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Pathophysiology I > Chapter 33: Diabetes > Flashcards

Chapter 33: Diabetes Flashcards

1
Q

What are the 2 different aspects of pancreatic function?

A

Exocrine Pancreas: digestive juices through duct into duodenum

Endocrine Pancreas: release hormones into blood

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2
Q

What is the endocrine section of the pancreas called?

A

Islets of Langerhans

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3
Q

What are the 4 type of cells and the hormones they secrete in the islets of langerhans

A

ALPHA: glucagon

BETA: insulin and amylin

DELTA: somatostatin

PP: pancreatic polypeptide

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4
Q

What does glucagon do in the body.

A

Causes cells to release stored glucose

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5
Q

What does insulin do in the body?

A

allows cells to uptake BG

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6
Q

What does amylin do in the body?

A

slows glucose absorption in small intestine and supresses glucagon secretion

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7
Q

What does somatostatin do in the body?

A

decreases GI activity and supresses glucagon and insulin secretion

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8
Q

When was diabetes mellitus first discovered?

A

in the 1st century AD

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9
Q

What are the 4 causes of diabetes mellitus?

A

1) absolute insulin DEFICIENCY
2) impaired RELEASE of insulin
3) inadequate or defective insulin RECEPTORS
4) production of INACTIVE insulin or DESTRUCTION of insulin

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10
Q

Describe DM type 1

A

it is absolute insulin deficiency d/t autoimmune destruction

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11
Q

What two autoantibodies can cause type 1 DM?

A

Islet cell autoantibodies

Insulin autoantibodies

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12
Q

What are 3 causes/RF of type 1 DM?

A

1) genetic predisposition (childhood onset)
2) environmental triggers
3) T-mediated hypersensitivity reactions against beta cell antigens

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13
Q

Describe DM type 1B

A

Intermittent ketoacidosis with remissions of VARIABLE insulin dependency

IDIOPATHIC with no sign of autoimmune destruction

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14
Q

What are the 2 RF for type 1B DM?

A

African or Asian decent

Strongly inherited

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15
Q

What percentage of DM is type 2?

A

90-95 percent

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16
Q

DM type 2 is a result of one or more of…. (3 things, list them)

A

1) Insulin resistance
2) Inc liver production of glucose
3) beta cell dysfunction

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17
Q

List the RF of DM type 2

A

Genetic
Environmental
Physical inactivity
OBESITY

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18
Q

What percentage of people with DM type 2 are obese?

A

90 percent

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19
Q

What type of obesity (body type) is most at risk for developing DM type 2

A

Apple shaped

Upper body obesity

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20
Q

Explain what insulin resistance is

A

Failure of target tissue to respond to insulin resulting in

1) decreased uptake
2) does not impair liver production of glucose, resulting in high glucose especially postprandial

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21
Q

What are the 6 things that beta cell dysfunction can be caused by.

A

Dec mass (genetic/prenatal

Inc apoptosis or dec regeneration

exhaustion (due to chronic insulin resistance)

desensitization (d/t chronic glucotoxicity)

destruction (lipotoxicity)

toxins/deposits (amyloid)

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22
Q

When DM type 2 is diagnosed, what can typically be said about beta cells?

A

dysfunction has already progressed

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23
Q

What is gestational diabetes mellitus?

A

Glucose intolerance developing during pregnancy

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24
Q

What are the RF for gestational diabetes mellitus (7)

A

1) Glycosuria
2) Family hx of type 2 DM
3) Hispanic, native American, African American descent
4) Severe obesity
5) Polycystic ovary disease
6) Prior h/o GDM
7) previous delivery of large baby

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25
Q

What are the fetal complications of gestational diabetes mellitus? (5)

A

MACROSOMIA: excessive birth weight

HYPOGLYCEMIA

HYPOCALCEMIA: d/t dec parathyroid gland function

POLYCYTHEMIA

HYPERBILIRUBINEMIA

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26
Q

What percentage of mothers with gestational diabetes progress to DM type 2 within 5-10 yrs

A

50 percent

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27
Q

Describe the onset of symptoms for DM type 1 and DM type 2

A

Type 1 is rapid onset

Type 2 is insidious

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28
Q

Which type of DM has weight loss and which has weight gain?

A

type 1: wt loss d/t fluid loss and use of fat stores

Type 2: weight gain

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29
Q

What are the three polys of DM? explain each

A

POLYURIA: glomeruli in kidneys unable to reabsorb glucose and glucose pulls water with it

POLYDIPSIA: loss of water -> intracellular dehydration -> thirst

POLYPHAGIA: (more with type 1) use of stores triggers this

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30
Q

List and describe the four general DM manifestations

A

BLURRED VISION: hyperosmolar fluid affects lens and retina

WKNESS/FATIGUE: dec fluid in cardiovascular system and inability to use glucose

PARESTHESIA: peripheral sensory nerve dysfunction

INFECTION: organisms thrive with abundant sugar

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31
Q

How long do you need to fast for Fasting Plasma Glucose test? what is the normal value?

A

8 hours

< 5.7 mmol/L

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32
Q

What is the random blood glucose test?

A

BG with no regard for last meal/glucose intake

Ex capillary BG (glucometer)

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33
Q

Describe what Oral Glucose Tolerance test is (OGTT).

A

measures ability to store glucose

75 g of concentrated glucose solution given at intervals

normal response is to return to normal BG levels in 2-3 hrs

2 hr GTT < 7.8mmol/L

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34
Q

Describe what the Glycosylated Hemoglobin test is. (A1C)

A

HGB becomes glycosylated to form A1C

Indicates average plasma glucose over long period (lvls for 6-12 wks)

sign of chronic hyperglycemia

Normal range 3.9-5.6 percent

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35
Q

When can Glycosylated Hemoglobin test (A1C) be misleading?

A

with anemia and pregnancy

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36
Q

For what type of DM is urine testing more important for?

A

For type 1 DM as a measurement of ketones

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37
Q

What is urine testing for sugar dependent on?

A

renal function and fluid intake

38
Q

What is the usual cause of DKA?

A

Type 1 DM

  • previously undiagnosed
  • can be triggered by stress, poor management, etc
39
Q

When does type 2 cause DKA?

A

when it is complicated by a major illness

40
Q

Describe the process of DKA

A

lack of insulin results in breakdown of E stores

LIVER:
converts glucose for use and mobilizes fatty acids for E

Ketones are produced when fatty acids are used, resulting in depletion of Bicarbonate and in acidosis

41
Q

With DKA what hormone levels increase?

A

Glucagon
Corticosteroids
Epinephrine
GH

42
Q

Describe the 5 diagnosis methods/criteria for DKA

A

HYPERGLYCEMIA: >13.8

Low bicarb

Low pH

Urine and serum ketones

Metabolic Acidosis

43
Q

What does hyperglycemia lead to in DKA?

A

Osmotic diuresis, dehydration, electrolyte loss

Water and K shifts from ICS to ECF

  • K may be low or high
  • Na+ usually low, but may be high
44
Q

What are DKA manifestations preceded by?

A

Polyuria, polydipsia, N and V, fatigue

45
Q

Describe the onset of manifestations for DKA

A

it is very rapid (<24 hrs)

46
Q

List the GI manifestations for DKA (3)

A

N and V, abd pain/tenderness, FRUITY BREATH

47
Q

List the 3 CVS manifestations for DKA

A

Dehydration
hypotension
tachycardia

48
Q

What type of respirations occur with DKA?

A

Kussmaul breathing (deep and rapid)

49
Q

Describe the 3 CNS manifestations of DKA

A

Confusion
Stupor
Coma

50
Q

Why are children at greater risk for CNS problems with DKA?

A

because their cerebral autoregulations are not fully developed

51
Q

List the four DKA treatment goals

A

1) Improve circulatory volume and tissue perfusion (IV fluids)
2) Decrease BG
3) Correct Acidosis
4) Correct electrolyte imbalance

52
Q

Why must insulin therapy to lower BG in DKA be done slowly?

A

Acidosis indicates insulin resistance

If you do too rapid, will rapidly lower serum osmolality resulting in cerebral edema

(brain cells have compensatory mechanisms to regulate intracellular osmolality and need time to adjust to the change in blood osmolality)

53
Q

What is hyperosmolar hyperglycemia defined as? (critical high)

A

> 33 mmol/L

54
Q

What does hyperglycemia do to the CNS?

A

suppress CNS

55
Q

What are the 5 RF for hyperosmolar hyperglycemic state?

A 
Type 2 DM
Acute pancreatitis
Sever infection
Myocardial infarction
TPN
56
Q

Describe what the insulin deficiency associated with hyperglycemic states causes (in terms of liver)

A

Results in HYPERGLUCAGONEMIA

1) glucagon causes glycogenolysis (breakdown of glycogen to glucose)
2) stimulates liver to convert amino acids into glucose (gluconeogenesis)

57
Q

What is one of the complications of a hyperosmolar hyperglycemic states in terms of fluid balance?

A

It causes glycosuria -> polyuria

and can result in dehydration

58
Q

Explain the impact of osmolarity in DM

A

The blood becomes hyperosmolar causing cells to shrivel

Neurons can regulate intracellular osmolarity and will increase it to compensate

If BG returns to normal too rapidly, neurons are hyperosmolar and swell

59
Q

Describe the 12 manifestations of a hyperosmolar hyperglycemic state (3 and then 9 CNS manifestations)

A

Poluria
Polydypsia
Dehydration

CNS: insidious, can mimic a stroke

Weakness, hemiparesis, aphasia, muscle fasciculations, hyperthermia, hemianopia, nystagmus, hallucinations, coma and ceisures

60
Q

What can be a complication of a hyperosmolar hyperglycemic state (1)

A

Thromboembolism

61
Q

Describe the treatment for HHS (hyperosmolar hyperglycemic state)

A

1) careful monitoring
2) replacement of fluid loss MUST be GRADUAL to avoid sudden cerebral edema
3) K+ lost during diuresis needs to be replaced carefully

Poor prognosis

62
Q

List 5 causes of hypoglycemia

A

1) insulin or oral hypoglycemia
2) alcohol
3) Exercise
4) dieting
5) endocrine disorders

63
Q

How can alcohol cause hypoglycemia?

A

it preoccupies the liver decreasing its ability to perform gluconeogenesis

64
Q

Describe the characteristics of hypoglycemia manifestations

A

Rapid onset and variable

65
Q

What age groups have vague symptoms like confusion for hypoglycemia?

A

Elderly and Children

66
Q

List the 10 manifestations of hypoglycemia.

A 
CNS:
h/a
difficulty problem solving
confusion
behavioural changes
coma and seizures

ANS:
PNS - hunger
SNS - anxiety, tachycardia, sweating, vasoconstriction of skin vessels

67
Q

Describe the treatment protocol for hypoglycemia

A

Rapid delivery of oral glucose 15g
- tabs or gel

D50W IV if emergency

Glucagon IM or SC if unable to take oral glucose

68
Q

What should the nurse consider about giving glucagon IV or SC in hypoglycemia.

A

that it releases glucose from livers, so if stores are depleted, will not be effective

69
Q

Explain what the Somogyi Effect is

A

it is a hypoglycemia and hyperglycemia cyclic response (rebound)

70
Q

Explain the mechanism/process for the somogyi effect

A

Insulin-induced hypoglycemia produces compensatory responses:

  • catecholamine
  • glucagon
  • cortisol
  • GH

Inc in BG resulting in some insulin resistance

Then more insulin is given and cycle starts over

71
Q

Explain how neuropathy can be caused by DM

A

blood vessel walls supplying the nerves thicken decreasing nutrients and O2

Demyelination occurs slowing nerve conduction

72
Q

What are the two types of neuropathy?

A

Somatic neuropathy

Autonomic neuropathy

73
Q

Describe the 4 ways that somatic neuropathy can present

A

1) Diminished SENSATION (especially in feet) leads to injuries
2) dec PROPRIOCEPTION leads to falls
3) DENERVATION of foot leads to clawing of toes
4) PAIN can result from diabetic neuropathy and HYPERSENSITIVITY

74
Q

There are four classifications of autonomic neuropathy. List them and describe the implications

A

VASOMOTOR CHANGES:
dizziness, syncope

BLADDER CONTROL:
retention -> infections, renal complications

GI MOTILITY:
Constipation, discomfort, N and V, postprandial V, bloating, can have diarrhea

SEXUAL DYSFUNCTION:
erectile dysfunction

75
Q

List the 5 RF for diabetic nephropathy

A 
Genetic/family
HTN
Poor BG control
Hyperlipidemia
Smoking
76
Q

What races are more at risk for diabetic nephropathy?

A

natives, Hispanic, african

77
Q

Explain the three processes that contribute to diabetic nephropathy.

A

1) Capillary basement membrane thickens:
- allows proteins to escape

2) NODULAR GLOMERULOSCLEROSIS
nodular lesions in glomerular capillaries dec blood flow leading to failure

3) KIDNEY ENLARGEMENT
d/t inc workload from attempting to filter excess glucose

78
Q

What is often the initial sign of capillary basement membrane thickening?

A

microalbuminuria

79
Q

Explain the process of diabetic retinopathy

A

1) altered vascular permeability
2) microaneurysm occurs
3) neovascularization (development of new, but weak vessels)
4) hemorrhage, scarring
5) retinal detachment

this is combined with neuropathic dmg to the optic nerve

80
Q

List the three RF for diabetic retinopathy

A

Poor BG control
HTN
Hyperlipidemia

81
Q

What does risk for diabetic retinopathy increase with?

A

Pregnancy
Puberty
Cataract surgery

82
Q

What percentage of newly diagnosed DM pts already have vascular issues?

A

50 percent

83
Q

Explain 3 vascular complications of DM

A

Atherosclerotic CAD
Cerebrovascular disease
Peripheral Vascular Disease

84
Q

What are the 9 RF for vascular complications

A 
Obesity
HTN
Hyperglycemia
Hyperlipidemia
Hyperinsulinemia
Altered platelet function
Endothelial dysfunction
Systemic inflammation
Elevated fibrinogen
85
Q

What are the 9 RF for vascular complications

A 
Obesity
HTN
Hyperglycemia
Hyperlipidemia
Hyperinsulinemia
Altered platelet function
Endothelial dysfunction
Systemic inflammation
Elevated fibrinogen
86
Q

How does glycosuria and hyperglycemia influence virulence

A

virulence is synonymous with growth

So increases it

87
Q

Which type of diabetes always needs insulin and which eventually requires insulin?

A

DM type 1 always does

DM type 2 eventually does

88
Q

What are the three routes of insulin?

A

SC
Inhalation
IV

89
Q

what are the three possible sources of insulin?

A

human/bovine/porcine

90
Q

What are the 4 types of insulin (in terms of action)

A

Short-acting (regular)
Rapid acting
Intermediate
Long-acting

Pathophysiology I (16 decks)

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