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Pharmacology 1 > Autacoids > Flashcards

Autacoids Flashcards

1
Q

Examples of first generation H1 antihistamines

A

Diphenhydamine
Promethazine
Cyclizine
Meclizine

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2
Q

Examples of second generation H1 antihistamines

A

Cetrizine
Levocitrizine

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3
Q

Pharmacological actions of antihistamines

A
  1. Antagonism of histamine
  2. Anti allergic
  3. CNS depression
  4. Anticholinergic action
  5. Overall fall in BP
  6. Local anesthetic
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4
Q

Difference between first gen and second gen H1 antihistamines

A

Second generation
1. Have no Anticholinergic action
2. No anitemetic property
3. No cns depression as it doesn’t cross bbb
4. Expensive
6. Do not impair psychomotor performance

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5
Q

Difference between first gen and second gen H1 antihistamines (uses)

A

First Gen uses for
1. Motion sickness
2. Drug induced parkinsonism
3. Muscular dystrophy
4. Allergy

Second gen used for
1. Only allergy

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6
Q

Uses of antihistamines

A
  1. Allergic disorders
  2. Insect bite and ivy poisoning
  3. Common cold
  4. Antipruritic
  5. Motion sickness
  6. Morning sickness
  7. Vertigo
  8. Pre anesthetic medication
  9. Cough
  10. Parkinsonism
  11. Acute muscle dystonia l
  12. Sedative in children
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7
Q

Vertigo use of antihistamines

A

Used as labrynthine suppressants
It suppresses end organ receptors and inhibit cholinergic pathway.
Used commonly In miniere disease

Eg: Cinnarizine

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8
Q

Action of prostaglandins in CNS

A

In CNs: sedation, rigidity, rise in body temperature
Inhibition of NA
Sensitize afferent nerves to pain

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9
Q

Action of prostaglandins in Eye

A

Decreases IOP by increases trabecular outflow

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10
Q

Action of prostaglandins in lungs

A

PGF PGD TXA2 bronchoconstrictors
PGI2 PGE2 bronchodilators

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11
Q

Action of prostaglandins in CVS

A

PGI2 vasodilation hence hypotensive
PGF vasoconstriction
PGE2 F2 stimulate heart. CO increases

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12
Q

Action of prostaglandins in GIT

A
  1. Muscle of gut contractions. Propulsive activity hence can cause diarrhea
  2. Decreases acid secretion, volume of pepsin and juice also decreased
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13
Q

Action of prostaglandins in Kidney

A

PGE2 PGI2 vasodilates hence diuretic action
PGD F TXA2 renal vasoconstrictions and release of renin

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14
Q

Action of prostaglandins in FGS

A

Uterine contraction
Cervical softening

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15
Q

Action of prostaglandins in MGS

A

Increases male sperm motility

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16
Q

Action of prostaglandins in bone

A

Increases bone resorption hence increase plasma ca2+

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17
Q

Action of prostaglandins in platelets

A

TXA2 cause platelet aggregation
PGI2 inhibits platelet aggregation
PGE2 at low doses causes and at high doses inhibits

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18
Q

Action of prostaglandins in endocrine

A

Increase release of acth insulin gh

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19
Q

Two classes of PG

A

Natural: dinoprostone, dinoprost, prostacyclin
Analogues: carboprost, misoprost, latanoprost

20
Q

Uses of PG

A
  1. FGS:
    Abortion
    Induce labor
    Cervical ripening/priming
    Postpartum hemorrhage
  2. MGS: impotency
  3. Glaucoma
  4. Pulmonary hypertension
  5. Peptic ulcer
  6. To avoid platelet aggregation in hemodialysis
  7. Peripheral vascular disease
21
Q

How many classes of NSAIDs are there and which are they

A

4 classes
Non selective cox inhibitor
Preferential cox 2 inhibitors
Selective cox 2 inhibitors
Antipyretic analgesic with poor anti inflammatory action

22
Q

Expand non selective cox inhibitors

A

Salicylates: aspirin
Propionic acid derivatives: ibuprofen, naproxen, ketoprofen
Fenamate: mephenamic acid
Acetic acid derivatives: indomethacin, ketorolac
Pyrazolone derivatives: phenylbutazone, oxyphenbutazone
Enolic acid derivatives: piroxicam, tenoxicam

23
Q

Examples of preferential cox 2 inhibitors

A

Diclophenac
Aceclophenac
Nimesulide

24
Q

Examples of selective cox 2 inhibitors

A

Celecoxib
Paracoxib

25
Q

Examples of analgesic antipyretic with poor anti inflammatory action

A

Para amino phenol: paracetamol
Benzoxazocine der: nefopam

26
Q

General Actions of NSAID

A

Antipyretic
Analgesic
Anti inflammatory
Dysmenorrhea
Closure of ductus arteriosus
Antiplatelet aggregatory

27
Q

General Side effects of nsaids

A
  1. Prolong Labour
  2. Gastric mucosal damage
  3. Renal effects
  4. Analgesic nephropathy
  5. Asthma
  6. Anaphylactoid reactions
  7. Bleeding
28
Q

Advantages of using selective cox 2 inhibitors ahead of non selective cox inhibitors

A
  1. No asthma induced
  2. No gastric mucosal damage
  3. No excessive bleeding due to anti platelet action
29
Q

Adverse effects of NSAID system wise

A
  1. GIT: nausea, anorexia, vomiting, epigastric distress, gastric ulceration, bleeding/perforation
  2. CNS: Tinnitus, Vertigo, Headache, mental confusion, hyperexcitability, seizures
  3. Hepatic: elevate transaminases, hepatic failure (rare), Reye’s syndrome
  4. CVS: increase BP, contraindicated in CHF
  5. Renal: Na+ and Water retention, edema, chronic renal failure
  6. Haematological: bleeding, thrombocytopenia, hemolytic anemia
  7. Others: asthma, angioedema, skin rash, pruritis
30
Q

Actions of aspirin

A
  1. Antipyretic, analgesic and anti inflammatory
  2. GIT irritation
  3. Blood: anti platelet
  4. Systemic effects at high doses of 3-5g/day:
    Increases cellular metabolism
    Increases glucose utilization
    Respiratory stimulation due to increased Co2
    Compensated Respiratory alkalosis
    Metabolic acidosis due to lactate, acetate, salicylic acid
    No effect on heart directly but indirectly increases CO
31
Q

Adverse effects in aspirin

A
  1. Side effects at 0.5-2g/day (analgesic dose): Nausea, Vomiting, increased blood loss, gastric mucosal damage, peptic ulceration
  2. Hypersensitivity
  3. Anti inflammatory doses at 3-5g/day: Salicylism, liver damage in children, Reye’s syndrome
  4. Acute salicylates poisoning at 15-30g/day
32
Q

Salicylism

A

Dizziness
Tinnitus
Vertigo
Reversible impairment of hearing and vision
Excitement
Hyperventilation
Electrolyte imbalance

33
Q

Acute salicylate poisoning

A

15-30g
Vomiting, dehydration, electrolyte imbalance, acidotic breathing, hypo/hyperglycemia, petechial hemorrhage, restlessness, delirium, hallucination, coma, death due to respiratory failure and cardiovascular collapse

Treatment: symptomatic
External cooling + IV fluids
Glucose if needed
Blood transfusion and Vit K to prevent bleeding

34
Q

Interactions of aspirin

A
  1. Displaces warfarin, phenytoin, sulfonylureas hence overdose symptoms
  2. At analgesic doses antagonizes probencid and inhibit tubular secretion of uric acid
  3. Aspirin blunts diuretics
35
Q

Uses of aspirin

A
  1. Analgesic at 0.5-2g/day
  2. Antipyretic
  3. Anti inflammatory at 3-5g/day
  4. Acute rheumatic fever
  5. Rheumatoid arthritis
  6. Osteoarthritis
  7. Post MI
  8. Prevention of preeclampsia
36
Q

Ketorolac

A

Potent analgesic and modest anti inflammatory
Used in post operative, dental and musculoskeletal pain

37
Q

Indomethacin

A

Potent anti inflammatory
Most common drug used in closure of ductus arteriosus

38
Q

Preferential COX2 inhibitors

A

Nimesulide
Relatively weak inhibitor of PG synthesis and moderately selective COX2 inhibitor
Anti inflammatory action by other mechanism
Useful in painful conditions like sports Injuries, sinusitis, bursitis, dental surgery, dysmenorrhea.

High chance of liver failure hence not used. Preferred in patients who are asthmatics and intolerance to aspirin

Diclophenac Sodium
Inhibit PG synthesis and somewhat COX2 selective
No COX1 action hence no cardioprotective action of low dose aspirin

39
Q

Selective COX2 inhibitors

A

Less gastric damage
Less occurrence of gastric ulcer and bleeding

Inhibit PGI2 and don’t inhibit TXA2 hence increases chance of thrombus. Therefore no cardioprotective action and only advices in patents prone to peptic ulcer, perforation or bleeds.

40
Q

Actions of Paracetamol

A

Central analgesic action by reducing pain threshold
Good antipyretic
Weak peripheral anti inflammatory action due to inability to inhibit COX when peroxides produced by cells of inflammation are present

41
Q

Manifestations of Acute paracetamol poisoning

A

Occurs in children having low hepatic glucoronide conjugating ability
>150mg/kg or >10g in adults

Early Manifestations include nausea, vomiting, abdominal pain, liver tenderness. After 12 hours: centrilobular liver necrosis, renal tubular necrosis, hypoglycaemia. After 2 days: Jaundice and liver failure followed by death

42
Q

Mechanism of acute paracetamol poisoning

A

N Acetyl P Benzoquinoneimine (NABQI) is a highly reactive minor metabolite of paracetamol. It is detoxified by conjugation with glutathione. When glutathione stores are saturated, it binds with proteins in liver and kidney and causes necrosis

43
Q

Treatment of acute paracetamol poisoning

A

Induced Vomiting or gastric lavage done
Activated charcoal given to stop further absorption
Antidote: N acetyl cysteine (replenishes glutathione stores)

44
Q

Examples of topical NSAIDs

A

Dicophenac
Ibuprofen
Naproxen
Nimesulide

45
Q

Classify drugs for gout

A

Acute gout: NSAId, colchicine, glucocorticoids
Chronic gout:-
Uricosurics: Probenecid
Synthesis inhibitor: Allopurinol

46
Q

Classy drugs for RA

A

DMARDS:
1. Non biological:
Immunosuppressants: Methotrexate, Cyclosporine, Azathioprine
Other immuno modulators: Sulfasalazine, Leflunomide, hydroxychloroquine
2. Biological agents:
TNF alpha antagonists: Etanercept, infliximab, adalimumab
IL1 antagonist: Anakinra
T cell modulating agent: Abatacept

Adjuvant drugs: prednisolone
B cell depletor: Rituximab

47
Q

First choice DMARD

A

Mtx

Pharmacology 1 (14 decks)

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