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Pharm + Thera > Anti-inflammatory drugs: NSAIDS + Glucocorticoids > Flashcards

Anti-inflammatory drugs: NSAIDS + Glucocorticoids Flashcards

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1
Q

Pain and inflammation results

A

Substance P, Bradykinin, Phospholipases, Prostaglandins, and serotonin all get released immediately

They all have an ability to bind and activate receptors on nerve endings

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2
Q

Prostaglandins and Inflammation

A

Injection of prostaglandins mimic aspects of the inflam response

Highly reactive oxidants also contribute to the inflammatory response and the formation of these compounds is inhibited by NSAIDS

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3
Q

All NSAIDS inhibit

A

Cyclooxygenase (COX)

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4
Q

If a drug does not inhibit COX

A

Does not have any anti- inflammatory activity

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5
Q

FEVER and PGE2

A

Immune cells respond to infections which produce cytokines (TNF, IL-6)

Cytokines release PGE2 by CNS vascular endothelial cells

PGE2 stimulates firing of HYPOTHALAMIC NEURONS, which raise the temp (fever)

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6
Q

NSAIDs + Fever

A

NSAIDS will lover fever but not lower body temp and have no impact on temp rising from exercise

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7
Q

Inhibitors of prostanoid Synthesis

A

phospholipase inhibitors corticosteroids

Lipoxygenase inhibitors

receptor antagonists

Colchicine

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8
Q

Acetyl Salicylic Acid

A

-Irreversible
Therapeautic Effects: Analgesia (reduces fever) and antipyretic within an hour
-non-selective COX 1/2 inhibitor
-anti-inflammatory effects after days (may take weeks for some conditions)

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9
Q

Theraputic effects of Acetyl Salictylic acid

A

Analgesia
-within an hour
-PGE2 sensitization of nociceptors
Antipyretic
-within an hour
-PGE2 in hypothalamus
Anti-inflammatory
-within says (could be weeks for some conditions)
-PGE2-mediated edema and leukocyte recruitment
Cardiac Protection: low dose therapy
-platelet thromboxane A2(reduce ability for platelets to be aggravated)
-although aspirin undergoes first-pass metabolism, the effect is on platelets in the bloodstream (portal vein has a lot of platelets)

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10
Q

What is Acetyl salicylic acid

A

Asprin

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11
Q

How is Acetyl salic acid metabolized?

A

Absorbed in the stomach and distributed throughout body tissues

-rapidly metabolized to salicylic acid. In GI cells, plasma and live.

-Further salicylate metabolism occurs in the liver (mostly Phase II)

-excreted by kidney

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12
Q

Undesired Effects of Aspirin

A

GI toxicity: dyspepsia, bleeding, ulceration, perforation. ADDITION of misoprostol (synthetic PGE) to NSAID formulation can be considered in patients at high risk of GI toxicity

Renal toxicity: inhibition of intrinsic PG system:hypovolemic patients at greatest risk

Salicylism: CNS toxicity (dizziness, headache, confusion)

platelet inhibition (can be deisred in lowering risk of cardiovascular disease)

Hepatotoxicity (liver toxicity)

Hypersensitivity reactions

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13
Q

PDR warning for…

A

Aspirin + all others NSAIDs

-can develop suddenly

-Serious GI toxicity such as bleeding, ulceration

-happens in people treated chronically with NSAIDS

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14
Q

RISK for NSAID induced GI complications

A
  1. Past complicated Ulcer
  2. Multiple NSAIDs
  3. High dose NSAID
  4. Anticoagulant
  5. Past uncomplicated ulcer
  6. Age > 70
  7. Steroids
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15
Q

Drug interactions

A

anticoagulants- combined activity
Alcohol- addictive irritant effect on gastric mucosa
Uricosuric Drugs- hyperuricemia at lower poses
Antihypertensive agents- generalized decrease in anti-hypertensice efficacy
diuretics- decreased effects of diuretic agents, increased risk of acute renal failure (particularly in the elderly who may already have reduced renal function// kidney damage)

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16
Q

How are the NSAIDS ibuprofen and Naproxen similar

A

-Cyclooxygenase inhibition (well-absorbed)
-hepatic metabolism
-adverse effects: GI, CNS, Renal toxicity, blood elements
-contraindications: hypersensitivity, peptic ulcer, hepatic disease
-less severe sside effects bc they are reversible inhibitors of COX 1/2

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17
Q

what are first line for mild pain and inflammation

A

Ibuprofen Naproxen

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18
Q

NSAID/PHARMACODNAMIC/HALFLIFE

A

Aspirin: COX 1/2 irreversible, half-life= 20 minutes but irreversible

Ibuprofen: COX 1/2 reversible: half-life 2 hours

Naproxen: COX 1/2 reversible: half-life 15 hours

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19
Q

COX-1 (from arachidonic acid)

A

constitutively expressed; Prostaglandins (Homeostatic Effects)

-Renal homeostasis

-Gastric mucosal protection

-Platelet function

From Physiologic stimulus comes through; the stomach, kidneys, intestine, platelets, endothelium all can be impacted. Things that come from COX-1 are: PGE2, TxA, PGI2: these things can impact physiologic functions

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20
Q

COX-2 (from arachidonic acid)

A

inducible; Prostaglandins (Inflammatory Effects)

-Pain

-Inflammation

-Fever

-Limited Homeostatic Effects

From Inflammatory stimuli; inflammatory sites (macrophages, synoviocytes) impacts: Inflammatory PGs, Proteases, O2: these things can impact inflammation

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21
Q

What is COX-2 selectively inhibited by

A

Celocoxib

In cox-2 there is a side pocked that was added; it fits into COX-2 side pocket

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22
Q

CELECOXIB

A

COX-2 Specific inhibitors

Benefits:
lower incidence of GI toxicity vs non-selective NSAIDS
Risks:
-inhibition may increase chance of thrombosis in patients at risk for this disease; it could be a key in generation of the prostacyclin. A PG that decreases platelet aggregation

  • Rofecoxib (Vioxx): thrombotic cardiac events

-COX-2 active in kidneys, the recommended doses of COX-2 inhibitors causes renal toxicities similar to what is associated with traditional NSAIDs

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23
Q

COX-1 and COX-2 impacts on thrombosis (formation of blood clots)

Study These Flashcards
A

they are different
COX-1 impacts thromboxane A2, which impacts TP receptors, which are pro-aggregatory, pro-adhesion, vasoconstrictor, increased vascular remodeling

COX1/2: impact prostacyclin- which impacts IP receptors- which are anti-aggregatory, anti-adhesion, vasodilator, reduced vascular remodelling, reduced cholesterol uptake

24
Q

What is Acetaminophen// paracetamol

25
Acetaminophen uses
effective analgesic(pain killing) -antipyretic(fever reducing) agent -weak anti-inflammatory activity -weak platelet inhibitor CNS actions: -inhibits cycooxygenase(enzyme that helps create the chemicals prostaglandin and thromboxane) in hypothalamus, this is where its analgesic(pain killing) + antipyretic(fever reducing) actions occur. (Prevents PGE2 production by CNS vascular endothelium) -may inhibit COX-3 -May act on Cannabinoid receptors (CB1)
26
Acetaminophen overdose+overuse
leading cause of acute liver failure in US -dose-dependent hepatotoxity (liver damage) and possibly acute renal failure (kidney failure) -chronic ingestion can lead to hepatotoxicity due to build-up of NAPQI or chonic analgesic nephropathy(kidney deterioration)
27
Acetaminophen and toxicity + symptoms +treatment
-safe at normal dosages -toxic to liver in overdose (more than 10g) -Medical emergency -Glutathione conjugation pathway(part of phase II of detoxification in the body) becomes overwhelmed Alternate metabolite is TOXIC SYMPTOMS: -vomit, lethargy, uper right abdominal pain TREATMENT N-acetylcysteine (NAC//Acetadote) -Detoxifies NAPQ( a toxic byproduct) -restores glutathione (GSH) -conjugates directly with NAPQI by serving as GSH substitute
28
What do all NSAIDS try to do
Target pain, and inflammation
29
Aspirin: Major indications, Mechanism, Adverse Effects, Distinctive PK + Notes
MI: pain+inflam, also antithrombotic (reduce blood clots) aget used in cardiovascular events Mechanism: Irreversibly inhibitor of COX1/2 Adverse Effects: Gastric ulceration, tinnitus, renal failure, interstitial nephritis, reye syndrome in children w/ viral infection Dinstincitive PK + notes: 20 minute half life, but irreversible. Overdose initially causes: hyperventilation (respitory alkalosis) and later a mixed metabolic acidosis/respiratory alkalosis
30
Ibuprofen Major indications, Mechanism, Adverse Effects, Distinctive PK + Notes
MI: Pain + inflam Mechanism: non-selective reversible COX inhibitor Distinctive PK/Notes: Daily max of 3000 mg
31
Naproxen MI, Mechanism, Adverse effects, and notes
MI: Pain + inflam Mechanism: non-selective reversible COX inhibitor notes: 15 hour half life BID dosing
32
Celeoxib MI, Mechanism, Adverse effects, and notes
(celebrex) Mechanism: selective reversible COX-2 inhibitor Notes: Fewer GI ulcers
33
Acetaminophen MI, Mechanism, Adverse effects, and notes
(Tylenol) MI: fever, pain Mechanism: Analgesic effect (pain relieving) not fully clear. Antipyretic effect from inhibition of hypothalamic heat-regulating center Adverse effects: OD= liver failure. Hepatotoxic metabolie NAPQI concentrations increase with as little as daily max 4g/ day Notes: 90% of normal dose is metabolized in the liver via glucuronidation and sulfate conjugation. Remaining 10% is metabolized by CYP2E1 to N-acetyl-p-benzoquinone imine (NAPQI)
34
N-Acettylcyteine MI, Mechanism
(NAC) MI: Acetaminophen overdose Mechanism: replenishes glutathione necessary to conjugate with hepatotoxic metabolite NAPQI
35
HPA feedback loop
Hypothalamus -Corticotrophin releasing factor CRF- anterior pituitary -ACTH adrenocorticotrophic hormone- Adrenal cortex- cortisol- which then increases blood glucose, BP, and amino acids... then cortisol exerts a negative feedback effect on the hypothalamus that inhibits further release of CRF.
36
Short term stress response
elevated bp, breathing, metabolic reate... change in blood flow patterns with increased alertness, decreased digestive and kidney activity
37
Long term stress response
Mineralocorticords -retention of sodium ions +water by kindeys Glucocorticoids: -proteins+fats broken down and converted to glucose.. elevated blood glucose -immune system supression
38
Steroid hormones
-derived from cholesterol -lipid soluble -regulation involves control of enzymes
39
Function of mineralocorticoids (aldosterone) also where it is produced
Adrenal cortex Maintains blood volume and BP by increasing sodium reabsorption by kidney
40
Glucocorticoids (cortisol) function + produced where?
Adrenal cortex; catabolic steroid. Promote gluconeogenesis; favor breakdown of fat and protein (fuel mobilization); anti inflammatory
41
Progesterone function + where its produced
ovaries primarily; prepares uterus lining for implantation of ovum
42
Androgens (strongest=testosterone) + where its produced
development of male secondary sex characteristics; prevents bone resorption
43
how does glucocorticoid signal
diffuses across the membrane and binds to steroid receptor in cytoplasm... receptor dimerizes and enters nucleus- then binds to glucocorticoid response element... DNA binding enhances expression of anti-inflam proteins
44
Glucocorticoids and inflamation
inhibit production of proinflammatory transcription factors, which results in less pro-inflam cytokines, adhesion molecules, and COX-2
45
Clinical use of glucocorticoids
Allergy; anaphylazis/asthma/dermatitis, prednisone. Endocrinology: -addisons disease -hydrocortisone Gastroenterology -colitis/chron's disease Hematology -leukemia/lymphoma -dexamethasone Rheumatology -arthritis
46
Steroids
hydrocortisone, prednisone, dexamethasone
47
Glucocorticoid effects of steroids in order of effect
Dexamethasone (most potent, longest duration of action)> prednisone> Hydrocortisone
48
issues with glucocorticoid therapy
Long term (several weeks) can cause HPA suppression, and Cushings syndrome
49
Recommended for glucocorticoid use
-short term for inflammatory flaire up -not used for prevention of inflammation -monitor symptoms for adrenal insufficiency/cushings -metabolism through CYP450 enzymes, possible drug interactions with other metabolized by CYP -taper dose to avoid adrenal insufficiency.
50
What is hydrocortisone major indication
cortisol replacement, dermatitis
51
what is hydrocortisones mechanism
activates glucocorticoid receptor, induces anti-inflam genes, suppresses inflammatory genes
52
Hydrocortisone adverse effects
mild cushings syndrome
53
Hydrocortisone pharmacokinetics and notes
LOW potency, short half-life CYP metabolism
54
Prednisone Major Indication, Mechanism, adverse effects, pk + notes
MI: Allergy and inflammatory conditions Mech:activates glucocorticoid receptor, induces anti-inflammatory genes, suppresses inflammatory genes Adverse: Adrenal insufficiency, cushings syndrome Pk/notes:Medium potency, medium half life, CYP metabolism taper dose.
55
What is Dexamethasones major indications, mechanism, adverse effects, PK + notes
MI:Allergy and inflammatory conditions, immune cell cancers (leukemia/lymphoma) Mechanism: Activates Glucocorticoid receptor induces anti-inflammatory genes, suppresses inflammatory genes, inhibits immune cell proliferation adverse effects: Adrenal insufficiency, Cushing's syndrome Notes: High potency, long half life, CYP metabolism taper dose

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