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PHAR 152 > Diabetes - Part 1 > Flashcards

Diabetes - Part 1 Flashcards

1
Q

What is diabetes mellitus?

A

A metabolic disorder characterized by the presence of hyperglycemia due to defective insulin secretion, insulin action, or both

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2
Q

What is the estimated economic impact of diabetes?

A

$30 million/yr

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3
Q

What are the long term complications of diabetes?

A

CVD, Kidney disease, blindness, neuropathy, amputation
~80% will die from heart disease or stroke

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4
Q

How much might diabetes shorten life expectancy but if not properly managed?

A

5-15 years

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5
Q

What is the pancreas composed of?

A

Acini and the islets of langerhans

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6
Q

What are the islet cells?

A

Beta (insulin) 60%
Alpha (glucagon) 30%
Delta (somatostatin) 10%

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7
Q

Beta cells

A

Compose about 50% of endocrine mass of pancreases
Produce insulin and amylin
Insulin released in response to elevated blood glucose levels

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8
Q

Alpha cells

A

Compromise about 35% of endocrine mass of pancrease
Produce glucagon
Glucagon released in response to low blood glucose levels

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9
Q

What does the pancreas release insulin?

A

After we eat and blood glucose rises

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10
Q

What brings blood glucose levels back down?

A

Glucose uptake in muscle and fat cells and glycogenesis and gluconeogensis in liver

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11
Q

When does blood glucose drop?

A

When we sleep

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12
Q

What is the fed state?

A

Insulin is released

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13
Q

What is the fasting state?

A

Glucagon released

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14
Q

How is glucose stored in the muscle?

A

As glycogen & used in energy metabolism (glycogenesis)

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15
Q

What are the other important counter-regulatory hormones?

A

Epinephrine, growth hormone, and cortisol

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16
Q

What is the major site of glucose uptake?

A

Muscle

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17
Q

What is the livers role?

A

Where glycogen is made, stored, and broken down

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18
Q

What does the liver do when you eat?

A

When the insulin is released it stimulates the liver to store glucose in the form of glycogen (glyconeogenesis)

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19
Q

What does the liver do when your not eating?

A

Glucagon is released and the liver provides glucose by:
- glycogenolysis
- gluconeogensis

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20
Q

When is insulin converted to fatty acids?

A

When the amount of glucose entering the liver is greater then the storage capacity for glycogen

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21
Q

What happens in the adipose tissue?

A

When excess CHOs are consumed that cannot be stored as glycogen they are converted to FFA’s and stored as TGs in adipose tissue

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22
Q

T or F: Insulin is a fat storing hormone

A

True

23
Q

What is lipolysis?

A

Starvation or insulin deficiency

24
Q

What role does the brain play?

A

The brain is constantly using glucose!
It uses ~20% of glucose
Glucose is its main energy source

25
Q

What are the different types of diabetes?

A

Prediabetes:
- impaired glucose tolerance (IGT)
- impaired fasting glucose (IFG)
Type 1
Type 2
And gestational diabetes

26
Q

What is T1DM?

A

Characterized by an absolute lack of insulin secretion
Primarily due to autoimmune (AI) beta-cel destruction
Not uncommon to see with other AI diseases

27
Q

How does T1DM usually present?

A

As acute metabolic symptoms of relatively short duration in a child, adolescent or young adult

28
Q

What does hyperglycemia happen?

A

When 80-90% of beta cells are destroyed

29
Q

What is the honeymoon phase of T1DM?

A

After diagnosis and initiation of insulin some patients go through a “honeymoon period”
- the correction of hyperglycemia causes insulin secretion to recover temporarily & insulin requirements may be quite low
- occurs in the days to weeks following diagnosis and initiation of insulin - can last for months

30
Q

What is prediabetes?

A

An intermediate state between normal glucose levels and diabetes
Includes IFG and IGT
It’s a strong predictor of T2DM and CVD

31
Q

What are the results for a diagnosis of prediabetes?

A

Fasting plasma glucose - 6.1-6.9 - IFG
2h PG in a 75g OGTT - 7.8-11.0 - IGT
A1C (%) - 6.0-6.4 - prediabetes

32
Q

What is T2DM?

A

Results from a combination of:
- impaired insulin secretion and insulin resistance
Accounts for ~90% of DM
Manifests only in those who lose the ability to produce sufficient quantities of insulin to maintain normal glycemic in the face of insulin resistance.

33
Q

What can cause T2DM?

A

The interaction of genetic and environmental factors:
Genetics - certain genes have been shown to determine risk for T2DM
Enviro: excessive caloric intake, sedentary lifestyle
Aging

34
Q

What are some risk factors for T2DM?

A

Age >/= 40
First degree relative with it
Overweight/obesity
History of prediabetes
History of GDM
Presence of end organ damage associated with diabetes:
- retinopathy, neuropathy, nephropathy
- CV (coronary, cerebrovascular, peripheral)
Vascular risk factors - low LDL, high TG, hypertension, overweight/obesity, smoking)
Medications

35
Q

Which medications may increase blood glucose?

A

Beta-blockers
Corticosteroids
Statins (but benefit usually outweighs risk)
Immunosuppressive agents
Niacin
Protease inhibitors (end in Vir)
Second gen antipsychotic agents
Thiazide or loop diuretics

36
Q

Why is there impaired insulin secretion in response to food for T2?

A

Impaired beta cell function
A reduced stimulus from incretin hormones

37
Q

What are the consequences of defective insulin secretion?

A

Hyperglycemia!
- first see a reduced early phase of insulin secretion -> elevated PPG
- then, late phase secretion diminishes -> elevated FPG

38
Q

What is insulin resistance?

A

There is decreased sensitivity of the actions of insulin by the target tissues (muscle, liver and adipocytes?
There will be less glucose being stored and/or used
And increased level of glucose in the blood

39
Q

What is the primary site of insulin resistance?

A

Skeletal muscle since it is the primary site of glucose disposal after a meal

40
Q

What is the ominous octet?

A

The defects that can cause hyperglycemia
- decreased incretin effect
- increased lipolysis
- increased glucose reabsorption
- decreased glucose uptake
- neurotransmitter dysfunction
- increased hepatic glucose production
- decreased insulin secretion and increased glucagon secretion
- inflammation

41
Q

Clinical presentation of type 1

A

Usually presents as acute symptoms of short duration
-polyuria
-polyphagia
-polydipsia
-weight loss
-fatigue
-blurred vision
-infections

42
Q

Clinical presentation of type 2

A

Commonly discovered incidentally, as patients may be asymptomatic
May have nonspecific symptoms (fatigue) or:
-polyuria
-polydipsia
-nocturia

43
Q

Fill in clinical features chart on slide 40

A

**

44
Q

What are the risk factors for type 2 diabetes in children?

A

T2DM in first or second degree relative
Member of a high risk ethnic or racial group
Obesity
IGT
PCOS
Exposure to diabetes in utero
Hypertension and dyslipidemia
Use of atypical antipsychotic medications

45
Q

What is gestational diabetes?

A

A condition that develops during pregnancy primarily due to insulin resistance
Overall prevalence: 4%; Indigenous women: 8-18%

46
Q

What are the risk factors for GDM?

A

Previous GDM
Member of high-risk population
Previous delivery of macroscopic infant
Age >35
Obesity
PCOS
Acanthodii’s nigricans
Corticosteroid use

47
Q

When should women be screened for GDM?

A

Between weeks 24-28 weeks and earlier if risk factors are present

48
Q

How can t2 be prevented?

A

Lifestyle modifications
Metformin
Acarbose
Pioglitazone
Rosiglitazone
Orlistat
Liraglutide

49
Q

What do we use for screening for T2?

A

FPG or A1C as initial screening tests

50
Q

How often should we screen for T2?

A

Every 3 years in people >40 or people at high risk

51
Q

At what screening results does someone become at risk?

A

FPG 5.6-6
A1C 5.5-5.9%

52
Q

At what screening results does someone become pre diabetic?

A

FPG 6.1-6.9
A1C 6.0-6.4%

53
Q

At what screening results does someone get diagnosed with diabetes?

A

FPG >/= 7.0
A1C >/= 6.5%

54
Q

What are the test results to diagnose diabetes?

A

FPG >/= 7.0mmol/L
AlC >/= 6.5%
2hPG in 75g OGTT >/= 11.1mmol/L
Random PG >/= 11.1mmol/L

PHAR 152 (10 decks)

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