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Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is T1D?

A

autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency

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2
Q

Symptoms of T1D

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
  4. Ketones in urine
  5. Acute onset
  6. Immediate and permanent insulin
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3
Q

What are the antibodies found in T1D?

A

anti-GAD antibodies

anti-islet cell antibodies

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4
Q

T2D

A

Ranging from predominant beta-cell deficiency to predominant insulin resistance

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5
Q

Epidemiology of T2D

A

o More common in Asian/African populations
• Onset in middle aged and elderly
• Associated with obesity and sedentary lifestyle

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6
Q

Metformin side effects

A

Nausea, anorexia, diarrhoea
Reduced vitamin B12 absorption
Lactic acidosis with severe liver disease or renal failure

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7
Q

Contraindications for metformin

A

Chronic kidney disease: NICE recommend that the dose should be reviewed if the creatinine is > 130 µmol/l and stopped if the creatinine is > 150 µmol/l

Metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration

Iodine-containing x-ray contrast media: there is an increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter

Alcohol abuse is a relative contraindication

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8
Q

Contraindications for metformin

A

Chronic kidney disease

Lactic acidosis if taken during tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration

Iodine-containing x-ray contrast media: increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter

Alcohol abuse is a relative contraindication

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9
Q

What is the 1st line treatment in T2D?

A

HbA1c below <48 - lifestyle
HbA1c up to 48-53 - Metformin + Lifestyle
HbA1c up to >58 - Metformin + 2nd drug

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10
Q

What is the 2nd line treatments in T2D?

A

HbA1c above 58mmol/mol

Metformin + gliptin
Metformin + sulphonurea
Metformin + pioglitazone
Metformin + SGLT-2

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11
Q

What is the 3rd line treatment for T2D?

A

If HbA1c remains above 58 despite 2nd line therpapy

metformin + gliptin + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + sulfonylurea + SGLT-2 inhibitor
metformin + pioglitazone + SGLT-2 inhibitor
OR insulin therapy should be considered

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12
Q

What is HbA1c?

A

Refers to glycated haemoglobin. It develops when haemoglobin, a protein within red blood cells that carries oxygen throughout your body, joins with glucose in the blood, becoming ‘glycated’.

By measuring HbA1c, clinicians are able to get an overall picture of what our average blood sugar levels have been over a period of weeks/months.

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13
Q

What is diabetes?

A

An elevation of blood glucose above a diagnostic threshold - Defining the threshold for diabetes is based upon risk of developing retinopathy

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14
Q

What is the threshold of diabetes based on?

A

Based upon risk of developing retinopathy

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15
Q

What are the threshold for diagnosis of diabetes?

A

Fasting Plasma Glucose = 126mg/dl = 7mmol/L
2-hour plasma glucose = 200mg/dl = 11.1 mmol/L
HbA1c = 6.5% = 48 mmol/mol and above

If asymptomatic a repeat confirmatory test is required

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16
Q

What are the normal glucose values in non-diabetics? (random 2-hour, fasting and HbA1c)

A

Fasting - 6mmol/L and below
2-hour plasma glucose = 7.7mmol/L and below
HbA1c = 41mmol/mol and below

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17
Q

What are the pre-diabetic glucose values in pre-diabetics patients? (random 2-hour, fasting and HbA1c)

A

Fasting - 6.1-6.9 mmol/L
2-hour plasma glucose = 7.8 - 11 mmol/L
HbA1c = 42 - 47 mmol/mol

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18
Q

What is the threshold of Gestational diabetes based on?

A

Threshold levels are NOT set by retinopathy risk but rather by risk to the fetus/neonate

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19
Q

What is C-peptide?

A

 C-peptide is co-secreted with insulin and is not part of injected insulin – so if c-peptide is present in the blood it must be coming from the person’s beta-cells

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20
Q

Symptoms of T2D

A

a. Polyuria
b. Thirst and polydipsia
c. Blurred vision
d. Genital Thrush
e. Fatigue
f. Weight loss

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21
Q

What are the 2 diabetic emergencies?

A

a. Diabetic Ketoacidosis

b. Hyperosmolar Hyperglycemic State

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22
Q

What are the macrovascular complications of diabetes?

A

Myocardial Infarction/ACS
Stroke
Peripheral Vascular Disease

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23
Q

What are the microvascular complications of diabetes?

A

Retinopathy
Neuropathy
Nephropathy

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24
Q

What are the targets for HbA1c?

A

An HbA1c target of 7.0% (53 mmol/mol) among people with type 2 diabetes is reasonable

For a patient on triple oral therapy or insulin – an HbA1c of 58 mmol/mol may be more appropriate

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25
Q

What kind of drug is metformin?

A

Biguanide

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26
Q

Describe the use of metformin in chronic renal disease

A

Metformin dose should be decreased as renal function falls
• Max dose 1g daily if eGFR <45ml/min
• Contraindicated if eGFR <30ml/min

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27
Q

What is the effect of metformin on weight?

A

Weight neutral or negative (weight losing)

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28
Q

Mechanism of action of sulphonylureas

A
  1. SUs bind to SUR1
  2. Closure of ATP sensitive K channel (KATP) occurs
  3. This leads to rise in membrane potential and triggers Voltage gated Calcium channel opening
  4. Calcium influx leads to insulin exocytosis - GLUCOSE INDEPENDENT INSULIN SECRETION EVEN WHEN GLUCOSE IS NOT INCREASED
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29
Q

What is the effect of sulphonylureas on weight?

A

Increase weight – by 1-2 kg on average

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30
Q

Side effects of sulphonylureas

A

Increase weight – by 1-2 kg on average

Risk of hypoglycemia

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31
Q

Example of sulphonylureas

A

Gliclazide.

Start at 40-80mg od; little benefit by increasing over 80mg bd although max dose 160mg bd.

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32
Q

SGLT2 inhibitors mechanism of action

A

Function through a novel mechanism of reducing renal tubular glucose reabsorption, producing a reduction in blood glucose without stimulating insulin release.

So SGLT2 inhibitors make you pee sugar - Weight loss will eventually plateau though

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33
Q

Side effects of SGLT2 inhibitors

A
  1. Genital mycotic infection (thrush)
  2. Fournier Gangrene
  3. Hypovolemia and hypotension
  4. Diabetic Ketoacidosis
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34
Q

Benefits of SGLT2 inhibitors

A

o Diuresis
o Improved myocardial energetics
o Renal protection
o Weight loss - will eventually plateau

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35
Q

Examples of SGLT2 inhibitors

A

Dapagliflozin, Canagliflozin, Empagliflozin

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36
Q

Mechanism of action of incretin drugs

A

Act via the GLP-1/GIP receptor – G Protein coupled receptors

Increase in cAMP acts in many ways (not fully understood) to:
o Close KATP channel (PKA)
o Modulate calcium currents (PKA)
o Directly on Insulin secretory mechanism

The net result is primarily augmentation of insulin secretion when the pathway is triggered (by glucose or sulphonylureas) = Therefore, NO HYPOGLYGAEMIA

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37
Q

DPP4 inhibitors (aka Gliptins) mechanism of action

A

Inhibit breakdown of GLP-1 and GIP

Augment insulin secretion so, like Sulphonylureas, are insulin secretagogues

As incretin action is glucose dependent – unlike Sulphonylureas, they do NOT cause Hypoglycaemia

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38
Q

What is the effect of DPP4 inhibitors on glucose lowering?

A

Weak glucose lowering. HbA1c reduction ~5-8 mmol/mol

39
Q

What is the effect of DPP4 inhibitors on weight?

A

Weight neutral (unlike SUs which increase weight)

40
Q

Side effects of DPP4 inhibitors

A

Generally, very well tolerated

Possible increased risk of pancreatitis

41
Q

Example of DPP4 inhibitors

A

Sitagliptin

42
Q

Mechanism of GLP-1 Receptor agonists

A

GLP-1 like molecules modified to avoid breakdown by DPP4. Act directly on the GLP-1 Receptor.

Act to promote insulin secretion (insulin secretagogues) in a glucose dependent mechanism (Better than SUs).

Act in many other tissues – especially hypothalamus to reduce appetite, and intestines to reduce gastric emptying.

43
Q

The effect of GLP-1 Receptor agonists on glucose lowering

A

Potent. HbA1c reduction ~11-15 mmol/mol

44
Q

The effect of GLP-1 Receptor agonists on weight

A

Weight loss - 2-3kg on average

45
Q

Example of a GLP-1 receptor agonist

A

Liraglutide

46
Q

Side effects of GLP-1 receptor agonists

A

Nausea and vomiting

Gallstones

47
Q

Mechanism of action of Thiazolidinediones (glitazones)

A

PPARg agonists – results in switching on 100s of genes

Net effect is to increase fat mass in subcutaneous depots and to ‘suck out’ fat from viscera (liver, pancreas) and muscle

Also increased adiponectin and reduced ‘inflammatory cytokines’ like TNFa and IL-6

48
Q

The effect of Thiazolidinediones (glitazones) on weight

A

Increase in weight – due to increase in fat mass and fluid retention

49
Q

The effect of Thiazolidinediones (glitazones) on glucose lowering

A

Good efficacy – 15-20mmol/mol HbA1c reduction; especially potent in obese women

50
Q

Examples of Thiazolidinediones (glitazones)

A

Pioglitazone

51
Q

Side effects of thiazolidinediones

A

Weight gain
Fluid retention
Fracture risk

52
Q

Delta cells

A

Part of the pancreatic islet cells - secrete somatostatin

53
Q

PP cells

A

Part of the pancreatic islet cells - secrete pancreatic polypeptide

54
Q

Example of an ultra long acting insulin

A

Insulin glargine

55
Q

Ultrafast/ultra-short-acting insulin

A

Insulin lispro

56
Q

Describe the production of insulin from beta cells

A

Glucose enters b cells through the GLUT2 glucose transporter and is phosphorylated by glucokinase

Increased metabolism of glucose leads to an increase in intracellular ATP concentration

ATP inhibits the ATP-sensitive K+ channel KATP

Inhibition of KATP leads to depolarisation of the cell membrane

Depolarisation of the cell membrane results in opening of voltage gated Ca2+ channels

An increase in internal Ca2+ concentration leads to fusion of secretory vesicles with the cell membrane and release of insulin

57
Q

Maturity onset diabetes of the young (MODY)

A

Monogenic disease with common clinical features to both type 1 and type 2 diabetes. Beta cell dysfunction but not autoimmune destruction.

58
Q

What are the two subunits of the kATP channel?

A

An inward rectifier subunit (KIR) - pore subunit – Kir6

A sulphonylurea receptor - regulatory subunit - SUR1

Both are required to form a functional channel
o Channel exists as an octomeric structure
o 4xSUR and 4xKIR

59
Q

Mutations of the glucokinase gene leads to what MODY condition?

A

MODY 2

60
Q

Mutations of the hepatocyte nuclear factor-4a gene leads to what MODY condition?

A

MODY 1

61
Q

Mutations of the hepatocyte nuclear factor-1a gene leads to what MODY condition?

A

MODY 3

62
Q

Mutations of the Insulin promoter factor 1 gene leads to what MODY condition?

A

MODY 4

63
Q

What are the 2 processes inhibited by insulin?

A

Lipolysis

Gluconeogenesis in liver

64
Q

Gluconeogenesis

A

Production of glucose from non-carbohydrate sources

65
Q

What processes are stimulated by Insulin?

A
  • Amino acid uptake in muscle
  • DNA synthesis
  • Protein synthesis
  • Growth responses
  • Glucose uptake in muscle and adipose tissue
  • Lipogenesis in adipose tissue and liver
  • Glycogen synthesis in liver and muscle
66
Q

Describe ketone body formation

A

Fatty acid (Beta) oxidation yields acetyl-CoA (from 3 hydroxybutyrate and acetoacetate) which enters the TCA cycle if fat and carbohydrate degradation are balanced

However, if supply of Pyruvate/Oxaloacetate is limited (e.g. if fat utilisation vastly outstrips glucose utilisation-no glycolysis) the Acetyl CoA is diverted to ketones.

Having no insulin reduces the amount of glucose being taken up by tissues from the blood and reduces glycolysis, making the body switch to fatty acid oxidation.

67
Q

Describe ketosis in glucose limiting conditions

A

> 

In starvation - Oxaloacetate is consumed for gluconeogenesis
When glucose is not available-fatty acids are oxidised to provide energy
Any excess acetyl-CoA (that can’t enter TCA cycle) is converted to ketone bodies, blood levels increase
Excessive accumulation of ketone bodies can lead to acidosis 
High glucose excretion also causes dehydration, exacerbates acidosis --> Coma, death

Diagnosed when high ketone and very high glucose, low or absent insulin and low pH in blood. Treat with insulin and rehydration

68
Q

Treatment of ketosis

A

insulin and rehydration

69
Q

LADA (Latent Autoimmune Diabetes in Adults):

A

A slow-progressing form of autoimmune diabetes. Like the autoimmune disease T1D, LADA occurs because your pancreas stops producing adequate insulin, most likely from some “insult” that slowly damages the insulin-producing cells in the pancreas. But unlike type 1 diabetes, with LADA, you often won’t need insulin for several months up to years after you’ve been diagnosed.

70
Q

What do the alpha cells of the pancreas produce?

A

Glucagon

71
Q

Role of glucagon

A

Glucagon acts on the liver to promote hepatic glucose production, raising blood glucose.

Glucagon secretion is elevated in the fed state in T2D and contributes to hyperglycaemia.

72
Q

Hyperglycaemic Hyperosmolar Non-ketotic Coma (HONK)

A

Coma resulting from very high blood glucose levels in a patient with normal ketone levels. If very high blood glucose levels are combined with high ketone levels, the state is likely to be ketoacidosis.

73
Q

Clinical signs of Hyperglycaemic Hyperosmolar Non-ketotic Coma (HONK)

A 
o	Polyuria
o	Polydipsia 
o	Altered mental status
o	Profound dehydration 
o      Hypernatremia
74
Q

Diagnosis of Hyperglycaemic Hyperosmolar Non-ketotic Coma (HONK)

A

o Gross hyperglycaemia (>30mmol/L)
o Dehydration
o Hyperosmolarity

75
Q

Investigations of Hyperglycaemic Hyperosmolar Non-ketotic Coma (HONK)

A 
o	Increased glucose (>30mmol/L)
o	Increased sodium
o	Increased urea
o	Normal ABGs (no acidosis – ketones)
o	ECG
o	CXR
76
Q

Treatment for Hyperglycaemic Hyperosmolar Non-ketotic Coma (HONK)

A

Aim is to gradually restore blood biochemistry
High risk of thromboembolism
Thromboprophylaxis (deltaparin or enoxaparin)
IV insulin

77
Q

Diabetic ketoacidosis

A

Type 1 DM - Uncontrolled catabolism associated with insulin deficiency

Diabetic ketoacidosis usually happens because your body doesn’t have enough insulin. Your cells can’t use the sugar in your blood for energy, so they use fat for fuel instead. Burning fat makes acids called ketones.

78
Q

ABGs for Diabetic ketoacidosis

A

o Acidosis
o Low bicarbonate
o Low CO2
o Metabolic acidosis with respiratory compensation

79
Q

Triggers for Diabetic ketoacidosis

A 
o	New onset diabetes 
o	Acute illness
o	Infection
o	Insulin omission
o	MI
o	Stroke
80
Q

Clinical signs of Diabetic ketoacidosis

A 
>	Dehydration
>	Tachycardia
>	Decreased blood pressure
>	Hyperventilation – kussmaul 
>	Sweet acetone breath (ketones)
>	Hyperglycaemia
>	Ketonuria
>	Ketonaemia
>	Acidosis
81
Q

Diagnosis of Diabetic ketoacidosis

A
  1. Hyperglycaemia (>14mmol/L)
  2. Metabolic acidosis
  3. Ketonuria/ketonaemia
82
Q

Management of Diabetic ketoacidosis

A
  1. Start IV fluids
  2. IV insulin (actrapid 50 units)
  3. Potassium
  4. LMWH
83
Q

What drugs cause galactorrhoea?

A

Chlorpromazine
Metoclopramide (and all dopamine antagonists)
Oestrogens

84
Q

What drugs cause hyperthyroidism?

A

Iodine

Amiodarone

85
Q

What drugs cause hypothyroidism?

A

Lithium

Amiodarone

86
Q

Kallman’s syndrome

A

(GnRH) deficiency, often with anosmia (can’t smell) and colour blindness
o Failure to start puberty or to fully complete puberty
o Also known as hypogonadotrophic hypogonadism

87
Q

Craniopharyngioma

A

Originates from rathke’s pouch between pituitary and 3rd ventricle floor

Rare, although most common childhood intracranial tumour, present with growth failure

88
Q

Robson mendenhall syndrome

A

Rare, autosomal recessive genetic trait, seen in children

Severe insulin resistance (decreased protein synthesis, glucose uptake, lipogenesis, glycogen synthesis)

Developmental abnormalities (head, face and nails), acanthosis nigricans, fasting hypoglycaemia, post prandial hyperglycaemia

Diabetic ketoacidosis

89
Q

What is the mode of inheritance for MODY?

A

Autosomal dominant

90
Q

Features of distal neuropathy

A

Warm, dry feet

Due to dilated vessels and diminished ability to sweat

91
Q

What conditions are associated with MEN 1

A
  1. Pituitary adenoma
  2. Parathyroid hyperplasia
  3. Pancreatic tumours
92
Q

MEN 2a conditions

A
  1. Parathyroid hyperplasia
  2. Medullary thyroid carcinoma
  3. Phaeochromocytoma
93
Q

MEN 2b conditions

A
  1. Mucosal neuromas
    2, Marfanoid body habitus
  2. Medullary thyroid carcinoma
  3. Phaeochromocytoma

Endocrinology (3 decks)

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