Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Block 2 > Terms > Flashcards

Terms Flashcards

1
Q 
Biogenic Amine
Cellular Source: Mast cells, basophils
Physiological response:
1. vasodilation
2. increased vascular permeability
3. pain
Mechanism: Activation of GPCRs
Pharmacology: Antihistamines (H1 antagonists)
A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q 
Peptide
Cellular Source: Endothelial cells
Physiological response: 
1. vasodilation
2. increased microvessel permeability
3. pain
Mechanism: activation of GPCRs
Pharmacology: receptor antagonists being tested
A

Bradykinin

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

Plasma proteins
Cellular Source: synthesized by liver, circulates in blood
Physiological response:
1. Chemotaxis: recruitment of inflammatory cells to site of injury
2. promote release of mediators from neutrophil
3. increase vascular permeability
4. excessive activation may contribute to tissue injury
Mechanism: complement protein complexes cause osmotic lysis, activation of GPCRs
Pharmacology: Eculizumab, APT070

A

Complement

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

Plasma protein
Cellular Source: produced in liver in response to cytokines, adipocytes
Physiological Response:
1. “acute phase reactant”
2. activates complement cascade
3. mediates phagocytosis
4. “marker of inflammation”
Mechanism: binds to phospholipids in bacteria and damaged cells, may be specific receptors in macrophages
Pharmacology: elevated CRP may be associated with increased risk of diabetes, hypertension and cardiovascular disease, statins may help

A

C-Reactive Protein

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

Secreted proteins (IL-a, IL-B, TNF-a)
Cellular source: nearly all inflammatory cells
Physiological response:
1. TNF-a: acute phase reaction, fever, sepsis
2. IL-1: acute phase reaction, fibroblast and lymphocyte proliferation, fever
Mechanism: bind to specific receptor proteins to induce gene expression in number of proteins via activation of NFkB and AP-1 –> increase COX and lipoxygenases, increase adhesion molecule expression, induce collagenase (fibrosis)
Pharmacology: etanercept, Infliximab

A

Cytokines

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

Purine Nucleotide
Cellular source: all cells
Physiological response:
1. Increased extracellularly during injury - anti-inflammatory
2. Inhibit cytokine action
Mechanism: activation of GPCRs
Pharmacology: Adenosine A2 agonists, Methotrexate, Folic acid antagonist

A

Adenosine

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

Family of Proteins
Cellular source: endothelial cells, platelets, leukocytes
Physiological response:
1. Leukocyte adhesion to endothelium
2. Endothelial adhesion molecules recruit activated platelets
Mechanism: contact molecules, calcium dependent
Pharmacology: Abciximab

A

Cell Adhesion Molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q 
Lipid Mediator
Cellular source: virtually all cells
Physiological response:
1. Vasodilation/vasoconstriction
2. pain
3. fever
4. platelet aggregation (via thromboxanes)
Pharmacology: NSAIDS
A

Prostaglandin

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

Lipid Mediator
Cellular source: macrophages, neutrophils
Physiological response:
1. Increased vascular permeability
2. Bronchoconstriction
Mechanism: activation of GPCRs
Pharmacology: Zileuton - 5 lipoxygenase inhibitor
Zafirlukast - cys-leukotriene receptor antagonist

A

Leukotriene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q 
Lipid Mediator
Cellular source: adrenal cortex
Physiological Response:
1. inhibition of cytokines
2. inhibition of phospholipase A2
3. inhibition of COX2
4. inhibition of cell adhesion molecules
Mechanism: activation of nuclear receptors
Pharmacology: steroids
A

Glucocorticoid

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

Physiological response:

  1. vasodilation
  2. increased vascular permeability
  3. pain
A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Physiological response:

  1. vasodilation
  2. increased microvessel permeability
  3. pain
A

Bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Physiological response:

  1. Chemotaxis: recruitment of inflammatory cells to site of injury
  2. promote release of mediators from neutrophil
  3. increase vascular permeability
  4. excessive activation may contribute to tissue injury
A

Complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Physiological Response:

  1. “acute phase reactant”
  2. activates complement cascade
  3. mediates phagocytosis
  4. “marker of inflammation”
A

C-Reative Protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Physiological response:

  1. TNF-a: acute phase reaction, fever, sepsis
  2. IL-1: acute phase reaction, fibroblast and lymphocyte proliferation, fever
A

Cytokines

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

Physiological response:

  1. Increased extracellularly during injury - anti-inflammatory
  2. Inhibit cytokine action
A

Adenosine

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

Physiological response:

  1. Leukocyte adhesion to endothelium
  2. Endothelial adhesion molecules recruit activated platelets
A

Cell Adhesion Molecules

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

Physiological response:

  1. Vasodilation/vasoconstriction
  2. pain
  3. fever
  4. platelet aggregation (via thromboxanes)
A

Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Physiological response:

  1. Increased vascular permeability
  2. Bronchoconstriction
A

Leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Physiological Response:

  1. inhibition of cytokines
  2. inhibition of phospholipase A2
  3. inhibition of COX2
  4. inhibition of cell adhesion molecules
A

Glucocorticoids

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

Exists as two isoforms, oxygenate and cyclize the precursor fatty acid to form cyclic endoperoxide (PGG), peroxidase activity converts PGG2 to PGH2
Inhibited by Aspirin

A

Cyclooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Constitutive

A

COX-1

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

Larger active site, inducible

A

COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Most abundant precursor of eicosanoids, concentration in cells is low, Found esterified to membrane phospholipids

A

Arachidonic Acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

LT1 and LT2

A

Cysteinyl Leukotriene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

PGE2

A

Lowers threshold of nociceptors in periphery
Activates spinal neurons and microglia that contribute to neuropathic pain
Fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what essential amino acid is serotonin synthesized from?

A

tryptophan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the rate-limiting enzyme in serotonin synthesis?

A

tryptophan hydroxylase?

29
Q

most of the serotonin in the body is found where?

A

GI system

30
Q

in the brain, cell bodies of serotonergic neurons are primarily located in?

A

raphe nucleus

31
Q

which serotonin receptor isn’t a GPCR?

A

5HT3

32
Q

what explains the GI complaints associated with aspirin use?

A

decreased production of PGs that promote mucus secretion

33
Q

why does aspirin increase bleeding time?

A

TXA2 production in platelets decreases

34
Q

general properties of NSAIDS?

A

anti-inflammatory, anti-pyretic, analgesic

35
Q

which medicine does not have anti-inflammatory properties?

A

acetaminophen

36
Q

which COX relates to PGs and inflammation?

A

COX 2

37
Q

mechanism of all NSAIDS?

A

inhibition of COX

38
Q

mechanism of acetylsalicylic acid

A

irreversible inhibitor of COX 1& 2, acetylation of serine moiety (covalent bonding)

39
Q

effect of aspirin on platelet cells

A

cannot regenerate without new platelet synthesis (no nucleus)

40
Q

unique effects specific to Aspirins (unrelated to COX inhibition)

A

uric acid excretion, CNS, respiration

41
Q

uricosuric agent/effects

A

increases rate of excretion of uric acid via competition with urate transporter

42
Q

low aspirin dose effect on uric acid (typical two 325 mg/4hrs)

A

decrease uric acid excretion

43
Q

large aspirin dose effect on uric acid

A

normal uricosuric effect: block reabsorption via interaction with transporter, OAT

44
Q

CNS effect of salicylates

A

stimulation followed by depression; tinnitus; nausea & vomiting

45
Q

adverse reactions to NSAIDs

A

GI (block production of protective PGs): ulceration and irritation
Renal: decrease RBF, Na/H20 retention (esp in CHF, renal disease, elderly)

46
Q

prostaglandins in GI

A

from COX-1, PGE2 and PGI2, inhibit acid secretion by stomach, promote secretion of cytoprotective mucus in intestine

47
Q

inhibition of platelet aggregation

A

PGI2

48
Q

stimulation of platelet aggregation

A

TXA2

49
Q

effect of PGE2 and PGI2 on kidney

A

increase RBF, increase salt and water excretion

50
Q

PGF2a (re: uterus)

A

pregnant uterus, contraction

51
Q

PGE2 (re: uterus)

A

pregnant uterus, contraction

maintain PDA

52
Q

PGI2 (re: uterus)

A

early pregnancy, dilation

53
Q

NSAIDs and pregnancy (SE)

A

increase risk of postpartum hemorrhage (TXA2), intrauterine closure of PDA, avoid use during 3rd trimester

54
Q

aspirin half-life during overdose

A

15-30 hours (zero order kinetics)

55
Q

Reye’s Syndrome

A

aspirin. children; acute encephalopathy, liver degeneration; follows viral illness; mitochondrial damage?

56
Q

side effects associated with all non-selective NSAIDs

A

GI irritation, inhibition of platelet aggregation/increased risk of bleeding, decrease in RBF in patients, hypersensitivity

57
Q

what do you give to manage acetaminophen toxicity?

A

N-acetylcysteine (replenishes glutathione stores)

58
Q

role of alcohol in acetaminophen toxicity?

A

EtOH induces P450 (2E1) involved in NAPIQ metabolite, also depletes glutathione

59
Q

location of histamine

A

tissues: mast cells
blood: basophils
non-mast cells (gastric mucosa cells, epidermis, neurons)

60
Q

drugs, peptides and venoms that promote histamine release

A

vancomycin, succinylcholine, morphine, curare

bradykinin, complement, substance P

wasp venom

61
Q

mechanism of histamine release

A

increase in intracellular calcium

62
Q

vancomycin-induced histamine reaction

A

red-man syndrome: follows rapid IV infusion, rash on face/neck/upper torso, hypotension, due to mast cell degranulation (not allergic rxn)

63
Q

mechanism of action of omalizumab

A

IgG that binds Fc portion of IgE; Fc portion cannot bind to mast cell

64
Q

H1 receptor G-protein coupling and 2nd messenger

A

Gq

Calcium

65
Q

H2 receptor G-protein coupling and 2nd messenger

A

Gs

cAMP

66
Q

H1 receptor effects on vasoconstriction and vascular permeability

A

acts on vascular smooth muscle

on post-capillary venules, causes endothelial cells to contract

67
Q

H1 effect on bronchioles, intestinal smooth muscle, peripheral nerve endings

A

contraction
contraction
pain and itching

68
Q

H2 effect on bronchioles, intestinal smooth muscle, peripheral nerve endings

A

relaxation
none
none

Pharmacology Block 2 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions