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PBL SEM 4 > diabetes complications and management of T1D > Flashcards

diabetes complications and management of T1D Flashcards

1
Q

what are micro vascular complications of diabetes?

A
  • diabetic retinopathy = leading cause of blindness in working-age adults
  • diabetic nephropathy = leading cause of end-stage renal disease
  • diabetic neuropathy = leading cause of non traumatic lower extremity amputations
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2
Q

what are macrovascular complications of diabetes?

A
  • stroke (2-4x increase in CV mortality and stroke)
  • heart disease
  • peripheral vascular disease
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3
Q

how is diabetic retinopathy classified?

A

RMP system

R = retinopathy
M = maculopathy
P = photocoagulation

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4
Q

summarise the R in the RMP system for diabetic retinopathy classification

A
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5
Q

summarise the M in the RMP system for diabetic retinopathy classification

A
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6
Q

summarise the P in the RMP system for diabetic retinopathy classification

A
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7
Q

what is responsible for our central vision, most of the colour vision and detailed vision?

A

macual

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8
Q

describe R3

A
  • new vessels on disc or elsewhere
  • fibrous proliferation on disc or elsewhere
  • haemorrhages - pre-retinal, vitreous
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9
Q

why do new vessels form in retinopathy (R3)?

A

due to ischaemia and secretion of growth factors

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10
Q

prevention of diabetic retinopathy

A
  • glycemic control
  • BP control
  • annual screening
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11
Q

treatment of diabetic retinopathy

A
  • photocoagulation
  • anti-VEGF therapy (anti-vascular endothelial growth factor injections) eg. Ranibizumab, Aflibercept
  • surgery to remove bleeding
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12
Q

what are the 4 most common forms of diabetic neuropathy?

A
  1. distal symmetrical sensorimotor polyneuropathy and small fibre neuropathy (lose sensation or develop pain distally)
  2. radiculopathies
  3. mononeuropathy - can affect cranial nerves - isolated nerve involvement
  4. autonomic neuropathy - internal organs affected
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13
Q

signs of peripheral neuropathy

A
  • PAIN : burning, parasthesia , persistent hyperaesthesia, nocturnal exacerbation
  • LOSS OF SENSATION : autonomic neuropathy — postural hypertension, diabetic gastroparesis, small bowel bacterial overgrowth, cardiac autonomic neuropathy, urogenital
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14
Q

neuropathy treatment

A

often hard to treat

  • 1st line agents for pain = duloxetine, pregabalin, gabapentin, amitriptyline
  • gastroparesis = prokinetics (eg. domperidone, metoclopramide), botox to pylorus (facilitates gastric emptying), gastric pacemakers
  • postural hypertension = fludocortisone, midodrine, compression stockings
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15
Q

what is a diabetic foot due to?

A

neuropathy and ischaemia (peripheral vascular disease)

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16
Q

where do ischaemic uclers tend to be?

A

in extremities

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17
Q

foot complications in diabetes prevelance

A
  • 20-40% have neuropathy
  • 5% have a foot ulcer
  • 5-7% 10 year cumulative incidence of amputation
  • increased morbidity, mortality and reduced QoL
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18
Q

how are foot uclers prevented?

A
  • education
  • good glucose control
  • regular foot checks to identify high risk feet
  • regular podiatry review of high risk feet
  • appropriate footwear
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19
Q

how are foot uclers treated?

A
  • food MDT
  • off-loading, debridement
  • antibiotics to treat infection
  • surgery
  • revascularisaton
20
Q

what is the commonest cause of renal failure?

A

diabetes

21
Q

what % of T1DM + T2DM patients develop diabetic nephropathy?

A

30% of t1d and 40% of t2d

22
Q

what is diabetic nephropathy often associated with?

A

retinopathy

23
Q

what is the first sign of diabetic kidney disease?

A

small amounts of albumin in urine

24
Q

what are the values of moderately increased albuminuria: increased albumin creatinine ration (ACR) for men and women?

A

men : ACR >_ 2.5 mg/mmol
women : ACR >_ 3.5 mg/mmol

or urinary albumin conc >_ 20mg/L in men and women

25
Q

ACR and urinary albumin conc in nephropathy?

A
26
Q

relationship between ACR and GFR and risk of adverse outcomes

A
27
Q

how it diabetic nephropathy treated?

A
  • BP control
  • RAS blockage eg. ACEI, ARB (eg. drugs like ramipril, irbesartan)
  • glycemic control
  • CVD risk management
  • management of the complications of renal failure
  • dialysis in end stage renal disease — haemodialysis, peritoneal
  • renal, pancreas and islet transplantation
28
Q

why are CHD symptoms in diabetics an unrelated guide to CHD severity and total ischaemic burden?

A

autonomic neuropathy, altered pain perception, possibly increased positive arterial remodelling

29
Q

what is the 1st presentation of CHD in DM in 50%?

A

angina

sudden death more common in DM

30
Q

target SBP?

A

130

31
Q

what is the most common and feared adverse effect of insulin therapy?

A

hypoglycaemia

32
Q

what does hypoglycaemia result from in diabetics?

A

absolute or relative hyperinsulinaemia and / or defective glucose counter regulation

33
Q

what are the key defences against hypoglycaemia?

A

adrenaline and symptoms

34
Q

what is lost when glucose levels drop in t1d?

A

inhibition of insulin, glucagon secretion, adrenaline, symptoms

35
Q

what can severe hypoglycaemia cause?

A

coma, seizures, strokes, arrhythmias and even death

36
Q

what are acute implications of hypoglycaemia?

A
  • negative effects on mood and emotions
  • impairs cognitive function; can affect performance of many activities
  • interference with balance, coordination, vision and level of consciousness can precipitate falls and injury
37
Q

what are the long term effects of hypoglycaemia?

A
  • fear of hypoglycaemia, elevated HbA1c —> complications
  • reduced QoL
  • weight gain
  • restrictions on employment
  • driving licensing restrictions
  • personal relationships disrupted
  • acquired hypoglycaemia-induced syndromes
  • cognitive decline (if recurrent hypos happen)
38
Q

how does t1d pose a big burden on the individual?

A
  • require life long insulin therapy
  • impose a heavy burden o the individual, family and healthcare systems
  • current treatment multiple daily injections or insulin pump therapy - requires multiple finger-stick measurements, carbohydrate counting and dynamic dose adjustments
  • many have poor control, glycaemic variability frustrates many; depression, anxiety and reduced QoL very common
  • impaired awareness of hypoglycaemia (IAH) affects 20-40% of T1DM, severe hypoglycaemia (SH) affects p to 30% of individuals with T1D
39
Q

what factors affect blood glucose?

A
40
Q

what factors contribute to high HvA1c sub-optimal diabetes (T1DM)?

A
  • fear and burden of hypoglycaemia
  • lack of access/non-engagement with high quality structured education (self-management skills)
  • burden of carbohydrate counting, injections, time and life, work pressures
  • depression, anxiety and lack of motivation
  • not monitoring glucose
  • variable insulin absoprtion and problems with insulin injection sites
  • lack of access to technology/HCP
  • clinical inertia
  • lack of access to insulin (global perspective)
41
Q

what are common analogue insulins used in T1D?

A
  • rapid-acting analogues (meal insulin) eg. novorapid, humalog, apidra
  • ultra-rapid acting analogue (meal insulin) - fiasp
  • long-acting insulins (16 to 24 hours) - levemir, lantus
  • ultra ling acting insulins (24+) - tresiba, toujeo
42
Q

what is an analogue insulin?

A

laboratory grown genetically modified sequence

43
Q

what is the current technology in type 1 diabetes?

A
44
Q

what is the target range for type 1 and 2 diabetes?

A

70-180 mg/dl = 3.9-10.0 mmol/L

45
Q

what is the HbA1c target for most adults?

A

<7% (<53mmol/mol)

46
Q

target SBP?

A

130mmHg for most adults, <130mmHg if tolerated, but not <120

PBL SEM 4 (50 decks)

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