Chemical transmission SNA/SNC

Acetylcholine release from cholinergic nerve stimuli stimulates: NO. NA. Ach. Prostaglandins. Endothelin.

Cotransmitters released from postganglionic sympathetic neurons include: Acetylcholine. Vasoactive intestinal peptide. Nitric oxide. Adenosine triphosphate. Gamma-amino butyric acid.

Bronchial osteoporosis occurs due to activation of: Adrenergic beta-1 receptors. Adrenergic beta-2 receptors. Muscarinic M1 receptors. Muscarinic M2 receptors. Muscarinic M3 receptors.

Activation of adrenergic beta-2 receptors results in: Contraction of the iris sphincter muscle. Relaxation of the iris sphincter muscle. Ciliary muscle relaxation. Ciliary muscle contraction. Lacrimal gland secretion.

The enteric (intestinal) nervous system is primarily considered to regulate: Urinary tract. Gastrointestinal motility or GIT motility. Male genitalia. Respiration. Vascular smooth muscle.

A co-transmitter known as a neuropeptide Y increases: Vasodilatory effect of acetylcholine. Vasodilatory effect of NO oxide. Vasodilatory effect of dopamine. Vasoconstrictive effect of norepinephrine / norepinephrine. Vasoconstrictive effect of endothelin.

The final step in releasing norepinephrine / norepinephrine from sympathetic neurons is: Docking. Loading. Diffusion. Synthesis. Exocytosis.

In the parasympathetic nervous system, neurotransmitter activity ends with: Synapse diffusion. Active reuptake / reuptake into presynaptic neurons. Inactivation by inhibitors. Enzymatic degradation. Endocytosis.

Enteric Nervous System: Receives input / input from sympathetic nervous system only. Receives input / (input, share, contribution) only from the parasympathetic nervous system. It releases many peptide neurotransmitters and NO. It cannot function without the central nervous system. It has cell bodies that lie in the plexus outside the intestinal / intestinal wall.

Fast neurotransmitters in CNS are: Glutamate. Dopamine. Substance P. Prostamoids. Nerve growth factor.

Slow neurotransmitters and neuromodulators work mainly through or through on: Ligand-gated ion channels; ligand-associated ion channels. G-protein coupled receptors. Enzymes. Transcription factors. Release of NOx NO.

The substances that the P-glycoprotein transports / transfers / transfers from vascular endothelial cells to the central nervous system are: Mostly non-polar (non-polar compounds). Amino acid derivatives such as e.g. Levodopa. Highly ionized. Many anti-tumor and anti-bacterial agents. Mostly mood-altering drugs. mood-altering substances.

The relationship between the biochemical and cellular effects of ZU and its behavior and therapeutic effects is better understood for the agents used in the treatment of: Mood depression. Epilepsy. Parkinson's disease. Schizophrenia. Mania.

Activation of muscarinic M2 receptors: Increases calcium conductivity / conductance. Increases the conductivity / conductance of potassium. Increases heart rate / rate (heart rate) and cardiac muscle contraction power. Causes central nervous system excitation. Causes relaxation of vascular smooth muscle.

Succinylcholine is a characteristic / characteristic agonist of: Muscarinic M1 receptors. Muscarinic M2 receptors. Muscarinic M3 receptors. Nicotinic receptors in skeletal muscle. Nicotinic receptors in the autonomic ganglia.

Secondary messengers / carriers that are formed after activation of muscarinic acetylcholine receptors are: Inositol triphosphate. Cyclic AMP. Cyclic GMP. Eicosanoids. Guanosine triphosphate.

Pilocarpine lowers intraocular pressure through: Reducing the aqueous humor formation. Iris sphincter muscle contractions. Ciliary muscle contractions. Iris sphincter muscle relaxation / release. Ciliary muscle relaxation / relaxation.

The increased release of potassium from denervated muscles by succinylcholine is due to: Cholinesterase inhibitions. Nicotinic receptor desensitization. Up-regulation of the nicotine receptor. Denervation of supersensitivity. destruction of the motor end plate.

Edrofonium / edrophonium causes reversible cholinesterase inhibition through: Bonds to the anionic site. Bindings to the ester site. Bonds to both the anionic and ester sites. Reversible attachments to the allosteric site. Formations of the complex with acetylcholine.

Pyridostigmine increases / promotes neuromuscular transmission / transmission in patients with myasthenia gravis via: Acetylcholine release increases. Inhibition of acetylcholine degradation. Causes of up-regulation / up-regulation of nicotine receptors. Cholinesterase reactivation / reactivation. Blocking auto-antibodies.

Activation of muscarinic M3 receptors leads to: Smooth muscle relaxations. Cardiac slowing. CNS stimulation. Vasoconstriction. Exocrine glands secretions.

Topical ocular administration of atropine produces effects that include: Miosis - narrowing of the pupil. Midriasis - dilation of the pupil due to nerve damage, injury or medication. Lacrimation. Reduction of intraocular pressure / pressure. Conjunctivitis.

If a test dose of edrophonium increases muscle weakness / weakness in patients with myasthenia gravis who are receiving or are treated with pyridstigmine, ie: The patient has essentially no myasthenia gravis. Pyridostigmine dose is too low. Pyridostigmine dose is too high. Atropine should be administered. None of the answers are correct.

Atropine intoxication in children typically results in: Respiratory depression. Muscular paralysis. Sweating. Hyperthermia / TT elevation. Sedation.

Persons with a genetic variant confirming abnormal plasma cholinesterase activity may exhibit prolonged muscle paralysis following administration: Tubocurarine. Pilocarpine. Pancuronium. Atracuria. Succinylcholine.

In the parasympathetic autonomic nervous system, M1 receptors are located in the respiratory tract and are pharmacodynamically most important. (first / second statement correct / incorrect). both incorrect.

Cholinergic neurons in the central nervous system produce at. Mood and emotions. Body temperature controls. Learning and memory. Food intake controls. Rhythm control of wakefulness / sleep.

The characteristics of the partial and full agonist action on the muscarinic receptor are: The partial agonist has an increasing maximum effect than the full agonist. The partial agonist has an increasing ED50 than the partial agonist. A partial agonist and a full agonist may also be one and the same drug. The partial agonist may also act as an antagonist. No claim is correct.

Acetylcholine release from cholinergic nerve endings is blocked by: Atropine. Bungarotoxin. Botulinum toxin. Batrachotoxin. Tetrodotoxin.

Scopolamine is used clinically as a preventative or in the treatment of: Travel weaknesses or. motion sickness. Asthma. Peptic ulcer. Glaucoma. Constipation.

Neuromuscular / neuromuscular blockage induced by atacurium can be nullified or eliminated. turn over with the application: Atropine. Neostigmine. Succinylcholine. Pilocarpine. Nicotine.

Transient muscular fasciculation following paralysis typically occurs after application: Succinylcholine. Tubocurarine. Vecuronium. Gallamina. Atropine.

Effect of muscarinic antagonists, surround the wrong. Miosis. Midriasis.

What Causes Cholinergic Agonists?. miosis. increased cardiac contractility. bronchodilation. bronchoconstriction and increased blood pressure.

What is the main clinical use of muscarinic agonists?. Asthma. Parkinson. Dementia. Glaucoma. Incontinence.

Some with receptors through which bronchoconstriction is triggered?. M3. M1. M2. beta 1. beta 2.