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Metabolism, Endocrinology, Haematology > Endocrinology Session 5 CLINICAL > Flashcards

Endocrinology Session 5 CLINICAL Flashcards

1
Q

What are the fuel sources normally available in blood?

A
  • Glucose

- Fatty acids

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2
Q

What are the fuel sources available in blood under special conditions?

A
  • Amino acids
  • Ketone bodies (when glucose critically short)
  • Lactate (anaerobic metabolism)
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3
Q

What are the glycogen stores?

A
  • Liver and muscle fuck medicine

- Made when glucose is in excess

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4
Q

What are the fat stores?

A
  • Made from glucose and dietary fats when excess

- Stored as TAG in adipose tissue

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5
Q

What are the muscle protein stores?

A
  • Used in emergenices

- Filled by normal growth and repair

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6
Q

What are the key features of metabolic control?*

A
  • Immediate metabolism supported by glucose
  • Making glycogen and fat stores
  • If no food for 8-10 hours, gluconeogenesis by using AAs, glycerol, lactate to make glucose for brain
  • Maintain blood glucose by using liver glycogen stores
  • Glucose preserved for the brain
  • Fatty acid metabolism producing ketone bodies which brain can adapt to using in starvation
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7
Q

What are anabolic hormones?

A

Hormones that promote fuel storage

  • Insulin
  • Growth hormone
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8
Q

What are catabolic hormones?

A

Hormones that promote release of fuel from stores and utilisation

  • Glucagon
  • Adrenaline
  • Cortisol
  • Growth hormone (lipolysis and gluconeogenesis)
  • Thyroid hormones
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9
Q

What does insulin STOP?

A
  • Gluconeogenesis
  • Glycogenolysis
  • Lipolysis
  • Ketogenesis
  • Proteolysis
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10
Q

What does insulin START?

A
  • Glucose uptake in muscle and adipose by GLUT4
  • Glycolysis
  • Glycogen and protein synthesis
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11
Q

What are the effects of FEEDING?

A
  • Increase in blood glucose stimulates insulin release
  • Insulin increases uptake and utilisation by muscle and adipose (GLUT4)
  • Promotes storage of glucose as glycogen
  • Promotes amino acid uptake and protein synthesis
  • Promotes lipogenesis and storage of fatty acids
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12
Q

What are the effects of FASTING?

A
  • Blood glucose falls
  • Less insulin
  • Low blood glucose stimulates glucagon
  • Stimulates glycogenolysis to use up glycogen stores and maintain blood glucose
  • Lipolysis to provide fatty acids for use by tissues
  • Gluconeogenesis to make glucose for the brain
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13
Q

What happens in energy starvation that goes on for a prolonged period of time?

A
  • Reduction of blood glucose stimulates release of cortisol from adrenal cortex and glucagon
  • Stimuates gluconeogenesis
  • Anti-insulin effects of cortisol and low insulin prevent tissues from using glucose to save it for brain
  • Tissues metabolise fatty acids
  • Glycerol for fat provides substrate for gluconeogenesis so reduced protein breakdown
  • Liver produces ketone bodies that brain starts to use
  • Kidneys contribute to gluconeogenesis
  • Once all depleted, using protein as fuel

Death due to loss of muscle mass

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14
Q

Why do metabolic and endocrine adaptation happen in pregnancy?*

A
  • Accommodate increased demands of developing fetus and placenta
  • Needs much energy and materials
  • Mother gains about 8kg
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15
Q

When does most fetal growth occur?*

A
  • 2/3rds over last 1/3 of pregnancy
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16
Q

What state is the mother at in early pregnancy?

A

ANABOLIC STATE

  • Increasing maternal fat stores
  • Small increase in insulin sensitivity
  • Nutrients stored to meet future demands of rapid growth and lactation after birth or later in pregnancy
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17
Q

What state is the mother at in late pregnancy?

A

CATABOLIC STATE

  • Decreased insulin sensitivity
  • Increase in maternal glucose and free FA concentration
  • Allows more substrate availability for growing fetus
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18
Q

How does placental transfer occur?*

A
  • Most by simple diffusion down concentration gradients
  • Some (AA) by active transport
  • Glucose is main fuel and transported via GLUT1
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19
Q

How is fetal growth and survival maintained?

A
  • Fetus controls maternal metabolism
  • Placenta, fetal liver create the fetoplacental unit
  • Placenta can secrete many hormones that control maternal hypothalamic pituitary axis
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20
Q

What hormones can the placenta secrete?

A
  • GnRH
  • TRH
  • GHRH
  • CRH (MAIN)
  • ACTH
  • hCG (human chorionic gonadotropin)
  • cCT (human chorionic thyrotropin)
  • hPL (human placental lactogen)
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21
Q

What are important placental STEROID hormones?

A
  • Oestriol

- Progesterone

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22
Q

What are the first changes in maternal metabolism related to?

A
  • Preparation for rapid growth, birth, lactation
  • Increase in maternal nutrient stores
  • Increase in insulin levels promotes anabolic state that stores more nutrients
23
Q

What are the second changes in maternal metabolism related to?

A
  • Adapting to meet demands
  • Reduced maternal glucose utilisation
  • Delayed disposal after meals
  • Releasing fatty acids from stores
  • Fetal-placental units produces anti-insulin hormones faster than production of maternal insulin, that cause insulin resistance
24
Q

What are the main anti-insulin hormones?

A
  • Corticotropin releasing hormone (maternal A. Pituitary desensitised)
  • Human placental lactogen
  • Progesterone
25
Q

Why can the anti-insulin hormones cause hypo and hyperglycaemia?

A
  • Hyperglycaemia AFTER MEALS: increased insulin resistance that cannot lower blood glucose well
  • Hypoglycaemia BETWEEN MEALS: continuous fetal glucose draw
26
Q

What do the oestrogens and progesterones do?

A
  • Increase sensitivity of maternal pancreatic B cells to glucose
  • Causes hypertrophy and hyperplasia
  • Increased insulin secretion and sensitivity
27
Q

What occurs if the B cells do not respond accordingly?

A

Blood glucose can be very elevated and gestational diabetes may develop

28
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

29
Q

What are the causes of gestational diabetes?

A

1) Autoantibody production
2) Genetic susceptibility
3) B cell dysfunction in setting of obesity and chronic insulin resistance (similar to T2 diabetes, most common)

30
Q

What are the clinical implications for gestational diabetes?*

A
  • 3-10% pregnancies
  • Increased miscarriage risk
  • 4x higher risk of congenital malformation
  • Fetal macrosomia
  • More adipose around shoulders = shoulder dystocia (stuck during birth)
  • Associated with preeclampsia and gestational hypertension

Reduced if managed

31
Q

What can determine if the mother will develop gestational diabetes?*

A
  • Starting point of insulin resistance
  • High risk women have a higher insulin resistance BEFORE pregnancy
  • Often develop type 2 diabetes later in life
32
Q

What are the risk factors for gestational diabetes?

A
  • Maternal age >25
  • BMI >25
  • Race/ethnicity - more common in Black, Asian, Hispanic
  • Family history of diabetes
33
Q

How to manage gestational diabetes?

A
  • Dietary modifications at first (initial)
  • Insulin injection if persistent hyperglycaemia)
  • Regular ultrasounds for fetal wellbeing
34
Q

What does the change in metabolic response to exercise ensure?

A
  • Enough to meet increase energy demands of skeletal and cardiac muscle (more energy stores mobilised)
  • Rate of mobilisation = rate of utilisation
  • Maintained glucose supply to brain
  • End products removed as fast as possible
35
Q

What does the magnitude and nature of response depend on?

A
  • Type of exercise (muscles used)
  • Intensity and duration
  • Physical conditions
  • Nutritional state of individual
36
Q

How is ATP rapidly resynthesised in increased metabolic demands?*

A
  • High muscle ATP turnover
  • Myosin ATPase (70%)
  • Rest from maintaining ionic gradients across cell membranes
37
Q

Where does energy to replenish ATP come from?*

A
  • Muscle creatine phosphate stores (immediate energy, only about 5 seconds of a 100m sprint)
  • Glycolysis (very low)
  • Oxidative phosphorylation (needs oxygen)

= DRAW ON ENERGY STORES TO PROVIDE SUBSTRATE FOR PATHWAYS

38
Q

What activates muscle glycogen phosphorylase to release glucose?

A
  • Adrenaline
  • AMP (allosteric)
  • PFK then stimulated by high AMP and pyruvate enters TCA cycle (aerobic) or lactate (anaerobic)
39
Q

What if the exercise is low intensity?

A
  • Enough O2 supplied for complete oxidation

- Glycogen stores can supply energy

40
Q

Where is blood glucose regulated?*

A

Liver (can also recycle lactate in Cori cycle)

41
Q

What does exercise do to the liver?

A

Increases hepatic blood glucose production by glycogenolysis and gluconeogenesis

42
Q

How does muscle take up blood glucose?

A
  • GLUT4

- GLUT1

43
Q

What is the insulin independent process of glucose uptake in exercising muscle?

A
  • High AMP stimulating AMPK that increases glucose translocation)
44
Q

Why must blood glucose levels be maintained?

A

Use by brain

45
Q

Why can fatty acids only be used for energy in aerobic conditions?

A
  • Slow release from adipose
  • Limited carrying capacity in blood
  • Limited carnitine shuttle uptake across membrane

Low ATP production but high capacity

46
Q

What happens in a 100m sprint?

A
  • Short and high intensity so cannot deliver enough O2
  • Anaerobic ATP creation so incomplete and inefficient
  • Lactate made (fatigue due to acidic condition because of rapid ATP hydrolysis)
  • Muscle store of glycogen spares blood glucose for the brain
47
Q

What happens in a 1500m middle distance run?

A
  • Medium intensity so can deliver some extra O2 (40% anaerobic)
  • Uses fatty acids and glucose
  • Initially creatine phosphate and anaerobic glycogen
  • Moves to aerobic from muscle glycogen
  • Final sprint again anaerobic metabolism
48
Q

What happens in a marathon?**

A
  • Long duration and low intensitiy
  • 95% aerobic
  • Muscle glycogen, liver glycogen, fatty acids used
  • Utilisation of fatty acids at about 20-30 min, muscle glycogen depleted in few mins
49
Q

What are the benefits of exercise?

A
  • Change of body composition to less fat and more muscle
  • Better glucose tolerance
  • Better insulin sensitivity of tissues
  • Blood TAG decrease (HDL higher)
  • Lower BP
  • Feeling better psychologically
  • Reverses progression of metabolic disease
50
Q

What happens in prolonged exercise to hormonal control?

A
  • Insulin levels fall slowly
  • Glucagon levels rise
  • Adrenaline and GH rise rapidly
  • Cortisol rises slow
51
Q

Why do insulin levels fall?

A

Secretion inhibited by adrenaline

52
Q

Why do glucagon levels rise?

A

Must mobilise energy stores

  • Activates glycogen phosphorylase (glycogenolysis)
  • Activates PEPCK and fructose-1,6-bisphosphate (gluconeogenesis)
  • Hormone sensitive lipase (lipolysis)
53
Q

Why do adrenaline and growth hormone rise?

A
  • Adrenaline to stimulate glycogenolysis and lipolysis

- GH stimulates gluconeogenesis and lipolysis

54
Q

Why does cortisol rise slowly?

A

To stimulate lipolysis and gluconeogenesis

Metabolism, Endocrinology, Haematology (16 decks)

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