Nokea
Which of the following statements about anticholinesterase drugs is WRONG:
- A. They can be divided into reversible and irreversible types
- B. They include neostigmine and physostigmine
- C. They can produce miosis and lacrimation
- D. They are useful bronchodilators
Correct Answer: D
Rationale: The correct answer is D because anticholinesterase drugs are not bronchodilators; they actually increase cholinergic activity by inhibiting the breakdown of acetylcholine. Reversible and irreversible types do exist (A), neostigmine and physostigmine are examples (B), and they can cause miosis and lacrimation due to increased cholinergic activity (C). Hence, D is the incorrect statement.
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The antagonistic hormone to calcitonin is _____.
- A. thyroxine.
- B. growth hormone.
- C. insulin.
- D. parathyroid hormone.
Correct Answer: D
Rationale: The correct answer is D: parathyroid hormone. Calcitonin and parathyroid hormone regulate calcium levels in the blood. Calcitonin lowers blood calcium levels by inhibiting bone resorption, while parathyroid hormone increases blood calcium levels by promoting bone resorption. Thus, they have opposite effects on calcium regulation, making parathyroid hormone the antagonistic hormone to calcitonin. Thyroxine (A), growth hormone (B), and insulin (C) do not directly oppose the action of calcitonin in regulating calcium levels.
Neostigmine is a drug useful in the treatment of myasthenia gravis, but it causes parasympathomimetic effects unless another drug is given first. This drug is:
- A. Atropine
- B. Epinephrine
- C. Isoproterenol
- D. Edrophonium
Correct Answer: A
Rationale: The correct answer is A: Atropine. Neostigmine is a cholinesterase inhibitor that increases acetylcholine levels leading to parasympathomimetic effects. Atropine, an anticholinergic drug, blocks the effects of acetylcholine, preventing excessive stimulation of cholinergic receptors. Administering atropine before neostigmine helps counteract the parasympathomimetic effects, making it a necessary pre-treatment. Epinephrine and isoproterenol are adrenergic drugs and wouldn't counteract the cholinergic effects of neostigmine. Edrophonium is another cholinesterase inhibitor like neostigmine, so it wouldn't be effective in preventing the parasympathomimetic effects.
Antidiuretic hormone _______________.
- A. controls metabolic rate
- B. controls the amount of urine one produces
- C. increases blood sugar
- D. controls reproduction
Correct Answer: B
Rationale: The correct answer is B: controls the amount of urine one produces. Antidiuretic hormone (ADH) acts on the kidneys to regulate water reabsorption, thereby controlling the amount of urine produced. It does not control metabolic rate (A), increase blood sugar (C), or control reproduction (D). ADH's main function is to maintain water balance in the body by reducing urine output.
Which of the following is not a steroid-based hormone?
- A. estrogen
- B. aldosterone
- C. epinephrine
- D. cortisone
Correct Answer: C
Rationale: The correct answer is C: epinephrine. Steroid-based hormones are derived from cholesterol and include estrogen, aldosterone, and cortisone. Epinephrine is a catecholamine hormone, not a steroid hormone. Catecholamines are derived from the amino acid tyrosine, not cholesterol like steroid hormones. Therefore, epinephrine does not belong to the category of steroid-based hormones.
When an action potential reaches the axon terminal, what happens next?
- A. The muscle fiber contracts
- B. Acetylcholinesterase breaks down acetylcholine in the synaptic cleft
- C. Endosomes containing neurotransmitter fuse to cell membrane, and release neurotransmitter into the synaptic cleft
- D. Sodium channels open at the motor end plate, moving the cell membrane closer to threshold
Correct Answer: c
Rationale: The correct answer is C because when an action potential reaches the axon terminal, endosomes containing neurotransmitters fuse with the cell membrane and release neurotransmitter into the synaptic cleft. This process is known as exocytosis. This neurotransmitter then binds to receptors on the postsynaptic neuron, initiating a new action potential.
Choice A is incorrect because the muscle fiber contraction is initiated by the binding of the neurotransmitter to receptors on the muscle cell, not directly by the action potential reaching the axon terminal.
Choice B is incorrect because acetylcholinesterase breaks down acetylcholine in the synaptic cleft after it has already been released and has completed its role in transmitting the signal.
Choice D is incorrect because sodium channels opening at the motor end plate is part of the process of muscle cell depolarization and contraction, not directly related to the release of neurotransmitter at the axon terminal.