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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
What are the fetal complications of gestational diabetes mellitus? (5)
MACROSOMIA: excessive birth weight HYPOGLYCEMIA HYPOCALCEMIA: d/t dec parathyroid gland function POLYCYTHEMIA HYPERBILIRUBINEMIA
26
What percentage of mothers with gestational diabetes progress to DM type 2 within 5-10 yrs
50 percent
27
Describe the onset of symptoms for DM type 1 and DM type 2
Type 1 is rapid onset Type 2 is insidious
28
Which type of DM has weight loss and which has weight gain?
type 1: wt loss d/t fluid loss and use of fat stores Type 2: weight gain
29
What are the three polys of DM? explain each
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
30
List and describe the four general DM manifestations
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
31
How long do you need to fast for Fasting Plasma Glucose test? what is the normal value?
8 hours < 5.7 mmol/L
32
What is the random blood glucose test?
BG with no regard for last meal/glucose intake Ex capillary BG (glucometer)
33
Describe what Oral Glucose Tolerance test is (OGTT).
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
34
Describe what the Glycosylated Hemoglobin test is. (A1C)
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
35
When can Glycosylated Hemoglobin test (A1C) be misleading?
with anemia and pregnancy
36
For what type of DM is urine testing more important for?
For type 1 DM as a measurement of ketones
37
What is urine testing for sugar dependent on?
renal function and fluid intake
38
What is the usual cause of DKA?
Type 1 DM - previously undiagnosed - can be triggered by stress, poor management, etc
39
When does type 2 cause DKA?
when it is complicated by a major illness
40
Describe the process of DKA
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
With DKA what hormone levels increase?
Glucagon Corticosteroids Epinephrine GH
42
Describe the 5 diagnosis methods/criteria for DKA
HYPERGLYCEMIA: >13.8 Low bicarb Low pH Urine and serum ketones Metabolic Acidosis
43
What does hyperglycemia lead to in DKA?
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
What are DKA manifestations preceded by?
Polyuria, polydipsia, N and V, fatigue
45
Describe the onset of manifestations for DKA
it is very rapid (<24 hrs)
46
List the GI manifestations for DKA (3)
N and V, abd pain/tenderness, FRUITY BREATH
47
List the 3 CVS manifestations for DKA
Dehydration hypotension tachycardia
48
What type of respirations occur with DKA?
Kussmaul breathing (deep and rapid)
49
Describe the 3 CNS manifestations of DKA
Confusion Stupor Coma
50
Why are children at greater risk for CNS problems with DKA?
because their cerebral autoregulations are not fully developed
51
List the four DKA treatment goals
1) Improve circulatory volume and tissue perfusion (IV fluids) 2) Decrease BG 3) Correct Acidosis 4) Correct electrolyte imbalance
52
Why must insulin therapy to lower BG in DKA be done slowly?
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
What is hyperosmolar hyperglycemia defined as? (critical high)
> 33 mmol/L
54
What does hyperglycemia do to the CNS?
suppress CNS
55
What are the 5 RF for hyperosmolar hyperglycemic state?
``` Type 2 DM Acute pancreatitis Sever infection Myocardial infarction TPN ```
56
Describe what the insulin deficiency associated with hyperglycemic states causes (in terms of liver)
Results in HYPERGLUCAGONEMIA 1) glucagon causes glycogenolysis (breakdown of glycogen to glucose) 2) stimulates liver to convert amino acids into glucose (gluconeogenesis)
57
What is one of the complications of a hyperosmolar hyperglycemic states in terms of fluid balance?
It causes glycosuria -> polyuria and can result in dehydration
58
Explain the impact of osmolarity in DM
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
Describe the 12 manifestations of a hyperosmolar hyperglycemic state (3 and then 9 CNS manifestations)
Poluria Polydypsia Dehydration CNS: insidious, can mimic a stroke Weakness, hemiparesis, aphasia, muscle fasciculations, hyperthermia, hemianopia, nystagmus, hallucinations, coma and ceisures
60
What can be a complication of a hyperosmolar hyperglycemic state (1)
Thromboembolism
61
Describe the treatment for HHS (hyperosmolar hyperglycemic state)
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
List 5 causes of hypoglycemia
1) insulin or oral hypoglycemia 2) alcohol 3) Exercise 4) dieting 5) endocrine disorders
63
How can alcohol cause hypoglycemia?
it preoccupies the liver decreasing its ability to perform gluconeogenesis
64
Describe the characteristics of hypoglycemia manifestations
Rapid onset and variable
65
What age groups have vague symptoms like confusion for hypoglycemia?
Elderly and Children
66
List the 10 manifestations of hypoglycemia.
``` CNS: h/a difficulty problem solving confusion behavioural changes coma and seizures ``` ANS: PNS - hunger SNS - anxiety, tachycardia, sweating, vasoconstriction of skin vessels
67
Describe the treatment protocol for hypoglycemia
Rapid delivery of oral glucose 15g - tabs or gel D50W IV if emergency Glucagon IM or SC if unable to take oral glucose
68
What should the nurse consider about giving glucagon IV or SC in hypoglycemia.
that it releases glucose from livers, so if stores are depleted, will not be effective
69
Explain what the Somogyi Effect is
it is a hypoglycemia and hyperglycemia cyclic response (rebound)
70
Explain the mechanism/process for the somogyi effect
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
Explain how neuropathy can be caused by DM
blood vessel walls supplying the nerves thicken decreasing nutrients and O2 Demyelination occurs slowing nerve conduction
72
What are the two types of neuropathy?
Somatic neuropathy Autonomic neuropathy
73
Describe the 4 ways that somatic neuropathy can present
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
There are four classifications of autonomic neuropathy. List them and describe the implications
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
List the 5 RF for diabetic nephropathy
``` Genetic/family HTN Poor BG control Hyperlipidemia Smoking ```
76
What races are more at risk for diabetic nephropathy?
natives, Hispanic, african
77
Explain the three processes that contribute to diabetic nephropathy.
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
What is often the initial sign of capillary basement membrane thickening?
microalbuminuria
79
Explain the process of diabetic retinopathy
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
List the three RF for diabetic retinopathy
Poor BG control HTN Hyperlipidemia
81
What does risk for diabetic retinopathy increase with?
Pregnancy Puberty Cataract surgery
82
What percentage of newly diagnosed DM pts already have vascular issues?
50 percent
83
Explain 3 vascular complications of DM
Atherosclerotic CAD Cerebrovascular disease Peripheral Vascular Disease
84
What are the 9 RF for vascular complications
``` Obesity HTN Hyperglycemia Hyperlipidemia Hyperinsulinemia Altered platelet function Endothelial dysfunction Systemic inflammation Elevated fibrinogen ```
85
What are the 9 RF for vascular complications
``` Obesity HTN Hyperglycemia Hyperlipidemia Hyperinsulinemia Altered platelet function Endothelial dysfunction Systemic inflammation Elevated fibrinogen ```
86
How does glycosuria and hyperglycemia influence virulence
virulence is synonymous with growth So increases it
87
Which type of diabetes always needs insulin and which eventually requires insulin?
DM type 1 always does DM type 2 eventually does
88
What are the three routes of insulin?
SC Inhalation IV
89
what are the three possible sources of insulin?
human/bovine/porcine
90
What are the 4 types of insulin (in terms of action)
Short-acting (regular) Rapid acting Intermediate Long-acting

Pathophysiology I (16 decks)

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