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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

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
What are the different types of diabetes?
Prediabetes: - impaired glucose tolerance (IGT) - impaired fasting glucose (IFG) Type 1 Type 2 And gestational diabetes
26
What is T1DM?
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
How does T1DM usually present?
As acute metabolic symptoms of relatively short duration in a child, adolescent or young adult
28
What does hyperglycemia happen?
When 80-90% of beta cells are destroyed
29
What is the honeymoon phase of T1DM?
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
What is prediabetes?
An intermediate state between normal glucose levels and diabetes Includes IFG and IGT It’s a strong predictor of T2DM and CVD
31
What are the results for a diagnosis of prediabetes?
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
What is T2DM?
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
What can cause T2DM?
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
What are some risk factors for T2DM?
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
Which medications may increase blood glucose?
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
Why is there impaired insulin secretion in response to food for T2?
Impaired beta cell function A reduced stimulus from incretin hormones
37
What are the consequences of defective insulin secretion?
Hyperglycemia! - first see a reduced early phase of insulin secretion -> elevated PPG - then, late phase secretion diminishes -> elevated FPG
38
What is insulin resistance?
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
What is the primary site of insulin resistance?
Skeletal muscle since it is the primary site of glucose disposal after a meal
40
What is the ominous octet?
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
Clinical presentation of type 1
Usually presents as acute symptoms of short duration -polyuria -polyphagia -polydipsia -weight loss -fatigue -blurred vision -infections
42
Clinical presentation of type 2
Commonly discovered incidentally, as patients may be asymptomatic May have nonspecific symptoms (fatigue) or: -polyuria -polydipsia -nocturia
43
Fill in clinical features chart on slide 40
**
44
What are the risk factors for type 2 diabetes in children?
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
What is gestational diabetes?
A condition that develops during pregnancy primarily due to insulin resistance Overall prevalence: 4%; Indigenous women: 8-18%
46
What are the risk factors for GDM?
Previous GDM Member of high-risk population Previous delivery of macroscopic infant Age >35 Obesity PCOS Acanthodii’s nigricans Corticosteroid use
47
When should women be screened for GDM?
Between weeks 24-28 weeks and earlier if risk factors are present
48
How can t2 be prevented?
Lifestyle modifications Metformin Acarbose Pioglitazone Rosiglitazone Orlistat Liraglutide
49
What do we use for screening for T2?
FPG or A1C as initial screening tests
50
How often should we screen for T2?
Every 3 years in people >40 or people at high risk
51
At what screening results does someone become at risk?
FPG 5.6-6 A1C 5.5-5.9%
52
At what screening results does someone become pre diabetic?
FPG 6.1-6.9 A1C 6.0-6.4%
53
At what screening results does someone get diagnosed with diabetes?
FPG >/= 7.0 A1C >/= 6.5%
54
What are the test results to diagnose diabetes?
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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