Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm Spring 2023 > NSAIDS, Corticosteroids > Flashcards

NSAIDS, Corticosteroids Flashcards

1
Q

Does Tylenol work well for inflammatory pain

A

No not really

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the indications to use acetaminophen (Tylenol)

A

Mild to moderate non-inflammatory nociceptive pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the role in therapy of acetaminophen (Tylenol)

A
  1. Fever
  2. Self-limiting painful conditions
  3. Osteoarthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mechanism of action of acetaminophen (Tylenol)

A
  1. Analgesic effects in CNS via COX inhibition, interacts with nitric oxide containing pathways, and blocking substance P actions
  2. Anti-pyretic
    *can use in children under 6 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the adverse effects of acetaminophen (Tylenol)

A
  1. Generally well tolerated
  2. Rare: Stevens-Johnson syndrome / Toxic Epidermal Necrolysis (TEN)
  3. BBW: Hepatotoxicity
    *can overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the roles of acetaminophen (Tylenol)

A
  1. Severe rash skin reactions SJS TEN = CI
  2. Caution in renal impairment
  3. BBW: Severe Hepatotoxicity
    *doses >4 grams a day
    *risk of dosing errors is 10x higher with injection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the maximum daily dose of acetaminophen

A

3,000mg per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

If someone overdoses on acetaminophen what is the antidote

A
  1. N-acetylcysteine
    *restores hepatic glutathione
    *helps to breakdown Tylenol
  2. Use Rumack-Matthew nomagram
    *input the serum acetaminophen level and time since ingestion to determine need for NAC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the COX-1 and 2 Non-selective NSAIDS

A
  1. Ibuprofen (Advil, Motrin)
  2. Naproxen (Aleve, Naprosyn)
  3. Indomethacin (Indocin)
  4. Ketorolac (toradol)
    *all have more GI problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the Increased COX-2 Selectivity NSAIDS

A
  1. Celecoxib (celebrex)
  2. Diclofenac (voltaren)
  3. Meloxicam (mobic)
    *2 is the most selective COX-2 available (less GI irritation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the indications for NSAIDs

A
  1. Mild to moderate pain suspected to be inflammatory, headache
  2. Fever reduction
  3. Arthritis
  4. Gout
  5. Closure of the patient ductus arteriosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the indications for Aspirin

A
  1. Prevention of myocardial infarcation/stroke
    *affects the platelets to be more thrombotic in nature
  2. Arthritis
  3. Headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the anti-inflammatory effects of NSAIDS and ASA

A

NSAIDS
1. Reversible inhibit COX1 and or 2 and the production of thromboxane, prostaglandins, and prostacyclin
ASA
1. Irreversible COX inhibition (inhibition of prostaglandins synthesis_
*have to eliminate the platelets before the effects wear off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the antipyretic effects of NSAIDS and ASA

A
  1. Inhibits the synthesis of fever inducing prostaglandins in the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the platelet effects of NSAIDS and ASA

A

NSAIDS
1. Inhibits platelet aggression (dont stick to each other, increased risk of bleeding)
ASA
1. Inhibits thromboxane synthesis (permanent)
*need new platelets (made every 8 to 10 days)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the analgesic effects of NSAIDS and ASA

A
  1. Reduced prostaglandin production at injured tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the effects of the Selective COX2 inhibition (NSAIDS)

A
  1. Do not affect platelet function at usual doses
    *do not inhibit platelet aggregation
  2. Less GI irritation
  3. Increased incidence of edema, hypertension, and maybe MI
  4. Nephrotoxicity (all NSAIDS) due to interfering with auto regulation of renal blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some pharmacokinetics pearls of NSAIDS

A
  1. Do not give and NSAID to a child <6 months old
    *can effect the development of kidneys, also why we avoid in pregnancy
  2. Highly protein-bound, typically to albumin
  3. Naproxen and piroxicam have longer half lives
    *N (14 hours) Piroxicam (57 hours)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the correlation between NSAIDS and their half lives

A

NSAIDs with shorter 1/2 life remain in the joints longer than anticipated T1/2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are some pharmacokinetics pearls of ASA

A
  1. First order renal elimination
  2. Anti platelet effects last 8 to 10 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the therapeutic dosing ranges for ASA

A

LOW (81-325mg/day)
1. Reduced platelet aggregation
Intermediate (300-2400mg/day)
1. Antipyretic and analgesic effects
HIGH (2400-4000mg/day)
1. Anti-inflammatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some adverse reactions of NSAIDs and ASA

A
  1. Stomach upset, abdominal pain NSAIDS <ASA
  2. GI bleed, clotting problems (increased bleeding time)
  3. Tinnitus, dizziness
  4. Worsening HTN, MI
  5. Hyperkalemia
  6. Impaired renal function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the rare but serious dermatological adverse reactions of NSAIDS

A
  1. Steven Johnson Syndrome (SJS)
  2. Toxic Epidermal Necrolysis (TEN)
24
Q

What are the rare but serious CNS adverse reactions of NSAIDS

A

Aseptic meningitis

25
Q

What are the rare but serious cardiovascular adverse reactions of NSAIDS

A
  1. MI
  2. Congestive heart failure
26
Q

What are the rare but serious Gastrointestinal adverse reactions of NSAIDS

A

Ulcer or bleeding

27
Q

What are the rare but serious hematologic adverse reactions of NSAIDS

A
  1. Thrombocytopenia
  2. Neutropenia
  3. Aplastic anemia
28
Q

What are the rare but serious hepatic adverse reactions of NSAIDS

A

Liver failure

29
Q

What are the cardiovascular warnings and risk of NSAIDS and ASA

A
  1. Increased risk of serious cardiovascular thrombotic events. MI, and stroke
  2. HTN
  3. Impaired renal function
30
Q

What are the gastrointestinal warnings and risk of NSAIDS and ASA

A
  1. Increased risk of serious GI adverse events (bleeding, ulceration, and perforation)
31
Q

What are the other warnings and risk of NSAIDS and ASA

A
  1. Hematological (anemia)
  2. Increased risk of MI and stroke
  3. Avoid in pregnancy
  4. Pre-existing asthma
    *severe bronchospasm
32
Q

What are the toxicities of ASA

A
  1. Higher doses / early overdose
    *respiratory alkalosis
    *tinnitus, vertigo, hyperventilation
  2. Very high doses/toxicity
    *above 300 mcg/mL clearly toxic
    *metabolic acidosis
  3. There is no antidote
    *use gastric lovage and charcoal
33
Q

What are the toxicities with ASA and children

A
  1. Children with viral infection if treated with salicylates will
    *have an increased risk for developing Reye’s syndrome
34
Q

What is Reye’s syndrome

A
  1. Rare but serious syndrome of rapid liver degeneration and encephalopathy
    *can be deadly
35
Q

What hormone is involved in corticosteroids

A

Cortisol
*important hormone involved with blood glucose, metabolism, inflammation
*produced in adrenal gland via cholesterol metabolism

36
Q

What does corticosteroids inhibit

A
  1. Induce synthesis of PLA2 inhibitor
  2. Decreased synthesis of COX2
37
Q

What are the anti-inflammatory and immunosuppressive effects of corticosteroids

A
  1. Inhibits some pro-inflammatory mediators and genes
    *affects transcription factors that control the synthesis of pro-inflammatory mediators
  2. Initiates upregulation of anti-inflammatory mediators
38
Q

What are the mechanisms of corticosteroids

A

When giving a corticosteroid it will
1. Shut down, the formation of inflammatory mediators
2. Will enhance anti-inflammatory mediators

39
Q

What are the least to most potent corticosteroids

A
  1. Cortisone
  2. Hydrocortisone
  3. Prednisone
  4. Prednisolone
  5. Methyprednisolone
  6. Triamcinolone
  7. Dexamethasone
  8. Betamethasone
40
Q

What are other corticosteroids to know

A
  1. Fluticasone
  2. Mometasone
  3. Budesonide
41
Q

What are the therapeutic uses for steroid (MAGIC PAUL)

A

M: multiple sclerosis
A: asthma/allergic rhinitis and hay fever
G: giant cell arteritis / polymyalgia rheumatica
I: inflammatory bowel disease
C: COPD
P: painful inflamed joints
A: atopic eczema
U: urticaria
L: lupus

42
Q

What are the adverse reactions of corticosteroids

A

Longer you’re on a steroid the more / worsening ADRs
1. Sick
2. Sad
3. Sex (decreased libido)
4. Salt (retain sodium and water)
5. Sugar (raises blood sugar)
*route matters

43
Q

What are the long term side effects of corticosteroids

A
  1. Growth suppression
  2. Osteoporosis
  3. Glaucoma
  4. Hyperglycemia
  5. Cushing syndrome
44
Q

Why do you need to taper a corticosteroid

A
  1. Can cause acute adrenal insufficiency
    *addisonian crisis
    *if ingested steroids are stopped suddenly it can cause addisonian crisis
45
Q

What is Cushing syndrome

A
  1. Adrenal gland produces too much cortisol or steroids are taken in high doses and the amount of cortisol is higher than natural
46
Q

What are the CI to corticosteroids

A

1.infections
2. Osteoporosis
3. Uncontrolled hyperglycemia
4. Diabetes
5. Glaucoma
6. Joint infection
7. Congestive heart failure
8. Uncontrolled hypertension

47
Q

What is the MOA of acetaminophen

A
  1. Likely affects pain signaling, possibly by affecting nitric oxide and blocking substance P
48
Q

What is the indication for lidocaine

A
  1. Useful for well-localized pain
  2. May be particularly preferred in elderly when concerned about CNS SE
49
Q

What is the MOA of lidocaine

A
  1. Inhibits sodium channels to reduce neuronal impulse inducing an anesthetic effect and reducing inflammation
50
Q

What are the ADRs of lidocaine

A
  1. Stinging / burning
  2. Localized numbness
51
Q

What are the clinal pearls to remember about lidocaine

A
  1. Topical
    *12 hrs on 12 off
  2. Max 3 patches for simultaneous use
  3. Does not accumulate with normal hepatic function
52
Q

What are the anti seizure effects of gabapentanoids (gabapentin / neurontin) (Pregabalin / lyrica)

A
  1. Decreases synaptic release of glutamate thereby reducing excessive neural excitivity contributing to the seizure prone environment
53
Q

What are the spasmolytic effects gabapentanoids (gabapentin / neurontin) (Pregabalin / lyrica)

A

Action on calcium channels theorized

54
Q

What are the analgesic effects of gabapentanoids (gabapentin / neurontin) (Pregabalin / lyrica)

A
  1. Action on voltage-gated calcium channels (may reduce current)
  2. Descending noradrenergic and serotonerigc pathway involvement
55
Q

What are the therapeutic uses of gabapentanoids

A
  1. Seizures
  2. Neuropathic pain
  3. Neuropathy
  4. generalized anxiety disorder
  5. Muscle spasms / spasticity
56
Q

What are the warnings or precautions of gabapentanoids

A
  1. Anaphylaxis
  2. Angioedma
  3. Somnolence, sedation
  4. Suicidal behavior and ideation
57
Q

What are the common SE of gabapentanoids

A
  1. Dizziness, somnolence, peripheral edema
  2. Pregabalin
    *dry mouth,
    *blurry vision
    *weight gain
    *abnormal thinking

Pharm Spring 2023 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions