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Metabolism > Type 1 Diabetes Management > Flashcards

Type 1 Diabetes Management Flashcards

1
Q

Insulin affects metabolism (generally) by

A

lowers blood sugar, inhibits dietary fat breakdown and dietary protein breakdown

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2
Q

Type I diabetes is caused by

A

absolute deficiency of insulin caused by autoimmune attack destroying pancreatic beta cells

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3
Q

What are the consequences of insulin deficiency?

A

hyperglycaemia, uncontrolled lipolysis, increased protein degradation (muscle wasting)

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4
Q

What is the presentation of Type I diabetes?

A

Weight loss associated with polyuria and polydipsia; uncontrolled lipolysis can lead to ketoacidosis

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5
Q

How does the pathophysiology of T1D differ from T2D?

A

T1D is an absolute deficiency of insulin; T2D is a relative deficiency of insulin

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6
Q

What year was insulin discovered?

A

1922

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7
Q

What year was insulin available in Australia?

A

1923

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8
Q

What are the different types of insulin for administration?

A

Long-acting insulin (24h)
Short-acting insulin
Pre-mixed insulin (short and long)
Insulin pumps

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9
Q

What are the different types of long-acting insulin?

A 
Isophane insulin (bovine)
Isophane insulin (human): human NPH and protaphane
Glargine insulin (Lantus)*
Detemir insulin (Levemir)*
*=genetically modified
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10
Q

Glargine insulin is modified to be long acting by

A

substitution of a Gly (on a-chain) and two Arg (on b-chain) - makes the molecule bind together and release slowly

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11
Q

Detemir insulin is modified to be long acting by

A

addition of a 14C FA to b chain - this binds the insulin to albumin protecting it from degradation and slowing release; it also allow the insulin to enter the brain and inhibit hunger - tf this is the only insulin that does not cause weight gain

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12
Q

What are the different types of short-acting insulin?

A 
Insulin neutral (bovine and human)
Insulin Glulisine (Apidra)*
Insulin Lispro (Humalog)*
Insulin Aspart (Novoprapid)*
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13
Q

The ‘action’ of insulin refers to

A

how fast it is absorbed from the subcutaneous depot after injection - NOT how quickly it binds to the receptor

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14
Q

What is the basal bolus regime of insulin administration?

A

typical regime to mimic physiology: one injection of LA insulin at bedtime (Glargine or Detemir) and one injection of SA insulin prior to meals (Aspart, Lispro, Glulisine)

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15
Q

How is insulin administered?

A

injections, pumps, artificial pancreas, transplantation

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16
Q

How are insulin injectables used?

A

needles that come in disposable pen form with a dial-able dose; 300 doses/pen; injected under the skin

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17
Q

How do insulin pumps work?

A

deliver SA insulin continuously at a background rate; patient presses a button to deliver bolus prior to each meal; it’s an open-loop system bc the patient has to control it

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18
Q

What is the idea behind an artificial pancreas?

A

allowing a continuous glucose sensor to determine the flow of insulin from the pump (closed loop system, not controlled by patient)

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19
Q

What is the benefit of an artificial pancreas/closed loop insulin delivery system (especially for children with T1D)?

A

closed-loop delivery of insulin may improve overnight control of glucose levels and reduce the risk of nocturnal hypoglycaemia - which can be fatal

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20
Q

What are the limitations to pancreas transplant?

A

Availability of tissue (human beta cells) and life-long immunosuppression that increases risk of cancer and infection

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21
Q

Elevated glucose causes damage particularly to

A

retina, kidney, and nerves

22
Q

What are the retinopathic complications of T1D?

A

proliferative and blindness - commonest cause of blindness in Australia

23
Q

What are the nephropathic complications of T1D?

A

renal failure requiring dialysis - commonest cause of going on dialysis and requiring transplant is now diabetes

24
Q

What are the neuropathic complications of T1D?

A

sensory (numb feet and poor circulation leads to gangrene - most common cause of amputations) and autonomic (problems with controlling BP, gastric stasis/emptying, ED in men)

25
Q

Complications arise in T1D because

A

blood sugar is not tightly controlled and blood glucose becomes elevated, which is toxic (esp to retina, kidneys, and nerves)

26
Q

What did the DCCT trial show in terms of complications?

A

tighter regulation of glucose levels leads to lower rates of complications; target range for HbA1C is 7%

27
Q

How is control of diabetes monitored?

A

measuring blood glucose
measuring HbA1C
measuring fructosamine
presence of complications

28
Q

How is blood glucose measured?

A

pinprick measurements with a glucose monitor; recorded in a table at breakfast, lunch, dinner, and bed with comments (eg reasons for hypo like exercise, hyper like pasta)

29
Q

When is blood glucose measured?

A

lecturer: just before meals and before bed as opposed to before and after to limit pricking; 4x daily, 2x daily (alternate times on alternate days), as little as 1x daily (rotating time of day) - have to balance what patient can manage with what data you need to keep them stable

30
Q

Stable morning sugars tell you what about a patient’s diabetes management?

A

Night-time long-acting dose is correct

31
Q

What type of glycosylation occurs when blood glucose is high?

A

non-enzymatic - glucose binds covalently and irreversibly to proteins at random - especially Hb in RBCs

32
Q

What is the rationale for measuring HbA1c?

A

Because glycosylation occurs on proteins and glucose moves in and out of RBCs readily, the amount of HbA1c (glycosylated Hb) gives an indirect measure of the average level of blood glucose (over the 3mo the RBC survives)

33
Q

When is HbA1c measured?

A

measured every 3-4 months; target as per DCCT and UKPDS is 7% (lower predisposes to hypos)

34
Q

If HbA1c is normal (~7%) but sugars are high (eg 10mmol/L), what is going on?

A

the patient is bleeding - could be slow gut from NSAIDs for eg - need to do FBC, iron levels

35
Q

What does measuring fructosamine tell us?

A

how good management has been for the past 6-8 weeks; beneficial if HbA1c is artificially low (for eg high numbers of reticulocytes/high red cell turnover)

36
Q

Retinal complications are assessed

A

once a year; preferably by an opthamologist or optometrist with drops to see the full retina; laser therapy can save vision

37
Q

Urinary microalbumin is measured

A

yearly at the beginning; after 5-10yrs+ every time you see the patient - measure albumin:creatinine to look for protein in urine which reflects kidney damage and early kidney failure

38
Q

Clinical examination of peripheral nerve sensation is performed

A

yearly; in addition to lying and standing BP, pulses, etc.

39
Q

What is hypoglycaemia?

A

Low blood glucose <4mmol/L

40
Q

What causes hypoglycaemia?

A

Too much insulin for the amount of blood glucose

41
Q

Symptoms of hypoglycaemia depend on

A

rate of fall and absolute glucose deficiency

42
Q

What are the two types of symptoms that can occur in hypoglycaemia?

A

if sugar falls rapidly it can trigger SNS activation releasing adrenaline (can cause MI and death in older pt due to silent angina), leading to tachycardia, anxiety, dry mouth, and tremor; slow fall/absolute low glucose levels lead to brain malfunction that can cause paralysis, coma, and death

43
Q

What is the most important reaction by the body to hypoglycaemia?

A

Glucagon - rises when insulin falls; glucagon deficiency causes a delay in recovery of glucose levels

44
Q

How is hypoglycaemia treated?

A

conscious: oral glucose + carbohydrate meal; diminished consciousness: IV glucose or glucagon; NEED TO INVESTIGATE WHY IT HAPPENED FOR PREVENTION!

45
Q

Ketosis can occur if a patient goes without insulin for

A

just a day in a long-standing T1D

46
Q

Ketosis occurs as a result of

A

inadequate insulin causes uncontrolled lipolysis producing ketone bodies

47
Q

Ketosis becomes ketoacidosis when

A

pH drops (hyperventilation, dehydration)

48
Q

What is the treatment for ketoacidosis?

A

gradual infusion of insulin and rehydration (IV saline), monitoring of potassium because insulin facilitates its uptake into cells and there is a risk of serum hypokalaemia and arrhythmia; takes 24hrs to stabilize; NEED TO INVESTIGATE WHY IT HAPPENED FOR PREVENTION!

49
Q

What is the commonest cause of ketoacidosis?

A

infection (insulin given is not enough); cessation of insulin (esp in adolescents with poor adherence), new onset, post-MI or pancreatitis, some have no cause

50
Q

What are the symptoms of ketoacidosis?

A

Polyuria, polydipsia, weight loss, drowsiness, coma

Metabolism (16 decks)

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