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ENDOCRINE > A. ACUTE AND SECONDARY COMPLICATIONS OF DIABETES > Flashcards

A. ACUTE AND SECONDARY COMPLICATIONS OF DIABETES Flashcards

1
Q

what are the 3 acute complications of diabetes

A
  1. hypoglycaemia (hypo) - T1DM and T2DM
  2. diabetic ketoacidosis (DKA) - T1DM
  3. hyperosmolar hyperglycaemia state (HHS) - T2DM
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2
Q

at what blood glucose level does hypoglycaemia occur

A

<4 mmol/L
(symptoms present at 3 mmol/L)

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3
Q

how might a type 1 diabetic get hypoglycaemia

A
  • insulin overdose
  • excessive exercise
  • inadequate CHO intake
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4
Q

how might a type 2 diabetic get hypoglycaemia

A
  • sulphonylureas as they stimulate insulin release (elderly)
  • hepatic or renal disease (don’t reabsorb glucose well)
  • some drugs (beta-blockers, diuretics and steroids)
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5
Q

side effects of hypoglycaemia

A

palpitations
tremors
sweating
anxiety

dizziness
hunger
irritability
headache
tingly lips

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6
Q

how does the body act to hypoglycaemia

A

counter-regulatory activity of SNS in order to increase glucose levels

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7
Q

what is neuroglycopenia/neuroglucopenia

A

glucose deficiency in brain

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8
Q

symptoms of neuroglycopenia

A

loss of concentration
slurred speech
behaviour mood changes
seizures
loss of consciousness

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9
Q

treatment of hypoglycaemia if conscious

A
  • sugary drink/food which is absorbed quickly
  • Glucogel: ie 40% dextrose (D-glucose) gel
  • 10-15 minutes for recovery then a snack (biscuit/bread) for sustained carbohydrates
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10
Q

treatment of hypoglycaemia if unconscious

A
  • IV glucose
  • IV/IM/SC glucagon but not after alcohol as works on liver
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11
Q

what is diabetic ketoacidosis (DKA)

A
  • diabetic coma
  • more likely in poorly-cotrolled T1DM
  • medical emergency
  • 10-20% mortality rate
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12
Q

what induces diabetic ketoacidosis (DKA)

A
  • hyperglycaemia and metabolic acidosis (ketosis) due to lots of ketones
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13
Q

what is DKA caused by

A
  • omission or reduction in insulin dose (inhibits ketogenesis and lowers blood glucose)
  • illness/infection
  • emotional upset
  • menstruation/pregnancy ketosis
  • rare syndromes of insulin resistance

*stress uses insulin more quickly

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14
Q

consequences of loss of insulin action

A

Liver:
- gluconeogenesis
- glycogen breakdown

Muscle:
- protein breakdown to amino acids

Adipose tissues:
- lipolysis to fatty acids and glycerol

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15
Q

what happens with the breakdown products: fatty acids, glycerol, amino acids

A

intermediates for gluconeogenesis
- lots of glucose produced
- lots of ketones produced

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16
Q

consequences of the increase in glucose

A

osmotic diuresis
- frequent passing of urine
- dehydration
- thirst as:
plasma glucose leads to filtered load (water taken with it) > renal absorption for glucose so get glycosuria

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17
Q

consequences of the ketone bodies

A

metabolic acidosis
- nausea, vomiting (due to change in pH)
- breathlessness (ventilation to change acid-base balance)
- abdominal pain

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18
Q

severe consequences of metabolic acidosis

A
  • CNS depression
  • diabetic coma
  • death
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19
Q

severe consequences of dehydration (low blood volume)

A
  • decreased peripheral circulatory volume:
  • renal failure
  • low cerebral blood flow
  • death
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20
Q

treatment of DKA

A
  • hospital
  • replacement of fluids, electrolytes (NaCl saline, KCl, glucose 10%)
  • IV infusion of insulin (suppress ketogenesis, reduce blood glucose, correct electrolyte imbalance)
  • treat cause
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21
Q

what is HHS

A
  • severe hyperglycaemia without ketosis (>40mmol/L)
  • managed as DKA but less insulin patients can still make insulin
22
Q

how to monitor blood glucose in primary care

A
  • HbA1c measurements every 3 months
23
Q

how to self-monitor blood glucose

A
  • capillary blood glucose testing (glucose meter and test strips)
  • continuous glucose monitoring:
    a) real time - all the Time
    b) flash - measures glucose in interstitial fluid

there is a time lag compared to direct blood glucose monitoring due to I.F being measured

24
Q

long term (chronic) microvascular complications of DM

A
  • retinopathy
  • nephropathy
  • neuropathy

specific to DM

25
Q

long term (chronic) macrovascular complications of DM

A
  • CVD (IHD)
  • cerebral vascular disease (stroke)
  • peripheral vascular disease

(accelerated atherosclerosis associated with DM)

26
Q

how do microvascular complications occur

A

damage of small vessels (capillaries) by hyperglycaemia (eg - sorbitol) and glycation of proteins - leads to advanced glycated end products

27
Q

how many patients get retinopathy after 20 years of DM

A

95%

28
Q

classification of retinopathy - background

A
  • microaneurysm (tiny areas of swelling in the blood vessels)
  • haemorrhages
  • exudates
29
Q

classification of retinopathy - pre-proliferative

A
  • bleeding into the retina
  • ‘cotton-wool spots’ indicates regions of ischaemia (blurring of vision)
30
Q

classification of retinopathy - proliferative

A
  • new blood vessels and scar tissue have formed on retina
  • new blood vessels can easily rupture
  • which can cause significant bleeding
  • can lead to retinal detachment, where the retina pulls away from the back of the eye
  • vitreous haemorrhage: reoccurrence common, 30% of eyes are blind within one year of first bleed
  • impairment of vision: floaters, clouding or loss of vision
31
Q

classification of retinopathy - maculopathy (retinal retraction)

A
  • blood vessels in macula (centre of eye involved in sharp vision) become leaky or blocked
  • retina can heal but there is severe scarring
  • scar tissue can peel away from back of eye
  • severe loss of vision
  • need annual eye checks
32
Q

optic disc of eye

A

where optic nerve and blood vessels exit the eye (near back of eye)

33
Q

macula of eye

A

central area of retina

34
Q

fovea

A

region of sharpest vision

35
Q

what is nephropathy

A

angiopathy of capillaries of glomeruli - narrowing and blocking so filter is damaged and proteins appear in urine
(glomerulosclerosis)

36
Q

symptoms of early nephropathy (5-10 years after diagnosis)

A
  • microalbuminuria
37
Q

symptoms of later nephropathy (10 years after diagnosis)

A
  • proteinuria
  • increased BP
  • decreased eGFR
38
Q

symptoms of advanced nephropathy (10 years after diagnosis)

A
  • end-stage renal disease
  • need dialysis or kidney transplant
39
Q

what drugs help limit nephropathy (ie - renoprotective)

A
  • ACE inhibitors: even if BP is normal
  • Primarily used for hypertension and heart failure but also in CKD to limit proteinuria
40
Q

what is neuropathy

A
  • family of nerve disorders caused by DM
  • affects cranial, autonomic, peripheral NS
41
Q

effects of neuropathy

A

erectile dysfunction
sweating
postural hypotension
bladder dysfunction
constipation/diarrhoea

42
Q

symptoms of neuropathy

A

loss of sensation
tingling
shooting pains
cramps
causalgia

*mainly in feet, increased risk of foot ulcers

43
Q

what is the leading cause of death in diabetes

A

ischaemic heart disease

44
Q

Ischaemic Heart Disease

A
  • develops prematurely
  • narrowed heart (coronary) arteries that supply blood to the heart muscle
  • myocardial infarction (heart attack) increases risk of complications like heart failure and rhythm disturbances
  • need to manage risk factors in diabetics (hypercholesterolaemia, hypertension, stop smoking)
45
Q

what is a stroke caused by

A
  • area of brain deprived of blood due to blood clot
  • 10-fold increase in younger patients
  • TIAs less likely
  • need to control hypertension
46
Q

what is peripheral vascular disease caused by

A
  • reduced circulation of blood to a body part other than the brain or heart
  • caused by a narrowed or blocked blood vessel
  • main cause is atherosclerosis - the build-up of fatty deposits that narrow a blood vessel, usually an artery
47
Q

effect of PVD

A

intermittent claudication (cramping) and ulcerations

48
Q

risks with PVD

A
  • gangrene/amputation
  • DVTs
  • pulmonary embolisms
49
Q

risk factors of DM

A
  • hyperglycaemia
  • hypertension
  • dyslipidameia
  • pro-coagulant state
50
Q

how to control microvascular effects

A
  • good glycemic control
  • control of hypertension with ACE1, AIIRA, CCB
  • T1DM recommended: 135/85mmHg
  • T2DM recommended:140/90 mmHg (<130/80 mmHg if renal impairment)
51
Q

how to control macrovascular effects

A
  • good glycaemic control
  • control of hypertension
  • control of dyslipidaemia (statin)
  • use anti-platelet drugs (clopidogrel)

ENDOCRINE (17 decks)

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