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Diabetes Flashcards

DM types 1 and 2 rare types: MODY

1
Q

What tests are available for screening for diabetes in high-risk individuals?

A
  1. Random capillary blood glucose
  2. Random venous blood glucose
  3. Fasting venous blood glucose
  4. HbA1c
  5. Oral glucose tolerance test (venous blood glucose 2h after oral glucose load).
    (lecture 19.4.18)
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2
Q

Other than identifying people at risk, give 3 ways of reducing the impact of diabetes and state whether they are primary, secondary of tertiary prevention.

A

(1. Identifying people at risk of diabetes)
2. Early prevention in those at risk (primary)
3. Early diagnosis of diabetes (secondary)
4. Supporting self-care for diabetes. (tertiary)

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3
Q

Give 3 examples of disability cause by diabetes

A

Blindess, renal failure, amputation.

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4
Q

How does the physical environment lead to diabetes?

A

Easy use of lifts, cars, remote controls and technology that leads to a sedentary lifestyle.

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5
Q

How does the economical environment lead to diabetes?

A

Fruit and vegetables, fitness classes, sports teams and gym memberships are expensive; it is cheaper to watch TV.

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6
Q

How does the sociocultural environment lead to diabetes?

A

People may have safety fears about walking around especially at night; family and social eating patterns affect diet.

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7
Q

What are the diagnostic criteria for diabetes mellitus?

A
  1. Symptoms of hyperglycaemia (eg polyuria, polydipsia and unexplained weight loss) and random blood plasma glucose ≥11mmol/l OR
  2. Fasting glucose ≥7mmol/L OR
  3. Oral glucose tolerance test 2h value ≥11mmol/L
    (lecture 20.4.18; OHCM)
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8
Q

Why would a DM patient present with thirst?

A

Diabetes causes osmotic activation of the hypothalamus.

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9
Q

How does insulin bring glucose into cells?

A

Insulin binds to insulin receptors eg in muscle cells and adipose tissue which activates them. They cause vesicles containing glucose transporter to fuse with the cell membrane, allowing glucose to move into the cell, decreasing the blood glucose level.
(osmosis youtube)

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10
Q

How does glucagon affect blood glucose level?

A

Glucagon is produced in the liver and causes gluconeogenesis (production of glucose from lactate, glycerol and amino acids) and glycogenolysis (breakdown of glycogen to glucose), increasing the level of glucose in the blood.

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11
Q

What is HLA and how does it increase the risk of diabetes?

A

The human leukocyte antigen system is a group of genes on chromosome 6 which encode the major histocompatibility complex which is important for self-tolerance and recognising foreign molecules. This increases risk of T1 diabetes. It does not affect T2 diabetes.

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12
Q

Which type of diabetes mellitus is more common?

A

Type 2 (90%)

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13
Q

Describe the pathophysiology of type 1 DM.

A

A genetic abnormality causes a decrease in self-tolerance among T cells which target the beta cell antigens. This allows the T cells to attack the beta cells. Loss of beta cells -> loss of insulin -> less glucose moving into cells -> more glucose in blood.

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14
Q

What is self-tolerance?

A

Ability of the immune system to recognise self-produced antigens as a threat while mounting an immune response to foreign antigens.

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15
Q

Why would a patient with type 1 DM have weight loss, fatigue and polyphagia?

A

Glucose is not getting into cells, so it cannot be used to make energy, so fat and muscle are metabolised. The person feels hungry.

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16
Q

What causes glycosuria in type 1 DM?

A

Some of the excess blood glucose spills into the urine.

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17
Q

What causes polyuria in type 1 DM?

A

Excess blood glucose spills into the urinary tract and this has an osmotic effect, causing water loss in urine and therefore lots of urine production.

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18
Q

What causes polydipsia in type 1 DM?

A

(polydipsia = thirst). Water is lost in urine due to polyuria (which is due to glycosuria which is due to hyperglycaemia)

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19
Q

Describe the physiology of ketogenesis.

A

Lipolysis of fat in adipose tissue makes free fatty acids, which are converted to ketone bodies in the liver. They can be used by cells for energy and are acidic.

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20
Q

Give an example of a ketoacid.

A

Acetoacetic acid.

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21
Q

What is ketoacidosis?

A

Excess ketoacids eg acetoacetic acid in the blood which can lead to death via circulatory collapse. Characterised by hyperglycaemia (<50ml/L(, Ketones (>2), and acidosis (HCO3 <15mmol/l).

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22
Q

What is Kussmaul breathing and how is it caused by ketoacidosis?

A

Deep, laboured breathing. Acidosis occurs and causes the body to compensate by expelling CO2 in breaths.

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23
Q

How does type 1 diabetes cause hyperkalaemia?

A

In order to decrease the acidity of blood, H+ is moved into cells by the K+/H+ transporter, which also moves K+ out of the cell. In addition, the lack of insulin means the Na/K/ATPase pump does not function, so K stays in the blood.

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24
Q

Why do Type 1 diabetes patients have a high anion gap?

A

Buildup of ketoacids causing large gap in the number of unmeasured ions. *?

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25
Q

How can stress and infection lead to a worsening of symptoms of hyperglycaemia?

A

Epinephrine is released, causing glucagon release, which causes hyperglycaemia and therefore dehydration etc.

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26
Q

How can infection cause ketoacidosis?

A

The body needs more energy to fight the infection, so more ketone bodies are generated by lipolysis.

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27
Q

Give 5 signs of ketoacidosis.

A

hyperventilation, cerebral oedema, fruity breath due to acetone (nail polish remover), dehydration, hypotension, tachycardia.

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28
Q

Describe the management of ketoacidosis.

A
  1. Fluids for dehydration
  2. insulin to lower blood glucose
  3. electrolytes to prevent hypokalaemia.
    When stable, treat underlying cause - this may be non-compliance so have discussion.
    Follow DKA protocol for your hospital!
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29
Q

Why are people with diabetes more prone to pruritis vulvae and balanitis?

A

Excess glucose sugar provides a favourable environment for fungi such as candida albicans to grow and colonise the vagina (pruritis vulvae) and head of the penis (balanitis).

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30
Q

How does diabetes cause blurry vision?

A

Uptake of glucose and therefore water into the lens.

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31
Q

What features are suggestive of type 1 diabetes?

A 
Lean body habitus
Onset in childhood/adolescence (but can be any age)
acute onset of osmotic symptoms
prone to ketoacidosis
high levels of islet autoantibodies.
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32
Q

What features are suggestive of type 2 diabetes?

A 
Usually presents in over-30s,
onset is gradual
family history/ sibling with condition
Hyperglycaemia can sometimes be controlled with lifestyle modification 
No HLA
Complications eg MI.
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33
Q

Give one autoantibody associated with type 1 diabetes.

A

Anti GAD, pancreatic islet cell ab, islet antigen-2 ab.

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34
Q

Give 3 autoimmune diseases associated with type 1 diabetes.

A

Hypothyroidism, Addison’s disease, coeliac disease.

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35
Q

Give 5 symptoms of ketoacidosis.

A

Nausea, vomiting, mental status changes, weakness, weight loss, abdominal pain, drowsiness/confusion.
(lecture 20.4.18)

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36
Q

Why do you need to give K+ as part of treatment for DKA?

A

At first, K+ shifts out of cells with acidosis, causing hyperkalaemia, but with insulin and rehydration, blood K+ levels will fall which can cause life-threatening hypokalaemia.

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37
Q

Why are urea and creatinine raised in diabetes?

A

Pre-renal failure.

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38
Q

Who is more at risk of cerebral oedema from DKA and why?

A

Children because their brains have not shrunk yet in relation to their skull, so ICP would rise more.

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39
Q

Give 3 complications of DKA.

A

Adult respiratory distress syndrome (due to hyperventilation?)
Thromboembolism - venous and arterial
Aspiration pneumonia (drowsy/comatose patients)
(lecture 20.4.18)

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40
Q

What are the key microvascular complications of type 1 diabetes?

A

Nephropathy (30%)

Neuropathy

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41
Q

How is type 1 diabetes managed?

A

Insulin treatment: previously twice daily and had to control diet, now you can do basal bolus: medium-acting insulin plus pre-meal quick acting insulin. This requires the patient to calculate their carbohydrate intake exercise but means they can live more normally.

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42
Q

Other than hunger, give 3 symptoms of hypoglycaemia.

A

Loss of concentration, confusion, sweating, tremor, palpitations, (hunger), irritability (adrenaline release)
(lecture 20.4.18)

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43
Q

What are the stages of hypoglycaemia?

A

Glucose level: <3.8mM: autonomic symptoms (sweating, tremor, palpitations)
<2.8mM: Neuroglycopaenia symptoms (confusion, behaviour change, drowsiness)
<1.5mM: severe neuroglycopaenia (coma, convulsions, hemiparesis)

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44
Q

What is the advantage and disadvantage of setting higher glucose targets? Why do some patients prefer to set high glucose targets?

A

Reduces risk of hypoglycaemia but increases risk of diabetic complications. Hypoglycaemia can be frightening and uncomfortable to patients often prefer to risk complications.

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45
Q

What should you consider in a patient with symptoms of type 1 diabetes with a parent affected by diabetes?

A

MODY: Maturity onset diabetes of the young. A type of monogenic diabetes which accounts for 1% of diabetes. Often diagnosed in non-obese people under 25, is autosomal dominant and occurs from a single gene defect altering beta cell function.
(lecture)

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46
Q

What is the most common form of MODY and how is it treated?

A

MODY-3 in which a hepatic nuclear factor (HNF)1-alpha mutations alter insulin secretion and cause beta cell proliferation. It is treated with sulphonylurea tablets, not insulin. (lecture 20.4)

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47
Q

What would indicate MODY in a patient with hyperglycaemia?

A

Parent affected with diabetes
Absence of islet autoantibodies
No ketosis, good control on low-dose insulin - suggests non-insulin dependence
Sensitive to sulphonylurea.

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48
Q

What is C peptide and what is it used for in practice?

A

A component of natural (but not synthetic) insulin which is negative after prolonged type 1 diabetes but persists in type 2 and MODY.

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49
Q

What should you consider in patients with diabetes symptoms who were diagnosed at birth?

A

Permanent neonatal diabetes. Small babies, epilepsy, muscle weakness. Treated with sulphonylureas.

50
Q

What rare type of diabetes can present with malabsorption, constipation and hearing impairment?

A

Maternally inherited diabetes and deafness. Due to a mutation in mitochondrial DNA.

51
Q

What is a genetic disorder associated with insulin resistance and hepatic steatosis?

A

Lipodystrophy - selective loss of adipose tissue.

52
Q

Give an inflammatory cause of diabetes

A
  1. Transient hyperglycaemia due to increased glucagon secretion in acute inflammation
  2. Chronic pancreatitis - formation of protein plugs which block pancreatic ducts and cause calculi formation
53
Q

What should you consider in patients with cirrhosis, diabetes and bronzed hyperpigmentation?

A

Hereditary haemochromatosis, where excess iron is deposited in the liver, pancreas, pituitary, heart and parathyroids. Most need insulin

54
Q

What could cause diabetes in patients with fatigue, weight loss, nausea/vomiting and jaundice?

A

Pancreatic neoplasia. Require insulin. Prone to hypoglycaemia due to loss of glucagon function.

55
Q

What can cause diabetes due to increased thickness of secretions?

A

Cystic fibrosis - increases thickness of secretions so blocks pancreatic ducts and cause fibrosis. Usually need insulin.

56
Q

How can a pituitary tumour cause diabetes?

A

Pituitary tumour presses on AP gland which produces excess GH causing acromegaly. Excess GH increases insulin resistance (like type 2 diabetes) and therefore decreased glucose uptake and increased output from the liver.

57
Q

How can cushing’s syndrome cause diabetes?

A

Cushing’s syndrome is excess glucocorticoid in blood. This increases lipolysis in fat, gluconeogenesis in the liver, and decreases glucose uptake by muscles.

58
Q

What is pheochromocytoma and how can it cause diabetes?

A

Neuroendocrine tumor of the medulla of the adrenal glands, causing catecholamine (mainly adrenaline) excess. Catecholamines increase gluconeogenesis and decrease muscle utilisation of glucose.

59
Q

Which drugs can cause diabetes?

A

Glucocorticoids (increase insulin resistance)

Thiazides/ protease inhibitors (HIV)/ antipsychotics (mechanism not fully understood)

60
Q

Give 3 symptoms of diabetic neuropathy.

A

Burning, shooting pain
Paraesthesia (pins and needles; abnormal sensation)
Hyperaesthesia (physical sensitivity)
Allodynia (increased pain sensation from areas that do not usually sense pain)
Nocturnal excacerbation
Autonomic: Diarrhoea, constipation, incontinence, erectile dysfunction.

61
Q

Give 3 complications of diabetic neuropathy.

A

Foot ulceration, leading to infection and amputation
Falls
Charcot foot (bone weakness)

62
Q

Describe the distribution of peripheral diabetic neuropathy and give a complication.

A

Glove and stocking distribution
Mortality due to cardiovascular disease
(leceture 20.4)

63
Q

Describe the management of diabetic painful neuropathy.

A 
Good glycaemic control
Tricyclic antidepressants, SSRIs
Anticonvulsants
Opioids
IV lignocaine
Capsaicin
64
Q

Give an example of a macrovascular complication of diabetes.

A

Cardiovascular complications

65
Q

Give 5 signs and symptoms of peripheral vascular disease.

A 
symptoms
1. Intermittent claudication (cramping induced by exercise, due to adenosine production by ischaemic muscle)
2. Rest pain - continuous pain when elevated.
signs
1. Diminished or absent pedal pulses
2. Coolness of feet and toes
3. Poor skin and nails
4. Hairless feet and legs
66
Q

How is PVD usually assessed?

A

Most commonly ankle brachial index (ABI). =Systolic pressure(ankle)/ systolic pressure(arm) <0.9.

67
Q

How is PVD managed?

A

Quit smoking
Walk through pain
Surgical intervention
Manage hypertension

68
Q

How can amputation be prevented?

A 
Screening for those at risk
Education and providing orthotic shoes
MDT foot clinic
Revascularisation
Antibiotics
69
Q

Give 3 examples of common mononeuropathies and their key features.

A

Third nerve - closed eye
Sixth nerve - nasally directed pupil
Seventh nerve - Bell’s palsy (half face affected)

70
Q

What increases the risk of diabetic retinopathy?

A 
Prolonged diabetes
Insulin treatment
Hypertension
Poor glycaemic control
Pregnancy
71
Q

How is DR prevented?

A

Primary prevention - screening in diabetics > 11 years old

72
Q

Describe the pathophysiology of DR.

A
  1. Occlusion of blood vessels causing ischaemic changes in the retina
  2. This causes basement membrane thickening, pericyte loss and decreased contact between endothelial cells
  3. This allows leakage of creatinine and albumin into the retina.
73
Q

What would an R1 retinopathy mean?

A

Background retinopathy

74
Q

What would an R2 retinopathy mean?

A

Pre-proliferative: multiple deep haemorrhages.

75
Q

What would an R3 retinopathy mean?

A

Proliferative: new blood vessels, pre-retinal fibrosis.

76
Q

What would an M retinopathy mean?

A

Maculopathy: exudate within the macula and fovea.

77
Q

Give one advantage and one disadvantage of laser therapy.

A

Laser therapy is the only treatment for DR. This does not improve sight but if given at the right time it effectively prevents deterioration. Side-effects can include difficulty with night vision (50%), loss of peripheral vision (20%) and vitreous haemorrhage.

78
Q

What is a P retinopathy?

A

photocoagulation

79
Q

What are the main characteristics of diabetic nephropathy?

A

Proteinuria followed by progressive decline in renal function.

80
Q

Give a complication of nephropathy.

A

CVD, ESCKD, amputation

81
Q

Give 2 risk factors for nephropathy.

A

Poor control of blood pressure and glucose.

82
Q

Describe the pathophysiology of diabetic nephropathy.

A

Glomerular injury causes the glomerulus to allow proteins to be filtered through when normally they would be too big.

83
Q

What is the main cause of death in diabetic nephropathy?

A

Cardiovascular disease.

84
Q

Describe the treatment of diabetic nephropathy.

A

BP and BG control (ARB/ ACEI)
Proteinuria control
Cholesterol control

85
Q

Give three vascular changes in diabetes.

A

Atherosclerosis
Arteriosclerosis
Inflammation
(Armando hasudungan)

86
Q

How does diabetes lead to an inflammatory plaque?

A

LDLs and monocytes can pass through gaps in endothelial cells to the tunica intima. The monocytes become macrophages and engulf the LDL, now becoming foam cells. The foam cells cluster together and rupture in the tunica intima, releasing lipids and inflammatory cells, causing an inflammatory plaque.

87
Q

Give one problem with suphonylureas and insulin

A

They cause weight gain - mostly insulin

lecture 23.4.18

88
Q

What is the advantage of metformin over insulin?

A

It does not cause weight gain, or causes it much less than insulin.

89
Q

Give 3 pharmacological alternatives to insulin for type 2 diabetes.

A 
Incretins
DPP-4 Inhibitors
GLP-1 analogues
TZDs
(lecture 23.4)
90
Q

Give an example of a DPP-4 inhibitor.

A

Sitagliptin.

91
Q

Give an example of a commonly used TZD

A

Pioglitazone.

92
Q

How do incretins work?

A
  1. They are released when food enters the small bowel and send signals to the brain to promote satiety.
  2. They increase insulin production by beta cells
  3. They slow gastric emptying so the person feels fuller.
    These mechanisms decrease appetite and blood glucose levels.
    (lecture 23.4)
93
Q

What is a healthy BMI?

A

18.5-24.9

94
Q

What BMI defines obesity?

A

30-39 (25-30 is overweight, 40+ is severe obesity)

95
Q

Which type of fat is most dangerous?

A

Abdominal (visceral) fat.

96
Q

Give 3 factors that decrease appetite

A

Feeling ill or nauseous
Incretin hormones eg glucagon-like peptide (GLP-1)
Neurotransmitters eg serotonin
Peptide YY - binds NPY receptors.

97
Q

Give 3 factors that increase appetite.

A

Neuropeptides eg NPY (neuropeptide Y) - causes growth of fat tissue.
Melanin-concentrating hormone (MCH)
Psychological - time of day, smells, social factors.
Orexin (hypocretin)
Ghrelin

98
Q

What is leptin?

A

A hormone expressed in white fat which decreases appetite. Without it, obesity and overeating occur.

99
Q

How does cholecystokinin decrease appetite?

A

It acts on receptors in the pyloric sphincter to cause delayed gastric emptying, gallbladder contraction and insulin release. It also produces a feeling of satiety via the vagus nerve.

100
Q

How does ghrelin increase appetite?

A

It is expressed in the stomach, and acts on hypothalamic cells to increase hunger and gastric acid secretion. Ghrelin levels increase when fasting.

101
Q

What could cause dehydration and increase in BMI?

A

ProOpioMelanoCortin (POMC) deficiency.

102
Q

What is shift work and why are shift workers more likely to gain weight?

A

Work outside of the 7am-7pm working day. Circadian rhythms change and this affects hormones released.

103
Q

Which arteries may be affected if the patient feels pain in the foot?

A

Tibial and peroneal

osmosis

104
Q

What is type 2 diabetes?

A

Diabetes caused by decreased insulin secretion with or without increased insulin resistance.
(OHCM)

105
Q

Why is type 2 diabetes increasing in prevalence? Give 3 reasons.

A

Changes in lifestyle - obesogenic environment
Better diagnosis
Improved longevity.

106
Q

Give 3 risk factors for type 2 diabetes.

A 
Asian
Male
Elderly
Obesity
Lack of exercise
Excess calorie and alcohol intake.
Strong genetic role
107
Q

What is impaired glucose tolerance?

A

Abnormality of glucose regulation with risk of progression to diabetes - window for intervention. Fasting plasma glucose <7mmol and OGTT 2h glucose ≥7.8<11.1mmol/L

108
Q

What is impaired fasting glucose?

A

Abnormality of glucose regulation with risk of progression to diabetes, window for lifestyle intervention. FPG ≥6.1<7mmol/L

109
Q

What is the management of IGT and IFG?

A

Lifestyle advice and annual review.

110
Q

How is glucose control monitored in type 2 diabetes?

A
  1. Fingerprick glucose if on insulin - pre-meal informs about long-acting insulin, post-meal informs about short-acting insulin.
  2. HbA1C
  3. Ask about hypoglycaemic attacks and whether they are symptomatic. Awareness may decrease in control is too tight and may return if control is loosened.
111
Q

Describe the general management of types 1 and 2 diabetes.

A
  1. Lifestyle advice, eg exercise to increase insulin sensitivity, decrease sat fats, increase starch carb
  2. Bariatric surgery?
  3. Set HbA1C target and review every 3-6 months.
  4. Assess global vascular risk, start high-intensity statin eg atorvastatin, control BP
  5. Foot care
  6. Advise informing DVLA and not to drive in hypogylcaemia.
112
Q

Describe the pharmacological management of type 2 diabetes.

A
  1. Monotherapy - 1st-line standard release metformin.
  2. If HbA1C rises, add alternative eg sitagliptin/sulphonylurea/empagliflozin/pioglitazone
  3. If HbA1C rises, add another
113
Q

How does metformin work?

A

Suppresses hepatic gluconeogenesis, lowering blood sugar.

114
Q

What class does sitagliptin belong to, how does it work and what is a side-effect?

A

DPP4 inhibitor, so DPP4 cannot destroy incretin, so more incretin stays in the blood and decreases blood glucose. Side effects (rare) include nausea.

115
Q

Pioglitazone class, mechanism, side-effect?

A

Glitazone. Increases insulin sensitivity. SE: hypoglycaemia, fractures, fluid retention, increased LFTs so stop is ALT increases 3fold.

116
Q

Glifazon class, mechanism, SE?

A

Selective sodium-glucose co-transporter-2 inhibitor (SGLTI)/gliflozin. Blocks reabsorption of glucose in kidneys and promotes excretion of excess glucose in the urine. SEs rare - UTI.

117
Q

When would you use ultra-fast acting insulin?

A

At the start of a meal, or just after (unless sugar-laden). Helps match what is eaten rather than what is planned as part of a QDS regimen.

118
Q

When would you use isophane insulin?

A

This is an intermediate-acting insulin. It is injected before meals, in conjunction with a short-acting insulin. Its activity peaks at 4-12 hours after injection. Inexpensive, favoured by NICE.

119
Q

When would pre-mixed insulins be administered?

A

Mixed short- and long-acting. Can be injected twice daily as part of a BD biphasic regimen.

120
Q

When would insulin glargine be administered?

A

This is a long-acting recombinant human insulin analogue. It is injected before the person goes to bed as part of a QDS or once-daily regimen, because there is no big peak, decreasing the risk of nocturnal hypoglycaemia.

121
Q

Liraglutide - class, mechanism, SE?

A

Glucagon-like peptide (GLP) analogue. Mimics incretins, which augment insulin release in the gut. Possible pancreatic cancer risk?

2a (75 decks)

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