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NURP 502 - Ex 3 > 8: Diabetes > Flashcards

8: Diabetes Flashcards

1
Q

Diabetes is a group of metabolic diseases, characterized by _____, resulting in defects in insulin secretion, insulin action, or both.

A

Diabetes is a group of metabolic diseases, characterized by hyperglycemia, resulting in defects in insulin secretion, insulin action, or both.

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2
Q

Diabetes is a progressive disease affecting the _____ functioning within the body.

A

Diabetes is a progressive disease affecting the fuel metabolism functioning within the body.

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3
Q

Which 3 races have the highest prevalence of diabetes?

A
  1. AA (14.7%)
  2. Native Americans (14.2%)
  3. Hispanics (11.8%)
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4
Q

DM is the leading cause of what 5 conditions?

A
  1. Kidney failure
  2. Nontraumatic lower limb amputations
  3. Blindness in adults
  4. Heart disease
  5. Stroke
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5
Q

What role does the pancreas play after a meal (hyperglycemia) in a normal person?

A

Pancreatic beta cells secrete insulin.

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6
Q

What 3 roles does the liver play after a meal (hyperglycemia) in a normal person?

A
  1. Glucose uptake
  2. Glycogen synthesis
  3. Triaglycerol synthesis
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7
Q

What 3 roles do muscles play after a meal (hyperglycemia) in a normal person?

A
  1. Increased glucose uptake and utilization
  2. Glycogen synthesis
  3. Protein synthesis
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8
Q

What 2 roles does adipose tissue play after a meal (hyperglycemia) in a normal person?

A
  1. Increased glucose uptake and utilization
  2. Triaglycerol synthesis
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9
Q

What role does the pancreas play during a fasting state (hypoglycemia) in a normal person?

A

Pancreatic islet cells secrete glucagon into plasma

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10
Q

What 3 roles does the liver play during a fasting state (hypoglycemia) in a normal person?

A
  1. Increased glycogenolysis
  2. Increased gluconeogenesis
  3. Increased ketone synthesis
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11
Q

What role do muscles play during a fasting state (hypoglycemia) in a normal person?

A

Proteolysis

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12
Q

What role does adipose tissue play during a fasting state (hypoglycemia) in a normal person?

A

Lipolysis

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13
Q

_____ hormones are released during meals from gut endocrine cells.

A

Incretin hormones are released during meals from gut endocrine cells.

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14
Q

What potentiates glucose-induced insulin secretion (and may be responsible for up to 70% of postprandial insulin secretion)?

A

Incretin

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15
Q

These 2 incretin hormones are thought to promote proliferation/neogenesis of beta cells and to prevent their decay (apoptosis). Both contribute to insulin secretion from the beginning of a meal; effects are progressively amplified as plasma glucose concentrations rise.

A
  1. GLP-1
  2. GIP
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16
Q

How does GLP-1 help in the GI tract?

A

Decreases gastric emptying

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17
Q

How does GLP-1 help in the liver?

A
  1. Increased glucose uptake
  2. Decreased glucose production
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18
Q

How does GLP-1 help in adipose tissue?

A
  1. Increased glucose uptake
  2. Increased lipolysis (possibly)
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19
Q

How does GLP-1 help in the brain?

A
  1. Increases satiety
  2. Decreases appetite
20
Q

How does GLP-1 help in skeletal muscle?

A
  1. Increases glucose uptake
  2. Decreases glucose utilization
  3. Increases glycogen synthase activity
21
Q

How does GLP-1 help in the pancreas?

A
  1. Increases insulin
  2. Decreases glucagon
  3. Increases beta cell proliferation
  4. Increases beta cell differentiation
  5. Decreases beta cell apoptosis
22
Q

What stimulates normal incretin secretion?

A

Food intake. Diminished secretion occurs in DM, but the response to incretin is preserved.

23
Q

In diabetes, insulin has decreased production, leading to _____ hepatic glucose production and _____ glucose uptake by muscles.

A

In diabetes, insulin has decreased production, leading to increased hepatic glucose production and decreased glucose uptake by muscles.

24
Q

Decreased muscular uptake of glucose leads to _____.

A

Decreased muscular uptake of glucose leads to insulin resistance.

25
Q

High serum glucose leads to renal excretory overload which causes _____.

A

High serum glucose leads to renal excretory overload which causes glucosuria.

26
Q

High serum glucose leads to osmotic diuresis and dehydration which causes _____.

A

High serum glucose leads to osmotic diuresis and dehydration which causes decreased cerebral blood flow.

27
Q

Increased lipolysis in adipose tissue leads to _____ synthesized by the liver, resulting in acidosis.

A

Increased lipolysis in adipose tissue leads to increased ketones synthesized by the liver, resulting in acidosis.

28
Q

What is insulitis?

A
  • Direct destruction of beta cells by virus or toxin → exposure of antigens to immune system.

or

  • Release of destructive cytokines that kill beta cells.

or

  • Programmed cell death (apoptosis) may be induced.
29
Q

Explain the pathway of islet cell destruction.

A
  • Activated cytotoxic T lymphocytes (CD8+) and macrophages attach to beta cells.
  • Release of cytokines from activated macrophages → cell destruction.
30
Q

3 classic symptoms of DM.

A
  1. Polydipsia (too much sugar in urine)
  2. Polyuria (too much peeing)
  3. Polyphagia (too much hunger, but still have weight loss)
31
Q

Clinical presentation of DMT1.

A
  • Wasting
  • Visual impairment
  • Orthostasis
  • Dry skin and mucus membranes
  • Impaired LOC, fruity breath (ketoacidosis)
32
Q

Glucose intolerance with onset or first recognition in pregnancy.

A

Gestational DM (GDM)

33
Q

What are 3 adverse effects of gestational DM (GDM)?

A
  1. Premature delivery
  2. Large babies
  3. Increased perinatal morbidity and mortality
34
Q

7 risk factors for gestational DM (GDM).

A
  1. Personal hx of DM or GDM
  2. PCOS
  3. Marked obesity
  4. Glycosuria
  5. Older age (25+)
  6. Family hx of DM
  7. Ethnicity
35
Q

When is testing for GDM conducted?

A
  • For those at high risk, early in 2nd trimester.
  • For those at normal risk, between weeks 24-28.
36
Q

What is the GTT?

A

Oral glucose test (75-gram load) performed after an overnight fast of at least 8 hours.

37
Q

What blood glucose values constitute GDM durin oral GTT?

  • Fasting: _____ mg/dl
  • 1 hour: _____ mg/dl
  • 2 hours: _____ mg/dl
A
  • Fasting: ≥92 mg/dl
  • 1 hour: ≥180 mg/dl
  • 2 hours: ≥153 mg/dl
38
Q

GDM increases risk of DMT2. When should women with GDM be rescreened?

A
  • 6-12 weeks PP.
  • If negative, check annually.
  • Lifelong screening at least every 3 years.
39
Q

What are predisposing factors for DMT2?

A
  • Heredity
    • 80% concordance rate in identical twins
    • 40% of siblings
    • 33% of offspring develop abnormal glucose tolerance or DM
  • Obesity (#1 cause)
  • Central adiposity
  • Inflammation
40
Q

It takes time to develop T2. What are the 3 phases?

A
  1. Plasma glucose normal despite insulin resistance because of hyperinsulinemia.
  2. Worsening insulin resistance; postprandial hyperglycemia despite hyperinsulinemia.
  3. Declining insulin secretion with insulin resistance → fasting hyperglycemia and overt DM.
41
Q

Insulin resistance in DMT2 is caused by what 2 factors?

A
  1. Increased hepatic glucose production
  2. Decreased muscle glucose uptake
42
Q

Impaired beta cell insulin secretion is exacerbated in DMT2 by the fact that _____ is not suppressed in hyperglycemia.

A

Impaired beta cell insulin secretion is exacerbated in DMT2 by the fact that glucagon secretion (by pancreatic alpha cells) is not suppressed in hyperglycemia.

43
Q

Since it takes time to develop T2, at what phase(s) can it still be aborted?

A

It can be aborted in Phases 1 and 2.

44
Q

What is Syndrome X?

A
  • Insulin resistance that is part of obesity in DMT2.
  • Components include:
    • Obesity
    • Glucose intolerance
    • HTN
    • Dislipidemia
    • Hyperglycemia
    • Hyperinsulinemia
45
Q

What is the subclassification for a non-obese person with DMT2?

A
  • Maturity-Onset Diabetes of the Young (MODY)
  • (Type 1.5 or monogenic diabetes)
  • It is considered a slowly evolving Type 1.
46
Q

Clinical presentation of DMT2.

A
  • Relatively asymptomatic
  • Symptoms of cardiac, skin, or neurological complications
  • Obese face, trunk, abdomen
  • Decreased peripheral sensation
  • Fundoscopic changes
  • Recurrent fungal infections, vaginal yeast infections
  • Intertrigo
  • Skin ulcers

NURP 502 - Ex 3 (37 decks)

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