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Diabetes Introduction Flashcards

1
Q

Diabetis mellitus definition

A

A metabolic disorder characterized by elevated blood glucose concentrations and disturbances of carbohydrates, lipids and protein due to defective insulin secretion and/or action.

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2
Q

What are the types and characteristics of diabetes

A

Type 1 DM

◦ Insulin-dependent (IDDM) - not used anymore

◦ Juvenile or growth onset- usually occurs before 20 yo
◦ Ketosis prone, could eventually become ketoacidosis

Type 2 DM
◦ Non-insulin dependent (mostly)

◦ Maturity onset (mostly)

◦ Not prone to ketosis due to insulin still being present

Gestational diabetes
◦ Diagnosed during pregnancy; goes away after pregnancy

  • women who develop GD are more likely to develop diabetes later on in life

Other types
◦ Genetic defects

◦ Pancreatopathy

Pre-diabetes- important to address and treat

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3
Q

Etiology of T1DM

what is the prevalence

A

Autoimmune or idiopathic destruction of pancreatic ß-cells → absolute deficiency in insulin production

5-10% of all diabetes cases

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4
Q

Etiology of T2DM

what is the prevalence

A
  • Cells do not respond normally to insulin (resistance)
  • Cells do not take up and utilize glucose efficiently → hyperglycemia
  • Pancreas may compensate or not with insulin production → hyperinsulinemia or normal levels
  • 10+ years of diabetes-> insulin levels decrease

90-95% of all cases

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5
Q

Which type of diabetes takes longer to develop

A

T2Dm

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6
Q

Out of 90-95 of T2DM patients, how many will be ketosis resistant? Ketosis prone?

Which of those will receive insulin treatment?

A

85-90 Ketosis resistant

5 Ketosis prone- will require insulin treatment

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7
Q

Out of 85-90 Ketosis resistant T2DM patients, how many will be obese? normal weigth?

A

75-80% obese

5-10% normal weight

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8
Q

What are the treatments prescribed to all ketosis resistant T2DM patients? (no matter obese or normal)

A

25% Diet Rx

50% Oral medication Rx

25% Insulin Rx- at later stages of diabetes

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9
Q

Is diabetes more prevalent in male or female canadians?

A

males

corresponds with higher obesity rates in males

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10
Q

How did prevalnce of diabetes change from 2011? from 2013?

A

Increase from 2011 (but not from 2013)

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11
Q

What is the prevalence of diabetes in Canada?

A

6.7% (2.0 million) of Canadians

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12
Q

How did prevalence amongst sexes change in Canada?

A

Slight increase in prevalence in males, slight decrease in females

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13
Q

What is the trend in diabetes prevalence across ages?

A

more in men
more in older people
new casses do not develop in people aged 60-75

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14
Q

Diabetes in Canada: Prevalence by Province and Territory

A

NL, NS and ON had the highest prevalence, while NU, AB and QC had the lowest.

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15
Q

Which populations are at hihger risk of diabetes

A

◦ South Asian, Asian, African, Hispanic descent
◦ Aboriginal, First Nations: 3-5 times more diabetes

◦ Overweight, older, low income

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16
Q

Policies and surveillance programs in Canada that are in place to help aboriginals

A

◦ Canadian Diabetes Strategy
◦ Aboriginal Diabetes Initiative
◦ Canadian Chronic Disease Surveillance System

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17
Q

what is the link between education and obesity?

A

Higher prevalence in lower educated demographic
Less access to healthy food

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18
Q

1/_ people with diabetes

A

1/12 people with diabetes

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19
Q

how many people with diabetes are unaware of it?

A

1 in 2

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20
Q

How is diabetes a burden?

A
  • High mortality
  • High costs
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21
Q

Type 1 Diabetes: Causes

A
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22
Q

T1DM Symptoms

Initial observations

Clinical laboratory tests reveal:

A

Initial observations

◦ Increased thirst (polydipsia)
◦ Increased urination (polyuria)
◦ Increased hunger (polyphagia)
◦ Weight loss (T1DM) or obesity (T2DM); happens very rapidly

Clinical laboratory tests reveal:
◦ Glycosuria
◦ Hyperglycemia
◦ Abnormal glucose tolerance (GTT)

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23
Q

Why is there increased hunger?

A

due to increased glucose excretion in urine-> caloric lose-> increased appetite
also cells are not taking up glucose -> increased energy need signals

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24
Q

What are the impacts of insulin?

A

↑ glucose uptake and storage

↓ glycogenolysis and gluconeogenesis = ↓endogenous glucose production

↑lipogenesis
↓ lipolysis
↑ protein synthesis

↓ proteolysis

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25
Insulin deficiency impacts
26
What are the cnages in usual insulin regulation in diabetes
Lypolysis occurs at higher levels due to the absence of supressing effect by insulin Higher levels of muslce breakdown No inhbibitory effect of insulin on gluconeogenesis in the liver
27
what is characteristic for the diabetic fasted state?
Increased lypolysis-\> FFA are used as a main energy store Excessive glucose levels due to high levels of gluconeogenesis and decreased uptake High glucose levels in urine
28
Diabetes fed state
29
Type 2 Diabetes: Causes
- Excessive food intake- more that calories burned - Lack of excercise - Genetic predisposition - constant Hyperinsulinemia (not only after meals, but also in fasted states) van contribute to obesity - Compensatory Hyperinsulinemia due to excessively high levels of glucose
30
What is inuslin resistance and what is it mostly due to?
Defined as a lesser sensitivity to insulin’s action in suppressing hepatic glucose production and stimulating glucose uptake Mostly due to defective insulin signaling within cells
31
Mechanism of insulin induced glucose uptake
32
Is insulin resistance cuased by the receptor?
insulin resistance mostly arises from the intercellular factors, not problems with the receptor itself
33
Insulin resistance: 2 cellular mechanisms
_Receptor defects: decreased number and affinity_ ◦ Rare cases of genetic mutations of INSR gene _Post-receptor second messenger signaling_ ◦ Most cases of IR
34
Insulin signaling cascade
insulin binds to the receptors Phosphorylation will occur IRS (insulin receptor substarte) will get phosphorylated; after that there are 2 possible pathways: 1) ERK-1 pathway (pathway fro insulin groeth and differentiation pathway) 2) PI3K-Akt pathway is connected to more acute effects of insulin e..g after meal consumption
35
Impacts of Pi3K-Akt pathway
Muscle: Increased glucose tranpsport (GLUT4), Increased glycogen synthesis Liver: Increased glycogen synthesis, Increased lipogenesis, decreased gluconeogenesis Fat: inceased glucose transport (GLUT4), Increased lipogenesis, decreased lipolysis
36
Akt mTORC1 connection
Akt controlls SREBP1C activity via mTORC1
37
Impacts of insulin resistance on liver, muscle, blood and adipocytes
Blood: Increased blood glucose and NEFA Muscle: decreased glucose uptake, decreased, GLUT4 expression transclocation, decreased glucose oxidation, decreased glycogenesis Liver: Increased gluconeogenesis Adipocytes: Increased lypolysis
38
Type 2 diabetes: Risk Factors
oAge oSex (male) ?- is it sexual difference in terms of hormones or in terms of obesity? oObesity oSedentary lifestyle oEthnicity (e.g. Aboriginal, African, South Asian, Hispanic) oPrediabetes: impaired fasting glucose or impaired glucose tolerance oFamily history oHistory of GDM oChild of a woman with poorly controlled diabetes during pregnancy oLow birth weight (\<2.5 kg) and high birth weight (\>4.0 kg) oPolycystic ovary syndrome (PCOS)
39
Insulin resistance: other related conditions
oObstructive sleep apnea oInfection- increased infections; high BG provides nutrition for pathogens oSteroid-induced oCushing’s syndrome oHemochromatosis oLipodystrophic diabetes oAcanthosis nigricans- results in blackening of the skin where the skin is bending oWerner’s syndrome (adult form of progeria) oIdiopathic
40
Metabolic staging of type 2 diabetes
Type-2 diabetes is characterized by a progressive decrease in insulin action, followed by an inability of the β-cell to compensate for insulin resistance. Insulin resistance is the first lesion, due to interactions among genes, aging, and metabolic changes produced by obesity. Insulin resistance in visceral fat leads to increased fatty acid production, which exacerbates insulin resistance in liver and muscle. The β-cell compensates for insulin resistance by secreting more insulin. Ultimately, the β-cell can no longer compensate, leading to impaired glucose tolerance, and diabetes.
41
Type 1 vs. Type 2 DM Onset Symptoms Control Stability
42
Type 1 vs. Type 2 DM Ketoacidosis Oral anti- hyperglycemic agents Insulin Tx Diet Complications
43
Diabetes Complications: Short-term (hours or days)
1. Hypoglycemic episodes 2. Diabetic ketoacidosis: life-threatening 3. Hyperglycemic hyperosmolar syndrome
44
What is one of the main complications of T1DM?
Hypoglycemic episodes
45
Describe diabetic ketoacidosis
* More in T1DM * ↑ risk during illness, infection, stress * Symptoms: N/V, stomach pain, acetone breath, rapid respirations, cognitive changes; can lead to coma * More rare than Hypoglycemic episodes * when a person is undiagnosed, or if someone uses insulin injection and forgets to inject it or stops to inject it * more dehydration is typical for DM-\> brain is affected-\> people forget to inject
46
Describe Hyperglycemic hyperosmolar syndrome
* More rare than Hypoglycemic episodes * More in T2DM * Seen with blood glucose \>33 mmol/L * excessivley high glucose levels-\> hyperosmolar situation * lost of glucose in urine-\> more dehydration-\> exacerbation * Infection and dehydration are precipitating factors
47
What is the BG levels in hypoglycemia
BG \< 3.9 mmo/L (but individual for symptoms)
48
What are the symptoms of hypoglycemia?
49
Common etiology of hypoglycemia
skipping or delaying meals, reduced CHO intake without med compensation, misdosage of insulin, unplanned exercise the more these occur, the less sensitive people become dangerous at night
50
Treatment of hypoglycemia
people sense the symotpms and need to take action as soon as they appear-\> fast action required ## Footnote **15-15 rule:** Give 15 g of fast absorbed CHO, check BG 15 min later, repeat if BG still low
51
What is the treatment for severe hypoglycemia? What are the dangers of this method
treatment (from care provider): injection of glucagon or glucose Glucagon works by telling your body to release sugar (glucose) into the bloodstream to bring the blood sugar level back up glucagon is not stable in the solution; stress of the situation affects the impact of injection thus, prevention is the best via education to feel the symptoms of hyperglycemia
52
Diabetes Complications: Long-term aka years
**Microvascular** * Retinopathy: cataracts, glaucoma, macular edema → blindness * Nephropathy: 20-40% of persons with DM * chronic kidney disease/failure → dialysis, transplantation * Neuropathy: ~ 50% of persons with DM * impaired sensation or pain in extremities → amputations * gastroparesis: ↓peristaltis -can lead to nausea and impaired digestion **Macrovascular**: CVD, CHD, stroke Other common complications: poor wound healing, erectile dysfunction, increased susceptibility to infections
53
Pathophysiology of diabetes complications
54
What is A1C an indicator of?
A1C is an indicator of long-term glycemic control because Hb half-life is about 3 months
55
What is the normal levels of A1C?
Measured as a % of Hb ◦ Normal: 4.3-6.0%
56
T1DM and dysplididemia
◦ HyperTG due to defective removal of chylomicrons and VLDL resulting from impaired LPL activity (insulin dependent) ◦ HDL and LDL-C may be normal
57
T2DM and dysplididemia
◦ HyperTG due to elevated de novo synthesis from glucose ◦ Low HDL-C (due to obesity) ◦ LDL-C often elevated but may be normal
58
Diabetes and heart disease
oDiabetic patients have 2-4 X risk of developing CVD: greater independent risk than smoking, hypertension, hypercholesterolemia, obesity oHeart disease is the major cause of death in DM: 65%
59
Recommendations for cardiovascular protection
the ABCDEs
60
Screening and diagnosis of T2DM in adults
61
FPG, OGTT, A1C, Random PG diabetes diagnosis criteria
62
OGTT Blood Glucose Curve
Blood glucose is measured at 2h mark
63
What are the 3 main markers for Diagnosis of prediabetes
oIFG oIGT oA1C 6.0%-6.4%
64
\_\_ can prevent diabetes onset
Intervention can prevent diabetes onset
65
Diabetes Prevention Program (DPP)
Benefit of diet and exercise or Metformin on diabetes prevention in at-risk patients Lifestyle changes had the biggest impact
66
ABCDES of diabetes care
67
Targets for glycemic control
68
Ideal, optimal, subotimal, inadequate Non-DM, DM taget, Consider action, Action required cut of levels for A1C, fasting glucose, glucose 2hrs PC
69
\_\_ results in reduction in incidence and progression of complications
Optimal glycemic control results in reduction in incidence and progression of complications
70
Which markers should be monitored in diabetes?
◦ SMBG: self-monitoring blood glucose ◦ Blood glucose ◦ Urine glucose ◦ Urine ketones ◦ Blood ketones ◦ Glycated proteins
71
Which device can be used for SMBG monitoring?
Glucometers
72
How frequently should SMBG be carried out?
Daily monitoring * TID (2 times/day) for type 1 ((conventional Tx), more with intensive Tx * variable for type 2
73
Coventional vs acute therapy
conventional therapy- fixed injection acute- calculating dose of insulin according to CHO ingested
74
In which populations is SMBG especially important? In which populations it may not be necessary?
Important for people on antihyperglycemic agents or insulin to prevent hypoglycemia May not be necessary for those only on diet Tx

NUTR 344 (22 decks)

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