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CLIs OMS I Fall 2013
Block 2
MOSBY’S
Cholesterol (166 – 170)
•
Normal Findings:
Adult: <200 mg/dL
Child: 120-200 mg/dL
Newborn: 53-135 mg/dL
• -Needed for production of steroids, sex hormones, bile acids, and
cellular membranes
• -The main lipid associated with arteriosclerotic disease
• -Metabolized by the liver
• -75% bound inside LDL and 25% is in HDL
• - Main component of LDL (minimal in HDL and VLDL)
• - Testing is typically part of a lipid profile (by itself is not an accurate
predictor of heart disease)
• - Individual cholesterol levels can vary daily by 15%
• -Positional changes affect levels (15% decrease seen in lateral
recumbent position, often seen in hospitalized patients)
• -Repeat tests should be done for abnormal values and an average will
be established
• -Used to predict risk of CHD within the Framingham Coronary
Prediction algorithm (determines overall risk of ischemic event)
Cholesterol (166 – 170)
• Increased levels: liver disease, pregnancy, oorophorectomy,
postmenopausal status, familial hyperlipidemias or
hypercholesterolemias, hypothyroidism, uncontrolled
diabetes mellitus, nephrotic syndrome, xanthomatosis,
hypertension, atherosclerosis, biliary cirrhosis, stress
• Drugs that increase levels: adrenocorticotropic hormone,
anabolic steroids, beta-adrenergic blocking agents,
corticosteroids, cyclosporine, epinephrine, oral contraceptives,
phenytoin, sulfonamides, thiazide diuretics, and vit D
Cholesterol (166 – 170)
• Decreased levels: liver disease, malabsorption, malnutrition,
acute myocardial infarction (6-8 weeks following), advanced
cancer, hyperthyroidism, cholesterol-lowering medication,
pernicious anemia, hemolytic anemia, sepsis, stress,
• Drugs that decrease levels: allopurinol, androgens, bile saltbinding agents, captopril, chlorpropamide, clofibrate,
colchicine, colestipol, erythromycin, isoniazid, liothyronine,
MAO inhibitors, niacin, nitrates, and statins
Creatine kinase, pp. 199-202
•
•
Adult/elderly (values higher after exercise): 55-170 units/L (males); 30-135 units/L (females)
Newborn: 68-580 units/L
• Isoenzymes: CK-MM: 100%, CK-MB: 0%, CK-BB: 0%
This test is used to support the diagnosis of myocardial muscle injury…it
can also be used to indicate neurologic or skeletal muscle diseases.
CK is predominantly found in heart muscle, skeletal muscle, and brain…CK
levels elevate when muscles or nerve cells are damaged:
• Rise within 6 hrs. after damage
• Levels peak at 18 hours (if damage is not persistent)
• Return to normal in 2-3 days
Interfering Factors:
IM injections, strenuous exercise, early pregnancy, muscle mass
Drugs that cause increased CK levels: alcohol, amphotericin B, ampicillin,
anesthetics, anticoagulants, aspirin, colchicine, dexamethasone, lithium,
lidocaine, morphine, statins.
Creatine kinase, pp. 199-202
Electrophoresis is used to detect the 3 CK isoenzymes:
• CK-BB (CK1): Found predominantly in the brain and lung
• CK-MB (CK2): specific for myocardial cells.
• Rise 3-6 hrs. post-infarction, levels peak at 12-24hrs., return to
normal in 12-48 hrs.
• Do not usually rise with transient chest pain cause by angina, PE, or
CHF.
• Will see a rise in patients with shock, malignant hyperthermia,
myopathies, or myocarditis.
• CK-MB levels used to determine the appropriateness of thrombolytic
therapy (MI)
• CK-MM (CK3): makes up almost all of the circulatory total CK enzymes in
healthy people. Increases in CK-MM suggest skeletal muscle damage.
*See Chart p. 201—levels of Troponin, CK-MB, and Myoglobin
post-MI*
Creatine kinase, pp. 199-202
CK is the main cardiac enzyme used to detect MI…others used include: Lactic
dehydrogenase (LDH), and aspartate amino transferase (AST)
*See Chart p. 201—levels of Troponin, CK-MB, and Myoglobin post-MI*
AVOID IM injections in patients with cardiac disease (they cause elevated CK levels)
Interfering Factors:
IM injections, strenuous exercise, early pregnancy, muscle mass
Drugs that cause increased CK levels: alcohol, amphotericin B, ampicillin,
anesthetics, anticoagulants, aspirin, colchicine, dexamethasone, lithium,
lidocaine, morphine, statins.
D-dimer, pp. 215-216
• Normal Findings: <0.4 mcg/mL
• ELISA and ELFA test, (Enzyme-linked fluorescent immunoassay is faster and more reliable)
• D-dimer is used to identify intravascular clotting by assessing
both thrombin and plasmin activity. (Disseminated
intravascular coagulation).
• D-dimer is a fibrin degradation fragment that is made through
lysis of cross-linked (d-dimerized) fibrin. The D-dimer assay
provides a highly specific measurement of the amount of
fibrin degradation that occurs…normal plasma does not have
detectable amounts of d-dimer fragments.
D-dimer, pp. 215-216
• D-dimer may be used in combination with the Fibrin Degradation
Products assay for high sensitivity and specificity of disseminated
intravascular coagulation (DIC).
• Levels of D-dimer will increase during thrombolytic therapy of fibrin
clots and can be used to determine the duration of anticoagulant
therapy in patients with DVT.
• High D-dimer levels are associated with PE, DVT, sickle cell anemia,
and thrombosis of malignancy.
Factor V-Leiden, pp. 244-245
• Normal: Negative FVL
• The test is used to diagnose factor V-Leiden thrombophilia
• Factor V is an important factor in reaction 4 (common pathway) of
normal hemostasis. The term “factor V-Leiden” refers to an
abnormal form of factor V in which there is a specific glutamine to
arginine substitution at nucleotide 1619 in the gene of factor V.
• FVL is inactivated 10 times slower than regular factor V due to a
mutation in the site where protein C normally binds to deactivate
and breakdown factor V. Result: increased thombin generation and
a mild hypercoagulable state.
•
FVL is the most common hereditary blood coagulation disorder in the US.(5% of Causcasian, 1.2% of Black
Americans). Only about 10% of patients with FVL experience a thrombotic event.
•
Testing for FVL is sometimes preceded by a screening coagulation test called the activated protein C (APC)
resistance test, used to identify the resistance of factor V to activated protein C.
Factor V-Leiden, pp. 244-245
• Individuals who are candidates for FVL testing include those
who have:
•
•
•
•
•
•
Experienced a thrombotic event without any predisposing factors
A strong family history of thrombotic events
Experienced a thrombotic event before 30 years of age
Experienced DVT during pregnancy or while on birth control pills
Had venous thrombosis at usual sites
Experienced an arterial clot
Lipoproteins, pp. 356-361
• Lipoproteins Should be collected after a 12-14 hour fast.
• Measured and classified by their density.
• Interfering Factors: smoking and alcohol ingestion decrease HDL,
binge eating alter lipoproteins, HDL values are age and sexdependent, HDL values (similar to cholesterol) decrease for 3
months post-MI, elevated HDL in hypothyroid, high triglyceride
levels make LDL calculations inaccurate.
• General Categories:
• Chylomicrons-carry TAGs from the intestine à liver, skeletal muscle, adipose
tissue
• VLDLs- carry newly synthesized TAGs from liver adipose tissue. VLDLs are the
predominant carriers of triglycerides. To a lesser degree, VLDLs are also
associated with increased risk of CAD because they can be converted to LDL
by lipoprotein lipase in skeletal muscle.
• IDLs- intermediates between VLDLs and LDLs, not detectable in blood
• LDLs- carry cholesterol from liver cells of the body. “bad cholesterol”
• HDLs- collects cholesterol from the body’s tissues and brings it back to the
liver, protective effect against heart disease. Out of the 5 subclasses of HDL,
only 2b is cardioprotective
Lipoproteins, pp. 356-361
• Risk for Coronary Heart Disease Based on Ratio of Cholesterol to
HDL
• High levels of LDLs are atherogenic…target levels vary according to
risk profile of patient (see p. 359). LDL= total cholesterol- ((TGs/5)HDL). SGGE divides LDL into 7 classes based on particle size. IIIa and
IIIb are the most commonly elevated forms, IVa and IVb are
associated with aggressive arterial plaques (nearly all patients with
IVa and IVb levels greater than 10% of total LDL have a
cardiovascular events within months!)
• LDL patterns have been identified to assess risk of CAD:
• (LDLs can be lowered with diet, exercise, and statins)
• LDL Pattern A: mostly large LDL particles, no increased risk for coronary
artery disease (CAD)
• LDL Pattern B: mostly small LDL particles associated with increased risk for
CAD
• Intermediate pattern: small and large LDL molecules, carries an intermediate
risk.
Lipoproteins (356 – 360)
• Lipoproteins- accurate predictor of heart disease
• -Proteins in the blood whose main purpose is to transport
cholesterol, triglycerides, and other insoluble fats
• -Used as markers to indicate the levels of lipids
Risk of CHD
Male
Female
½ the average
3.4
3.3
Average (3:1)
5.0
4.4
2x average (moderate)
10.0
7.0
3x average (high)
24.0
11.0
Risk for Heart Disease
Male
Female
High
60 mg/dL
70 mg/dL
Moderate
45 mg/dL
55 mg/dL
Low
25 mg/dL
35 mg/dL
Prothrombin time (448-451)
• Adequacy of extrinsic system and common pathway
• Activation of factor X in the presence of factor V and
phospholipid and calcium
• Stimulates platelet aggregation and converts fibrinogen to
fibrin in clot stabilization
• Tests:
• Factors I (fibrinogen), II (prothrombin), V, VII, and X
PT
• Hepatocellular liver disease (cirrhosis, hepatitis, neoplastic
invasive processes) Factors I, II, V, VII, IX, X
• Obstructive biliary disease bile necessary for fat absorption
decreases A,D,E and K are all fat soluble. II, VII, IX, X all dependent
on vitamin K, differentiate from liver disease because it responds
to vitamin K
• Coumarin ingestion (warfarin) interfere with vitamin K associated
factors; effects long lasting, can be fixed by vitamin K. Monitors
warfarin tx.
PT and INR
• Evaluate extrinsic and common pathway
• Fibrinogen, prothrombin, V, VII, X
• Decreased levels: hepatocellular disease affect factors I, II, V, VII, IX,
and X
• Obstructive biliary disease causes fat malabsorption A, D, E, and K
affected
• Coumarin (warfarin) ingestion
• INR is a stardardized ratio to correct for laboratory, environmental
variations in clotting time, unrelated to sample quality.
• Warfarin interferes with vitamin K may be enhanced by aspirin,
quinidine, sulfa, and indomethacin
• Barbituates, chloral hydrate and oral contraceptives cause increased
coumarin drug binding decreasing the effects
• Alcohol can prolong
• Diet high in fat or leafy vegetables may shorten OT
• Diarrhea or malabsorption can prolong
Partial thromboplastin time (PTT)
• Assess the intrinsic system and common pathway of clot
formation and to monitor heparin therapy
• First phase of reactions is intrinsic system: factor XII forms
complex on subendothelial collagen
• Extrinsic factors include thromboplastin
• Prothrombin becomes thrombin converts fibrinogen to fibrin
• Plasmin degenerates
• Evaluates fibrinogen II (prothrombin, V, VIII, IX, X, XI, and XII
• If any of these exist in inadequate quantities then PTT is
prolonged
PTT
• Vitamin K deficiency can prolong PTT II, IX, and X are
dependent
• Coag factors are made in the liver so hepatocellualr disease
will prolong
• Heparin inactivates prothrombin (II) not thromoplastin
• Monitor heparin whose effects are short-lived if too much is
given protamine sulfate can reverse
PTT
• Assess the intrinsic and common pathway of coag
• Evaluates fibrinogen, prothrombin, V, VIII, IX, X, XI, and XII
• Hepatocellular disease prolongs PTT and obstruction which
precludes GI absorption of fat soluble vitamins prolongs time
• Heparin prolongs PTT so it is used for therapy monitoring
• Antihistamines, ascorbic acid, chlorpromazine, heparin and
salicylates prolong PTT
• Early DIC and extensive cancer causes decreased levels
Triglycerides (521 – 522)
Adult: Male 40-160 mg/dL
Female 35-135 mg/dL
Critical: >400 mg/dL
•
•
•
•
•
•
-Produced in the liver using fatty acids and glycerol
-Transported by VLDL and LDL
-When levels are high, triglycerides are deposited in fatty tissues
-Constitute most of the fat of the body
-Measured as part of a lipid profile
Indications: TGs identify the risk of CHD. This test, along with
Lipoproteins and Cholesterol create the lipid profile for the patient.
This test may also be used to detect fat metabolism disorders.
• Test explanation: TGs are circulating fats in the blood that are
attached to VLDL or LDL, act as a storage source for energy. When
TG levels in the blood are high, TGs are deposited in the fatty
tissues.
Triglycerides (521 – 522)
• Increased levels: ingestion of fatty meals, alcohol, pregnancy, glycogen storage disease,
apoprotein CII deficiency, hyperlipidemias, hypothyroidism, high carb diet, nephrotic
syndrome, chronic renal failure
• Drugs that may increase levels: cholestyramine, estrogens, and oral contraceptives
• Decreased levels: malabsorption, malnutrition, abetalipoproteinemia, hyperthyroidism
• Drugs that may decrease levels: ascorbic acid, asparaginase, clofibrate, colestipol, fibrates,
and statins
• Interfering factors:
•
•
•
•
•
ingestion of fatty meals can cause elevated TG levels
ingesting alcohol causes increased VLDL levels, which increases TG
Pregnancy causes increased levels
Drugs causing increased TG levels: estrogen, oral contraceptives, cholestyramine
Drugs causing decreased TG levels: ascorbic acid, asparaginase, clofibrate, fibrates, statins.
Troponins, pp. 530-532
• Normal Findings: Cardiac Troponin T: <0.2 ng/mL
• Cardiac Troponin I: <0.03 ng/mL
• This test is performed on patients experiencing chest pain to
determine if the pain is caused by cardiac ischemia. It is a
specific indicator of cardiac muscle injury.
• Cardiac troponins are biochemical markers for cardiac disease
and can actually be used in patients with unstable angina to
determine the likelihood of a cardiac event. Their sensitivity
and specificity are similar to that of CK-MB (but troponins are
even more sensitive)—Cardiac troponin levels become
elevated as early as 3 hrs. post-myocardial injury and stay
elevated for 7-14 days (7-10 days for troponin I, 10-14 days
for troponin T)
•
ELISA method w/monoclonal Abs—fast, can be done bedside.
Troponins, pp. 530-532
• If reinfarction is suspected, troponins may not be as helpful
because levels could still be elevated from the first ischemic event.
[Stay elevated longer than CK-MB]
• Cardiac troponins are useful for the following situations:
•
•
•
•
•
•
Evaluation of patient with unstable angina
Detection of reperfusion associated with coronary recanalization
Estimation of MI size
Detection of perioperative MI
Evaluation of severity of PE
Congestive heart failure
• Interfering factors: Troponin T levels are falsely elevated in dialysis
patient.
Oximetry (1173-1174)
• >95% is normal
• Monitors arterial oxygen saturation in patients at risk for
hypoxemia. Surgery, cardiac stress testing, mechanical
ventilation, heavy sedation, lung function testing or trauma
• Non-invasive measures how many hemoglobin have oxygen
attached to them
• Fetal oxygen saturation monitoring: if heart is in distress but
saturation is fine you can avoid c-section, placed on cheek
between 30 and 70%
Radiology 101:Pages 16-23
Reading frontal chest x-ray
• Designed to look at lungs, not trauma to the ribs etc.
• R marker should be on your left side
• Glance over the image for any obvious abnormality always
look at your four corners
• Anterior posterior and posteroanterior
• Start at top and make sure trachea is midline
• Move to heart, transverse diameter of cardiac silhouette
should not be more than 50% transverse diameter of
thoracic cage
• Greater the distance between and object and film, the greater
the magnification
Radiology 101:Pages 16-23
Frontal chest X-ray (continued)
• Right heart convex, left cardiac border at the top should be
concave
• Left ventricle makes up left heart
• SVC makes straight right border
• In enlargement left superior border becomes convex
• Left enlargement cardiac apex moves down and out
• Right enlarges right border is more protuberant
• Left and right pulmonary arteries form hilar shadows, left
should be more cephalad
• Aorta forms knob
• Aortopulmonary window between knob and pulmonary
artery shadow; should be concave or suspect mass or
adenopathy
Radiology 101:Pages 16-23
Frontal chest X-ray (continued)
• Mediastinum shadow is caused by great vessels and vascular
pedicle
• Pedicle extends from thoracic inlet to base of heart; right
border is SVC left is aortic knob
• Divide lungs into horizontal thirds
• Domed diaphragm with right side higher than left
• Lateral costophrenic angles should be sharp and acute
• Look at lower cervical spine and ribs
• Ribs we see are posterior arcs anterior ribs are angled
downward
Radiology 101:Pages 16-23
Lateral radiograph
•
•
•
•
•
Right ventricle is anterior border
Left ventricle is inferior-posterior cardiac border
Left atrium forms superior-posterior cardiac border
IVC can be seen as it enters from abdomen
If left ventricle is 2 cm or more posterior to IVC then it is
enlarged
• Evaluating hila left is posterior to line drawn down from
tracheal air column and one third the size of the right
• Silhouette sign when two objects of similar density are in
direct juxtaposition interface or borders are lost
DRUGS TO KNOW
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Aspirin
(ASA)
Prophylaxis against transient
ischemic attack, MI, acute
coronary syndrome, prevent
reocclusion, arthritis, mild pain
or fever
GI bleeding, acute renal
insufficiency,
thrombocytopenia, Reye dz,
asthma, tinnitus, dyspepsia,
occult bleeding, prolonged
bleeding, rash
NSAID induced sensitivity,
chickenpox of flu like symptoms,
G6PD deficiency
Bleeding like hemophilia, von
Willebrand thrombocytopenia
Inhibit both Cox 1 and 2
Use cautiously with GI
bleeds impaired renal
function, vit K deficiency,
purpura, hepatic
impairment
MOA-Inhibits
synthesis of
prostaglandin by
cyclooxygenase;
inhibits platelets
aggregation; has
antipyretic (antifever) and
analgesic activity.
Metabolized by
the liver.
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Atenolol
HTN, angina, thyroid storm, HF
AV block, bradyarrythmia,
sedation, decreased libido,
mask hypoglycemia,
depression, dyspnea,
wheezing
Bronchial asthma, COPD,
cardiogenic shock,
decompensated heart failure, 2nd
and 3rd degree AV block, severe
sinus bradycardia
Beta one selective
adrenergic antagonists
MOA: Blocks
response to betaadrenergic
stimulation; cardio
selective for beta 1
receptors at low
doses with little to
NO effect on beta
two (safer in
asthmatics)
Limited
metabolization in
liver.
Beta-blocker (B1
specific)
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Atorvastatin
Pg 330
Class: Inhibitor of cholesterol
synthesis (Statin)
Mech: inhibits HMG-CoA
reductase
Indications:
•
Hypercholesterolemia
•
Familial
hypercholesterolemia
•
Coronary
atherosclerosis
•
Prophylaxis for coronary
aterosclerosis
•
• Active liver disease
• Pregnancy and lactation
• Up to 60% dec. in LDL
• 10% HDL increase
• 40% Triglyceride dec.
MOA: HMG-COA
reductase
inhibitor, inhibits
rate-limiting step
in cholesterol
biosynthesis by
competitively
inhibiting HMGCOA reductase
•
•
•
•
Myopathy-increased
risk
Rhabdomyolysis
Hepatotoxicity
Abdominal pain
(constipation,
diarrhea, nausea)
Headache
• Drug of choice
for lowering LDL,
one of the most potent
• Metabolism by P450
3A4
• Combo with bile acid
sequestrant yields
lower LDL
• Co-admin with Niacin->
inc. risk of myopathy
• Co-admin with
gemfibrozil can induce
rhabdomyolysis
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Atropine
Anticholinergic Agent,
Anticholinesterase
overdose, bradycardia,
excessive salivation and
mucus production during
surgery
Narrow Angle glaucoma
marginal nicotinic effect;
more effective at reversal
of exogenous rather than
endogenous cholinergic
activity
parasympathetic
sites in smooth
“No See, No Pee, No Spit,
No Sh*t”
Blurry vision,
xerostomia (dry mouth),
constipation, urinary
hesitancy, increased
IOP, loss of taste,
hypotension, confusion,
coma, ataxia, insomnia,
headache,
muscle, CNS, and
secretory glands.
Actions of PNS inhibited
MOA: Antimuscarinic;
inhibits action of
acetylcholine at
Increases cardiac
output and dries
secretions.
Metabolized: Liver
Drug
Uses
Side effects
Contraindications
Therapeutic
considerations
Clopidogrel (Plavix)
ACS, recent MI, stroke,
peripheral artery disease, CAD,
cardioembolic stroke
1-10% URI, chest pain,
headache, flu like syndrome,
arthralgias, pain, dizziness,
diarrhea, depression, rhinitis,
rash, UTI <1% neutropenia,
acute liver failure, TTP,
hypotension, hepatitis,
myalgia, eczema
Active bleeding disorder
Needs loading dose. Less
side effects tha ticlopidne
MOA: Inhibitor of
adenosine (ADP)induced pathway
for platelet
aggregation.
Metabolized in
liver by CYP450
enzymes.
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Eptifibatide (integrelin)antiplatelet agent
Acute coronary syndrome,
percutaneous coronary
intervention
Major bleeding,
intracerebral hemorrhage,
hypotension, bleeding
History of bleeding, recent
major surgery, recent
stroke, intracranial
hemorrhage, uncontrolled
hypertension
Don’t give with second ,
second anti GIIb-IIIa agent,
minimize arterial and
venous puncture, synthetic
peptide as parenteral
MOA: blocks binding of
fibrinogen & von
willebrand factor of
glycoprotein IIB/IIIA
receptor on platelet
surface.
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Heparin- Anticoagulant
Prevent embolism,
thrombosis, prevent
systemic embolism with
MI, unstable angina, open
heart surgery, DIC,
maintain patency IV cath
Hemorrhage, heparin
induced
Heparin induced
thrombocytopenia, active
major bleeding, bleeding
tendencies, open
ulcerative wounds,
conditions that increase
capillary permeability,
severe HTN, bacterial
endocarditis
Unfractionated
causes
thrombocytopenia
more than LMW,
MOA:
Low dose: inactivates
factor Xa and inhibits
conversion of
prothrombin to thrombin
High dose: inactivates
factor IX, X, XI, & XII and
thrombin and inhibits
conversion of fibrinogen
to fibrin
Also inhibits activation of
factor VIII
thrombocytopenia,
hypersensitivity, prolonged
clotting time, mucosal
ulceration, hematoma
antihistamines, cardiac
glycosides, nicotine and
tetracycline affect ability
Cephalosporins, penicillins,
oral anticoagulants,
platelet inhibitors may
increase affects
Don’t use ginger, garlic,
ginkgo
Drug
Clinical app
Adverse effects
Contraindications
Isosorbide mononitrate
Prophylaxis of angina,
treatment of chronic
ischemic heart disease
Refractory hypotension,
palpitations, tachycardia,
syncope, flushing,
headache
Severe hypotension, shock
or acute MI with low left
ventricular filling pressure,
increased intracranial
pressure, angle closure
glaucoma, co
administration of
phosphodiesterase
inhibitor type V [These are
viagra and it’s relatives ]
Class: Nitrate
MOA- Donate NO, which
activates guanylyl cyclase
and increase
dephosphorylation of
myosin light chain in
vascular smooth muscle,
causing vasodilation.
Therapeutic considerations
venous dilation greater
than arterial, can lead to
tolerance
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Metoprolol (Lopressor) –
Beta Blockers, Beta 1
selective
AMI, CHF, HTN, Angina,
Hyperthyroidism, Acute
Tachy,
Side Effects: 1-10%
Dizziness, headache,
tiredness, depression,
diarrhea, pruritus,
dyspepsia, heart failure,
wheezing, nausea
Asthma or COPD,
cardiogenic shock,
Decompensated cardiac
failure, 2nd & 3rd degree
AV
Beta 1 selective adrenergic
antagonists
MOA: Blocks response to
beta-adrenergic
stimulation; cardio
selective for beta 1
receptors at low doses
with little to NO effect on
beta two (safer in
asthmatics) [B2 are in
bronchiole smooth muscle,
blocking causes
bronchoconstriction]
Metabolized in liver by
CYP2D6
.
Drug
Clinical app
Adverse effects
Contraindications
Therapeutic considerations
Nitroglycerin
(Nitrostat) – Nitrate
Short acting, short term
treatment of acute anginal
attacks
Refractory hypotension,
palpitations, tachycardia,
syncope, flushing,
headache
Severe hypotension, shock or
acute MI with low left
ventricular filling pressure,
increased intracranial
pressure, angle closure
glaucoma, co administration
of phosphodiesterase
inhibitor type V,
transdermal contraindicated
in patients allergic to skin
tape, IV contraindicated in
tamponade, restrictive
cardiomyopathy, constrictive
pericarditis
Preferred due to longer
half life, better absorption,
nonsusceptibility to
extensive first pass, less
rebound angina, greater
efficacy, venous dilation
greater than arterial, can
lead to tolerance
shorter half life than
isosorbide mononitrate
Nitrate enters vascular
smooth muscle and
converted to Nitric Oxide
(NO) leading to activation
of cGMP and vasodilation,
thus also reducing
preload.
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Ramipril (Altace) – ACE
Inhibitor “End in pril”
Hypertension, heart
failure, diabetic
nephropathy, myocardial
infarction
>10% Cough (if cough
switch to an ARB),
hypotension, 1-10%
headache, angina,
dizziness, N/V, postural
hypotension, syncope,
vertigo, <1% angioedema
Hx of angioedema,
bilateral renal artery
stenosis [They depend on
RAA axis for renal
perfusion], renal failure,
pregnacny
3 patterns of metabolism:
1) active drug --> active
metabolite 2)prodrug ->active drug 3) active drug
and excreted unchanged.
MOA: Competitively
inhibits angiotensinconverting enzymes,
resulting in decreased
plasma angiotensin II
concentrations; BP may be
reduced in part through
decreased vasoconstriction
increased renin, activity,
and decreased aldosterone
secretion; increases renal
blood flow
Cough and
angioedema are
caused by
bradykinin action:
potentially lifethreatening. Delay
progression of
cardiac contractile
dysfunction in heart
failure and after MI,
and delay progression
of diabetic
nephropathy
Drug
Clinical app
Adverse effects
Contraindications
Therapeutic considerations
Simvastatin
(Zocor) – Lipid Lowering
Agent, Statin
Hypercholesteremia,
familial, coronary
atherosclerosis,
prophylaxis for coronary
atherosclerosis
Myopathy,
rhaddomyolysis,
hepatotoxicity,
dermatomyositis,
abdominal pain,
constipation, diarrhea,
nausea, headache
Active liver disease
pregnancy and lactation
Lowering LDL metabolized by
P450, 3A4 inhibitors increase
risk of myopathy, combo with
bile acid sequestrant or
cholesterol absorption
inhibitor additive decrease in
LDL, combo with niacin
maybe used in high LDL and
low HDL increases risk of
myopathy, gemfibrozil
decreases statin clearance
induce rhabdo
MOA: HMG-COA reductase
inhibitor, inhibits ratelimiting step in cholesterol
biosynthesis by
competitively inhibiting
HMG-COA reductase
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Tissue plasminogen
activator (t-PA) (Alteplase,
Activase) – Thrombolytics
AMI = acute MI, PE, Acute
Ischemic Stroke
pulmonary edema, arterial
embolism, bleeding, DVT,
hypotension, intracranial
hemorrhage, stroke, fever,
chills, N/V, sepsis, shock
Internal bleeding,
intracranial/spinal
trauma, surgery, masses,
recent stroke,
uncontrolled hypertension
Binds to newly formed
thrombi with high affinity,
causing fibrinolysis at the
site of a thrombus
Can generate a systemic
lytic state and cause
unwanted bleeding
MOA: Recombinant
human tissue-type
plasminogen activator (tpa); produces local
fibrinolysis. Promotes
thrombolysis by
converting plasminogen to
plasmin which degrades
fibrin and fibrinogen.
Drug
Clinical app
Adverse effects
Contraindications
Therapeutic considerations
triamterene/
Hydrocholorothiazide
(Maxide,Dyazide) – Thiazide
Combos, HTN
HTN, adjunct in
edema states
associated with HF,
cirrhosis, renal
dysfunction,
corticosteroid and
estrogen
Arrhythmia, stevens-johnson,
pancreatitis, hepatotoxicity,
SLE, hypotension, alkalosis,
vasculitis, photosensitivity,
electrolyte abnormalities,
impotence, restlessness,
blurrred vision, headache,
hyperglycemia, hyperuricemia
Anuria, hypersensitivity to
sulfonamides, co
administration with agents
that prolong QT
First line in treating HTN,
diminish hypercalcuria in
patients at risk for
nephrolithiasis, decreases
glucose tolerance may
unmask diabetes, don’t
use with antiarrhythmic
Triamterene – Direct effect on
renal distal tubule to inhibit Na
reabsorption. Inhibits Na/KATPase, decreases Ca and MG
and hydrogen excretion
=Postassium sparing diuretic
HCTZ- inhibits Na reabsorption in
distal renal tubules; results in
increased excretion of Na and
water also K and H ions.
-is a sulfa drug
Drug
Clinical app
Adverse affects
Contraindications
Therapeutic
considerations
Warfarin (Coumadin) –
Anticoagulants
Venous Thrombosis, DVT,
Afib, Cardiac Valve
Replacement, Post MI
1-10% Intraocular
Hemorrhage, UNK Freq –
abd pain, rash, pruritus,
tissue necrosis, headache,
lethargy, anemia,
hemorrhage, fever, purple
toe syndrome,
Pregnancy, Hemorrhage,
Bleeding tendency,
uncontrolled Hypertension
Monitor with PT/INR.
Many drug-drug
MOA: Interferes with
hepatic synthesis of
vitamin K dependent
clotting factors II, VII, IX, &
X as well as proteins C and
S.
interactions, never
give to pregnant
woman, can cause skin
necrosis, receive fresh
frozen plasma if
hemorrhaging occurs