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Diabetes mellitus Flashcards

1
Q

normal blood glucose range

A

4.0 - 5.4 mmol/L (72 to 99 mg/dL) when fasting

Up to 7.8 mmol/L (140mg/dL) 2 hours after eating

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2
Q

secondary causes of DM

A

chronic pancreatitis
endocrine: acromegaly + Cushing’s syndrome
drug induced: thiazide diuretics + corticosteroids

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3
Q

principle organ of glucose homeostasis

A

liver

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4
Q

Aetiology/path of T1DM

A

AI destruction of pancreatic B cells
? genetic susceptibility + env triggers
autoantibodies against insulin + islet cell antigens

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5
Q

Aetiology/path T2DM

A 
Polygenic
Env factors (notably central obesity) trigger it in those genetically susceptible

B cell mass is 50% of normal at time of Dx
Hyperglycaemia is from decreased insulin secretion (that’s inappropriately low for the glucose level) + peripheral insulin resistance

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6
Q

Acute presentation

A

young, 2-6wk Hx of thirst, polyuria + weight loss

ketoacidosis

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7
Q

What stimulates thirst in acute presentation?

A

fluid + electrolyte loss

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8
Q

what causes weight loss in acuts presentation?

A

fluid depletion + breakdown of fat

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9
Q

cause of polyuria in acute presentation of DM?

A

osmotic diuresis from when blood glucose levels exceed renal tubular abortive capacity

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10
Q

subacute presentation

A

older patients

same as acute. additional features:

  • lethargy
  • visual problems
  • pruritus
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11
Q

Diagnostic investigations

A

Fasting plasma glucose > 7.0
Random plasma glucose > 11.1

1 lab value is diagnostic in a pt with hyperglycaemic symptoms

2 lab values needed if asymptomatic

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12
Q

What’s the glucose tolerance test used for?

A

mainly for epidemiological studies

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13
Q

Aims of the MDT approach to management

A
  1. good glycemic control
  2. weight loss
  3. aggressive Tx of hypertension + hyperlipidaemia
  4. regular checks of metabolic control
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14
Q

Dietary Tx T2DM

A

basically just a healthy diet

e. g.
- carb sources: high fibre, low glycaemic index
- Low fat dairy products & oily fish

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15
Q

Biguanide Tx for T2DM

+ SEs

A

(metformin) - reduces glucose production by the liver + sensitises target tissues to insulin

SEs: anorexia + diarrhoea

1st line & should be offered if HbA1c rises to 48mmol/mol (6.5%) on lifestyle interventions

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16
Q

Sulphonylureas for Tx of T2DM

A

promote insuline secretion

Glibenclamide. SEs: hypoglycaemia

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17
Q

What do incretins do? Tx of T2DM

A

mimic 2 pancreatic hormones (GIP + GLP-1) and promote insulin release after an oral glucose load

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18
Q

What is insulin treatment?

A

synthetic human insulin subcut injection in abd, thighs or upper arm.

must inform the DVLA if you’re on it

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19
Q

3 categories of insulin treatment

A
  1. short-acting (soluble) insulins: work within 30-60 mins. Last 4-6hrs.
  2. rapid-acting insulin analogues e.g. insulin aspart. Faster onset + shorter duration of action.
    - used for nocturnal hypoglycaemia
  3. longer-acting insulins: premixed with retarding agent (zinc or prolamine)
    - intermediate (12-24hrs)
    - long acting (24hrs+)
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20
Q

What would you start a young pt on?

What would the targets be?

A

Intermediate insulin, 30 mins before breakfast and evening meal

–> Honeymoon period

–> Multiple injection regimen

Glucose targets:
5-7 on waking
4-7 mol before meals at other times of day
4-10 after

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21
Q

complications of insulin therapy

A

hypoglycaemia
injection site: lipohypertrophy, local allergic reactions
insulin resistance
weight gain

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22
Q

how is metabolic control of diabetes measured at home?

A

finger prick

urine testing for glucose + ketones

23
Q

how is metabolic control of diabetes measures in hospital/clinic?

A

Glycated Hb (HbA1c)

  • produced by the attachment of glucose to Hb
24
Q

pathogenesis of diabetic ketoacidosis

A

uncontrolled catabolism associated with insulin deficiency

DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

25
how does DKA result in dehydration?
unrestrained increase in hepatic gluconeogenesis --> high circulating glucose levels --> osmotic diuresis --> dehydration
26
how does DKA result in metabolic acidosis?
peripheral lipolysis --> increase in circulating FFAs. Converted in the liver to acidic ketones --> metabolic acidosis
27
DKA clinical features
profound dehydration (H20 + electrolyte loss at kidneys, exacerbated by vomiting) sunken eyes, decreased tissue turgor, dry tongue, low BP Kussmaul's resp (deep hyperventilation) Ketone breath ('pear drops' smell) Abdo pain Polyuria, polydipsia, Some conscious disturbance
28
Diagnostic Ix DKA
- hyperglycaemia (>11mmol) / known DM - acidosis (pH <7.3) - bicarbonate <15 mmol/l - ketones >3 mmol/l or urine ketones ++ on dipstick U&E: urea and creatinine often raised from dehydration
29
Mx DKA
ABC ITU - replace fluid, electrolyte loss + insulin, restore acid-base balance over 24hrs - correction of hypokalaemia - LA insulin should be continued, SA insulin should be stopped Watch out for cerebral oedema
30
Hyperosmolar hyperglycaemic state
Life threatening | Marked hyperglycaemia, hyperosmolality + mild/NO ketones
31
Cause hyperosmolar hyperglycaemic state
uncontrolled T2DM | infection is most common precipitating cause (pneumonia)
32
Clinical features hyperosmolar hyperglycaemic state
insulin reduced but sufficient to inhibit ketoacidosis, glucose production is unrestrained Profound dehydration (secondary to osmotic diuresis) Neuro : decreased level of consciousness, headaches, papilloedema, weakness General : fatigue, lethargy, N&V Haematological: hyperviscosity (?> MI, stroke) CV : dehydration, hypotension, tachy
33
Mx hyperosmolar hyperglycaemic state
LMWH (as at risk of occlusive events from hyperosmolar state) Rehydrate slowly Replace K+ when urine starts to flow
34
Macrovascular complications of DM
Macrovascular: atherosclerotic risk
35
Microvascular complications DM
specific to diabetes - small vessels throughout body are affected - 3 danger sites: retina, renal glomerulus + nerve sheath
36
2 major forms of diabetic retinopathy
non-proliferative + proliferative absence or presence of abnormal neovascularization arising from the retina
37
Presentation maculopathy
macula oedema | perimacular hard exudates
38
How to treat new vessel formation + maculopathy?
laser photocoagulation of the retina
39
what accelerates development + progression of retinopathy?
poor glycemic control hypertension smoking
40
Diabetic nephropathies
secondary to glomerular disease | thickening of GBM + later, glomerulosclerosis
41
Whats the earliest clinical evidence of glomerular damage? And what does it progress to?
microalbuminuria --> albuminuria --> persistent proteinuria --> renal failure
42
Mx diabetic nephropathy
**BP control** ACE-i. 130/80
43
Ischeamic lesions (nephropathy)
arteriolar lesions with hypertrophy + hyalinisation of the vessels affect both afferent and efferent arterioles
44
What are isolated mononeuropathies the result of?
occlusion of vasa nervorum Vasa nervorum are small arteries that provide blood supply to peripheral nerves. These vessels supply blood to interior parts of nerves and their coverings.
45
what are more diffuse neuropathies the results of?
accumulation of fructose + sorbitol which disrupts the structure + function of the nerve
46
what is the most common diabetic neuropathy?
symmetrical mainly sensory neuropathy affects feet first unrecognised trauma --> ulceration neuropathic arthropathy - Charcot's joints learn foot care principles (as at risk of insensitive foot ulceration)
47
Acute painful neuropathy | and Tx
burning/crawling pains in lower limbs, worse at night tricyclic antidepressants carbamazepine - a benzodiazepine (anticonvulsant + analgesic)
48
What is the neuropathy that presents with painful wasting, often asymmetrical, of quads
diabetic amytrophy
49
presentation of autonomic neuropathy in cvs system (also effects GI, bladder and erections)
CVS: resting tachycardia, loss of sinus arrhythmia, postural hypotension, peripheral vasodilation, warm foot, bounding pulse
50
the diabetic foot
reduced sensation to vib, temp + pinprick thin skin, no hair, bluish, cooler, absent pulses infection, ischaemia + neuropathy all --> tissue necrosis
51
why are iinfections a complication of DM
DM impairs the function of polymorphonuclear leucocytes + confers increased risk of infection, particularly UT and skin
52
skin complications of DM
lipohypertrophy: avoid by varying injection site vitiligo: seem in DM and other organ-specific AI diseases
53
Pre-diabetes diagnosis
Fasting plasma glucose: 5;5mmol/L to 6.9 mmol/L HbA1c: 24 to 47 mmol/mol (6.0 to 6.4%)

Endocrinology (14 decks)

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