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year two sem two > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

Define the major neurotransmitters of the parasympathetic and sympathetic nervous systems ?

A
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2
Q

What parts of the autonomic nervous system does acetylcholine act ?

A
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3
Q

How does stimulation of the parasympathetic system affect the following body systems ?

A

Parasympathetic stimulation through Acetylcholine

  • decrease HR, conduction velocity, contractile force
  • salivary glands, lacrimal glands increase secretion
  • Gastrointestinal tract increase motility, tone, relax sphincters, increase secretions and increase contraction of the gall bladder and ducts
  • Lungs = bronchial constriction, increase secretion and decrease RR
  • Bladder contraction fundus and relaxation sphincter
  • Causes contraction of the sphincter muscle of the Iris ciliary muscle
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4
Q

Describe the synthesis, storage and release of Acetylcholine ?

A

Synthesis and storage, release ACTH

  • Synthesised by Choline acetyltransferase
  • This catalyses the transfer of an acetyl group from acetyl coenzyme A to choline
  • ACHT is stored in a bound form within vesicles
  • Choline must be pumped into the cholinergic neuron, and the action of the cholinergic transporter is the rate limiting step
  • An action potential in the cholinergic neuron terminal evokes the opening of voltage sensitive calcium channels and the release of ACHT - by exocytosis to trigger a post synaptic physiological response.
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5
Q

Describe how Acetylcholine is broken down and how this is important ?

A

Acetlycholine breakdown

  • Broken down by Acetylcholinesterase (ACHE)
  • rapidly hydrolyses ACH into choline and acetic acid
  • Thus Acetylcholine has a rapid, discrete and localized action
  • True AChE is localised in the synaptic cleft at cholinergic synapses.
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6
Q

Describe the two different cholinergic receptors, and where they act ?

A

The effects of ACh is mediated via cholinergic receptors. These receptors are classified to their responsiveness to 2 agonist (nicotine and muscarine)

Mascarinic receptors

  • postganglionic parasympathetic neurons eg heart muscle, smooth muscles and secretory glands
  • presynaptic noradrenic and cholinergic nerve terminals
  • non inervated sites in vascular endothelium
  • spinal cord and brain
  • G protein coupled receptor

Nicotinic receptors

  • sympathetic and parasympathetic ganglia
  • adrenal medulla
  • neuromuscular junctions (skeletal muscle)
  • spinal cord and brain
  • ligand gated ion channel
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7
Q
A

Question answers

  1. Choline acetyltransferase
  2. action of choline transporter into the cholinergic neuron
  3. Acetylcholinesterase (ACHE)
  4. muscarinic and nicotinic
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8
Q

Describe the different types of muscarinic receptors, and what physiological response occurs when they are stimulated ?

A
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9
Q

Identify three direct esters, what are these drugs mode of action ?

A

Parasympathomimetic Cholinomimetic Esters

Carbachol, Bathanecol, and Methacholine

Stimulation of the parasympathetic nervous system by acting directly upon postsynaptic receptors

  • Acetylcholine naturally occurs in the body as an Ester
  • ACH however is rapidly degraded, where as the artificial esters are longer lasting
  • these drugs may be selected to act specifically on muscurinic or nicotinic receptors

Methacholine and bethanechol activate muscurinic but not nicotinic receptors

Carbachol has both muscurinic and nicotinic activity

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10
Q

Describe the three different types of Parasympathomimetic drugs and their action ?

A
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11
Q

Provide six indications of Parasympathomimetic drugs?

A

Indications for Parasympathomimetic drugs ?

  • Urinary bladder atony in cats (urolithiasis)
  • Rumen atony
  • Colic and impaction of the intestinal tract
  • Retained placenta still birth
  • Glaucoma
  • Anti-curae, and myasthenia-like symptoms in dogs
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12
Q

Describe the mechanism of action and toxiticity of cholinomimetic

alkaloids ?

A

Parasympathomimetic cholinomimetic alkaloids

Pilocarpine, Muscarine and Slaframine

Mode of action = directly stimulate postsynaptice muscurinic receptors

  • minimal activation of nicotinic receptors
  • do not depend on naturally produced ACH for activity
  • long duration of action
  • Pilocarpine only alkaloid frequently used in clinical practice

Toxicity

  • diarrhoea
  • colic
  • bronchoconstriction
  • dyspnea
  • hypotension
  • bradycardia (too slow)
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13
Q

Provide examples of Cholinesterase inhibitors, mode of action and affects of toxicity ?

A

Cholinesterase inhibitors

Reversable inhibitors = Physostigmine, Neostigmine, Pyridostigmine and Edrophonium

Irreversable Inhibitors = Organophosphates, Diisopropyl fluorophosphate, Echothiophate

Mechanism of action = Inhibits the breakdown of ACH to potentiate and prolong cholinergic neurotransmission.

  • classified according to the duration of action
  • Neostigmine and Physostigmine can be hydrolysed by ACHE, however at a slower rate
  • organophosphates form a more stable enzyme-inhibitor complex
  • Neostigmine and Pyridostigmine exhibit a greater effect at the neuromuscular blockers - these drugs can be used to reverse the effects of neuromuscular blockers.
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14
Q

Describe the potential toxic affects of Cholinesterase inhibitors ?

A

Toxic affects of Cholinesterase inhibitors

Physostigmine = like most organophosphates can cross the blood brain barrier freelyleading to convulsions, CNS depression, unconsiousness and respiratory failure.

  • ACHE inhibitors may cause synergistic effects with phenothiazine tranquilizers
  • contraindicated during succinyl choline administration
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15
Q
A

Questions

Receptor types involved = muscarinic receptors

Organ funtion specific effects

  • Heart and vasculature = slow heart rate (bradycardia) and high blood pressure
  • Lung = bronchoconstrictions + increase in secretions
  • Gastrointestinal = increase motility and secretions + relaxed sphincters
  • Urogenital = increased contraction + relaxation of sphincter

Treatment options and rationale

  • Atropine muscurinic receptor antagonist
  • dilution of poison and expulsion
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16
Q

If no mechanical block is identified what is a suitable drug to treat gluacoma in cats ?

A

Glaucoma

Pilocarpine

C) Stimulation of Muscarinic receptors

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17
Q
A

E = Expulsion of a retained placenta following farrowing in pigs

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18
Q
A

E. O-Isopropyl-methylphosphono fluridate sarin

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19
Q
A

E. Organophosphate poisoning

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20
Q

Provide two examples of Muscarinic receptor antagonist and their pharmacological affects ?

A

Muscarinic receptor antagonist

Atropine and (Glycopyrrolate synthetic derivative)

Pharmacological affects

competitive antagonism

  • inhibition of glandular secretions
  • low dose transient reflex (bradycardia HR too slow)
  • high dose tachycardia (HR too high) due to increased inhibition of pacemaker activity
  • pupillary dilation (impairment of near vision)
  • relax smooth muscles spasmolytic
  • treatment of acute asthma attacks
  • treatment of organophosphate poisoning
  • treatment of muscarine poisoning
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21
Q

Describe the important clinical applications of using the muscarinic recetor antagonist of Atropine or Glycopyrrolate ?

A

Clinical applications of Atropine and Glycopyrrolate

  • Pre-medication for anaesthesia inhibits bronchial and saliva secretions + prevent bronchial constriction
  • Induction of pupil dilation and paralysis of accomodation
  • Spasmolytics (muscle relaxannts GI, uterine, bronchial etc)
  • Asthma
  • Treatment of organophosphate poisoning
  • Treating muscarine poisoning
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22
Q

Detail the toxicity of Atropine ?

A

Toxicity Atropine

  • species and rout of administration dependant
  • it is dependant upon the route of administration and species involved ( horses and ruminants are more susceptable to parental doses).

Symptoms

  • dry mouth thirst
  • constipation colic
  • tachycardia
  • ataxia (reduced coordination)
  • dysphagia
  • mydriasis
  • hyperpnea
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23
Q

Detail the clinical application of 2-Pralidoxime (2-PAM)

A

2-PAM

Organophosphate poisoning = action is by inhibition of Acetylcholinesterase enzyme (ACHE), this prevents the breakdown of ACH and results in excessive activation of the parasympathetic response

  • used in the treatment of organophosphates time dependant
  • dissociates the organophosphate from ACHE active site
  • 2-PAM is usually used concurrently with a muscarinic receptor blocker eg Atropine

Note over time the organophosphate becomes covalently bonded and irreversable - time dependant

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24
Q

How do you distinguish between depolarising and non-depolarising nicotinic blockers and provide examples?

A

A depolarizing nicotinic blocker such as Succinylcholine acts similarly to ACH by causing depolarisation of the postsynaptic memebranes. Unlike ACTH Succinylcholine is not readily broken down resulting in stimulation followed by a period of paralysis normally lasting 5mins as the synapse is fatigued.

  • succinylcholine, nicotine, suxamethonium, and decamethonium

A non depolarising agent such as Atracurium or Pancuronium dose not result in depolarisation. It’s action is elicited by competitive inhibition of the nicotinic receptor.

  • Atracurium, Pancuronium
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25
When using Succinylcholine what is a phase one and phase two block ?
26
A = Atropine Muscarine is a alkaloid which causes stimulation of muscarinic receptors - Atropine is a muscarinic receptor antagonist
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B. 2-PAM dissociates organophosphate from the recepyor It's action is time dependant as as the interaction with organophosphates becomes covalent and irreversable
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C. Acetylcholine and nicotinic receptors
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D. Succinylcholine
30
Provide two examples of non depolarizing neuromuscular blocking agents ?
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A. Atracurium
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D. Muscarinic subtype M2 via acetylcholine
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5A = pilocarpine, bethanecol, pilocarpine 5B = atropine, scopolamine, glycopyrrolate 5C = neostigmine, physostigmine and organophosphates
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AA
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C.
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E.
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D.
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E.
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A.
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E.
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B.
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A. C.
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B.
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A.
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A.
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B. Beta 1 receptors ## Footnote 1) Alpha 1 receptors Adrenaline, Noreadrenaline and dopamine 2) Selective alpha 2 receptor agonist = Xylazine, Medetomidine 3) Apha 1, Beta1 and Beta 2 agonist = Adrenaline, Noreadrenaline 4) Selective Beat 2 agonist = Salbutamol, Terbutaline, and Clenbuetrol 5) Dopamine, Alpha1 and Beta1 agonist = Dopamine
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B. Beta 1 receptors excitory selective for the heart Dobutamine
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D. Highly selective for Beta 1 receptors
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C. Beta 2 agonist Salbutamol avoids a systemic response
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C. Noreadrenaline releasing agent
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A.
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D. Propanolol In the heart these detrimental effects are driven by Beta 1 receptors. Therefore it is wise to use a Beta one antagonoist such as Propanolol.
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This is an epinephrine/norepinephrine reversal effect. As alpha receptors are blocked, adrenaline preferentially activated Beta receptors. At beta 2 receptors in the large blood vessels, the net effect is vasodilatory thus decreasing blood pressure.
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A. Xylazine and medetomidine
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A, B, C, D, E, G, H, I, and J A pheochroimocytoma = tumor in the adrenal gland.
63
Describe the synthesis of catecholamines ?
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Provide an overview of the control and secretion of catecholamines ?
65
Identify the five adrenergic receptors ?
66
Describe where about in the body Beta 1 receptors are located, mode of activation, effects and relative strength of agonist ?
67
Provide common antagonist of Beta 1 receptors within the sympathetic system, what are the effects of antagonism ?
* Propanolol * Atenolol This causes a decrease in heart rate as beta 1 receptors are primarly located in the heart (somewhat in the kidneys)
68
Detail the mechanism of action when Beta one receptors are stimulated ?
69
Discuss where Beta 2 receptors are located, their mechanism of action, effects and relative strengths of angonist ?
70
Detail the location of Alpha one receptors, their mechaism of action and strength of agonist ?
71
Provide the name of two Alpha two antagonist ?
* Phenoxybenzamine * Prazosin
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* B Terbutaline a selective Beta 2 agonist * D Salbutamol a selective Beta 2 agonist
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Detail the mechanism of action for a Alpha one receptor agonist ?
74
Describe the location, mechanism of action, effects and strength of agonist for Alpha two receptors ?
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Identify the antagonist for Alpha two receptors ?
* Antipamezole * Tolazoline * Yohimbine
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Describe the effects of Alpha two stimulation ?
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Describe the location of Dopaminergic receptors and the effects of stimulating them ?
78
Describe the effects of Sympathetic stimulation on the heart, blood vessels, endothelium, GI tract, lungs, eye, bladder and sweat glands ?
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Describe how sympathetic stimulation affects the glands and fat cells of the body ?
80
Identify the agonist of Alpha one and two, and Beta one and two receptors ?
81
Identify agents which work as indirect sympathetic agonist ?
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Identify the Beta one and Beta two antagonist ?
84
Provide a summary of sympathetic agonist, and the receptors they act upon ?
85
Identify Beta two agonist to stimulate bronchodilation in the lungs, why should we avoid the use of Norepinephrine ?
86
What agents can be used to treat systemic hypotension?
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What agent can be utilised to manage acute systolic cardiac dysfunction ?
88
Identify agents to be used to treat incontinence and to stimulate mydriasis ?
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What agents can be used to stimulate alpha 2 receptors to induce sedation, and what is the mechanism of action ?
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Identify Sympathomimetic toxicities ?
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What is epinephrine reversal ?
92
Identify hemostatic agents ?
Hemostatic agents = agents which can be used to cause a blood clot Topical use * Diathermy = application of pressure * Thromboblastin * Thrombin * Fibrin * Oxidised cellulose * Epoinephrine + Noreepinephrine Systemic hemostatic agents * Blood or plasma * Vitamin K * Tranexamic acid
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Tumour development Step wise tumour development - cumulative effect of multiple genetic (and epigenetic) changes over a long time course that creates a tumour. Many genes are required to direct and control the steps within the normal cell cycle Oncogenesis = is the complex process by which neoplastic cells develop. DNA mutations can occur in one or many of the different genes that normally regulate cell growth and differentiation- * proto oncogenes - regulate cell growth and differentiation * tumour suppressor genes such as p53 - slow * genes which code for DNA repair proteins * telomerases
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Describe the actions of ACH through a muscarinic receptor in the heart, and in the smooth muscle of the intestine ?
ACH ACH lacks sensitivity, it is active at multiple sites (autonomic, peripheral nicotinic and muscarinic receptors. Effects of ACH release and stimulation of cholinergic receptors may be 1. Excitatory eg smooth muscle of the gastrointestinal tract due to depolarisation of the postsynaptic membrane which increases peristalsis 2. Inhibitory as seen in the myocardium (due to inhibition of the G protein couple receptor) linked to inhibition of adenyl cyclase which lowers HR.
96
What are parasympathomimetics, and their two modes of action ?
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Identify reversable and irreversible inhibitors of cholinesterase activity ?
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1. Autoimmune disease which acts to destroy nicotinic receptors 2. Goal is to increase the concentration of acetylcholine at nicotinic receptors treatment = neostigmine
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E. only
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E. Sarin
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Answer E only
102
What are the effects of atropine poisoning, and how can we treat it ?
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Depolarising Neuromuscular blocking agents Depolarising (agonist), muscle relaxants Succinylcholine, Nicotine, Suxamethonium and Decamethonium Mode of action = These drugs cause skeletal muscle paralysis and relaxation, by interfering with the ACH mediated depolarisation of presynaptic membranes at neuromuscular junctions. * action nicotinic receptors * unlike ACH not readily broken down, leading to prolonged depolarisation * succinylcholine stimulates nicotinic receptors for around 5 30secs followed by a period of paralysis lasting around 5 mins after a single dose - this is known as a phse one block * Phase 2 block = repeated dose od succinylcholine causes the accumulation of metabolite succinylmonocholine which has a curae like (non - depolarising ) block affect. The short action of succinylcholine makes it useful for such procedures as intubation.
104
Non - depolarising neuromuscular blockers Atracurium and Pancuronium These are antagonist for nicotinic acetylcholine receptors on skeletal muscle. They block ion channels at **motor end plates but have no depolarizing activity.** They are commonly used during surgery to cause complete muscle relaxation
105
Discuss the pathophysiological control mechanisms of the airways ?
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Describe the five classes of respiratory pharmacological agents and provide examples ?
108
Mechanism of action glucocorticoids Examples = prednisone, prednisolone and fluticasone (inhaler) * they are mediated by the glucocorticoid receptor * inhibition of chemotaxis by decreasing mediators eg prostaglandins, leukotrienes, and platelet activation factor * increase the expression of Beta two receptors hence their synergistic effects with Beta 2 agonist * transcriptional regulation of genes (chemokines, adhesion molecules) involved in the activation of mast cells, eosinophils and lymphocytes * inhibit spasmogens
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Beta two agonist Albuterol, Terbutaline and Clenbuterol * mostly inhalation, short acting * first choice in acute asthma attacks - decrease mast cell degeneration * bronchodilation * spasmolytic - relief of spasms Indications * airway disease including acute inflammation * allergic bronchitis and feline “asthma” * recurrent airway obstruction “heaves”
110
Identify the three drug types which can be used to cause bronchodilation ?
Three types of bronchodilators Beta 2 agonist = Albuterol, Terbutaline and Clenbuterol Xanthine derivatives = Theophylline Anticholinergic (M3) = Glycopyrrolate and Ipratropium
111
What is a antitussive pharmacological agent, provide examples ?
Antitussives Butorphanol, codeine and Dextromethorphan medicines which suppress coughing
112
Describe the mechanism of action for Beta two agonist ?
113
Theophylline and Aminophylline * increase cellular cAMP * inhibit calcium influx and mast cell degranulation * may increase CNS mediated increases in respiration
114
Discuss the bronchodilators muscarinic antagonist, provide examples and their mode of action ?
115
1 - D 2 - I 3 - J
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1 = E 2 = I 3 = A
117
1 = K 2 = indicated for maladaptive dry cough which interferes with rest. Cough may be productive and characterised by the presence of excess sputum and may be associated with chronic bronchitis 3 = respiratory depression, drowsiness, euphoria and constipation
118
Decongestants saline, bromhexine and N - acetylcysteine these compounds will decrease the viscosity by dissociation of disulphide bonds in mucoproteins (PH 7-9), or by endonuclease activity
119
Describe beta one receptors and their agonist ?
Beta one receptors * predominantly expressed in the myocardium (sino atrial and atrio - ventricular) * kidneys * G protein couple recetor (GPCR) causing an increase in cyclic adenosine mono-phosphate (cAMP) * activation of beta one receptors causes positive inotropic, chronotropic and dromotropic effects
120
Agonist Endogenous = Epinephrine \> Norepinephrine, dopamine Synthetic = Isoprotenol, Dobutamine Antagonist Propranolol, Atenolol
121
Widely distributed, but predominantly * expressed in lungs, smooth muscle * large vessels in the skeletal muscle * hepatocytes * peripheral vasculature * some visceral non innervated organs Causes a cellular response activation of Gs subunit of GPCR with an increase in cAMP but other mechanisms may be involved * mediates smooth muscle relaxation * bronchodilation, vasodilation, dilates GIT and urinary sphincters * induces skeletal muscle tremor * stimulates glucogenolysis
122
Describe what pharmacological agents could be used as an agonist and antagonist on B2 receptors ?
Agonist Isoproterenol \> Epinephrine \> Norepinephrine Salbutamol, Terbutaline Antagonist
123
Describe the effect of Alpha one receptor stimulation ?
Alpha one receptor stimulation * Alpha one receptors are widely distributed but mostly expressed in the innervated vasculature, smooth muscle and visceral organs * cellular responses involves activation of G9/PLC/IP3 and DAG with an increase in cellular Ca2+ - this propels most of the physiological changes Changes induced * constriction of vasculature * constriction smooth muscle sphincters * dilation / relaxation of GI smooth muscle etc
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Alpha one receptors Agonist Noreadrenaline \> Adrenaline \>\>Isoprotenol others = phenylephrine, methoxamine, isoproterenol, Antagonist Phenoxybenzamine, prazosin
125
Alpha two receptors Alpha two receptors are widely distributed but predominate the CNS (particularly the brain stem, and limbic system). They are also expressed in the vasculature, GI, pancreatic islets, presynaptic membranes and non - innervated tissues eg. thrombocytes and endothelial cells. Cellular response involves a G1 subunit of GPRC, decreasing cAMP and increasing K+ conductance. Physiological changes * reduced insulin secretion * reduced CNS sympathetic flow * inhibition of presynaptic neurotransmitter
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Alpha two receptors Agonist = Xylazine, Detomidine, Medetomidine Antagonist = Atipamezole, Tolazoline and Yohimbine
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Describe dopamine receptors ?
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What is the affect of dopamine ?
Dopamine Dopamine increases HR and myocardial contractility vi B1 and vasoconstriction via A1 receptors
129
Describe the sympathetic drugs used as antogonist and agonist of the sympathetic system ?
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131
Epinephrine reversal phenomenon and severe hypotension * Epinephrine has a higher affinity for alpha one receptors, however, these are blocked (alpha 1 = constriction of vasculature, constriction smooth muscle sphincters) * Thus epinephrine enacts its actions through stimulation of beta two receptors. (beta two expressed in lungs, smooth muscle thus bronchodilation, vasodilation)
132
Identify selective beta 2 agonist, and what are they used for ?
Beta 2 agonist (selective Salbutamol, Terbutaline, clenbuterol) and (non selective adrenaline) * metered dose inhaler salbutamol * or parentally for turbutaline and clenbuterol * commonly used as bronchodilators * stimulation of the beta 2 receptors in smooth muscle of the alveoli
133
What four physiological factors affect gastric motility and secretion ?
134
Calcium chelators Heparin sodium
135
Heparin or low molecular weight Reviparin, Daltaparin Potentially could cause haemorrhage, thrombocytopaenia, immune mediated reactions
136
These agents act by preventing the activation of vitamin K dependant coagulation factors 2,7,9 and 10. The time lag allows for complete depletion of preformed coagulation factors.
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Meloxicam like Aspirn are non steroidal anti inflammatory drugs (NSAIDS). That have antiplatelet aggregation activity via inhibition of cyclooxygenase -1on platelets and thus the production of thromboxane. In essence this drug prevents the formation of a clot hence excessive bleeding. j
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1 = Tranexamic acid 2 = A synthetic amino acid and competitive inhibitor of serine protease inhibitor. This protease activity activates plasminogen to plasmin which which prevents fibrinolysis and clot break down. 3 = Any condition which predisposes to excessive coagulation
140
1 = coumarin and derivatives 2 = inhibitors of vitamin K epoxide reductase 3 = there is a lag period as the vitamin K dependant clotting factors are utilised 2,7,9 and 10 4 = calves have lower hepatic function to clear poison 5 = vitamin K

year two sem two (7 decks)

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