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Gen Med > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the pathophysiology behind T1DM

A

Autoimmune destruction of beta cells in the pancreas which causes an absolute deficiency of insulin

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2
Q

How does type 1 DM present

A

Shorter history

  • Weight loss - unable to use glucose for energy so use fat and muscle instead
  • Polydipsia - incresed thirst due to lots of urine produced
  • Polyuria - glucose lost in urine
  • tiredness
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3
Q

Which infections are more common in diabetics and why

A

Thrush and UTIs

Due to high sugar environment easier for bacteria to multiply

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4
Q

What is LADA

A

Latent autoimmune diabetes of adults

Form of T1DM with slower progression to insulin dependence

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5
Q

What are the glucose targets for T1DM patients

A

5-7mmol/L on waking

4-7mmol/L before meals and at other times of the day

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6
Q

How many times do T1DM patients need to monitor their insulin a day

A

4x a day including before each meal and before bed

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7
Q

How is DM diagnosed

A

Random blood glucose >11mmol/L
fasting glucose >7mmol/L
Oral glucose tolerance tests 2hrs later after 75g of glucose 2x venous gluose >11mmol/L
HbA1c >6.5% (>48mmol/L)

1 positive test result and symptomatic
or 2 positive test results and asymptomatic

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8
Q

Which HbA1c results suggest prediabetes

A

42-47mmol/L

5.7-6.4%

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9
Q

What is the pathophysiology behind T2DM

A

Normal or increased insulin secretion but relative insulin resistance
Resistance due to increased blood glucose levels so muscle and adipose tissue stop taking up glucose if oversaturated
Increased insulin production so increased absorption of glucose in cells (already overaturated)
therefore exhaustion of beta cells

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10
Q

How might T2dm present

A 
Polydipsia
Polyuria 
Hx of blurred vision
Itchiness 
Peripheral neuropathy 
Recurrent thrush/UTIs 
Fatigue
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11
Q

How is T2DM managed

A

Diet and exercise to decrease insulin resistance
If HbA1c 6.5% (48mmol/L)
oral hypoglycaemics - metformin 1st line

1st intensification HbA1c (7.5%) 
Metformin + DPP4 i e.g. sitagliptin 
Metformin + pioglitazone 
Metformin + sulfonylurea e.g. gliclazide 
Metformin + SGLT 2 inhibitor

Aim for a HbA1c of 7.0%

2nd intensification
Triple therapy on insulin based therapy
HbA1c therapy >7.5%

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12
Q

When are rapid acting insulins used

A

Taken before a meal used with long acting insulins e.g. Novorapid

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13
Q

When are short acting insulins used

A

30mins before meal e.g. Actrapid

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14
Q

When are intermediate acting insulins used

A

covers blood glucose when rapid stops working. Works for about 7hours
given at bedtme to cover night time
Patients should be aware of the risk of becomig hypoglycaemic

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15
Q

When are long acting insulins used

A 
Given at bedtime to cover overnight 
Combined with rapid and short acting 
Taken OD or BD 
e,g. Levemir 
Glargine
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16
Q

What are the BM targets whilst on insulin therapy

A

Fasting 5-7mmol/L

before meals 4-7mmol/L

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17
Q

What is the MOA of metformin

A

Increases insulin sensitivity

Decrease hepatic gluconeogenesis

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18
Q

What are the side effects of metformin

A

GI upset - nausea, diarrhoea

Lactic acidosis

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19
Q

Which patients cannot take metformin

A

Patients with an eGFR of <30ml/min

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20
Q

What is the MOA of sulfonylureas

A

Stimulates beta cells to secrete insulin

  • Glicazide
  • Glimepinide
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21
Q

What are the side effects of Sulfonylureas

A

Hypoglycaemia
Weight gain
Hyponatraemia

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22
Q

What is the MOA of pioglitazone

A

Activates PPAR gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

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23
Q

What are the side effects of pioglitazone

A

Weight gain

Fluid retention

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24
Q

What is the MOA of DPP4 inhibitors (gliptins)

A

Increases incretin levels which inhibit glucagon secretion e.g. sitagliptin

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25
Q

What are the side effects of gliptins

A

increased risk of pancreatitis

however generally well tolerated

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26
Q

What is the MOA of SGLT-2 inhibitors (-gliflozins)

A

Inhibits reabsorption of glucose in the kidney e.g Dapagliflozin

27
Q

What are the side effects of SGLT-2 inhibitors

A

UTIs

Typically result in weight loss

28
Q

What is the MOA of GLP-1 agonists

A

Incretin mimetic which inhibits glucagon secretion e.g. Exenatide
Given via SC

29
Q

What are the side effects of GLP-1 agonists

A

Nausea and vomiting
Pancreatitis
typically result in weight loss

30
Q

What is the MOA of insulin

A

Direct replacement for endogenous insulin

31
Q

What are the side effects of insulin

A

Hypoglycaemia
Weight gain
Lipodystrophy

32
Q

What is given if Metformin is not tolerated or contraindicated e.g. eGFR <30ml

A

Gliptin
Sulfonylurea
Pioglitazone

33
Q

When is insulin therapy considered in T2DM

A

Considered when the HbA1c reaches 7.5% and drug therapy is not controlling blood glucose (after first intensification)

34
Q

Which drug should be continued when insulin therapy is started and why

A

Metformin because it reduces insulin resistance, reduces hyperinsulinaemia and counteracts weight gain

35
Q

What is the target BP for diabetics

A

140/80 for diabetics with no end organ damage

130/80 for end organ damage

36
Q

What are the microvascular complications of Diabetes

A

Neuropathy
Nephropathy
Retinopathy
Cardiomyopathy

37
Q

What is the pathophysiology of diabetic neuropathy

A

Less blood flow to nerves due to narrowing of blood vessels due to damage of walls becuase high glucose content of blood

38
Q

How may diabetic neuropathy present

A

Stock and glove distribution - same as b12

Absent ankle relfexes

39
Q

How does diabetic nephropathy present

A

Proteinuria - turbid, frothy urine
Oedema - decreased serum protein
Increased BP

40
Q

How is diabetic nephropathy treated

A

first line is ACE inhibitors

41
Q

How might diabetic retinopathy present

A

Floating spots in vision
blurred vision
sudden loss of vision

42
Q

What would fundoscopy show in diabetic retinopathy

A 
Cotton wool spots 
microaneurysms 
haemorrhages 
new vessel formation  
papilloedema
43
Q

What are the macrovascular changes in Diabetes

A

Peripheral vascular disease - ulcers
Atherosclerosis
Coronary heart disease
Stroke/TIA - statins given

44
Q

What is acanthosis nigricans

A

Dark velvety patches - sign of insulin resistance in obesity, diabetes, in cushings, hypothyroidism, PCOS

45
Q

What are secondary causes of hyperglycemia

A

Drugs - steroids, beta blockers, adrenaline, thiazides, some antipsychotics
Acute stress events - stroke, MI, sepsis, encephalitis
endocrine dysfunction - pancreatic disease and pancreatitis - CF
Thyroid, adrenal or pituitary dysfunction
Endocrine tumours - increased production of GH, glucocorticoids, catecholamines, glucagon, somatostatin

46
Q

Why do diabetics get foot ulcers

A

Loss of sensation therefore cannot feel damage to feet so will continue to walk on them
There will also be reduced circulation to the feet decreasing the healing
More likely to become infected because of high glucose in blood - better environment for organisms to grow

47
Q

Which staging system is used for diabetic ulcers

A

Wagners
Grade 1: superficial
Grade 2: involves ligament, tendon, joint capsule or fascia - no abscess or osetomyelitis
Grade 3: deep ulcer with abscess or osteomyelitis
Grade 4: gangrene to portion of mid foot
Grade 5: extensive gangrene of foot

48
Q

If an ulcer involves ligaments, tendons or the joint capsule which grade on the wagners classification is it?

A

Grade 2 - no abscess or osteomyelitis

49
Q

How are diabetic foot ulcers treated

A

Prevention: remove dead skin regularly and keep foot clean to prevent infection
Abx therapy
Grade 1: mild - flucloxacillin QDS or Doxycycline OD 2 weeks
Grade 2/3: moderate - flucloxacllin 1g QDS + Ciprofloxacin 500mg BD 2 weeks
Systemic toxicity: Severe - In patient IV Tazocin + Vancomycin + Vascular surgery referral

50
Q

How is osteomyelitis treated in diabetic foot ulcers

A

If confined to one bone, hole can be drilled into it and filled with abx cement

51
Q

How can neuropathy be tested for in diabetic foot disease

A

Using a 10g monofilament on various parts of the foot

52
Q

How would you investigate diabetic foot disease

A 
Check foot pulses 
ABPI - may be higher than 1 due to calcification of arteries. may also be reduced due to peripheral arterial disease 
X ray foot - signs of osteomyelitis and charcots arthopathy 
measure depth of ulcer
note which structures are affected 
Sensation of foot using monofilament 
Temperature of foot 
Check BP
53
Q

What is charcots arthropathy

A

Microtrauma and peripheral neuropathy - fractures and progressive destruction and damage to bones and joints e.g. ankle
Reduced autonomic nervous system
Less vasoconstriction
Increased blood flow to the bones
Increase osteoclast activity and reabsorption of the bone
Weakens bone

54
Q

How may charcots arthropathy present

A

Warmer than other foot
Red, swollen and oedematous
Pain and soreness of foot - less than expected due to diabetic neuropathy
Normally unilateral

55
Q

How is charcots arthropathy diagnosed

A

Xray and MRI

56
Q

What are the signs of charcots arthropathy on X ray

A 
Distended joint 
Disorganisation 
Destruction 
Dislocation 
Increased density 
Production of debris
57
Q

How is charcots arthropathy treated

A

Immobilise - prevent further destruction

  • full contact cast
  • walking brace
58
Q

What is the definition of hypoglycaemia

A

Plasma glucose of <3mmol/L

59
Q

What are the symptoms of hypoglycaemia

A

Autonomic

  • sweating
  • tremour
  • Anxiety
  • hunger
  • Palpitations
  • dizziness

Neuroglycopenic

  • confusion
  • drowsiness
  • visual trouble
  • seizures
  • coma
60
Q

When might post prandial hypoglycaemia occur

A

After gastric or bypass surgery (dumping syndrome - surge in insulin production)
and in t2dm
will have a prolonged OGTT

61
Q

How would you investigate hypoglycaemia

A 
Bedside Obs - BM, urine dip 
Bloods 
- FBC 
- blood glucose 
- U+Es 
- LFTs
- CRP
- TFTs
62
Q

What are the causes of hypoglycaemia

A

In diabetics

  • insulin
  • sulfonylureas
    e. g. increased activity, missed meal, accidental/non-accidental OD
Non diabetic EXPLAIN 
Exogenous drugs e.g. insulin, oral hypoglycaemics, alcohol binge with no food, aspirin poisoning, ACE inhibitors 
Pituitary insufficiency 
Liver failure
Addisons disease
Islet cell tumour
Non-pancreatic neoplasm
63
Q

What are the risk factors for developing diabetes

A 
Obesity 
Acromegaly
Steroid use - long term 
Lack of exercise 
Calorie/alcohol excess 
Cushing's
Pancreatic surgery/pancreatitis 
CF
haemochromatosis

Gen Med (10 decks)

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