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MCQs 24

The document summarizes the hormonal functions of the pancreas, detailing the roles of insulin, glucagon, somatostatin, and pancreatic polypeptide. It explains how insulin facilitates glucose entry into cells and its effects on potassium levels, as well as the conditions of diabetes mellitus. Additionally, it includes multiple-choice questions related to the hormonal functions and interactions within the body.

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0% found this document useful (0 votes)
287 views3 pages

MCQs 24

The document summarizes the hormonal functions of the pancreas, detailing the roles of insulin, glucagon, somatostatin, and pancreatic polypeptide. It explains how insulin facilitates glucose entry into cells and its effects on potassium levels, as well as the conditions of diabetes mellitus. Additionally, it includes multiple-choice questions related to the hormonal functions and interactions within the body.

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9johnwick1
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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CHAPTER SUMMARY (24)

■■Four polypeptides with hormonal activity are secreted by the pancreas:


insulin, glucagon, somatostatin, and pancreatic polypeptide.
■■Insulin increases the entry of glucose into cells. In skeletal muscle cell
it increases the number of GLUT-4 transporters in the cell membranes. In
liver it induces glucokinase, which increases the phosphorylation of
glucose, facilitating the entry of glucose into the cell.
■■Insulin causes K+ to enter cells, with a resultant lowering of the
extracellular K+ concentration. Insulin increases the activity of Na, K
ATPase in cell membranes, so that more K+ is pumped into cells.
Hypokalemia often develops when patients with diabetic acidosis are
treated with insulin.
■■Insulin receptors are found on many different cells in the body and
have two subunits, α and β. Binding of insulin to its receptor triggers a
signaling pathway that involves autophosphorylation of the β subunits on
tyrosine residues. This triggers phosphorylation of some cytoplasmic
proteins and dephosphorylation of others, mostly on serine and threonine
residues.
■■The constellation of abnormalities caused by insulin deficiency is
called diabetes mellitus. Type 1 diabetes is due to insulin deficiency
caused by autoimmune destruction of the B cells in the pancreatic islets.
Type 2 diabetes is characterized by the dysregulation of insulin release
from the B cells, along with insulin resistance in peripheral tissues such
as skeletal muscle, brain, and liver.

MULTIPLE-CHOICE QUESTIONS
For all questions, select the single best answer unless otherwise
directed.
1. Which of the following are incorrectly paired?
A. B cells: insulin
B. D cells: somatostatin
C. A cells: glucagons
D. Pancreatic exocrine cells: chymotrypsinogen
E. F cells: gastrin

2. Which of the following are incorrectly paired?


A. Epinephrine: increased glycogenolysis in skeletal muscle
B. Insulin: increased protein synthesis
C. Glucagon: increased gluconeogenesis
D. Progesterone: increased plasma glucose level
E. Growth hormone: increased plasma glucose level
3. Which of the following would be least likely to be seen 14 days
after a rat is injected with a drug that kills all of its pancreatic B
cells?
A. A rise in the plasma H+ concentration
B. A rise in the plasma glucagon concentration
C. A fall in the plasma HCO3 – concentration
D. A fall in the plasma amino acid concentration
E. A rise in plasma osmolality

4. When the plasma glucose concentration falls to low levels, a


number of different hormones help combat the hypoglycemia. After
intravenous administration of a large dose of insulin, the return of a
low blood sugar level to normal is delayed in
A. adrenal medullary insufficiency.
B. glucagon deficiency.
C. combined adrenal medullary insufficiency and glucagon deficiency.
D. thyrotoxicosis.
E. acromegaly.

5. Insulin increases the entry of glucose into


A. all tissues.
B. renal tubular cells.
C. the mucosa of the small intestine.
D. most neurons in the cerebral cortex.
E. skeletal muscle.

6. Glucagon increases glycogenolysis in liver cells but ACTH does not


because
A. cortisol increases the plasma glucose level.
B. liver cells have an adenylyl cyclase different from that in
adrenocortical cells.
C. ACTH cannot enter the nucleus of liver cells.
D. the membranes of liver cells contain receptors different from those in
adrenocortical cells.
E. liver cells contain a protein that inhibits the action of ACTH.

7. A meal rich in proteins containing the amino acids that stimulate


insulin secretion but low in carbohydrates does not cause
hypoglycemia because
A. the meal causes a compensatory increase in T4 secretion.
B. cortisol in the circulation prevents glucose from entering muscle.
C. glucagon secretion is also stimulated by the meal.
D. the amino acids in the meal are promptly converted to glucose.
E. insulin does not bind to insulin receptors if the plasma concentration of
amino acids is elevated.
Chapter 24
1. E 2. D 3. D 4. C 5. E 6. D 7. C

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