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Sem 2 - MEH > Special Circumstances > Flashcards

Special Circumstances Flashcards

1
Q

What fuel sources are usually available in the blood?

A
  • Glucose
    • Glucose is the preferred fuel source
    • Little (about 12g) free glucose available
    • More glucose (about 300g) stored as glycogen
  • Fatty Acids
    • Can be used as fuel by most cells except red blood cells, brain and CNS.
    • Stored as triacylglycerol (fat) in adipose
    • 10-15 kg fat in a 70kg man (about 2 months fuel supply)
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2
Q

What other fuel sources are available for the body to use under special condition?

A
  • Amino Acids
    • ​Some muscle protein (about 6kg) can be broken down to provide amino acids for fuel
    • Converted to glucose or ketone bodies
    • about 2 weeks supply of energy
  • Ketone bodies
    • ​Mainly from fatty acids
    • Used when glucose is critically short
    • Brain can metabolsie instead of glucose
  • Lactate
    • ​Product of anaerobic metabolism in muscle
    • Liver can convert back to glucose (Cori cycle) or can ve utilised as fuel source for TCA cycle in other tissues (e.g. heart)
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3
Q

What energy stores are available in our body?

A
  • Glucogen (400g)
    • Readily available source of glucose
    • Made and sotred in liver and muscle
    • Made when glucose is in excess in blood
  • Fat (10-15kg)
    • Made from glucose and dietary fats when in excess
    • Stored as triacylglycerol in adipose tissue
    • Source of
      • Fatty acid
      • Glycerol
  • Muscle protein (6kg available)
    • Used in emergency
    • Amino acids can be:
      • Glucogenic (Ala and Val)
      • Ketogenic (Lys and Leu)
      • Both (Tyr and Phe)
    • Store filled by normal growth and repair processes

Food is consumed episodically leading to intermittent supply

Absorbed nutrients are sometimes available in excess and sometimes unavailable (feed / fasting cycle, starvation)

Body needs to be able to draw upon long and short energy stores

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4
Q

What are the key features of metabolic control?

A
  • Up to two hours after eating (glucose and fat available from gut):
    • Immediate metabolism suported by glucose
    • Speed up growth and repair processes
    • Make glycogen as rapidly as possible
    • Increase fat stores
  • 2-10 hours after eating (glucose and fats no longer absorbed):
    • Maintain blood glucose by drawing on glycogen stores
    • Support other metabolic activity with fatty acids released from stores
    • Preserved blood glucose for brain
  • 8-10 hours after eating (Glycogen stores depleted)
    • Need to make more glucose for brain from amino acids, glycerol and lactate
    • Continue to support other metabolism with fatty acids
  • Starvation
    • Need to reduce protein breakdown
    • Fatty acid metabolism produces ketone bodies
    • Brain becomes able to metabolise ketome bodies (reduces need for glucose)
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5
Q

What are the roles of anabolic hormones in metabolism?

A
  • Promote fuel storage
  • Insulin
  • Growth hormone (increases protein synthesis)
  • Lack of insulin = catabolic state
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6
Q

What are the roles of catabolic hormones in metabolism?

A

Promote and release from stores and utilisation

  • Glucagon
  • Adrenaline
  • Cortisol
  • Growth hormone (increases lipolysis and gluconeogenesis)
  • Thyroid hormones
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7
Q

What are the roles of insulin?

A

It inhibits:

  • Gluconeogenesis
  • Glycogenolysis
  • Lypolysis
  • Ketogenesis
  • Proteolysis

It promotes:

  • Glucose uptake in muscle and adipose (GLUT4)
  • Glycolysis
  • Glycogen synthesis
  • Protein synthesis
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8
Q

What are the effects of feeding?

A

Increase in blood glucose stimulates pancreas to release INSULIN

  • increases glucose uptake and utilisation by muscle and adipose (GLUT4)
  • Promotes amino acid uptake and protein synthesis in liver and muscle
  • Promotes lipogenesis and storage of fatty acids as triacylglycerols in adipose tissue.
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9
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 to maintain blood glucose for brain and other glucose dependant tissues
    • Lipolysis in adipose tissue to provide fatty acids for use by tissues
    • Gluconeogenesis to maintain supplies of glucose for the brain
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10
Q

What are the effects of energy starvation?

A
  • Reduction of blood glucose stimulates release of cortisol from adrenal cortex and glucagon from pancreas
  • Stimulate gluconeogenesis and breakdown of protein and fat
  • Reduction in insulin and anti-insulin effects of cortisol prevent most cells from using glucose and fatty acids are preferentially metabolised
  • Glycerol from fat provides important substates for gluconeogenesis, reducing the need for breakdown of proteins.
  • Liver starts to produce ketone bodies and brain starts to utilise these sparing glucose requirement from protein
  • Kidney begin to contribute to gluconeogenesis
  • Once fat stores depleted, system must revert to use of protein as fuel.
  • Death related to lass of muscle mass (resp muscle - infection)
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11
Q

What adaptations occur during pregnancy? When are these most important?

A

A number of alterations to the maternal metabolism and endocrine system accomodate the increased demands of the developing foeus and placenta.

The growth of foetus requires lots of energy and raw materials!

The mother has a net weight gain of about 8 kg by the end of pregnancy

2/3rds of foetal growth occurs over the last 1/3 of pregnancy. From 28 weeks onwards the foetus grows from 1kg to 3.5kg

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12
Q

What ate the two main phases of metabolic adaptation during pregnancy?

A

Anabolic phase - preparatory increase in maternal nutrient stores (especially adipose)

Catabolic phase - maternal metabolism adaps to meet an increasing demand by foetal-placental unit.

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13
Q

What happens in the amabolic phase of pregnancy?

A

In early pregnancy, mother is in an anabolic state

  • Increase in maternal fat stores
  • Small increase in level of insulin sensitivity

Nutrients are stored to meet future demands of rapid foetal growth in late gestation and lactation after birth.

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14
Q

What happens in the catabolic phase pf pregnancy?

A

Late pregnancy is characterised as a catabolic state.

  • decreased insulin sensitivity (increased insulin resistance)

Increase in insulin resistance results in an increase in maternal glucose and free fatty acid concentration.

Allows for greater substrate availability for foetal growth.

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15
Q

How do substances transfer across the placenta?

A

Most substances transfer by simple diffusion down concentration gradients (some active transport e.g. amino acid transporters)

Glucose is principle fuel for foetus and transfer facilitated by transporters (mainly GLUT1)

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16
Q

What does it mean by the “aggressive parasite”?

A
  • Feotus controls maternal metabolism to ensure its own survival.
  • The placenta, fetal adrenal glands and fetal liver, constituve a new endocrine entity, known as the foetalplacental unit.
  • Placenta secretes a wide range of proteins that can control maternal hypothalamic pitiitary axis.
  • Important placental steroid hormones include: Oestriol and progesterone.
17
Q

What are the maternal metabolic changes during the first half of pregnancy?

A
  • Changes to maternal metabolism during first 20 weeks of pregnancy are related to a preparatory increase in maternal mutrient stores (mainly adipose tissue)
  • In preparation for:
    • Rapid growth rate of foetus
    • Birth
    • Subsequent lactation
  • Increasing levels of insulin (increase insulin: anti-insulin ratio) promotes an anabolic state in mother that results in increased nutrient storage.
18
Q

What maternal metabolic changes occur during the second half of pregnancy?

A
  • Maternal metabolism adapts to meet increasing demands
  • 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
  • Maternal insulin levels continue to increase but the production of anti-insulin hormones by tbe foetal-placental unit increases at an even faster rate and the insulin:anti-insulin ratio therefore falls.
19
Q

What are anti-insulin hormones?

A

Placenta secretes several hormones that excert an anti-insulin effect on maternal metabolism

  • Corticotropin releasing hormone (increases x1000) - This means the maternal anterior pituitary becomes desensitised resulting in a more modest increase in ACTH and cortisol
  • Human Placental Lactogen
  • Progesterone

Tend to result in transient hyperglycaemia after means because of increased insulin resistance

Overall, late pregnancy has blood glucose about 10% lower since insulin levels are about 1.65x higher in fasting state and 3x higher in postprandial state,

Hypoglycaemia can occur between meals and late at night because of the continuous foetal draw of glucose.

20
Q

How does insulin secretion change during pregnancy?

A
  • Increased appetite in pregnancy means more glucose is ingested
  • Oestrogen and progesterone increase sensitivity of maternal pancreatic B-cells to blood glucose
    • B cell hyperplasia
    • B cell hypertrophy
  • Leads to increased insulin synthesis and secretion
  • If B-cells do not respond normally, blood glucose may become seriously elevated and Gestational diabetes may occur.
21
Q

What is gestational diabetes?

A

A disease in which pancreatic B-cells do not produce sufficient insulin to meet increased requirement in late pregnancy

22
Q

What are the three known underlying causes of gestational diabetes?

A
  • Autoantibodies similar to those characteristic of type I DM (less than 10% of cases)
  • Genetic suseptibility similar to maturity onset diabetes (rare - 1-5% of cases)
  • B-cell dysfunction in setting of obesity and chronic insulin resistance i.e. “evolving” type II DM (vast majority of women with GDM)
23
Q

What are the clinical implications of gestational diabetes?

A
  • Affects 3-10% of pregnancies
  • Increased incidence of miscarriage
  • Incidence of congenital malformation - 4x higher
  • Foetal macrosomia (means ‘large body’)
    • Disproportionate amount of adipose arounf shoulders and chest could lead to shoulder dystoia (shoulders getting stuck during birth)
  • Associated with hypertensive disorders of pregnancy such as Gestational hypertension and Preeclampsia (high BP, protein in urine, swollen limbs)
  • Risk of complications greatly reduced if gestational diabetes is diagnosed and managed.
24
Q

What is a key factor in deciding if a patient is likely to develop Gestational diabetes?

A

Insulin resistance BEFORE PREGNANCY is crucial in whether or not a women will develop gestational diabetes

25
Q

What are the risk factors for gestational diabetes?

A
  • Maternal age over 25
  • BMI over 25kg/m2
  • Race / ethnicity
    • More common in asian, black and hispanic ethnic groups
  • Personal or family history of diabetes
  • Family history of macrosomia
26
Q

How do you manage gestational diabetes?

A
  • Initial dietary modification including calorific reduction in obese patients
  • Insulin injection if persistant hyperglycaemia is present
  • Regular ultrasound scans to assess foetal growth and wellbeing.
27
Q

What systems need to rapidly adapt to exercise?

A
  • Muscoskeletal system
  • Cardiovascular system
  • Respiratory system
  • Temperature regulation
28
Q

What does the metabolic response to exercise need to ensure?

A
  • Increased energy demands of skeletal and cardiac muscle are met by mobilisation of energy stores
  • Minimal disturbances to metabolic homeostasis by keeping rate of mobilisation equal to rate of utilisation.
  • Glucose supply to brain is maintained
  • End products of metabolism are removed as quickly as possible.
29
Q

What does the magnitide and nature of response to exercise depend on?

A
  • Type of exercise (muscle used)
  • Intensity and duration of exercise
  • Physical condition and nutritional state of individual
30
Q

Where does the energy used in exercise come from?

A
  • ATP“stores” are limited - last 2 seconds during a sprint.
  • This means it must be rapidly resynthesised at a rate that meets the metabolic demands placed upon the cell. Different strateries are employed by different rells to match the rate of re-synthesis with hydrolysis.
  • Muscle creatinine phosphate stores (about 17mmol/kg muscle) can rapidly replenish ATP to provide immediate energy
  • Still only enough for about 5 seconds worth of energy during a 100m sprint
  • Beyond initial burst of energy, further ATP must be supplied by:
    • Glycolysis (Inefficient, 2 ATP net per glucose)
    • Oxidative phosphorylation (Required oxygen!)
  • Must therefore draw on energy stores to provide substrate for these pathways.
31
Q

When is muscle glycogen used as an energy store?

A
  • Additional intensive exercise (anaerobic) for up to two minutes can be sustained by breakdown of muscle glycogen.
  • If exercise is low intensity enough, oxygen can be supplied for complete oxidation of glucose and glycogen stores (from muscle and liver) could theoretically last for about 60 mins (e.g jogging)
32
Q
A
33
Q

How is blood glucose regulated during exercise?

A
  • Liver is principal organ for regulating blood glucose
  • Exercise results in an increase in hepatic blood glucose production through glycogenolysis and gluconeogenesis
  • Liver recycles lactate produced by anaerobic metabolism (Cori cycle)
  • Muscle takes up blood glucose vis GLUT4 transporter (insulin promotes translocation to plasma membrane) and GLUT1 (constitutively active)
  • Exercising muscle also has insulin independatn process of glucose uptake (increase in AMP stimulates AMPK resulting in signalling cascade which increases GLUT4 translocation)
  • Rate of glucose production form liver however is insufficient to meet full demands of exercising muscle
  • Essential that blood glucose levels maintained for use by brain
34
Q

How are fatty acids used as a fuel?

A
  • Major store of triacylglycerol in adipose (15kg) but also some muscle itself
  • Theoretically cound provide enough energy for anout 48 hours of low intensity exercise
  • Can only be used in aerobic condition
    • Slow release from adipose tissue
    • Limited carrying capasity in blood
    • Capasity limited by uptake across mitochondrial membrane (carnitine shuttle)
  • Low rate of ATP production but high capasity for sustained production.
35
Q

What energy stores are used in a 100m sprint?

A
  • Short, high intensity exercise
  • Cannot deliver sufficient oxygen to muscles in time
  • Once hgih energy phosphate stores used (about 5 seconds) must creat ATP anaerobically
    • Inefficient
    • Incomplete metabolism of glucose
  • Produces lactate (lactic acid) with sunsequent build up in H+ produces fatigue
  • Cannot deliver extra lucose to muscle cells fast enough
  • Need muscle store of glycogen
  • Helps to spare blood glucose for brain
36
Q

What energy stores are used in 1500m middle distance race?

A
  • Medium intensity
  • Can deliver some extra oxygen to muscles
  • However, stil about 40% anaerobic
  • Aerobic metabolismcan use fatty acids as well as glucose

Three phases to race:

  • Initial start uses creatine phosphate and anaerobic glycogen metabolism.
  • Long middle phase in which ATP is produced aerobically from muscle glycogen (relies on adequare supply of O2 to muscle)
  • Final finishing sprint relies again on the anaerobic metabolism of glycogen and produces lactate.
37
Q

What energy stores are used when running a marathon?

A
  • Low intensity, long duration
  • 95% aerobic
  • Use of
    • Muscle glycogen
    • Liver glycogen
    • Fatty acids
  • Muscle glycogen depleted in a few minutes. Glucose from liver glycogen peaks at about an hour then declines steadily.
  • Utilisation of fatty acids rises steadily from 20-30 minutes.
38
Q

How are hormones used to control the metabolic response to exercise?

A

Over the course of running a marathon:

  • Insulin levels fall slowly (inhibiton of secretion by adrenaline)
  • Glucagon levels rise:
    • Stimulates glyconeogenolysis (activates glycogen phosphorylase)
    • Stimilates gluconeogenesis (PEPCK and fructose 1,6 bisphosphate)
    • Stimulates lipolysis (Hormone sensitive lipase)
  • Adrenaline and growth hormone rise rapidly
    • Adrenaline stimulates glycogenolysis and lipolysis
    • Growth hormome stimulates lipolysis and gluconeogenesis
  • Cortisol rises slowly
    • Stimulates lipolysis and gluconeogenesis
39
Q

What are the benefits of exercise?

A
  • Body composition changes (incease muscle, decrease adipose)
  • Glucose tolerance improves (increase muscle glycogenesis)
  • Insulin sensitivity of tissues increases
  • Blood triglyceries decrease (decrease VLDL and LDL, increase HDL)
  • Blood pressure falls
  • Phsychological effects (feeling of wellbeing)
  • Reverse progression of metabolic diseases
  • More successful than pharmacological intervention for treatment of T2DM

Sem 2 - MEH (22 decks)

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