type 2 diabetes PAT202

Question 1

what are risk factors of type 2 diabetes?

Answer 1

• age, obesity
• HTN
• physical inactivity
• family hx
• affects both adult and children
• genetics
• environmental factors

Question 2

presence of antibodies in type 2 diabetes?

Answer 2

-islet cells antibodies not prevalent

Question 3

insulin resistance in type 2?

Answer 3

insulin resistance is generally caused by altered cellular metabolism and an intracellular post receptor defect

Question 4

insulin secretion in type 2?

Answer 4

typically increased at time of diagnosis, but progressively declines over the course of the illness

Question 5

what are the characteristics of type 2?

Answer 5

• usually not insulin dependent but may be insulin requiring
• individuals not ketosis prone (but may form ketones under stress)
• obesity is common in the abdomen region
• strong genetic predisposition
• often associated w/ HTN and dyslipidemia

Question 6

what are the three core mechanisms of type 2?

Answer 6

• insulin resistance
• beta cell dysfunction
• glucagon

Question 7

what happens in beta cell dysfunction?

Answer 7

• beta cell mass is decrease

- inflammation and changes occur in adipokines

Question 8

factor of glucagon and type 2?

Answer 8

-pancreatic alpha cells are less responsive to glucose inhibition; hyperglycemia- abnormally high levels of glucagon increase hepatic production of glucose

Question 9

why is recurrent infections (boils, and carbuncles, skin infections, prolonged wound healing a factor of type 2?

Answer 9

-growth of microorganisms is stimulated by increased glucose levels, impaired blood supply hinders healing; decline in immune protection

Question 10

genital prutits why does it happen in type 2?

Answer 10

hyperglycaemia and glycosuria favour fungal growth’ candidal infections, resulting in pruritus are a common presenting symptom in women

Question 11

why does visual changes happen in women?

Answer 11

blurred vision occurs as water balance in the eye fluctuates b/c of elevated blood glucose levels; diabetic retinopathy is another cause of visual loss

Question 12

why does paresthesias occurs in type 2?

Answer 12

common manifestations of diabetic neuropathies

Question 13

why is fatigue a factor in type 2?

Answer 13

metabolic changes result in poor use of food products, contributing to lethargy and fatigue

Question 14

acanthosis nigricans and type 2?

Answer 14

brown to black pigmentation in body folds associated w/insulin resistance

Question 15

do we need to screen for type 1 diabetes?

Answer 15

NO

-there is insufficient evidence for interventions to prevent or delay type 1 diabetes

Question 16

how do we screen for type two diabetes?

Answer 16

• screen every three years for individuals over 40 yrs of age or individuals a high risk using a risk calculator
• Screen earlier and/or more frequently (every 6 to 12 months) in people with additional risk factors for diabetes or for those at very high risk using a risk calculator

Question 17

what is a normal FPG /A1C (fasting plasma glucose)?

Answer 17

-FPG <5.6 mmol/L and/or A1C <5.5%

Question 18

what is an at risk FPG/A1C?

Answer 18

FPG 5.6-6.0 mmol/L and/or A1C 5.5-5.9%*

RESCREEN MORE OFTEN

Question 19

what is a prediabetic FPG/A1C?

Answer 19

FPG 6.1-6.9 mmol/L and/or A1C 6.0-6.4%**

rescreen more often

Question 20

what is a diabetic A1C/FPG?

Answer 20

FPG ≥7.0 mmol/L and/or A1C ≥6.5%

Question 21

FPG (mmol/L) of 6.1-6.9- what is the prediabetic category?

Answer 21

impaired fasting glycaemia (IFG)

Question 22

2h PG in a 75g OGTT (mmol/L)

oral glucose tolerance test OF 7.8-11.0. what is the prediabetic category?

Answer 22

impaired glucose tolerance (IGT)

Question 23

A1C (%) of 6.0-6.4 is _?

Answer 23

prediabetes

Question 24

what is the diagnosis of diabetes?

Answer 24

-Glycosylated hemoglobin (HgA1C) levels
permanent attachment of glucose to hemoglobin molecules; reflects average glucose exposure over life of a red blood cell (RBC) (approximately 90-120 days)
-Fasting plasma glucose (FPG) levels
-Two-hour plasma glucose during oral glucose tolerance testing (OGTT) using a 75-g oral glucose load
-Random glucose levels in an individual with symptoms

Question 25

diagnostic criteria for diabetes?

Answer 25

-FPG ≥7.0 mmol/L
-Fasting = no caloric intake for at least 8 hours
or
-A1C ≥6.5% (in adults)
or
-2hPG in a 75 g OGTT ≥11.1 mmol/L
or
-Random PG ≥11.1 mmol/L
-Random = any time of the day, without regard to the interval since the last meal
or
-Client with classic symptoms of hyperglycemia or hyperglycemic crisis, a random PG ≥11.1 mmol/L

Question 26

what is obesity?

Answer 26

• Characterized by abnormal or excessive body fat (adiposity)
• Excessive adiposity is source of adipokines and inflammatory mediators that alter glucose and fat metabolism leading to increased risk of CV disease, type 2 diabetes, and many other health complications
• those with central or visceral obesity are at increased risk for developing insulin resistance and type 2 diabetes

Question 27

what mechanisms does obesity act on?

Answer 27

• alteration in production of adipokines by adipose tissue
• elevated serum free fatty acids and intracellular lipid deposits
• release of inflammatory cytokines from adipose tissue
• reduced insulin-stimulated mitochondrial activity
• obesity-associated insulin resistance

Question 28

what is adipose tissue?

Answer 28

it is an endocrine organ
-Contains
macrophages, mast cells, neutrophils, fibroblasts, endothelial cells, blood vessels, nerves, and adipocytes

-Adipocytes
most are considered white adipose tissue (WAT)

-WAT secretes numerous adipokines that function like hormones
actions necessary for metabolic functions and immune responses

Question 29

Adipose tissue localized around abdomen and upper body

Answer 29

-central or visceral obesity
results in apple shape
-excess causes adipocyte dysfunction and dysregulation of adipokines

Question 30

Increase in adipocyte size

Answer 30

• exceeds supporting vascular supply resulting in hypoxia and inflamed and fibrotic adipose tissues
• leads to dysregulation of adipokines, macrophage infiltration, insulin resistance, chronic proinflammatory state, and altered lipid metabolism

Question 31

Excess lipolysis leads to increased release of free fatty acids (FFAs) into circulation

Answer 31

-excess FFAs are distributed to nonadipose cells, and when their utilization capacity is exceeded cellular dysfunction or death occurs (lipotoxicity)

Question 32

More on The Consequences of Increased FFAs (free fatty acids)

Answer 32

-Diversion of excess FFAs to nonadipose tissues

-pancreatic beta cells
FAAs cause beta cell dysfunction (lipotoxicity)

-skeletal muscle
FAAs cause insulin resistance & ↓ glucose use in peripheral tissues

-liver
↑ FFAs and ↑ triglycerides → ↓ hepatic insulin sensitivity → ↑ hepatic glucose production → hyperglycemia
uptake of FFAs from portal circulation → hepatic triglyceride accumulation → non-alcohol fatty liver disease (NAFLD)

-heart
CAD

Question 33

alternations in adipokines

Answer 33

-Adipocytes release a number of hormones that are altered in obesity and have an important adverse effect on insulin sensitivity

-Adipokines or adipocytokines are cytokines (cell signalling proteins) secreted by WAT adipocytes and other tissues
contribute to insulin resistance → increased BG levels

-Adipokines primarily from WAT
leptin
adiponectin

Question 34

what is leptin?

Answer 34

• Expressed primarily by adipocytes
• Regulates hepatic gluconeogenesis, insulin sensitivity, and glucose and lipid metabolism in liver, muscle, and adipose tissue

-Leptin levels increase as number of adipocytes increase
but…increased levels cause body to not respond to leptin the way is it supposed to!
leads to dysregulation and leptin resistance

-Leptin resistance results in
insulin resistance, hyperglycemia, hyperinsulinemia, and hyperlipidemia
stimulates macrophages and endothelial cells to produce proinflammatory mediators

Question 35

adiponcetin

Answer 35

-Produced primarily by visceral adipose tissue
insulin-sensitizing
antiinflammatory
antiatherogenic
BUT plasma levels decrease w/ visceral obesity=contributes to insulin resistance

Question 36

Role of The Gut Microbiome

Answer 36

• Changes in intestinal microbiome associated with obesity
• Microbes (mostly bacteria) found in high concentration in lower GI tract

-Among other roles, gut microbial bacteria participate in inflammatory responses
affect host inflammation

-Gut microbiota may have a causal role in the development of obesity and insulin resistance

Question 37

how does all this r/t metabolic syndrome?

Answer 37

Visceral obesity =chronic increase FFAs = lipotoxicity = pancreatic beta cell dysfunction, insulin resistance & glucose underutilization in peripheral tissues (inhibits glucose uptake), ↓hepatic insulin sensitivity (hepatic glucose production and hyperglycemia)

Insulin resistance
effects of insulin are less than expected for glucose disposal in skeletal muscle and suppression of glucose production by liver
increase risk of developing type 2 diabetes

Question 38

metabolic syndrome

Answer 38

-Develops during childhood, is highly prevalent among overweight children and adolescents, and affects millions of adults
-Is a cluster of disorders
-central/visceral obesity
distribution of body fat is localized around abdomen and upper body (apple shape)
-dyslipidemia
↑ triglycerides
↓ HDL-C
↑ BP
↑ FBG/FPG