Pharmacology Block 2 > Terms > Flashcards

Terms Flashcards

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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11
Q

Physiological response:

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

Histamine

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12
Q

Physiological response:

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

Bradykinin

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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

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14
Q

Physiological Response:

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

C-Reative Protein

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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

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16
Q

Physiological response:

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

Adenosine

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17
Q

Physiological response:

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

Cell Adhesion Molecules

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18
Q

Physiological response:

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

Prostaglandins

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19
Q

Physiological response:

  1. Increased vascular permeability
  2. Bronchoconstriction
A

Leukotrienes

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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

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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

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22
Q

Constitutive

A

COX-1

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23
Q

Larger active site, inducible

A

COX-2

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24
Q

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

A

Arachidonic Acid

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25
LT1 and LT2
Cysteinyl Leukotriene
26
PGE2
Lowers threshold of nociceptors in periphery Activates spinal neurons and microglia that contribute to neuropathic pain Fever
27
what essential amino acid is serotonin synthesized from?
tryptophan
28
what is the rate-limiting enzyme in serotonin synthesis?
tryptophan hydroxylase?
29
most of the serotonin in the body is found where?
GI system
30
in the brain, cell bodies of serotonergic neurons are primarily located in?
raphe nucleus
31
which serotonin receptor isn't a GPCR?
5HT3
32
what explains the GI complaints associated with aspirin use?
decreased production of PGs that promote mucus secretion
33
why does aspirin increase bleeding time?
TXA2 production in platelets decreases
34
general properties of NSAIDS?
anti-inflammatory, anti-pyretic, analgesic
35
which medicine does not have anti-inflammatory properties?
acetaminophen
36
which COX relates to PGs and inflammation?
COX 2
37
mechanism of all NSAIDS?
inhibition of COX
38
mechanism of acetylsalicylic acid
irreversible inhibitor of COX 1& 2, acetylation of serine moiety (covalent bonding)
39
effect of aspirin on platelet cells
cannot regenerate without new platelet synthesis (no nucleus)
40
unique effects specific to Aspirins (unrelated to COX inhibition)
uric acid excretion, CNS, respiration
41
uricosuric agent/effects
increases rate of excretion of uric acid via competition with urate transporter
42
low aspirin dose effect on uric acid (typical two 325 mg/4hrs)
decrease uric acid excretion
43
large aspirin dose effect on uric acid
normal uricosuric effect: block reabsorption via interaction with transporter, OAT
44
CNS effect of salicylates
stimulation followed by depression; tinnitus; nausea & vomiting
45
adverse reactions to NSAIDs
GI (block production of protective PGs): ulceration and irritation Renal: decrease RBF, Na/H20 retention (esp in CHF, renal disease, elderly)
46
prostaglandins in GI
from COX-1, PGE2 and PGI2, inhibit acid secretion by stomach, promote secretion of cytoprotective mucus in intestine
47
inhibition of platelet aggregation
PGI2
48
stimulation of platelet aggregation
TXA2
49
effect of PGE2 and PGI2 on kidney
increase RBF, increase salt and water excretion
50
PGF2a (re: uterus)
pregnant uterus, contraction
51
PGE2 (re: uterus)
pregnant uterus, contraction | maintain PDA
52
PGI2 (re: uterus)
early pregnancy, dilation
53
NSAIDs and pregnancy (SE)
increase risk of postpartum hemorrhage (TXA2), intrauterine closure of PDA, avoid use during 3rd trimester
54
aspirin half-life during overdose
15-30 hours (zero order kinetics)
55
Reye's Syndrome
aspirin. children; acute encephalopathy, liver degeneration; follows viral illness; mitochondrial damage?
56
side effects associated with all non-selective NSAIDs
GI irritation, inhibition of platelet aggregation/increased risk of bleeding, decrease in RBF in patients, hypersensitivity
57
what do you give to manage acetaminophen toxicity?
N-acetylcysteine (replenishes glutathione stores)
58
role of alcohol in acetaminophen toxicity?
EtOH induces P450 (2E1) involved in NAPIQ metabolite, also depletes glutathione
59
location of histamine
tissues: mast cells blood: basophils non-mast cells (gastric mucosa cells, epidermis, neurons)
60
drugs, peptides and venoms that promote histamine release
vancomycin, succinylcholine, morphine, curare bradykinin, complement, substance P wasp venom
61
mechanism of histamine release
increase in intracellular calcium
62
vancomycin-induced histamine reaction
red-man syndrome: follows rapid IV infusion, rash on face/neck/upper torso, hypotension, due to mast cell degranulation (not allergic rxn)
63
mechanism of action of omalizumab
IgG that binds Fc portion of IgE; Fc portion cannot bind to mast cell
64
H1 receptor G-protein coupling and 2nd messenger
Gq | Calcium
65
H2 receptor G-protein coupling and 2nd messenger
Gs | cAMP
66
H1 receptor effects on vasoconstriction and vascular permeability
acts on vascular smooth muscle | on post-capillary venules, causes endothelial cells to contract
67
H1 effect on bronchioles, intestinal smooth muscle, peripheral nerve endings
contraction contraction pain and itching
68
H2 effect on bronchioles, intestinal smooth muscle, peripheral nerve endings
relaxation none none
Pharmacology Block 2
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