Brainscape's Knowledge GenomeTM

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


See full index

Y2B2 - Musculoskeletal πŸ“— > Pharmacology πŸ’Š > Flashcards

Pharmacology πŸ’Š Flashcards

1
Q

what is the definition of Rheumatoid arthritis (RA)?

A

a chronic, progressive inflammatory disease; characterized by symmetric small joint inflammation, swelling, and deformity and systemic manifestations.

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

Patho-Physiology of Rheumatoid arthritis (RA)

A
  • The exact aetiology is unclear. However, genetic factors play an important role.
  • Activated T cells, B cells, polymorphonuclear leukocytes (PMLS), macrophages, and complement system β€”-> production of soluble mediators (lysosymes, cytokines, e.g. TNF-a, IL-1, etc.) β€”> cause joint inflammation, cartilage destruction, bone erosion, and deformity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the clinical manifestations of Rheumatoid arthritis (RA)?

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

Diagnosis of Rheumatoid arthritis (RA)

A

Serological
- Abnormal blood antibodies (rheumatoid factor) β€”> in 80% of RA patients.
- Elevated CRP & ESR
- Positive anti-CCP antibodies.

Joint X-ray
- can show joint swelling and bony erosions typical of RA.

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

what are the aim of drug treatment of Rheumatoid arthritis (RA)?

A
  • To reduce pain, Stiffness & improve joint function (Symptomatic drug treatment)
  • To prevent chronic deformity by arresting the inflammation that results in joint destruction (DMARDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

symptomatic treatment of Rheumatoid arthritis (RA)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the importance of symptomatic treatment of Rheumatoid arthritis (RA)?

A
  • NSAIDs and/or corticosteroids are used as a (bridge therapy) —–> provide symptomatic relief till the therapeutic effect of DMARDs is observed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the action done by DMARDs?

A

They prevent disease progression and slow down joint destruction by modifying the immune reactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when should DMARDs be started? and how many should be used?

A
  • They should be started as early as possible (within 3 months of symptom onset) -> more favorable outcome.
  • 1 or more DMARDs are used depending on disease severity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How long is the lag between starting therapy by DMARDs & observing an effect?

A

There is a lag between starting therapy and observing an effect (3 weeks to 3 months).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

It is usual to continue DMARDs with conventional NSAIDs drugs.

A

..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the mechanism of action of Methotrexate?

A
  • It is a folic acid antagonist β€”-> cytotoxic and immuno suppressant properties β€”-> inhibits cytokine production & nucleic acid biosynthesis β€”-> inhibits activation & proliferation of PMLs, T cells, and macrophages.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

usage of Methotrexate

A
  • It is used in more than 60% of RA cases.
  • It is given once weekly orally.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how are the toxic effects of Methotrexate reversed?

A

by the subsequent administration of folinic acid (leucovorin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

adverse effects of Methotrexate

A

1) GIT: nausea and mucosal ulceration.

2) Myelosuppression especially leucopenia (periodic CBC).

3) Hepatotoxicity is common (monitoring liver functions is essential)

4) Acute pneumonia-like syndrome.

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

what is the mechanism of action of Leflunomide?

A

It inhibits the mitochondrial enzyme, dihydroorotate dehydrogenase (DHODH) β€”> inhibits pyrimidine base synthesis β€”-> suppresses T cell and B cell proliferation & activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the adverse effects of Leflunomide?

A

1) GIT: nausea & diarrhea
2) Hepatotoxicity
3) Hypokalemia
4) Alopecia & rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the mechanism of action of Hydroxychloroquine?

A

unknown, but might be:
- Inhibition of phagocytic functions.
- Stabilization of lysosomal membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the side effects of Hydroxychloroquine?

A
  • GIT: diarrhea
  • Corneal deposits & Retinopathy: the most disturbing toxic effect, rare, is a result of gradual accumulation of the drug in the retina β€”> irreversible retinal damage with permanent blindness
  • Skin discoloration & rash
  • Hemolysis in G6PD deficiency.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the mechanism of action of Sulphasalazine?

A
  • A prodrug β€”> cleaved by gut bacteria - 5-aminosalicylic acid & sulfapyridine.
  • Sulfapyridine is thought to be the principal anti-rheumatic agent.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

adverse effects of Sulphasalazine

A
  • GIT: nausea, vomiting, diahrrea
  • Myelosuppression: Occasional leucopenia and thrombocytopenia.
  • Hemolysis in G6PD deficiency.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the mechanism of action of Cyclosporine?

A
  • Cyclosporine β€”> bind cyclophilin β€”-> inhibit calcineurin β€”-> inhibit dephosphorylation of NFAT β€”-> decrease gene expression of IL-2 β€”-> inhibit T cell proliferation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

adverse effects of Cyclosporine

A
  • Nephrotoxicity
  • HTN, Hyperkalemia, Hirsutism, gingival Hyperplasia β€œ4H”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what plays a central role in RA?

A

Inflammatory cytokines

25
Q

what are biological DMARDs? and what is their method of adminstration?

A
  • Biological DMARDs are antibodies and antibody fusion proteins that inhibit the action of cytokines by blocking the cytokine from binding to its specific receptor
  • administered S.C or i.v.
26
Q

what are the groups of antibodies used in treatment of RA?

A

chimeric antibodies, humanized antibodies, and human antibodies.

27
Q

what are cytokine inhibitors used in treatment of RA

A

Cytokine inhibitors used in the treatment of RA are:
1) Inhibitor of IL-1 (anakinra),
2) Inhibitors of INF (infliximab, etanercept, and adalimumab)
3) Inhibitor of IL-6 (tocilizumab).

28
Q

which has stronger effect, Biologic DMARDs or methotrexate?

A

biologic DMARDs

  • Methotrexate + any biological agent -> more effective than methotrexate
29
Q

Examples of biologic DMARDs

A
30
Q

what are the main side effects of Biologic DMARDs?

A
  • injection/infusion-related reactions
  • infections (TB, fungal, sepsis, and reactivation of hepatitis B) β€”> never use 2 biologic DEMARDs together.
  • Increased risk of lymphoma and other cancers.
31
Q

when is the use of TNF-alpha inhibitors contraindicated?

A

1) Acute and chronic infections
2) Recent malignancies
3) Live virus vaccination
4) Demyelinating disorders
5) Class III or IV heart failure

32
Q

what are prostaglandins considered as members of?

A

PGs are members of fatty acid derivatives

33
Q

what are prostaglandins derived from?

A

Prostaglandins are derived from arachidonic acid (derived from membrane phospholipid) by the action of cyclooxygenase (COX) enzyme

34
Q

what are the forms of COX?

A
35
Q

classification of NSAIDs

A
36
Q

absorption of Acetylsalicylic acid (Aspirin)

A

absorbed Orally completely from the stomach and GIT

37
Q

distribution of Acetylsalicylic acid (Aspirin)

A
  • widely distributed to all tissues, including CNS
  • Plasma protein binding is high
38
Q

metabolism of Acetylsalicylic acid (Aspirin)

A

metabolism of salicylates Occurs by hepatic microsomal enzymes

39
Q

excretion of Acetylsalicylic acid (Aspirin)

A

Increased by alkalinization of urine (pH 8).

40
Q

what is the mechanism of action of Acetylsalicylic acid (Aspirin)?

A
  • Non-selective irreversible inhibition of COX leading to inhibition of both PGs and TXs synthesis.
  • Other NSAIDs produce reversible inhibition.
41
Q

what are the pharmacological effects of Aspirin?

A
  • Analgesic affects
  • Antipyretic affects
  • GIT effects
  • Hepatic effects
  • Hematologic effects
  • Respiratory effects
  • Renal Effects
  • Other effects
42
Q

Analgesic effects of Aspirin

A

For mild to moderate intensity pain (not severe pain)

43
Q

antipyretic affects of Aspirin

A

Aspirin is antipyretic but not hypothermic agent

44
Q

GIT effects of aspirin

A

Salicylates can produce 2 types of gastric ulcer:

Acute gastric ulcer
- Occurs as a result of acute ingestion of large doses of salicylates.

Chronic gastric ulcer
- Occurs as a result of chronic ingestion of therapeutic doses of salicylates.

45
Q

hepatic affects of aspirin

A

Salicylates can produce 2 types of hepatic injury:

Mild hepatic injury
- It is dose-dependent, reversible & asymptomatic.
- There may be mild increase in serum transaminases (SGOT & SGPT).

Severe hepatic injury
(Reye’s syndrome)

  • A rare & fatal condition occurs if aspirin is used to control fever of some viral infections (e.g. chicken pox, influenza, etc.) in children below 12 years.
  • There is severe hepatic injury associated with encephalopathy.
  • The etiology is unknown.
46
Q

hematologic affects of aspirin

A

Antiplatelet action
- Aspirin in low dose (75-150mg) inhibit platelet aggregation by Irreversible inhibition of COX enzyme β†’ ↓↓ TXA2 β†’ ↓↓ platelet aggregation.

Anticoagulant action
- Aspirin in high doses (> 6 gm /day) inhibits hepatic synthesis of vit K dependent coagulation factors (treated by vit K).

47
Q

respiratory effects of aspirin

A

Aspirin induced asthma.

48
Q

renal effects of aspirin

A

Analgesic nephropathy:
- It is chronic renal failure due to chronic abuse of analgesics, which produce chronic renal ischemia due to decrease synthesis of renal PGE2 and PGI2.

Salt & water retention:
- Due to decrease RBF and increase aldosterone

Antagonize diuretic effect of diuretics:
- Due to decrease synthesis of vasodilator PGs

49
Q

other effects for aspirin

A
  • Anti-inflammatory.
  • Anti-immunological.
  • Anti-rheumatic effects.
50
Q

what are the therapeutic uses of salicylates?

A
51
Q

what are the side effects of salicylates?

A
52
Q

precautions and contraindications of using aspirin

A
  1. GIT disorders: peptic ulcer and gastritis.
  2. Hemorrhagic disorders: hemophilia, thrombocytopenia..
  3. Chronic renal diseases.
  4. Severe hypertension.
  5. Pregnancy.
  6. Chronic liver diseases.
  7. Before surgery.
  8. Children <12 years old.
53
Q

drug interactions of aspirin

A
  1. It antagonizes the diuretic effect of diuretics, and the anti-hypertensive effect of anti-hypertensives (e.g. Ξ²-blockers, ACEIs).
  2. It increases the plasma concentrations of anticoagulants (heparin and warfarin), phenytoin, thyroxin, and other drugs (by displacement) leading to increase their effect and toxicity.
  3. Antacids decrease aspirin absorption.
54
Q

compare between nonselective COX inhibitors and selective COX-2 inhibitors in terms of:

  • Mechanism
  • Pharmacological effects
  • Gastric side effects
  • Renal side effect
  • Thrombotic side effect
  • Hypersensitivity reactions
A
55
Q

what is the mechanism of action of Acetaminophen (Paracetamol)?

A

It is a selective Cox III inhibitor so it inhibits PGs synthesis in the brain only.

56
Q

what are the pharmacological effects of Acetaminophen (Paracetamol)?

A
  • It has analgesic & antipyretic actions without anti-inflammatory action.
  • It has little or No effects on the CVS, GIT, respiratory or platelet functions.
57
Q

what is the therapeutic uses of Acetaminophen (Paracetamol)?

A
  • As analgesic & antipyretic when aspirin is contraindicated (e.g. patients with peptic ulcer, hemophilia, etc).
  • Used in pregnancy with greater safety than aspirin.
58
Q

what are the adverse effects of Acetaminophen (Paracetamol)?

A

At therapeutic doses:
Acetaminophen is well-tolerated but may cause:
- Skin rash& drug fever (as allergic reactions).
- Hemolytic anemia in patients with G-6-PD deficiency.
- Long term use may lead to renal failure.

At toxic doses:
- Dose dependent hepatotoxicity (hepatic necrosis).

Y2B2 - Musculoskeletal πŸ“— (8 decks)

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