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Diabetes Therapeutics > Diabetes General > Flashcards

Diabetes General Flashcards

1
Q

Overall, well-controlled diabetes is the leading cause of…..

A

NOTHING

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2
Q

Define 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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3
Q

In regards to aging and diabetes, what is the current trend?

A

Being accelerated due to advancing age of baby boomers (1946-1965)
Gap is widening from those 0-14yo (15.6%)

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4
Q

What is the economic impact of diabetes?

A

Estimated economic impact: $30 billion/yr
(SK: $100 million/yr in direct costs)
Medical costs are 2-3x higher in those with diabetes

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5
Q

What are some of the complications associated with diabetes? What is the major cause of death?

A

CVD, kidney dx, blindness, neuropathy, amputation……
~80% will die from heart disease or stroke

CVD is a major way people with diabetes die

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6
Q

Un-controlled diabetes life expectancy

A

If not properly managed, diabetes may shorten life expectancy by 5-15 years

Poorly controlled diabetes decreases a persons lifespan

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7
Q

The pancreas is composed of…..

A

Acini (exocrine) and Islets of Langerhans (endocrine)

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8
Q

The islet cells of Langerhans types and functions

A

a) Delta –> Somatostatin –> 10%
b) Beta –> Insulin –> 60%
c) Alpha –> Glucagon –> 30%

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9
Q

What is euglycemia? How is it maintained?

A

Euglycemia (sugar at correct levels) is maintained by these 3 hormones (somatostatin, insulin, glucagon) working together

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10
Q

One of somatostatins function is…

A

Inhibition of glucagon and insulin secretion

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11
Q

Beta Cells compromise what % of endocrine mass? What do they produce? What is the response?

A
  • Comprises about 50% of endocrine mass of the pancreas
  • Produces insulin and amylin
  • Insulin released in response to elevated blood glucose levels
  • Amylin is a hormone that can help with satiety (feeling of fulnness)
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12
Q

What hormone is released in response to elevated blood glucose levels?

A

Insulin

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13
Q

What hormone helps with the feeling of satiety?

A

Amylin

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14
Q

Alpha Cells compromise what % of endocrine mass? What do they produce? What is the response?

A
  • Compromise about 35% of endocrine mass
  • Produce glucagon
  • Glucagon released in response to low blood glucose levels
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15
Q

What hormone is released in response to low blood glucose levels?

A

Glucagon

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16
Q

What is the normal blood glucose levels for people?

A

4-6 millimoles/L

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17
Q

Describe the cycle of glucose homeostasis?

A

1) Ingestion of a meal
2) Blood glucose increases
3) Pancreas secretes insulin
4) Insulin acts on muscle, adipose and the liver

  • Muscle and Adipose –> Glucose Uptake
  • Liver –> Increased glycogenesis, decreased gluconeogenesis

5) Blood glucose levels decrease to normal
6) Absence of meal/Night-time –> Blood glucose decreases
7) Pancreas secretes glucagon
8) Glucagon acts on the liver to increase glycogenolysis and gluconeogenesis
9) Blood glucose increases to normal levels

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18
Q

What are the stimulus for secretion of insulin?

A

Increased serum glucose
Increased serum amino acids
Increased serum free fatty acids
Glucagon
GH (growth hormone)
Cortisol
GIP (Gastric Inhibitory hormone)

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19
Q

What are the stimuluses for Glucagon secretion?

A

Decreased serum glucose
Decreased serum amino acids
Epinephrine and Norepi

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20
Q

Insulin works at what targets? What occurs as a result?

A

a) Liver
- Increases glycogenesis
- Decreased gluconeogenesis

b) Muscle
- Increases protein synthesis
- Increased glycogenesis

c) Adipose Tissue
- Increased lipogenesis

d) Pancreas
- Decreased glucagon secretion

e) Miscellaneous
- Increased K+ uptake into cells
- Increased cholesterol synthesis

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21
Q

Glucagon works at what targets? Function?

A

a) Liver
- Increased glycogenolysis
- Increased gluconeogenesis

b) Adipose Tissue
- Increased lipolysis

c) Pancreas
- Decreased insulin secretion

d) Miscellaneous
- Decreased K+ uptake into cells
- Decreased cholesterol synthesis

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22
Q

What are some other important counter-regulatory hormones? What do these hormones do?

A

Epinephrine/Norepi
Growth Hormone
Cortisol

Increase serum sugar

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23
Q

Insulin is released in the….

A

Fed State

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24
Q

Glucagon is released in…

A

Fasting State

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25
Q

Does glucagon have any effect on muscle?

A

NO

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26
Q

What is the net effect of insulin? What mechanisms does this occur by?

A
  • Decreased serum glucose
  • Increased storage of energy by increasing protein synthesis, fat synthesis, and glycogen synthesis
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27
Q

What is the net effect of glucagon? What mechanisms does this occur by?

A
  • Increased serum glucose
  • Increased energy release by increasing protein and fat catabolism and by gluconeogensis
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28
Q

Insulins Role Simple

A
  • Drives sugar out of the blood stream and into cells
  • Insulin is key for helping cells uptake glucose from the blood
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29
Q

What is the major site of glucose uptake?

A

Muscle

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30
Q

After a meal and excess CHO, insulin functions to….

A

With the ingestion of a meal and excess CHO, insulin stimulates the uptake of glucose in skeletal muscle

Glucose is stored as glycogen in muscle & used in energy metabolism (glycogenesis)

Further, the presence of insulin stimulates production of proteins from amino acids

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31
Q

Does insulin only effect glucose? If not, what does it effect?

A

Insulin stimulates production of proteins from amino acids

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32
Q

What occurs in between meals in regards to protein?

A

In-between meals: body still has energy demands, so in attempt to produce energy, proteins are converted into AA’s
AA’s –> transported to liver –> converted to glucose via gluconeogenesis (formation of glucose from a non-carbohydrate source)

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33
Q

Why can insulin stimulate protein formation from amino acids?

A

Insulin is an Anabolic Agent

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34
Q

In regards to diabetes, what is happening in regards to insulin?

A

In diabetes there is either lack of, or impairment of insulin action, and glucose is not able to be taken up by the muscle cells

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35
Q

The liver is the site of….

A

Glycogen production, storage and break down

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36
Q

After a meal, what hormone has an effect on the liver? Function?

A

When you eat –> insulin is released it and stimulates the liver to store glucose in the form of glycogen (glycogenesis)
Insulin also suppresses gluconeogenesis (glucose from a non-carb source)

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37
Q

When one is not eating, what hormone has an effect on the liver? Function?

A

When you are not eating –> glucagon is released and the liver provides glucose by:

a) Glycogenolysis (liver glycogen is split back into glucose)
b) Gluconeogensis (formation of glucose from non-CHO sources (i.e. AA’s)

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38
Q

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

A

If the amount of glucose entering the liver is greater than the storage capacity for glycogen, insulin promotes its conversion to fatty acids

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39
Q

How are excess CHO’s stored? When does this occur?

A

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

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40
Q

Insulin is a ______ storing hormone

A

FAT

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41
Q

How does insulin act as a fat storing hormone?

A

It stimulates the conversion of glucose to glycerol phosphate & free fatty acids (FFA’s) and is stored as TG’s in fat cells

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42
Q

In starvation or insulin deficiency, _____ occurs. Describe such process?

A

LIPOLYISIS

TG’s split back to glycerol and FAs –> Metabolism of FFA’s –> β-hydroxybutyrate, acetoacetic acid, and acetone (ketone bodies)

These ketone bodies can be used as an energy source

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43
Q

What organ uses glucose constantly? Percentages?

A

The Brain

Brain accounts for ~2% of body weight but uses ~20% of glucose

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44
Q

What is the main energy source for the brain? Why is this concerning/important?

A

Glucose is its main energy source (does not depend on presence of insulin for its use – no ‘key’ required)

The brain is very sensitive to reduced glucose levels - this can lead to states of confusion to unconsciousness (or worse)

45
Q

What are some types of diabetes?

A

1) Pre-diabetes
- Impaired glucose tolerance (IGT)
- Impaired fasting glucose (IFG)
2) Type 1
3) Type 2
4) Gestational Diabetes (GDM)
5) Others: LADA (latent autoimmune diabetes in adults), MODY (maturity-onset diabetes in the young), Type 3c

46
Q

Type-1 Diabetes Definition

A
  • Characterized by an absolute lack of insulin secretion
47
Q

Type-1 Diabetes Cause

A
  • Primarily due to autoimmune (AI) beta-cell destruction
48
Q

In Type-1 Diabetes, a clinician would typically see examples of ______. Examples?

A
  • Typically see markers of immune destruction
    –> Islet cell antibodies, insulin antibodies, and GAD (glutamic acid decarboxylase) antibodies
49
Q

Type-1 Diabetes is commonly seen with….

A

Other auto-immune diseases –> Celiacs being a common one

50
Q

Type-1 Diabetes initial presentation…..

A
  • Usually presents as acute metabolic symptoms of relatively short duration in a child, adolescent, or young adult
51
Q

Can type-1 diabetes occur in older generations?

A

Yes

52
Q

If a clinician can not tell if Type-1 or type-2, they can…..

A

Can do tests to see if immune destruction has occurred

53
Q

In type-1 diabetes, hyperglycemia occurs when beta cells….

A
  • 80-90% of beta-cells are destroyed
  • Threshold to start feeling symptoms
54
Q

Describe the timeline of type-1 diabetes manifestations?

A
  • Beta-cell mass near 100%
  • Genetic Predisposition
  • Immunologic Trigger –> Toxin, viruses, etc.
  • Decrease in beta-cell mass due to immunologic abnormalities, progressive impairment of insulin release
  • Decrease of beta-cell mass to an 80-90% decrease, diabetes

(If destruction is less than 80-90%, no diabetes)

55
Q

What is the honeymoon phase of type-1 diabetes? What is important in regards to counselling pts?

A

Upon diagnosis of diabetes and initiation of insulin some patients go through a “honeymoon period”

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

This period is transient, hence:
Must continue to receive insulin
Monitor for hypoglycemia

56
Q

Pre-diabetes is….

A

An intermediate state between normal glucose levels and diabetes

  • Not at threshold for type-2 diabetes
57
Q

Pre-diabetes includes…..

A

Includes IFG (impaired fasting glucose) and IGT (impaired glucose tolerance)

58
Q

Pre-diabetes is a strong predictor of what?

A

Type-2 Diabetes
Cardiovascular Disease

It’s estimated 30-60% will develop T2DM in the following 8-10 years

59
Q

Can interventions in pre-diabetes prevent type-2 diabetes?

A

Many trials have shown diabetes can be prevented in those with prediabetes with lifestyle interventions or medications – many will revert to normoglycemia

60
Q

What is a 2 H PG in a 75g OGTT (mmol/L) test?

A

Testing with a 2 Hour Plasma Glucose in a 75 gram oral glucose tolerance test

Includes collection of fasting plasma glucose after an 8-hour fast, followed by consumption of glucose drink, and blood collected at 1 hour and 2 hours post-drink for plasma glucose

61
Q

Diagnosis of prediabetes (test values) includes:

A

a) Fasting Plasma Glucose (mmol/L) = 6.1-6.9 –> indicates impaired fasting glucose of prediabetes category

b) 2h PG in a 75 g OGTT (mmol/L) = 7.8-11.0 –> Indicates impaired glucose tolerance of prediabetes category

c) A1C (%) = 6.0-6.4 –> indicates prediabetes

62
Q

What is the relation between A1C and the 5 year incidence of diabetes?

A

A1C Category - 5-year Incidence of Diabetes

5.0-5.5 - <5 to 9%
5.5-6.0 - 9 to 25%
6.0-6.5 - 25 to 50%

63
Q

Type-2 Diabetes accounts for _____ % of Diabetes Mellitus

A

90%

64
Q

Type-2 Diabetes results from…..

A

Impaired insulin secretion
Insulin resistance

65
Q

When does Type-2 Diabetes Manifest in a person?

A
  • Only manifests in those who lose the ability to produce sufficient quantities of insulin to maintain normoglycemia in the face of insulin resistance
66
Q

Type-2 Diabetes involves the interaction of….

A

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

67
Q

What are some risk factors for T2DM?

A

Age ≥40 years
First-degree relative with type 2 diabetes
Member of high-risk population (e.g., African, Arab, Asian, Hispanic, Indigenous or South Asian descent, low socioeconomic status)
Overweight / obesity
History of prediabetes
History of GDM
History of delivery of a macrosomic infant (big baby, greater than 9 llbs)
Presence of end organ damage associated with diabetes:
Microvascular (retinopathy, neuropathy, nephropathy)
CV (coronary, cerebrovascular, peripheral)
Associated diseases
Vascular Risk Factors
Medications

68
Q

Associated diseases that are a risk fcator for Type-2 Diabetes include….

A

Acanthosis nigricans (darkening, velevety thickening of skin)
PCOS (polycystic ovarian syndrome)
obstructive sleep apnea
HIV infection
psychiatric illnesses (schizophrenia, bipolar)
gout
non-alcoholic steatohepatitis
cystic fibrosis
history of pancreatitis

69
Q

Vascular risk factors for T2DM include….

A

low HDL, high TG, hypertension, overweight/obesity, smoking)

70
Q

What are some medications that may increase blood glucose? Which one is considered okay?

A

5-fluoruracil
Beta-blockers
Corticosteroids
Diazoxide
Immunosupressive Agents
Second-generation anti-psychotic agents –> clozepine, olanzepine, quitipiene, risperidone

HMG-CoA reductase Inhibitors –> Statins –> (Benefit of these medications outweighs the risk)

71
Q

What population is insulin resistance found in?

A

Obese people –> To some degree

72
Q

_____ can be used as an indicator of T2DM; however ____ is better.

A

The degree of obesity (BMI) correlates with degree of insulin resistance.

Visceral adipose tissue (VAT):
- Fat cells within the abdominal cavity
- Especially resistant to insulin action
- A stronger predictor of T2DM than BMI

73
Q

In regards to waist circumference, what value leads to a 90% chance of resistance?

A

Male >102cm
Female >88cm

= 90% chance of resistance

74
Q

What is the relation of T2DM and beta cells?

A

T2DM patients have a significantly decrease β-cell mass, as well as a β-cell secretory defect….this continues to deteriorate with time

75
Q

In Type-2 diabetes, there is _______ in response to food because……

A
  • Impaired Insulin secretion in response to food
  • Impaired β-cell function
  • A reduced stimulus from incretin hormones (go and tell pancreas to pump out insulin to bring sugars down)
76
Q

What is the main effect of defective insulin secretion? How does this manifest?

A

Hyperglycemia!
- First see a reduced early phase of insulin secretion –> elevated PPG (post-prandial glucose)
- Then, late phase secretion diminishes –> elevated FPG

77
Q

How is insulin released?

A

Insulin is released in phases

78
Q

In type-2 diabetes, where does insulin resistance occur?

A

There is decreased sensitivity to the actions of insulin by the target tissues (muscle, liver, adipocytes)

79
Q

What is the primary site of insulin resistance? Why? What is the response?

A

SKELETAL MUSCLE

Primary site of glucose disposal after a meal, and hence the primary site of insulin resistance
Muscle is resistant to insulin actions hence there is decreased glucose uptake by it

80
Q

Insulin resistance at the liver has what effect?

A

Resistance to insulin action on the liver results in the inability to suppress hepatic glucose production

81
Q

Insulin resistance at the adipose tissue manifestation?

A

Adipocytes become resistant to antilypolytic effects of insulin which leads to ↑ lipolysis

Leads to elevated FFA’s in the circulation which can stimulate liver glucose production, impair skeletal muscle sensitivity & impair insulin release

82
Q

Insulin resistance net effect

A

Greater serum glucose concentration

83
Q

What is the ominous octet?

A

Multiple pathophysiologic abnormalities associated with type-2 diabetes

Hyperglycemia is a result of:

1) Pancreas
- Decreased insulin secretion by beta cells
- Increased glucagon secretion by alpha cells

2) Gut
- Decreased incretin effect

3) Adipocytes
- Increased lipolysis

4) Kidneys
- Increased glucose reabsorption

5) Muscle
- Decreased glucose uptake

6) Inflammation

7) Brain
- Neurotransmitter dysfunction

8) Liver
- Increased hepatic glucose production

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84
Q

Why is early detection important for Type-2 diabetes?

A
  • T2DM is progressive
  • Macrovascular and microvascular complications are occurring before an actual diagnosis
  • Earlier detection and intervention may help to prevent complications earlier
85
Q

What is the clinical presentation of type-1 diabetes?

A

Usually presents as acute symptoms of SHORT duration:
Polyuria
Polyphagia
Polydipsia
Weight loss (some due to cells starving, pee out a lot of sugar)

Fatigue
Blurred vision
Infections

20-40% present with DKA (diabetic ketoacidosis) after several days of the above symptoms –> Very sick –> Nauseau, vomiting, etc

86
Q

What is the clinical presentation of type-2 diabetes?

A

Is commonly discovered incidentally, as patients may be asymptomatic

May have nonspecific symptoms (i.e. fatigue) or:
polyuria
polydipsia
nocturia

May already have established diabetic complications at diagnosis (damage to micro and macrovascular system)

87
Q

Comparison of Type-1 and Type 2?

a) Age of Onset
b) Weight
c) Islet Auto-antibodies
d) C-peptide
e) Onset/Symptoms
f) First Line Tx
g) Microvascular Complications
h) DKA

A

a) Age of Onset
1 - Most <25 but can occur at any age (but not before the age of 6 months)
2 - Usually >24 but incidence increasing in adolescents due to increasing rate of obesity in children and adolescents
b) Weight
1- Usually thin, but with obesity epidemic, can have overwieght or obesity
2- >90% at least overweight
c) Islet Auto-antibodies
1- Usually present (approx. 90%)
2 - Absent
d) C-peptide
1- undetectable/low
2- Normal/high
e) Onset/Symptoms
1- Abrupt/symptomatic
2- Gradual/asymptomatic
f) First Line Tx
1- Insulin
2- Non-insulin antihyperglycemic agents, gradual dependence on insulin may occur
g) Microvascular Complications
1- Absent at diagnosis
2- Present at diagnosis
h) DKA
1- Common
2- Rare

88
Q

C peptide is a measurement of…..

A
  • A measurement to determine whether one is still producing insulin or not
89
Q

genetic pre-disposition is higher in….

A

Type 2

90
Q

What are the risk factors for the growing incidence of type-2 in children?

A

T2DM in a first- or second-degree relative
Member of a high risk ethnic or racial group
Obesity
IGT
PCOS
Exposure to diabetes in utero
Acanthosis nigricans
Hypertension and dyslipidemia
Nonalcoholic fatty liver disease (NAFLD)
Use of atypical antipsychotic medications

91
Q

What is gestational diabetes?

A

A condition that develops during pregnancy primarily due to insulin resistance

92
Q

Gestational diabetes effects in fetus?

A

GDM increases the risk of fetal hyperinsulinemia, heavier birth weight (future predicter of type-2), higher rates of cesarian deliveries, and neonatal hypoglycemia

93
Q

Gestational Diabetes is associated with what risk?

A

↑ risk of developing T2DM in both mother and child

94
Q

Screening for GDM should be conducted when….

A

Weeks 24-28 of pregnancy

95
Q

Risk Factors for GDM

A

Previous GDM
Member of high-risk population
Previous delivery of macrosomic infant
Age ≥ 35yo
Obesity
PCOS
Acanthosis nigricans
Corticosteroid use

96
Q

Recommendations for screening of GDM. What type of screening is done?

A

All women should be screened for GDM between weeks 24-28 weeks of pregnancy; earlier if risk factors are present
Screening may be a 1-step or sequential 2-step process (FPG, A1C, OGTT)

97
Q

Can Type-1 diabetes be prevented?

A

No

Has been and continues to be researched
Immunosuppresive agents
Excluding cow’s milk protein
Immunomodulator agents
Low-dose insulin injections

No successful preventive interventions thus far

98
Q

Can type-2 diabetes be prevented? Who do we target?

A

If intervention occurs early, may be preventable

Primarily involves targeting high risk individuals (IGT or obesity to prevent progression)

99
Q

How can type-2 diabetes be prevnted?

A

***Lifestyle modification
Diabetes Prevention Program (DPP) study and Finnish Diabetes Prevention Study (DPS)
Metformin (DPP)
Acarbose (STOP-NIDDM)
Pioglitazone (PIPOD, ACT NOW, PROactive)
Rosiglitazone (DREAM, RECORD)
Orlistat (XENDOS)
Liraglutide (SCALE)

100
Q

Is screening required for type-1 diabetes?

A

Screening not recommended due to:
overall low prevalence
no identifiable intervention which will prevent it

101
Q

Is screening required for type-2 diabetes?

A

Important as a large amount of people are undiagnosed (up to 1/3 of all cases)
Use FPG or A1C as initial screening tests

102
Q

Is there any difference in the tests used to screen for type 1 and 2?

A

No

The same tests are used to screen & diagnose

103
Q

Describe the screening algorithm for type-2 diabetes

A

Look at Slide 56 in lecture deck

104
Q

What is CANRISK?

A

A validated tool (in those >40yo) for a variety of populations to help assess risk of type-2 diabetes

Available in 13 languages

Quick and easy

Stratifies people into low, medium, and high risk of having prediabetes or type 2 diabetes

Helps identify patients who should be referred to physicians for further work -up

105
Q

Diagnosis of Diabetes Values

A

FPG ≥7.0 mmol/L
Fasting = no caloric intake for at least 8 hours
or
A1C ≥6.5% (in adults)
Using a standardized, validated assay in the absence of factors that affect the accuracy of the A1C and not for suspected type 1 diabetes
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

106
Q

What are the advantages and disadvantages of FPG?

A

Advantages:
- Established standard
- Fast and Easy

Disadvantages:
- Inconvenient
- Less sensitive than OGTT

107
Q

What are the advantages and disadvantages of A1C?

A

Advantages:
- Convenient
- Better predictor of CVD
- No day-to-day variability

Disadvantages:
- Cost
- Not valid for all medical conditions (e.g. anemia, hemoglobinopathesis)
- Altered by ethinicty and aging
- Not to be used for children, GDM, suspected T1DM

108
Q

What are the advantages and disadvantages of 2 hr PG 75 g OGTT?

A

Advantages:
- Established standard

Disadvantages:
- Inconvienient
- Taste
- Cost

Diabetes Therapeutics (4 decks)

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