Review Session Questions/IRATs/In class case Q's

Question 1

1. Phentolamine treatment for high blood pressure is associated with orthostatic hypotension . What is the most likely explanation for this phenomenon?
   a. Phentolamine stimulates Nitric Oxide production
   b. Phentolamine stimulates beta -2 receptors in the vasculature
   c. Phentolamine blocks alpha-1 receptors in the vasculature
   d. Phentolamine inhibits the reuptake of Norepinephrine.

Answer 1

c. Phentolamine blocks alpha-1 receptors in the vasculature

Question 2

Phentolamine treatment is also associated with tachycardia. A related drug, prazosin, is less likely to cause tachycardia. Why is this?

a. Prazosin blocks both alpha- and beta-receptors.
b. Prazosin blocks only the alpha -1 receptors.
c. Prazosin increases vagal tone.
d. Phentolamine is also a beta-1 agonist

Answer 2

b. Prazosin blocks only the alpha -1 receptors.

Question 3

Isoproterenol infusion would likely result in which hemodynamic profile?

a. Increased heart rate, increased diastolic blood pressure.
b. Decreased heart rate, decreased diastolic blood pressure.
c. Increased heart rate, decreased diastolic blood pressure.
d. Decreased heart rate, increased diastolic blood pressure.

Answer 3

c. Increased heart rate, decreased diastolic blood pressure.

Question 4

1. Darifenacin is commonly used to treat incontinence. Based on its mechanism of action, which of the following conditions would be considered likely side effects from its use?
   a. Hot dry skin
   b. Diarrhea
   c. Difficulty focusing on far objects
   d. Excess Salivation

Answer 4

a. Hot dry skin

Question 5

An intercostal nerve block can be done to numb up a dermatome. Intercostal nerves are located between which layers in the thoracic body wall?
A. External intercostal and internal intercostal muscles.
B. Innermost intercostal muscles and parietal pleura.
C. Internal intercostal and innermost intercostal muscles.
D. Parietal pleura and visceral pleura.
E. Superficial fascia and deep fascia.

Answer 5

C. Internal intercostal and innermost intercostal muscles.

Question 6

A 12-year-old girl complains of chest discomfort. No masses are found upon palpation of her chest wall and neck. A CT scan reveals a mass directly behind the sternal angle that is compressing the brachiocephalic veins. The mass is most likely associated with which of the following structures?

a. Esophagus.
b. Heart.
c. Middle lobe of right lung.
d. Thymus.
e. Thyroid gland.

Answer 6

D. thymus

Question 7

A man tells his physician that he has three testes. The physician examines him and finds no masses in the groin region. His scrotum is not painful, nor greatly enlarged, but finds a soft, scrotal mass that feels like cooked spaghetti. What is the man’s probable condition?

a. He has three testes.
b. Hydrocele.
c. Inguinal hernia.
d. Varicocele.
e. Triple cryptorchidism.

Answer 7

d. varicocele

Question 8

A 45yo male was seen with groin pain and a palpable mass just superior to the inguinal ligament. The patient was diagnosed with a hernia and a surgical repair was performed. During the operation the surgeon found a loop of bowel passing through the deep ring. Which type of hernia was this?

a. Direct inguinal.
b. Epigastric.
c. Femoral.
d. Indirect inguinal.
e. Umbilical

Answer 8

d. Indirect inguinal

Question 9

Next series of Q’s from what dr. charyk said to review for quiz.
What is the effect of hyperkalemia on a typical cell membrane potential?
a. Depolarization
b. Hyperpolarization
c. No change

Answer 9

A. depolarization

When there is increased K+ extracellularly, there is less driving force for K+ to leave the cell, which makes it more depolarized.

Question 10

Based on your reading, which ion channel mutation most commonly leads to symptoms of Hyper-PP (Hyperkalemic period paralysis)?

a. KCNJ18 K+ channel
b. SCN4A Na+ channel
c. CLCN1 Cl- channel
d. nACh receptor
e. Any of these

Answer 10

“B” is the answer. Mutations in the SCN4A are autosomal dominant traits.

Myotonias can also be caused by “C” because chloride is used by skeletal muscle cells to repolarize the membrane; when the CLCN1 channel does not work properly, chloride cannot enter and the cell depolarization is prolonged, leading to symptoms of myotonia (e.g. clenching his fist). “D” would cause muscle weakness.

Question 11

Q#2: What ion causes the rising phase of the action potential?

a. Potassium
b. Sodium
c. Calcium
d. Chloride
e. All of these

Answer 11

The correct answer is B. Na+ channels open in response to increase in depolarization caused when the nAChR channel is activated by ACh and Na+ rushes into the cell at the end plate. The voltage gated Na+ channels located nearby on the sarcolemma sense the voltage change, leading to a Hodgkin & Huxley positive feedback cycle.

Question 12

Q#3: What causes the falling phase of the action potential?

a. Potassium channel inactivation
b. Potassium channels opening
c. Sodium channel inactivation
d. Na+/K+ ATPase
e. More than one of these

Answer 12

The correct answer is E. But which ones??? “A” is incorrect – Inactivation of K+ channels would lead to depolarization because the K+ would not be able to leave the cell. “B” is correct – K+ channels are activated when Na+ channels are, but have a DELAY in opening. This allows the action potential to have both a rising and falling phase which creates the traveling, propagating signal down the membrane. “C” is also correct because Na+ channels open but then quickly close (inactivate). The channels remain closed until the membrane repolarizes to a level close to the membrane potential (inactivation is responsible for the refractory period). “D” only plays a very small role in repolarizing the membrane. It is more important for the maintenance of the steady state during rest. So “B” & “C” are best answers.

Question 13

Q#4: How does a mutation in a sodium channel SCN4A lead to Hyper-PP?

a. Potassium concentration increases in the cell because sodium cannot enter
b. Increased Sodium concentration exacerbates the activity of the Na + /K+ ATPase
c. Na + channels remain inactivated so no new action potentials can be produced
d. Potassium builds up in the cell which stimulates endocytosis of Na + channels

Answer 13

The correct answer is C. With this mutation, 50% of the Na+ channels (the mutants) get stuck open (slow/no inactivation) and these keep the cell from returning to normal resting potential. The other 50% (the normal subpopulation of channels – it’s an autosomal dominant disease) get stuck closed (inactivated) and their unresponsiveness makes the cell inexcitable. Sustained depolarization, as occurs in hyperkalemia, inactivates the voltage-gated Na+ channels, which remain inactivated until the membrane repolarizes, thus blocking action potential generation. If action potentials are generated, their amplitude would reduce because ENa decreases (use Nernst equation to prove it). “A” is not correct because Na/K ATPase pump is responsible for maintaining levels of these ions and it is not mutated. “B” is not correct because if the pump was more active, even more Na+ would be extruded from the cell which would cause hyperpolarization, not depolarization. “D” is not correct; there is no evidence that prolonged hyperkalemia changes the level of Na+ channels in the membrane.

Question 14

What drug could you use to confirm that the elevated resting HR in the transplant patients is due to the loss of predominantly parasympathetic tone?
	A. Atropine
	B. Cevimeline
	C. Epinephrine
	D. Propranolol
	E. succinylcholine

Answer 14

A. Atropine. It will increase resting heart rates in the innervated control subjects and not in the uninnervated transplant patients

Question 15

If transplanted hearts are uninnervated, why does peak HR increase in transplant patients after exercise?

Answer 15

Adrenal medulla increases release of catecholamines

Question 16

What drug could you use to confirm that the increased peak HR in transplant patients is due to the actions of catecholamines?

	A. Albuterol
	B. Botulinum toxin
	C. Epinephrine
	D. Prazosin
	E. propranolol

Answer 16

E. You could use a beta adrenergic receptor antagonist such as propranolol, it will block the increase in heart rates in both the controls and the transplant patients.

Question 17

What is myasthenia gravis?

Answer 17

It is an autoimmune disease where Ab’s attack nAChR. Decreases # of receptors from Ab induced endocytosis, damages muscle due to complement-mediated membrane damage.

Question 18

What is the decremental response in myasthenia?

What causes it?

Answer 18

Decreased muscle contraction following repetitive nerve stimulation. Muscle may have robust initial response, but decreased ability to sustain muscle activity.

Repeated nerve stimulation causes decrease in amount of Ach released (depletes stores), this doesn’t have as large of an effect in normal patients due to “safety factor” (more Ach released than needed to activate enough AChRs to get maximal contraction.

Question 19

What can ameliorate the neuromuscular weakness caused by myasthenia gravis?

Answer 19

An acetylcholinesterase inhibitor (pyridostigmine). Increases lifetime of Ach so more AChR can be activated.

Question 20

What are some unwanted side effects after administration of an AChE inhibitor?

Answer 20

Increases Ach at cholinergic sites as well as neuromuscular - increased sweating, salivation, miosis, diarrhea

Question 21

What would you give to treat the unwanted side effects of an AChE inhibitor?

Answer 21

Since the cholinergic receptors are mediated by muscarinic receptors, you could administer a mAChR antagonist like atropine

Question 22

How can you tell if neuromuscular weakness is due to too much AChE inhibitor (due to an amelioration of underlying disease such as myasthenia gravis) or too little AChE inhibitor (due to exacerbation of disease)

Answer 22

Edrophonium is a rapidly reversible inhibitor of AChE. If they get better, there is too little pyridostigmine, if they get worse there is too much pyridostigmine.