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Year 3 OSCE > Case 5- Diabetes Mellitus > Flashcards

Case 5- Diabetes Mellitus Flashcards

1
Q

Causes of DM

A

Steroids
Pancreatitis
Pancreatic surgery
Acromegaly
Pregnancy

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2
Q

Metformin

A

Increased insulin sensitivity
Decreases hepatic gluconeogenesis

GI disturbance (if intolerable, the MR version can be trialled)
Lactic acidosis
Contraindicated in reduced eGFR (below 30)
Stop in MI (due to lactic acidosis)

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3
Q

Pioglitazone (Thiazolidineione)

A

Activate PPARgamma receptors in adipocytes to promote adipogenesis and fatty acid uptake and reduce peripheral insulin resistance

Weight gain
Fluid retention (contraindicated HF)
Bladder cancer
Liver impairment
Increase fracture risk

NB- rarely Used second line

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4
Q

Sulfonylurea (glicazide/glimperide)

A

Stimulate pancreatic beta cells to secrete insulin

Weight gain (apetite)
Hypoglycaemia
Hyponatraemia (due to SIADH)
Hepatotoxicity (cholestasis)
Increased risk of CVD when used as a mono therapy

Avoid in breast feeding and pregnancy
Overdose- hyperinsulinaemia and increased C peptide levels

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5
Q

DPP4 Inhibitor (sitagliptin)

A

Increases incretins (inhibits breakdown) which inhibit glucagon secretion

GI disturbance
Pancreatitis

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6
Q

GLP 1 Mimetics (liraglutide/ exenatide)

A

Incretin mimetic which inhibits glucagon secretion

GI disturbance
Weight loss
Pancreatitis

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7
Q

SGLT 2 Inhibitors (empaglifozin)

A

Inhibits glucose resorption in kidney (proximal convoluted tubule SGLT2 transporter), increases urinary glucose

Glucose excreted in urine- UTI
Reduced risk of CVD
Weight loss
DKA
Necrotising fasciitis if the genitalia or perineum eg. Fourniers gangrene
Increased risk of lower limb amputation

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8
Q

Meglitinides SE

A

Hypoglycaemia
Weight gain

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9
Q

DM blood glucose ranges

A

Random >11.1
OGTT >11.1
Fasting >7
HbA1c >48

NB- OGTT: don’t eat for 8-12 hours prior

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10
Q

HbA1C Targets

A

48 if on one medication
53 if one 2 or more/ hypo risk drug monotherapy/ elderly at risk of fall
If above 58- step up management
If above 80- need insulin

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11
Q

Symptoms of hypoglycaemia

A

Autonomic- tremor, pallor, anxiety, tachycardia, palpitations, hunger, nausea and vomiting

Neuroglycopenic- agitation, confusion, behavioural changes, seizures, somnolence

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12
Q

Hyperglycaemia symptoms

A

Polyuria, polydipsia, n & v, volume depletion signs, altered mental status, lethargy, coma, blurred vision, weakness

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13
Q

Diabetes Mellitus type 1 Sx

A

Typical hyperglycaemia Sx eg. Polyuria

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14
Q

Diabetes type 2 investigations and management

A

Finger prick BM
Urine- ketones and glucosuria
Bloods- HBA1c, OGTT, plasma ketones, fasting blood glucose, UE (diabetic nephropathy)
Tests for complications- fundoscopy and diabetic foot exam

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15
Q

DKA and HHS Investigations

A

Urinalysis- ketones
Bloods- FBC, ketones, UE (K will be normal but it is extra cellular so need to replace to make it intra cellular), ABG (metabolic acidosis, resp compensation), blood cultures, BM
ECG and CXR

Needs acidaemia, ketonaemia, hyperglycaemia

Replace potassium!

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16
Q

C peptide levels

A

Indicate amount of endogenous insulin being produced- very low levels indicative of type 1

NB- GAD autoantibodies serve as a marker for autoimmune diabetes in adults

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17
Q

HHS vs DKA

A

No ketones or acidaemia in HHS, and history is usually longer (glucose often more than 35 in DKA)

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18
Q

Diabetic foot exam

A

Compare one foot to another (inspection and all other steps)

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19
Q

Statins

A

QRISK greater than 10% (and no known heart disease) for type 2 diabetics or T1DM or CKD if eGFR less than 60, offer 20mg OD atorvastatin

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20
Q

Diabetes type 2 management

A

Lifestyle modifications- diet, exercise, weight loss, smoking cessation, statin and ACE-I (ARB if Afro Caribbean)
Monitoring for complications

Drug therapy- as per the 2 diagrams on passmedicine

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21
Q

Normal blood glucose ranges

A

Random <7.8
OGTT <7.8
Fasting 4-6.0
HBA1c <42

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22
Q

Hall marks of DKA

A

Acidaemia
Ketonaemia
Hyperglycaemia

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23
Q

Hallmarks of HHS

A

Hyperglycaemia
Hyper osmolarity
Volume depletion
NO KETOSIS

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24
Q

Diagnose DKA

A

pH <7.3 (or bicarbonate <15)
Ketones >3 or more than 2+ on dipstick
BM >11 or known diabetic

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25
Q

Diagnose HHS

A

Glucose >11
Osmolarity >320
Absence of significant ketosis

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26
Q

Management of HHS

A

IV fluids
IV Insulin (sometimes not even needed)
Stop metformin for 2 days
Prophylactic LMWH

NB- continue long acting insulin but stop other forms

27
Q

Management of DKA

A

IV fluids (0.9% saline/isotonic)
IV insulin (0.1unit/kg/hour)- 5% dextrose when glucose starts dropping below 15
Potassium replacement (after first saline bag)- if potassium is within 3.5-5.5
Treat cause

NB- continue long acting insulin but stop other forms

28
Q

Impaired glucose tolerance (pre diabetes) ranges

A

Random 7.8-11.1
OGTT 7.8-11.1
Fasting 6.1-7.0
HBA1c 42-47

29
Q

Investigations for type 1 DM

A

Finger prick BM
Urine- ketones and glucosuria
Bloods- OGTT, plasma ketones, fasting blood glucose, UE (diabetic nephropathy), c peptide (low), diabetes specific autoantibodies
Tests for complications- fundosdopy and diabetic foot exam

NB- HbA1c isn’t helpful in T1DM

30
Q

Diagnosing between T1DM and T2DM

A

See gallery

For those in whom there is a doubt, C-peptide levels (low in T1DM) and diabetes-specific autoantibodies are the investigations of choice (positive in T1DM)

31
Q

Diagnosing type 1 diabetes

A

Fasting greater than 7 or Radom glucose/ OGTT greater than 11.1
If patient is asymptomatic, above criteria must be demonstrated on 2 separate occasions

32
Q

Diagnosing type 2 diabetes

A

Fasting greater than 7, Radom glucose/ OGTT greater than 11.1, HBA1c measurement of 48 or greater
If patient is asymptomatic, above criteria must be demonstrated on 2 separate occasions (even HBA1c)

33
Q

What is type 1 DM

A

Autoimmune disorder where insulin producing beta cells of islet of langerhans in pancreas are destroyed by immune system

34
Q

What is type 2 DM

A

Relative deficiency of insulin due to an excess of adipose tissue

35
Q

Maturity onset diabetes of the young (MODY)

A

A group of inherited genetic disorders affecting the production of insulin
Young patients with symptoms similar to T2DM eg. Asymptomatic hyperglycaemia
Autosomal dominant condition

36
Q

Latent autoimmune diabetes of adults (LADA)

A

A small group of patients who develop autoimmune diabetes later in life (check c peptide and diabetes as often misdiagnosed as T2DM)

37
Q

Side effects of insulin therapy

A

Hypoglycaemia (tell patients about symptoms, 10-20g of short acting carb, glucagon kit at home)
Weight gain
Lipodystrophy (rotate injection site, causes erratic insulin absorption)

38
Q

Management of T1DM

A

Monitor HBA1c every 3-6 months
Self monitor blood glucose 4 times a day (before each meal and before bed- more if unwell, during and after sport, should be 5-7 on waking and 4-7 at other times of day)
Insulin

39
Q

Hypertension and type 2 diabetes

A

Blood pressure targets are the same as those without diabetes
ACE-I is preferred except in Afro-Caribbean patients where ARB is first line

40
Q

Ramadan and diabetes

A

Eat a long acting carbohydrate meal prior to sunrise
Patients should have access to BM monitoring
Some changes with metformin and glicazide (sulfonylureas)

41
Q

Diabetes Mellitus sick day rules

A

Increase frequency of blood glucose monitoring (should be able to access urinary ketone monitoring too)
Increase fluid intake (3 litres in 24 hours)
Drink sugary drinks if can’t eat
Continue taking oral hypoglycaemics (don’t take metformin in dehydration)
Don’t stop insulin

NB- low threshold of admitting these patients eg. Persistent vomiting, no one at home in case they are unconscious, persistently high BM’s

42
Q

Features of DKA

A

Abdominal pain
Polyuria, polydipsia, dehydration
Deep hyperventilation (Kussmaul breathing)
Acetone breath (pear drops)

43
Q

Resolution of DKA

A

Ketonaemia and acidosis should resolve within 24 hours
If labs suggest it has resolved and patient is eating and drinking normally, revert to insulin regime

44
Q

Complications of DKA

A

VTE
Arrhythmia
Gastric stasis
ARDS
AKI
Cerebral oedema (children)- headache, irritability, visual disturbance, focal neurology (usually 4-12 hours post treatment)

45
Q

Management of diabetic neuropathy

A

Optimise glycaemic control
Amitriptyline, duloxetine, gabapentin, or pregabalin (if one doesn’t work, try another one)
Tramadol for exacerbations
Topical capsaicin
Pain management clinics if persistent

46
Q

Gastrointestinal autonomic neuropathy

A

Gastroporesis- Erratic blood glucose control, bloating, vomiting
Chronic diarrhoea
GORD

47
Q

DVLA and diabetes

A

Diet controlled- no need to inform
If on tablets- no need to inform
If on sulfonylurea (glicazide) or hypo causing tablet, mustn’t have had more than 1 episode of hypoglycaemia requiring the assistance of another on the preceding 12 months
If on insulin- tell DVLA, need hypoglycaemic awareness, no visual impairment, mustn’t have had more than 1 episode of hypoglycaemia requiring the assistance of another on the preceding 12 months

Drivers on insulin can have type 2 (HGV) license but need to follow standards above and do regular glucose monitoring (machine with a memory function), no complications of disease, there has not been any severe hypoglycaemic event in the previous 12 months

48
Q

Causes of a reduced HBA1c (reduced RBC life span)

A

Sickle cell anaemia
GP6D deficiency
Hereditary spherocytosis

NB- haemolysis/increased turnover

49
Q

Causes of an increased HBA1c

A

Iron deficiency anaemia
Vitamin B12 or folate deficiency
Splenectomy

NB- reduced turnover ie. less Fe/B12 to create new cells

50
Q

Insulinoma

A

Tumour derived from pancreatic islets of langerhans cells (endocrine tumour)

Weight gain, high insulin, hypoglycaemia, high c peptide
Symptoms and signs of hypoglycemia
Plasma glucose < 2.5 mmol/L
Reversibility of symptoms on the administration of glucose

Diagnose- prolonged fasting (72 hours), CT pancreas
Management- surgery or diazoxide/somatostatin

NB- C-peptide production does NOT fall on exogenous insulin injection in patients with an insulinoma (it does with self-administration of insulin)

51
Q

Kallman’s syndrome

A

Delayed puberty secondary to hypogonadotropic hypogonadism (x Linked recessive)
Usually anosmia in a boy with delayed puberty

Other features- cryptorchidism, hypogonadism, low sex hormone levels, LH and FSH levels are low/normal, normal or above average height

May also have cleft lip/palate and visual/hearing defects

52
Q

Management of hypoglycaemia

A

Unconscious- 150ml 10% glucose IV or glucagon 1mg IM

Conscious can’t swallow- 2 tubes glucose gel around teeth

Conscious can swallow- 15-30g fast acting carbs eg. 5-7 glucose tabs or 150ml fruit juice, and long acting carbs eg, biscuit, toast

53
Q

Estimate serum osmolarity

A

2 x Na+ + glucose + urea

54
Q

In newly diagnosed adults with type 1 diabetes, what is the first-line insulin regime

A

basal–bolus using twice‑daily insulin detemir

55
Q

Causes of hypoglycaemia

A

Diabetics;

Insulin or sulfonylurea treatment with an increase in activity or a missed meal or non-accidental overdose.

Non-diabetics (EXPLAIN);

Exogenous drugs such alcohol, aspirin poisoning, pentamidine, quinine sulfate, ACE-inhibitor
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours eg insulinoma
Non-pancreatic neoplasms

56
Q

Causes of hypoglycaemia

A

Diabetics;

Insulin or sulfonylurea treatment with an increase in activity or a missed meal or non-accidental overdose.

Non-diabetics (EXPLAIN);

Exogenous drugs such alcohol, aspirin poisoning, pentamidine, quinine sulfate, ACE-inhibitor
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours eg insulinoma
Non-pancreatic neoplasms

57
Q

Impaired fasting glucose and impaired glucose tolerance

A

NB- 2 different things

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

58
Q

Thiazides and glucose tolerance

A

Thiazides worsen glucose tolerance (and predispose to digoxin toxicity)

59
Q

Diabetic medications and elective surgery

A

Omit agents that can precipitate hypoglycaemia ie. glicazide (but continue others ie. metformin)

60
Q

Diabetic medications and elective surgery

A

Omit agents that can precipitate hypoglycaemia ie. glicazide (but continue others ie. metformin)

61
Q

Conditions where HBA1c cannot be used for diagnosing diabetes

A

haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)

62
Q

T1DM and BMI 25+

A

NICE recommend considering adding metformin if the BMI >= 25 kg/m²

63
Q

Metformin and surgery

A

OD or BD: take as normal
TDS: miss lunchtime dose
assumes only one meal will be missed during surgery, eGFR > 60 and no contrast during procedure

64
Q

Adding and sglt2 inhibitor

A

add even if diabetes is well controlled ie. hba1c is <48

Year 3 OSCE (61 decks)

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