Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology 1 > Autacoids > Flashcards

Autacoids Flashcards

(47 cards)

Start Studying
1
Q

Examples of first generation H1 antihistamines

A

Diphenhydamine
Promethazine
Cyclizine
Meclizine

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

Examples of second generation H1 antihistamines

A

Cetrizine
Levocitrizine

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

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

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

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

Action of prostaglandins in CNS

A

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

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

Action of prostaglandins in Eye

A

Decreases IOP by increases trabecular outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Action of prostaglandins in lungs

A

PGF PGD TXA2 bronchoconstrictors
PGI2 PGE2 bronchodilators

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

Action of prostaglandins in CVS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Action of prostaglandins in Kidney

A

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

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

Action of prostaglandins in FGS

A

Uterine contraction
Cervical softening

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

Action of prostaglandins in MGS

A

Increases male sperm motility

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

Action of prostaglandins in bone

A

Increases bone resorption hence increase plasma ca2+

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

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

Action of prostaglandins in endocrine

A

Increase release of acth insulin gh

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

Two classes of PG

Study These Flashcards
A

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

20
Q

Uses of PG

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

Diclophenac
Aceclophenac
Nimesulide

24
Q

Examples of selective cox 2 inhibitors

Study These Flashcards
A

Celecoxib
Paracoxib

25
Examples of analgesic antipyretic with poor anti inflammatory action
Para amino phenol: paracetamol Benzoxazocine der: nefopam
26
General Actions of NSAID
Antipyretic Analgesic Anti inflammatory Dysmenorrhea Closure of ductus arteriosus Antiplatelet aggregatory
27
General Side effects of nsaids
1. Prolong Labour 2. Gastric mucosal damage 3. Renal effects 4. Analgesic nephropathy 5. Asthma 6. Anaphylactoid reactions 7. Bleeding
28
Advantages of using selective cox 2 inhibitors ahead of non selective cox inhibitors
1. No asthma induced 2. No gastric mucosal damage 3. No excessive bleeding due to anti platelet action
29
Adverse effects of NSAID system wise
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
Actions of aspirin
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
Adverse effects in aspirin
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
Salicylism
Dizziness Tinnitus Vertigo Reversible impairment of hearing and vision Excitement Hyperventilation Electrolyte imbalance
33
Acute salicylate poisoning
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
Interactions of aspirin
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
Uses of aspirin
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
Ketorolac
Potent analgesic and modest anti inflammatory Used in post operative, dental and musculoskeletal pain
37
Indomethacin
Potent anti inflammatory Most common drug used in closure of ductus arteriosus
38
Preferential COX2 inhibitors
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
Selective COX2 inhibitors
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
Actions of Paracetamol
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
Manifestations of Acute paracetamol poisoning
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
Mechanism of acute paracetamol poisoning
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
Treatment of acute paracetamol poisoning
Induced Vomiting or gastric lavage done Activated charcoal given to stop further absorption Antidote: N acetyl cysteine (replenishes glutathione stores)
44
Examples of topical NSAIDs
Dicophenac Ibuprofen Naproxen Nimesulide
45
Classify drugs for gout
Acute gout: NSAId, colchicine, glucocorticoids Chronic gout:- Uricosurics: Probenecid Synthesis inhibitor: Allopurinol
46
Classy drugs for RA
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
First choice DMARD
Mtx

Pharmacology 1 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions