complications Flashcards

1
Q

Why would you get dehydration in DM?

What’s the difference in terms of onset of T1DM and T2DM?

A

Due to osmotic diuresis

T1DM - relatively sudden
T2DM - slow progression

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2
Q

What are 3 main acute complications that can arise from DM? Which ones tend to happen in which DM?

A

acute:

  • hypoglycaemia
  • diabetic ketoacidosis (hyperglycaemia T1DM)
  • hyperosmolar hyperglycaemic state (T2DM)
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3
Q

Below what blood glucose level does symptoms of hypoglycaemia present?

A

<4mmol/L

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4
Q

Explain some causes of hypoglycaemia in either types of DM

Explain some of the symptoms seen in hypoglycaemia

A

T1DM - insulin overdose, excessive exercise, inadequate CHO intake

T2DM - sulphonylureas (elderly), hepatic/renal disease, drugs

Symptoms:
palpitations, tremors, sweating, anxiety (counter-regulartory activity of SNS)
loss of conc, slurred speech, behaviour/mood changes, seizures (glucose deficiency in brain)

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5
Q

Treatment for hypoglycaemia? (conscious and unconscious)

A

conscious - sugary drink/food, then sustained carb snack
unconscious - glucose or glucagon i.v/i.m
glucagon can’t be used after alcohol

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6
Q

What is diabetic ketoacidosis?

A

diabetic coma - hyperglycaemia and metabolic acidosis

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7
Q

What’s insulin’s normal function on adipose tissue, SKM, and liver?

A

adipose tissue- increase glucose uptake (GLUT-4), lipogenesis, decr in lipolysis
SKM - increase glucose uptake and protein synthesis, decr protein breakdown
liver - increase glycogen synthesis, decr glycogen breakdown and gluconeogenesis

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8
Q

What are the 4 processes that happen if you loose the insulin signal? (In liver, adipose and muscle tissue)

A

liver - gluconeogenesis and glycogen breakdown
adipose - lipolysis
SKM - protein breakdown

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9
Q

Explain the process by which you get hyperglycaemia and ketosis during uncontrolled T1DM

A
all intermediates/products bc of processes feed into liver to feed ketogenesis and cause hyperglycaemia 
The FFAs (from lipolysis) go through beta-oxidation and go through ketogenesis, forming acetoneacetate, beta-hydroxybutyrate and acetate
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10
Q

Clinical signs and symptoms of hyperglycaemia and ketosis?

A

hyperglycaemia: peripheral circulatory failure, renal failure, low cerebral blood flow
metabolic acidosis - CNS depression and diabetic coma

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11
Q

More severe consequences of hyperglycaemia and ketosis?

A

DEATH

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12
Q

What’s the treatment for diabetic ketoacidosis?

A
  • insulin i.v (supress ketogenesis, reduce blood glucose, correct electrolyte imbalance)
  • replacement of fluids, electrolytes
  • treat underlying cause
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13
Q

What is HHS? What’s the blood glucose level for it?

A

hyperosmolar hyperglycaemic state
v high blood glucose >40 mmol/L
severe hyperglycaemia without ketosis

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14
Q

What are 3 tests done to monitor glucose control?

What’s the recommended range for HBA1C?

A

urine testing - ketones and glucose
blood glucose testing
HbA1C test (recommended range 48-59 mmol/mol)

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15
Q

What are some long-term complications of DM? (think in terms of micro and macrovascular)

A

microvascular: retinopathy, nephropathy, neuropathy
macrovascular: CVD, cerebral vascular disease (stroke), peripheral vascular disease.

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16
Q

Why does microvascular damage happen in DM?

A

damage of small vessels by hyperglycaemia and glycation of proteins

17
Q

What are the different stages of retinopathy?

A

background - no symptoms but visable in opthalmoscope
pre-proliferative - new blood vessels developing bc of the damaged ones
proliferative
maculopathy - the macula is affected

18
Q

One way that kidneys get damaged due to DM?

A

sclerosis - build-up deposits in arterioles, narrowing blood vessels.
glomerulosclerosis

19
Q

What changes are seen across the different stages of nephropathy?

A

early - microalbuminuria
later - proteinuria, higher bp, low eGFR
advanced - end-stage renal disease

ACEi help limit nephropathy even if bp normal

20
Q

What are diabetic foot ulcers (also think of why they happen more often in patients w/ DM) and what problem do they pose?

A

neuropathy - affect peripheral NS and - poor sensation in feet - don’t notice they have a scratch, poor healing

susceptible to infection - hyperglycaemia makes you more attractive target for pathogen