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Pharmacology > Ganglioblockers and MR > Flashcards

Ganglioblockers and MR Flashcards

1
Q

What are ganglioblockers?

A

Drugs that inhibit the effects of acetylcholine on Nn receptors which are localized and sympathetic and parasympathetic autonomic ganglia, adrenal medula, and sinus caroticus.

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2
Q

What is an example of a ganglioblocker?

A

Trimethaphan or Arfonad which is highly hydrophilic

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3
Q

What are the pharmacodynamics of ganglioblockers?

A
  1. They block Nn receptors
  2. they cause pharmacological denervation since they block both PNS and SNS
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4
Q

what is the effect of ganglioblockers on arteries?

A

Vasodilation, improvement of peripheral circulation, and decrease of BP

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5
Q

what is the effect of ganglioblockers on veins?

A

Vasodilation, decrease often return, and decrease of stroke volume

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6
Q

what is the effect of ganglioblockers on the heart?

A

It causes tachycardia and stimulates negative inotropic effect

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7
Q

what is the effect of ganglioblockers on eye?

A

Mydriasis and cycloplegia

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8
Q

what is the effect of ganglioblockers on GIT?

A
  • Decrease of tone and peristalsis
  • Constipation
  • decrease of secretion
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9
Q

what is the effect of ganglioblockers on urinary bladder?

A

It causes urine retention

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10
Q

what is the effect of ganglioblockers on exocrine glands?

A

Xerostomia and anhidrosis

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11
Q

what are the effects of ganglioblockers blocking sympathetic ganglions?

A
  1. Decrease of blood pressure
  2. inhibition of the secretion of vasopressin
  3. dilation of arteries and veins causing orthostatic collapse
  4. relaxation of precapillary sphincters and improving tissue blood supply and microcirculation
  5. decrease of preload and post load of the heart due to dilation of veins and arteries
  6. improvement of contractile function of the left ventricle of the heart
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12
Q

what are the effects of ganglioblockers blocking Parasympathetic ganglions?

A
  1. Tachycardia due to the decrease of effective vagus nerve and reflective response because the fall of blood pressure and vein return decrease
  2. relaxation of smooth muscles like bronchi, intestines, bile ducts, and urinary tract
  3. decrease of secretor function of salivary, sweat, guacamole, and stomach glands
  4. dilation of pupil and paralysis of accommodation
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13
Q

what are the pharmacokinetics of ganglioblockers?

A
  • Quaternary amines absorption from GIT isn’t full and is unpredictable
  • after absorption they are usually distributed and extracellular spaces and eliminated through kidneys usually unchanged
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14
Q

What are the uses of ganglioblockers?

A
  1. It is used in surgical interventions to obtain controllable hypertension for prevention of bleeding
  2. hypertensive crisis and aortic aneurysm to inhibit sympathetic reflexes
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15
Q

what are the side effects of ganglioblockers?

A
  1. Orthostatic collapse
  2. stimulation of angina pectoris
  3. inhibition of exocrine gland and gastric juice secretion
  4. atonic Constipation and development of paralytic ileus
  5. mydriasis, increase of intraocular pressure, and paralysis of accommodation
    dryness of skin and mouth, dysarthria, and dysphagia
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16
Q

what is the mechanism of action of central Myorelaxants?

A

They act on appropriate centers of the spinal cord

17
Q

what is an example of central Myorelaxant?

A

Tizanidine or Sirdalud

18
Q

what is the mechanism of action of Peripheral Myorelaxants?

A

They bind to Nm receptors of neuromuscular synapses and block the neurotransmission on the postsynaptic level and close reduction of skeletal muscle tone bringing to the development of paralysis

19
Q

what is the classification of peripheral Myorelaxants?

A
  1. Depolarizing myorelaxants like Succinylcholine, Dimythylinym, or Suxamethionium
  2. Nondepolarizing myorelaxants
20
Q

What are the different types of non depolarizing myorelaxants?

A
  1. Competitively acting
  2. non competitively acting like prestonalum
21
Q

what are the different types of competitively acting non depolarizing myorelaxants?

A
  • Long duration of 80 to 180 minutes
    1. Tubocurarine
    2. Pancuronium
  • intermediate duration of 30 to 40 minutes
    1. vecuronium
    2. atracurium
  • short duration of 10 to 20 minutes like mivacurium
22
Q

describe the pharmacodynamics of non depolarizing myorelaxants.

A
  • In case of competitive mechanisms they compete with acetylcholine for the same receptors and they usually have more affinity but no memetic activity
  • noncompetitive binds to the other subunits of receptors preventing the binding of acetylcholine with receptors
23
Q

describe the pharmacodynamics of depolarizing myorelaxants.

A
  • They have affinity toward receptors and intrinsic chromatic activity
  • they opened sodium channels of receptors causing depolarization of skeletal muscles and at the beginning can cause convulsions and tremor
  • After biting to the receptors they are not disassociated quickly and cause lung depolarization of muscle cells which results in sodium channel deactivation due to which effects of acetylcholine are inhibited and activation of muscle fiber is prevented
24
Q

how do myorelaxants effect skeletal muscles?

A
  • Non depolarizing type by IV administration calls the relaxation of skeletal muscles from mimic muscles of face, finger muscles, hands, legs, intercostal muscles, and diaphragm and brings to the stoppage of respiration
  • depolarizing type causes constriction of muscles before paralysis which lasts shortly only for seconds
25
Q

how do myorelaxants effect autonomic ganglia?

A
  • Competitive causes and significant ganglion blockage at which the main receptors are nicotinic and this effect is more prominent for tubocurarine but not the new drugs
  • succinylcholine can activate the ganglia because it has an agonistic activity on receptors
26
Q

how do myorelaxants effect autonomic ganglia?

A
  • Competitive causes and significant ganglion blockage at which the main receptors are nicotinic and this effect is more prominent for tubocurarine but not the new drugs
  • succinylcholine can activate the ganglia because it has an agonistic activity on receptors
27
Q

how do myorelaxants effect cardiovascular system?

A
  • Tubocurarine decreases blood pressure by blocking vegetative ganglia, histamine release, reduced vein flow, and paralysis of legs and respiratory muscles
  • due to inhibition of vagus nerve tachycardic and develop
28
Q

how do myorelaxants effect GIT?

A

Competitive type can worsen the post operative atonia of intestines

29
Q

what is the pharmacokinetic of myorelaxants?

A

There are quaternary substances used by IV and not enterally

30
Q

what are the usages of myorelaxants?

A
  1. Surgical interventions for achieving myorelaxation
  2. myorelaxation for intratracheal intubation
  3. inhibition of spontaneous respiration to achieve artificial respiration
  4. prevention of convulsions when anti epileptic drugs are absent
  5. myorelaxation in case of bone fracture
31
Q

what are the side effects of myorelaxants?

A
  • Long paralysis of respiratory muscles and apnea
  • hypertension caused by tubocurarine
  • release of histamine by tubocurarine and atracurium which causes bronchospasm, increased activity of exocrine glands of upper Airways, hypersalivation, and full of BP
  • succinylcholine may cause severe complications in patients with hereditary absence of pseudocholinesterase enzyme and the effects can be reversed by injection of fresh blood plasma
  • depolarizing type can cause minor trauma and muscle pain
  • depolarizing type can cause arrhythmias or heart arrests
  • malignant hyperthermia due to mutations of calcium ion channels leading to release of calcium from sarcoplasmic reticulum and activation of catabolism at which dantrolene is used as an antidote
32
Q

what are the advantages of new myorelaxants?

A
  1. Less ganglion blocking activity and less cardiovascular effects
  2. less or absence of histamine release
  3. short duration of action and easy recovery of their effects

Pharmacology (11 decks)

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