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Y2 Endocrine > Diabetes: Science and Clinical > Flashcards

Diabetes: Science and Clinical Flashcards

1
Q

The exocrine pancreas produces… [physiology]

A

watery, alkaline secretions and digestive enzymes to the duodenum

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2
Q

The endocrine pancreas has 4 groups of cells which are: [physiology]

A
  1. beta cells (insulin)
  2. alpha cells (glucagon)
  3. D-cells (somatostatin)
  4. F cells (pancreatic polypeptide)
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3
Q

Where are b-cells found? [physiology]

A

centrally within the islets of langerhans

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4
Q

Role of somatostatin [physiology]

A

released in response to increased BG and amino acides. slows rate of digestion to prevent excess nutrients in the plasma

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5
Q

Role of pancreatic polypeptide [physiology]

A

reduces appetite and food intake

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6
Q

promotes the acitivity of which enzyme [Insulin]

A

Glycogen synthase

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7
Q

inhibits the activity of which enzyme [Insulin]

A

lipase

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8
Q

[carbohydrates] insulin has 4 effects on carbohydrates

A
  1. facilitates transport into cells via GLUT 4
  2. stimulates glycogenesis
  3. inhibits glycogenolysis
  4. inhibits gluconeogenesis
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9
Q

[fat] insulin has 4 effects on fat

A
  1. increases fatty acid uptake into adipose tissue
  2. increased transport of glucose into adipose tissue via GLUT 4
  3. Promotes use of fatty acid in reactions
  4. inhibits lipolysis
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10
Q

[proteins] insulin has 3 effects on protein

A
  1. promotes active transport of amino acids into muscles
  2. increases amino acid incoporation into protein
  3. inhibits protein degradation
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11
Q

main driver of release of insulin [insulin; physiology]

A

an increase in blood sugr

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12
Q

5 steps of insulin release in the cell [insulin; cellular release]

A
  1. glucose enters b-cell via GLUT 2 facilitated diffusion
  2. glucose is metabolised to G-6-P and then to ATP
  3. ATP:ADP ratio increases causing ATP-K sensitive channel to close
  4. reduced K exit depolarises cell and opens VGCC
  5. Ca enters b-cell and stimulates release of insulin
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13
Q

insulin is produced as a polymer with what other protein [insulin]

A

C-peptide
*this can be measured in T1 diabetics to monitior the decrease in insulin production however may take 3-4 years to disappear so is not a reliable indicator

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14
Q

what is the physiological difficulty with diabetes mellitus? [DM; physiology]

A

An inability to produce any or sufficient endogenous insulin

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15
Q

Why do complications occur in DM? [DM; physiology]

A

As a result of high blood sugar as insulin is the only hormone able to reduce BG

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16
Q

Criteria for diagnosis from a random BG [DM; diagnosis]

A

> 11.1 mmol/L with symptoms OR

7.8 - 11 mmol/L on two occassions with symptoms

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17
Q

Criteria for diagnosis from 2hr OGTT [DM; diagnosis]

A

> 11.1mmol/L and above

7.8-11 is pre-diabetes

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18
Q

Criteria for diagnosis from FG [DM; diagnosis]

A

> 7.0mmol/L

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19
Q

Criteria for diagnosis from HbA1c [DM; diagnosis]

A

48 mmol/L and above

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20
Q

Three forms of microvascular complications [DM; complications]

A

Retinopathy, neuropathy, nephropathy

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21
Q

Process underlying retinopathy [DM; Complications]

A
  1. formations of microaneurysms in the eye.

2. proteins cause the BM of the eye to become thickened and more permeabel –> fibrous response –> destroys the retina

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22
Q

Process underlying nephropathy [DM; Complications]

A

Vascular disease in the kidney leads to kidney failure

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23
Q

Process underlying neuropthy [DM; Complications]

A

PVD may affect the nerves causing a loss of sensation and higher chance of foot ulcers

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24
Q

Forms of macrovascular complications [DM; Complications]

A

MI, Stroke and CVD - need to tightly control blood pressure as all vascular disease is accelerated, 50-70% of diabetics die from CVD

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25
Q

Pathophysiology of T1DM [T1DM]

A

Autoimmune destruction of the pancreatic b-cells leading to inability to produce insulin and control blood sugar. Usually occurs in adolescence but can occur at any age

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26
Q

Genetics associated with T1DM [T1; Science]

A

90% of T1DM carry HLA DR3+DR4; those with a first degree relative with T1DM have a 5-6% chance of developing the disease

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27
Q

Autoantibodies associated with T1DM [T1; science]

A

ICA (islet cell antibodies) and GAD (anti-glutamic acid decarboxylase)

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28
Q

What is LADA? [T1; science]

A

A form of T1 that presents in adults but presents with a slower onset and slower progression to insulin dependence

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29
Q

Symptoms associated with T1 (5/9 for 5*) [T1; symptoms]

A

Polyuria; polydipsia; weight loss; tiredness; ketosis; thirst; thrush; many and persistent infections; blurred vision

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30
Q

Treatment of T1 [T1; Treatment]

A

Insulin regimes, DAFNE

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31
Q

Example of long acting insulin [T1; treatment]

A

lantus

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32
Q

Example of rapid acting insulin [T1; treatment]

A

novorapid

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33
Q

A finger prick before a meal informs the patient of the long/short acting dose? [T1; treatment]

A

A long acting dose is monitored before a meal

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34
Q

A finger prick after a meal informs the patient of the long/short acting dose? [T1; treatment]

A

A short acting dose is monitored after the meal

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35
Q

What sort of adjustment might be made to insulin when exercising for a short period and why? [T1; treatment; physiology]

A

Increased dose of insulin as a short burst of exercise will increase the amount of adrenalin produced. Adrenaline pushes BG up and thus more insulin is required to counteract this.

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36
Q

What sort of adjustment might be made to insulin when exercising for a longer period and why? [T1; treatment; physiology]

A

Decreased dose of insulin as the prolonged exercise will deplete BG availability and thus less insulin is required

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37
Q

What sort of adjustment might be made to insulin when feeling unwell and why? [T1; treatment; physiology]

A

More insulin is likely to be required especially if the patient is not eating or is vomiting and becoming dehydrated. This is because the stress hormone cortisol is produced in higher quantities and is likely to push BG up. Not controlling insulin properly when unwell is more likely to result in DKA

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38
Q

What is ketoacidosis? [T1; phsyiology]

A

ketoacidosis is an alternative pathway used in the starvation states in order to produce energy. It is less efficient and produces acetone as a by-product.

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39
Q

What is diabetic ketoacidosis? [T1; physiology; complications]

A

In T1DM, blood glucose may be high, glucose cannot enter the cells without insulin. Thus the cells act as if in starvation state and use the ketosis pathway to generate energy

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40
Q

Typical signs and symptoms of DKA [T1; complications; symptoms]

A
  1. Drowsiness
  2. Vomiting and dehydration
  3. Abdominal pain
  4. Kussmaul Breathing
41
Q

In which patients should you test BG? [Signs and symptoms; T1; complications]

A

Unexplained vomiting, abdominal pain, polyuria, polydipsia, lethargy, ketotic breath, dehydration, coma, anorexia, kussmaul breathing

42
Q

What is Kussmaul breathing? [T1; complications; signs and symptoms]

A

Deep, laboured hyperventilation

43
Q

What is the main driver of acidaemia in DKA? [T1; science]

A

beta-hydroxybutarate

44
Q

3 criteria for diagnosis of DKA [T1; diagnosis; complications]

A
  1. acidaemia
  2. hyperglycaemia
  3. ketonuria
45
Q

Investigations to order in suspected DKA + justification [T1; complications; diagnosis; investigations]

A
  1. ECG - cardiac cause
  2. CXR - pulmonary cause
  3. Urine dipstick - ketones, nitrates, leucocytes (infection)
  4. capillary and lab glucose - hyperglycaemia (lab more accurate)
  5. U&Es - monitor K+
  6. HCO3
  7. a-amylase - acute pancreatitis
  8. ABG/VBG - acidosis
  9. FBC
  10. Cultures - sepsis/infection
46
Q

Common complications of DKA [T1; complications]

A

Cerebral oedema (kids); aspiration pneumonia; hypokalaemia; hypomagnesia; hypophosphataemia; thromboembolism

47
Q

Treatment steps of DKA (4/6 for 5*) [T1; complications; treatment]

A
  1. 0.9% saline 500ml bolus (established IV access, may need to run more than one bolus)
  2. when BG <15mmol/L switch to dextrose
  3. contact senior help to start insulin regime (?0.1units/kg/hour?) 4. Start of LMWH heparin
  4. monitor ABG/VBG and K+
  5. continue fluids to rehydrate
    * *caution with replacing bicarbonate as may increase risk of cerebral oedema**
48
Q

Hypoglycaemia for any diabetic? [T1/T2; complications; diagnosis]

A

4mmol/L

49
Q

Complication of persistent Hypo’s [T1/2; complications]

A

those who have many hypos are less able to recognise them

50
Q

Risk factor for becoming hypo and why [T1; complications; physiology]

A

binge-drinking as the liver does not create any glycogen stores at this time

51
Q

Symptoms of hypos [T1/2; complications]

A

Usually rapid onset and may be preceeded by odd behaviour; sweating; tachycardia; seizures

52
Q

Treatment of a hypo in a patient who is able to swallow [T1/2; complications; treatment]

A

15-20g of glucotabs; 60ml glucojuice; 170ml lucozade or a sugary alterantive

53
Q

Treatment of a hypo in a patient who is concious but confused [T1/2; compliations; treatment]

A

1-2 tubes of glucogel

54
Q

Treatment of a hypo in the unconcious patient [T1/2; complications; treatment]

A

IV glucose (10-20g) or 200-300ml of dextrose. 1mg IM Glucagon (500mg in kids)

55
Q

Exceptions to use of IM Glucagon in hypos [T1/2; complications; treatment]

A

Patients who are frail, malnourished or have been drinking heavily

56
Q

Follow up to initial treatment of hypo [T1/2; complications; treatment]

A

Re-check BG after 15 minutes and repeat steps if still hypo. After recovery to normal BG, patient should have a snack of something including complex carbs and the insulin regime should be reviewed if necessary

57
Q

Pathophysiology behind T2DM [T2; physiology]

A

Decreased insulin secretion AND/OR increased insulin resistance

58
Q

Associations of T2DM [T2; epidemiology]

A

obesity, lack of exercise, calorific excess and alcohol excess

59
Q

Genetics associated with T2DM [T2; genetics]

A

strong genetic component; 80% concordance with twins

60
Q

Presentation of T2DM [T2; Signs and symptoms]

A

May be incidental finding or present similarly to T1

61
Q

What is metabolic syndrome? [T2; risk factors]

A

A syndrome including 3 of the following which puts an individual at significantly increased risk of CVD:
central obesity + BMI >30 + 2 of the following:
- BP >130/85
- Triglycerides >1.7 mmol/L
- HDL <1.03(M) or 1.29(F) mmol/L
- Fasting glucose >5.6 mmol/L

62
Q

Overview of treatment for T2DM [T2; treatment]

A

Diet and exercise advice; podiatry and opthalmology screening; realistic HbA1c targetting; pharmacy

63
Q

First line treatment in most T2 [T2; treatment]

A

Metformin

64
Q

Mechanism of action of Metformin [T2; treatment; physiology]

A

biguanide that increases insulin sensitivity and aids weightloss - not associated with hypos

65
Q

Dosing of metformin [T2; treatment]

A

500mg BD after food, may be increased to 1g BD

66
Q

Contraindications to metformin [T2; treatment]

A

Renal disease

67
Q

Side effects of metformin [T2; treatment]

A

nausea, diarrhoea, abdo pain

68
Q

Example sulphonylurea [T2; treatment]

A

Gliclazide

69
Q

Dose of Gliclazide [T2; treatment]

A

40mg OD

70
Q

Mechanism of action of SUs [T2; treatment; physiology]

A

increases insulin action by acting on the K-ATP channel

71
Q

Contraindications of SUs [T2; treatment]

A

Hepatic and renal impairement or if prone to hypos

72
Q

Side effects of SUs [T2; treatment]

A

hypoglycaemia and weight gain

73
Q

Example of a Glitazone [T2; treatment]

A

Pioglitazone

74
Q

Mechanism of action of glitazone [T2; treatment; physiology]

A

PPARy agonist - acting on lipoprotein lipase and GLUT 4, only used in combination with Metformin or SUs

75
Q

Contraindications of glitazone [T2; treatment]

A

hepatotoxicity, osteoporosis

76
Q

Side effects of glitazones [T2; treatment]

A

hepatotoxicity, fractures, weight gain, fluid retention

77
Q

Example of SGLT2 inhibitors [T2; treatment]

A

Dapagiflozin

78
Q

Mechanism of action of SGLT2 inhibitors [T2; treatment; physiology]

A

Act to selectively block the reabsorption of glucose by SGLT2 in PROXIMAL tubule causing glucosuria and calorific loss; very good for those who need to lose weight and little chance of Hypos

79
Q

Contraindications of SGLT2 inhibitors [T2; treatment]

A

avoid in those prone to UTIs

80
Q

Example of DPP4 inhibitors [T2; treatment]

A

Sitagliptin

81
Q

Mechanism of action of DPP4 inhibitors [T2; treatment, physiology]

A

inhibits the actions of DPP4 which inhibits GLP 1 however requires a certain number of b-cells to work

82
Q

Side effects of DPP4 inhibitors [T2; treatment]

A

nausea

83
Q

Examples of GLP-1 analogues [T2; treatment]

A

Exenatide

84
Q

Mechanism of action of GLP-1 analogues [T2; treatment, physiology]

A

binds to receptors that increase IC cAMP conc. and increase insulin secretion, decrease glucagon secretion and slows gastric emptying leading to a decreased appetite ***modest weight loss and reduces hepatic fat accumulation

85
Q

Administration of GLP-1 analogues [T2; treatment]

A

SC injection 2 x daily

86
Q

Side effects of GLP-1 analogues [T2; treatment]

A

nausea, hypos, protentially pancreatitis

87
Q

Example of a-glucosidase inhibitors [T2; treatment]

A

a-carbarose

88
Q

Mechanism of action of a-carbarose [T2; treatment]

A

inhibits breakdown of starch to sugar via inhibition of a brush border enzyme

89
Q

Side effects of a-carbarose [T2; treatment]

A

GI problems associated with excess glucose in intestine - not popular

90
Q

Hyperosmolar Hyperglycaemic Non-ketotic Coma (HONK) compared to DKA [T2; complications]

A

Frequently occurs in older and T2 patients; history is longer than for DKA and has marked dehydration and glucose >35mmol/L; acidosis is absent as there is no switch to ketone metabolism

91
Q

Signs and symptoms of HONK [T2; complications; signs and symptoms]

A
  1. hypovolaemia
  2. hyperglycaemia
  3. hyperosmolar >320mosmol/kg
    significant renal impairment is common
92
Q

Calculation for osmolarity [T2; complications; science]

A

2 x [Na+/-K] + urea + glucose

93
Q

2 x [Na+/-K] + urea + glucose [T2; complications; science]

A

Calculation for osmolarity

94
Q

Calculation for osmolarity [T2; complications; science]

A

2 x [Na+/-K] + urea + glucose

95
Q

2 x [Na+/-K] + urea + glucose [T2; complications; science]

A

Calculation for osmolarity

96
Q

Normal osmolarity range [T2; complications; science]

A

285-295 mosmol

97
Q

Medications that may predispose to HONK [T2; complications; causes]

A

steroids or diuretics

98
Q

Treatment steps (4/6 for 5*) in HONK [T2; complications; treatment]

A

Caution not to fluid overload

  1. 0.9% saline over 48 hours or 0.45% if fluctuating Na+
  2. add K+ when urine starts to flow
  3. care with insulin as may not need
  4. LMWH unless contraindicated
  5. screen for vascular events and sepsis as co-morbidities are likely
  6. keep BG slightly higher for first 24 hours to avoid cerebral oedema

Y2 Endocrine (4 decks)

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