Diabetes Introduction Lecture Flashcards

1
Q

What is diabetes?

A

Metabolic disorder characterised by chronic hyperglycaemia due to defects in insulin secretion and/or action

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2
Q

Normal fasting and 2h OGTT

A

Fasting <6.1 mmol/mol
OGTT <7.8 mmol/mol

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3
Q

Diabetes fasting glucose value

A

Value >7 mmol/mol

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4
Q

D

Diabetes OGTT 2hr value

A

Value ``>11.1 mmol/mol

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5
Q

Impaired glucose tolerance values

A
  • Impaired Fasting glycaemia - 6.1 - 6.9
  • Impaired glucose tolerance - 7.8 - 11
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6
Q

Impaired fasting glucose value

A

5.5 - 6.9 mmol/mol

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7
Q

Different types of classifications of Diabetes

A
  • Type 1 (beta cell destruction, 5-10%)
  • Type 2 (insulin secretion defect, 90%)
  • Genetic defects of beta cell function - mitochondiral or neonatal diabetes
  • Genetic defects in insulin action
  • Disease of exocrine pancreas
  • Endocrinology problems
  • Infections - CMV, congenital rubella
  • Drugs
  • Syndrome - downs, klinefelter, turners
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8
Q

Genetic defects of insulin secretion

A
  • Lipodystrophy
  • Type 1 insulin resistance
  • anti-insulin receptor antibodies
  • Insulin signalling defects
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9
Q

Gold standard for diagnosing diabetes

A
  • 2hr OGTT
  • HbA1C
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10
Q

Value of HbA1C suggesting diabetes

A

48mmol/mol. (6.5%)

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11
Q

Causes of secondary diabetes

A
  • Pancreas problems - pancreatitis, cancer of pancreas
  • Medication - eg steroids, antipsychotics
  • Cushings
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12
Q

Type 1 diabetes vs type 2 age of onset

A

Type 1: 12 years old
Type 2: 60

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13
Q

Presentation of Type 1 diabetes vs type 2

A

Type 1 - osmotic symptoms eg polyuria, polydipsia, weight loss, DKA
Type 2 - Diabetic complications, or found on routine testing, hyperglycaemia symptoms

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14
Q

Cause of type 1 vs type 2

A

Type 1 - beta cell autoimmune destruction
Type 2 - beta cell dysfunction and insulin resistance

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15
Q

Type 1 vs type 2 treatment

A

Type 1 - insulin as insulin dependent
Type 2 - diet (obesity is often co-existing), oral hypoglycaemic agentsm insulin last

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16
Q

Complications of diabetes - macrovascular

A
  • TIA
  • Stroke
  • Angina
  • MI
  • Heart failure
  • Peripheral vascular disease
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17
Q

Complications of diabetes - microvascular

A
  • Retinopathy - non-proliferative, proliferative, macular oedema
  • Nephropathy - microalbuminuria, macroalbuminuria, end stage renal disease
  • Neuropathy - autonomic, peripheral
  • Osteomyelitis
  • Amputation
  • Erectile dysfunction
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18
Q

Non-proliferative retinopathy vs proliferative on fundoscopy

A

Non-proliferative - haemorrhageem aneurysm and hard exudate on fundoscopy
Proliferative - growrth of abnormal blood vessels

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19
Q

Classification of diabetic retinopathy

A
  • Background retinopathy - R1 - microaneurysms, dot haemorrhages, cottton wool spots and hard exudate
  • Pre-proliferative - R2 - multiple blots, venous bleeding, intraretinal microvascular abnormalities
  • Proliferative - R3 - retinal neovasculariation, retinal detachment, vitreous haemorrhage
  • M1 - maculopathy
  • O - other diabetic lesion
  • P - previous laser therapy/photocoagulation
  • U - unclassified often due to cataract
20
Q

When do immediate refer to opthalmologist?

A
  • Neovascular glaucoma/ rubeosis iridis (new vessels causing glaucoma or new vessels on iris)
  • Vitreous haemorrhage
  • Retinal detachment
21
Q

When to urgent refer to ophthalmologist (<2 weeks)?

A

R3 - proliferative retinopathy

22
Q

When to routine refer to opthalmologist (<13 weeks)?

A

R2 - preproliferative retinopathy
M1 changes

23
Q

Treatment for diabetic retinopathy - medical

A
  • Gllycaemic control
  • BP control
  • Lipid control
  • Antiplatelets
  • Smoking cessation
24
Q

Treatment for diabetic retinopathy - surgical

A
  • Laser therapy
  • Vitrectomy
  • Intravitreal VEGF
25
Q

What is diabetic nephropathy?

A

Presence of proteinuria +ve on dipstick (albumin conc of 300mg/g over 24hrs or 200 mcg/min)

26
Q

Microalbuminuria value

A

30-300mg/g

27
Q

CKD classification values using eGFR

A
  • G1 (normal or high) - 90 or more
  • G2 (mild decrease) - 60-89
  • G3a (mild-moderate decrease) - 45-59
  • G3b (moderate to severe decrease) - 30-44
  • G4 - ( severe decrease) - 15-29
  • G5 (kidney failure) - <15
28
Q

CKD albuminuria values

A
  • A1 (normal-mild increase) - <30mg/g or <3mg/mmol
  • A2 (moderate increase) - 30-300mg/g or 3-30 mg/mmol
  • A3 (severely increased) - >300mg/g or >30mg/mmol
29
Q

What are the changes seen in microscopic kidney during nephropathy?

A
  • Early - kidney enlarged due to tubular hypertrophy and hyperplasia
  • 5 years - increased GBM and matrix accumulation
  • Glomerulosclerosis - diffuse
  • Nodular glomeruloscelrosis - Kimmelstiel-Wilson nodules
  • Tubulointersititial changes - nephron loss and direct disease
30
Q

Treatment for diabetic nephropathy

A
  • Glycaemic control
  • BP control - ACEi, ARBs for BP <130/80
  • Lipid control
  • Diet - protein <0.8g/kg
  • Manage anaemia, hyperPO4, hyperkalaemia, Vit D deficiency
31
Q

When to refer nephropathy to nephrologist?

A
  • CKD stage 4 or worse (15-29 eGFR)
  • Rapid decline eGFR (>5ml/min/1/73m2/year)
  • Microscopic/macroscopic haematuria
  • Systemic distease - SLE, Sjogrens syndrome
  • Uncontrolled BP despite 4 drugs
  • Proteinuria >1g/day or ACR >70mg/mmol
  • Suspected renal artery stenosis
  • FH of genetic disorder eg PCKD
32
Q

Cause of diabetic neuropathy

A
  • Distal axonal loss with focal demyelination and attempts at nerve regeneration
  • Changes to vasa nervorum - nutrients to nerve
  • = partial/complete loss of nerve function
33
Q

Classifications of neuropathy

A
  • Sensory-motor - acute/chronic, large fibre or small fibre, distal to proximal loss
  • Autonomic neuropathy - erectile dysfunction, gastroparesis, postural hypotension
  • Proximal motor neuropathy - loss of proximal, AKA diabetic amyotrophy, often in quads
  • Mononeuropathy and entrapment neuropathy eg carpal tunnel syndrome/ulnar nerve/lat popliteal
34
Q

Treatment for neuropathy

A

Treat the pain - start on SNRI eg duloxetine and then maybe add opioids/anticonvulsant like pregabalin

Cau use:
* Anticonvulsant - eg pregabalin
* SNRI - eg duloxetine
* TCA - eg amitryptyline
* Opioid - eg morphine

35
Q

Treatment for autonomic neuropathies

A
  • Treat symptom eg postural hypotension - steroid like fludrocortisone
  • Sildenafil for ED
36
Q

Consequences of gastroparesis and treatment

A
  • Vomitting
  • Flatulence
  • Constipation
  • Bloating
    Due to not enough force
    Treat with metoclopramide/stomach pacemaker
37
Q

Diabetic foot examination steps

A
  • Inspect - colour, ulcers, hair loss
  • Between toes - inspect for small ulcers
  • Palpate - assess each side comparing temp
  • Capillary refill and pulses (dorsalis pedis and posterior tibial, popliteal fossa if possible)
  • Sensation - test on clavicle, then to crude touch (cotton), fine touch (monofilament needs to BEND), pain (sharp), vibration and proprioception
  • If loss vibration on toe, move to malleolus, tibia and then anerior spine of hip
  • Ankle reflex
  • Gait
  • Assess shoes
38
Q

Two types of diabetic foot

A
  • Neuropathic feet
  • Ischaemic feet
39
Q

Features of neuropathic diabetic foot

A
  • Warm
  • Dry skin
  • Palpable pulses
  • Not painful
  • Callus present
40
Q

Features of ischaemic diabetic foot

A
  • Cold/cool
  • Atrophic/hairless
  • No palpable pulses
  • Tender/painful
  • Claudication/rest pain
  • Skin blanches on elevation and reddens on dependency
41
Q

Grading system used for diabetic foot

A

Wangers classfication
0 - high risk, no ulcers
1- superficial ulcer, no infection
2 - deep ulcer, no abscess/bone involved
3 - deep ulcer, abscess or bone involved
4 - localised gangrene
5 - gangrene of whole foot

42
Q

What causes Charcot foot?

A
  • Increased blood flow due to loss of sympathetic nerves
  • Osteoclast activty then increases and increased bone turnover
43
Q

X-ray signs Charcot foot

A
  • Osteolysis and joint subluxation/dislocation
  • Consider MRI/bone scan
44
Q

Treatment for Charcot foot

A

Immobilise 2-3 months

45
Q

Appearance of charcto foot

A

Tarsal-metatarsal region or MTP joints involved
Warm/hot, swollen and often painful
If untreated - ‘rocker bottom’ deformity or medical convexity

46
Q

UK prevalance of type 1 vs type 2

A

Type 1 - 0.25%
Type 2 - 5-7%