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Clinical Nutrition 3 > Diabetes Intro > Flashcards

Diabetes Intro Flashcards

1
Q

How is glucose produced?

A
  • Endogenously under the control of glucagon, catecholamines, cortisol and GH
  • In the liver and kidney
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2
Q

How is insulin used?

A

With insulin, uptake in muscle adipose and liver tissues

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3
Q

Where does glucose from the CNS and other organs originate from?

A

-Liver

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4
Q

Where does glucose from the liver, muscle/fat and kidney originate from?

A

-Kidney

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5
Q

___ of glucose is produced by liver, and ___ of glucose produced by the kidney

A

90%, 10%

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6
Q

What does the post-prandial glucose flux feed?

A
  • CNS and other organs
  • Liver
  • Muscle and fat
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7
Q

Discuss glucose regulation in a healthy individual PP

A

Low at baseline, will spike a meal and then quickly return to baseline

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8
Q

Discuss glucose regulation in a T2DM PP

A

-Higher at baseline, will peak at meal and stay higher for longer before returning to a higher baseline

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9
Q

Discuss insulin release in the healthy individual

A

-Low at baseline, and will drastically spike at meals an then gradually return to low baselin

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10
Q

Discuss insulin release in the T2DM individual

A
  • Low at baseline, will slightly increase but will not achieve a true “spike”
  • Delayed and reduced insulin response
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11
Q

Discuss glucagon in the healthy individual

A

High in fasted state, an will drastically drop upon insulin release to shut off endogenous processes, then slowly increase ~ hr later

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12
Q

Discuss glucagon in T2DM

A

Will remain high as insulin resistance is reduced and insufficient

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13
Q

Anabolic effects of insulin of glucose? (Insulin stimulates)

A
  • Glucose transport
  • Glycolysis
  • Glycogenesis
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14
Q

Anti-catabolic effect of insulin on glucose? (Insulin inhibits)

A
  • Gluconeogenesis

- Glycogenolysis

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15
Q

Anabolic effect of insulin on lipid?

A
  • Lipogenesis, synthesis of TG and FFA

- Lipoprotein lipase activity (clearing lipid from the blood)

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16
Q

Anti-catabolic effect of insulin on lipid?

A
  • Lipolysis
  • LPL in muscle
  • FA oxidation in the liver (B-oxidation)
  • Ketogenesis
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17
Q

Anabolic effects of insulin on protein?

A
  • Increase transport of AA and protein synthesis

- Electrolyte homeostasis: Allow for potassium to enter into the cell

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18
Q

Anti-catabolic effects of insulin on protein?

A

-Protein catabolism

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19
Q

What is released alongside insulin from the B-cell? What is this indicative of?

A
  • C-peptide
  • If we want to see if there is any production of “self” insulin, we can check for presence of C-peptide
  • Helpful in T1DM or overt T2DM
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20
Q

What is the key concept regarding insulin and glucagon in T2D?

A
  • Delayed or reduced insulin

- Excessive glucagon

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21
Q

How many phases of insulin are there?

A

-2

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22
Q

1st phase of insulin? (Acute)

A
  • 5-10 mins after B-cell is exposed to rapid increase in glucose
  • Important for decreasing hepatic glucose production, decreasing lipolysis and to prepare target cells of the action of insulin
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23
Q

2nd phase of insulin?

A

Insulin secretin will rise more gradually, and is directly related to the degree (meal composition, absorption) and duration of the stimulus

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24
Q

Initial observations of onset of diabetes?

A
  • Polydipsia
  • Polyuria
  • Polyphage
  • Weight loss (type I) or obesity (type 2)
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25
Q

Clinical lab tests to asses for diabetes?

A
  • Hyperglycemia
  • Glucosuria
  • Abnormal Glucose Tolerance Test
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26
Q

Diabetes is similar to a ___ but not as efficient

A

fasting

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27
Q

What occurs during the absence of insulin? (1/2)

A
  • Liver is producing glucose via gluconeogenesis
  • Muscle and adipose use ketone and fatty acids
  • Glycolytic enzyme activity decreases
  • Hypoglycemia is more pronounced than fasting
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28
Q

What occurs in the absence of insulin (2/2) ?

A
  • Liver increased VLDL production
  • Muscle glycogen and protein used for energy
  • Cardiac and skeletal muscles rely on KB
  • Adipose releases FFA
  • Hexokinase increased, hyperG and complications
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29
Q

Is there a difference between glucose levels after nutrition administered orally vs IV?

A

No

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30
Q

Is there a difference between insulin levels after nutrition administered orally vs IV?

A
  • Yes, when feeds are oral, insulin release is higher and normal
  • Response to glucose given if given IV is lower, resembles what is seen in T2DM (delayed and reduced insulin secretion)
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31
Q

What can explain the difference in insulin release between oral and IV feeds

A

-In parenteral nutrition, we bypass the gut which means that we bypass the incretins

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32
Q

What are the two main incretins?

A

-GLP-1 and GIP

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33
Q

What is the mechanism of action of incretins?

A

When glucose enters the enterocytes, incretin will be released from the GI which will elicit an even greater release of insulin

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34
Q

Besides incretins and glucose, what else can determine plasma glucose concentration?

A
  • CHO composition of foods
  • Rate of gastric emptying
  • Rate of glucose absorption
  • Concurrent rate of glucose disposal
  • Diurnal change in insulin sensitivety
  • Activity of hormones
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35
Q

How can change in exercise modulate plasma glucose concentration?

A

Aerobic exercise may decrease blood glucose, and could counteract hyperglycemia during exercise. Anaerobic exercise, may increase blood glucose

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36
Q

What else may modulate plasma glucose levels?

A
  • Consumption of alcohol
  • Acute illness
  • Emotional stress
37
Q

What is type I diabetes?

A

Pancreatic beta cell destruction which usually leads to absolute insulin deficiency. Can be (1) immune mediated or (2) idiopathic

38
Q

What is type II diabetes?

A

May range from predominately insulin resistance with insulin deficiency to a predominantly secretory defect with insulin resistance

39
Q

What is gestational diabetes?

A

-Glucose intolerance with onset or first recognition in pregnancy

40
Q

What is monogenic diabetes?

A

MODY, special type of diabetes which will require genetic testing and a specific genetic tx as their responsiveness varies greatly

41
Q

T1DM onset?

A

usually <25 but can occur at any age (but not before age of 6 months)

42
Q

T1DM weight?

A

Usually thin, but with obesity epidemic can have overweight/obesity (now complicates w/ insulin resistance)

43
Q

T1DM presence of islet auto-bodies?

A

Present

44
Q

T1DM insulin production?

A

Absent

45
Q

T1DM Family hx?

A

Infrequent (5-10%)

46
Q

T1DM DKA?

A

Common

47
Q

T2DM age on onset?

A

Usually >24 but incidence increasing in adolescents, paralleling increasing rate of obesity in children and adolescents

48
Q

T2DM weight?

A

> 90% at least overweight

49
Q

T2DM islet auto-bodies?

A

Absent

50
Q

T2DM C-peptide?

A

-Normal/high

51
Q

T2DM insulin production?

A

Present

52
Q

T2DM first line-tx?

A
  • Healthy lifestyle intervention
  • Non-insulin antihyperglycemic agents
  • Gradual dependence on insulin may occur
53
Q

T1DM first-line tx?

A

Insulin

54
Q

T2DM family hx?

A

Frequent (75-90%)

55
Q

T2DM DKA?

A

Rare

56
Q

What is the consequence of the obesity epidemic and Type 1 DM?

A

Type 1 Diabetics may now be obese, therefore they have insulin resistance as well as insulin deficiency

57
Q

What is usually required prior to the onset of T1DM?

A
  • A genetic predisposition

- The “natural” history

58
Q

Discuss the onset of T1DM

A

There will be a genetic predisposition, and then a trigger to decrease insulin production until in consequently halts (Silent insulin)
-Clinical diabetes is observed when there is no insulin (or C-peptide) released.

59
Q

(T/F) There is a greater genetic risk factor for the offspring of an affected father with T1DM compared to an affected mother

A

F, greater in mother (1 in 50)

60
Q

Where is there a greater incidence of T1DM? What is a potential hypothesis?

A
  • North America and Australia

- Potentially Vitamin D, but not confirmed

61
Q

Why isn’t T1DM considered a children’s disease anymore?

A

42% of people with T1DM will receive their diagnosis between the ages of 31 and 60

62
Q

What is the clinical presentation of T1DM?

A

Diabetic Ketoacidosis (DKA)

63
Q

Discuss DKA

A

The complication of severe insulin deficiency leading to hyperglycemia, causing glucosuria, dehydration and ketogenesis to the eventual acidosis

64
Q

What are common symptoms of DKA?

A
  • Vomiting
  • Abdo pain
  • Hyperventilation
  • Lethargy
  • Confusion
  • Dehydration
  • Fruity Breath
65
Q

What would we expect in terms of insulin-mediated glucose uptake and mean plasma insulin during OGTT of someone lean and NGT?

A

-Smaller amount of insulin for same insulin-mediated glucose uptake with normal glucose levels

66
Q

What would we expect in terms of insulin-mediated glucose uptake and mean plasma insulin during OGTT of someone obese and NGT?

A

-More insulin required for less insulin mediated glucose uptake with normal glucose levels

67
Q

What would we expect in terms of insulin-mediated glucose uptake and mean plasma insulin during OGTT of someone obese and IGT?

A

-Much higher insulin for much less insulin mediated glucose uptake, and glucose levels begin to rise (higher baseline)

68
Q

What would we expect in terms of insulin-mediated glucose uptake and mean plasma insulin during OGTT of someone Obese and Diabetic (w/ residual insulin signalling)?

A
  • Slightly declining insulin (compared to IGT) for same less amount of insulin-mediated glucose levels
  • Glucose levels continue to climb to a higher baseline
69
Q

What would we expect in terms of insulin-mediated glucose uptake and mean plasma insulin during OGTT of someone obese and diabetic (overt)?

A

-Exhaustion of plasma insulin, very little insulin mediated glucose uptake and highest baseline glucose levels

70
Q

How do we measure beta cell function?

A

By decreases in either mass, or function

71
Q

When we have a decrease of ___ of b-cell mass we begin to see insulin resistance, or Impaired glucose tolerance

A

50%

72
Q

Name 5 pathogenic feature of hyperglycemia in type II diabetes

A
  • Decreased incretin effects
  • Increased lipolysis and decreased glucose uptake in adipose
  • Increased glucose reabsorption and excretion in kidneys
  • Increased hepatic glucose prodocution
73
Q

What are the standard insulin requirements?

A

0.5-1.0 U/kg/day

74
Q

What are the 3 key impacts of insulin resistance?

A

Will decrease:

1) Ability of insulin to suppress endogenous glucose production in the liver
2) Uptake of glucose in tissues with insulin-dependent glucose transporters (mainly in skeletal muscle)
3) Inhibition of lipolysis

75
Q

Under normal conditions, how does the pancreatic B-cell compensated for insulin resistance?

A

Will detect the higher-than-normal levels of glucose to:

Hyper-secretion –> Hyperinsulinemia —> Formal FPG

76
Q

4 populations who are usually insulin sensitive?

A
  • Children with T1DM
  • Lean people with T1DM
  • Conditioned athletes
  • Newly diagnosis with T1DM
77
Q

6 populations who are usually insulin resistant?

A
  • Children in puberty
  • People with T2Dm
  • Late term pregnant women
  • People ill w/ infections
  • People on steroids
  • People w/ high stress
78
Q

What are the 4 way to diagnose diabetes?

A
  • FPG
  • A1C
  • 2hPG in a 75 g OGTT
  • Random PG?
79
Q

Diabetes diagnosis FPG?

A 
>/= 7.0 mmol/L
-Fasting = no caloric intake for at least 8 hours
80
Q

Diabetes diagnosis A1C?

A

> /= 6.5%

81
Q

Diabetes diagnosis in 2hPG in a 75g OGTT?

A

> /= 11.1 mmol/L

82
Q

Diabetes diagnosis Random PG?

A

> /= 11.1 mmol/L

83
Q

Normoglycemia ranges for fasting glycemia and post-prandial glycemia?

A

1) 5.6-6.1

2) 7.8

84
Q

Range for IFG? (fasting glycemia)?

A

5.6-6.1 - 7.0

85
Q

Range for IGT? (post-prandial glycemia)?

A

7.8-11.1

86
Q

When is diabetes indicated with postprandial glycemia?

A

When greater than 11.1

87
Q

When is diabetes indicated with fasting glycemia?

A

When greater than 7

88
Q

(T/F) A patients IFG is 6.2 (IFG) but his A1C is 6.6%, this is a diagnosis of diabetes.

A

T

Any time that A1C is >6.5%, even if other values indicate only IGT or IFG

Clinical Nutrition 3 (30 decks)

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