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Endocrinology semester 1 > endocrine pancreas, Diabetes Mellitus > Flashcards

endocrine pancreas, Diabetes Mellitus Flashcards

1
Q

what cells make up the Islets of Langerhans?

A

α cells
β cells
δ cells
PP cells

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2
Q

what do α cells secrete?

A

glucagon

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3
Q

what do β cells secrete?

A

Insulin and Amylin

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4
Q

what do δ cells secrete?

A

Somatostatin

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5
Q

what do PP cells secrete?

A

Pancreatic Polypeptide

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6
Q

what is insulin?

A

polypeptide hormone with 2 amino acid chains

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7
Q

how are the 2 amino acid chains of insulin liked?

A

2 disulphide bonds

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8
Q

how is insulin secretion regulated?

A

Insulin secretion is tightly regulated and is controlled by blood levels of various nutrients, neural stimulation and hormones.

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9
Q

what is the principle stimulus to insulin secretion?

A

glucose

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10
Q

what are the endogenous factors controlling insulin secretion?

A

incretins
GIP: glucose-dependent insulinotropic peptide
GLP-1: glucagon-like peptide-1

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11
Q

where is insulin released into?

A

into the portal vein

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12
Q

what is the half life of insulin in plasma?

A

5-6 minutes

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13
Q

what is the half life of proinsulin in plasma?

A

17 minutes

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14
Q

what is the half life of C peptide in the plasma?

A

30 minutes

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15
Q

How does the degradation of insulin occur?

A

Proteolytic degradation of insulin occur mainly in liver, kidney & muscle usually after internalisation of insulin

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16
Q

what is the main hormone in controlling metabolism of carbohydrate, fat and protein?

A

insulin

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17
Q

what is the most obvious cause effect of insulin?

A

reduce the blood glucose and is the only hormone capable of reducing blood glucose level.

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18
Q

what are long term effects of insulin?

A

Increase & decrease of key enzymes &

Stimulates cell proliferation

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19
Q

what are the effects of insulin on the liver?

A

Increased glycogen synthesis (↑glycogenesis)
Increased use of glucose for the energy (↑glycolysis)
Increased fat synthesis (↑lipogenesis)
Decreased synthesis of ketone bodies (↓ketosis)

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20
Q

what metabolic process of the liver does insulin decrease?

A

ketosis - synthesis of ketone bodies

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21
Q

what are the actions of insulin on fatty tissues?

A

Increased glucose uptake
Increased fatty acid uptake
Increased fat synthesis
Increased glycolysis

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22
Q

what are the actions of insulin on muscle?

A

Increased glucose uptake
Increased uptake of amino acids
Increased glycogenesis
Increased glycolysis

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23
Q

what is glucagon?

A

Single chain peptide of 29 amino acids synthesized by α cells of pancreatic islets.

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24
Q

what is the main physiological stimuli of glucagon?

A

amino acids in plasma

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25
Q

Do high or low concentrations of fatty acids and glucose stimulate glucagon secretion?

A

low concentrations

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26
Q

Do high or low concentrations of fatty acids and glucose inhibit glucagon secretion?

A

high concentration

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27
Q

how does somatostatin impact glucagon release?

A

Somatostatin inhibits glucagon release

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28
Q

how do catecholamines and cholinergic impact glucagon release?

A

Catecholamines & cholinergic stimulation both increase glucagon release

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29
Q

what is the half life of glucagon?

A

3-6 minutes

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30
Q

where is the primary site of action for glucagon?

A

liver

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31
Q

where does glucagon increase glycogenolysis?

A

liver

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32
Q

where does glucagon increase gluconeogenesis?

A

liver and kidney

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33
Q

where does glucagon reduce glycogen synthesis?

A

liver

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34
Q

where does glucagon reduce glucose oxidation?

A

liver

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35
Q

where does glucagon increase lipolysis?

A

liver and fat

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36
Q

where does glucagon increase ketogenesis?

A

liver

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37
Q

where does glucagon reduce lipogenesis?

A

liver

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38
Q

where does glucagon increase proteolysis?

A

liver

39
Q

what is amylin?

A

37 amino acids peptide co-stored with insulin and release with insulin by β-cells

40
Q

what is the function of amylin?

A

Complement insulin action by reducing gastric emptying, antagonizing glucagon effects and reducing food intake

41
Q

what is function of somatostatin?

A

Inhibits insulin & glucagon release.

Inhibits growth hormone & TSH release from pituitary

inhibits release of various GI hormones

42
Q

how can diabetes mellitus be characterised?

A

hyperglycaemia - raised blood glucose level

43
Q

what is the normal range of blood glucose levels?

A

3.5 - 7 mmol/L

44
Q

how is normal glucose levels reached in a fasting state?

A

decreased blood glucose –> release of glucagon –> glucagon action

45
Q

how is normal glucose levels reached after a meal?

A

increased blood glucose –> release of insulin from the pancreas –> insulin action

46
Q

what are the 2 types of diabetes mellitus?

A

type 1 or insulin dependent diabetes mellitus

type 2 or non-insulin dependent diabetes mellitus

47
Q

what is the pathophysiology of Type 1 diabetes?

A

beta cells of pancreas which produce insulin are completely destroyed

48
Q

what is the pathophysiology of Type 2 diabetes?

A

beta cells produce too little insulin too late

tissue responses to insulin may also be decreased (Insulin resistance) especially in overweight people

49
Q

what are the 3 classic symptoms of diabetes?

A

polydipsia (extreme thirst)
polyuria (excessive urine output)
feeling tired and lethargic

50
Q

what are some other symptoms of diabetes?

A

Genital itching
Fluctuating vision,
Night cramps
Weight loss (particularly in type 1)

51
Q

why do polydipsia and polyuria occur?

A

high blood glucose –> glucose in urine –> loss of water with glucose loss –> increased urine output –> dehydration/increased serum osmolality –> extreme thirst

52
Q

what are the tests conducted for the diagnosis of diabetes?

A

blood glucose level

presence of glucose in the urine

53
Q

when is a diagnosis of diabetes made?

A

Fasting plasma glucose ≥ 7 mmol/L and/or

Random plasma glucose ≥ 11.1 mmol/L

54
Q

what are the acute metabolic complications associated with diabetes?

A

Ketoacidosis (Type 1)
Non-ketotic Hyperosmolar Hyperglycaemic State (Type 2)
Hypoglycaemia

55
Q

what are the microvascular long term complications associated with diabetes?

A

retinopathy (Damage to retina)
neuropathy (Nerve damage)
nephropathy (Kidney damage)

56
Q

what are the macrovascular long term complications associated with diabetes?

A

Diabetes is a risk factor for
heart attack
stroke
decreased blood circulation leading to gangrene (e.g. foot)

57
Q

what are the clinical features of ketoacidosis?

A 
Thirst
Polyuria
Vomiting
Hyperventilation
Weakness
Confusion & Coma
58
Q

what is the treatment for ketoacidosis?

A

Fluid, insulin and potassium in hospital

59
Q

when does non-ketotic hyperosmolar hyperglycaemic state (HHS)?

A

Occurs in people with Type 2 diabetes, who may be experiencing very high blood glucose levels (often over 40mmol/l)

60
Q

how fast is the development of HHS -?

A

usually develops over a course of weeks

61
Q

what are the clinical features of non-ketotic hyperosmolar hyperglycaemic state?

A 
Thirst
Polyuria
Weakness
Confusion & Coma
But no ketoacidosis, so no hyperventilation
62
Q

what is hypoglycaemia?

A

Blood glucose <4 mmol/L

63
Q

when can hypoglycaemia occur?

A

Major source of anxiety for insulin treated diabetic patient

Could also occur in patients treated with insulin secretagogues such as sulphonylureas

64
Q

what are the autonomic signs and symptoms of hypoglycaemia?

A

Anxiety, tremor, palpitations, sweating etc.

65
Q

what are the neuroglycopenic signs and symptoms of hypoglycaemia?

A

Dizziness, blurred vision, headache, tiredness, inability to concentrate, hunger, shivering etc.

66
Q

what are the aims of diabetes management?

A

alleviate symptoms

prevent acute metabolic complications

prevent long term complications

67
Q

what are some ways to manage diabetes?

A

Patient education

Control of diet

Drug therapy

Detection & treatment of early signs and symptoms of long-term complications

68
Q

what are some antidiabetic drugs?

A

sulphonylureas, biguanides

69
Q

what are examples of sulphonylureas?

A

Chlorpropamide, Glibenclamide, Gliclazide, Glimepiride, Glipizide & tolbutamide

70
Q

what are examples of biguanides?

A

Metformin

71
Q

what are the type of insulins used?

A

Short-acting insulins

Intermediate- and long-acting insulins

72
Q

what is the mode of action for sulfonylureas?

A

stimulate insulin secretion from beta cells

73
Q

what are side effects of sulfonylureas?

A 
Weight gain  . 
Hypoglycaemia                        
GI disturbances
Sensitivity reactions                              
Facial flushing with Chlorpropamide
74
Q

what is the mode of action for biguanides?

A

Increases glucose uptake by peripheral tissue
Reduces hepatic gluconeogenesis
Reduces appetite

75
Q

what are side effects of biguanides?

A

GI disturbances
Weight loss (useful in overweight patients)
Lactic acidosis (should not be given to patients with renal disease or severe pulmonary or cardiac disease )
Decreased Vitamin B12 absorption

76
Q

why doesn’t Hypoglycaemia occur with metformin?

A

it has no effect on insulin secretion

77
Q

what is the mode of action for acarbose?

A

delays the digestion and absorption of starch & sucrose by inhibiting alpha glucosidase enzymes

78
Q

what are the side effects of Acarbose?

A

Flatulence .

Abdominal distention or pain, diarrhoea

79
Q

what is the mode of action for meglitinides?

A

Stimulate insulin secretion from pancreas which is claimed to be glucose dependent

80
Q

what are the side effects of meglitinides?

A

Weight gain
Hypoglycaemia
GI disturbances
sensitivity reactions

81
Q

what is the mode of action for thiazolidinediones/glitazones?

A

PPARγ agonists

82
Q

what are the side effects of Thiazolidinediones or glitazones?

A

Pioglitazone should not be used in patients with heart failure or history of heart failure

83
Q

what is the mode of action for Dipeptidylpeptidase-4 Inhibitors?

A

Inhibitor of DPP-4 inhibitor; DPP-4 break down endogenous incretins GIP and GLP-1

84
Q

what is the mode of action for incretin mimetic drugs?

A 
Peptide GLP-1 receptor agonists
Glucose dependent stimulation of insulin secretion
Inhibits glucagone secretion
Delays stomach emptying
Promote weight loss
85
Q

what are the side effects of incretin mimetic drugs?

A

Nausea, vomiting and diarrhoea

Can cause hypoglycaemia when combined with sulphonylureas

86
Q

what is the mode of action for sodium-glucose co-transporter 2 (SGLT2) inhibitor?

A

improves both fasting and post-prandial plasma glucose levels by reducing renal glucose reabsorption leading to urinary glucose excretion

87
Q

what are the side effects of sodium-glucose co-transporter 2 (SGLT2) inhibitor?

A

Urinary tract infections

88
Q

what are the sources of Insulin treatment?

A

beef, pork but mainly human (by recombinant DNA technology)

89
Q

what are the short acting insulins?

A

Soluble insulin
Insulin aspart
Insulin glulisine
Insulin lispro

90
Q

what are the intermediate- and long-acting insulins?

A

Isophane
Insulin detemir, Insulin glargine
Protamine zinc insulin

91
Q

what are the 3 types of insulin preparations?

A

short acting insulins
intermediate- and long-acting insulins
biphasic insulins

92
Q

what are some examples of normal insulin regimens?

A

Short-acting insulin mixed with intermediate-acting insulin: twice daily (before meals);

Short-acting insulin mixed with intermediate-acting insulin: before breakfast

Short-acting insulin: before evening meal

93
Q

how is diabetes monitored?

A

blood glucose levels, urine glucose, urine ketones, blood pressure, lipid profile, obesity, smoking

94
Q

what are some programmes and help available to prevent long-term complications of diabetes?

A

Such as retinal screening

Screening for microalbuminuria

Foot care from Chiropodist etc.

Endocrinology semester 1 (10 decks)

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