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Pharm Block 2 > Intro and Eicosanoids > Flashcards

Intro and Eicosanoids Flashcards

1
Q

What drug is PGE2 and what is it used for?

A

Dinoprostone

  • Cervical ripening, cervical gel (0.5mg to 1.5mg/24hours), promotes cervical breakdown by activating collagenase, relaxes smooth muscle via EP4 receptor
  • Termination of early pregnancy/abortion, vaginal suppository (20mg to max dose of 240mg), causes uterine contraction via EP1/3 receptors
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2
Q

Adverse effects of PGE2?

A

Think cervical ripening and termination of early pregnancy

  • GI-related (nausea, vomiting, diarrhea)
  • Fever
  • Uterine rupture
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3
Q

What drug is PGF2alpha and what is it used for?

A

Carboprost

  • Termination of 2nd trimester/week 13-20 pregnancy, IM injection 250ug/no more than 12mg, stimulates uterine contractility via FP receptors
  • Control postpartum hemorrhage when conventional methods fail, IM injection, 250ug/no more than 2mg, causes myometrial contractions via FP receptors
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4
Q

Are the effects of carboprost mediated by calcium and/or cAMP?

A

Termination of pregnancy and postpartum hemorrhage control are both mediated by an INCREASE IN CALCIUM via FP receptors

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5
Q

Are the effects of dinoprostone mediated by calcium and/or cAMP?

A

Cervical ripening is mediated by an INCREASE IN cAMP via EP4 receptors

Early termination of pregnancy is mediated by an INCREASE IN CALCIUM via EP1/3 receptors

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6
Q

Misoprostol is an analogue of which prostaglandin?

A

PGE1

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7
Q

What is misoprostol used to treat? How is it administered?

A

Ulcers induced by long term NSAID use

Oral prep, 4x/day

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8
Q

What is the mechanism of misoprostol? Calcium or cAMP mediated?

A

Suppresses gastric acid secretion by parietal cells via EP3 receptors, DECREASE in cAMP, increasing mucin and bicarbonate secretion

Increases mucosal blood flow via EP2/4, INCREASE in cAMP

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9
Q

Major side effect of misoprostol?

A

Diarrhea

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10
Q

Contraindication of misoprostol?

A

Pregnancy

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11
Q

Other than misoprostol, what is another drug that is PGE1?

A

Alprostadil

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12
Q

What is Alprostadil used for? How is it prepared? Mechanism/Ca or cAMP?

A
  • Erectile dysfunction, intracavernous injection, relaxes trabecular smooth muscle and dilation of cavernous arteries, leads to entrapment of blood and causes erection. Via EP2/4 receptors and INCREASE in cAMP
  • Temporary maintenance of patent ductus arteriosus until surgical correction, IV infusion, relaxation of ductus smooth muscle via EP2/4 receptors and INCREASE in cAMP.
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13
Q

Adverse effects of alprostadil?

A

For erectile dysfunction: priaprism (erection

For keeping ductus open: apnea in about 10% of neonates; <2kg weight

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14
Q

Which drug is used as a PGI2 analogue?

A

Epoprostenol

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15
Q

What is epoprostenol used to treat? How is it administered?

A

Primary pulmonary hypertension, rare idiopathic disease mostly seen in young adults (seen more in females, causes right heart failure, often fatal

Continuous IV infusion (central venous catheter)

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16
Q

What is the mechanism for epoprostenol, receptor, cAMP or Ca2+?

A

IP receptor, cAMP-mediated dilation of pulmonary artery VSM

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17
Q

Adverse effects of epoprostenol?

A

Nausea, vomiting, headache, flushing

18
Q

Bimatoprost is an analogue for ___ and is used to treat ______ & ______ and is administered as _______

A
  • PGF2-alpha
  • Glaucoma
  • Eyelash hypotrichosis
  • Ophthalmic solution
19
Q

How does bimatoprost treat glaucoma and eyelash hypotrichosis; mechanism?

A

Increases OUTFLOW of aqueous humor via EP2/4 receptors and INCREASED cAMP

Increases the percent and duration eyelashes are in the growth phase

20
Q

Adverse side effects of bimatoprost?

A

For glaucoma: eye redness, itching, changing in eye color, increases length and number of eyelashes

For eyelash hypotrichosis: eye redness, itching, excess unwanted hair growth, brown iris pigmentation

21
Q

What are characteristics of acute inflammation? Main cell type?

A 
Rapid onset (minutes), short duration (hours-days)
Main characteristic: EDEMA
Main cell type: Leukocytes, mainly PMNs
22
Q

What are the characteristics of chronic inflammation? Main cell type?

A 
Prolonged duration (weeks or months)
May follow acute inflammation or start without any manifestations of an acute reaction
Main characteristic: FIBROSIS
Main cell type: monocyte
23
Q

What are the differences in how acute and chronic infections are triggered?

A

ACUTE: infection, microbial toxins, trauma, foreign bodies (splinters, dirt, etc)

CHRONIC: Immune-mediated inflammatory disease like RA, MS, allergic diseases OR prolonged exposure to potentially toxic agents

24
Q

inflammation protects against foreign objects and necrosis but it itself can NOT cause tissue damage. True or false?

A

FALSE; it IS capable of causing tissue damage

25
Q

What is the mediatory theory?

A

Signs and symptoms of inflammation are caused by the release of chemicals (pro vs anti-inflammatory)

26
Q

Give some examples of acute vs chronic infections

A

Acute:
Sore throat, reaction to burn or insect bite
Chronic:
TB, RA, ulcerative colitis, Crohn’s disease, asthma

27
Q

In what cells do you find histamine?

A

Stored in mast cells and basophils

28
Q

Cellular source of bradykinin? What kind of receptor does it use?

A

Endothelial cells; series of proteolytic reactions in tissues give rise to bradykinin

Acts through B2 (GPCR) receptor

29
Q

Complement; cellular source? what does it do and mechanism?

A

Synthesized in liver, circulate in blood

  • Chemotaxis: recruit inflammatory cells to sites of injury
  • Promote release of mediators from PMNs
  • Increase vascular permeability
  • Too much causes tissue injury

Complexes of complement aggregate on cell surface to cause osmotic lysis via GPCR

30
Q

What is an “acute phase protein”?

A

A protein whose plasma concentration changes from baseline by at least 25% during inflammation

31
Q

What is a C-reactive protein? Source, response, mechanism?

A 
Plasma protein - pentameric shape/25kDa that binds to C polysaccharide of bacterial cell walls
Synthesized by liver and fat cells
ACUTE PHASE PROTEIN
Activates complement cascade
Mediates phagocytosis
Marker of inflammation

Binds to phosphitidylcholine-containing substances in bacteria and damages cells, calcium dependent binding

32
Q

Too much CRP is associated with:

A

Increased risk of diabetes, hypertension and CV disease

33
Q

What’re some examples of cytokines and what they do? Source?

A

Secreted proteins made by nearly all cells
TNF-alpha; fever, sepsis
IL-1; fever, fibroblast and lymphocyte proliferation

34
Q

What role does Adenosine have on inflammation? Source?

A

Purine nucleoSIDE formed from ATP; all cells

Increases extracellularly during injury and acts as an anti-inflammatory agent to inhibit cytokine action via GPCRs

35
Q

What are cell adhesion molecules? Source? Importance?

A

Family of proteins including Ig-like CAMs, integrins, selectins, cadherins (glycoproteins on cell surface to mediate CONTACT)

From endothelial cells, platelets, leukocytes

Leukocyte adhesion to endothelium is important for repair, also endothelial adhesion molecules contribute to recruitment of activated platelets

36
Q

Which cells make oxygen derived free radicals and why are they important?

A

All cells make them (superoxide, hydroxyl radicals)
- Important for intracellular killing of bacteria by neutrophils via protein oxidation, lipid peroxidation, DNA mutations

37
Q

What do leukotrienes do? Cellular source?

A

From macrophages, neutrophils

Increase vascular permeability and bronchoconstriction

38
Q

What physiological responses do glucocorticoids carry out?

A

Inhibit:

cytokines, PLA2, COX-2, CAM

39
Q

What does LTB4, LTC4 and LTD4 do?

A

Leukotrienes;

  • LTB4 is a chemoattractant for PMNs
  • LTC4 and LTD4 increase vascular permeability
40
Q

What kind of molecules are etanercept and infliximab?

A

Both are inflammatory cytokine INHIBITORS

  • Etanercept: is a soluble receptor that binds/inhibits TNF-alpha
  • Infliximab: is a chimeric monoclonal antibody that binds TNF-alpha

Pharm Block 2 (7 decks)

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