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7. Endocrinology (Medical Knowledge)a > The Endocrine Pancreas 2 > Flashcards

The Endocrine Pancreas 2 Flashcards

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USMLE® Step 1 flashcards
1
Q

What class of hormone is glucagon?

A

Peptide hormone

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2
Q

What is the primary function of glucagon?

A
  • raise blood glucose
  • glucose mobilising hormone that mainly acts on the liver
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3
Q

What is the plasma half life of glucagon?

A

5-10 minutes

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4
Q

Where is glucagon mainly degraded?

A

In the liver

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5
Q

What system does glucagon form part of, which opposes the actions of insulin?

A

Glucose counter-regulatory control system

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6
Q

What does the glucose counter regulatory control system consist of?

A

Glucagon

Epinephrine

Cortisol

Growth hormone

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7
Q

Is glucagon most active in the absorptive or post-absorptive state?

A

Post-absorptive state

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8
Q

What kind of receptors are glucagon receptors?

A

G-protein coupled receptors linked with adenylate cyclase/cAMP system

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9
Q

What does the activation of glucagon receptors cause?

A
  • increased glycogenolysis
  • increased gluconeogenesis
  • ketogenesis (formation of ketones from fatty acids (lipolysis)
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10
Q

What effect does increased blood glucose have on insulin and glucagon?

A

Increased insulin secretion

Decreased glucagon secretion

Decreased blood glucose has the opposite effects

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11
Q

How do amino acids impact the release of insulin and glucagon?

A
  • stimulates release of both
  • an adaptation to adjust for the composition of a meal very high in protein
  • if not for this effect on glucagon then the insulin stimulating effects would result in very low [BG]
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12
Q

What is meant by obligatory glucose user?

A

Endocrine system ensures there is enough glucose circulating to supply the needs of the brain

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13
Q

Other than the brain, what can tissues use when glucose is not available?

A

Free fatty acids and ketones to produce energy

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14
Q

What are examples of stimuli that promote glucagon release?

A
  • low [BG] : <5mM
  • high [amino acid]: prevents hypoglycaemia following insulin response to amino acids
  • sympathetic innervation and epinephrine, b2 effect
  • cortisol
  • stress: eg exercise, infection
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15
Q

What are examples of stimuli that inhibits glucagon release?

A
  • glucose
  • free fatty acids (FFA) and ketones
  • insulin (fails in diabetes so glucagon levels rise despite high [BG]
  • somatostatin
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16
Q

How does parasympathetic activity (vagus nerve) impact Islet cells?

A

Increases insulin and to a lesser extent increases glucagon, in association with the anticipatory phase of digestion

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17
Q

How does sympathetic activity impact Islet cells?

A
  • promotes glucose mobilisation
  • increased glucagon
  • increased epinephrine
  • inhibition of insulin

all appropriate for fight or flight response

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18
Q

Give a summar of glucose counter regulatory controls for:

muscle glycogenolysis

liver glycogenolysis

gluconeogenesis

inhibition of glucose uptake

lipolysis

protein catabolism

A
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19
Q

What class of hormone is somatostain?

A

Peptide hormone

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20
Q

What is somatostatin produced by?

A

D cells of the pancreas

Hypothalamus

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21
Q

What is somatostatin also known as?

A

Growth hormone inhibiting hormone (GHIH)

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22
Q

What is the main action of somatostatin?

A
  • inhibit activity in GI tract
  • slow down absorption of nutrients
  • to prevent exaggerated peaks in plasma concentration
23
Q

What can synthetic somatostatin (SS) be used for clinically?

A

To help patients with life-threatening diarrhoea associated with gut or pancreatic tumours

24
Q

What effect does somatostatin have on insulin and glucose?

A
  • not a counter-regulatory hormone in the control of blood glucose
  • strongly suppresses the release of both insulin and glucagon in a paracrine fashion
25
Q

What effect does somatostatin have on growth hormone?

A

Inhibits its release from anterior pituitary

26
Q

What can disruption of the steady state be caused by?

A
  • exercise
  • starvation
  • diabetes
27
Q

How does exercise affect the entry of glucose into skeletal muscle?

A

increased during exercise, even in the absence of insulin

28
Q

How does exercise impact the insulin sensitivity of a muscle?

A

causes an insulin-independent increase in the number of GLUT-4 transporters incorporated into muscle membrane

29
Q

What is the difference in migration of GLUT-4 transporters during exercise and when not exercising?

A

When not exercising, requires insulin to activate

When exercising, can migrate to membrane without insulin being present

30
Q

How does the body get energy during starvation?

A

when nutrients are scarce the body relies on stores for energy

  • adipose tissue is broken down - fatty acids are released and FFA can be used by most tissues to produce energy
  • liver will convert excess to ketone bodies - provide additional source of energy for brain and muscles
31
Q

Why does the brain adapt after a period of starvation to use ketones?

A

To save proteins that would otherwise be broken down to provide gluconeogenic substrates

32
Q

Can be brain always use ketones as fuel?

A

No, it needs to adapt to be able to use them - which it does after a period of starvation

33
Q

Why are proteins of the body the last store to be depleted in starvation?

A

It is very weakening and leaves you vulnerable to infection

34
Q

What are the 2 main forms of diabetes?

A

Type 1

Type 2

35
Q

What is type 1 diabetes also known as?

A

Insulin dependent diabetes mellitus (IDDM)

36
Q

What does IDDM stand for?

A

Insulin dependent diabetes mellitus

37
Q

What is type 1 diabetes?

A
  • autoimmune destruction of pancreatic B cells
  • loss of ability to produce insulin
  • compromised ability to absorb glucose from plasma
38
Q

What percentage of diabetic patients have type 1 diabetes?

A

10%

39
Q

Why do type 1 diabetics take daily injections and not an oral tablet?

A

Peptide hormones cannot be given orally

40
Q

What would happen to a type 1 diabetic who did not take insulin injections?

A
  • excessively wasted
  • develop ketoacidosis
  • coma
  • death
41
Q

What is a consequence of the body thinking it is starving in diabetes?

A

Liver produces glucose which makes the problem worse

42
Q

Why does ketoacidosis occur in diabetes?

A
  • when nutrients are scarce body relies on stores for energy (adipose tissue broken down and free fatty acids release)
  • in poorly controlled insulin dependent diabetes a lack of insulin depresses ketone body uptake
  • they build up rapidly in the plasma
  • because they are acidic create life threatening acidosis
  • (ketoacidosis or ketosis) with plasma pH < 7.1
43
Q

What are indicators of ketoacidosis?

A

Ketones are detectable in urine and produce distinctive acetone smell to breath

44
Q

What is type 2 diabetes also called?

A

Non-insulin dependent diabetes mellitus (NIDDM)

45
Q

What does NIDDM stand for?

A

Non-insulin dependent diabetes mellitus

46
Q

What happens in type 2 diabetes?

A
  • peripheral tissues become insensitive to insulin (called insulin resistance)
  • muscle and fat can no longer respond to normal levels of insulin, either due to abnormal response of insulin receptors or a reduction in their number
  • B cells remain intact (may even be insulinaemia)
47
Q

What percentage of diabetics are type 2?

A

90%

48
Q

What is type 2 diabetes typically associated with?

A

Obesity and usually appears >40 years but age is decreasing

49
Q

What is the treatment for type 2 diabetes?

A
  • restore insulin sensitivity of tissues with exercise and dietary changes
  • if this fails, oral hypoglycaemic drugs will be used
  • eventually end up taking insulin
50
Q

What is a glucose tolerance test?

A
  • patient ingests glucose load after fasting
  • [BG] measured
  • [BG] will normally return to fasting levels within an hour
  • elevation after 2 hours is indicative of diabetes
51
Q

Can a glucose tolerance test distinguish type 1 from type 2 diabetes?

A

No, it cannot

52
Q

What are examples of diabetic complications?

A

Retinopathy

Neuropathy

Nephropathy

Cardiovascular disease

53
Q

What are complications of hypoglycaemia in diabetes?

A
  • cognitive dysfunction
  • lethargy
  • coma
  • convulsions
  • permanent brain damage and death

7. Endocrinology (Medical Knowledge)a (28 decks)

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