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Life Maintenance > Diabetes Complications > Flashcards

Diabetes Complications Flashcards

1
Q

What are the Sx of peripheral Arterial disease?

A

asymptomatic

claudication (leg cramping relieved at rest)
leg pain at rest
ulceration
gangrene

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2
Q

What is an abnormal ABPI?

A

ABPI = anke-brachial-pressure index)
ABPI < 0.9 suggests arterial disease
ABPI < 0.5 suggests severe arterial disease

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3
Q

What are the general complications of DM?

A
  • metabolic (acute vs chronic)

- vascular

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4
Q

What acute metabolic complications can be used by DM?

A
  • DKA

- hyperosmolar hyperglycaemic state (HHS)

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5
Q

Why does DKA occur in T1DM?

A

Complete deficiency in insulin production (no suppression of ketosis generating ketone bodies)

Compensatory hormones released (GCG, catecholamines, GH)

Acidosis results from ketone bodies

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6
Q

What is the pathophysiology in DKA that results in the Sx?

A

insulin deficiency -> ketosis -> acidosis

insulin deficiency -> hyperglycaemia -> osmotic diuresis -> dehydration

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7
Q

Which electrolytes are depleted/lost through osmotic diuresis in DKA?

A
  • (water)
  • Na+
  • total K+ (ICF+ECF)
  • Cl-
  • Ca2+
  • PO4
  • Mg2+
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8
Q

What are the preliminary (resuscitation) steps in Mx of DKA?

Step 1 in Mx

A
  • insert 2x IV cannula (large bore) for fluid resuscitation
  • FBCs, U&Es, BM, lactate, VBG and blood culture
  • urinalysis, ECG, CXR, urine culture (also check for other infective sources)
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9
Q

What investigations should be performed in DKA?

A
  • BM
  • Glucose (venous blood test)
  • ketones
  • ABG
  • osmolality
  • MSU
  • blood cultures
  • ECG
  • amylase
  • CXR
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10
Q

How is DKA clinically managed?

A
  • sliding scale of insulin
  • fluid resuscitation
  • correct metabolic abnormalities

LOOK FOR AND Rx PRECIPITANTS

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11
Q

What fluid resuscitation steps should be taken for DKA?

Step 2 in Mx

A

NaCl saline 0.9% (without K+)
1L over 10-15 mins

NaCL 0.9% (without K+)
1L over 1hr

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12
Q

What clinical steps should be taken to correct the hyperglycaemia?

Step 3 in Mx

A
  • prescribe IV insulin at a fixed rate of 6 units/hr via infusion pump
  • if BM < 14mmol/L then infuse 10% glucose at 100ml/hr and 0.9% saline
    then reduce IV insulin rate to 3-5 units/hr
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13
Q

What is the on-going management for DKA?

A
  • Hourly MEWS and BM testing
  • hourly fluid balance
  • check electrolytes via VBG (especially K+)
  • Catheterise if oliguric
  • Adjust insulin so glucose is falling at rate of >3mmol/L until <14mmol/L
  • Then at BM <14mmol/L, infuse 10% glucose along with insulin at 6 units/hr
  • refer to DM team for early input
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14
Q

What is the hyperosmolar hyperglycaemic state?

A

HHS

= marked hyerglycaemia (>30mmol/L) without significant ketosis or acidosis
There is usually dehydration with some reduced consciousness (GCS)

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15
Q

How is HHS defined clinically?

A

hyperglycaemia, BM > 30mmol/L

plasma osmolality > 320 mOsm/L

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16
Q

What is the epidemiology of HHS?

A
  1. 83/1000 in total population

- higher in Afro-Carribean population

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17
Q

What are the presenting/clinical Sx of HHS?

A
  • elderly
  • confused
  • vomiting
  • dehydration
  • pyrexia
  • focal neurology
  • COMA
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18
Q

What is the Mx for HHS?

A

similar to DKA

  • Be more cautious with fluid replacement
  • give less insulin
  • MUST use prophylactic heparin
  • low threshold for central venous line insertion
  • maintain glucose, such that is doesn’t change >10mmol/L/24hr
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19
Q

How may insulin delivery change post-HHS?

A

may need to switch to subcutaneous (SC) insulin for 2 months post-HHS

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20
Q

What are the chronic complications of DM?

A

MICROVASCULAR

  • nephropathy
  • retinopathy
  • neuropathy

MACROVASCULAR

  • CHD/CVA
  • peripheral vascular disease
  • hypertension
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21
Q

What is the pathophysiology for vascular complications in DM?

A
  • leakage of PAS POSITIVE glycated proteins
  • increase in ECM
  • hypertrophy and hyperplasia of endothelium
  • acute reversible alterations in metabolism
  • cumulative irreversible change in proteins and nucleic acids
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22
Q

How can chronic uncontrolled hyperglycaemia result in cellular damage?

A

MITOCHONDRIAL OVERPRODUCTION OF ROS

stimulated PARPs in nucleus (increased DNA damage)

suppression of GAPDH and other proteins

Also creates NAD+ excess, which is damaging

results in activation of NF-kB proteins and cellular stress and death

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23
Q

How are glycation products made in DM?

A

non-enzyme linked reaction

excess of glucose in blood will eventually attach to the plasma proteins (e.g. Hb) over time

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24
Q

What are the cellular consequences of glycan product accumulation?

A

REDUCED
myo-inositol synthesis (signalling molecule, PI3K)

INCREASED

  • vascular permeability
  • vasoactive hormone production
  • basement membrane synthesis
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25
Q

What are the main mechanisms by which DM increases risk of CHD?

A
  • vasoconstriction (by endothelin etc, causing hypertension)
  • inflammation (e.g. IL-1 and ICAM-1)
  • Thrombosis (Tissue factor etc) causes hyper coagulation and platelet activation
26
Q

What is the relationship between HbA1c control and DM complications?

A

T1DM: early good HbA1c linked to long term benefit

27
Q

What are the main uncontrollable risk factors for microvascular complications?

A
  • disease duration
  • gender
  • age
  • ethnicity
  • T1DM
  • pregnancy
  • genetic factors
28
Q

What are the types of diabetic retinopathy?

A 
Type 1
rare: <5 years of DM
incidence peaks at 15-20yr of DM
severe + proliferative 
(incidence increases for DM <20yr)

Type 2
can be present at Dx
increased risk of macular oedema

29
Q

What are the risk factors for diabetic retinopathy?

A
  • poor glycaemic control
  • genetic factors
  • high BP
  • smoking
30
Q

What are the main sub-types of diabetic retinopathy?

A
  • non-proliferative

- proliferative

31
Q

What are the main types of non-proliferative diabetic retinopathy?

A
  • without maculopathy
  • with maculopathy

(i.e. macular oedema)

32
Q

In non-proliferative diabetic retinopathy, what are the clinical signs of increased retinal vascular permeability?

A
  • dot and blot retinal hemes
  • micro-aneurysms
  • retinal oedema (usually around macula)
  • exudates with micro-aneurysms
33
Q

What are the main features of non-proliferative diabetic retinopathy?

A
  • increased retinal vascular permeability
  • venous beading (= ischaemia, seen as saccular bulges in endothelium)
  • intra-retinal microvascular abnormalities
  • severe retinal haemorrhage and micro-aneurysms
34
Q

What is the pathophysiology of PROLIFERATIVE diabetic retinopathy?

A

new vessels arise from venous side of circulation

at junction between perfused and ischaemic areas

proliferation is unusual and will have branching pattern with loops

new vessels can be drawn forward by retinal detachment

35
Q

How is maculopathy imaged?

A

Digital retinal photograph

36
Q

What is type 1 diabetic nephropathy?

A
  • associated with duration of DM
  • M>F
  • higher incidence in patients who develop DM before 15yo
37
Q

What are the risk factors for type 1 nephropathy?

A
  • age at DM onset
  • poor glycemic control
  • genetic factors
  • high BP
  • smoking
38
Q

What is the epidemiology of diabetic nephropathy?

A

leading cause of end stage renal failure in UK

25-45% in T1DM
20-30% in T2DM

39
Q

What are the 3 methods by which you can screen for microalbuminuria?

A
  • albumin:creatinine ratio (random spot collection)
  • 24hr urine collection with creatinine (eGFR)
  • timed collection (4h or overnight)
40
Q

What are the advantaged of using the albumin:creatinine ratio to assess microalbuminuria?

A
  • eliminates dilution effect

- more sensitive

41
Q

What is a big risk factor and clinical indicator of diabetic nephropathy?

A

microalbuminuria

42
Q

what are the clinical stages in diabetic nephropathy?

A
  • normoalbuminuria
  • hyperfilturation
  • micralbuminuria
  • macroalbuminuria
  • azotemia/renal failure
  • end stage renal disease (ESRD)
43
Q

What are the modifiable risk factors for renal disease progression in DM?

A
  • hypertension
  • albuminuria
  • Dyslipidemia
  • HbA1c
  • Anaemia
  • Ca-PO4
44
Q

What are the non-modifiable risk factors for renal disease progression in DM?

A
  • age
  • gender
  • ethnicity
45
Q

What are the main ways diabetic nephropathy can be prevented/treated?

A
  • tight glycemic control
  • BP control
  • ACEi
  • low protein diet
  • lipid control
46
Q

What are the different types of diabetic neuropathy?

A
  • peripheral sensory
  • acute painful neuropathy
  • diabetic amyotrophy
  • diffuse motor neuropathy
  • focal neuropathy (e.g. carpel tunnel)
  • autonomic neuropathy
47
Q

How may diabetic peripheral neuropathy present?

A
  • decreased sensation
  • parasthesia
  • decreased motor function
  • pain
  • decreased perception of joint position (e.g. Charcot joint)
48
Q

What is Charcot joint?

A

aka neuropathic joint of Charcot

destructive joint disorder in patients with abnormal pain sensation and proprioception
Bony destruction and ulcers are often present

49
Q

What is (diabetic) autonomic neuropathy?

A

damage to nerves supplying major organs

rare complication in DM

Sx: dizziness (hypotension), vomiting (delayed gastric emptying), sweating whilst eating, bladder dysfunction etc

50
Q

What are the macrovascular complications of DM?

A
  • ischaemic heart disease
  • cerebrovascular disease
  • peripheral vascular disease
51
Q

What are the main risk factors for microvascular disease?

A
  • hypertension
  • dyslipidaemia
  • smoking
  • FHx
  • hyperglycaemia
  • ins resistance
52
Q

What is peripheral vascular disease?

A
  • affects lower extremity
  • gangrene
  • claudication

results from tissue ischaemia

53
Q

What is the classic dyslipidaemia profile in T2DM/IR?

A
  • low HDL
  • high VLDL
  • hypertriglyceridaemia
  • post-prandial hyperlipidaemia
  • elevated ApoB-100
  • polygenic hypercholesteraemia
54
Q

What are the HbA1c targets in T2DM?

A

General target: HbA1c = 6.5% or 48mmol/mol

For patients on drug with hypo risk, target is higher
HbA1c = 7.0%, 53mmol/mol

55
Q

When may the target HbA1c level be relaxed?

A
  • patients who are unlikely to achiever longer term risk reduction benefits
  • high risk of hypos
  • intensive Mx is not appropriate
56
Q

What is the nemonic use to summarise diabetic Mx?

A 
A: advice (smoking/exercise)
B: BP
C: cholesterol
D: diabetic control
E: eye care
F: foot care
G: guardian drugs
57
Q

What are GUARDIAN DRUGs in DM?

A

A guardian drug may be given in addition to your diabetes medicine, in order to decrease your risk of further diabetes complications

e.g. aspirin, ACEi, statins

58
Q

What is the Glasgow prognostic criteria?

A

= indicates severity of acute pancreatitis

The criteria are;
Age >55 years
WBC >15 x 109/L
Urea >16 mmol/L
Glucose >10 mmol/L
pO2 <8 kPa (60 mm Hg)
Albumin <32 g/L
Calcium <2 mmol/L
LDH >600 units/L
AST/ALT >200 units

Score > 3
severe pancreatitis likely

59
Q

What complication can be caused by insulin therapy applied to the same part of the abdomen? How can it be avoided?

A

lipodystrophy

  • typically presents as lumps of sc fat
  • can cause erratic insulin absorption
  • avoided by rotating injection sites
60
Q

What is gastroparesis?

A

possible complication of T2DM

  • autonomic neuropathy
  • causes delayed gastric emptying

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