Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BI316 Pharmacology and Toxicology > lecture 7 pt 2 > Flashcards

lecture 7 pt 2 Flashcards

1
Q

The ANS has sympathetic and parasympathetic divisions consisting of what type of nerves

A

efferent and afferent nerves

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

In organs innervated by both divisions of the ANS how do they respond

A

Both branches of the ANS serve their own physiological functions and are thus more or less active in a particular tissue according to the specific need of the body at that given moment.

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

At rest how does the ANS response

A

“Housekeeping” during inactivity is carried out by the Parasympathetic NS while the Sympathetic NS is inactivated

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

During stress how does the ANS respond

A

Mobilisation during activity is carried out by Sympathetic NS while the Parasympathetic NS is inactive

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

Drugs can principally influence the chemical transmission process during the….

A

synthesis, storage, release, degradation or reuptake of the neurotransmitter:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Potential sites of drug action at chemical transmission via a cholinergic synapse

A

(1) Uptake of precursor
(2) Synthesis of transmitter
(3) Storage of transmitter in vesicles
(4) Degradation of surplus transmitter
(5) Depolarization by prolonged action potential
(6) Calcium influx in response to depolarization
(7) Exocytotic release of transmitter
(8) Diffusion to post-synaptic membrane
(9) Interaction with post-synaptic receptors
(10) Inactivation of transmitter
(11) Reuptake of degraded transmitter
(12) Interaction with pre-synaptic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

in a chemical synapse, In response to an action potential what follows

A

Ca2+ enters the presynaptic neuron axon terminal, the vesicle then fuses with the plasma membrane, releasing neurotransmitter molecules into the synaptic cleft. The neurotransmitter molecules then bind to receptors in the plasma membrane of the postsynaptic cell causing ion channels to open, which in turn changes the membrane potential of the postsynaptic cell.

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

Sites of drug action at a nicotinic cholinergic synapse

A

The neurotransmitter Acetylcholine (ACh) is release from the synapse into the synaptic cleft and acts post- synaptically on a nicotinic ACh receptor complex that intrinsically controls the physiological activity of a cation channel

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

Muscarinic acetylcholine receptor

A
  • M-AChR are activated by agonist ACh
  • Pharmacologically type 2 class of metabotropic receptors
  • G-protein coupled class of receptors
  • ACh effects at postganglionic parasympathetic synapses are mediated via m-AChR:
  • Heart
  • Smooth muscle - Glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what can activate and block mAChRs

A

All mAChRs are activated by Ach and blocked by Atropine

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

Muscarinic AChRs are G-protein-coupled receptors causing:

A
  • Activation of phospholipase C, triggering production of second messengers
  • Formation of inositol trisphosphate
  • Diacylglycerol
  • Inhibition of adenylyl cyclase
  • Activation of potassium channels
  • Inhibition of calcium channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how Manu Muscarinic acetylcholine receptors are there and what are they called

A

5 main subtypes (M1 to M5)

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

M1 ‘NEURAL’ mAChR

A
  • Mostly found in cerebral cortex, autonomic ganglia, gastric glands, salivary glands
  • Functional response: CNS excitation, gastric secretion
  • Selective M1 antagonist is the blocker Pirenzepine (treatment of peptic ulcers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

M2 ‘CARDIAC’ mAChR

A
  • Mostly found in the heart and presynaptic terminals of peripheral and central neurons
  • Functional response: Cardiac inhibition, neural inhibition
  • Selective blocker Gallamine (obsolete muscle relaxant with unwanted cardiac side
    effects - tachycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

M3 ‘GLANDULAR’ mAChR

A
  • Mostly found in glands and smooth muscle
  • Functional response: Gastric secretion, salivary secretion, smooth muscle
    contraction
  • Selective blocker Darifenancin (treatment of urinary incontinence)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the main effect of muscarinic cholinomimetics that resembles parasympathetic stimulation

A
  • Vasodilation
  • Decreased heart rate
  • Decreased blood pressure
  • Contraction of gut smooth muscle - Exocrine secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What problems are associated with Muscarinic agonists

A

Muscarinic agonists are poorly absorbed from the GI-tract and furthermore exhibit considerable side effects which excludes many pharmacological applications.

18
Q

Muscarinic agonists

A
  • Acetylcholine (physiological ligand)
  • Muscarine Acetylcholine - Carbachol
  • Methacholine
  • Pilocarpine
  • Betanechol
  • Oxotremorine
  • Cevimeline
19
Q

Muscarinic agonist used for the reduction of intraocular pressure (IOP) in glaucoma

A

Pilocarpine increases aqueous outflow via contraction of the ciliary muscle, which opens fluid pathway

20
Q

what is the normal IOP and what is that of Glaucoma

A

– IOP Normal: 15 mm Hg (10-20 range)
– IOP Glaucoma: > 21 mm Hg

21
Q

Substances acting antagonistically at the M-cholinoceptor mAChR are termed what

A

Parasympatholytics

22
Q

what is a prototype of a parasympatholytic muscarinic antagonist

A

Atropine

23
Q

Properties of atropine

A
  • plant alkaloid
  • occurs in deadly nightshade (Atropa belladonna)
24
Q

Examples of Parasympatholytics:

A
  • Atropine
  • Hyoscine
  • Tiotropium
  • Cyclopentolate
  • Pirenzepine
25
Q

Effects of the typical muscarinic antagonist atropine:

A
  • Cardio Acceleration
  • Inhibition of exocrine gland function
  • Effects on the eye
  • Relaxation of smooth muscle
  • CNS- attenuating effects
26
Q

Cardio Acceleration

A

Tachycardia is triggered through block of cardiac mAChRs. However, tachycardia is modest: 90 beats/min

27
Q

Inhibition of exocrine gland function

A

Decreased secretion of salivary, bronchial and sweat glands

28
Q

Effects on the eye

A

Dilation of pupil; relaxation of the ciliary muscle causes paralysis of accommodation causing impaired near vision; increase of intraocular pressure

29
Q

Relaxation of smooth muscle

A

Bronchial and urinary tract smooth muscle are relaxed. Also gastrointestinal motility is inhibited

30
Q

CNS-attenuating effects

A

Dose-dependent effects through blockade of brain mAChR (low dose: restlessness; toxic dose: hyperactivity and disorientation)

31
Q

Atropine poisoning due to Ingestion of deadly nightshade berries is characterized by the following effects:

A

Peripheral effects and Central effects

32
Q

Peripheral effects

A
  • Tachycardia
  • Dry mouth
  • Hyperthermia
  • Constipation
33
Q

Central effects

A
  • Motor restlessness
  • Psychic disturbances
  • Disorientation
  • Hallucinations
34
Q

what therapy can be used for severe atropine intoxication to Indirectly increase ACh levels

A

Administration of phyostigmine, an indirect parasympathomimetic drug (anti-AChE)

35
Q

clinical use of muscarinic antagonists: Premedication before inhalation anesthesia

A

Due to relaxation of bronchial smooth muscle, atropine prevents a possible hyper-secretion of bronchial mucus that cannot be expectorated by coughing during anesthesia.
Potential side effects: Dry mouth, blurred vision, urinary retention

36
Q

Clinical use of muscarinic antagonists: Relaxation of gastrointestinal smooth muscle

A

Hyoscine butylbromide for the facilitation of endoscopy and gastrointestinal radiology

37
Q

Clinical use of muscarinic antagonists: Prophylaxis of kinetosis

A

Prevention of motion sickness using hyoscine orally or transdermally

38
Q

Clinical use of muscarinic antagonists: Inhibition of gastric secretion

A

Pirenzepine is used for the treatment of peptic ulcer

39
Q

Clinical use of muscarinic antagonists: Bronchodilation in bronchial asthma and spastic bronchitis

A

Administration of Tiotropium by inhalation causes bronchodilation in conditions of increased airway resistance

40
Q

Clinical use of muscarinic antagonists: Treatment of bradycardia

A

Intravenous atropine may be used in bradycardia to raise the heart rate after myocardial infarction

41
Q

Clinical use of muscarinic antagonists: Urinary incontinence

A

Selective M3 receptor antagonist Darifenacin acts on bladder muscle contraction

42
Q

Clinical use of muscarinic antagonists: Symptomatic treatment in Parkinsonism

A

Centrally acting M1 antagonist Benztropine is useful to counteract tremor at rest and muscle rigidity

BI316 Pharmacology and Toxicology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions