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Pharmacology > B2 > Flashcards

B2 Flashcards

1
Q

Describe the therapeutic uses of pilocarpine & cevimeline

A

Directly acting cholinomimetic drugs which acts on M3 receptors

Pilocarpine ( natural alkaloids)
I) act as sialogoagues to treat xerostomia , Sjogren’s syndrome
II) treatment of glaucoma -> stimulate pupil contraction ( miosis) -> ciliary muscle contract -> trabecular mesh work opens -> allows aq. humour to flow out -> reduce intraocular pressure
- can lead to pulmonary edema as it increases pulmonary secretions

Cevimeline
I) Sialogogue to treat xerostomia due to cancer chemotherapy
- less toxic than pilocarpine hence it is used as an alternative
- benthanechol can also be used as a sialagogue alternative to pilocarpine

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2
Q

An example of a cholinomimetic drug which can cross BBB is …

A

Physostigmine

  • a reversible anticholinesterase (natural alkaloid)
  • Why? Because it is a tertiary ammonium alkaloid —others are quadternary , cannot cross BBB
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3
Q

List adverse effect of Oraganophosohate

A

DUMBBELS ( cholinergic overdose )

Diarrhoea , Urination , Miosis , Bradycardia , Bronchoconstriction , Lacrimation ,

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4
Q

The competitive antagonists of AcH & cholinomimetic drugs is ( ………….)

A

The competitive antagonists of AcH & cholinomimetic drugs is ( atropine )

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5
Q

Classification of antimuscarinic / anticholinergic drugs

A

1) Plant ( Atropa Belladonna )
I) Atropine
II) Scopolamine

2) Semisynthetics derivatives
I) Atropine methonitrate
II) Hyoscine butylbromide

3) Synthetics compounds
I) Glycopyrrolate

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6
Q

Explain the pharmacological action of atropine on CNS , CVS , EyE, respiratory system , GIT , urinary system , and body temperature.

A

On CNS

  • excitatory effects
  • restlessness , irritability , hallucinations , delirium
  • uses : to treat Parkinson disease ( benztropine )

On CVS

  • prevent the inhibitory effect of M2 receptor
  • tachycardia , increase conduction velocity
  • uses : Treat MI , abolish reflex vagal cardiac slowing

On eye

  • cause mydriasis ( dilation of pupils) , dry eyes due to reduced lacrimation , cycloplegia ( loss of accommodation ) due to relaxation of ciliary muscle
  • worsen glaucoma
  • uses : fundoscopy

On respiratory system

  • stimulate bronchodilator , acitivity of RS gland are inhibited -> drying and mucociliary clearance is inhibited
  • uses : prevent reflex bronchioconstriction during intubation , COPD

On GIT

  • decrease tone & motility of GIT — prolong gastric emptying time , contracts sphincters , decrease in peristalsis
  • Relaxes the bile duct & gall bladder ( prevent release of bile )
  • decrease in glandular secretions ( saliva -> dry mouth , gastric acid )
  • uses : prevent biliary & intestinal colic , diarrhea , motion sickness treat peptic ulcer.

On genitourinary tract

  • relaxation of bladder & ureter , contraction of urethral sphincter causing urinary retention
  • uses : prevents involuntary micturition

On body temperature

  • causes rise in body temperature due to hyperactivity , restlessness which is attenuated by abolishment of sweating
  • uses : treat hyperhydrosis

Also treats :
I) Mushroom poisoning
II) Organphosphorus poisoning ***

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7
Q

Activation of alpha- adrenoreceptor will usually lead to ( …………… ) of all types of smooth muscle Except ( …………… )

Activation of beta p- adrenoreceptor will usually lead to ( ……………. ) of all types of smooth muscle

A

Activation of alpha- adrenoreceptor will usually lead to ( contraction ) of all types of smooth muscle Except ( GIT )

Activation of beta p- adrenoreceptor will usually lead to ( relaxation ) of all types of smooth muscle

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8
Q

Describe the therapeutic uses of adrenaline

A

Anaphylactic shock
- administer 0.3-0.5 mg IM in 1:1000 solution

Bronchial asthma
- in salbutamol longer acting in widen of airways

Cardiac arrest

Duration of LA

Epistaxis

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9
Q

Classify the Adrenergic drugs based on their usage ( PCBL NUMA)

A

Pressor agents - increase BP ( alpha 1 receptor )
: NE , dopamine

Cardiac agents: increase contraction ( beta 1 receptor )
:adrenaline , isoprenaline

Bronchodilators ( beta 2 receptor )
- salbutamol

Local vasoconstrictor effect - for homeostasis , prolong effect of LA ( alpha1 receptor ) 
Nasal decongestant ( alpha1 receptor ) 
\: phenylephrine
Uterine relaxant ( beta 2 receptor ) 
- salbutamol

Mydriatics -pupil dilation ( alpha 1 receptor ) - cause the constrictor of pupillary ciliary muscle

Anorexiants - suppress appetite

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10
Q

Describe the role of alpha agonists ( adrenaline ) in dental practice

A

Hemostasis

  • used in 1:10000 or 1:20000 solution
  • used following tooth extraction for homeostasis as it causes local vasoconstriction

Prolong duration of LA

  • used in 1:100000 solution
  • due to local vasoconstriction effect
  • prevent systemic absorption & reduce toxicity of LA

Anaphylactic shock

  • 1:1000 solution 0.3-0.5ml ,IM
  • drugs like LA , penicillin can cause anaphylactic shock
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11
Q

Describe the role of adrenaline in anaphylactic shock

A

0.3-0.5mg in 1:1000 solution administered IM

  • acting beta 1 receptor , it increases HR ( chronotropic ) and FOC ( inotropic )
  • acting on beta 2 receptor , it increase bronchodilation and reduced release of mediator from mast cells
  • acting on alpha 1 receptor , it causes vasoconstriction of blood vessels , increasing blood pressure .
  • acting on alpha 1 receptor , it reduced mucosal / laryngeal edema
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12
Q

Give the classification of Adrenergic antagonists ( beta-blocker )

A

Non-selective ( acts on both beta 1 & beta 2 receptors ) (ptps)

  • propranolol
  • Timolol
  • pindalol
  • sotalol

Cardioselective / B1blocker (babem)

  • bisoprolol
  • atenolol
  • betasolol
  • esmolol ***shortest acting blocker
  • metoprolol

Beta-blocker with additional vasodilatory effect ( alpha-1 blocking action )

  • labetalol
  • carvedilol
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13
Q

Describe the action of propranolol on CVS , RS , metabolism , eye and skeletal muscle

A
  • it antagonists B1 and B2 receptor

On CVS

  • blocks beta 1 receptor
  • hence reduces conduction velocity , HR , FOC ,CO causing decreasing BP
  • AV conduction decreases , increasing PR interval
  • cardiac work decreases , decreasing O2 requirement of myocardium
  • On kidney , decreases renin secretion causing decreased BP

On Respiratory system

  • blocks B2 receptors , causing bronchoconstriction
  • can lead to bronchospasm in asthmatic & COPD patients
  • cardioselective beta- blockers ( metoprolol , bisoprolol ) less likely to cause bronco spasm in asthmatic patients

On eye

  • acts on beta 2 receptors
  • decreases secretion of aq . humour , reducing IOP, & glaucoma
  • no effect on pupil size
  • timolol is drug of choice

On metabolism

  • acting beta2 receptors , decrease glycogenolysis and glucagon secretion
  • contraindicated for diabetic patient

On skeletal muscle

  • act on beta 2 receptor , causes decreased blood flow to skeletal muscle & lead to muscle fatigue due to decreased in CO
  • inhibit tremors

On CNS

  • decreases anxiety symptoms in short term
  • causes behavioural changes , forgetfulness , nightmares in long term
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14
Q

(……………….) ( an opioid anatagonist ) can precipitate withdrawal symptoms in morphine & heroin addicts , hence it cannot be directly use to treat addicts

Instead , (……………………) should be given then only (………)

It is used in case of opoid overdose / poisoning in which it reverses the RS depressive effects

A

( IV naloxone , naltrexone , nalmefene ( an opioid anatagonist ) can precipitate withdrawal symptoms in morphine & heroin addicts , hence it cannot be directly use to treat addicts

Instead , ( methadone ) should be given then only ( naloxone )

It is used in case of opoid overdose / poisoning in which it reverses the RS depressive effects

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15
Q

Classify NSAID according to their selectivity to COX

A

Non COX selective inhibitors ( inhibits COX1 and COX 2)
- aspirin , ibuprofen , diclofenac

Preferential COX2 inhibitors

  • diclofenac
  • aceclofenac

Highly selective COX2 inhibitors ( coxibs )
I) Celecoxib

Analgesic and antipyretic but poor anti inflammatory effect
I) paracetamol

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16
Q

Describe the pharmacological actions of NSAIDS

A

1) Analgesic effects
- NSAIDS inhibits COX-2 enzymes , reducing synthesis of prostaglandins
- The role of these prostaglandins is to increase the sensitivity of central & peripheral pain receptors to inflammatory mediators eg , bradykinin
- hence , decrease PG synthesis -> decreased pain receptor sensitivity -> increased pain threshold

2) Antipyretic effect
- prostaglandins released due to the tissue damage , malignancy , graft injection etc set the hypothalamic heat regulating centre to a higher level cause hyperpyrexia
- hence NSAID which inhibits production of PG will reset the thermostat to normal body temperature.

3) Anti-inflammatory effect
- PG synthesis reduced -: less vasodilation , vascular permaebility decrease , edema decrease.
- NSAIDs also inhibit granulocyte adherence to the damaged vasculature
- NSAID also cause modulation of T cell function , stabilisation , of lysosomal membrane & inhibit chemotaxis

4) Antithrombotic effect ( blood thinning )
- aspirin inhibit TXA2 thus inhibit platelet aggregation , reducing risk of thrombi

17
Q

State the function of TXA2 and PG

A

TXA2
-induce platelet aggregation

PG - vasodilation
- Inhibit platelet aggregation

18
Q

Describe the adverse effect of NSAID

A

1) Gastric mucosal damage
- - due to inhibition of COX1 enzyme ( offers gut mucosa protection ) causing reduced PG ( PGE2 and PGI2) synthesis
- - PG acts as cytoprotectic agents by decreasing gastric acid production , stimulating mucous & HCO3 production and dilating mucosal blood vessels
- prevented by
I) Taking NSAID after food
II) Using Selective COX-2 inhibitors
III) Use proton pump inhibitors / H2 blockers / misrostol with NSAID
IV) paracetamol ( for cases of mild inflammation )
- hence contraindicated in patients with peptic ulcers

2) Renal dysfunction
- Prostalglandin cause vasodilation in kidney and help in salt and water excretion . In hypovolemia , the kidney blood flow is maintained Antihypertensives and diuretics produce some of their actions through prostaglandins .

  • Inhibitor of PG mediated compensatory vasodilation and salt and water excretion
    3) Hypersensitivity & asthma

4) Increase bleeding tendency ( anti platelet effect )
- due to inhibition of COX-1
- long term of aspirin decrease prothrombin levels by decreasing factor V ( proconvertin )
- hence non selective NSAID are contraindicated in Hemophilia and dengue & should be stopped 1 week before surgery

5) Reye’s syndrome

19
Q

MOA of paracetamol

A

Produces analgesia centrally by inhibiting COX-3 enzyme and via activation of decreasing serotonergic pathways

Or it may produce effect by acting as cannabinols agonist and by antagonising NMDA and substance P in the spinal cord

20
Q

Unlike other NSAID , paracetamol does not have ( …………. ) or ( …………….. ) effects

It is preferred in condition like :

  • children < 12 yrs
  • pt with history of peptic ulcer
  • pt with bronchial asthma
  • pt with bleeding disorder
  • pt on anticoagulants
  • pg with hypertension
  • pregnancy
A

Unlike other NSAID , paracetamol does not have ( gastric side) or ( platelet ) effects

It is preferred in condition like :

  • children < 12 yrs
  • pt with history of peptic ulcer
  • pt with bronchial asthma
  • pt with bleeding disorder
  • pt on anticoagulants
  • pg with hypertension
  • pregnancy
21
Q

Mechanism of paracetamol toxicity

A

> 10 gum

  • usually pcm is metablized by glucoronide & sulfate conjugation ( major pathway )
    Phase 1 metabolism ( oxidation by CYP50 , minor pathway ) of PCM produces NAPQI , highly toxic minor metabolite which usually get detoxified by glutathione conjugation
  • with toxic doses PCM , glutathione stores plummet & large number of toxic metabolites accumulate form covalent bonds with hepatic renal ellualr proteins
  • cause necrosis of the organs and eventual death.
    Treantment
  • oral methionine or IV N-acetylcholine cysteine -> replenish glutathione stores in liver
22
Q

Classify local anaesthetics based on their duration of action

A

1) Short acting , low potency
- procaine , chlorprocaine

2) Intermediate acting & potency
- lignocaine , prilocaine

3) Long acting , high potency
- tetracaine , bupivacaine , ropivacaine , dibucaine

23
Q

What are advantages of amides LA over ester LA

A

1) Amide LA have long per duration of action -> greater efficacy
- as they are not hydrolysed by esterases ( which are found throughout the body )
- instead they are metabolised in the liver only

2) Hypersensitivity reactions are less with amides LAs

24
Q

Describe the advantages and disadvantages of adding adrenaline to LA

A

Advantages
A) Increases the duration of action of LA
-Vasoconstriction reduces blood flow -> less absorption to systemic circulation -> drugs stays in tissue longer

B) Decreases systemic toxicity
- As drug is less absorbed into systemic circulation

C) Provide a bloodless field to surgery

D) Provides additional analgesic effect
- Due to alpha2 receptor stimulation -> decreased release of substance P

Disadvantages
A) Can make the injection more painful
B) Increased the chance of local tissue oedema
C) Delayed wound healing - due to vasoconstriction reducing blood flow
D) May raise BP & promote arrhythmias
E) If used on tissue with end arterial circulation may cause necrosis
- due to vasoconstriction and lack of collateral blood supply
- Lead to ischemia of the tissue

25
Q

Describe the mechanism of action of local anaesthetics

A

LA in its unionised form crosses the nerve membrane

Then, it binds to the intracellular portion of Na+ voltage channnel in its ionised form
Inactive ( but open ) Na channels are most sensitive to LA — charged LA can only access to its binding site when the Na+ channels is open

Blocks Na+ voltage gated channels on neurons

Influx of Na during depolarisation is inhibited
Generation of AP& propagation of impulses is inhibited

26
Q

Describe the adverse effect of local anaesthetics

A
  • mainly involve CNS & CVS
    I) CNS
  • mix of depressant & stimulant effects
  • tremor , restlessness , convulsions , disorientation , twitching , dizziness , AV disturbance , respiratory depression

II) CVS

  • depressant effect on heart
  • decreased excitability , contractility & conduction due to inhibition of NA+voltage gated channels
  • vasodilation of arterioles
  • can lead to bradycardia , hypotension , arrhythmia , heart block

III) Hypersensitivity reactions
- more common in ester linked LAs

IV) Metheglobinemia

27
Q

Describe surface anesthesia

A
  • topical application of LA to mucus membrane / abraded skin
  • LA used :
    I) Eutectic mixture of lignocaine-prilocaine ( EMLA ) — the only preparation that can anaesthetise intact skin
28
Q

Describe infiltration anaesthesia

A
  • Subcutaneous injection of LA directly into tissue without taking into consideration the direction of cutaneous nerves
  • only sensory nerve endings are blocked
  • onset is immediate , duration is shorter than nerve block
  • use : minor operation
  • LA used : lignocaine
29
Q

Describe the field block

A
  • Subcutaneous injection of LA to anesthetiser the area distal to the site of injection
  • All nerves coming to a particular field are blocked
  • Lesser LA needed vs infiltration ananesthetia
30
Q

Describe nerve block

A
  • Injection LA closer to nerve trunks ( brachial plexus , intercostal , trunk of mandibular nerve , cervical plexus )
  • leads to both sensory and motor paralysis
  • drugs used : lignocaine ,mepivacaine , bupivacaine

Pharmacology (4 decks)

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