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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is diabetes?

A

A syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both

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2
Q

Give 5 serious complications of diabetes

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. Diabetic neuropathy
  4. Stroke
  5. CVD
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3
Q

What is the range for normal blood glucose?

A

3.5-8.0mmol/L

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4
Q

Why can the brain not use free fatty acids for fuel?

A

They cannot cross the blood brain barrier

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5
Q

What happens to glucose taken up by muscles?

A

It is stored as glycogen or metabolised to lactate or CO2 and H2O

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6
Q

What does the GLUT1 transporter do?

A

Enables basal non-insulin-stimulated glucose uptake into many cells

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7
Q

What does the GLUT2 transporter do?

A
  • Found in the β cells of the pancreas, the renal tubules and hepatocytes
  • Transports glucose into the β cells which enables the cells to sense the glucose levels
  • A low affinity transporter – only allows glucose in when there is a high concentration of glucose
  • This means the β cells can detect the high glucose levels and release insulin in response
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8
Q

What does the GLUT3 transporter do?

A

Enables non-insulin-mediated glucose uptake into the brain, neurones and placenta

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9
Q

What does the GLUT4 transporter do?

A

Mediates most of the peripheral action of insulin - enables the uptake of glucose into muscle and adipose tissue cells following stimulation of the insulin receptor by insulin binding to it

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10
Q

Name the 7 types of diabetes

A
  1. Type 1 diabetes
  2. Type 2 diabetes
  3. Mongenic types diabetes e.g. MODY
  4. Pancreatic diabetes
  5. Endocrine diabetes
  6. Malnutrition related diabetes
  7. Diabetes insipidus
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11
Q

Which type of diabetes does gestational and medication induced diabetes fall under?

A

Type 2 diabetes

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12
Q

What are the measurements to diagnose diabetes?

A
  • Symptoms and random plasma glucose >11mmol/L
  • Fasting plasma glucose >7mmol/L
  • No symptoms – glucose tolerance test (GTT = 75g glucose) fasting >7mmol/L or 2h value >11mmol/L (repeat on 2 occasions)
  • HbA1c of >48mmol/L or >6.5%
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13
Q

What is type 1 diabetes?

A

A disease of insulin deficiency usually caused by autoimmune destruction of β cells of the pancreas

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14
Q

In the fasting state, is insulin low or high?

A

Low

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15
Q

Where is ingested glucose distributed to?

A
  • 40% to the liver to restore glycogen stores

* 60% to the periphery (mostly muscles) for fuel

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16
Q

What is the name for the cells in the endocrine pancreas?

A

The islets of Langerhans

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17
Q

Where are insulin and glucagon secreted from?

A

In the islets of Langerhans:
• Glucagon - α cells
• Insulin - β cells

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18
Q

What is the mechanism of insulin secretion?

A
  1. Glucose enters pancreatic cell by GLUT2 glucose transporter and helped by glucokinase
  2. Ca2+ enters the cell via the calcium channels
  3. K+ enters via Kir6.2 potassium channels (ATP dependent)
  4. Glucose is metabolised in the cell and generated ATP/ADP to close potassium channel
  5. The membrane depolarises for Ca2+ to enter and stimulate the insulin secretory granules
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19
Q

What happens in diabetic ketoacidosis(DKA)?

A
  1. Reduced glucose supply and increased fatty acid oxidation
  2. Increased production of acetyl-CoA leads to ketone production that exceeds the ability of the peripheral tissues to oxidise them so blood pH lowers
  3. Acidic blood impairs the ability of haemoglobin to bind to oxygen
  4. The patient’s breath will smell of ketones
  5. Patient likely becomes acidotic, anorexic and dehydrated leading to AKI, hyperglycaemia and eventually death
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20
Q

What are the crucial factors normally associated with type 2 diabetes?

A
  • Obesity
  • Lack of exercise
  • Calorie and alcohol excess
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21
Q

Why is ketoacidosis almost never seen in T2DM compared to T1DM?

A

In type 2 there are always detectable insulin levels and even low levels of insulin prevent muscle catabolism and ketogenesis so profound muscle breakdown and gluconeogenesis are restrained and ketone production is rarely excessive in type 2

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22
Q

What would you usually see in acute presentation (2-6 weeks) of diabetes mellitus?

A
  • Polyuria and nocturia
  • Polydipsia (thirst)
  • Weight loss
  • Ketouria (and may progress to ketoacidosis)
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23
Q

What would you usually see in subacute presentation (months to years) of diabetes mellitus?

A
  • Present but less marked polyuria, polydipsia and weight loss
  • May complain of lack of energy, visual blurring, pruritus vulvae or balanitis (due to Candida infection)
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24
Q

What are complications that patients may present with that suggest diabetes mellitus?

A
  • Staphylococcal skin infection
  • Retinopathy found during visit to optician
  • Polyneuropathy causing tingling and numbness in the feet
  • Erectile dysfunction
  • Arterial disease resulting in MI or peripheral gangrene
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25
Q

How would you treat diabetes mellitus type 1?

A
  1. Educate the patient on the disease and risks
  2. Lifestyle modification e.g. smoking, exercise, diet
  3. Good glyacemic control
  4. Treat hypertension and hyperlipidaemia
  5. Give insulin in type 1
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26
Q

What is the 1st line treatment for type 2 diabetes mellitus?

A
  • Educate the patient on the disease and risks
  • Lifestyle modification e.g. smoking, exercise, diet
  • Good glyacemic control
  • Treat hypertension and hyperlipidaemia
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27
Q

What is the 2nd line treatment for type 2 diabetes mellitus?

A
  1. Oral metformin
  2. If HbA1c >53mmolL after 16 weeks on metformin then add a sulfonylurea e.g. oral gliclazide
  3. If HbA1c >57mmol/L at 6 months consider adding insulin, a glitazone, sulfonylurea receptor binder or a GLP analogue
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28
Q

What does oral metformin do?

A
  • Reduces the rate of liver gluconeogenesis
  • Increases cell sensitivity to insulin
  • Reduces diabetes CVS risk
  • Doesn’t cause hypoglycaemia
  • Contraindicated in heart failure, liver disease and renal disease (can induce lactic acidosis)
29
Q

What do sulfonylureas do?

A
  1. Promotes insulin secretion
  2. Avoided in pregnancy
  3. Can cause hypoglycaemia
30
Q

What are the 3 main types of insulin?

A
  1. Short acting soluble insulins
    - Start working within 30-60 mins and last for 4-6hrs
  2. Short acting insulin analogues
    - Fast onset and short duration
  3. Longer-acting insulins
    - Can be immediate (12-24hrs) or longer-acting (>24hrs)
31
Q

Give 4 complications of insulin treatment

A
  1. Hypoglycaemia – most common, also caused by sulfonylurea
  2. Injection site – lipohypertrophy
  3. Insulin resistance – mild and associated with obesity
  4. Weight gain – insulin makes people feel hungry
32
Q

Why should insulin therapy for type 1 diabetics not be stopped?

A

It greatly increases the risk of diabetic ketoacidosis. Insulin may need adjusting up or down but should never be stopped

33
Q

What is the clinical presentation of DKA?

A
  • Excess ketones in the urine and can be detected on the breath
  • Gradual drowsiness, vomiting and dehydration
  • Kussmaul’s respiration (deep rapid breathing)
  • Disturbance of consciousness
  • Coma in 5% of cases
34
Q

How would you diagnose DKA?

A
  • Hyperglycaemia – blood glucose >11mmol/L
  • Raised plasma ketones >3mmol/L
  • Acidaemia – blood pH <7.3
  • Metabolic acidosis with bicarbonate <15mmol/L
  • Urine testing dipstick -> glycosuria and ketonuria
  • Raised U+Es due to dehydration, low body K+ but usually high serum K+
35
Q

What investigations would you do to exclude differential diagnoses in DKA?

A
  • Do FBC and blood and urine cultures to check for infection

* ECG and cardiac enzymes to look for MI

36
Q

How would you treat DKA?

A
  1. ABC management
  2. 0.9% fluid saline
  3. Restore electrolyte loss (K+)
  4. Restore acid-base balance over 24hrs
  5. Replace deficient insulin
  6. Monitor blood glucose
37
Q

Name 4 macrovascular complications of diabetes

A
  1. Atherosclerosis
  2. Stroke
  3. Ischaemic heart disease leading to MI
  4. Peripheral vascular disease
38
Q

Name 4 microvascular complications of diabetes

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. Diabetic neuropathy
  4. Cataracts develop earlier
39
Q

What are some signs and symptoms of peripheral vascular disease?

A 
• Symptoms
- Intermittant claudication
- Rest pain
• Signs
- Diminished or absent pedal pulses
- Coolness of the feet and toes
- Poor skin and nails
- Absence of hair on feet and legs
40
Q

What is the role of laser therapy in diabetic retinopathy?

A

To stabilise retinal deteriation and decrease the progression of sight loss but doesn’t restore sight

41
Q

How would you detect diabete nephropathy?

A

Albumin : creatinine ratio >3 indicates microalbuminuria (dipstick doesn’t detect it)

42
Q

Give some clinical features of diabetic neuropathy

A
  • Pain (like burning) and paraesthesia
  • Autonomic problems e.g. GI problems, erectile dysfunction
  • ‘Glove and stocking’ sensory loss
43
Q

How is hypoglycaemia defined?

A

Plasma glucose <3mmol/L

44
Q

What are the causes of hypoglycaemia?

A

• Diabetes
- Due to insulin or sulfonylurea treatment
• Non-diabetics (EXPLAIN)
- Ex -Exogenous drugs - insulin, oral hypoglycaemic, alcohol binge with no food
- P - Pituitary insufficiency
- L - Liver failure
- A - Addison’s disease
- I - Islets cell tumour and immune hypoglycaemia
- N - Non-pancreatic neoplasm

45
Q

What are clinical presentations of hypoglycaemia?

A

• Autonomic
- Sweating, anxiety, hunger, tremor, palpitations, dizziness
• Neuroglycopenic
- Confusion, drowsiness, visual trouble, seizures, coma
- Focal symptoms (rarely)

46
Q

How would you diagnose hypoglycaemia?

A
  • Finger-prick during attack
  • Take drug history and exclude liver failure
  • Bloods – glucose, insulin, C-peptide, plasma ketones
47
Q

How would you treat hypoglycaemia?

A
  • Oral sugar and long-acting starch e.g. toast
  • If cannot swallow give 50% IV glucose or IM glucose if no IV access
  • Re-educate diabetics on insulin use
48
Q

What is diabetes insipidus?

A

The passage of large volumes of dilute urine (>3L/day) due to impaired water reabsorption in the kidney

49
Q

What are the 2 types of diabetes insipidus?

A
  1. Cranial DI

2. Nephrogenic DI

50
Q

What is the underlying pathlogical reason for cranial diabetes insipidus?

A

Reduced ADH secretion from the posterior pituitary

51
Q

Give some causes for Cranial DI

A
  • Idiopathic
  • Congenital defects in ADH gene
  • Hypothalamic disease
  • Tumour
  • Trauma
  • Infiltrative disease (e.g. sarcoidosis)
52
Q

What is the underlying pathlogical reason for nephrogenic diabetes insipidus?

A

Impaired response of the kidney due to ADH

53
Q

Give some causes for Nephrogenic DI

A 
• Hypokalaemia
Hypercalcaemia
• Drugs
• Renal tubular acidosis
• Sickle cell disease
• Prolonged polyuria of any cause
• Familial - mutation of ADH receptor
54
Q

What are the 3 key features of diabetes insipidus?

A
  1. Polyuria
  2. Polydipsia
  3. No glycosuria
55
Q

Give 3 differential diagnoses for diabetes insipidus

A
  1. Diabetes mellitus
  2. Hypokalaemia
  3. Hypercalcaemia
56
Q

How would you diagnose diabetes insipidus?

A
  • Measure urine volume (unlikely if vol<3L/day)
  • Check blood glucose
  • Water deprivation test
57
Q

How would you differentiate between cranial and nephrogenic DI?

A

When desmopressin is givin during the water deprivation test, there is response in cranial (urine osmolality increases) but there is no response in nephrogenic

58
Q

How do you treat cranial diabetes insipidus?

A
  1. Find cause

2. Give synthetic analogue of ADH (e.g. oral desmopressin)

59
Q

How do you treat nephrogenic diabetes insipidus?

A
  1. Treat cause
  2. Give thiazide diuretics
  3. NSAIDs
60
Q

What are the monogenic causes of diabetes?

A
  1. Maturity-onset diabetes of the young (MODY)
  2. Permanent neonatal diabetes
  3. Maternally inherited diabetes and deafness (MIDD)
  4. Lipodystrophy
61
Q

Are MODY patients dependent on insulin?

A

No

62
Q

What factors would contribute to a diagnosis of MODY?

A
  • Parents have diabetes
  • Absence of islet antibodies
  • Evidence of non-insulin dependence
  • Sensitive to sulphonurea
63
Q

Give 3 pints which would be evidence of non-insulin dependence

A
  1. Good control on low dose insulin
  2. No ketosis
  3. Measurable C-peptide
64
Q

What are 4 signs of permanent neonatal diabetes?

A
  1. Diagnosis age <6months (usually at birth)
  2. Small babies
  3. Epilepsy
  4. Muscle weakness
65
Q

What is maternally inherited diabetes and deafness (MIDD)?

A

Loss of beta cell mass due to a mutation in the mitochondrial DNA

66
Q

What is lipodystrophy?

A

Selective loss of adipose tissue

67
Q

Give 5 exocrine pancreasis conditions that can cause diabetes

A
  • Inflammation (acute or chronic pancreatitis)
  • Hereditary hemochromatosis
  • Deposition e.g. amyloidosis
  • Pancreatic neoplasia
  • Cystic fibrosis
68
Q

Name 3 potentially reversible endocrine causes of diabetes

A
  1. Acromegaly
  2. Cushing’s syndrome
  3. Pheochromocytoma
69
Q

Name 4 types of drugs which can induce diabetes

A
  1. Glucocorticoids
  2. Thiazides
  3. Protease inhibitors
  4. Antipsychotics

Endocrine (7 decks)

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