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NURS 416 > Week 3a Glucose Regulation > Flashcards

Week 3a Glucose Regulation Flashcards

1
Q

biguanides do not?

A

increase insulin resistance

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2
Q

Where does blood from the islets drain into?

A

the hepatic portal vein

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3
Q

Promotes conversion of monosaccharides, lipids and amino acids into storage forms of polysaccharides, triglycerides and proteins

A

Insulin

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4
Q

Glucagon

A

promotes conversion of glycogen, proteins and lipids into glucose (gluconeogenesis) and release of glucose into the blood

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5
Q

How do catchecholamines affect blood glucose?

A

they help to maintain blood glucose levels in times of stress

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6
Q

How does growth hormone affect blood glucose?

A

increases protein synthesis in all cells of the body, mobilizes fatty acids from adipose tissue and antagonizes the effects of insulin

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7
Q

How do glucocorticoids affect blood glucose?

A

They are critical to survival during periods of fasting and starvation. They also stimulate gluconeogensis by the liver.

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8
Q

What is the main stimulant for insulin secretion?

A

high serum glucose

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9
Q

What are the 3 functions of Insulin?

A

1) glucose uptake by cells
2) facilitates storage of glucose and glycogen and triglycerides
3) Prevents breakdown of other sources

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10
Q

What does a C-peptide level suggest?

A

It distinguishes between type 1 diabetes or type 2

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11
Q

Why is C-peptide level measured instead of insulin?

A

can assess a persons own insulin even if they receive injections

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12
Q

Gluconeogenesis

A

generation of glucose

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13
Q

Glycogenolysis

A

the breakdown of glycogen

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14
Q

What functions and the beta cell glucose sensor?

A

Glucokinase

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15
Q

What can mutations in glucokinase lead to?

A

early onset of mild diabetes (maturity-onset diabetes of the young - MODY)

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16
Q

What is the most potent stimulator of insulin release?

A

Glucose

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17
Q

Incretin-like drugs for the treatment of type 2 DM, unlike sulfonylureas, are less likely to induce?

A

hypoglycaemia

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18
Q

What is insulin secretion inhibited by?

A

catecholamines and somatostatin

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19
Q

Where are the majority of insulin receptors?

A

liver, muscle and fat tissue

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20
Q

Where are GLUT-4 ?

A

muscle cells and adipose tissue

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21
Q

GLUT -2

A

beta cells and liver cells.

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22
Q

GLUT - 1

A

all tissues, basal glucose uptake. Does not require the actions of insulin. Nervous system.

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23
Q

When does endogenous insulin peak?

A

35-40 mins post meal

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24
Q

What does endogenous insulin return to baseline after a meal?

A

2-3 hours

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25
Q

What is diabetes mellitus characterized by?

A

hyperglycaemia, polydipsia, polyuria and glycosuria

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26
Q

Diagnosis of type 1 DM includes a fasting glucose of?

A

> 7mmol/L

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27
Q

Type 1A DM involves?

A

a hypothetical triggering event that involves an environmental agent that incites an immune response

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28
Q

In Type 1B DM, there is no evidence of?

A

autoimmunity

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29
Q

Which type of people is Type 1B DM most common in?

A

African or asian descent

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30
Q

Type 1 B DM is strongly?

A

Inherited

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31
Q

What is the difference between latent autoimmune diabetes of adult hood and Type 1 DM?

A

LADA occurs when the body stops producing adequate insulin. LADA progresses slowly and insulin may still be produced even after diagnosis

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32
Q

What kind of gene condition is Maturity Onset Diabetes of the Young (MODY)

A

it is a single gene mutation that disrupts insulin production. It is also a dominant genetic condition

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33
Q

Neonatal DM

A

a monogenic form of diabetes, like MODY

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34
Q

What are the 3 metabolic abnormalities in Type 2 diabetes?

A

1) impaired beta cell function and insulin secretion
2) Peripheral insulin resistance
3) Increased hepatic glucose production

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35
Q

What are 3 major causes of beta cell dysfunction in diabetes?

A

1) Chronic hyperglycaemia that results in beta cell desensitization
2) Chronic elevation of free fatty acids
3) Amyloid deposition in the beta cells

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36
Q

metabolic syndrome

A

cluster of conditions such as increased blood pressure, excess body fat around the waist and abnormal cholesterol or triglyceride levels

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37
Q

What are some of the signs and symptoms of metabolic syndrome?

A
  • elevated triglycerides
  • Low HDL
  • HTN
  • Systemic inflammation
  • Fibrinolysis
  • abnormal function of the vascular endothelium
  • Macrovascular disease
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38
Q

What are some consequences of reduced glucose uptake?

A
  • lipolysis
  • proteolysis
  • endothelial dysfunction
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39
Q

How does ketonuria result?

A

Liver metabolism of excessive amounts of fatty acids which results in ketogenesis and ketonuria

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40
Q

What are some acute complications of diabetes?

A

1) Diabetic ketoacidosis
2) hyperosmolar hyperglycaemic state
3) hypoglycaemia

41
Q

when are people with type 2 DM particularly susceptible to DKA?

A

during infections

42
Q

In DKA what occurs in response to the marked increase in plasma osmolarity?

A

cellular dehydration

43
Q

What electrolyte supplementation is routinely given in the treatment of DKA?

44
Q

What is a tell-tale symptom of DKA?

A

rapid breathing (kussmals respirations)

45
Q

Unlike DKA, hyperosmolar nonketotic coma does not affect?

46
Q

excessive thirst, dry mouth, increased urination, warm dry skin, fever, drowsiness, confusion and hallucinations are symptoms of?

A

Hyperosmolar hyperglycemic state

47
Q

What are some chronic complications of diabetes mellitus?

A
  • diabetic nephropathy
  • diabetic retinopathy
  • vascular disease
  • diabetic neuropathy
48
Q

When is short-acting insulin usually given?

A

with one or more meals per day. It should be injected 30-45 minutes before the start of a meal

49
Q

When is long acting insulin usually administered?

A

once daily at bedtime

50
Q

Onset of rapid acting insulin

A

10-15 minutes

51
Q

Peak of rapid acting insulin

52
Q

Duration of rapid acting insulin

53
Q

onset of long-acting insulin

A

90 minutes

54
Q

How long does long-acting insulin plateau for?

55
Q

Short acting insulin is also called

A

regular insulin

56
Q

onset of short acting insulin

A

30 minutes

57
Q

Peak of short acting insulin

58
Q

Duration of short acting insulin

A

6.5 hours but is dose dependent

59
Q

Which type of insulin can be given IV for ketoacidosis?

A

Short-acting insulin

60
Q

what are some examples of short acting insulin

A

Novolin ge toronto and Humulin R

61
Q

what is the onset of intermediate acting insulin?

62
Q

What is the peak of intermediate acting insulin

63
Q

What is the duration of intermediate acting insulin?

A

up to 18 hours but is dose dependent

64
Q

what are some of the symptoms of hypoglycaemia?

A

tachycardia, confusion, sweating, drowsiness, convulsions, coma and death if it is not treated

65
Q

what is the treatment for a conscious patient experiencing hypoglycaemia?

A

4 glucose tablets, 175 mL of apple juice or 15 mL of honey

66
Q

What is the treatment for an unconscious patient experiencing hypoglycaemia?

A

50% dextrose IV and/or glucagon IM

67
Q

what is the calculation for the total daily insulin dose?

A

0.3 units x patients weight in kg

68
Q

What is the recommended % of carb intake for a diabetic patient?

69
Q

What is the recommended % of fat intake for a diabetic patient?

70
Q

What is the recommended % of protein intake for a diabetic patient?

71
Q

what do secretagogues do?

A

increase insulin release

72
Q

2 examples of secretagogues

A

sulfonylureas and meglitinides

73
Q

2 examples of drugs that increase sensitivity to insulin

A

biguanides and Thiazolidinediones

74
Q

what do glucosidase inhibitors do?

A

reduce absorption of glucose by preventing digestion of carbs

75
Q

What do incretin enhancers do?

A

reduce metabolism of insulin and decrease the rate of digestion of carbs

76
Q

when should you take alpha-glucosidase inhibitors

A

with meals

77
Q

What is the action of biguanides?

A

increase sensitivity to insulin. Decrease production and release of glucose from the liver, increases cellular uptake of glucose, lowers lipid levels and promotes weight loss

78
Q

Incretin enhancers have a low risk of?

A

hypoglycaemia

79
Q

Meglitinides can cause?

A

hypoglycaemia

80
Q

Nursing considerations for biguanides

A

risk for lactic acidosis, avoid alcohol, low risk for hypoglycaemia

81
Q

sulfonylureas can cause?

A

hypoglycaemia

82
Q

Action of Thiazolidinediones

A

increases insulin sensitivity in fat and muscle tissue

83
Q

Nursing considerations for Thiazolidinediones

A

can cause fluid retention and worsening of heart failure

84
Q

what is first line treatment for type 2 DM?

A

Biguanides (metformin)

85
Q

Actions of biguanides

A

1) reduce gluconeogenesis
2) reduce glucose absorption
3) increase cell glucose uptake
4) do not increase insulin release

86
Q

Onset of metformin

87
Q

Peak of metformin

A

10-16 hours

88
Q

Contrainsidcations of metformin

A

CHF, hepatic disease, alcoholism, renal disease, diuretics, antibiotics, ginseng, garlic, juniper, coriander, fenugreek

89
Q

Actions of sulfonylureas

A

1) stimulate release of insulin

2) increase sensitivity of insulin receptors

90
Q

example of a sulfonylurea?

A

glyburide (DiaBeta)

91
Q

Onset of sulfonylureas?

92
Q

Duration of sulfonylureas?

A

10-24 hours

93
Q

How is sulfonylureas usually administered?

94
Q

taking alcohol and/or aspirin with a sulfonylurea drug can cause the development of?

A

hypoglycaemia

95
Q

Adverse effects of Thiazolidinediones?

A

fluid retention, headache, weight gain and hepatotoxicity

96
Q

does hypoglycaemia occur with Thiazolidinediones?

97
Q

what is an example of a incretin enhancer?

A

sitagliptin

98
Q

what do SGLT2 inhibitors fo?

A

increase glucose dieresis

99
Q

what is important to asses with SGLT2 inhibitors?

A

renal function

NURS 416 (17 decks)

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