Unit 3 - Pharmacology

Front 1

Diphenhydramine

Back 1

Antihistamine/Antimuscarinic (H1 and M1); motion sickness;

Front 2

Lorazepam and diazepam

Back 2

GABAR; Reduce N&V from central cortical regions; used for anticipatory nausea

Front 3

Scopolamine

Back 3

Muscarinic antagonist; used to PREVENT but not tx motion sickness

Front 4

Prochlorperazine, metoclopramide

Back 4

DA antagonist; DA blockers stop emesis; used to tx chemotherapy induced, estrogen induced and other blood borne causes of N&V

Front 5

Odansetron

Back 5

5HT3 antagonist; 5HT3R found in area prostrena, peripheral sensory and enteric nerves;

Decrease emesis in chemo and radiation and posteroperatively

Front 6

Dexamethasone

Back 6

Corticosteroids; inhibits inflammatory mediated gut 5HT release

Front 7

Loperamide and Diphenoxylate

Back 7

Opiate antidiarrheal; decrease GI motility;

Front 8

Precaution with loperamide and diphenoxylate (opiates) for antidiarrheal

Back 8

Increases oral bioavailability of other drugs

Front 9

Nabilone and dronabinol

Back 9

CB1 agonists; used to tx NV after chemo

Front 10

Psyllium (metamucil)

Back 10

Absorbant; used for mild diarrhea and constipation; absorbs water

Front 11

Cholestyramine

Back 11

Bile binding resin; absorbant; antidiarrheal; inactivates osmotic activity of bile acids; used to tx bile acid induced diarrhea due to bile malabsorption or during tx for cholelithiasis with bile acids; binds bile acids

Front 12

Bismuth Subsalicylate (Pepto-Bismol)

Back 12

Tx acute diarrhea (traveler's diarrhea); mechanism not understood; temp black tongue and black stools may confound melena

Front 13

Why might you not want to get an antimcirobial agent during acute diarrhea?

Back 13

Diarrhea plays a protective role in expelling pathogenic organisms/toxins; don't want to interfere with that

Front 14

Cascara and Senna

Back 14

Anthraquinones; laxative; needs bacteria to convert into emodium which stimulates gut motility

Front 15

Phenolphthaline and Bisacodyl

Back 15

Stool softener/surfactant; Laxative; must be absorbed into blood and eliminated in the bile as the active glucuronide;

Detergent -> stool softener

Front 16

What must be a consideration when giving Phenolphthaline and Bisacodyl

Back 16

Needs to follow enterohepatic metabolism; won't work in patients taking cholestyramine (bile binding resins) or in pts with bile duct obstruction

Front 17

Castor Oil

Back 17

Laxative; converted to ricinoleic acid by pancreatic lipase which acts as an irritant promoting GI motility

Front 18

Lubiprostone (PGE1 analog)

Back 18

Laxative; enhances chloride secretion into intestinal lumen

Front 19

Dioctyl Sodium Sulfosuccinate

Back 19

Stool softener or surfactant

Front 20

MgS04

Back 20

water retaining -> increased intraluminal pressure

Front 21

Bisacodyl

Back 21

Direct intestinal walls stimulant

Front 22

Methylcellulose

Back 22

Collects water and swells -> increased bulk

Front 23

Docusate

Back 23

Detergent -> stool softener

Front 24

Mineral oil

Back 24

Lubricant

Front 25

Lactulose

Back 25

Hyperosmotic (also indicated for systemic encephalopathy); non-absorable sugar

Front 26

Psyllium [Metamucil]

Back 26

Collects water and swells -> increased bulk (could stimulate motility when touches gut wall or inhibit diarrhea by absorbing water)

Front 27

Oral Nalaxone

Back 27

Opiod antagonist; increases gut motility; doesn't interfere w/ hydroxodone

Front 28

Almivopan

Back 28

Opiod antagonist; increases gut motility

Front 29

Methylnaltrexone (Relistor)

Back 29

Opiod antagonist; increases gut motility

Front 30

Erythromicin

Back 30

Tx constipation; cholinergic agonist -> motility

Front 31

Neostigmine

Back 31

Tx constipation; increases ACh stimulation by preventing ACh breakdown; used after surgery to stimulate bowel movement

Front 32

Antacids (NaHC03), Al(OH)2, Ca(CO)3, Mg(OH)2

Back 32

Ca, Mg and Al hydroxides neutralize protons in the gut lumen

AluMINIMUm amount of feces (Al = constipation)
Mg = Must Go to the bathroom (Mg = diarrhea)
Together they balance eachother out and have a high acid neutraizing capability

Front 33

Ranitidine, Cimetidine

Back 33

H2R antagonist; indirectly decrease proton pump activity

Front 34

Omeprazole (-prazoles)

Back 34

PPI; tx GERD, NSAID PUD, Zollinger Ellison

May cause hypergastrinemia as well as anemia

Front 35

Pirenzepine

Back 35

M1 Muscarinic Antagonist; reduces gastric acid secretion;

Front 36

Misoprostol

Back 36

PGE1 analog; increases production and secretion of gastric mucous barrier; decreased acid production; tx NSAID ulcers

Front 37

Sucralfate

Back 37

Bind ulcer base, proving physical protection; allows HC03 secretion to reestablish pH gradient in mucous layer; increase ulcer healing, traveler's diarrhea

Front 38

PPI + Clarithryomycin + Amoxacillin or Metronidazole

Back 38

Combo used to kill H. Pylori (Metronidazole used when pt is allergic to penicillin)

Front 39

N-acetylcysteine (NAC)

Back 39

Tx acetaminophen hepatoxicity; NAPQ1 metabolite of acetominophen is very toxic; NAC supplies -SH groups for it to react with

Front 40

Chenodeoxycholic acid, Ursodeoxycholic acid

Back 40

Tx gallstones; increase conc. of bile acids in gall bladder -> reduces bile lipis and cholesterol concentration which causes gallstones; dissolves slowly

Front 41

How can Lactulose tx liver failure

Back 41

Degraded by colonic bacteria into lactic acid; protonated ammonia which then stays in lumen and is excreted

Front 42

Rifaximin

Back 42

Tx liver failure; eliminate urease producing bacteria and reduce the amount of ammonium produced

Front 43

Interferon Alpha

Back 43

Tx Chronic hepatitis C; IFN activates JAK-STAT which transcribes viral resistance proteins

Front 44

Ribavirin

Back 44

Tx chronic hepatitis C; inhibit viral RNA polymerases

Front 45

Lamivudine and Entecavir

Back 45

Tx chronic hepatitis B; inhbiit viral reverse transcriptase

Front 46

Uncoated lipase + PPI

Back 46

Steatorrhea due to pancreatitis; Failure to secrete lipase = steatorrhea; uncoated so it will activate in duodenum to replace lost; need PPI bc gastric acid will degrade lipase

Front 47

Protease

Back 47

Chronic pancreatitis; failure to secrete proteases results in pain; without protease (trypsin) can't inactivate CCK releasing peptide, which causes colonic pressure; give protease to prevent pain and replace lost protease

Front 48

Ferrous Sulfate

Back 48

Tx microcytic, hypochromic anemia; must continue to be given even after anemia is fixed to replenish ferritin; doses >100-200mg/day saturate active transport mechanism thus no additional benefit

Front 49

Ferrous Gluconate (oral)

Back 49

Tx microcytic, hypochromic anemia; must continue to be given even after anemia is fixed to replenish ferritin; doses >100-200mg/day saturate active transport mechanism thus no additional benefit

Front 50

Iron Dextran

Back 50

Tx microcytic, hypochromic anemia; perenteral; only used when oral iron replacement therapy is not enough

Front 51

What is the only type of anemia that will respond to iron supplementation?

Back 51

Iron deficiency; hypochromic, microcytic

Front 52

Deferoxamine

Back 52

Treat acute iron overdoses (A parenteral iron chelator, complex is excreted in urine)

"Defer Iron"

Front 53

Hydroxycobalamin (Vitamin B12)

Back 53

Used to tx macrocytic hyperchromic (megaloblastic) anemia; co enzyme for tetrahydrofolate (needed for nucleotide synthesis)

Front 54

Folic Acid

Back 54

Tx macrocytic hyperchromic (megaloblastic) anemia; precursor for tetrahydrofolate (needed for nucleotide synthesis)

Front 55

Erythropoietin EPO)

Back 55

Tx microcytic anemia of CHRONIC inflammatory dx; also pts w end stage renal failure and normocytic anemia (increases RBC production)

Front 56

Methotrexate

Back 56

Tx rheumatoid arthritis; impedes tumor growth; can cause macrocytic hyperchromic anemia; no amount of dietary folates or folic acid supplements will overcome reductase inhbiition by MTX

Front 57

Leucovorin (tetrahydrofolate)

Back 57

Given to rescue BM & GI cells AFTER doses of MTX; do not take WHILE on MTX

Front 58

Imatinib = Gleevec (Novartis)

Back 58

Tx CML; binds bcl-abl TK to block uncontrolled proliferation and induce apoptosis of cells with the philadelphia chromosome

Front 59

Trastuzumab = Herceptin

Back 59

Tx breast cancer; anti HER2 Ab

Front 60

Filgrastim (G-CSF)

Back 60

Stimulates production of neutrophils; used for marrow recovery

Front 61

Azathioprine

Back 61

Immunosuppresive oral med for organ transplantation pts and autoimmune disorders; impairs T&B lymphocyte proliferation. Converts to 6 mercaptopurine

Toxic if combined with allopurinol

Front 62

Cyclophosphamide

Back 62

Tx lymphomas, leukemia, and somes olid tumors; alkylating agent that slows/stops cell growth

Front 63

Cyclosporine (and tacrolimus)

Back 63

Lipid soluble peptide antibiotic that improves organ and bone marrow graft survival; impairs differentiation and activation of CD4+ T cells; does not cause bone marrow suppression

Front 64

Mycophenolate

Back 64

Prevent organ transplant rejection; blocks purines ynthesis

Front 65

Methotrexate

Back 65

1. Immunosupressive, 2. anticancer cytotoxic drug (impede tumor growth) 3. tx RA
can cause macrocytic hyperchromic anemia

Front 66

Prednisone

Back 66

Immunosuppressive glucocorticoids (inhibits inflammatory response); tx arthritis, modulate allergic response, also used in organ transplant, autoimmune dx (autoimmune hemolytic anemias)

Front 67

Asprin

Back 67

Antiplatelet drug; Irreversibly inhibits COX in platelets = decreased activation
Low doses prevent MI and recurrence; Inhibits platelet enzyme that makes TXA2; also an NSAID with analgesic, antiptyretic and anti-inflammatory properties (irreversible inhbiits COX1&2)

Front 68

Clopidogrel

Back 68

Antiplatelet drug; irreversible inhbiits platelet ADP-R; used after pt has balloon angiopalsty in coronary artery

Front 69

Warfarin

Back 69

Indirect anticoagulant; Vit K antagonist in the liver; prevent or tx venous thrombosis and prevent emboli from atrial fibrillation or synthetic heart valves

Teratogenic

Front 70

Heparin

Back 70

Immediately inhibits coagulation; used to manage acute thromboembolic disorders (pulmonary embolism); can result in severe thrombocytopenia

Front 71

Tissue Plasminogen Activator (rtPA) (tenecteplase)

Back 71

Thrombolytic (dissolver of blood clots); converts plasminogen to plasmin to dissolve clots; thrombolytic tx of acute phase of MI

Front 72

INR

Back 72

A high INR level indicates that there is a high chance of bleeding; The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and
international normalized ratio (INR) are measures of the extrinsic pathway of
coagulation. They are used to determine the clotting tendency of blood, in the
measure of warfarin dosage, liver damage, and vit. K status.

Front 73

EXPLAIN THE MECHANISMS BY WHICH ASPIRIN AND CLOPRIDOGREL INHIBIT
PLATELET-DRIVEN THROMBOSIS.

Back 73

Platelets do not interact with the lining of normal, healthy
blood vessels; however, when the subendothelium is exposed/damaged platelets stick
to the injured tissue and release (TxA2 and ADP). They also express gpIIb/IIIa that
causes other platelets, fibrinogen and vWF to form a clot. Until it is reinforced by fibrin, this
clot can break away and form an embolus. This matters because… Aspirin inhibits the
platelet enzyme that makes Thromboxane A2 (TxA2) and Clopidogrel inhibits platelet
ADP receptors. So, NO clot!

Front 74

LET’S TALK ABOUT ARACHIDONIC ACID (AGAIN):

Back 74

Arachidonic Acid is converted to PGH2 which can then become either of
the following depending on which tissue it is in …
(1) In PLATELETS (with COX-1) it is converted to THROMBOXANE, which
stimulates platelet activation and constricts blood vessels
(2) In VESSEL WALLS (with COX1&2) it is converted to PROSTACYCLIN,
which inhibits platelet activation and dilates blood vessels.
This matters because… Low dose aspirin stays in the liver and only
inhibits COX-1 making it very effective to stop platelet activation and
dilate blood vessels. A high dose gets past the liver and interacts with
the blood vessel walls to be counter-therapeutic since it would stimulate
platelet activation and constrict vessels.