Glossary of Drug flashcards for Second Semester Pharm

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Ferrous Sulfate- Use
2. Toxicity
Oral Treatment for Iron Defieciency
2. Acute-Children (10 tablets), treat with whole bowel irrigation or Defoxamine Chronic- Hemochromatosis
Iron Dextran-Use
Injectable from used for iron deficiency
Injectable form used for people with kidney disease on top of iron definiency.
Inactive form of b12 that has a longer half-life and is more bound to plasma proteins. Given parenterally. Patient has a lifetime of once a month injections.
Folic Acid-Absorbed where?
2. Stored?
3. Excreted?
4. Deficiency?
5. Enzyme Cofactor for?
6. Cancer?
2. Liver
3. Urine and stool
4. Inad. dietary intake(organic meats, beans, green veggies) alcoholics, poor diet adn reduced absorption
5. Dna syn, b12 methionine prod. purine synthesis
6. Methotextrate blocks folate reductase to tetrahydrofolate.
Epoetic Alpha-Use
Problem solved-given with what?
Recombinant human erythropoietin
used to treat low levels of EPO. (chronic renal failure, can be given with iron and sulfate, given IV and subcutaneous)
Filgastrin (G-CSF)-Uses
2. Toxicity
3. Half-life
Used to stimulate proliferation of neutrophils. Given for severe neutropenia,
2. Can cause bone pain
3. 2-3 hours
Sargramosim (GM-CSF)
Used to stimulate macrophages and neutrophils. Wider range of action, can stimulate stem cells
conjugation product of filgastrin and polyethylene glycol with much longer half-life (15-80 hours)
A 20-yr-old female complains of lethargy and is found to have a blood hemoglobin concentration of 10 g/dl (normal = 12-16g/dl), a low mcv and a low mean corpuscular hemoglobin concentration
Ferrous sulfate
A 54-yr-old female exhibits severe neutropenia following a course of doxorubicin therapy for breast cancer
A 65-yr-old female with progressive fatigability and anorexia is found to have a low blood hemoglobin concentration and an elevated mean corpuscular volume, and an elevated serum concentration of methylmalonic acid.
A 64-yr-old male with diabetic neuropathy and end-stage renal disease exhibits peripheral reticulocytopenia and anemia.
What are some reasons why Fe supplementation may not correct anemia?
Anemia may not be due to iron deficiency, can't give in hemolytic anemia
How does Iron get from the burger to the RBC? What might decrease amount of Fe from burger?
iron is absorbed from the duodenum and proximal jejunum. Fe 2 best absorbed, reduced form, ready to bind to oxygen. Transferrin takes iron to RBC's.
small, hemoglobin deficient RBC.
Macrocytic anemia- B12 or folate deficiency. Accumulation of large RBC precursor cells.
What to do if give too much iron?
Give deferoxamin or do a whole bowel irrigation.
What is the methylfolate trap?
b12 is needed to convert n5methyltetrahydrofolate into tetrahydrofolate (active form)
n5methyltetrahydrofolate builds up due to low b12
Hydroxocbalamin is most effective given how?
Hydroxocobalamin is best given parenterally due to normal problems with absorption.
What does rHuEpo do? When is it indicated?
Indicated in chronic renal failure, cancer patients, bone marrow, aids or cancer. Stimulates bone marrow to make more rbcs.
What are some adaptations to chronic anemia?
tachycardia, increased cardiac output, vasodilation
Warfarin?? Action
Adverse effects
Oral, Blocks vitamin K reductase and prevents carboxylation of clotting factors. Strcture similar to Vitamin K. Hemorrhage, Fetal abnormalites (fetal warfarin syndrome, chondrodysplasia punctata.
What drugs increase Pt (longer to clot)
1. Cimetidine (inhibit metabolism)
2. Aspirin (high dose)
3. Cephalosporins (kill bacteria)
4. Heparin, Hepatic Disease (less clearance
What drugs decrease Pt?
1. Barbituates (decrease hepatic enzymes)
2. Rifampin
3. Diuretics
4. Vit K
5. Heriditary resistance
Uses of warfarin?
Atrial Fib
Artificial heart valves
Stroke or MI prevention
Heparin? Action

Adverse effects
NOt absorbed orally given IV or subcut, Binds and inactivates AT-III, inactivates activated clotting factors (thrombin, 10, and others) IMMEDIATE
Hemorhage (elderly, renal failure) thrombocytopenia (antibody causes aggregation), hyperkalemia (inhibits aldosterone), osteoporosis
Clinical uses of Heparin?
Acute thromboembolism (venous thrombosis, pulmonary embolism, DIC) also-cardio surgery, a-fib, renal dialysis, blood transfusion
Treatment of Heparin overdose?
STOP heparin, give protamine sulfate, fresh frozen plasma
What is fondaparinux?
A synthetic pentasaccharide heparin
What is enoxaparin?
LMWH(less effective than HMW, but has a greater bioavailability and works selectively at 10a INDERECT
What is dalteparin?
LMWH(less effective than HMW, but has a greater bioavailability and works selectively at 10a and AT III DOES NOT WORK AT Thrombin, INDERECT
What is ximelagatran?
Direct thrombin inhibitor but banned due to liver toxicity.
What is bivalirudin?
Direct thrombin inhibitor, synthetic peptide, blocks at the catalytic site and at the substrate recognition site. Used for acute coronary syndrome
What is argatroban?
Direct thrombin inhibitor, used for heparin induced thrombocytopenia, DOES NOT CROSS THE PLACENTA.
What is protamine sulfate?
Given to stop bleeding from too much heparin, antagonizes heparin
Action of aspirin?
Blocks platelet aggreagation by inhibiting TXA2 thru COX. Less effect on prostacycli. Used in unstable angina, transient ischemic attacks and stroke prevention, acute MI
What does clopidogrel do?
Blocks ADP receptors on platelets, reduces expression of GP receptors, inhibits platelet aggregation.
What does abciximab do?
Monoclonal antibody to GP receptors, blocking platelet aggregation
what does tiroFIBan do?
Analog of sequence of Fibrinogen, binds and prevents platelet aggregation
What does epifibitide do?
Analog of sequence of Fibrinogen, binds and prevents platelet aggregation
What does alteplase do?
This acts as a DIRECT tissue plasminogen activator, it can be used in ACUTE MI, ISCHEMIC STROKE, AND PULMONARY EMBOLISM iv infusion
What does reteplase do?
Slightly faster onset of action than alteplase, lasts longer, and given in bolus form
What does tenecteplase do?
Slightly faster onset of action than alteplase, lasts longer, and given in bolus form
What does streptokinase do?
Inderect plasminogen activator that forms a complex with endogenous plaminogen.
What does urokinase do?
DIRECTLY Converts plasminogen into plasmin.
What does aminocaproic acid do?
Inhibits plasmin activation
What does vitamin K do?
Large doses to reverse warfarin excess
What are contraindications of fibrinolytic drugs?
active bleeding
Severe hypertension
intracranial surgery
surgery, disease, drugs
Who should heparin not be given to?
Elderly women, people in renal failure, people bleeding
Emergency room, likely a stroke, not hemorrhaging, I should administer
A man requires prophylactic treatment for transient ischemia (stroke), however, he is allergic to aspirin
Ticlopidine or clopidegrol
A woman has an abrupt onset of blurred vision, hemiparesis, and headache and is found to have a thrombus within a large intracranial artery
23-yr-old pregnant woman has been treated with iv heparin for DVT and has developed heparin-induced thrombocytopenia. What treatment is advised for DVT in this case?
22 yr-old woman in her 2nd trimester of pregnacy presents at ER with pain and swelling in right leg. Ultrasound indicated thrombosis in popliteal vein and she was treated for 7 days with iv UFH. Given she lives 100 miles from nearest hospital, what is th
Low molecular weight heparin
Where do chylomicrons come from?
they come from the diet. Intestine----Blood---Peripheral cells
Where is VLDL synsthesized from?
Triglycerides from hepatocytes.
Liver---Blood---Peripheral cells
Where does LDL come from?
From VLDL after the TG is removed. Blood--Peripheral cells, and liver
What is the function of HDL?
It takes cholesterol from periphery to the liver for breakdown
What is hypertryglyceridia?
overprodution of VLDL, low LPL activity.
What is chylomicronamia?
LPL and cofactor deficiency (Apo C-2)
What is combined hyperlipidemia?
Inc. VLDL production and conversion to LDL
What is dysbetapoproteinemia?
lack APOE3 and 4
What is hypercholesterinemia?
LDL receptor defect
What is ligand defective apolipoprotein b?
defect in ligand domain of apob100
What are some secondary lipoprotein disorders?
Drug induced-diuretics, beta blockers, isotretinoin, oral contraceptives
Other-diabetes, hypothyroidism, alcoholism-increased vldl, renal or liver disease.
What are the four drug therapies for high cholesterol?
Statins, niacin, bile acid binding resins, or fibrates.
What are the two prodrug statins?
Lovastatin and Simvastatin
Which statin is absorbed 100% but is also the least potent?
What is the longest acting and most potent statin?
How do statins work?
These drugs inhibit HMG CoA reductase, decrease hepatic cholesterol synthesis, upregulate hepatic LDL receptors, increase uptake of LDL cholesterol and decrease serum total and LDL cholesterol.
What are the pharmokinetics of the statins?
Most have a short half-life
They are administered at night because of the noncturnal peak in cholesterol synsethesis
Absoprtion of LOVATATIN increased by food.
What is special about Atorvastatin?
It has a long half life, can be given once a day, and can be administered anytime
What are most of the statins metabolized by?
Which statin is not metabolized by the CYP 3A system?
What are some common CYP 3A inhibitors
erythromycin, azole antifungal drugs, antidepressants and HIV protease inhibitors
What are some side effects?
Drugs which inhibit metabolism should not be given, increases hepatotoxicity.
Can also have muscle pain and increased myositis and myalgia
An adult female is diagnosed with hypercholesterolemia. In addition to diet modification and increased physical activity, statin therapy should be initiated. The patient requested that any drugs needed would only require a single dose that did not necess
Describe Type 1 hypercholesternemia
What causes this?
Increase in coronary heart diseae?
Drug therapy
Massive fasting hyperchylomicronemia, even following normal dietary fat intake causes increased TG levels.
Caused by low LPL
No increase
no drug therapy, low-fat diet
Type 2A?
Due to?
Cause increase in heart disease?
Elevated LDL with normal VLDL
Block in LDL degradation (block in synthesis or processing of receptors)
Diet, cholestyramine, niacin or statin
Type 2B?
Elevated LDL and VLDL = increased serum TG and cholesterol.
Increase VLDL syn in the liver
Same as 2A -Diet, cholestyramine, niacin or statin
Type III?
serum concentration of IDL are increased
underproduction of Mutant APOLipo E or overproduction of IDL
Xanthomas and accelerated vascular diseae
Diet, drug therapy, niacin, and fenofibrate.
Type IV?
VLDL levels are increased, LDL is normal, normal to elevated cholesterol, and greatly increased circulating TG levels.
Diet, or niacin and fenofibrate
Type V?
Serum VLDL and chylomicrons are elevated. LDL is normal or decreased.
Either increased VLDL or chylomicrons or decreased clearance.
What are the three bile acid binding resins?
Colestipol, cholestyramine, colesevelam.
What are two indicators for statins?
Increased cholesterol and after MI
What is the mechanism of the bile acid binding resins?
Bind to bile acids in the GI tract, prevent reabsorption of bile acids=increase utilization of cholesterol to replace bile acids. They also increase LDL receptor synthesis.
Where is it important for the bile acid binding resins to work at?
the lumen of the intestine (jejunum and ileum).
When are these typically used?
when people are not tolerating other drugs, or as an additive affect.
When are bile acid resins given?
Absorbed from gut?
Before meals and at bedtime
inhibit absorption of digoxin, thyroid hormone and other drugs
What are the adverse effects of the resins?
Bloating constipation and gritty taste.
Which drug is an inhbitor of intestinal sterol absorption?
What is ezetimibe's mech. of action>
Localized in brush border of small intestine, inhibits absoprtion of cholesterol.
What effects does ezetimibe have?
decreases LDL, triglyceride and increase HDL
Where is ezetimibe absorbed from?
What are some adverse effects and how is it used?
from the small intestine, half life of 22 hr, metabolized by conjugation with glucoronate-more active. Mainly excreted in the feces.
Few adversed effects and used alone or with a statin.
What is vitorin?
Ezetimibe plus simvastatin, synergistic relationship, simvastatin must also be activated in the gut.
What are the two fibric acid drugs?
How are they best absorbed?
Gemfibrozil and fenofibrate
What's up with Gemfibrozil?
Absorbed in intestine, increase bound to plasma protein, half-life of 1 hour 30 min, 70% renal elimination
What's up with Fenofibrate?
completely hydrolized in the intestine
What is the mechanism of action of the fibrates?
Bind PPAR--transcriptional induction--increase LPL and HDL apoprotein--Increase fatty acid catabolism, decrease VLDL production by liver and increase VLDL clearance by HDL apolipoprotein.
What is the use of fibrates?
Treat hypertriglyceridemia
treat low HDL levels
What are the adverse affects of fibrates?
myopathy, rhabdomyolysis, bone marrow suppression, exfoliative dermatitis
Potentiates effects of warfarin.
How does niacin work?
Inhibits VLDL secretion by activating LPL. Nicotinc receptors on adipocytes-decrease release of fatty acids and decrease VLDL secretion.
What are the uses of Niacin?
hypercholesteremia, hypertriglyceremia, low hdl
What are the adverse effects of Niacin?
cutaneous flushing, hepatitis, increase blood glucose, aggravate peptic ulcer, myopathy, rhabdomyolysis.
What to use for cholesterol?
What to use for Tris?
What to use for all?
What can be used with any of the other drugs?
What can be used with statins?
What do you want to avoid?
Gemfibrozil and niacin combination
What should you use caution with?
Gemfibrozil and niacin
Drugs that will increase LDL receptor expression include?
Bile acid binding resins, Statins,
Which drugs act at the level of transcription?
the Fibrates
The treatment of cholesterol with gemfibrozil plus a statin leads to increased risk of ?
What is inflammation?
A normal, protective response to tissue injury caused by physical trauma, noxious chemicals or microbiologic agents. It is the bodie's attempt to inactivate or destroy invading organisms.
What happens with inflammation?
response to injury or insult, blood vessels dilate, increase vascular permeability, increase leukocyte production.
What all mediators control infflammtion?
Histamine, kinins, neuropeptides, cytokines. and Eicosanoids (MOST IMPORTANT FOR NSAIDS)
What is the mechansim of action for prostaglandins?
Sensitize spinal neurons, enhance synaptic efficacy as well as a direct and indirect stimulationof peripheral nerve endings
What are prostaglandins?
Unsat. fatty acid derivatives with 20 carbon atoms, produced in minute quantities by all tissues, act locally on tissues where they are produced, rapidly metabolized at site of action, DO NOT CIRCULATE.
What are the indications for NSAIDS?
Inflammation (erythema, edema, hyperalgesia)
What is the mech of fever?
Pyrogenic stimulus releases cytokines, increases PG in hypothalamus, increase temp and decreased heat loss
Do NSAIDS inhibit lipooxygenase?
NO, they only hit cox
When is cox-1 expressed ?
Alway on platelets, kidneys and the GI tract
When is cox-2 expressed?
It is inducible and is associated with inflammation.
What is a side effect of Cox-1 inhibition?
Inability to form stomach protecting prostaglandins
What keeps most aspirin in a non-ionized form?
low gastric pH keeps most ASA in non-ionized form, which enhances absorption.
What causes irritation of mucousal lining?
How can this be decreased?
rapid absorption leads to high concentration in gastric mucousal cells and irriation of mucousal lining.
buffering (pH above 3.5) can decrease irritation by slowing the absorption rate
What is the phase 1 metabolism of aspirin?
It is hydrolyzed to acetic acid and salicylate by esterases in tissues and blood
What is the phase 2 metabolsim of aspirin?
conjugation with glycine, water soluble excretion in urine.
Why is it that seemingly low doses of aspirin after several 700 mg doses can result in toxicity?
Saturation of phase 2 metabolism of aspirin causes a shift from first to zero order kinetics--subsequent small doses result in rapid build up of salicylate.
What are the mech of action of
irreversible COX inhibitor
reversible cox inhibitor

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