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MEH > 20. Metabolic And Endocrine Control During Special Cirumstances > Flashcards

20. Metabolic And Endocrine Control During Special Cirumstances Flashcards

1
Q

What are the fuel sources normally available in the blood?

A

Glucose

Fatty acids - except RBC, brain and CNS

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2
Q

What fuel sources are available under special conditions?

A

Amino acids
Ketone bodies
Lactate

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3
Q

What are the anabolic hormones in metabolic control and what do they do?

A

Insulin
Growth hormone - increased protein synthesis

Promote fuel storage

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4
Q

What are the catabolic hormones in metabolic control and what do they do?

A 
Glucagon
Adrenaline
Cortisol
Growth hormone - increases lipolysis and gluconeogenesis
Thyroid hormones

Promote release from stores and utilisation

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5
Q

What does insulin prevent?

A 
Gluconeogenesis
Glycogenolysis
Lipolysis 
Ketogenesis
Proteolysis
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6
Q

What does insulin promote?

A

Glucose uptake in muscle and adipose (GLUT4)
Glycolysis
Glycogen synthesis
Protein synthesis

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7
Q

What are the effects of feeding?

A

Increase in blood glucose stimulates pancreas to release insulin
Increase glucose uptake and utilisation by muscle and adipose (GLUT4)
Promotes storage of glucose as glycogen in liver and muscle
Promotes amino acid uptake and protein synthesis in liver and muscle
Promotes lipogenesis and stage of fatty acids as triacylglycerol in adipose tissue

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8
Q

What are the effects of fasting?

A

Blood glucose falls and insulin secretion depressed
Reduces uptake of glucose by adipose and muscle
Low blood glucose stimulates glucagon which stimulates:
- glycogenolysis in liver
- lipolysis in adipose tissue
- gluconeogenesis to maintain supplies of glucose for brain

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9
Q

What does the reduction of blood glucose stimulate the release of?

A

Cortisol from adrenal cortex

Glucagon from pancreas

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10
Q

What processes does energy starvation stimulate?

A

Gluconeogenesis and breakdown of protein and fat

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11
Q

What does the reduction in insulin and anti-insulin effects of cortisol do?

A

Prevent most cells from using glucose and fatty acids are preferentially metabolised

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12
Q

What does the liver start to produce in energy starvation?

A

Keaton bodies and brain starts to utilise these sparing glucose requirement from protein

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13
Q

What are the 2 main bases of metabolic adaptation during pregnancy?

A

Anabolic phase

Catabolic phase

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14
Q

What happens in the anabolic state in pregnancy?

A

In early pregnancy
Increase in maternal fat stores
Small increase in level of insulin sensitivity
Nutrients are stored to meet future demands of rapid fetal growth in late gestation and lactation after birth

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15
Q

What happens in the catabolic state in pregnancy?

A

Late pregnancy
Decreased insulin sensitivity
Increase in insulin resistance results in an increase in maternal glucose and free fatty acid concentration
Allows for greater substrate availability for fetal growth

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16
Q

How are substances transferred across the placenta?

A

Not substances transfer by simple diffusion down concentration gradients
Glucose is principal fuel for fetus and transfer facilitated by transporters (GLUT1)

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17
Q

What is the fetoplacental unit?

A

The placenta, fetal adrenal glands and fetal liver constitute a new endocrine entity

18
Q

What does the placenta secrete?

A

Wide range of proteins that can control the maternal hypothalamic pituitary axis

19
Q

What are the hypothalamic like releasing hormones?

A

Corticotropin releasing hormone (CRH)
Gonadotropin releasing hormone (GnRH)
Thyrotropin releasing hormone (TRH)
Growth hormone releasing hormone (GHRH)

20
Q

What are the pituitary like hormones?

A

ACTH
Human chorionic gonadotropin (hCG)
Human chorionic thyrotropin (cCT)
Human placental lactose needs (hPL)

21
Q

What are the important steroid hormones released?

A

Oestriol

Progesterone

22
Q

Why does the maternal metabolism change during the first 20 weeks of pregnancy?

A

Related to a preparatory increase in maternal nutrient stores (mainly adipose tissue)
In preparation for rapid growth rate of fetus, birth, subsequent lactation

23
Q

What are the maternal metabolic changed during the second half of pregnancy?

A

Concentration of nutrients in the maternal circulation kept relatively high by:

  • reducing maternal utilisation of glucose by switching tissues to use of fatty acids
  • delaying maternal disposal of nutrients after meals
  • releasing fatty acids from stores built up during 1st half of pregnancy
24
Q

What happens to the maternal insulin in the second half of pregnancy?

A

Levels continue to increase but the production of anti-insulin hormones by the fetal-placental unit increases at an even faster rate and the insulin/anti-insulin ratio therefore falls

25
Q

What are the anti-insulin hormones?

A

Corticotropin releasing hormone
Human placental lactogen
Progesterone

26
Q

How does corticotropin releasing hormone work?

A

Maternal anterior pituitary becomes desensitised resulting in s more modest increase in ACTH and cortisol

27
Q

What do oestrogens and progesterone do in terms of insulin secretion in pregnancy?

A

Increase sensitivity of maternal pancreatic beta-cells to blood glucose
Beta-cell hyperplasia
Beta-cell hypertrophy
Leads to increased insulin synthesis and secretion

28
Q

What happens if beta cells do not respond normally in pregnancy?

A

Blood glucose may become seriously elevated and gestational diabetes may develop

29
Q

What is gestational diabetes?

A

Disease in which pancreatic beta cells do not produce sufficient insulin to meet increased requirement in later pregnancy

30
Q

What are the 3 known underlying causes of gestational diabetes?

A

Autoantibodies similar to those characteristic of type 1 DM
Genetic susceptibility similar to maturity onset diabetes
Beta cell dysfunction in setting of obesity and chronic insulin resistance

31
Q

What are the clinical implications of gestational diabetes?

A

Increased incidence of miscarriage
Incidence of congenital malformation 4x higher
Fetal macrosomia - leading to shoulder dystocia
Associated hypertensive disorders of pregnancy such as gestational hypertension and preeclampsia

32
Q

What are the risk factors of gestational diabetes?

A 
Maternal age >25 years
BMI >25kg/m^2
Race/ethnicity - more common in Asian, black and Hispanic ethnic groups
Personal or family history of diabetes
Family history of macrosomia
33
Q

What is the management of gestational diabetes?

A

Initial dietary modification including calorific reduction in obese patients
Insulin injection if persistent hyperglycaemia is present
Regular ultrasound scans to assess fetal growth and well being

34
Q

Where does energy come from for exercise?

A

Muscle creatine phosphate stores can rapidly replenish ATP to provide immediate energy
Still only enough for 5 seconds worth of energy during a 100m sprint

Beyond initial burst of energy, further ATP supplied by glycolysis and oxidative phosphorylation

35
Q

What can additional intensive exercise (anaerobic) for up to 2 mins be supplied by?

A

Breakdown of muscle glycogen

36
Q

What is the cori cycle?

A

Glucose used up in muscles, produces lactate
Lactate transported to liver via blood
Liver recycles lactate into glucose
Glucose transported back to muscles via blood

37
Q

How does muscle take up blood glucose?

A

Via GLUT4 transporter and GLUT1

38
Q

When can fatty acids be used as fuel?

A

In aerobic conditions

  • slow release from adipose tissue
  • limited crying capacity in blood
  • capacity limited by uptake across mitochondrial membrane (carnitine shuttle)
39
Q

What is the hormonal control of the metabolic response to prolonged exercise?

A

Insulin levels fall slowly
Glucagon levels rise - stimulates glycogenolysis, gluconeogenesis and lipolysis
Adrenaline and growth hormone rise rapidly
Cortisol rises slowly - stimulates lipolysis of gluconeogenesis

40
Q

What are the benefits of exercise?

A 
Body composition changes
Glucose tolerance improves
Insulin sensitivity of tissues increases
Blood triglycerides decrease
Blood pressure falls
Psychological effects

MEH (22 decks)

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