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Endocrine > Diabetes Tutorial > Flashcards

Diabetes Tutorial Flashcards

1
Q

What will T1DM look like histologically?

A

Insults typical of insulin diabetes causing beta cell destruction
Loss of beta cell secreting insulin

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2
Q

What will T2DM look like histologically?

A

Amyloid disposition within islet cells

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3
Q

What is monogenic diabetes?

A

Diabetes due to a mutation in a gene regulating insulin secretion or action e.g. MODY, neonatal diabetes and mitochondrial diabetes

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4
Q

What can cause secondary diabetes?

A 
Cushing's
Acromegaly
Haemachromatosis
Chronic and acute pancreatitis
CF
HIV drugs 
Post organ transplantation
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5
Q

What is the WHO criteria for diabetes?

A

Fasting plasma glucose =>7.0 mmol/L

Plasma glucose after a 75g oral glucose load or a random glucose >= 11.1 mmol/L

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6
Q

What is significant in a history taking of someone who might have diabetes?

A

Symptoms of hyperglycemia, rapidity of onset, weight loss
Diet - lots of sugar
Medication - corticosteroids
PMH - pancreatitis, heavy alcohol consumption
FMx of diabetes/ autoimmune conditions/ of insulin resistance: CVS, Stroke, Hypertension, high lipids

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7
Q

How can diabetes be investigated?

A

Confirm hyperglycemia
Ketonuria
Check for GAD antibodies
Insulin conc

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8
Q

What can be done in a clinical exam of diabetes?

A

General incuding fluid status - tachycardia, postural hypotension
Signs of infection that may be precipitated infection
Microvascular disease? Fundoscopy, foot exam
Features of secondary diabetes? Cushingoid, bronze pigementation, acanthosis

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9
Q

What causes DKA?

A

Absolute or relative lack of insulin
Increased glucose production but reduced glucose uptake
Increased tissue fatty acid metabolism producing ketone bodies

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10
Q

What are the symptoms of DKA?

A

Increased weakness and muscle cramps
Nausea and vomiting
Kussmaul’s breathing
Tired, drowsy, confused Coma

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11
Q

What are the symptoms of dehydration?

A

Polyuria and thirst

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12
Q

How can an MI cause DKA?

A

Increased counterregulatory hormones such as catecholamines, glucagon, GH and cortisol causing increased glucose production and reduced glucose uptake

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13
Q

What can cause diabetic nonketotic hyperosmolar coma in type 2 patients?

A

Relative lack of insulin
Increased glucose production and lack of glucose utilisation
Increased blood glucose
Osmotic diuresis causing dehydration leading to polyuria, thirst and an increased sodium and urea in blood
This leads to drowsiness, confusion and a coma

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14
Q

How is plasma osmolality calculated?

A

Plasma osmolality = 2 x (plasma sodium + plasma potassium + plasma urea + plasma glucose)

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15
Q

What are the normal values for plasma osmolality?

A

285 - 295

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16
Q

What leve of plasma osmolality can cause impaired consciousness?

A

340

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17
Q

How is DKA diagnosed?

A

Confirm diabetes - high lab glucose
Confirm ketosis - blood or urine ketones high
Confirm acidosis - low venous bicarb or acidosis on blood gas

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18
Q

How is DKA managed?

A

ABC
Hx and exam to look for cause; infection, surgical abdomen, silent MI
Cardiac monitor and other non invasive monitoring
IV fluids - N/Saline 1 litre quickly
IV insulin - 6 units hourly but NO bolus insulin
Watch potassium and replace aggressively to prevent hypokalemia and cardiac arrest. Insulin drives K+ into cells and therefore can drop quickly

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19
Q

What is the first line drug in the treatment of T2DM?

A

Metformin with a target HbA1c to 53 mmol/mol

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20
Q

What is the second line drug in T2DM if metformin doesn’t create adequate glycaemic control?

A

Sulphonylurea

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21
Q

What is the side effect of sulfonylurea?

A

Hypoglycemia

Weight gain

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22
Q

What can be used if hypoglycemia is a concern with SU as a second line drug?

A

Thiazlidinedione

23
Q

What can be used if there are concerns over weight gain in SU as a second line drug?

A

Gliptin - DDP4 inhibitor

24
Q

What is the third line in T2DM?

A

Insulin
Thiazolidinedione
Exenatide

25
Q

What is the mechanism of action of thiazolidinediones?

A

Activators of the transcription factor called PPAR-gamma. Activates hundreds of genes to promote pre-adipocyte differentiation into mature adipocytes
Insulin sensitivity improves at liver and muscle

26
Q

What are the common side effects of pioglitazone?

A

Fluid retention
Pathological fractures
Severe peripheral neuropathy
Heart failure

27
Q

What are the CI’s of glitazones?

A

Heart failure

Possibly increases risk of IHD

28
Q

What is the mechanism of action of sulphonylureas?

A

Act on the beta cells to augment insulin secretion. The act at the beta cell kATP channel to close the channel and stimulate insulin secretion. This is unregulated and therefore insulin secretion continues in the presence of normal or low blood glucose

29
Q

What are the common side effects of sulphonylureas?

A

Weight gain

Hypoglycemia

30
Q

What is the mechanism of action of metformin?

A

The drug of choice for overweight/ obses diabetic patients
Improves insulin action at the liver as it acts to decrease hepatic glucose production.
Decreases macrovascular outcomes
Weight neutral

31
Q

What are the side effects of metformin?

A

GI - diarrhoea, constipation

Lactic acidosis

32
Q

How is metformin excreted?

A

Via the kidneys

33
Q

What are the issues surrounding metformin excretion and renal failure?

A

Should not be used with renal impairment (eGRF <40mls/min; creatinine >150micomol/L)

34
Q

What class of drug is metformin?

A

Biguanide

35
Q

What is an example of a GLP-1 activator?

A

Exenatide

36
Q

What is the mechanism of action of GLP-1 activators?

A

Gut peptide that is released to a meal and acts at the pancreatic beta-cells to augment insulin secretion - only stimulate insulin production in the presence of elevated blood glucose - does not cause hypoglycemia

37
Q

How is exenatide administered?

A

Not orally active so given by sub-cutaneous injection

38
Q

What are the side effects of exenatide?

A

Delay gastric emptying and act centrally to decrease appetite and therefore associated with nausea and 3/4kg of weight loss

39
Q

What is the mechanism of action of DDP-IV inhibitors?

A

Inhibits the enzyme DDP-IV which breaks down GLP-1, therefore increasing the plasma levels of GLP-1

40
Q

What is the mechanism of action of acarbose?

A

Inhibits alpha-glucosidase which is involved in carbohydrate absorption and therefore less carb is absorbed from any meal

41
Q

What are the natural roles of incretins?

A

Beta cell: enhances glucose dependent insulin secretion in the pancreas
Alpha cell: suppresses postprandial glucagon secretion
Liver: reduces hepatic glucose output
Stomach: slows gastric emptying
Brain: promotes satiety and reduces appetite

42
Q

What is the polyol pathway?

A

Sorbitol accumulates in cells causing osmotic damage in the lens and neural tissue
Increased total body sodium which predisposes to hypertension and causes an altered redox state of pyridine nucleotides

43
Q

What are the acute reversible effects of hyperglycemia?

A

Increased polyol pathway: increased sorbitol, decreased myoinositol and protein kinase C
Early glycosylation products

44
Q

What are the cumulative changes of hyperglycaemia?

A

AGE - in ECM and nucleic acids
Disordered arrangement of collagen and basement membrane
Increased genetic mutations

45
Q

What does AGE interfere with?

A 
Function of: 
Proteoglycans
Basement membranes
Enzyme activity 
Cellular receptors
Increased nucleic acid damage
46
Q

What are the grades of retinopathy?

A 
R0 - no retinopathy
R1 - BDR mild retinopathy
R2 - BDR moderate retinopathy
R3 - BDR severe retinopathy
R4 - proliferative retinopathy
47
Q

What can be seen in retionpathy R1?

A

At least one dot haemorrhage or microaneurysms with or without hard exudates
Cotton wool spot
< 4 blot haemorrhages

48
Q

What can be seen in retinopathy R2?

A

4 or more haemorrhages in one hemi-field only

49
Q

What can be seen in retinopathy R3?

A

4 or more blot haemorrhages in both inferior and superior hemi-fields
Venous bleeding
intro-retinal microvascular abnormality (IRMA)

50
Q

What can be seen in proliferative retinopathy?

A

New vessel at disk or elsewhere

Vitreous haemorrhages

51
Q

What are low risk diabetic feet?

A

Sensation and pulses normal
Able to self care
No structural abnormalities

52
Q

What are moderate risk diabetic feet?

A

Imparied sensation OR impaired pulses

Low risk feet AND inability to self care and/or structural abnormalities

53
Q

What are the high risk diabetic feet?

A

Impaired sensation AND impaired pulses
Previous foot ulcer
Moderate risk feet AND inability to self care and/or structural changes

Endocrine (35 decks)

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