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Pharmacology > Pharm Exam 4 Factoids > Flashcards

Pharm Exam 4 Factoids Flashcards

0
Q

Catalyzes production of leukotrienes, HETES and HPETES

A

Lipoxygenase

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1
Q

Enzyme required for release of arachundonic acid from membrane phospholipids

A

Phospholipase A2

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2
Q

Catalyzes production of prostaglandins and thromboxane

A

Prostaglandin H synthase

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3
Q

Enzyme

Arachidonic acid to 5-HPETE

A

5-LOX

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4
Q

Enzyme

5-HPETE to LTA4

A

LTA synthase

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5
Q

Enzyme

LTA4 to LTB4

A

LTA4 hydroxylase

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6
Q

Enzyme

LTA4 to LTC4

A

LTC synthase

GSH

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7
Q

Function of 5-HETE

A

Chemotaxis for leukocytes

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8
Q

Function of LTB4

A

Chemotaxis
Aggregation
Adhesion
All for leukocytes

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9
Q

Function of LTC4, LTD4, LTE4

A

Vasoconstriction
Bronchospasm
Increase vascular permeability

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10
Q

Function of PGI2

A

Vasodilation
Decrease platelet aggregation
Distribution: endothelium, kidney, platelets, brain

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11
Q

Function of theomboxane TxA2

A

Vasoconstriction
Increase platelet aggregation
Distribution: platelets, vascular smooth muscle, macrophages, kidney

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12
Q

Function of PGD2, PGE2, PGF2a

A

Vasodilation
Potentiation of edema, pain and fever
Distribution PGD: mast cells, brain, airways, lymphocytes, eosinophils
PGE: brain, kidney, vascular smooth muscle cells, platelets
PGF: uterus, airways, vascular smooth muscles, eye

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13
Q

Features of COX-1

A

Arachidonic acid to PGG2
Constitutive expression
Functions: housekeeping, cytoprotective, maintains gastric mucosal integrity, mediates normal platelet function
Not inducible, regulated developmentally

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14
Q

Features of COX2

A

Arachidonic acid to PGG 2
Inducible
Constitutive in areas of the brain, kidney, vas deferens, GI tract
Not in platelets
Functions: inflammation, memory, salt/ water balance, uterine contractions, colon and breast cancer
Inducers: bacteria, tissue damage, growth factors, inflammatory cytokines

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15
Q

Metabolizes of Arachidonic acid on smooth muscle

A 
PGE2 and PGI2 relax
TxA2 contracts
PGD2 either constricts or dilates
Ductus arteriousus sensitive to vasodilators effects of PGE and PGI2
Uterine contraction is PGE2 or PGF2alpha
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16
Q

Cytoprotective metabolites

A

PGE2 and PGI2 inhibit gastric acid secretion
PGE2 increase mucus secretion
PGI2 regulate mucosal blood flow

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17
Q

Platelet regulation metabolites

A

TxA2 promote platelet aggregation

Prostacyclin PGI2 inhibits aggregation

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18
Q

Fever and pain metabolites

A

PGE2 increased concentration in hypothalamus

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19
Q

Therapeutic uses of NSAIDS

A 
Reduce pain
Reduce fever associated with inflammation, tissue damage or disease
Close ductus arteriousus 
Prophylactic of thromboembolic disorders
Decrease risk of colon cancer
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20
Q

Side effects of NSAIDS and reason why

A 
Gastric or intestinal irritation
NSAID induced gastric or duodenal ulcer
Due to decreases synthesis of cytoprotective PGs (COX-1)
Increased bleeding
Prolonged gestation
Renal injury/ failure
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21
Q

Overcoming gastric irritation

A

Co administration of a proton pump inhibitor

Selective blockade of COX2

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22
Q

Salicylate poisoning

A

Uncoupling of oxidative phosphorylation in mitochondria-hyperventilation and respiratory alkalosis, compensatory bicarbonate secretion

Large doses and small children medullary response depressed-hypoventilation and respiratory acidosis

Both have metabolic acidosis-toxic plasma concentrations of salicylates, decreased renal excretion of acids, impaired metabolism of carbs leading to increased lactic & pyruvic acid

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23
Q

High incidence of severe headaches

A

Indomethacin-acetic acid derivative

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24
Q

Causes peri operative pain

A

Etodolac and ketorolac

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25
Q

TNF facts

A

Pro inflammatory cytokines
Activates NFkB leading to production of pro inflammatory mediators
Activates MAP kinase pathways especially JNK leading to transcription factor activation, changes in signaling, proliferation, differentiation, and apoptosis of cells
Stimulates acute phase response, attracts neutrophils, stimulates phagocytosis by macrophages
Receptors: TNFR1 expressed widely, TNFR2 expressed on immune cells

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26
Q

TNF Ab causing TB

A

Certolizumab pegol

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27
Q

Define gout

A

Hyperurecemia caused by overproduction of uric acid and/or decreased ability to excrete it
Deposition of monosodium urate in tissues, particularly joints and kidneys
Cause inflammation

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28
Q

Contraindications examples ( reasons to withhold treatment)

A 
Coma
Convulsions
Strong acids or bases
Petroleum distillates
Heart disease
Pregnancy 
CNS stimulants
29
Q

Causes emesis (vomiting)

A

Ipecac, mustard powder, apomorphine

30
Q

Steps to treat poisonings before arrival

A 
Obtain useful information 
Emesis
Adsorbents: activated charcoal
Decontaminate skin and eyes
Get to treatment center
31
Q

Steps to treat poisoning at treatment center

A
  1. Emergency management
  2. Initial exam-consistent symptoms
  3. Remove unabsorbed toxicant:emesis, gastric lavage, whole bowel irritation (sorbitol, Na2SO4, MgSO4), adsorbents
  4. Supportive treatment
  5. Hasten elimination of absorbed toxicant-diuresis, urinary ph adjustment, dialysis, hemodialysis-slowly eliminated toxicants and small MW
32
Q

Receptor ligand interactions toxicity examples

A

Nicotine, organophosphates, TCDD (dioxin)

33
Q

Interference with excitable membranes examples

A

Saxitoxin, tetrodotoxin-block Na channels
Organic solvents-alter membrane fluidity
DDT: interferes with Na channel closing
Organophosphates, carbamates: inhibit AChe

34
Q

Examples of interference with energy production

A 
Carbon monoxide
Nitrite
Cyanide, hydrogen sulfide, azide 
Nitrophenols
Fluoroacetate
ATP depletion affects membrane integrity, ion pumps, protein synthesis 
Heart and Brain most sensitive
35
Q

Examples of calcium homeostasis disrupters

A

Nitro phenols, quinones, peroxides, aldehydes, dioxins, heavy metal ions

36
Q

Periods of teratogenic susceptibility

A

Early: lethal effects
Late: no major structural malformations instead growth retardation, functional disorders, Carcinogenesis
Organogenesis: period of high susceptibility

37
Q

Malignant hyperthermia pharmacogenomics

A

Idiosyncratic response to general anesthetics such as halothane in combo w/ succinylcholine
Rigidity of skeletal muscles, tachycardia, and hyperthermia
MOA: increased release of Ca from sarcoplasmic reticulum leads to increased muscle contractions and heat production
Change from lys to arg in ryanodine receptor
Treat with dantrolene

38
Q

GP6D deficiency pharmacogenomics

A

Erythrocyte Glucose 6 phosphate dehydrogenase deficiency occurs in 1 in 10 Africans
X-linked recessive
Resistance to plasmodium falciparum Malaria
Lowers NADPH and GSH
Drugs produce H2O2 which oxidizes glutathione
G6PD deficiency leads to premature rupture or red blood cells
Drugs: primaquine, quinine, quinidine, sulfonamides, dapsone, methylene blue

39
Q

Isoniazid and N-Acetyltransferase-2 SNPs (NAT-2) pharmacogenetics

A 
Rapid metabolizers (more NAT-2) have an inadequate response for TB to isoniazid 
Poor metabolizers (less NAT-2) may exhibit toxicity 
Egyptians, Africans and Caucasians most likely slow acetylators
40
Q

Aldehyde dehydrogenase pharmacogenetics

A

10 human ALDH and 13 alleles result in autosomal dominant trait that lacks catalytic activity if one subunit is inactive
ALDH-2 deficiency leads to accumulation of acetylaldehyde leading to facial flushing, palpitations, and tachycardia
Absent in 45% of Chinese but not in Caucasians or Africans
Involved in alcohol metabolism

41
Q

CYP450 2C19 pharmacogenetics

A

Cure rate for helicobacter pylori infection is greater in patients who are poor metabolizers of omeprazole
CYP2C19 poor metabolizers: Filipinos, Japanese, Chinese Taiwanese
100% vs 25% cure rate

42
Q

Cytochrome P450 CYP2D6 pharmacogenomics

A

Low to absent in 7% of Caucasians and 2% of Asians and Africans
Causes poor analgesia with acetaminophen plus codeine
Ultra rapid metabolizers carry multiple copies of CYP2D6 gene-10% of Spanish, 1-2% of Swedish and 30% of Ethiopian
Inhibited by fluoxetine, paroxetine, haloperidol, quinidine, ritonavir

43
Q

Thioopurine methyl transferase pharmacogenomics

A

TPMT Catalyzes S-methylation of Azathioprine and 6-mercaptopurine
Very low or no activity occurs in <.5% of populations
Can have fatal consequences for children treated with 6-mercaptopurine for acute lymphocytic leukemia and cause inability to tolerate Azathioprine
Autosomal co dominant
Deficiency leads to accumulation of XC thioguanine nucleotides leading to bone marrow toxicity

44
Q

Polymorphic beta 2 receptor pharmacogenomics

A

SNPs have been associated with abnormal receptor expression, signaling and down regulation
Have clinical importance in asthma and hear failure

45
Q

Drugs that cause type I hypersensitivities

A 
Chimeric monoclonal Abs
Immunoglobulin preparations
NMJ blockers
Quinolone antibiotics
Beta lactam antibiotics-penicillins, cephalosporins 
Toluene diisocyanate-symptoms persist
Apamin-bees
46
Q

Examples of type II hypersensitivities

A

Beta lactam antibiotics
Penicillins-hemolysis, less likely thrombocytopenia
Cephalosporins-hemolysis less likely thrombocytopenia
Aspirin, quinidine or phenytoin cause thrombocytopenic purpura

47
Q

Drugs that cause type III hypersensitivity reactions

A 
Beta lactam antibiotics
Sulfonamides
Nonsteroidal antiinflammatory drugs 
Hydralazine-lupus like 
Procainamide
48
Q

Drugs that cause Type IV hypersensitivity

A

Beta lactams-penicillins, cephalosporins

Sulfonamides-May be severe, Steven Johnson syndrome or toxic epidermal

49
Q

Anaphylactoid reaction

A

Non IgE mediated histamine release
Dose dependent
Rechallenge can be done-premedicate with antihistamine
No cross reactivity within same class/chemical

50
Q

Type I hypersensitivity

A

Allergic reaction
Rechallenge OK
Immediate after non Reactive first exposure
B and T cells-> T cells activist ate B cells -> histamine, heparin, platelet activating factor

51
Q

Type II hypersensitivity

A

Desensitization and rechallenge not recommended
Targets blood cells or platelets
Immediate if previous exposure, 5-8 days first time

52
Q

Type III hypersensitivity

A

Rechallenge not recommended
Targets Vascular endothelium, skin, joints, kidney
Immune complex deposition
Joints-arthalgia, skin-purpura, kidneys-glomeruli nephritis, systemic-serum sickness, vasculitis
Immediate if previous exposure, 10-14 days if first time

53
Q

Type IV hypersensitivity

A

Delayed
T cells exposed then rexposure activates memory T cells releasing cytokine and Chemokines attracting macrophages
Skin reactions-hives, morbilliform Rash, eczema
Rechallenge after desensitization
7-20 days onset on average

54
Q

Drugs that cause anaphylactoid reactions

A

Codeine or morphine-high doses or epidural
Vancomycin-red neck syndrome
Radio contrast media
Caspofungin-decreased histamine

55
Q

Drugs frequently causing allergic reactions

A

Antimicrobials, anticonvulsants, cardiovascular drugs, macromolecules, antiinflammatory, antineoplastic

56
Q

Type A adverse reactions

A 
Account for 2/3 of ADRs
Predictable and dose dependent
Include anaphylactoid   
Extension of pharmacological effect
Preventable
57
Q

Type B adverse reactions

A

Idiosyncratic or immunologic reaction

Rare and not predictable

58
Q

Type C adverse reactions

A

Long term use

Drug accumulation

59
Q

Type D adverse reactions

A

Delayed effects-dose independent
Carcinogenicity
Terarogenecicity

60
Q

P-glycoproteins

A

Efflux pump in epithelial cells with an excretory function in gut wall
Induced by rifampin
Inhibited by quinidine, verapamil, itraconazole, erythromycin

61
Q

Inducers of cyp450 metabolism

A 
Phrnoarbital
Carbamazepine
Phenytoin
Rifampin
Cigarette smoking
Tobacco
Chronic ethanol use
62
Q

Inhibitors of cyp450 metabolism

A 
Cimetidine
Omeprazole
Fluoxetine 
Ciprofloxacin
Clarithromycin
Erythromycin
Grapefruit juice
Itraconazole 
Ciprofloxacin
Ritonavir
63
Q

Competition for secretion in proximal tubule

A

Probenecid and ampicillin

Ibuprofen and hydrochlorothiazide

64
Q

Slows hepatic blood flow

A

Propranolol

65
Q

Food that binds to drug and prevent absorption

A

Milk and tetracycline

66
Q

Drug that is increased in absorption with food

A

Fatty meal and griseofulvin

67
Q

Protective food

A

All foods and ibuprofen on gastric mucosa

68
Q

Food and inhibition of p450 metabolism

A

Grapefruit and lovastatin

69
Q

Grapefruit effects

A

Inhibits intestinal p450 responsible for first pass metabolism
May Inhibit P glycoproteins In intestinal brush border

70
Q

Interaction causing increased BP

A

MAO inhibitors and tyrannies containing foods

71
Q

Interaction that causes decreased anti coagulation effects

A

High vitamin K foods (green leafy veggies)

And warfarin

Pharmacology (15 decks)

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