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FMS > FMS Week 10: Pharmacotherapy of Inflammation & SLE > Flashcards

FMS Week 10: Pharmacotherapy of Inflammation & SLE Flashcards

1
Q

Histamine Synthesis

A
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2
Q

Functions of Histamine

4 Listed

A
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3
Q

Histamine Storage Sites

3 Listed

A
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4
Q

Histamine Receptors

4 Listed

A
  • H1
  • H2
  • H3
  • H4
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5
Q

Histamine Receptor: H1

Signaling Pathway and Receptor locations

6 Listed

A
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6
Q

Histamine Receptor: H2

Signaling Pathway and Receptor locations

6 Listed

A
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7
Q

Histamine Receptor: H3

Signaling Pathway and Receptor locations

3 Listed

A
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8
Q

Histamine Receptor: H4

Signaling Pathway and Receptor locations

3 Listed

A
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9
Q

Organ Systems that respond to H1 and H2

4 Listed

A
  • Cardiovascular
  • Gastrointestinal
  • Pulmonary
  • Nervous System
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10
Q

What kind of receptor are the Histamine receptors

A

7TM G protein-coupled receptors

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11
Q

Cardiovascular interactions with histamine and receptor type

3 Listed

A
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12
Q

Histamine Interactions with Gastrointestinal System and receptor type

1 Listed

A
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13
Q

Histamine Interactions with Pulmonary System and receptor type

1 Listed

A
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14
Q

Histamine Interactions with Nervous System and receptor type

1 Listed

A
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15
Q

Intradermal Wheal-and-flare Response Properties

3 Listed

A
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16
Q

Mechanism of histamine-induced vasodilation

A

Increase in NO

Increase in PGI2

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17
Q

Mechanism of histamine-induced edema

A
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18
Q

Histamine Antagonists AKA

A

Anti-histimines

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19
Q

1st Generation H1 receptor competitive antagonists Examples

3 Listed

A
  • Chlorpheniramine
  • Diphenhydramine
  • Promethazine
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20
Q

1st Generation H1 receptor competitive antagonists Duration

A

Short duration 3 - 6 hours

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21
Q

1st Generation H1 receptor competitive antagonists additional effects

A
  • anticholinergic
  • anti-α-adrenergic
  • antiserotonergic
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22
Q

1st Generation H1 receptor competitive antagonists: Do they cause Sedation?

A

Yes, causes sedation

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23
Q

1st Generation H1 receptor competitive antagonists additional effects additional uses

2 Listed

A
  • Antiemetic (against vomiting and nausea
  • Anti-motion sickness
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24
Q

2nd/3rd Generation H1 Receptor Competitive Antagonists Additional Effects

A

Not useful for nausea or motion sickness

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25
Q

2nd/3rd Generation H1 Receptor Competitive Antagonists: Do they cause sedation

A

Less sedation than 1st generation H1 blockers

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26
Q

2nd/3rd Generation H1 Receptor Competitive Antagonists Duration

A

Long Duration 12-24 hours

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27
Q

2nd/3rd Generation H1 Receptor Competitive Antagonists Examples

A
  • Ioratadine
  • fexodenadine
  • cetirizine
  • desloratadine
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28
Q

2nd/3rd Generation H1 Receptor Competitive Antagonists Other Receptor Activity

A

Little-to-no

  • anticholinergic
  • anti-α-adrendergic
  • anti-serotonergic

actions

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29
Q

Uses of H2 receptor antagonists

6 Listed

A
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30
Q

NSAIDS AKA

A

Nonsteroidal Anti-inflammatory Drugs

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31
Q

Aspirin is an acid or a base?

A

Aspirin is a weak acid

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32
Q

Aspirin is a ________ NSAID

A

Classic

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33
Q

Aspirin effects

4 Listed

A
  • Analgesic (pain reliever)
  • antipyretic (reduces fever)
  • anti-platelet (prevents thrombosis)
  • anti-inflammatory agent
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34
Q

Aspirin qualities of absorption

A
  • rapidly and completely absorbed from the stomach and intestine in unionized form
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35
Q

Aspirin Mechanism of Action

A

Irreversibly inhibits prostaglandin biosynthesis by acetylating the enzyme cyclooxygenase (COX)

**********************************************************************************

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36
Q

Aspirin reduces risk in people 50 and older

A
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37
Q

Common to all Salicylate-like NSAIDs

7 Listed

A
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38
Q

Aspirin and Cancer risk

4 listed

A
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39
Q

Prostaglandins and Cyclooxygenase

6 listed

A

Cyclooxygenase converts Arachidonic acid into cyclic endoperoxide intermediates and prostaglandins

  • PGF2
  • PGE1
  • PGE2
  • PGD2
  • Prostacyclin (PGI2)
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40
Q

Cyclooxygenase 1 vs 2

4 Main things Listed

A
  • Cox-1 is constitutive
  • Cox-1 Homeostasis
  • Cox-2 is inducible
  • Cox-2 inflammation
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41
Q

PGE2 is involved in all processes leading to?

3 listed

A

The classic signs of inflammation

  • redness
  • swelling
  • pain
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42
Q

PGI2 is rapidly produced following?

A

Tissue Injury

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43
Q

PGI2 is an important mediator of?

3 Listed

A

edema and pain associated with acute inflammation

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44
Q

PGI2 is most abundant prostanoid in?

A

Synovial fluid in Human arthritic knee joints

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45
Q

PGD2 is produced by?

2 Listed

A

antigen-presenting dendritic cells and Th2 cells

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46
Q

PGD2 is suggested to play a role in?

A

antigen-specific immune system responses

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47
Q

Elevated levels of PGF2α has been reported in patients suffering from…

4 Listed

A
  • Rheumatoid arthritis
  • Psoriatic arthritis
  • Reactive arthritis
  • Osteoarthritis
48
Q

Traditional NSAIDs inhibit?

A

Both COX-1 and COX-2

49
Q

Examples of Traditional NSAIDs

2 Listed

A
  • Ibuprofen
  • Meclofenamate
50
Q

Some NSAIDs that show some selectivity for COX-2 in-vitro

4 Listed

A
  • Diclofenac
  • Etodolac
  • Meloxicam
  • Nabumetone
51
Q

Diclofenac indomethacin and possible meloxicam are associated with increased risk of?

A

Cardiovascular events (predominantly myocardial infarction)

52
Q

NSAIDs associated with increased risk of cardiovascular events

3 Listed

A
  • Diclofenac
  • Indomethacin
  • Meloxicam
53
Q

NSAID side effects and toxicities involving inhibition of COX-1

4 Listed

A
  • Stomach irritation
  • Prolonged bleed time
  • renal toxicity
  • CNS effects
54
Q

Aspirin Allergy effects

A
  • Angioedema
  • Anaphylaxis
  • Respiratory Symptoms
  • Skin Reactions (increased leukotrienes)
55
Q

Reye’s Syndrome

A

NSAID side effects and toxicities

56
Q

NSAID efficacy table

A
57
Q

NSAID Toxicity Table

A
58
Q

NSAID GI Complications

3 Listed

A
  • The incidence of dyspepsia is >// to 40%
  • often amenable to treatment with an H2 receptor antagonist or proton pump inhibitors (PPI)
  • Incidence of complicated or symptomatic ulcer is 2-5% may be life-threatening
59
Q

NSAID Preexisting conditions and risk factors to consider

A
  • Stomach Ulcer or bleeding
  • Heart disease: Including heart attack or stroke; July 2015 (non-aspirin)
  • Kidney disease or high blood pressure
  • co-administered meds and supplements
60
Q

Non-aspirin risk of heart attack or stroke

A
61
Q

Acetaminophen: The Non-________

A

NSAID

62
Q

Acetaminophen is an acid or a base?

A

A weak base

63
Q

Acetaminophen: Effects

A
  • Analgesic
  • Antipyretic
  • NOT ANTI-INFLAMMATORY
64
Q

Acetaminophen anti-iflammatory

A

Acetaminophen is NOT ANTI-INFLAMMATORY

65
Q

Acetaminophen: Platelet effects

A

no Anti-platelet effects

66
Q

Acetaminophen: overdose

4 Listed

A
  • severe hepatotoxicity caused by reactive quinone metabolites
  • usually, these metabolites are rapidly inactivated by conjugation with glutathione
  • with toxic levels of the drug, hepatic glutathione becomes depleted
  • The drug N-acetylcysteine is used to prevent hepatotoxicity
67
Q

N-AcetylCysteine is used to?

A

Prevent Hepatotoxicity from Acetominaphen overdose

68
Q

Selective COX-2 Inhibitors benefits

A

drugs having selectivity for COX-2 over COX-1 should cause significantly fewer severe side effects in the GI tract than traditional NSAIDs

69
Q

COX-2-selective Inhibitors Examples

3 Listed

A
  • Celecoxib
  • Etoricoxib
  • Lumiracoxib
70
Q

The only selective COX-2 inhibitor currently approved by the FDA?

A

Celecoxib (Celebrex)

71
Q

Celecoxib GI complicaitons

A

has not been shown to be any better than NSAIDs for upper GI (stomach) complications but has been shown to be associated with a significantly reduced incidence of small bowel inflammation and mucosal breaks than traditional NSAIDs

72
Q

Celecoxib is a _________ (drug structure) and ____________ (Drug type)

2 Listed

A
  • Sulfonamide
  • Selective-COX-2 Inhibitor
73
Q

Celecoxib metabolism

A
  • t1/2 = 6-12 hours
  • metabolized by CYP2C9
  • Inhibits CYP2D6
  • Significant first-pass metabolism (20-60% bioavailability)
74
Q

Celecoxib is approved as an analgesic for

3 Listed

A
  • Rheumatoid Arthritis
  • Osteoarthritis
  • NOT FOR GENERAL PAIN
75
Q

CYP2D6 metabolizes…

3 Listed

A
  • Metoprolol
  • SSRIs
  • TCAs
76
Q

Comparisons of NSAIDS and GI complications

A
77
Q

In addition to inflammation, COX-2 plays a role in?

3 Listed

A

physiologic processes such as

  • bone remodeling
  • ulcer repair activity
  • COX-2 derived prostaglandins are involved in renal function: Inhibition of COX-2 reduces water and salt excretion by the kidney which can lead to peripheral edema, hypertension, exacerbation of pre-existing hypertension
78
Q
A
79
Q

Celecoxib decreases __________ in animal studies

A

fetal survival rates

80
Q

COX-2 inhibitors in Aspirin-Induced Asthma

A
81
Q

Leukotrienes from the ____________ pathway

A

Lipoxygenase

82
Q

Leukotriene pathway inhibitors Examples

3 Listed

A
  • Zileuton
  • Zafirlukast
  • Montelukast
83
Q

Zileuton inhibits

2 Listed

A
  • 5-Lipoxygenase
  • CYP3A4 (can influence the metabolism of terfenadine, warfarin, theophylline)
84
Q

Zileuton Route of administration

A

Orally Active

85
Q

Zileuton Indicated uses

A

for mild to moderate asthma

86
Q

Considered to be an alternative to low-dose inhaled corticosteroid

3 Listed

A
  • Zileuton
  • Zafirlukast
  • Montelukast
87
Q

Zafirlukast & Montelukast Inhibits

4 Listed

A
  • LTD4 - receptor antagonists
  • CYP3A4
  • CYP2C9
  • Increased warfarin t1/2
88
Q

Zafirlukast & Montelukast Route of Administration

A

Orally Active

89
Q

Zafirlukast & Montelukast Indicated uses

A

For mild to moderate asthma

90
Q

HPA Axis and Cortisol

2 Listed

A

Negative Feedback on the Hypothalamus

  • decreased CRH (Corticotropin-Releasing Hormone)

Negative feedback on the Anterior Pituitary

  • Decreased ACTH (Adrenocorticotropic Hormone)
91
Q

Cortisol is the primary?

A

Glucocorticoid in humans

92
Q

The primary glucocorticoid in humans is?

A

Cortisol

93
Q

Glucocorticoids exert a wide range of physiologic effects including:

3 listed

A

regulation Of

  • Immune
  • Growth
  • carbohydrate, fat, and protein Metabolism
94
Q

Classic MOA of Glucocorticoids

A
95
Q

Glucocorticoid resistance

2 Listed

A
96
Q

Patients with inflammatory diseases can have reduced responsiveness to glucocorticoids, these conditions are?

3 Listed

A
  • Rheumatoid arthritis
  • asthma
  • inflammatory bowel disease
97
Q

Glucocorticoid effects on immune cells

Inhibits 9

Stimulates 2

A

Inhibits:

  • Neutrophils
  • B cells
  • Th1
  • Th2
  • Th17
  • Mast Cells
  • Basophils
  • Eosinophils
  • DCs

Stimulates

  • Treg
  • Macrophages
98
Q

Potential mechanisms of GC resistance

4 Listed

A
99
Q

Synthetic Glucocorticoids Pharmacokinetics

3 Listed

A
100
Q

Chronic use of Glucocorticoids is associated with risk for?

& Short Term use risks

A

Adverse effects

Short term use: Sepsis, venous thromboembolism, fracture

101
Q

Side effects of prolonged Glucocorticoid therapy Main organ systems & tissues

11 Listed

A
102
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Adrenal gland

2 Listed

A
  • Adrenal atrophy
  • Cushing’s syndrome
103
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Cardiovascular System

2 Listed

A
  • Hypertension
  • Thrombosis
104
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: CNS

3 Listed

A
  • changes in behavior
  • cognition
  • memory
105
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: GI Tract

3 Listed

A
  • GI Bleeding
  • Pancreatitis
  • Peptic Ulcer
106
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Immune System

1 Listed

A

Immunosuppression

107
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Integument

3 Listed

A
  • Delayed wound healing
  • Erythema
  • Dlucocorticoid-induced acne
108
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Eyes

2 Listed

A
  • Cataracts
  • Glaucoma
109
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Kidneys

2 Listed

A
  • Increased sodium reabsorption
  • increased potassium excretion
110
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Reproductive System

3 Listed

A
  • Delayed puberty
  • Fetal growth retardation
  • Hypogonadism
111
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Bone

2 Listed

A
  • inhibits bone formation
  • Stimulates bone resorption
112
Q

Side Effects of high dose or prolonged Glucocorticoid therapy: Growth and Development

1 Listed

A

Inhibits growth in children

113
Q

Systemic corticosteroid use considerations

A
114
Q

Synthetic Glucocorticoid Anti-inflammatory activity in comparison to cortisol

4 Listed

A
115
Q

synthetic Glucocorticoids Examples

4 Listed

A
  • Cortisone
  • Prednisone
  • Triamcinolone
  • Dexamethasone

FMS (34 decks)

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