Case 5 - Diabetes Flashcards

1
Q

What are the different types of diabetes?

A
  • Type 2
  • Type 1
  • MODY
  • LADA
  • Gestational
  • Drug induced (steroids, anti-psychotics)
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2
Q

What is MODY?

A

Maturity onset diabetes of the young – Genetic defects of beta cell function or insulin action.

  • Like T2DM but young
  • Strong FH
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3
Q

What is LADA?

A

Some insults causes pancreas to stop producing adequate insulin by damaging beta cells.
- Think of this in older patient with T1DM presentation or not responding to anti-hyperglycaemic agents.

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4
Q

What is pre-diabetes?

A

Blood glucose levels are higher than normal but not high enough to be called diabetes.

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5
Q

What is type 1 diabetes?

A

Result of an autoimmune response that triggers the destruction of β cells in the pancreas and results in an absolute insulin deficiency.

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6
Q

What are the causes of type 1 diabetes?

A
  • Genetic
  • Autoimmune response with production of antibodies
  • Viral: enterovirus
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7
Q

What anti bodies are associated with T1DM?

A
  • ICA: Islet cell antibodies

- GAD: Glutamic acid decarboxylase

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8
Q

When is T1DM presented?

A

Childhood onset <20 years

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9
Q

What are the risk factors of diabetes?

A
  • Black/Hispanic/Native -
  • America/ South Asian origin are 6x more likely to develop diabetes – non-modifiable
  • Family history of diabetes – non-modifiable
  • High waist to hip ratio – modifiable
  • Older age – non-modifiable
  • Hypertension
  • Dyslipidaemia
  • Physical inactivity – modifiable
  • Dyslipidaemia
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10
Q

What are the symptoms of T1DM and T2DM?

A
  • Polyuria - Glucosuria leads to polyuria in diabetic patients;
  • Polydipsia – due to excessive thirst
  • Polyphagia – increase in appetite
  • Fatigue
  • Visual disturbances – blurred vision
  • Calf cramps
  • Poor wound healing
  • Pruritus – due to poor circulation, dry skin or yeast infection
  • Candida infections
  • Weight loss: T1DM
  • Weight gain: T2DM
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11
Q

What is type 2 diabetes?

A
  • Insulin resistance and pancreatic β cell dysfunction resulting in relative insulin deficiency.
  • Over time insulin sensitivity goes down leading to increased blood glucose.
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12
Q

How to diagnose diabetes?

A
  • HBA1c
  • OGTT
  • C peptides
  • Fasting plasma glucose
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13
Q

What is fasting glucose test?

A
  • Test after min 8 hours fast

- DM: ≥ 126 mg/dL (≥ 7.0)

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14
Q

C-peptide test results

A
  • Increased: T2DM

- Decreased: T1DM

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15
Q

What is oral glucose tolerance test?

A
  • Give 75g oral glucose, wait 2 hours.
  • Given to fasting patient.
  • DM: ≥ 200 mg/dL (≥ 11.1)
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16
Q

What are the normal levels for the different diabetes test?

A
  • HBA1c: <42mmol/mol
  • Fasting glucose: < 100 mg/dL (< 5.6)
  • OGTT: < 140 mg/dL (< 7.8)
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17
Q

What specific tests are done for T1DM?

A
  • Anti-GAD

- ICS antibody

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18
Q

What is the treatment for T1DM?

A

Life long insulin

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19
Q

What is the conservative management for diabetes?

A
  • Weight loss (T2)
  • Increased physical activity
  • Balanced diet (reduced carbohydrate intake)
  • Smoking cessation
  • Reduced hypertension
  • High fibre diet
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20
Q

How are complications monitored?

A
  • Yearly retinal screening
  • Foot exam for ulcers + neuropathy
  • Annual urine testing for kidney function
  • Weight/BP/lipids
  • Education on complications
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21
Q

What are the different types of insulin?

A
  • Rapid-acting (10min-4h) - Novorapid
  • Short-acting (30min-8h) - Actrapid
  • Intermediate-acting (1h-16h) - Insulatard
  • Long-acting (1h-24h) - Lantus
  • Combination (intermediate: rapid-acting) - Humalog 25 (25:75), Humalog 50 (50:50), Novomix 30 (30:70)
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22
Q

What is T2DM anti-hyperglycaemic therapy algorithm?

A

1st - General measures
2nd - Metformin
3rd - Metformin + another drug
4th - Metformin + 2 other drugs OR metformin + insulin

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23
Q

Which DM meds work by increasing insulin sensitivity?

A
  • Metformin

- Pioglitazone

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24
Q

Which DM meds work by increasing insulin secretion?

A
  • DPP4 inhibitors (gliptin)
  • GLP1 agonists (glutide)
  • Meglitinides (glinide)
  • Sulfonylurea (zide)
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25
Q

Which DM med works by increasing renal excretion of glucose?

A

SGLT2 inhibitors (flozin)

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26
Q

Which DM meds increase weight?

A
  • Sulfonylurea
  • Insulin
  • Pioglitazone
27
Q

Which DM meds reduce weight?

A
  • GLP1 agonists

- SGLT2 inhibitors

28
Q

Which DM meds have the highest risk of hypoglycaemia?

A
  • Insulin

- Sulfonylurea

29
Q

What type of drug is metformin?

A
  • Biguanide
  • Increases insulin sensitivity
  • Decreases hepatic glucose production
30
Q

What are the side effects of metformin?

A
  • Diarrhoea
  • Abdominal discomfort
  • Lactic acidosis (don’t prescribe if they have impaired renal function, eGFR <36)
31
Q

What type of drug is glicazide?

A
  • Sulfonylurea

- Stimulates insulin release

32
Q

What are the side effects of sulfonylurea?

A
  • Weight gain

- Hypoglycaemia

33
Q

What type of drug is sitagliptin?

A
  • DPP4 inhibitors (incretin)

- Increase insulin secretion

34
Q

What are the side effects of DPP4 inhibitors?

A
  • GI disturbances
  • URTI symptoms
  • Pancreatitis
35
Q

What type of drug is liraglutide?

A
  • GLP1 agonist

- Increase insulin secretion

36
Q

What are the side effects of GLP1 agonists?

A
  • GI disturbances
  • Weight loss
  • Dizziness
37
Q

What type of drug is empagliflozin?

A
  • SGLT2 inhibitors

- Stops glucose reabsorption

38
Q

What are the side effects of SGLT2 inhibitors?

A
  • Weight loss

- Glucosuria (risk of UTI)

39
Q

What are the acute complications of diabetes?

A
  • Hyperosmolar hyperglycaemic state
  • Diabetic ketoacidosis
  • Hypoglycaemia
40
Q

What are microvascular complications?

A
  • Retinopathy
  • Nephropathy
  • Neuropathy: peripheral and autonomic
41
Q

What are the macrovascular complications?

A
  • Stroke
  • MI
  • Peripheral vascular disease
  • Coronary heart disease
  • Diabetic cardiomyopathy
42
Q

How are eyes affected in retinopathy?

A
  • Loss of central vision: due to capillary leakage into retina causing intra-retinal haemorrhage. Seen as hard exudates
  • Total blindness: Retinal ischaemia leads to new but poor quality (non-functional) vessels forming. Occurs due to capillary occlusion.
43
Q

How to minimise blindness?

A
  • Blood glucose and BP control
  • Annual retinal screening
  • Vitrectomy
44
Q

How to minimise end stage kidney disease?

A
  • Bood glucose control
  • Early detection of nephropathy (albumin:creatnine)
  • BP control: ACEi
  • Dialysis + transplantation
45
Q

Which genes are associated with T1DM?

A

HLA D3/4

46
Q

What are neuropathic pain symptoms?

A

Burning, cold, tingling, stabbing, toothache, walking on glass, contact sensitivity, allodynia, numbness, restlessness, worse at night, eased by exercise or counter irritation.

47
Q

What is a neuropathic foot ulcer?

A

Loss of protective sensation and abnormal foot function (putting pressure in affected areas, making them worse).

48
Q

How is a neuropathic foot ulcer presented?

A
  • Callus present near metatarsal heads causing toes to be retracted
  • Blistering due to toes
49
Q

What are the features of Charcot neuropathy?

A

Pes cavus, claw toes, loss of transverse arch, rocker-bottom deformity

50
Q

How can diabetes in pregnancy affect foetus + mother?

A

1st trimester - congenital abnormalities

2nd/3rd trimester - accelerated growth and lead to cardiomypothay, difficult birth, neonatal mortality

51
Q

What is DKA?

A
  • Absolute insulin deficiency (T1DM)
  • Increased glucagon, catecholamine, cortisol and G: leading to excess glucose
  • Fats are broken down into ketones: leads to H+ release causing hyperventilation and CO2 retention. Causes metabolic acidosis.
52
Q

What are the potential triggers of DKA?

A
  • Infection
  • Lack of adherence to medication
  • Alcohol
  • Steroids
  • Injury/surgery
  • Pregnancy
  • Menstruation
  • Diabulemia
53
Q

What are the symptoms of DKA?

A
  • Gradual drowsiness
  • Vomiting
  • Dehydration
  • Abdominal pain - ketoacidosis leads to irritation of the peritoneum.
  • Polyuria/dipsia
  • Lethargy
  • Ketotic breath – fruity breath
  • Kussmasul breathing
54
Q

How to diagnose DKA?

A
  • Acidaemia: pH <7.3 or HCO3- <15mmol/L)
  • Hyperglycaemia: >11mmol/L or known DM
  • Ketonaemia: ≥3mmol/L or ketonuria ++ on dipstick
55
Q

How to investigate DKA?

A
  • Blood glucose
  • Ketone levels
  • pH, U+Es, HCO3-
  • Urine dip
56
Q

How to manage DKA?

A
  • Fluids: IV 0.9% saline with potassium
  • Add potassium to second bag onwards depending on serum K+
  • Insulin e.g. 0.1unit/kg/h fixed rate - Glucose when glucose <14mmol/L after insulin to prevent hypoglycaemia
57
Q

What is HHS?

A
  • Small amounts of insulin being secreted
  • Associated with T2DM: develops slowly (days to weeks)
  • Develops as a result of illness/dehydration
  • Don’t get ketosis or acidosis like you do in DKA
58
Q

What are the symptoms of HHS?

A
  • Polyuria
  • Polydipsia
  • Leg cramps
  • Nausea and vomiting
  • Neurological abnormalities
  • Altered mental status
  • Lethargy
  • Coma/ decreased conscious level
  • Dehydration
59
Q

How to treat HHS?

A
  • Rehydration
  • Prophylactic LMWH
  • Fixed rate insulin infusion
  • Monitor/replace K+
60
Q

What is the cause of hypoglycaemia?

A
  • In diabetics due to drugs

- Causes of blood glucose levels to reach <3.3 mmol/L (<60 mg/dL).

61
Q

What are the symptoms of hypoglycaemia?

A
  • Adrenergic (sweating, tremor, hunger) THEN

- Neruoglycopenia (blurred vsion, confusion, parasthesia)

62
Q

What is hypoglycaemia unawareness?

A

After several episodes or very low hypoglycaemia, body gets used to adrenergic symptoms and doesn’t display them.

63
Q

How to treat hypoglycaemia?

A
  • Able to Cooperate - 30ml Lucozade and 15 g slower acting carbohydrate
  • Unable to Cooperate but Conscious - 1.5/2 tubes of glucose gel onto buccal membrane
  • Comatose, Fitting - Glucagon (SC, IM, IV)