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Pharm Flashcards

1
Q

Histidine–>Histamine via what?

A

Histidine decarboxylase

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2
Q

Where do we find histamine?

A

All tissues, especially GI, lungs, skin

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3
Q

How is histamine packaged?

A

inactive form, complexed to heparin inside mast cell/basophil granules

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4
Q

What triggers mast cell degranulation?

A

binding of allergens–>crosslinking IgE Fc receptors
Bacterial toxins/insect stings
trauma/cold

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5
Q

What are the triple responses of Lewis?

A

response to scratching skin-redness, flare, wheal

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6
Q

What are autocoids?

A

biologically active substance with sort half life. They act near the site of synthesis

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7
Q

What are the two autocoids and what are their differences?

A
  1. Vasoactive amines (histamine, serotonin)=mast cells and basophils (histamine only), platelets
  2. Eicosanoids (prostaglandins, leukotrienes)=all leukocytes, platelets (prostaglandins only)
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8
Q

Peripheral effects of H1

A

increase naso/broncho mucous production
bronchoconstruction
pruritis (itching)
inflammation

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9
Q

Effect of H1 on IP3 and DAG?

A

increase

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10
Q

CNS effects of H1

A

Decrease BP, increase HR
Increases neurotransmission
Decreases sedation

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11
Q

H2, H3, H4 affect on cAMP

A

H2 increases

H3 and H4 decreases

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12
Q

H1, H2, H3, H4…which ones are Gs, Gi, Gq?

A

Gs: H2
Gi: H3, H4
Gq: H1

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13
Q

H2 effects

A

increase gastric acid secretion
decrease BP, increase HE
inflammation

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14
Q

H3 effects?

A

presynaptic inhibition of CNS neurotransmitter release

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15
Q

H4 effects?

A

Mast cell chemotaxis

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16
Q

Examples of 1st generation H1 Antagonist

A

Diphenhydramine, chorpheniramine, dimenhydrinate, doxylamine

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17
Q

Mechanism of 1st generation H1 Antagonist

A

competitive, reversible inhibition of H1 receptors in PNS and CNS. results in decreased DAG/IP3

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18
Q

Effects in periphery of 1st generation H1 Antagonist

A

decrease mucous production, bronchoconstriction, itching

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19
Q

CNS effects of 1st generation H1 Antagonist

A

increased sedation, decreased NT release/cognitive

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20
Q

Major SE of 1st generation H1 Antagonist

A

Sedation. Also some sympathetic effects, hypotension/dizziness, tachy

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21
Q

Examples of 2nd generation H1 antagonist

A

Cetirixine, loratidine, fexofenadine

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22
Q

Mechanism of 2nd generation H1 antagonist

A

competitive, reversible inhibition of H1 receptors in PERIPHERY only (does not cross BBB)

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23
Q

SE of 2nd generation H1 antagonist compared to 1st?

A

less than 1st gen due to greater specificity and no CNS effects

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24
Q

Examples of H2 antagonist?

A

cimetidine, ranitidine, famotidine, nizatidine

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25
Mechanism of H2 antagonist?
inhibition of H2 receptor, decreases cAMP
26
Effects of H2 antagonist?
decrease gastric acid secretion
27
SE of H2 antagonist?
Anti-androgenic effects (prolactin release results in man boobs)...this is mostly with cimetidine **possibly some cytochrome p450 inhibition
28
H2 antagonist use?
peptic ulcer disease, GERD, gastritis
29
What kind of inhibitors are NSAIDs?
non-selective COX1 and COX2
30
The desired effect of NSAIDs due to what receptor?
COX2 inhibition
31
SE of NSAIDs due to?
COX1 inhibition
32
Mechanism of ASA?
acetylates serine residue in COX active site. More COX1 selective and thus, higher dose is needed for COX 2 inhibition
33
ASA use?
4 As low doses: Anti-platelet (TIAs, stroke, MI proph) Intermediate doses: Analgesic, Anti-pyretic (medium to low grade fever) High doses: Anti-inflammatory (arthritis, joint swelling)
34
SE of ASA?
GI bleeding (gastric mucosal damage due to decreased PGE2 and PGI2)
35
What is Reye's syndrome?
febrile viral illness in children under 16 with ASA
36
Mechanism of Propionic Acid?
competitively reversibly binds COX active site
37
Use of Propionic Acid?
anti-inflammatory, analgesic, antipyretic
38
SE of Propionic ACid?
Less G distress and ulcers than ASA | Acute renal insufficiency and chronic interstial nephritis
39
COX-2 Selective inhibitors example
Celecoxib, rovecoxib
40
Why doesn't Cox-2 selective inhibitors bind the COX-1 site?
its fatass is too big
41
Use of COX-2 selective inhibitors?
osteoarthritis, RA, familial adenomatous polyposis, dysmenorrhea, acute pain
42
GOAL ofCOX-2 selective inhibitors?
decrease the GI and vascular SE common with other NSAIDS
43
SE of Cox-2 inhibitors?
increases risk in adverse thrombotic CV events
44
Indomethacin mechanism
decreases movement of granulocytes in affected area
45
Use of indomethacin?
close a PDA, acute gout
46
Acetaminophen mechanism
conjugates with arachidonic acid in CNS
47
Acetaminophen inhibits COX1 or COX2?
both
48
Uses of acetaminophen
pain/fever control in children with viral infections and adults with bleeding/GI risks
49
When does acetaminophen become toxic?
When Glutathione is used up. Remember that it gets degraded via the Cytochrome p450 pathway
50
Steroids are released by the body from where and why?
released from zona fasciculata in adrenal gland in response to pituitary release of ACTH. It's part of a negative feedback that inhibits ACTH release in the pituitary
51
Mechanism of steroids?
binds nuclear receptors in cell cytoplasm. This changes the protein levels in cells and possibly indirect inhibition of phosphilipase Ax and reduced expression of COX2
52
SE of steroids?
Osteoporosis (suppresses Ca absorption) | Cushing's Syndrome
53
Synthetic Prostanoids is AKA
misoprostol
54
Mechanism of synthetic prostanoids?
enhances normal PGE and decreases acid production
55
When is synthetic prostanoids used?
maintenance of PDA also induces liver prevents NSAID induced peptic ulcers
56
SE of synthetic prostanoids?
NEVER give to pregnant patients...abortifacient
57
Type I hypersensitivity rxn in asthma early response is
bronchoconstriction
58
What is the pathophys of type 1 hypersensitivity rxn
antigen binds preformed IgE on mast cells. This leads to degranulation of leukotrienes, prostaglandins and histamines. Ultimate results? inflammation and bronchoconstriction
59
First line therapy of bronchoconstriction work in what way?
They are short acting beta2 agonists (SABAs)
60
Albuterol and terbulatine are what?
First line therapy SABAs
61
LABAs example?
Salmeterol, formoterol
62
When do we use LABAs instead of SABAs?
Adjunctive therapy with corticosteroids and for long term management
63
SE of SABAs and LABAs?
tachy, hyperglycemia, hypokalemia, hypomagnesemia
64
Corticosteroids/Glucocorticoids example?
Beclamethasone, fluticasone, prednisone
65
When do we use corticosteroids/glucocortoids?
Long term management by reducing inflammatory response.
66
What is the action of salmeterol and fluticasone?
inhibits inflammatory cascade and bronchodilates
67
What is ipratropium?
Second line bronchoconstriction blocker
68
Mechanism of ipratropium?
Muscarinic receptor antagonist, blocks vagally mediated bronchoconstriction
69
What is the mechanism of montekulast?
binds cysteinyl leukotriene receptor and blocks action of leukotriend D4 (which prevents bronchoconstriction)
70
What is montekulast?
A second line bronchoconstriction blocker
71
What is a major SE of montekulast?
Churg-Strauss syndrome (autoimmune vasculitis)
72
How does cromyln work?
prevents degranulation of mast cells
73
When is cromolyn used?
asthma prophylaxis only
74
What is the mechanism of Zileuton?
inhibits 5-lipoxygenase which decreases leukotriene synthesis
75
What are the two main characteristics of RA?
1. lymphocutic infiltration in synovial joints and 2. granulomatous extra-articular nodules
76
Pathophys of RA?
positive rheumatoid factor (anti-IgG antibodies). This promotes release of IL-1, IL-6, TNF-alpha and activates T cells, which activates B cells to release antibodies and synovial inflammation
77
What is methotrexate?
RA therapy
78
Mechanism of methotrexate?
low dose: inhibition of lymphocyte proliferation (blocks purine synthesis) High dose: folate antagonist
79
Major SE of methotrexate?
Nausea
80
Mechanism of Leflunomide (LEF)?
LEF is a tx for RA. Blocks pyrimidine synthesis, acts on dihydroorotate dehydrogenase to inhibit lymphocyte proliferation in the autoimmune system.
81
Sulfasalazine (SSZ) mechanism?
anti-inflammatory, antimicrobial
82
How is SSZ used?
In combination with MTX for autoimmune disorders
83
Hydroxychloroquinone mechanism?
interferes with antigen processive and inhibites phospholipase A
84
When to use hydroxychloroquinone?
MALARIA. in combination with MTX/SSZ for autoimmune disorders
85
SE of hydroxychloroquinone?
retinopathy
86
What are Anti-TNF-alpha antibody examples?
infliximab, adalimumab
87
Use of anti-TNF-alpha antibodies?
combination with MTX (otherwise body develops antibodies to drug)
88
Ethanercept mechanism?
binds TNF-alpha to prevent downstream signaling and destruction symptoms
89
SE of ethanercept?
local inflammation at injection site and increased risk of infection
90
What is hyperuricemia?
acute monoarticular arthritis due to deposition of monosodium urate crystals
91
Presentation of Gout?
sudden onset of pain in first MTP then becomes tender joint
92
What drug is a risk factor for gout?
thiazide diuretics
93
How is Lesh-Nyhan syndrome related to gout?
increases risk because it decreases uric acid excretion and impairs purine metabolism
94
Pathophys of gout?
purines bcome uric acid via xanthine oxidase. Increasing uric acid retention results in crystalization
95
Why can't you treat gout with ASA?
competes with uric acid for secretion via proximal kidney tubule
96
How does indomethacin treat gout?
It's an NSAID that reduces movement of granulocytes to the affected area
97
How do NSAIDs work on gout?
decrease PGH2 via COX1/COX2 inhibition
98
Allopurinol purpose and mechanism?
treats chronic primary gout, purine analog--competitive inhibition or uric acid synthesis, less likely to form crystals
99
How does Colchicine help in gout?
decrease granulocyte ability to migrate to the affected area
100
SE of colchicine?
small therapeutic window
101
Probenecid/Sulfinpyrazone mechanism?
inhibits urate-anion exchanges in order to promote clearance of uric acid
102
When do prescribe probenecid/sulfinpyrazone?
chronic hyperuricemia
103
Prbenecid SE?
drug-drug interaction

Pharmacology (4 decks)

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