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Thompson- spring > Diabetes Part 1.PP slides 1-43 > Flashcards

Diabetes Part 1.PP slides 1-43 Flashcards

1
Q

Where is the pancreas?

A
  • The pancreas located deep to the stomach
  • Stretches across the abdomen with

–Head adjacent to the duodenum

–Tail adjacent to the spleen

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2
Q

Another picture of the pancreas

A
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3
Q

What two major types of tissues make up the pancreas and what do they secrete?

A
  1. Acini- secrete digestive juices into the duodenum (exocrine)
  2. Islets of Langerhans- secrete insulin and glucagon directly into the blood (endocrine)
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4
Q

4 types of cells contained in the Islets

How are they distinguished from one another?

A
  1. α-
  2. β-
  3. δ-
  4. PP

–Types are distinguished from one another by their morphological and staining characteristics

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5
Q

3 fun facts about β-cells

(not really fun, but let’s pretend)

A
  1. Constituting about 60% of all the cells of the islets
  2. Lie mainly in the middle of each islet
  3. Secrete insulin and amylin (inhibits insulin secretion, any other effects unknown)
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6
Q

How many α-cells are in the Islets roughly? What do they secrete?

A
  • about 25% of the total
  • Secrete glucagon
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7
Q

How many δ-cells are in the Islets roughly? What do they secrete?

A
  • About 10% of the total
  • Secrete somatostatin
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8
Q

How many PP cells are in the Islets roughly? What do they secrete?

A
  • Very few in number
  • Secretes a hormone of uncertain function called pancreatic polypeptide
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9
Q

What does PP stand for in PP cells?

A

Pancreatic Polypeptide

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10
Q

Point about communication among cells in pancreas

A

The close interrelations among these cell types allow cell-to-cell communication and direct control of secretion of some of the hormones by the other hormone

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11
Q

What does insulin inhibit?

A

glucagon secretion

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12
Q

What does amylin inhibit?

A

insulin secretion

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13
Q

What does somatostatin inhibit?

A

the secretion of both insulin and glucagon

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14
Q

What is Diabetes Mellitus?

A

Chronic disorder caused by either deficient insulin, or defective insulin action

–Hyperglycemia

–Disruption of metabolism of carbohydrates, fats, and proteins

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15
Q

Diabetes Mellitus is the leading cause of what 3 things?

A
  1. ESRD (end stage renal disease)
  2. blindness
  3. non-traumatic amputation of LE

*has cascading effect on other diseases

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16
Q

What are the effects of insulin on the metabolism?

A
  1. Increase carbohydrates storage as glycogen mainly in the liver and muscles
  2. Increase amino acid uptake and protein synthesis
  3. Increase fatty acid storage in adipose tissue
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17
Q

Basic explanation of how insulin is involed in Type 1 and 2 Diabetes

A
  • Type I DM – little or no insulin produced
  • Type 2 – defective insulin and/or impaired cell receptor binding of insulin
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18
Q

What happens with carbohydrate metabolism with glucose uptake in the muscle?

A

–Activity – increase membrane permeability to glucose during moderate or heavy exercise

–Carbohydrate consumption - Insulin can increase the rate of transport of glucose into the resting muscle cell by at least 15-fold

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19
Q

What is the purpose of GLUT1 transporters in the brain?

A

Brain has GLUT1 transporters so glucose uptake in brain not directly insulin dependent

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20
Q

True or False: Critical blood glucose level for normal brain function is > 20-50 mg/dl which is relatively high.

A

False

It is relative low

21
Q

What can happen to the brain if a person becomes too hyperglycemic or hypoglycemic?

A

Hypoglycemic shock with fainting, seizures, and even coma

Hyperglycemia shows a progressive loss of consciousness leading to coma

*Both have the capcity to slowly shut the brain down

22
Q

3 major insulin effects that lead to fat storage in adipose tissue

A
  1. Increases the utilization of glucose will decrease the utilization of fat, thus functioning as a fat sparer (allows us to use readily availible glucose)
  2. Promotion of fatty acid synthesis
  3. Increase uptake of glucose by adipose cells and conversion into fatty acids as just discussed
23
Q

Relationship between insulin and plasma cholesterol (3)

(Include: How much does plasma lipoproteins change?)

A
  • Insulin deficiency promotes increase plasma cholesterol and phospholipid synthesis from fatty acids in the liver.
  • Occasionally the plasma lipoproteins increase as much as 3X in the absence of insulin
  • This high lipid concentration-especially the high concentration of cholesterol-promotes the development of atherosclerosis in people with deficient insulin action
24
Q

What effect does does ketoacidosis have on a diabetics breath?

A

It gives a fruity breath smell

25
Q

Relationship between insulin and ketoacidosis (4)

A
  • Insulin deficiency promotes ketoacidosis
  • When fats are used for metabolism b-oxidation of the fatty acids produces acetyl-CoA
  • Excessive acetyl-CoA forms ketone bodies and decrease pH – ketoacidosis
  • Ketoacidosis, if severe, can lead to coma and death
26
Q

Example of a ketogenic diet

A

Atkins

High in fat and protein

Low in Carbs

*Research being done on effects of ketogenic diet and kids with autism and seizures

27
Q

Relationship between increased protein synthesis and insulin storage (5)

A
  • Stimulates transport of many amino acids into the cells
  • Increase the translation of messenger RNA, thus forming new proteins
  • Increase the rate of transcription of selected DNA genetic sequences in the cell nuclei, thus forming increased quantities of RNA and still more protein synthesis
  • Maintains high levels of amino acids by inhibiting deamination & decreased rate of gluconeogenesis
  • Inhibits the catabolism of proteins by cellular lysosomes
28
Q

What is normal for blood glucose? (3)

A

–Usually between 70 and 120 mg/dl of blood in the fasting person each morning before breakfast (some references 70-100)

–Increase to 120 to 140 mg/100 ml during the first hour or so after a meal

–Blood glucose concentration back to fasting level usually within 2 hours after the last absorption of carbohydrates

*may have a variation of 10mg/dl

29
Q

How does a lack of insulin affect protein metabolism? (3)

A
  • Increase protein catabolism and decreased rate of protein synthesis
  • Increase [amino acid] in blood due to amino acid dumping by tissue
  • Protein wasting leading to extreme weakness as well as many deranged functions of the organs can result from insulin deficiencies
30
Q

Factors and conditions that increase Insulin secretion (3)

A
  • Insulin resistance
  • If cell receptors become damaged, glucose cannot be absorbed from the bloodstream, prompting ↑ insulin production to overcome the resistance
  • Obesity – “belly fat” hormones (metabolic syndrome causing insulin resistance, ↑BP, ↑lipids, cardiovascular disease)
31
Q

A game that encourages diabetes

A
32
Q

When is insulin produced?

A

Immediately after we eat

33
Q

How does liver function as a blood glucose buffer system? (4)

A
  • 2/3 of the glucose absorbed from the gut is stored in the liver in the form of glycogen under the stimulation of increase insulin secretion
  • Subsequently when blood [glucose] and the rate of insulin secretion fall, the liver releases the glucose back into the blood
  • In this way, the liver decreases the fluctuations in blood glucose concentration to about 1/3 of what they would otherwise be
  • Patients with severe liver disease have problems maintaining a narrow range of blood glucose concentration (vulnerable to diabetes)
34
Q

True or False: Insulin functions as primary controller in feedback control systems for maintaining a normal blood [glucose]

A

True

35
Q

How do the feedback controls look for maintaining a normal blood glucose?

A
  • Increase blood glucose, insulin is secreted & causes the blood [glucose] to decrease toward normal
  • Decrease in blood [glucose], decrease insulin secretion
36
Q

4 reasons it is critical that blood glcose does not rise too much

A
  1. Glucose can exert a large amount of osmotic pressure in the extracellular fluid

–If the glucose concentration rises to excessive values, this can cause considerable cellular dehydration

  1. An excessively high level of blood glucose concentration causes loss of glucose in the urine.
  2. Loss of glucose in the urine also causes osmotic diuresis by the kidneys, which can deplete the body of its fluids and electrolytes
  3. Long-term increase in blood glucose may cause damage to many tissues, especially to blood vessels. Vascular injury, associated with uncontrolled diabetes mellitus, leads to increased risk for heart attack, stroke, end-stage renal disease, and blindness
37
Q

Some stats about rising incidence of diabetes

A

–Increase per year

–Increase by age group

  • 18-44 stable with slight rise
  • Greatest increase 45-64 & 65-79 age groups

Dr. T attributes this to diet and exercise a long with added stress

38
Q

Characteristics of Type I Diabetes (4)

A
  • Formerly Insulin Dependent (IDDM) or juvenile onset
  • Autoimmune destruction of b-cells often with serologic evidence of autoimmune disease and certain genetic markers
  • Prone to ketoacidosis and demonstrate the metabolic derangements associated with hyperglycemia
  • Requires exogenous (injectable) insulin
39
Q

Characteristics of Type II Diabetes (4)

A
  • formerly Non-Insulin Dependent (NIDDM) or adult onset
  • Produced by a combination of cellular resistance to insulin and lack of a compensatory increase in production of insulin.
  • Not as likely to exhibit ketoacidosis and the metabolic derangements associated with hyperglycemia
  • Can often be corrected by diet, exercise and oral hypoglycemic agents
40
Q

Differences between Type I and II

onste and etiology

A
41
Q

Differences between Type I and II

risk factors

A
42
Q

Difference between Type I and II

lots of other categories

A
43
Q

Highlighted risk factor in power point for Type II

A

–High risk individuals are aged 55 or older, have a BMI > 30 & have a family history of diabetes

–19.9% of these high risk individuals developed Type 2 diabetes in 5 years

44
Q

True or False: Gestational diabetes is associated with pregnancy, and gets worse post partum

A

False

Usually return back to normal

45
Q

Fasting blood glucose level

NEED to KNOW

A

70-90 mg/dl

46
Q

2 hour post meal blood glucose level

NEED to KNOW

A

120-140 mg/dl

47
Q

What is the HbA1c test (hemoglobin A1c test, glycosylated hemoglobin A1c test, glycohemoglobin A1c test)?

A
  • Long-term assessment of blood glucose levels
  • Reveals average blood glucose over a period of two to three months (life span of a RBC).
  • It measures the number of glucose molecules attached to hemoglobin, a substance in RBCs.
  • Norm is 4-6%
  • Definition of diabetes presence is when HbA1c ≥7%
  • A1C is considered truth serum because it represents multiple days (ultimately the length of the life of a RBC). The HbA1c “big picture” complements the day-to-day “snapshots” obtained from the self-monitoring of blood glucose (mg/dl)
48
Q

3 tests used to diagnose diabetes and results for each resulting in a diagnosis of diabetes

A
  1. HbA1c- greater than or equal to 6.5%
  2. Fasting glucose levels- greater than or equal to 126 mg/dL
  3. 2-hour glucose tolerance test- greater than or equal to 200mg/dL
49
Q

Role of Insulin and Glucagon in Homeostasis (3)

A
  • Insulin secreted by beta cells in response to high blood sugar. After a meal, blood glucose ↑ and insulin ↑
  • In response to insulin, cells take in glucose from the blood for nutrition; both blood glucose and insulin levels go back to resting range (70-120 for glucose)
  • When blood glucose ↓ (between meals and during exercise), glucagon is activated to cause the liver to release stored glucose

Thompson- spring (13 decks)

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