobramycin
Bacteriostatic–binds to 30S
SE: Nephrotoxicity and ototoxicity
Mainly active against G-
Can combine with beta lactams for G+ coverage
Monitor renal function and levels
Tetracyclines
- Method of action
- SE
- Coverage
Bacteriostatic–binds to 50S
SE: GI distress, gray-brown discoloration of the teeth, photosensitivity
Broad spectrum–G+, G-, atypical
Can be used for acne, walking pneumonia, chlamydial infections and PID, tick infections
Sulfonamides
- Method of action
- SE
- Coverage
Bacteriostatic–inhibits folic acid
SE: GI distress, rash, fever, steven johnson syndrome and vasculitis
G+ and G- (except pseudomonas and GAS)
Vancomycin
- Method of action
- SE
- Coverage
Bactericidal–inhibits d-alanyl-d-alanine portion of cell wall
SE: fever, chills, phlebitis, red man syndrome, nephrotoxicity
Active mostly against MRSA
Oxazolidinones
- Method of action
- SE
- Coverage
Linezolid + Tedizolid Oral tx for MRSA Bacteriostatic--bind to 50S se: GI distress, thrombocytopenia, leukopenia G+ only--MRSA, VRE
Clindamycin
- Method of action
- SE
- Coverage
Bacteriostatic–binds to 50S
SE: diarrhea and C. DIff colitis
Active against G+ and G- anaerobic
Used for anaerobic respiratory infections, skin infections, PID
Metronidazole
- Method of action
- SE
- Coverage
Bactericidal–inhibition of DNA protein synthesis
SE: GI distress, seizures, peripheral neuropathy
G- coverage only
DOC for abdomen and GU system (H Pylori, C. Diff, bacterial vaginosis, trich)
Chloramphenicol
- Method of action
- SE
- Coverage
Variably bactericidal–binds to 50S
SE: Gray baby syndrome, optic neuritis, fatal aplastic anemia
Broad spectrum: G+, G-, anaerobic
Rifampin
- Method of action
- SE
- Coverage
Variably bactericidal–inhibits DNA
SE: GI distress, headache, fever, discolors body fluids to orange
Mostly against G+ with some G- coverage
DOC for TB
Nitrofurantoin
Variably bactericidal–interferes with cell wall synthesis
SE: N/V and pulmonary reactions, hepatotoxicity, peripheral neuropathy
Only used for uncomplicated UTI
First line treatment for HSV-1
Topical acyclovir or penciclovir
Second line treatment for HSV-1
Systemic acyclovir, famciclovir, valacyclovir
First line treatment for VZV
Systemic antiviral if <72 hours from outbreak or patient is immunocompromised
Treatment of warts
Salicyclic acid
Keratolytic peeling agent
CI in diabetes or impaired circulation
Medications that may cause an increase in blood pressure
Oral contraceptives, nicotine, steroids, appetite suppressants, TCA’s, cyclosporine, NSAID’s, some nasal decongestants
Diagnostic criteria for hypertension
> 150/90 in adults >60
140/90 in adults <60
Must have 3 readings at least 1 week apart
When to initiate emergency BP treatment
If above 180 systolic
3 factors associated with resistant hypertension
Obesity, impaired renal function, diabetes
Hypertension in blacks
Occurs at an earlier age, more severe, results in organ damage more often
Isolated or predominant systolic hypertension is secondary to
Aorta artery stiffening secondary to advancing age
Main causes of secondary hypertension
CKD, renovascular hypertension, hypothyroidism, hyperparathyroidism, pheochromocytoma, sleep apnea, primary aldosteronism
Stimulation of alpha 1
Vasoconstriction of arterioles and veins
Stimulation of beta 2
Vaso dilation
Stimulation of beta 1
Increase in HR and contractility
What to avoid before BP readings
Smoking 30 minutes before and caffeine 1 hour before
Goals of BP treatment
<140/90 for general population
<130/80 for people with co-morbidities
Follow up every month until BP is at goal and then every 3-6 months
Tx for hypertension without compelling indications
Stage 1: thiazide diuretics for most; can consider ACEI, ARB, Beta blocker, calcium channel blocker
Stage 2: combination of drugs including a thiazide diuretic
Tx for hypertension for diabetics
ACEI or ARB
Can combine with calcium channel blocker, thiazide diuretic or beta blocker
Tx for hypertension for CKD
ACEI or ARB
Tx for hypertension for CAD
ACEI or ARB
+ Beta blocker if recent MI or angina
Tx for hypertension for heart failure
ACEI + beta blocker + loop diuretic
Tx for hypertension for African American
Thiazide diuretic or calcium channel blocker or combination
What to monitor with thiazide diuretics
Serum electrolytes, glucose, uric acid
Excessive fluid loss
Sexual dysfunction
What to monitor with calcium channel blockers
Headache, dizziness, peripheral edema, drug interactions (grapefruit juice, clarithromycin, erythromycin)
What to monitor with ACEI and ARBs
BUN, Cr, potassium
Thiazide diuretics
- MOA
- SE
- CI
Hydrochlorothiazide
inhibit reabsorption of Na + Cl in distal tubules
Takes several days for effect
Causes potassium and bicarb excretion but decreased Ca excretion
Causes uric acid retention
CI: Allergy to sulfa, anuria
Preg Cat B
SE: hypokalemia, hypomagnesia, hypercalcemia, hyperuricemia, hyperglycemia, tinnitus, paresthesia, N/V, diarrhea, impotence, hyperlipidemia, anorexia
Loop diuretics
- MOA
- SE
- CI
Bumetanide, furosemide, torsemide
Inhibits reabsorption of Na + Cl at proximal and distal tubules and loop of Henle
Indicated for edema d/t CHF, hepatic cirrhosis, renal disease
CI: anuric or severe electrolyte depletion and allergy to sulfa
Preg Cat C
SE: Hypocalcemia, hypokalemia, hypomagnesia
Reserved for patients with renal dysfunction over thiazide diuretics
Potassium sparing diuretics
- MOA
- SE
- CI
Amiloride, Spirinolactone
Interfere with sodium reabsorption at distal tubule, decreasing K+ secretion
True benefit for HF patients
CI: severe renal impairment, K+>5, acute renal insufficiency, anuria, Addison’s disease
SE: gynecomastia, hyperkalemia, hyponatremia, hirsutism, menstrual irregularities, drowsiness, confusion, headache, rash
First line diuretic for uncomplicated hypertension
Thiazide
Loop is second (especially if renal dysfunction)
Treatment considerations of potassium sparing diuretics
Use in combination with thiazides to augment diuresis and blunt hypokalemic effects
Beta Blockers MOA
Block central and peripheral beta receptors–results in decreased cardiac output and sympathetic outflow
Selective beta blockers
A-M
Better for patients with asthma, COPD, and peripheral vascular disease
At higher doses, lose cardioselectivity and may aggravate bronchospasm
Beta blockers with intrinsic sympathomimetic activity
Pindolol and Acebutolol
Reduce HR and contractility during excessive sympathetic outflow, but in resting states HR and contractility are maintained
Beta blockers in CHF
Decreases mortality and decreases vascular remodeling
Discontinue if patient has acute decompensation
Tapering of beta blockers
Taper gradually over 14 days when discontinuing to prevent withdrawal symptoms–unstable angina, MI, death
Beta blockers are CI in
Sinus bradycardia, asthma, COPD, AV block, cardiac failure, Severe PVD
Pregnancy category for beta blockers
Cat C
But best for lactation
In diabetic patients, beta blockers
Can mask all symptoms of hypoglycemia with the exception of sweating
ACE Inhibitors MOA
-pril
Inhibits ACE enzyme, which decreases production of angiotensin II (decreases vasoconstriction and decreases aldosterone effects of water retention)
Also inhibits degradation of bradykinin and increases synthesis of vasodilating prostaglandins
ACEI CI in
Bilateral renal artery stenosis + pregnancy (cat d)
SE ACEI
Chronic dry cough, rashes, dizziness, angioedema
ACEI decreases mortality in patients with
CHF, post MI, and systolic dysfunction
ARB’s MOA
-sartan
Block vasoconstriction and aldosterone secreting effects of angiotensin II by blocking angiotensin receptor
ARBs indicated for
Hypertension, nephropathy in type 2 DM, heart failure, those who can not tolerate ACEI
SE ARBs
Dizziness, upper respiratory tract infections, cough, viral infection, fatigue, pharyngitis, rhinitis
Red flags with ACEI or ARB’s
Swelling, SOB, difficulty swallowing, hives, uritcaria, fainting, cloudy urine ,sore throat, abdominal pain, irregular HR, leg weakness, numbness and tingling, extreme nervousness
Renin Inhibitors
Aliskiren
Blocks conversion of angiotensinogen to angiotensin I
CI in pregnancy (Cat X)
SE: diarrhea and rare angioedema
Ca channel blockers MOA
Inhibits movement of Ca ions across the cell membrane, which causes cardiovascular relaxation and vasodilation
CI in pregnancy Cat C
Non-dihydropyridine Ca Channel blockers
Verapamil + Diltiazem
Decrease HR + slow conduction at AV node
Avoid in patients with AV block and caution with heart failure
SE: GI upset, peripheral edema, hypotension
Dihydropyridine Ca channel blockers
-dipine
Potent vasodilators
SE: headache, flushing, palpitations, peripheral edema, gingival hyperplasia (nifedipine)
Recommended for use of ca channel blockers
Blacks, hypertension associated with ischemic heart disease, prinzmetal angina
Special factors of nifedipine
Cause potent peripheral vasodilation–most likely to cause peripheral edema
Special factors of amlodipine
Best for blacks, elderly, people with high cholesterol
Not likely to cause peripheral edema
Peripheral alpha 1 blockers
-zosin
Effective in BPH and not usually prescribed for htn
Dilates arterioles and veins
CI in presence of cardiovascular disease
Relaxes smooth muscle in bladder neck + prostate
SE: first dose phenomenon, vivid dreams and depression
Central alpha 2 agonists
Clonidine, methyldopa, guanabenz, guanfacine
Decreases release of NE
May cause fluid retention (can combine with diuretic)
Usually used in STAT management of htn
Do not abruptly stop
SE: fluid retention, sedation, dry mouth, dizziness, syncope
Direct vasodilators
Hydralazine + Minoxidil
Arteriolar smooth muscle relaxation
Reserved for essential or severe hypertension
May cause fluid retention and reflex tachycardia (combine with beta blocker and diuretic)
SE: dermatitis, drug fever, peripheral neuropathy
Direct vasodilators CI in
CAD, acute MI, aortic aneurysm
Adrenergic antagonists
Resperine, guanethidine, guanadrel
Inhibits SANS by decreasing NE stores
May cause depression
DOC for htn in pregnancy
Methyldopa
Medications used in hypertensive emergency
Hydralazine Nitrates Nicardipine + Clevidipine Labetalol + Esmolol Phentolamine Enalapril
Contributing factors to hyperlipidemia
Beta blockers, oral contraceptives, diabetes, pregnancy, diets high in fat and cholesterol, lack of exercise, obesity, smoking, hypertension, age
Chylomicrons
largest lipoproteins, composed mainly of triglycerides
Produced in the guy from dietary fat and cholesterol
VLDL
Composed of cholesterol and triglycerides
Converted to LDL when triglyceride content decreases
LDL
Contains mostly cholesterol
50% taken up by the liver and 50% taken up by the peripheral cells
Primary symptom of atherosclerosis
Angina–due to compromised blood flow
4 major statin benefit groups
- Have clinical atherosclerotic cardiovascular disease
- No disease but LDL >190
- No disease, 40-75 yo, DM, LDL 70-189
- No disease, 40-75 yo, LDL 70-189, 10 year risk of disease >7.5%
If patient is not having an expected response to statins…
Monitor every 3-12 months for continued assessment
Most common complaint with statins
Muscle related–increases risk of myopathy
If symptoms resolve after discontinuation and patient has no other CI, Restart the same statin at a lower dose or different statin at a low dose
Statin MOA
Block conversion of HMG-CoA to mevalonate–rate limiting step in production of cholesterol by the liver
Increases number of LDL receptors on liver
Decreases triglyceride levels and moderately increases HDL
Maximum effect after 4-6 weeks
Best to take at night time
Statin CI
Pregnancy, breastfeeding, active liver disease
Ezteimibe
Cholesterol absorption inhibitor at the brush border of small intestine; decreases delivery of cholesterol to liver and increases clearance of cholesterol from blood
Complements statins
Cholestytramine
Bile acid resins
Bind bile acids in the intestines to be excreted in feces–decreases return of cholesterol to the liver and increases LDL receptors
Increases triglyceride levels
Max effect seen in 3 weeks
Adjunct therapy to diet therapy
Not absorbed systemically–do not need to monitor liver levels
SE: bloating, abdominal pain, heartpain, constipation
Bile acid resins CI in
biliary obstruction, chronic constipation, triglycerides >300
Niacin
B vitamin–take in higher doses
Decreases VLDL synthesis, inhibits lipolysis in adipose tissue, increases lipoprotein lipase activity
Decreases triglycerides and LDL and increases HDL
Most people can not tolerate adverse effects–pruritus and flushing
Niacin CI
Hepatic dysfunction, severe hypotension, hyperglycemia, gout, A Fib, peptic ulcers
Baseline monitoring for niacin
Glucose and uric acid levels
Fibric acid derivatives
Gemfibrozil + Fenofibraic
Mainly affects triglycerides and HDL
CI in history of gallstones + severe hepatic/renal dysfunction
SE: Myopathy when combined with statins, hepatotoxicity, cholestatic jaundice, leukopenia, anemia, thrombocytopenia
First, second, third line for hyperlipidemia
First: statins
Second: cholesterol absorption inhibitors, niacin, bile acid resins
Third: fibric acid derivatives
S/S angina
Left sided chest pain, discomfort, heaviness or pressure, sensation radiating to back, jaw, neck, throat or arms lasting 1-15 minutes, SOB, fatigue
Modifiable risk factors for angina
Cigarette smoking, hypertension, dyslipidemia, diabetes, obesity, physical inactivity
Non-modifiable risk factors for angina
Age, heredity, men
Atherosclerosis pathophys
Fatty streak –> fibrous plaque –> complicated lesion
Nonpharmacologic therapy for angina
Decrease weight, smoking cessation, exercise
Drug choices for angina
ACEI/ARBs, nitrates, beta blockers, calcium channel blockers, antiplatelet therapy
What should you assess when starting someone on an ACEI or ARB
Renal function and serum potassium within 1-2 weeks of starting
ACEI + Lithium
Patients taking lithium and ACEI are at increased risk of toxicity due to decreased renal excretion
Nitrates MOA
Decreases preload through dilation of veins and decreases afterload by causing dilation of arteries
Increases blood flow and O2 supply to myocardium through artery dilation
SE: headache, flushing, dizziness, weakness, orthostatic hypotension, reflex tachycardia
Do not stop abruptly–can cause rebound hypertension
Sublingual nitroglycerine
Nitrol + Isordil
First line therapy for managing angina acutely
Relieves in 1-5 minutes
Long acting nitrates
Isosorbide Dinitrate, isosorbide mononitrate, nitroglycerine (transdermal)
Used for chronic prophylaxis of angina
Nitrate tolerance
Can occur in 7-10 days
Have one 10-12 hour nitrate free interval per day
CI combo of nitrate +
Phosphodiesterase-5 inhibitors (viagra)
Beta blockers particularly helpful for what type of angina
Exertional angina
Decreases HR + contractility which decreases the workload of the heart and decreases O2 demand
Aspirin
Irreversible enzyme antagonism to block prostaglandin synthesis–blocks formation of TAX-2
Recommended to take 75-162mg daily for patients with acute/chronic ischemic heart disease
SE: dyspepsia, bruising, bleeding
Clopidogrel
Decreases ADP induced platelet activation
First line, second line, third line for chronic prophylaxis angina
All patients should receive daily aspirin and short acting nitrate for acute attacks
First: beta blockers
Second: beta blocker + calcium channel blocker or long acting nitrate
Third: 3 drug combination
Highest risk factors for heart failure
CAD, hypertension, cardiomyopathy
Other risk factors: acute MI, arrhythmias, pulmonary embolism, sepsis
Drugs that may worsen heart failure
NSAIDs, steroids, hormones, antihypertensives, sodium containing drugs, lithium, amphetamines, cocaine, alcohol
S/S left sided heart failure
Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, nocturia
Cardiomegaly, S3 heart sound, signs of pulmonary edema, tachycardia, increased RR
S/S right sided heart failure
Peripheral pitting edema, abdominal pain, anorexia, bloating, constipation, nausea, vomiting
Hepatomegaly, distention of jugular veins, hepatojugular reflex, signs of portal htn, ascites, splenomegaly
4 levels of heart failure
- No limitation of physical activity
- Slight limitation; comfortable at rest
- Marked limitation; less than ordinary activity causes dyspnea
- Unable to carry out physical activity without symptoms; symptoms present at rest
In patients with a history of reduced ejection fraction, what can be used to prevent HF
ACEI or ARBs
In patients with an MI and reduced ejection fraction, what should be given to prevent HF
Beta blockers
Which ACEI have been shown to prolong survival for patients with LV dysfunction
Enalapril, Captopril, Lisinopril
ACEI for heart failure
indicated for patients who present with fatigue or mild dyspnea on exertion and who do not have any other signs of symptoms of volume overload
Decreases preload and afterload, increases cardiac index and increases ejection fraction
Diuretics for heart failure
Loop diuretics are more potent
Combine with ACEI and beta blocker
Decreases preload by reducing volume overload
Dose is increased until urine output increases and weight decreases
NSAIDs may decrease effects
May decrease lithium clearance
ARBs for heart failure
Decreases blood pressure, decreases vascular resistance, decreases pulmonary capillary wedge pressure, decreases HR, and increases cardiac index
Decreases HF exacerbation
Beta blockers for heart failure
Metoprolol, Bisoprolol, Carvedilol
All patients with stage 2-4 HF should receive
Should not be used in unstable patients or acutely ill patients
Symptomatic improvement may not be seen for 2-3 months
Digoxin
Can prevent clinical deterioration in patients with heart failure but does not decrease mortality
Mild inotropic effect by inhibiting cell membrane Na/K ATPase, increases Ca entry into the cell, and increases force and velocity of contraction
Must monitor renal function
Signs of digoxin toxicity
N/V, anorexia, headache, fatigue, disorientation, confusion, seizures, arrhythmias
Digoxin should be discontinued if the following occur
Elevated digoxin level, substantial reduction in renal function, toxicity symptoms, conduction abnormality, increase in arrhythmias
Drugs that will increase digoxin levels
Quinidine, amiodarone, flexainide, propafenone, spironolactone, verapamil, antibiotics, anticholinergics
Drugs that decrease digoxin levels
Antacids, cholestyramine, neomycin, kaolin-pectin
First, second, third line for HF
First: ACEI with or without a diuretic depending on fluid retention
Second: ACEI + beta blocker + diuretic (loop preferred)
Third: ARB + beta blocker + aldosterone antagonist + diuretic + digoxin
Pediatrics tx of HF
Class I: IV inotropes (not digoxin) + IV diuretics
Class II: + Digoxin
Class III: + O2
Monitoring for heart failure
Serum electrolyte levels, renal function, blood pressure, weights
Conditions that may cause arrhythmias
myocardial ischemia, chronic HF, hypertension, valvular heart disease, hypoxemia, thyroid abnormalities, electrolyte disturbances, drug toxicity, increased caffeine, increased alcohol, anxiety, exercise
Phases of cardiac AP
Phase 0: Rapid depolarization due to influx of Na
Phase 1: brief initial repolarization due to inactivation of inward Na and activation of outward K
Phase 2: plateau period no change in potential
Phase 3: repolarization due to K efflux
Phase 4: depolarization of cell with Na leaking into cell as K leaves
Catecholamine stimulation leads to
Shorter AP duration
Vagal stimulus and endogenous purines leads to
Inhibition of depolarization
After-depolarization
Abnormal impulse formation due to intracellular calcium overload
May occur in response to hypothermia, electrolyte imbalance, catecholamine excess, or stress
Supraventricular arrhythmias
Atria, SA and AV nodes
Not usually life threatening but can lead to decreased ventricular filling and decreased CO
Ex: sinus tachy, PSVT, sinus brady, A fib, A tach
Ventricular arrhythmias
Originate in ventricles or bundle of His
Usually symptomatic and require immediate intervention
Ex: Premature ventricular contractions, v tach, v fib, tdp
Risk factors for arrhythmias
Previous CAD, MI, cardiomyopathy, hypertension, valvular heart disease, alcohol or drug use
Class 1 AAD’s
Na channel blockers
Class 1A
Procainamide, quinidine, disopyramide
Intermediate onset/offset
Treatment of supraventricualr and ventricular arrhythmias
Widens QRS complex, prolongs QT and PR
Potent anticholinergic effects
Blocks alpha 1- can cause vasodilation and hypotension
SE: GI distress, tdp, hemolytic anemia, AV block, hypotension
Class 1B
Lidocaine + Mexiletine
Fast onset/offset
Decreases automaticity + conduction velocity + shortens refractoriness
Primarily effects ventricular myocardium–selective to ischemic tissue
Eliminated via liver
SE: CNS dizziness, paresthesia, disorientation, tremor, agitation
Class 1c
Flecainide + Propafenone
Slow onset and offset
Most used for supraventricular arrhythmias
Potent negative inotropic effects
SE: blurred vision, dizziness, headache, tremor, nausea, vomiting, bronchospasm, heart block, ventricular arrhythmias
Class 2 AAD
Beta blockers
Useful for ventricular and supraventricular arrhythmias
Helpful when combined with other AAD’s
Decreases O2 consumption, decreases HR, decreases BP, decreases contractility and CO
Class 3 AAD
Amiodarone, dronedarone, sotalol, dofetilide, ibutilide
K+ channel blockers
Used to treat a Fib primarily
Prolong QT interval
Amiodarone
Has characteristics of all 4 AAD classes
no negative inotropic effects
Approved for life threatening recurrent ventricular arrhythmias
Requires loading dose, large Vd and high lipophilicity–potential to accumulate and cause adverse effects in numerous organs
Perform thyroid function tests every 6 monyhs and assess pulmonary function annually
SE: optic neuritis, GI distress, tdp
Dronedarone
Shorter half life than amiodraone
CI in HF
No loading dose needed
Sotalol
Reverse use dependence effects
Can maintain SR in patients with A Fib
Eliminated by kidneys–assess renal function routinely
Most SE due to beta blocking ability
Class 4 AAD
Non-dihydropyridine calcium channel blockers
Verapamil + Diltiazem
Used for supraventricular arrhythmias
Slows conduction and prolongs refractoriness
Negative inotropic and chronotropic effect
CI in HF
Digoxin as AAD
Stimulates PANS–Increases vagal tone and slows conduction
Used primarily to slow ventricualr rate in supraventricular arrhythmias
Electrolyte imbalances that can precipitate digoxin toxicity
Hypokalemia, hypomagnesia, hypercalcemia
Adenosine
Converts PSVT to SR
Activates potassium channels – hyperpolarizes membrane, which decreases spontaneous nodal depolarization
Atropine
Enhances both sinus nodal automaticity and AV nodal conduction for use in symptomatic bradycardia
First line treatment for A Fib
Goal: control ventricular rate
If hemodynamically unstable, immediate DCC
If hemodynamically stable:
-Normal LV systolic function: IV diltiazem, verapamil or beta blocker
-EF<40%: IV beta blocker or digoxin
-IV amiodarone for ventricular rate control
Second line treatment for A Fib
If it persists, DCC or give warfarin as anticoagulant for 2-3 weeks and then cardioversion
PO diltiazem or verapamil or beta blocker or digoxin
Treatment of paroxysmal supraventricular tachycardia
If hemodynamically unstable: DCC or vagal maneuvers
DOC is adenosine
If persistent, try IV diltiazem, verapamil or beta blocker
Treatment of non-sustained ventricualr tachycardia
Terminates within 30 seconds; drugs not necessary if asymptomatic If symptomatic: beta blockers, non-dihydropyridine calcium channel blockers, class 1C AAD
Treatment for ventricular tachycardia
If unstable DCC
If stable: IV amiodarone, procainamide, or sotalol
After acute episode is terminated, ICD is indicated
Treatment for pulseless VT/VF
CPR + AED
If persists, vasopressor therapy with epinephrine
If persists, DOC is IV amiodarone
Treatment of bradycardia
IV atropine if s/s poor perfusion
If not effective, give dopamine or epinephrine through continuous infusion
Pediatrics and arrhythmias
Usually due to respiratory origin
PSVT is most common–occurs in children with congenital heart disease
Bradycardia is ominous sign in seriously ill children
What should you avoid when being treated with AAD
Licorice (Can cause hypokalemia), alcohol, excessive salt intake, caffeine
Venous thromboembolism
Venous thrombi form due to venous stasis, vascular endothelial wall injury, and hypercoagulability (virchow triad)
Risk factors for venous thromboembolism
Prolonged immobility, varicose veins, obesity, pregnancy, recent surgery, thrombophilia, central venous catheters, oral contraceptives, age >40
Source of 90% of pulmonary embolisms
Lower extremity DVT
Where do proximal DVT’s develop
in the popliteal, femoral or iliac veins above the knee
Atrial fibrillation
Loss of coordination of electrical and mechanical activity in the atria
Thrombi can form in the left atrial appendage due to impaired ventricle filling and incomplete emptying of the atria
Clot may travel to brain–stroke
Goals of tx of A Fib
Prevent TIA with anticoagulants, restore SR, control ventricular HR
Risk factors for developing stroke with A Fib
History of stroke, increased age, hypertension, HF with impaired systolic function, DM
Indications for prosthetic valve
Mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation
Valves in the mitral position are more thrombogenic than aortic
Mechanical prosthetics require lifelong anticoagulation
Final step in clotting cascade
Formation of thrombin (IIa), which converts fibrinogen to fibrin to form a clot
Platelets in clotting
Adhere to the site of injured blood vessels, attracting other platelets and forming large platelet aggregates that help stabilize the platelet-fibrin clot
When platelets are activated, receptors for clotting factors are exposed; this provides a stable environment for the initiation of the clotting cascade
Extrinsic pathway
Initiated by components from blood
Factor 7 is initiating factor
Intrinsic pathway
When blood comes into contact with a foreign surface, such as a prosthetic device
Factor 11 is initiating factor
Both clotting pathways converge at
Factor 10
Converts prothrombin to thrombin
Antithrombin III
Inhibits active clotting factors 2a, 7a, 9a, 10a, 11a, 12a
Protein C, S, Z
Prevent excess clot formation by inactivating 5a and 8a
Deficiency in these proteins creates a predisposition to pathologic thrombosis
Venous thrombi
Form in areas of sluggish blood flow and contain primarily red cells held together with fibrin
Arterial thrombi
Form in areas of high blood flow and are composed primarily of platelets bound with fibrin strands
S/S venous thromboembolism
Erythema, pain, swelling, venous distention, warmth
50% have no symptoms
Increased D-dimer >500
Diagnostic method of choice for DVT
Compression ultrasonography
S/S A fib
Palpitations, chest pain, SOB, weakness, decreased BP, dizziness, syncope, irregular pulse, irregular jugular venous pulsations
Absence of P waves
Diagnostic tests for ischemic stroke
Blood glucose, electrolytes, CBC with platelets, ECG, cardiac enzymes, prothrombin time, INR, aPTT, O2 saturation
Non contrast CT or MRI to diagnose
CI to anticoagulation
Recent hemorrhagic stroke, active major bleeding, recent trauma or surgery, immediate postop after CNS/ocular surgery, spinal catheters, aneurysms
Warfarin CI in pregnancy
Heparin indications
Treatment of acute venous or arterial thrombosis and prophylaxis of VTE
Un-fractionated Heparin MOA
Inhibits reactions that lead to clotting but does not alter concentration of normal clotting factors
Binds to antithrombin III and increases inactivation rate of intrinsic clotting cascade pathway (12, 11, 10, 9) and thrombin (2)
Prevents conversion of fibrinogen to fibrin
Can not inactivate clot-bound thrombin or activated factor X
Immediate onset
Must be given IV or SC
Limitations of un-fractionated heparin
Variability in size, highly bound to plasma proteins, some people have heparin resistance, can cause heparin induced thrombocytopenia
Lab monitoring for un-fractionated heparin
aPTT
Low molecular weight heparin
Dalteparin, enoxaparin, tinzaparin
Produce major effect via thrombin and factor X
Long half life than un-fractionated
SC administration
Less binding to proteins
Less intense lab monitoring and more predictable effect than un-fractionated
Lab monitoring for LMWH
Anti-Xa activity
Warfarin MOA
Inhibits activation of clotting factors in liver than depend on vitamin K: 2, 7, 9, 10 and protein C, Z, S
Does not affect function of existing clotting factors or thrombus
Long offset of effect–8-14 days for full effect (must heparinize initially)
Causes a quick fall in protein C–temporary hypercoagulable state
Long half life
Lab monitoring for warfarin
INR every 4-6 weeks
Narrow therapeutic index
Multiple drug-drug interactions
Direct acting oral anticoagulants
Dabigatran, rivaroxaban, apixaban, edoxaban
Faster onset than warfarin
Adv: Fixed dosing, no dietary interaction, no intense monitoring
Disadv: No antidote, more expensive, faster offset
Antidote of warfarin
Oral vitamin K, fresh frozen plasma, four factor prothrombin complex concentrates
Antidote of heparin
Protamine sulfate
Heparin induced thrombocytopenia
Anti-body mediated prothrombotic reaction
Diagnosed by ELISA antibody test
Discontinue heparin and give alternative anticoagulant
Anti-platelet agents indications
Prevention and treatment of stroke, add on therapy to anticoagulants, prevent CV death, MI, or stroke following acute coronary syndrome
Asprin MOA
Prevents prostaglandin synthesis in platelets by irreversibly inhibiting COX, which usually catalyzes conversion of arachidonic acid to TXA2)
Onset of effect is within 5 minutes
Effect lasts 7-10 days after discontinuing
Clopidogrel
Inhibits ADP, which is a promoter of platelet receptor binding
Extensively metabolized by liver from prodrug
Common SE is diarrhea
First line therapy for DVT or PE
Bolus IV of unfractionated heparin followed by continuous IV infusion
Injectable UFH/LMWH followed by warfarin or direct thrombin inhibitor for at least 3 months
First line therapy for prophylaxis of DVT or PE
For patients undergoing orthopedic surgery
LMWH, Warfain, direct oral anticoagulants, aspirin
First line for prevention of non-cardioembolic ischemic stroke and transient ischemic attack
First: aspirin
Second: Clopidogrel
First line therapy for stroke prevention in nonvalvular atrial fibrillation
Warfarin or direct acting oral anticoagulant
First line therapy for prophylaxis against systemic embolism in patients with prosthetic heart valves
Long term anticoagulation with warfarin alone or in combination with aspirin
Potential causes of anemia
Blood loss, nutritional deficiency, malabsorption syndromes, sickle cell disease, thalassemia, hemoglobinopathy, treatment of cancer, HIV, hepatitis C
Normal Hgb and MCV values
MCV: 80-96
Men Hgb: 13
Women Hgb: 12
S/S of rapid onset of anemia
Tachycardia, light headedness, breathlessness
S/S of chronic anemia
Fatigue, weakness, headache, vertigo, faintness, sensitivity to cold, pallor, loss of skin tone
Smokers normal RBC values
Higher than normal levels of RBC’s
Microcytic anemias
Thalassemia, iron deficiency, chronic disease, sideroblastic
Normocytic anemias
Acute blood loss
Macrocytic anemias
Folate or vitamin B12 deficiency
Immediate therapy for acute post-hemorrhagic anemia/chronic blood loss
Hemostasis, restoration of blood volume, treatment of shock with blood transfusion
Patients with sickle cell anemia are susceptible to
Infection, particularly strep pneumoniae and haemophilus influenzae
Important education for patients with sickle cell anemia
Folic acid supplementation and vaccinations
Hydroxyurea
Can be used for prophylaxis of sickle cell crises
Increases Hgb F, Increases water content of RBC, increases deformability of sickled cells and alters RBC adhesions
Do not use if pregnant
SE of hydroxyurea
Myelosuppression, risk of cancer, cutaneous hyperpigmentation, alopecia, xerosis, nail pigmentation, leg ulcers
Pain management for sickle cell crises
Hydration, aggressive pain relief with analgesics and opiates–NSAIDs, acetaminophen, morphine, hydromorphone
Causes of iron deficiency anemia
Deficient diet, decreased absorption, pregnancy and lactation, blood loss, chronic alcoholism
Can be exacerbated by chronic intestinal blood loss due to parasitic and malarial infections
Drugs that may cause iron deficiency
Fluoroquinolones, tetracyclines, H2 blockers, proton pump inhibitors, calcium supplements
Diagnostic lab findings in iron deficiency anemia
Decreased serum iron, decreased ferritin, increased TIBC, decreased Hgb, decreased Htc
Low ferritin is earliest and most sensitive indication
Treatment of iron deficiency anemia
Dietary supplementation and iron preparation
May take 6-8 weeks for hemaglobin to improve and 6 months to completely restore iron stores
SE iron supplements
Discolored feces, anorexia, constipation or diarrhea, N/V
What affects absorption of iron supplements
Vitamin C will increase
Milk and tea will decrease
Antacids, proton pump inhibitors and H2 antagonists will also decrease
Indications for use of IV iron
Chronic bleeding, intestinal malabsorption, intolerance to oral iron, nonadherence, hemoglobin <6 with signs of poor perfusion
Anemia of chronic renal failure
-Causes and Tx
Decreased EPO production by kidney due to decreased GFR
Give iron supplementation first, then treat reversible causes of decreased renal function, then give recombinant EPO
Diagnostic lab findings in anemia of chronic disease
Decreased serum iron, decreased transferrin, decreased TIBC
Tx of anemia of chronic disease
Increased doses of EPO administered subcu
Tx of thalassemia
If severe, regular transfusions and folate supplementation
Tx of vitamin B12 deficiency
Parenteral administration of B12–must receive every month for rest of life
Tx of folate deficiency
Oral folate replacement until numbers are restored
Tx for aplastic anemia
RBC transfusions and platelets given for bleeding, antibiotics given for infections
Severe forms may require hematopoietic stem cell transplant and immunosuppression therapy
Geriatric Hgb <10
Negative outcomes–decreased physical performance, increased number of falls, increased frailty, decreased cognition, increased dementia, increased hospitalizations, increased mortality
What makes fibric acid derivatives ineffective?
Alcohol
Antidote to dabigratran (direct acting oral anticoagulant)
Idarucizumab
Different types of iron supplements
Ferrous gluconate has less iron in it but causes less constipation than ferrous sulfate
Sickling causes patients to be at high risk for
Pain, infection, gall stones, renal failure
How long can you store B12 for
3 years
Deficiency is not an acute condition
Deficiency can cause permanent neurological issues
How long can you store folate for
3 months
Distinguish between folate and B12 deficiency
B12: increase in homocysteine and MMA
Folate: Increase in homocysteine onlu, normal MMA
What do antiretrovirals do
Inhibit transcriptase
Normal total cholesterol
Less than 200
Normal LDL
Less than 130
Normal triglyceride
Less than 150
Normal HDL
Over 40
Statins + calcium channel blocker requires
PT/INR monitoring due to risk of bleeding
What cholesterol medication should not be dosed with a statin
Fibric acid derivatives
Unless under the care of a cardiologist
Patient education for digoxin
Check HR before taking, routine lab work to check levels (dig toxicity and potassium)
1st line agent for heart failure
ACEI
Labs for hypertensive medications
Liver + renal, electrolytes
If experiencing bad peripheral edema with nifedipine, switch to
Amlodipine
If a patient has an allergic reaction to penicillin, give
Macrolide
What antibiotic to give if pregnant
Macrolide
Adenosine
Converts PSVT to SR
Activates potassium channels by increasing outward K+
current and hyper-polarizing membrane, which decreases spontaneous SA node depolarization
Amiodarone
Class 3 AAD: K+ channel blocking
Has properties from all 4 classes
Good for treating ventricular arrhythmias orimarily
Many toxic side effects: pulmonary toxicity, retinal toxicity, liver, and thyroid toxicity
Prolongs QT interval
DOC for lyme disease
Doxycycline
Where to place transdermal nitrate patch
Place away from the chest area–on the extremities
SE of gentamycin (aminoglycoside)
Ototoxicity
Furosemide may cause
Ototoxicity
If patient has not responded to penicillin or doxycycline
Give a fluoroquinolone
Concerns with levofloxacin
Neurotoxicity and tendon rupture
If a beta blocker is making a patient tired…
Can decrease the dose
Labs to monitor with statins
CK and kidney function
Liver function tests
Always treat hypertension with what first
Thiazide diuretic
Coronary artery spasm education
Give sublingual nitroglycerine up to 3 doses 5 minutes apart
