Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Diabetes mellitus > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

secondary causes of DM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

principle organ of glucose homeostasis

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aetiology/path of T1DM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acute presentation

A

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

ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What stimulates thirst in acute presentation?

A

fluid + electrolyte loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes weight loss in acuts presentation?

A

fluid depletion + breakdown of fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cause of polyuria in acute presentation of DM?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

subacute presentation

A

older patients

same as acute. additional features:

  • lethargy
  • visual problems
  • pruritus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What’s the glucose tolerance test used for?

A

mainly for epidemiological studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sulphonylureas for Tx of T2DM

A

promote insuline secretion

Glibenclamide. SEs: hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

complications of insulin therapy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

how does DKA result in dehydration?

A

unrestrained increase in hepatic gluconeogenesis –> high circulating glucose levels –> osmotic diuresis –> dehydration

26
Q

how does DKA result in metabolic acidosis?

A

peripheral lipolysis –> increase in circulating FFAs. Converted in the liver to acidic ketones –> metabolic acidosis

27
Q

DKA clinical features

A

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
Q

Diagnostic Ix DKA

A
  • 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
Q

Mx DKA

A

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
Q

Hyperosmolar hyperglycaemic state

A

Life threatening

Marked hyperglycaemia, hyperosmolality + mild/NO ketones

31
Q

Cause hyperosmolar hyperglycaemic state

A

uncontrolled T2DM

infection is most common precipitating cause (pneumonia)

32
Q

Clinical features hyperosmolar hyperglycaemic state

A

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
Q

Mx hyperosmolar hyperglycaemic state

A

LMWH (as at risk of occlusive events from hyperosmolar state)

Rehydrate slowly

Replace K+ when urine starts to flow

34
Q

Macrovascular complications of DM

A

Macrovascular: atherosclerotic risk

35
Q

Microvascular complications DM

A

specific to diabetes

  • small vessels throughout body are affected
  • 3 danger sites: retina, renal glomerulus + nerve sheath
36
Q

2 major forms of diabetic retinopathy

A

non-proliferative + proliferative

absence or presence of abnormal neovascularization arising from the retina

37
Q

Presentation maculopathy

A

macula oedema

perimacular hard exudates

38
Q

How to treat new vessel formation + maculopathy?

A

laser photocoagulation of the retina

39
Q

what accelerates development + progression of retinopathy?

A

poor glycemic control
hypertension
smoking

40
Q

Diabetic nephropathies

A

secondary to glomerular disease

thickening of GBM + later, glomerulosclerosis

41
Q

Whats the earliest clinical evidence of glomerular damage?

And what does it progress to?

A

microalbuminuria –> albuminuria –> persistent proteinuria –> renal failure

42
Q

Mx diabetic nephropathy

A

BP control ACE-i. 130/80

43
Q

Ischeamic lesions (nephropathy)

A

arteriolar lesions with hypertrophy + hyalinisation of the vessels affect both afferent and efferent arterioles

44
Q

What are isolated mononeuropathies the result of?

A

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
Q

what are more diffuse neuropathies the results of?

A

accumulation of fructose + sorbitol which disrupts the structure + function of the nerve

46
Q

what is the most common diabetic neuropathy?

A

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
Q

Acute painful neuropathy

and Tx

A

burning/crawling pains in lower limbs, worse at night

tricyclic antidepressants
carbamazepine - a benzodiazepine (anticonvulsant + analgesic)

48
Q

What is the neuropathy that presents with painful wasting, often asymmetrical, of quads

A

diabetic amytrophy

49
Q

presentation of autonomic neuropathy in cvs system (also effects GI, bladder and erections)

A

CVS: resting tachycardia, loss of sinus arrhythmia, postural hypotension, peripheral vasodilation, warm foot, bounding pulse

50
Q

the diabetic foot

A

reduced sensation to vib, temp + pinprick

thin skin, no hair, bluish, cooler, absent pulses

infection, ischaemia + neuropathy all –> tissue necrosis

51
Q

why are iinfections a complication of DM

A

DM impairs the function of polymorphonuclear leucocytes + confers increased risk of infection, particularly UT and skin

52
Q

skin complications of DM

A

lipohypertrophy: avoid by varying injection site
vitiligo: seem in DM and other organ-specific AI diseases

53
Q

Pre-diabetes diagnosis

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions