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A Physiology > Hormonal regulation of intermediary metobolism IV. > Flashcards

Hormonal regulation of intermediary metobolism IV. Flashcards

1
Q

I. Phases of fasting
1. What are the 4 phases of fasting?

A
  1. Postpandrial phase
  2. Interdigestive phase/Early fasting (0-24 hrs)
  3. Short-term fasting (24-72 hrs)
  4. Long-term fasting (>72 hrs)
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2
Q

I. Phases of fasting
2A. What happen in Postpandrial phase?

A
  1. High insulin level
    a. Storage of nutrients
    - Glycogen synthesis
    - Protein synthesis
    - Lipogenesis
    b. + non-obligatory glucose utilizing tissues also use glucose for energy production
    - Glycolysis
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3
Q

I. Phases of fasting
2B. What is the Goal of Postpandrial phase?

A

1/ Storage of nutrients
2/ To prevent the high levels of transport nutrients (glucose)

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4
Q

I. Phases of fasting
3A. What happen in liver during Interdigestive phase/Early fasting (0-24 hrs) phase?

A
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5
Q

I. Phases of fasting
3B. What happen in muscle during Interdigestive phase/Early fasting (0-24 hrs) phase?

A
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6
Q

I. Phases of fasting
3C. What happen in fat tissue during Interdigestive phase/Early fasting (0-24 hrs) phase?

A
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7
Q

I. Phases of fasting
3D. During 1. Interdigestive phase/Early fasting (0-24 hrs), does plasma glucose cc. reduce?

A

Plasma glucose cc. does not reduce

Insulin↓
glucagon↑
cortisol = but necessary

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8
Q

I. Phases of fasting
4. What happen here?

A
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9
Q

I. Phases of fasting
5A. What happen in liver during 2. Short-term fasting (24-72 hrs)?

A
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10
Q

I. Phases of fasting
5B. What happen in muscle during 2. Short-term fasting (24-72 hrs)?

A
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11
Q

I. Phases of fasting
5C. What happen in FAT TISSUE during 2. Short-term fasting (24-72 hrs)?

A
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12
Q

I. Phases of fasting
6. Does Plasma glucose cc. decrease during 2. Short-term fasting (24-72 hrs)?

A
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13
Q

I. Phases of fasting
7. What are the important values during muscle proteolysis?

A

7-12 g Nitrogen
Corresponding to 50-75 g protein
Daily weight loss: 250-375 g

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14
Q

I. Phases of fasting
8A. What happen in liver during 3. Long-term fasting (>72 hrs)?

A
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15
Q

I. Phases of fasting
8B. What happen in muscle during 3. Long-term fasting (>72 hrs)?

A
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16
Q

I. Phases of fasting
8A. What happen in liver during 3. Long-term fasting (>72 hrs)?

A
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17
Q

I. Phases of fasting
8C. What happen in FAT TISSUE during 3. Long-term fasting (>72 hrs)?

A
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18
Q

I. Phases of fasting
9. What happen to plasma glucose cc. during 3. Long-term fasting (>72 hrs)?

A
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19
Q

I. Phases of fasting - 3. Long-term fasting (>72 hrs)
10. Does Gluconeogenesis happen in kidney?

A

Yes

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20
Q

I. Phases of fasting - 3. Long-term fasting (>72 hrs)
11. How does proteolysis occur in 3. Long-term fasting (>72 hrs)?

A

Proteolysis is reduced by time
- Urea exretion reduces (10-15 g → 1g by the 6. week)
- When insreases again→ perimortal proteolysis

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21
Q

I. Phases of fasting - 3. Long-term fasting (>72 hrs)
12. Explain the peak of ketogenic capacity

A

Peak of ketogenic capacity on the 3rd day
- BUT the uptake of keton bodies decreases continously
- Concentration of keton bodies increases for weeks (2-3 mM)

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22
Q

I. Phases of fasting
13. Make a schematic diagram about hepatic glucose release during glucose production in starvation

A
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23
Q

I. Phases of fasting
14. Make a schematic diagram about renal glucose release during glucose production in starvation

A
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24
Q

I. Phases of fasting
15. Make a schematic diagram about Glucose consumption of the body during prolonged fasting

25
Q

I. Phases of fasting
16. Make a schematic diagram about Anorexia nervosa

26
Q

II. Catabolic response to stress
1. Make a schematic diagram about Catabolic response when catecholamines are involved

27
Q

II. Catabolic response to stress
2. Make a schematic diagram about Catabolic response when glucocorticoids are involved

28
Q

II. Catabolic response to stress
3. What are these points when it comes to Stress induced hyperglycemia?

29
Q

II. Catabolic response to stress
4. What are Metabolic changes during physical exercise?

30
Q

III. Disturbances of the intermediary metabolism
1. What are the 2 types of Diabetes mellitus?

A

Type 1
Insulin dependent IDDM, T1D
Juvenile

Type 2
Non insulin dependent NIDDM, T2D

31
Q

III. Disturbances of the intermediary metabolism
2A. What are the features of diabetes type 1?

A

1/ Insulin dependent diabetes mellitus
2/ Type 1, IDDM
3/ An autoimmune process deteriorates the β cells of the Langerhans islets

32
Q

III. Disturbances of the intermediary metabolism
2B. What are the molecular events of diabetes type 1?

A

1/ After 60%- β-cell loss exogenous hyperglycemia
-> blood glucose level ↑ only after carbohydrate consumption (reduced carbohydrate tolerance)

2/ Later endogenous hyperglycemia
-> even the fasting blood glucose level is higher; the source of the glucose during fasting is the inappropriately high gluconeogenesis.

33
Q

III. Disturbances of the intermediary metabolism
2C. Make a schematic diagram about Abnormal metabolic processes in insulin dependent diabetes mellitus

34
Q

III. Disturbances of the intermediary metabolism
2D. What are the classic symptoms of diabetes type 1

A
  • Weight loss
  • Polyuria
  • Polydipsia
  • Pluritus
  • Confusion/coma
35
Q

III. Disturbances of the intermediary metabolism
3. Diagnosis of DM - the evaluation of the oral glucose tolreance test
-> Draw the glucose curve of diabetes mellitus and normal range

36
Q

III. Disturbances of the intermediary metabolism
4A. What are the Rules of OGTT?

A

*It should be performed in the morning after at least 10 hours of fasting.
*Unrestricted, but minimum 150 g glucose containing diet must be consumed during the previous 3 days of the test.
*The patient should have average physical activity during the previous days.
*The examination should be done in resting conditions without physical activity and smoking.
*Any circumstances that can alter the results of the examination (infections, drugs, etc.) should be taken into consideration – in some cases the postponement of the OGTT may be warranted.
*75 g glucose is required for the test which should be disolved in 250-300 ml of water, and should be consumed within 5 minutes. (For children 1.75 g/body weight kg, but maximum 75 g is suggested.)
*For the categorization of carbohydrate metabolism, the measurement of the 0- and 2-hour values is sufficient.

37
Q

III. Disturbances of the intermediary metabolism
4B. When is OGTT contraindicated?

A

If fasting glucose is ≥7mmol/L the OGTT is contraindicated!

38
Q

III. Disturbances of the intermediary metabolism
5A. What are the important values in Evaluation of the OGTT?

39
Q

III. Disturbances of the intermediary metabolism
6. Make a schematic diagram about type 2 diabetes and normal range blood glucose cc.

40
Q

III. Disturbances of the intermediary metabolism
7. What is Degree of hemoglobin glycation (HbA1c) ?

A

Degree of hemoglobin glycation (HbA1c) reflects the average blood glucose level over a prolonged previous period (3-4 months)

41
Q

III. Disturbances of the intermediary metabolism
7B. What are the important values of Degree of hemoglobin glycation (HbA1c) ?

42
Q

III. Disturbances of the intermediary metabolism
7c. What is Target value in treatment? (Degree of hemoglobin glycation (HbA1c))

43
Q

III. Disturbances of the intermediary metabolism
8A. What are the characteristics of Type 2 diabetic?

A

1/ Type 2 or non insulin dependent diabetes mellitus (T2D, NIDDM)
2/ Most abundant endocrine disorder: high plasma glucose level despite of high plasma insulin concentration
3/ Relative insulin deficiency/ insulin resistance -> complex metabolic disorders affecting many tissues
4/ Heterogeneous etiology, multicomponent:
– Obesity,eatinghabits,geneticfactors,etc.
– Can be caused by: overproduction / administration of hormones that increase
glucose levels (glucocorticoid, GH, T3 …: secondary diabetes)
5/ In later stages, insulin secretion decreases (β-cells are depleted)

44
Q

III. Disturbances of the intermediary metabolism
8B. What are the molecular events in plasma in obesity?

A

1/ In obesity, greater insulin secretion is required to ensure the same blood glucose levels
2/ Daily changes of plasma : glucose, C peptide, insulin levels
3/ in normal weight and obese patients.

45
Q

III. Disturbances of the intermediary metabolism
8C. What are the expression that Determination of insulin resistancy and ß cell function?

A

HOMA-IR and HOMA %B index

46
Q

III. Disturbances of the intermediary metabolism
8D. How to use HOMA-IR index?

47
Q

III. Disturbances of the intermediary metabolism
8E. How to use HOMA %B index?

48
Q

III. Disturbances of the intermediary metabolism
9/ Make a schematic diagram about Insulin resistance, ß-cell dysfunction and the appearance of the disease?

49
Q

III. Disturbances of the intermediary metabolism
10/ What does Increased body mass index show?

A

+ correlation with the non-insulin dependent diabetes mellitus (NIDDM)

50
Q

III. Disturbances of the intermediary metabolism
11/ ___ and ___ correlates to central obesity

A

Insulin resistance and T2D correlates to central obesity

51
Q

III. Disturbances of the intermediary metabolism
12. What is the Progression of type2 diabetes

52
Q

III. Disturbances of the intermediary metabolism
13. Describe Gestational diabetes mellitus (GDM)

A
  • Gestational diabetes mellitus is a carbohydrate metabolism disorder diagnosed during pregnancy
  • Incidence is 2-6 %
  • General screening is performed between the 24-28th gestational week with a
    standard OGTT with 75g glucose
  • GDM is diagnosed if fasting glucose ≥7 mmol/l (recently ≥ 5.6mmol/l) and/or 2 hour glucose ≥ 7.8 mmol/l.
  • Six weeks after delivery OGTT should be performed to reconsider the diagnosis
  • Short and long term complications
  • Mother: delivery complications, cesarean section, later diabetes and
    cardiovascular diseases
  • Child: LGA, hypoglycemia, later obesity, diabetes, cardiovascular diseases
53
Q

III. Disturbances of the intermediary metabolism
14A. What are the options to ameliorate NIDDM?

A

1/ Diet
2/ exercise
3/ sulfanylurea
4/ GLP (analogues) dipeptidyl peptidase inhibition
5/ TZD (tiazolidin-dion drugs)
6/ biguanidins (metformin)
7/ SGLT- inhibition
8/ insulin

54
Q

III. Disturbances of the intermediary metabolism
14B. Why is diet an option to ameliorate NIDDM?

A

reduces the lipid content of the adipose tissue
-> increases adiponectin secretion ↑, in other insulin target tissues triglicerid ↓ (insulin resistance ↓) , resistin, TNFα and IL6 secretion ↓
8/ insulin

55
Q

III. Disturbances of the intermediary metabolism
14C. Why is excercise an option to ameliorate NIDDM?

A

excercise
=> GLUT-4 translocation to the plasma membrane, blood plasma [glucose]↓

56
Q

III. Disturbances of the intermediary metabolism
14D. Why is sulfanylurea an option to ameliorate NIDDM?

A
  • sulfanylurea
    -> KATP inhibition
    -> insulin secretion↑
57
Q

III. Disturbances of the intermediary metabolism
14D. Why is GLP (analogues) an option to ameliorate NIDDM?

58
Q

III. Disturbances of the intermediary metabolism
14E. Why is TZD (tiazolidin-dion drugs) an option to ameliorate NIDDM?

59
Q

III. Disturbances of the intermediary metabolism
14F. Why is SGLT- inhibition an option to ameliorate NIDDM?

A
  • SGLT- inhibition -> plasma [glucose]↓

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