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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
2nd/3rd Generation H1 Receptor Competitive Antagonists: Do they cause sedation
Less sedation than 1st generation H1 blockers
26
2nd/3rd Generation H1 Receptor Competitive Antagonists Duration
Long Duration 12-24 hours
27
2nd/3rd Generation H1 Receptor Competitive Antagonists Examples
* Ioratadine * fexodenadine * cetirizine * desloratadine
28
2nd/3rd Generation H1 Receptor Competitive Antagonists Other Receptor Activity
Little-to-no * anticholinergic * anti-α-adrendergic * anti-serotonergic actions
29
Uses of H2 receptor antagonists 6 Listed
30
NSAIDS AKA
Nonsteroidal Anti-inflammatory Drugs
31
Aspirin is an acid or a base?
Aspirin is a weak acid
32
Aspirin is a ________ NSAID
Classic
33
Aspirin effects 4 Listed
* Analgesic (pain reliever) * antipyretic (reduces fever) * anti-platelet (prevents thrombosis) * anti-inflammatory agent
34
Aspirin qualities of absorption
* rapidly and completely absorbed from the stomach and intestine in unionized form
35
Aspirin Mechanism of Action
Irreversibly inhibits prostaglandin biosynthesis by acetylating the enzyme cyclooxygenase (COX) \*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*
36
Aspirin reduces risk in people 50 and older
37
Common to all Salicylate-like NSAIDs 7 Listed
38
Aspirin and Cancer risk 4 listed
39
Prostaglandins and Cyclooxygenase 6 listed
Cyclooxygenase converts Arachidonic acid into cyclic endoperoxide intermediates and prostaglandins * PGF2 * PGE1 * PGE2 * PGD2 * Prostacyclin (PGI2)
40
Cyclooxygenase 1 vs 2 4 Main things Listed
* Cox-1 is constitutive * Cox-1 Homeostasis * Cox-2 is inducible * Cox-2 inflammation
41
PGE2 is involved in all processes leading to? 3 listed
The classic signs of inflammation * redness * swelling * pain
42
PGI2 is rapidly produced following?
Tissue Injury
43
PGI2 is an important mediator of? 3 Listed
edema and pain associated with acute inflammation
44
PGI2 is most abundant prostanoid in?
Synovial fluid in Human arthritic knee joints
45
PGD2 is produced by? 2 Listed
antigen-presenting dendritic cells and Th2 cells
46
PGD2 is suggested to play a role in?
antigen-specific immune system responses
47
Elevated levels of PGF2α has been reported in patients suffering from... 4 Listed
* Rheumatoid arthritis * Psoriatic arthritis * Reactive arthritis * Osteoarthritis
48
Traditional NSAIDs inhibit?
Both COX-1 and COX-2
49
Examples of Traditional NSAIDs 2 Listed
* Ibuprofen * Meclofenamate
50
Some NSAIDs that show some selectivity for COX-2 in-vitro 4 Listed
* Diclofenac * Etodolac * Meloxicam * Nabumetone
51
Diclofenac indomethacin and possible meloxicam are associated with increased risk of?
Cardiovascular events (predominantly myocardial infarction)
52
NSAIDs associated with increased risk of cardiovascular events 3 Listed
* Diclofenac * Indomethacin * Meloxicam
53
NSAID side effects and toxicities involving inhibition of COX-1 4 Listed
* Stomach irritation * Prolonged bleed time * renal toxicity * CNS effects
54
Aspirin Allergy effects
* Angioedema * Anaphylaxis * Respiratory Symptoms * Skin Reactions (increased leukotrienes)
55
Reye's Syndrome
NSAID side effects and toxicities
56
NSAID efficacy table
57
NSAID Toxicity Table
58
NSAID GI Complications 3 Listed
* 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
NSAID Preexisting conditions and risk factors to consider
* 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
Non-aspirin risk of heart attack or stroke
61
Acetaminophen: The Non-\_\_\_\_\_\_\_\_
NSAID
62
Acetaminophen is an acid or a base?
A weak base
63
Acetaminophen: Effects
* Analgesic * Antipyretic * NOT ANTI-INFLAMMATORY
64
Acetaminophen anti-iflammatory
Acetaminophen is NOT ANTI-INFLAMMATORY
65
Acetaminophen: Platelet effects
no Anti-platelet effects
66
Acetaminophen: overdose 4 Listed
* 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
N-AcetylCysteine is used to?
Prevent Hepatotoxicity from Acetominaphen overdose
68
Selective COX-2 Inhibitors benefits
drugs having selectivity for COX-2 over COX-1 should cause significantly fewer severe side effects in the GI tract than traditional NSAIDs
69
COX-2-selective Inhibitors Examples 3 Listed
* Celecoxib * Etoricoxib * Lumiracoxib
70
The only selective COX-2 inhibitor currently approved by the FDA?
Celecoxib (Celebrex)
71
Celecoxib GI complicaitons
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
Celecoxib is a _________ (drug structure) and ____________ (Drug type) 2 Listed
* Sulfonamide * Selective-COX-2 Inhibitor
73
Celecoxib metabolism
* t1/2 = 6-12 hours * metabolized by CYP2C9 * Inhibits CYP2D6 * Significant first-pass metabolism (20-60% bioavailability)
74
Celecoxib is approved as an analgesic for 3 Listed
* Rheumatoid Arthritis * Osteoarthritis * NOT FOR GENERAL PAIN
75
CYP2D6 metabolizes... 3 Listed
* Metoprolol * SSRIs * TCAs
76
Comparisons of NSAIDS and GI complications
77
In addition to inflammation, COX-2 plays a role in? 3 Listed
**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
79
Celecoxib decreases __________ in animal studies
fetal survival rates
80
COX-2 inhibitors in Aspirin-Induced Asthma
81
Leukotrienes from the ____________ pathway
Lipoxygenase
82
Leukotriene pathway inhibitors Examples 3 Listed
* Zileuton * Zafirlukast * Montelukast
83
Zileuton inhibits 2 Listed
* 5-Lipoxygenase * CYP3A4 (can influence the metabolism of terfenadine, warfarin, theophylline)
84
Zileuton Route of administration
Orally Active
85
Zileuton Indicated uses
for mild to moderate asthma
86
Considered to be an alternative to low-dose inhaled corticosteroid 3 Listed
* Zileuton * Zafirlukast * Montelukast
87
Zafirlukast & Montelukast Inhibits 4 Listed
* LTD4 - receptor antagonists * CYP3A4 * CYP2C9 * Increased warfarin t1/2
88
Zafirlukast & Montelukast Route of Administration
Orally Active
89
Zafirlukast & Montelukast Indicated uses
For mild to moderate asthma
90
HPA Axis and Cortisol 2 Listed
Negative Feedback on the Hypothalamus * decreased CRH (Corticotropin-Releasing Hormone) Negative feedback on the Anterior Pituitary * Decreased ACTH (Adrenocorticotropic Hormone)
91
Cortisol is the primary?
Glucocorticoid in humans
92
The primary glucocorticoid in humans is?
Cortisol
93
Glucocorticoids exert a wide range of physiologic effects including: 3 listed
regulation Of * Immune * Growth * carbohydrate, fat, and protein Metabolism
94
Classic MOA of Glucocorticoids
95
Glucocorticoid resistance 2 Listed
96
Patients with inflammatory diseases can have reduced responsiveness to glucocorticoids, these conditions are? 3 Listed
* Rheumatoid arthritis * asthma * inflammatory bowel disease
97
Glucocorticoid effects on immune cells Inhibits 9 Stimulates 2
Inhibits: * Neutrophils * B cells * Th1 * Th2 * Th17 * Mast Cells * Basophils * Eosinophils * DCs Stimulates * Treg * Macrophages
98
Potential mechanisms of GC resistance 4 Listed
99
Synthetic Glucocorticoids Pharmacokinetics 3 Listed
100
Chronic use of Glucocorticoids is associated with risk for? & Short Term use risks
Adverse effects Short term use: Sepsis, venous thromboembolism, fracture
101
Side effects of prolonged Glucocorticoid therapy Main organ systems & tissues 11 Listed
102
Side Effects of high dose or prolonged Glucocorticoid therapy: Adrenal gland 2 Listed
* Adrenal atrophy * Cushing's syndrome
103
Side Effects of high dose or prolonged Glucocorticoid therapy: Cardiovascular System 2 Listed
* Hypertension * Thrombosis
104
Side Effects of high dose or prolonged Glucocorticoid therapy: CNS 3 Listed
* changes in behavior * cognition * memory
105
Side Effects of high dose or prolonged Glucocorticoid therapy: GI Tract 3 Listed
* GI Bleeding * Pancreatitis * Peptic Ulcer
106
Side Effects of high dose or prolonged Glucocorticoid therapy: Immune System 1 Listed
Immunosuppression
107
Side Effects of high dose or prolonged Glucocorticoid therapy: Integument 3 Listed
* Delayed wound healing * Erythema * Dlucocorticoid-induced acne
108
Side Effects of high dose or prolonged Glucocorticoid therapy: Eyes 2 Listed
* Cataracts * Glaucoma
109
Side Effects of high dose or prolonged Glucocorticoid therapy: Kidneys 2 Listed
* Increased sodium reabsorption * increased potassium excretion
110
Side Effects of high dose or prolonged Glucocorticoid therapy: Reproductive System 3 Listed
* Delayed puberty * Fetal growth retardation * Hypogonadism
111
Side Effects of high dose or prolonged Glucocorticoid therapy: Bone 2 Listed
* inhibits bone formation * Stimulates bone resorption
112
Side Effects of high dose or prolonged Glucocorticoid therapy: Growth and Development 1 Listed
Inhibits growth in children
113
Systemic corticosteroid use considerations
114
Synthetic Glucocorticoid Anti-inflammatory activity in comparison to cortisol 4 Listed
115
synthetic Glucocorticoids Examples 4 Listed
* Cortisone * Prednisone * Triamcinolone * Dexamethasone

FMS (34 decks)

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