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PHAR 152 Diabetes > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is our number one resource for Diabetes?

A

Diabetes Canada Guidelines

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2
Q

What is Diabetes Mellitus?

A

Metabolic disorder characterized by the resence of hyperglycemia due to defective insulin secretion, insulin action, or both.

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3
Q

What percent of Canadians live with diabetes? Percent of undiagnosed, prediabete, diagnosed?

A

10% & 30%

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4
Q

How much higher are medical costs for those with diabetes?

A

2-3x higher

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5
Q

Which major complications lead to mortality in diabetes?

A

Heart attack and Stroke (CVD) ~80% of death in daibetes

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6
Q

What 3 hormones work together to maintain Euglycemia?

A

Somatostatin
Glucagon
Insulin

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7
Q

What hormone is produced from alpha islet cells? beta islet cells? Delta cells?

A

alpha- glucagon
beta- insulin
delta - somatostatin

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8
Q

Describe beta cells.

A

~50% of endocrine mass of pancreas
produce insulin and amylin
insulin released in response to elevated blood glucose levels

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9
Q

Describe alpha cells.

A

~35% of endocrine mass of pancreas
produce glucagon
Glucagon released in response to low blood glucose levels

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10
Q

How does insulin affect glycogenesis and gluconeogenesis?

A

Increases glycogenesis
Decreases gluconeogenesis

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11
Q

How does glucagon affect glycogenolysis and gluconeogenesis?

A

increases glycogenolysis
Increases gluconeogenesis

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12
Q

Which hormone is released in fasting state? Fed state?

A

Fasting: Glucagon
Fed: insulin

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13
Q

What is the major site of glucose uptake?

A

Muscles

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14
Q

Where is glycogen made, stored and broken down?

A

The liver

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15
Q

What happens if the amount of glucose entering the liver is greater than the storage capacity of glycogen?

A

Insulin promotes its conversion to fatty acids

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16
Q

What happens to TG’s when there is insulin defeciency or starvation?

A

Lipolysis occurs and TG’s split back to glycerol and FA’s, ketone bodies used as an energy source.

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17
Q

How much glucose does the brain use?

A

~20%

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18
Q

T or F. The brain needs insulin to use glucose.

A

False; insulin is not required for the brain to uptake glucose

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19
Q

What are the 2 types of prediabetes?

A

IGT (impaired glucose tolerance)
IFG (imapired fasting glucose)

20
Q

Describe Type 1 Daibetes.

A

Absolute lack of insulin secretion
Primarily due to autoimmune disease causing beta-cell destruction
Usually presents as acute metabolic symptoms of relatively short duration in a child, adolescent or young adult.

21
Q

What is the prevalence of type 1 diabetes in children?

A

~95% –> 5 % type 2

22
Q

What is the honeymoon phase of T1DM?

A

Correction of hyperglycemia causing insulin secretion to revocer temporarily & insulin requirements may be quite low
Is transient so must continue to recieve insulin and monotor for hypoglycemia

23
Q

what percent of people develop T2DM from prediabetes over 8-10 years?

A

30-60%

24
Q

What is the fasting plasma glucose range for IFG prediabetes daignosis

A

6.1-6.9

25
Q

what is the 2h PG in a 75g )GTT range for IGT prediabetes diagnosis?

A

7.8-11.0

26
Q

What is the A1C (%) range do diagnose prediabetes?

A

6.0-6.4

27
Q

What A1C range has a 5 year incedence of daibetes percent range of 5-9%?

A

5.0-5.5

28
Q

What A1C range has a 5 year incedence of daibetes percent range of 9-25% ?

A

5.5-6.0

29
Q

What A1C range has a 5 year incedence of daibetes percent range of 25-50 % ?

A

6.0-6.5

30
Q

What is T2DM a combination of?

A

impaired insulin secretion and insulin resistance

31
Q

When does T2DM manifest?

A

Once a person loses the ability to produce sufecient quantities of insulin to maintain normoglycemia in the face of insulin resistance

32
Q

What are some risk factors of T2DM?

A

obesity
age older than 40
history
high risk population
vascular risk factors
medications
etc.

33
Q

T or F the degree of Obesity does not correlate with the degree of insulin resistance.

A

False; BMI correlates with insulin resistance

34
Q

What is a stronger predictor of T2DM than BMI?

A

Visceral adipose tissue;
- fat cells within the abdominal cavity
- especially refractory to insulin action

35
Q

What happens to beta cell mass and beta cell secretion in T2DM?

A

Both significantly decrease, continue to deteriorate over time

36
Q

Why is there impaired insulin secretion in response to food?

A

Impaired beta-cell function
Reduced stimulus from incretin hormones

37
Q

What are the consequences of defective insulin secretion?

A

Hyperglyceimia;
- 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

decreased sensitivity to the actions of insulin by the target tissues

39
Q

What is the Ominous Octet? (Leading to hyperglycemia)

A
  1. decreased incretin effect
  2. increased liplysis
  3. increased glucose reabsorption
  4. decreased glucose uptake (cells)
  5. Neurotransmitter dysfunction
  6. increased hepatic glucose production
  7. decreased insulin secretion
  8. increased glucagon secreation
    (Inflammation also affects)
40
Q

What are the clinical presentation of T1DM?

A

Usually presents as acute symptoms of short duration
- polyuria
- polyphagia
- polydipsia
- weight loss
- fatigue
- blurred vision
- infections
- 20-40% ;resent with DKA after several days of the above symptoms

41
Q

What are the clincial presentations of T2DM?

A

commonly discovered incidentally, as pts may be asymptomatic
- may have nonspecific symptoms; polyuria, polydipsia, nocturia
- may already have established diabetic complications at diagnosis

42
Q

Compare and contrast T1DM and T2DM clinical features.

A

Age: most under 25 vs susually over 24 but increasing in adolescents (correlation with obesity rates)
Weigth: usually thin, obesity increasing vs >90% at least overweight
Islet autoimmune antibodies: usually present (~90%) vs absent
C-peptide: undetectable/low vs normal/high
Onset/symptoms: Abrupt/symptomatic vs Gradual/asymptomatic
First line treatment: Insulin vs Non-insulin antihyperglycemic agents, gradual dependance on insulin may occur
Microvascular complications: absent at diagnosis vs present at diagnosis
DKA: common vs rare

43
Q

What is Gestational diabetes melitus (GDM)?

A

Condition develops during pregnancy primarily due to insulin resistance
increased risk of developing T2DM in both mother and child

44
Q

Can T1DM be prevented?

A

No successful preventative interventions thus far

45
Q

Can T2DM be prevented?

A

Yes;
- involves targeting high risk individuals
- lifestyle modifications
- metformin
- Acarbose
- Pioglitazone
- Rosiglitazone
- Orlistat
- Liraglutide

PHAR 152 Diabetes (1 decks)

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