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NUTR 3090 > DIABETES MELLITUS > Flashcards

DIABETES MELLITUS Flashcards

1
Q

explain what is diabetes mellitus

A

-chronic disease
-insulin deficiency or resistance
-hyperglycemia bc of lipid, cho, protein metabolism disturbances

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2
Q

Mechanism of diabetes insipidus?

A

-hyperglycaemia bc of excessive water loss
= hypertonic blood volume
-antidiuretic hormone dysregulation
-not insulin related

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3
Q

what is amylin?
Where and how much secreted?

A

peptide hormone thats released with insulin by beta cells (100:1 insulin)

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4
Q

what cells secrete insulin? glucagon? somatostatin?

A

insulin = beta
glucagon = alpha
somatostatin = delta

all in the pancreas

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5
Q

Purpose of amylin?

A

blood glucose regulation via
1. decreased food intake
2. delayed gastric emptying
3. decreased glucose production

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6
Q

how would amylin delaying gastric emptying help regulate blood glucose?

A

delayed absorption of glucose
= slower time from GIT to bloodstream
=stable post-meal glucose levels

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7
Q

Explain the role of insulin

A
  1. Mediates transport of glucose from blood to muscle or adipose cells
  2. inhibit glycogenolysis and gluconeogenesis
  3. promotes energy storage via glycogen/fat production and body tissues building via proteins
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8
Q

is insulin catabolic?

A

No anabolic bc it creates molecules in body and uses energy in process

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9
Q

role of glucagon?

A
  1. promote glycogenolysis + gluconeogenesis
  2. inhibit energy storage (glycogen and fat production) and building of tissue via proteins
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10
Q

is glucagon anabolic?

A

no its catabolic bc breaks down molecules and releases energy.

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11
Q

what GLUT transporter is mediated by insulun, and where can we find it?

A

GLUT-4

-commonly in muscle and adipose tissues

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12
Q

List GLUT transporters

A

GLUT 1 - RBC, brain
GLUT 2 - liver * fruc and galac too
GLUT 3 - brain
GLUT 4 - skm and adipose
GLUT 5 - fructose in intestinal level

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13
Q

classifications of DM

A
  1. pre diabetes (IFG or IGT)
  2. t1d
  3. t2d
  4. pre existing DM in pregnancy (T1 or T2)
  5. GDM
  6. hypoglycemia
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14
Q

Improvements in Canada for diabetes needed?

A

treatment, screening, access and education

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15
Q

whats the differences between IFG vs IGT?

A

higher levels of glucose fasted state vs hyperglycemia post prandial

new vs more established

risks of diabetes and CVD vs higher risk of CVD

both show no symptoms

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16
Q

blood levels for IGT? IFG?

A

IGT : 7.8-11

IFG: 6.1 -6.9

17
Q

what is the overload hypothesis?

A

related to the development of T1D
stress exposure to fetus = autoimmune response triggered

18
Q

explain the etiology of T1D

A

autoimmune disease/susceptible

typically have antibodies for beta cells, insulin or beta cell antigens that destroy them

  • development of autoantibodies triggered via environment-gene interaction
  • around 2 years of life then manifested later in life

huge genetic component

19
Q

in t1d, what is the thresholfd for when minimal insulin is secreted

A

loss of 80-90% beta cells

20
Q

Acute effects of T1DM

A
  1. hyperglycemia
  2. glucosuria (glucose spills into urine)
  3. polyuria - osmotic diuresis bc glucose spills into urine
  4. polydipsia - thirst
  5. polyphagia -increased food intake
  6. dehydration
  7. fatigue
  8. weight loss even with increased apetite
21
Q

why do T1D patients lose weight even tho they are more hungry?

A

combination of all the acute effects
- inability to uptake glucose in cells so body perceives this as a state of energy deficit even tho you have high blood glucose levels
-protein and fat broken down instead of cho
-excretion of water
-loss of calories through urine

22
Q

severe effects of T1D?

A

Ketones broken down for fuel

-ketosis- acumulation of ketones in blood
-ketoacidosis - lower blood PH bc of uncontrolled ketosis
-diabetic ketoacidosis DKA - lowered blood pH

23
Q

What happens during DKA?

A

complete deficiency in insulin

blood pH decrease = hyperapnea
brain uses ketones for energy
= stupor
=coma

24
Q

Can we prevent or treat T1D?

A

yes, we can delay the onset

-manage life stressors
-avoid autoimmune responses that triggers inflammation (gluten ex.)

25
Q

What is T2D?

A

-chronic disease
-mainly insulin resistance
-overtime pancreas may stop making insulin
-disease of aging and obesity rather than genetics and environmental factors

26
Q

T2D etiology

A
  1. Genetic
  2. Obesity
  3. Diet high in ADDED saturated fats and low GI/GL foods
27
Q

what percentage of diabetics are obese (BMI>30)

A

60-80%

28
Q

Explain the progression to T2D over the years

A
  1. insulin resistance
  2. hyperinsulinemia
  3. Prediabetes - IGT/IFG
  4. T2D
29
Q

what is hyperinsulinemia

A

high levels of insulin in the blood due to IR
–pancreas secreting more insulin to manage glucose levels but body not responding

30
Q

short term effects of t2d

A
  1. classic symptoms of DM
  2. mild fatigue
  3. mild or no weight loss
  4. mild ketosis NOT DKA
31
Q

2 types of hypoglycemia

A
  1. fasting/spontaneous
  2. Reactive/ functional
32
Q

Explain fasting/spontaneous hypoglycemia

A

-Due to tumours, liver disease, alcoholism, endocrinopathies
-relative of absolute lack of insulin relative to counter-reg hormones

33
Q

explain reactive functional hypoglycemia

A

-post prandial/absorptive
-occurs in DM when too much insulin OR too little food (intake vs insulin mismatch)
-can be DM prior diagnosis (insulin release vs sensitivity mismatch)

34
Q

what type of hypoglycemia would you see in dm patients?

A

reactive functional

35
Q

hypoglycemia bc of too much insulin or too little food is…

A

mismatch between insulin and food intake

36
Q

hypoglycemia in prediabetes is an example of

A

insulin release and sensitivity mismatch

37
Q

symptoms of hypoglycemia
specific to DM patients treated with insulin

A

insulin shock
=fatigue
coma
sometimes death

38
Q

what is brittle DM

A

diabetes thats hard to control due to fluctuations of blood sugar
-mostly in type 1
-anxiety around controlling levels
-brain damage if not controlled

NUTR 3090 (9 decks)

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