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Pharm > 06a: Anti-Inflammatories, Immunosuppressants > Flashcards

06a: Anti-Inflammatories, Immunosuppressants Flashcards

1
Q

List the physiological roles of histamine.

A
  1. Allergic/inflammatory reactions
  2. Gastric acid secretion
  3. Neurotransmission
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2
Q

List some CNS effects of His.

A

Arousal, neuroendocrine (ACTH, ADH), thermoregulation, hunger/satiety

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3
Q

T/F: Distribution and storage of His found in nearly all tissues.

A

True

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4
Q

His stored in (X) in mast cells and basophils. It’s in (active/inactive) form and (free/bound).

A

X = secretory granules
Inactive
Bound (to heparin and anionic protein)

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5
Q

His release from (X) cells in GI tract is mediated by which NT/hormones?

A

X = ECC

ACh and gastrin

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6
Q

T/F: Both His receptor subtypes H1 and H2 are RTK receptors.

A

False - both GPCR

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7
Q

His H1 receptor utilized which 2nd messenger pathway?

A

Increase IP3/DAG (thus increase Ca)

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8
Q

His H2 receptor utilized which 2nd messenger pathway?

A

Increase cAMP

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9
Q

List the two important antagonists for the H1 receptor.

A
  1. Diphenhydramine (Benadryl)

2. Loratadine (Claritin)

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10
Q

List the H1 receptor responses on vasculature.

A
  1. Vasodilation of arterioles/venules (via NO)
  2. Increase cap permeability
  3. Vasoconstriction of large a and v
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11
Q

List the non-vascular H1 receptor responses.

A
  1. Bronchial smooth muscle constriction
  2. Stimulation of nerve endings (itch, flare, pain)
  3. CNS arousal
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12
Q

List the H2 receptor responses. Star the responses only present if high His levels.

A
  1. Gastric acid secretion
  2. Vasodilation (smooth muscle relaxation)*
  3. Increased HR, contractility*
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13
Q

Diphenhydramine, aka (X), is in what class of drugs?

A

X = benadryl

First generation anti-histamines

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14
Q

Loratadine, aka (X), is in what class of drugs?

A

X = claritin

Second generation anti-histamines

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15
Q

T/F: First generation anti-histamines have weak selectivity for H1 v H2 receptors.

A

False

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16
Q

T/F: First generation anti-histamines have CNS access.

A

True

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17
Q

First generation anti-histamines had which secondary effects, due to weak selectivity?

A
  1. Local anesthetic activity
  2. Muscarinic and alpha-adrenergic antagonism
  3. Sedation
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18
Q

(First/second) generation anti-histamines helped develop other classes of drugs to treat (X).

A

First;

X = psychosis

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19
Q

Weak selectivity of first generation anti-His results in side effects including: urinary (incontinence/retention), (hyper/hypo)-tension, (tachy/brady)-cardia.

A

Retention (anti-muscarinic), hypotension and reflex tachycardia (anti-alphaR)

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20
Q

(First/second) generation anti-histamines used to treat Type 1 hypersensitivity reaction. And asthma?

A

Neither for neither!! Need Epi; anti-his are not bronchodilators

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21
Q

(First/second) generation anti-histamines used to treat nausea/vomiting and motion sickness.

A

First - can access CNS

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22
Q

T/F: First generation anti-histamines can be bought OTC for sleep aid.

A

True

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23
Q

Toxicity of first gen anti-his presents similarly to toxicity by (X) drug.

A

X = Atropine (muscarinic antagonist)

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24
Q

Compared to first gen, second generation anti-his have (extra/missing) (X) group that limits CNS access. This lowers incidence of which side effect?

A

Extra;
X = carboxylate
Sedation

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25
Q

Cases of sudden death due to ventricular arrhythmia (inhibited K channel) was seen in which class of drugs?

A

Older 2nd gen anti-his (taken off market)

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26
Q

Mechanism of NSAIDS primarily mediated by:

A

Ihibition of cyclooxygenase (COX)

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27
Q

NSAIDS and aspirin-like drugs used to treat (generally) which symptoms?

A

Pain, inflammation, fever

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28
Q

T/F: Second-gen anti-his help reduce watery eyes, rhinorrhea, and sneezing.

A

True

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29
Q

T/F: Second-gen anti-his help reduce nasal itching and congestion.

A

False - not nasal congestion

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30
Q

PGE2 (prostaglandin) causes (increase/decrease) body temp. Also (increase/decrease) pain and (X) in response to autocoids.

A

Increase;
Increase
X = edema

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31
Q

(PGE2/PGF2a) prostaglandins affect GI tract. In which way(s)?

A

Both;

  1. Increase GI motility/secretion and cytoprotection
  2. Decrease gastric secretions
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32
Q

Prostaglandins (PGE2/PGF2a) (increase/decrease) uterine contraction.

A

Both

Increase

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33
Q

Prostacyclin is metabolite of (X), made in (Y) cells. What are its functions?

A 
X = arachidonic acid (via COX pathway)
Y = endothelial
  1. Inhibits platelet aggregation
  2. Vasodilation
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34
Q

Thromboxane A2 (TXA2) is metabolite of (X), made in (Y) cells. What are its functions?

A 
X = arachidonic acid (via COX pathway)
Y = platelet
  1. Stimulates platelet aggregation
  2. Vasoconstriction
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35
Q

COX (1/2) is constitutively expressed in (X) cells and is “good” for its effects on:

A

1;
X = all

Gastric cytoprotection, vascular homeostasis, platelet aggregation, kidney function

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36
Q

COX (1/2) is constitutively expressed in (X) cells and is also induced by (Y).

A

2
X = brain, kidney, bone, GI tissues
Y = cytokines, GFs, tumor promoters

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37
Q

COX-2 is associated with which physiological/pathological conditions?

A

Inflammation and cancer

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38
Q

“Traditional” non-selective NSAIDs, such as (X), inhibit COX (1/2). Is this optimal?

A

X = ibuprofen
Both;

No.. COX-1 inhibition, to some extent, mediates many adverse events

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39
Q

COX-2-selective agents, such as (X): preferred over traditional NSAIDs due to less adverse effects, especially on (Y) system.

A 
X = Celecoxib
Y = GI
40
Q

T/F: Acetaminophen is an NSAID.

A

False - not anti-inflammatory

41
Q

Acetaminophen generally provides what kind of relief?

A

Antipyretic (reduce fever) and analgesic (reduce pain)

42
Q

Acetaminophen acts by (reversibly/irreversibly)

(stimulating/inhibiting) (X). Its effects are (stronger/weaker) than NSAIDs and salicylates.

A

Reversibly inhibiting;
X = COX (in CNS!!)
Weaker

43
Q

Acetaminophen lacks (X) effect due to poor ability to inhibit COX in presence of (Y).

A 
X = anti-inflammatory
Y = peroxides (at sites of inflammation)
44
Q

(X) is the preferable antipyretic analgesic for patients with increased risk of NSAID toxicity.

A

X = acetaminophen

45
Q

(NSAIDs/Acetaminophen/Aspirin) are problematic in excess due to buildup of (conjugated/non-conjugated) metabolite that causes centrilobular hepatic necrosis.

A

Acetaminophen;

Non-conjugated

46
Q

List conditions that increase risk of centrilobular hepatic necrosis via metabolite of (X) drug.

A

X = Acetaminophen

  1. Inducers of CYP enzymes (CYP2E1, CYP3A4)
  2. Alcohol (CYP induction, hepatotoxicity)
  3. Glutathione depletion (less conjugation)
47
Q

Drug of choice for children with viral infections is (NSAID/Acetaminophen/Aspirin).

A

Acetaminophen

48
Q

List some “traditional” NSAIDs.

A

Ibuprofen, Aspirin, Non-acetylated salicylates

49
Q

(X) drug irreversibly inactivates COX via (Y) modification.

A 
X = aspirin
Y = acetylation
50
Q

Aspirin has (short/long) half-life and is converted to (active/inactive) metabolite (X).

A

Short;
Active (antipyretic, analgesic, anti-inflamm)
X = sodium salicylate

51
Q

NSAIDs: Antipyretic effects via (increase/decrease) in cutaneous blood flow and (increase/decrease) sweating.

A

Increase; increase

52
Q

Avoid (X) drug class for children with viral infections due to association with (Y) Syndrome.

A 
X = salicylates
Y = Reyes'
53
Q

Primary mechanism of NSAIDs to relieve pain.

A

Inhibit PGE2 synthesis in periphery

54
Q

List the mechanism of NSAIDs to reduce inflammation.

A
  1. Inhibition of COX-2

2. Inhibit activation of TF (NF-kB)

55
Q

The transcription factor NF-kB has key role in (X). (Stimulating/inhibiting) its activation is a role of which drugs?

A

X = cytokine and pro-inflammatory mediator production
Inhibiting;
NSAIDs

56
Q

Baby aspiring taken daily provides some selective inhibition of (X) and stimulation of (Y). This makes it CV-protective.

A 
X = thromboxane (in platelet)
Y = prostacyclin (in endothelial cell)
57
Q

Role of NSAIDs in (stimulation/inhibition) of (X) synthesis makes (coagulation/bleeding) an adverse effect of the drugs.

A

Inhibition;
X = thromboxane
Bleeding

58
Q

A single analgesic dose of (X) increases bleeding time by factor of (1/2/3/4/5) for how long?

A

X = aspirin (irreversibly inactivates COX-1 in platelets)
2;
Life of platelet (4-7 days)

59
Q

T/F: Acetaminophen does not affect platelet function, so bleeding isn’t adverse effect.

60
Q

Aspirin requires relatively smallest dose for its (anti-inflamm/anti-platelet/analgesic) effect than (anti-inflamm/anti-platelet/analgesic) effects.

A

Anti-platelet (80 mg/day);
Analgesic (700-1000 mg/day)
Anti-inflamm (3 g/day)

61
Q

Chronic use of (X) associated with “analgesic nephropathy”, specifically which renal outcomes?

A

X = NSAIDs, acetaminophen

Papillary necrosis and interstitial nephritis

62
Q

NSAIDs renal toxicity greater in patients with renal/CV diseases due to which side effects?

A

Na/water retention and edema

63
Q

Most common side effect of NSAIDs involves (CNS/GI/Renal) toxicity, caused by (stimulation/inhibition) of (X) enzyme.

A

GI;
Inhibition
X = COX-1

64
Q

List the GI toxicity effects of NSAIDs.

A

Bleeding, erosions, ulcers

65
Q

Pt comes in with bronchospasm, rhinorrhea, and hives after taking aspirin. This is case of aspirin (allergy/intolerance). It’s mediated by (X).

A

Intolerance (NOT allergy, no Ab)

X = leukotrienes

66
Q

T/F: Aspirin and acetaminophen intolerance will present similar to allergic reaction.

A

False - not acetaminophen

67
Q

Aspirin intolerance more likely seen in (X) patient population due to (higher/lower) levels of and sensitivity to (Y).

A

X = asthmatics
Higher;
Y = leukotrienes

68
Q

Rofecoxib, a(n) (X) drug, was taken off market for increasing risk of CV events (MI, stroke). Do other (X) drugs also have this risk?

A

X = COX-2 inhibitor

Yes (Celecoxib, for ex), but not any more toxic than traditional NSAIDs

69
Q

Active center of COX(1/2) has larger side pocket. Thus, (ibuprofen/celecoxib) is bulkier.

A

COX-2;

Celecoxib (selective)

70
Q

T/F: Celecoxib, unlike Ibuprofen, has no GI or renal toxicity.

A

False - less GI toxicity, but still Na retention/edema (renal toxicity)

71
Q

T/F: There’s a CV (boxed) warning for all NSAIDs.

A

False - not aspirin

72
Q

Glucocorticoids, such as (X), have which effects on immune system?

A

X = cortisol

Anti-inflammatory and immunosuppressant

73
Q

T/F: Cortisol has equal affinity for glucocorticoid and mineralocorticoid receptors.

74
Q

In (X) locations, cortisol converted to (Y) by 11-b-hydroxysteroid DH. (Y) is (active/inactive) and has which important characteristic?.

A 
X = kidney, colon, salivary glands
Y = cortisone

Active;
selective to glucocorticoid receptors

75
Q

Glucocorticoids (stimulate/inhibit) arachidonic acid pathway by (increasing/decreasing) transcription of:

A

Inhibit;
Increasing: Lipocortin (inhibits phospholipase A2)
Decreasing: COX-2 transcription

76
Q

(X) drugs (increase/decrease) synthesis of IkB, which (stimulates/inhibits) NF-kB, thus (increasing/decreasing) its function of:

A

X = glucocorticoids
Increase;
Inhibits;
Decreasing

Transcription of pro-inflammatory proteins

77
Q

(X) anti-inflammatory drugs decrease synthesis of adhesion factors affecting leukocyte localization.

A

X = glucocorticoids

78
Q

List the advantages of anti-inflammatory synthetic steroids (over cortisol, for example).

A
  1. Greater selectivity (glucocorticoid v mineralocorticoid receptors)
  2. Longer half-life and duration of action
79
Q

List examples of anti-inflammatory synthetic steroids, specific for glucocorticoid receptors.

A
  1. Dexamethasone

2. Prednisone

80
Q

List three therapeutic uses for glucocorticoids.

A
  1. Adrenal disorders (replacement therapy)
  2. Immunosuppressant effect (for autoimmune/transplants)
  3. Anti-inflammatory (for RA, lupus)
81
Q

Postural hypotension is symptom of glucocorticoid (toxicity/insufficiency) along with which other symptoms?.

A

Insufficiency;

Nausea/vomit, anorexia, joint/muscle pain, fever

82
Q

T/F: Glucocorticoids used to treat severe allergic reactions.

83
Q

T/F: Glucocorticoids are ineffective treatments for GI disorders.

A

False - used for UC and Crohn’s

84
Q

(X) anti-inflammatory drugs used to treat cerebral edema (from tumor).

A

X = glucocorticoids

85
Q

(X) anti-inflammatory drugs used to neural inflammation (i.e. Bell’s palsy).

A

X = glucocorticoids

86
Q

T/F: Glucocorticoid toxicity could cause immune cell malignancies.

A

False - used to treat them (i.e. leukemia, lymphoma)

87
Q

Prolonged treatment of glucocorticoids is not safe for which reasons?

A
  1. Toxicity
  2. Suppresses HPA axis
  3. Abrupt termination is life-threatening
88
Q

Upon cessation of long-term glucocorticoid administration, (X) gland is (hypertrophied/atrophied). Thus, you’ll see a surge in (ACTH/Cortisol) and lag in (ACTH/Cortisol) levels.

A

X = adrenal cortex
Atrophied;
ACTH;
Cortisol

Over the time-course of months!

89
Q

T/F: Glucocorticoids used to treat infection.

A

False - immunosuppressive (infection is consequence of GC long-term use)

90
Q

Long-term GC use: (hyper/hypo)-tension, (hyper/hypo)-glycemia, and muscle (hyper/a)-trophy.

A

Hypertension, Hyperglycemia, and muscle atrophy (wasting)

91
Q

(Local/systemic) administration of GC is preferred for which reason? Provide some examples of this admin method.

A

Local to reduce toxicity;

Nasal spray, topical admin, joint injection, slow-release capsule (high first pass effect)

92
Q

Methotrexate used as (X) drug and functions to (stimulate/inhibit) (Y) process in high doses.

A

X = immunosuppressant
Inhibit;
Y = pyrimidine synthesis (arrest DNA replication/cell division)

93
Q

Methotrexate used as (X) drug and functions to (stimulate/inhibit) (Y) process in low doses.

A

X = immunosuppressant
Inhibit;
Y = de novo purine synthesis

94
Q

Infliximab is (low/high) MW drug that acts to:

A

High (Ab);

Block TNF-alpha (immunosuppressant)

95
Q

Abatacept (increases/decreases) immune function by binding APC at (MHC/Co-stim ligand) and (stimulating/inhibiting) T-cell activation.

A

Decrease (immunosuppressant);
Co-stim ligand;
Inhibiting

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