Pharm 22 Objectives Flashcards

1
Q

What are eicosanoids?

A

signaling molecules made up of 20-carbon fatty acids found in the cell membrane

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2
Q

How are eicosanoids produced?

A

Inflammation causes arachidonic acid to create eicosanoids

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3
Q

What are the three main types of eicosanoids?

A

Prostaglandins (COX)

Thromboxane (COX)

Leukotrienes (Lipoxygenase)

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4
Q

What are the steps inhibited by NSAIDs?

A

Drugs such as NSAIDs block the synthesis of prostaglandins and COX

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5
Q

Role of eicosanoids in: smooth muscle function

A

stimulates uterine contractions
and
Increases GI motility

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6
Q

Role of eicosanoids in: platelet function

A

Maintains bicarbonate gel layer lining of GI mucosa

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7
Q

Role of eicosanoids in: renal function

A

increase sodium and water excretion

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8
Q

Role of eicosanoids in: inflammation, pain, and fever

A

Actives specific prostanoid receptors in target tissue

released by physical trauma or chemical stimuli

promote tissue inflammation

affect smooth muscle and platelet aggregation

target tissues vary by PG, some PBs bind to sites better than others

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9
Q

Role of COX-2

A

mediate pain, fever, and inflammation

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10
Q

What is the main target of NSAIDs

A

COX-2

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11
Q

Role of COX-1

A

Support and protects GI mucosa

Increases mucosal blood flow, production of mucus, and bicarbonate

Stimulates epithelial cells that line GI tract

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12
Q

COX-1 catalyzes thromboxane A2 in platelets which results in

A

a trigger for platelet aggregation

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13
Q

Advantages of selective COX-2 inhibitors?

A

Less GI distress

Less incidence of GI Bleed

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14
Q

Clinical utilization of COX-2 selective NSAIDS

A

Osteoarthritis (100-200mg daily/100mg BID)

Rheumatoid arthritis (100-200mg BID)

Dysmenorrhea (400mg x 1/200mg BID)

Acute Pain (400mg x1/200mg BID)

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15
Q

Disadvantages of selective COX-2 inhibitors?

A

Cost

Increase risk for cardiac events

Prescription is needed

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16
Q

Advantages for nonselective COX inhibitors

A

minimal downiness

Anti-inflammatory action

No risk of abuse or diversion

OTC choices are available

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17
Q

Disadvantages for nonselective COX inhibitors

A

Only best for mild to moderate pain

Anti-inflammatory action is delayed about 3-5 days

GI tox and renal effects

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18
Q

Analgesic dose of aspirin?

A

300 - 600 mg q6 hrs

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19
Q

Cardiovascular dose of aspirin?

A

75 - 100 mg daily

20
Q

What is the most commonly used salicylates for GI disorders?

A

Aminosalicylates

21
Q

Aminosalicylates clinical uses?

A

Inflammatory bowel disease specifically Ulcerative colitis and Crohns disease

22
Q

What are the available formations of aminosalicylates?

A

Sulfasalazine- PO tab

Mesalamine- rectal suppository or suspension and delayed-release tab.

23
Q

Explain the MOA of Acetaminophen

A

Antipyretic action: direct action on hypothalamic heat regulating center

Almost as potent as ASA inhibiting prostaglandin synthesis in the CNS

24
Q

What effect does acetaminophen have outside the CNS and inflammation?

A

Minimal effect outside the CNS

Little to no anti-inflammatory effect

25
Q

Advantages of Acetaminophen?

A
  • Inexpensive
  • No risk of dependence, addiction or diversion
  • Antipyretic as well as analgesic
  • No effect on platelets
  • Very low risk of GI bleeding
  • Very low risk of renal dysfunction unless overdosed
  • Little to no drowsiness
  • use in chronic pain
26
Q

Disadvantages of Acetaminophen?

A
  • only useful in mild to moderate pain
  • risk of overdose
  • total daily dose is a limiting factor for combination products
  • confusion about which products contain APAP.
27
Q

If drinking and/or have liver disease what dose of Acetaminophen is safe?

A

NO APAP dose is safe due to lack of glutathione

28
Q

If you are not drinking but have liver disease what dose of Acetaminophen is safe?

A

2.0 grams/day

29
Q

Wher is acetaminophen metabolized?

A

Extensively metabolized by the liver

30
Q

What occurs when pt OD with acetaminophen?

A

Overdoses use up glutathione then metabolites bind to liver cells.

31
Q

What is the MAX dose limits of acetaminophen in healthy adults?

A

4.0 grams

32
Q

What is the MAX dose limits of acetaminophen in elderly OR mild liver dysfunction?

A

3.1 grams

33
Q

What is the MAX dose limits of acetaminophen in moderate liver dysfunction OR etoh use?

A

2.0 grams

34
Q

S/S of acute acetaminophen poisoning?

A

N/V

Drowsiness

Liver tenderness

Chronic/acute hepatotoxicity

Acute renal failure

35
Q

Describe the psychological process and pathway that regulate cortisol production and release.

A
  • CRH stimulates release of ACTH from pituitary gland
  • ACTH stimulates release of cortisol from adrenal cortex
  • Adrenal cortex releases cortisol into the bloodstream and inhibitory feedback to they hypothalamus
36
Q

Describe the effects of short term use of glucocorticoids

A

Stimulation/agitation (euphoria, psychosis, insomnia)

Hyperglycemia

Appetite changes (increase or decrease)

37
Q

Describe the effects of long term use of glucocorticoids.

A

Cushingoid features (full face (moon face) and weight gain)

Thinning of bones (osteopenia, osteoporosis)

Impaired immune response

Thinning skin

38
Q

How does systemic glucocorticoid administration at pharmacologic doses affect the HPA axis?

A

Doses can cause suppression of HPA axis

Give dose in AM to minimize suppression.

Alternate-day therapy, in which all or most of the dose is given on alternate days.

39
Q

Duration of glucocorticoid that may cause withdrawal/rebound?

A

> 10 days of corticosteroid Tx = Watch out for rebound!

Between 7 – 10 days Tx MAY cause withdrawal/rebound

40
Q

What is the clinical application of corticosteroids in tx of IBS?

A

Hydrocortisone rectal foam or enema 100mg/60ml (Cortenema®)

Systemic needed for more severe/less localized symptoms

Systemic oral (prednisone) helpful for achieving remission

41
Q

Tx options for other GI disorders such as UC and crohns disease?

A

Hydrocortisone and other glucocorticoids have been extensively used for the treatment of both ulcerative colitis and Crohn’s disease.

42
Q

Specific tx for mild UC?

A

Rectal corticosteroid

43
Q

Specific tx for severe UC?

A

Orally or parenteral corticosteroids, specifically Budesonide

44
Q

Tx for maintaining remission of UC?

A

Sulfasalazine, olsalazine, and their active metabolite mesalamine are used to induce and maintain the remission of ulcerative colitis

45
Q

Describe how to administer glucocorticoids for acute disorders?

A

Give in large doses that are gradually tapered over several days until treatment is discontinued

46
Q

Describe how to administer glucocorticoids for severe disorders?

A

Large doses of steroids must be given daily for several months until remission is achieved, then the dose is slowly tapered, and continued for 1 to 2 years or longer.

47
Q

Why use depo glucocorticoid shot?

A

Depot preparations are useful in providing a sustained level of the drug for several week