26 Endocrine pancreas Flashcards

1
Q

State all cell types in the pancreas and the hormones they secrete respectively.

A
  1. beta cells: insulin
  2. alpha cells: glucagon
  3. delta cells: somatostatin
  4. F/PP cells: pancreatic polypeptide
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2
Q

Briefly describe how different cell types are distributed in the pancreatic islet of the pancreas.

A

Alpha cells and delta cells: more on the periphery;

beta cells: within the center

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3
Q

Which of the following is false about the pancreas?
A. acetylcholine is the NT that affects glucagon and insulin secretion
B. Pancreas is only under autonomic control
C. effect of catecholamines on pancreatic hormone is to inhibit insulin and stimulate glucagon

A

B only

  1. Pancreas is innervated by autonomic nerve = autonomic control
  2. Pancreas is also under sympathetic control: epinephrine + hormonal control

C is true!

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4
Q

Describe the direction of blood flow in the pancreas islets. What is its significance?

A

From the core to the periphery, such that insulin can inhibit secretion of glucagon and maybe also somatostatin

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5
Q

Which of the following is false?
A. When high insulin is detected but there is normal level of C peptide, it indicates overdose of exogenous insulin
B. All proinsulin will have complete cleavage to insulin
C. in the regulated pathway, some maturing secretory granules will form lysosome
D. constitutive pathway may be caused by insulinoma

A

B

2 pathways in generating insulin:
1. Regulated pathway
○ Complete cleavage of proinsulin to insulin
○ 95% of beta cell insulin secretion
2. Constitutive pathway
○ Insulinoma
○ Releasing large amounts of unprocessed proinsulin
○ 5%
○ Discharge of proinsulin/insulin into circulation without signals
Lead to high insulin and proinsulin levels

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6
Q

List 2 stimulators, 2 amplifiers and 2 inhibitors of insulin secretion.

A

Stimulators:

  1. high blood glucose levels
  2. amino acids
  3. parasympathetic stimulation via acetylcholine
  4. free fatty acids and ketones

Amplifiers:
Incretins (GI hormones)
1. GIP
2. GLP-1 (glucagon-like peptide 1)

Inhibitors:

  1. somatostatin
  2. hypoglycemia
  3. catecholamines from sympathetic nerve innervation and secreted by adrenal medulla
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7
Q

Which of the following is true?
A. Glucose-induced insulin secretion is by insulin binding to GLUT4 transporter to activate glucokinase and G6P…

B. Sulphonylurea drugs are used for treating diabetic patients

C. Sulphonylurea drugs works by binding to SUR-1 receptors, which is made up of ATP-sensitive K+ channels, causing it to open

D. Incretin amplifies glucose-induced insulin release by genomic action

A

B only

A: should be GLUT2 transporters
C: should be causing it to close
D. should be by second messenger system: through PKA > cAMP > Ca2+

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8
Q

Biphasic release of insulin appears to originate from a readily releasable and reserve pool of insulin.
What happens to patients with Type 2 DM?

A

Loss of first-phase of insulin secretion due to the deterioration of beta-cell function with depleted store of insulin, loss of sensitivity and responsiveness to glucose

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9
Q

Why is an OGTT but not IV injection of glucose more suitable to test for insulin function?

A

Oral dose can stimulate a greater rise in insulin secretion that IV > can test for maximum insulin secretory response.
Presence of incretin in gut has amplifying effect on insulin

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10
Q

Post-translational processing of preproglucagon generates __________ in intestinal L cells and glucagon in pancreatic A cells.

A

GIP-1 (Glucagon-like peptide)

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11
Q

Which of the following is true about the actions of GIP-1?

A. It promote satiety
B. It slows gastric emptying
C. It inhibits glucagon secretion 
D. It restores beta cell function
E. it promotes beta cell differentiation
A

all of the above

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12
Q

What drug class does exenatide and liraglutide belongs to?

A

They belong to GIP-1 receptor agonists.

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13
Q

Which of the following is false about GIP-1 receptor agonists?

A. They are used because GIP-1 has short biological half life due to the degradation of DPP-4
B. They have longer biological half lives due to their binding to albumin
C. Most of them are taken orally.
D. Lixisenatide is one of the examples
E. They pose hypoglycemic risk

A

C
most of them are given by subcutaneous injection
DPP-4 inhibitors can also be used, taken orally

E as well
no hypoglycemic risk

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14
Q

How can we treat DM2 patients in the renal perspective?

A

Give inhibitors of SGLT 2 (sodium-glucose transporters) to increase glucose excretion, no risk of hypoglycemia

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15
Q

Which of the followings about insulin effects is/are false?
A. it promotes the release of K+ ions from cells
B. It promotes protein synthesis
C. It promotes glycolysis
D. It inhibits ketogenesis
E. It inhibits glycogenolysis

A

A

Should be promote the uptake of K+ ions

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16
Q

How does insulin lower blood glucose levels during the process of stimulating glucose uptake in cells?

A

Insulin lowers blood glucose levels by inducing translocation of GLUT-1 to cell surface of skeletal muscles and adipocytes.
Insulin also induces glucokinase expression in hepatocytes.

17
Q

List a clinical significance of knowing insulin lowers K+ by stimulating uptake of K+ in cells.

A

During insulin infusion, K+ has to be infused as well as insulin will cause hypokalemia

18
Q

Give 2 stimulators and 2 inhibitors of glucagon.

A

Stimulators

  1. Hypoglycemia
  2. amino acids from protein intake
  3. parasympathetic stimulation (via acetylcholine)
  4. sympathetic stimulation (beta 2)

Inhibitors:

  1. hyperglycemia
  2. somatostatin
  3. insulin
  4. GLP-1
19
Q

Which of the followings is not an effect of glucagon?

A. increase glycogenolysis and gluconeogenesis
B. promote ketogenesis
C. weak lipolytic effect on adipose tissue
D. stimulate glycogenolysis in muscles

A

D

That’s why we need Cori cycle

20
Q

State the 2 conditions in which secretion of insulin and glucagon are both stimulated.

A
  1. Increase in plasma levels of amino acids from protein intake
  2. Parasympathetic stimulation (e.g. food intake)
21
Q

Differential diagnosis of hypoglycemia:
state what to check:
1. Is it due to high insulin concentrations?
2. Is the hyperinsulinemia endogenous?
3. Has it been stimulated by sulphonylurea?
4. If no, insulinoma likely

A
  1. check insulin levels
    if no: deficiency counter regulatory hormones
  2. check C-peptide, if low, = exogenous insulin administration
  3. sulphonylurea screen
  4. diagnostic imaging
22
Q

Why does Type 1 diabetes have ketoacidosis?

A
  • Absolute or severe insulin deficiency lifts inhibition on hormone sensitive lipase allowing increased lipolysis
  • Glucagon in the absence of insulin leads to inhibition of acetyl CoA carboxylase > drop in malonyl CoA levels> removes inhibition on CPT-1 on outer mitochondrial membrane, allowing long chain FA to be shuttled from cytosol to mitochondrial matrix for beta-oxidation and ketone body production
23
Q

Which of the following is false relating to non-ketotic hyperosmolar hyperglycemic state (HHS)?

A. It is common in Type 1 DM
B. There is hyperglycemia, extreme dehydration and hyperosmolar plasma
C. Hyperglycemia causes decreased glucose utilization due to insulin deficiency
D. Hyperglycaemia leads to glucosuria and osmotic diuresis.

A

A should be type 2 DM

  • Hyperglycaemia leads to glucosuria and osmotic diuresis. The development of hyperosmolar hypoglycaemia occurs when dehydration leads to hypovolemia
    which eventually results in a “shoutdown” of glomerular filtration and worsening of hyperglycaemia.
24
Q

Give the concentration of normal HbA1c and that of a patient with poor glycemic control.

A
  • In normal subjects, concentration of HbA1c is <5.7% of total HbA.
  • Levels between 5.7% and 6.4% are considered as pre-diabetes and those at
    >6.5% are considered as diabetes with poor glycemic control.
25
Q

Which of the following is/are long term complications of DM?

A. Autonomic neuropathy: diarrhea, impotence
B. Diabetic foot: peripheral neuropathy and ischemia, foot ulcers, amputations
C. Retinopathy: visual impairment and blindness
D. Macroangiopathy: coronary heart disease and peripheral vascular disease
E. Neuropathy: renal failure

A

All of the above