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NURP 502 - Ex 3 > 8: Diabetes > Flashcards

8: Diabetes Flashcards

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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?

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A
  1. Increases satiety
  2. Decreases appetite
20
Q

How does GLP-1 help in skeletal muscle?

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

How does GLP-1 help in the pancreas?

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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?

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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.

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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 _____.

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A

Decreased muscular uptake of glucose leads to insulin resistance.

25
High serum glucose leads to renal excretory overload which causes \_\_\_\_\_.
High serum glucose leads to renal excretory overload which causes **_glucosuria_**.
26
High serum glucose leads to osmotic diuresis and dehydration which causes \_\_\_\_\_.
High serum glucose leads to osmotic diuresis and dehydration which causes **_decreased cerebral blood flow_**.
27
Increased lipolysis in adipose tissue leads to _____ synthesized by the liver, resulting in acidosis.
Increased lipolysis in adipose tissue leads to **_increased ketones_** synthesized by the liver, resulting in acidosis.
28
What is insulitis?
* 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
Explain the pathway of islet cell destruction.
* Activated cytotoxic T lymphocytes (CD8+) and macrophages attach to beta cells. * Release of cytokines from activated macrophages → cell destruction.
30
3 classic symptoms of DM.
1. Polydipsia (too much sugar in urine) 2. Polyuria (too much peeing) 3. Polyphagia (too much hunger, but still have weight loss)
31
Clinical presentation of DMT1.
* Wasting * Visual impairment * Orthostasis * Dry skin and mucus membranes * Impaired LOC, fruity breath (ketoacidosis)
32
Glucose intolerance with onset or first recognition in pregnancy.
Gestational DM (GDM)
33
What are 3 adverse effects of gestational DM (GDM)?
1. Premature delivery 2. Large babies 3. Increased perinatal morbidity and mortality
34
7 risk factors for gestational DM (GDM).
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
When is testing for GDM conducted?
* For those at high risk, early in 2nd trimester. * For those at normal risk, **_between weeks 24-28_**.
36
What is the GTT?
Oral glucose test (75-gram load) performed after an overnight fast of at least 8 hours.
37
What blood glucose values constitute GDM durin oral GTT? * Fasting: _____ mg/dl * 1 hour: _____ mg/dl * 2 hours: _____ mg/dl
* Fasting: **_≥92_** mg/dl * 1 hour: **_≥180_** mg/dl * 2 hours: **_≥153_** mg/dl
38
GDM increases risk of DMT2. When should women with GDM be rescreened?
* 6-12 weeks PP. * If negative, check annually. * Lifelong screening at least every 3 years.
39
What are predisposing factors for DMT2?
* 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
It takes time to develop T2. What are the 3 phases?
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
Insulin resistance in DMT2 is caused by what 2 factors?
1. Increased hepatic glucose production 2. Decreased muscle glucose uptake
42
Impaired beta cell insulin secretion is exacerbated in DMT2 by the fact that _____ is not suppressed in hyperglycemia.
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
Since it takes time to develop T2, at what phase(s) can it still be aborted?
It can be aborted in Phases 1 and 2.
44
What is Syndrome X?
* Insulin resistance that is part of obesity in DMT2. * Components include: * Obesity * Glucose intolerance * HTN * Dislipidemia * Hyperglycemia * Hyperinsulinemia
45
What is the subclassification for a non-obese person with DMT2?
* **Maturity-Onset Diabetes of the Young (MODY)** * (Type 1.5 or monogenic diabetes) * It is considered a slowly evolving Type 1.
46
Clinical presentation of DMT2.
* 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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