Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Pharm Exam 4 Factoids > Flashcards

Pharm Exam 4 Factoids Flashcards

0
Q

Catalyzes production of leukotrienes, HETES and HPETES

A

Lipoxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Enzyme required for release of arachundonic acid from membrane phospholipids

A

Phospholipase A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Catalyzes production of prostaglandins and thromboxane

A

Prostaglandin H synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Enzyme

Arachidonic acid to 5-HPETE

A

5-LOX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Enzyme

5-HPETE to LTA4

A

LTA synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Enzyme

LTA4 to LTB4

A

LTA4 hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Enzyme

LTA4 to LTC4

A

LTC synthase

GSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Function of 5-HETE

A

Chemotaxis for leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Function of LTB4

A

Chemotaxis
Aggregation
Adhesion
All for leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Function of LTC4, LTD4, LTE4

A

Vasoconstriction
Bronchospasm
Increase vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Function of PGI2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Function of theomboxane TxA2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cytoprotective metabolites

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Platelet regulation metabolites

A

TxA2 promote platelet aggregation

Prostacyclin PGI2 inhibits aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fever and pain metabolites

A

PGE2 increased concentration in hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Overcoming gastric irritation

A

Co administration of a proton pump inhibitor

Selective blockade of COX2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

High incidence of severe headaches

A

Indomethacin-acetic acid derivative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Causes peri operative pain
Etodolac and ketorolac
25
TNF facts
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
26
TNF Ab causing TB
Certolizumab pegol
27
Define gout
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
28
Contraindications examples ( reasons to withhold treatment)
``` Coma Convulsions Strong acids or bases Petroleum distillates Heart disease Pregnancy CNS stimulants ```
29
Causes emesis (vomiting)
Ipecac, mustard powder, apomorphine
30
Steps to treat poisonings before arrival
``` Obtain useful information Emesis Adsorbents: activated charcoal Decontaminate skin and eyes Get to treatment center ```
31
Steps to treat poisoning at treatment center
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
Receptor ligand interactions toxicity examples
Nicotine, organophosphates, TCDD (dioxin)
33
Interference with excitable membranes examples
Saxitoxin, tetrodotoxin-block Na channels Organic solvents-alter membrane fluidity DDT: interferes with Na channel closing Organophosphates, carbamates: inhibit AChe
34
Examples of interference with energy production
``` Carbon monoxide Nitrite Cyanide, hydrogen sulfide, azide Nitrophenols Fluoroacetate ATP depletion affects membrane integrity, ion pumps, protein synthesis Heart and Brain most sensitive ```
35
Examples of calcium homeostasis disrupters
Nitro phenols, quinones, peroxides, aldehydes, dioxins, heavy metal ions
36
Periods of teratogenic susceptibility
Early: lethal effects Late: no major structural malformations instead growth retardation, functional disorders, Carcinogenesis Organogenesis: period of high susceptibility
37
Malignant hyperthermia pharmacogenomics
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
GP6D deficiency pharmacogenomics
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
Isoniazid and N-Acetyltransferase-2 SNPs (NAT-2) pharmacogenetics
``` 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
Aldehyde dehydrogenase pharmacogenetics
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
CYP450 2C19 pharmacogenetics
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
Cytochrome P450 CYP2D6 pharmacogenomics
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
Thioopurine methyl transferase pharmacogenomics
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
Polymorphic beta 2 receptor pharmacogenomics
SNPs have been associated with abnormal receptor expression, signaling and down regulation Have clinical importance in asthma and hear failure
45
Drugs that cause type I hypersensitivities
``` Chimeric monoclonal Abs Immunoglobulin preparations NMJ blockers Quinolone antibiotics Beta lactam antibiotics-penicillins, cephalosporins Toluene diisocyanate-symptoms persist Apamin-bees ```
46
Examples of type II hypersensitivities
Beta lactam antibiotics Penicillins-hemolysis, less likely thrombocytopenia Cephalosporins-hemolysis less likely thrombocytopenia Aspirin, quinidine or phenytoin cause thrombocytopenic purpura
47
Drugs that cause type III hypersensitivity reactions
``` Beta lactam antibiotics Sulfonamides Nonsteroidal antiinflammatory drugs Hydralazine-lupus like Procainamide ```
48
Drugs that cause Type IV hypersensitivity
Beta lactams-penicillins, cephalosporins | Sulfonamides-May be severe, Steven Johnson syndrome or toxic epidermal
49
Anaphylactoid reaction
Non IgE mediated histamine release Dose dependent Rechallenge can be done-premedicate with antihistamine No cross reactivity within same class/chemical
50
Type I hypersensitivity
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
Type II hypersensitivity
Desensitization and rechallenge not recommended Targets blood cells or platelets Immediate if previous exposure, 5-8 days first time
52
Type III hypersensitivity
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
Type IV hypersensitivity
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
Drugs that cause anaphylactoid reactions
Codeine or morphine-high doses or epidural Vancomycin-red neck syndrome Radio contrast media Caspofungin-decreased histamine
55
Drugs frequently causing allergic reactions
Antimicrobials, anticonvulsants, cardiovascular drugs, macromolecules, antiinflammatory, antineoplastic
56
Type A adverse reactions
``` Account for 2/3 of ADRs Predictable and dose dependent Include anaphylactoid Extension of pharmacological effect Preventable ```
57
Type B adverse reactions
Idiosyncratic or immunologic reaction | Rare and not predictable
58
Type C adverse reactions
Long term use | Drug accumulation
59
Type D adverse reactions
Delayed effects-dose independent Carcinogenicity Terarogenecicity
60
P-glycoproteins
Efflux pump in epithelial cells with an excretory function in gut wall Induced by rifampin Inhibited by quinidine, verapamil, itraconazole, erythromycin
61
Inducers of cyp450 metabolism
``` Phrnoarbital Carbamazepine Phenytoin Rifampin Cigarette smoking Tobacco Chronic ethanol use ```
62
Inhibitors of cyp450 metabolism
``` Cimetidine Omeprazole Fluoxetine Ciprofloxacin Clarithromycin Erythromycin Grapefruit juice Itraconazole Ciprofloxacin Ritonavir ```
63
Competition for secretion in proximal tubule
Probenecid and ampicillin | Ibuprofen and hydrochlorothiazide
64
Slows hepatic blood flow
Propranolol
65
Food that binds to drug and prevent absorption
Milk and tetracycline
66
Drug that is increased in absorption with food
Fatty meal and griseofulvin
67
Protective food
All foods and ibuprofen on gastric mucosa
68
Food and inhibition of p450 metabolism
Grapefruit and lovastatin
69
Grapefruit effects
Inhibits intestinal p450 responsible for first pass metabolism May Inhibit P glycoproteins In intestinal brush border
70
Interaction causing increased BP
MAO inhibitors and tyrannies containing foods
71
Interaction that causes decreased anti coagulation effects
High vitamin K foods (green leafy veggies) | And warfarin

Pharmacology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions