Lecture 16: Diabetes

Question 1

Polydipsia

Answer 1

thirst

Question 2

Polyuria

Answer 2

frequent urination

Question 3

Polyphagia

Answer 3

inc appetite

Question 4

Diabetes diagnostic criteria

Answer 4

just one of the following:
-A1C > 6.5%
-FPG > 126 mg/dL
-2h PG > 200mg/dL
-random PG > 200 mg/dL w sx

Question 5

Type I diabetes (IDDM)

Answer 5

-10% of DM
-glucose intolerance
-no insulin secretion
-almost no pancreatic beta cells
-need exogenous insulin
-ketoacidosis tendencies

Question 6

Type I Diabetes onset

Answer 6

-early (age 12)
-autoimmune response that kills pancreatic B cells
-might be triggered by viruses, chemicals, etc in predisposed individuals
-often no family hx
-aka juvenile onset DM (JODM)

Question 7

Loss of B-cell mass (BCM) in type I

Answer 7

-gradual loss
-FPG normal until 70% of BCM lost
-C-peptide is a maker for insulin secretion when injected insulin present

Question 8

C-peptide

Answer 8

-part of insulin processing
-C-peptide present = little bit of BCM left
-once gone there’s no more BCM

Question 9

Stage 1 type 1 diabetes BCM

Answer 9

-ICA and IAA become positive (autoantibodies)
-normal glucose stimulated insullin release
-BCM declines but FBG stays same*

Question 10

Stage 2 type 1 diabetes

Answer 10

-gradual loss of insulin release
-abnormal OGTT
-FBG starts to increase* (about 70% of BCM loss)

Question 11

Stage 3 type 1 diabetes

Answer 11

-BCM depletes
-FBG spikes
-C-peptide present vs absent?
-overt diabetes
-OGTT will detect hyperglycemia

Question 12

Autoantigens associated w type I 1A-2 (islet antigen)

Answer 12

-57% sensitivity = 57% will develop
-99% selectivity = 99% have Abs

-presence of ANTIBODIES against B cell proteins is a risk factor for type 1

-IA-2, ZnT-8, GAD65, Ca1.3, VAMP-2

Question 13

Type 2 Diabetes

Answer 13

-non-insulin dependent
-insulin resistance or not enough secretion
-NIDDM
-family history present
-non-obese vs obese

Question 14

Non-obsese NIDDM

Answer 14

-10%
-onset < 25 (MODY)
-low insulin secretion
-mutations in specific proteins

Question 15

Obese NIDDM

Answer 15

-80%
-fastest growing type of DM around the world
-onset > 35
-low insulin secretion for body mass
-insulin resistance/decreased BCM

Question 16

Consequence of lack of insulin

Answer 16

-Hyperglycemia
-Glucosuria
-Hyperlipidemia
-Uninhibited glucagon

Question 17

Hyperglycemia

Answer 17

-dec glucose uptake in cells where uptake is insulin dependent (skeletal muscle uptakes the most)
-dec glYcogen synthesis (stored glucose in liver)
-inc conversion of aas to glucose (inc gluconeogenesis (inhibited by insulin))

Question 18

Glucosuria

Answer 18

-glucose in urine
-lose more water = dehydration and polydipsia

Question 19

Hyperlipidemia

Answer 19

-inc fatty acid mobilization from fat cells
-inc fatty acid oxidation = KETOACIDOSIS
-ketone bodies (acetoacetate, hydroxybutyrate)
-unchecked bc low insulin

Question 20

Uninhibited Glucagon

Answer 20

-inc levels in the presence of inc blood glucose levels
-opposite of insulin
-stimulates release of glucose from liver
=hyperglycemia

Question 21

Complications of low insulin

Answer 21

1. CV: angiopathies (blood vesels)
2. Neuropathy: inc use of polyol pathway (aldose reductase) (uses all NADPH which cant be used for oxidative protection)
   -water accumulation in neurons and reduced protection from oxidative damage (neuropathies/nerve pain)
   -Nephropathy: changes to renal vasc and glomerular basement membrane (kidneys/nephropathies)
   -occular: cataracts, microaneurysms, (disrupted blood flow) hemorrhage (retinopathies)
   -inc susceptibility to infections

Question 22

Past goals of insulin therapy and monitoring

Answer 22

-reduce symptoms: polyuria, dehydration, ketoacidosis

Question 23

Current goals of insulin therapy

Answer 23

-keep AVERAGE BG levels < 150 mg/dL
-prevent/delay onset of complications
-increased risk of hypoglycemia
-A1C < 6 or 7

Question 24

why risk hypoglycemia to tx diabetes?

Answer 24

-retinopathy risk increases over A1c
-better to keep it low
-hyperglycemia worse

Question 25

Diabetes

Answer 25

-type 1 and 2
-results from HYPERglycemia

Question 26

Type I DM sx

Answer 26

-polydipsia
-polyuria
-polyphagia
-potential ketoacidosis

Question 27

Diabetic ketoacidosis

Answer 27

-uncontrolled oxidation of fatty acids
-accumulation of ketone bodies

Question 28

Ketoacidosis

Answer 28

-using FA for food
-oxidation of fat
-build up of ketones
-lack of insulin makes it harder to shut off FA oxidation

Question 29

T/F: ICA and IAA are only detectable after the onset of diabetes

Answer 29

FALSE

Question 30

Why does uncontrolled type 1 often result in ketoacidosis?

Answer 30

-glucose is not available as fuel
-body utilizes fatty acids
-insulin inhibits use of fatty acids (cant do in DM)
-ketone bodies are acidic