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Medicine Year 1 - Semester 2 - Part 1 > Metabolic Changes in Health and Disease > Flashcards

Metabolic Changes in Health and Disease Flashcards

1
Q

Catabolism

A

Weight Loss

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2
Q

Anabolism

A

Weight Gain

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3
Q

How much body energy is lost as heat ?

A

60%

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4
Q

What does chronic, low-grade systemic inflammation cause ?

A

As a result of obesity :

Increases the risk of cancer, cardiovascular disease, osteoarthritis and other diseases.

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5
Q

What does obesity cause ?

A

Increases risk of developing metabolic syndrome and type 2 diabetes.

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6
Q

What controls appetitie enhancement / suppression?

A

Neuronal and hormonal factors regulate food intake

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7
Q

Describe the role of insulin in metabolism

A

Insulin :

Hypoglycaemic / Anabolic hormone

  • Acts to decrease blood glucose / fuel storage
  • Lock nutrients away in storage molecules
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8
Q

Describe the role of glucagon in metabolism

A

Glucagon :

Hyperglycaemic / Catabolic hormone

  • Acts to increase blood glucose levels
  • Mobilise energy stores
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9
Q

State the hyperglycaemic hormones

A

Glucagon
Adrenalin

Cortisol
Growth hormone
(not directly related to absorptive/postabsorptive events)

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10
Q

Give some functions of insulin

A

Stimulates :

  • glucose uptake by cells
  • amino acid uptake by cells
  • glucose catabolism for energy
  • lipogenesis & fat storage
  • protein synthesis

Inhibits :

  • gluconeogenesis
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11
Q

Give some functions of glucagon

A

Stimulates :

  • glycogenolysis
  • lipolysis and fat mobilisation
  • gluconeogenesis
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12
Q

Function of metabolic homeostasis

A

Aims to ensure a constant supply of glucose for the brain (which uses 60% of all glucose produced)

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13
Q

Why does the brain require a constant supply of glucose ?

A

It is unable to store glycogen or utilise fatty acids (due to blood brain barrier).

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14
Q

State the key regulator of blood glucose

A

Liver

Buffering via :

  • Glycogenesis
  • Glycogenolysis
  • Gluconeogenesis
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15
Q

State the normal blood glucose range

A

4-7 mmol/L

OR

70-110 mg/dL

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16
Q

How much energy does a 70kg person use per day ?

A

1600kcal/day

(up to 5000 active state)

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17
Q

How long do carbohydrate stores last ?

A

1 day or less - blood glucose will fall

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18
Q

Metabolic changes associated with short-term starvation

A

Proteins can yield glucose (deamination and gluconeogenesis), but need to be preserved as much as possible.

Muscle shifts to using fatty acids as primary fuel.

Triglycerides have limited ability to be converted to glucose.

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19
Q

Describe glucose sparing for the brain

A

Muscle shifts to using fatty acids as primary fuel.

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20
Q

Metabolic changes associated with long-term starvation

A

Ketone bodies build up

Over the 1st few days, the brain becomes more tolerant to lower glucose - uses ketone bodies

Over time the brain gradually increases the use of ketone bodies

The body preserves valuable protein reserves, as need for amino acids to fuel glucogenesis reduced (muscle preserved)

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21
Q

Describe a key feature of long term starvation

A

Ketone body build up
Brain increases use of ketone bodies (need for glucose reduced)

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22
Q

What is the cause of ketone body build up ?

A

A consequence of fatty acid breakdown of acetyl-CoA and reduced activity of the citric acid cycle.

23
Q

State the metabolic changes in fasting

A

Brain :

  • Can only use glucose and ketones for energy

Liver :

  • glycogen becomes glucose

Adipose :

  • Lipids become free fatty acids and glycerol that enter the blood.

Muscle :

  • Glycogen can be used for energy.
  • Muscle can use fatty acids
  • Muscle protein broken down to amino acids to enter blood
24
Q

Describe the function of the pancreas

A

Acts as both an endocrine and exocrine gland

25
Q

Describe the exocrine function of the pancreas

A

Digestive enzyme production

26
Q

Describe the endocrine function of the pancreas

A

Islets of Langerhans (endocrine cells) are embedded within exocrine tissue

27
Q

Describe Islets of Langerhans

A

Composed of 4 cell types, secreting hormones directly into the bloodstream.

  • Glucagon in alpha cells
  • Insulin in beta cells
  • Somatostatin in delta cells
  • Polypeptides in PP cells
28
Q

Exocrine cells

A

Acinar cells

29
Q

Endocrine cells

A

Islets of Langerhans
2% of pancreas mass
Found in clusters of cells

30
Q

Amylin

A

Hormone which is involved in regulating appetite and inhibiting glucagon activity.

31
Q

Insulin

A

Directs the events of the absorptive state - hypoglycaemic hormone

32
Q

When are beta cells stimulated to release insulin ?

A

Rising blood glucose levels

Glucose dependent insulinotropic peptide (GI tract hormone)

Parasympathetic nervous system

33
Q

When insulin binds to membrane receptors on target cells what is stimulated ?

A

Translocation of Glut transporters

Facilitated diffusion - 20 fold increase in glucose uptake

Glycogen synthesis (liver/muscle)
Glycolysis

Triglyceride and protein synthesis

34
Q

Glucagon

A

Controls blood glucose levels in the post-absorptive/fasting state - hyperglycaemic hormone.

35
Q

When are alpha cells stimulated to release glucagon ?

A

Secrete glucagon in response to low glucose

36
Q

Where does glucagon act ?

A

Acts mainly on liver (muscle doesn’t have glucagon receptors) :

stimulating :

  • glyconeolysis
  • gluconeogenesis
37
Q

What determines the state of metabolism ?

A

Circulating levels of insulin and glucose

38
Q

What hormone dominates in the :

a) fed state
b) fasted state

A

a) Insulin
b) Glucagon

39
Q

Where is adrenalin & noradrenaline synthesised ?

A

The adrenal medulla (modified sympathetic ganglion)

40
Q

Function of catecholamines (adrenaline / noradrenaline)

A

Targets mainly muscle for glucose

Lower glucose uptake by muscle - metabolise fatty acids instead (glucose sparing)

Increase glucagon secretion / inhibit insulin secretion

41
Q

Function of the sympathetic nervous system ?

A

Plays a crucial tole in increasing glucose

Adipose tissue also supplied with sympathetic fibres : growth hormone, thyroxine.

42
Q

What is diabetes mellitus ?

A

Chronic metabolic disease resulting form deficient secretion or action of insulin.

43
Q

How is diabetes mellitus characterised ?

A

BY elevated blood glucose / chronic hyperglycaemia.

44
Q

What causes Type 1 diabetes ?

A

10% of cases

An autoimmune condition in which Beta cells are destroyed - no insulin released.

Genetic predisposition ?
Environmental trigger

45
Q

What causes Type 2 diabetes ?

A

90% of cases

Mostly associated with lifestyle
Genetic component (also)

46
Q

Describe the results of Type 2 diabetes

A

Tissues become insensitive to the effects of insulin-resistance

47
Q

Treatment of Type 2 diabetes

A

Lifestyle changes - diet + exercise
Hypoglycaemic drugs (insulin)

48
Q

Health consequences of hyperglycaemia

A

Lack of sensitivity to insulin (increase in blood glucose)

Dehydration

Tissue Injury

Peripheral Neuropathy

Autonomic Nerve Dysfunction

49
Q

Describe tissue injury caused by hyperglycaemia

A

Prolonged hyperglycaemia damages blood vessels
Poor circulation
Increased risk for MI
Stroke
Kidney disease
Blindness

50
Q

Describe dehydration caused by hyperglycaemia

A

Osmotic pressures caused by glucose in renal tubules
Decreased water reabsorption
Polyuria
Intra/extra cellular dehydration
Increased thirst and hunger

51
Q

Describe how excess urination occurs

A

XS glucose cannot be reabsorbed via the proximal convoluted tubules.

Increased osmotic strength of urine - less water reabsorbed

Urine volume greatly increases and this explains sweet urine.

IN serve cases, acidic ketone bodies add to osmotic strength.

52
Q

State the metabolic consequences of hyperglycaemia

A

Due to lack of insulin/insulin resistance, metabolism is similar to prolonged fasting/starvation.

High glucose availability.

53
Q

Describe what happens when there is an increased utilisation of fats

A

Glycolysis slows

Gluconeogenesis stimulated (using amino acids)

New glucose and ketone bodies circulate in blood

Metabolic acidosis - increased ketone bodies

Medicine Year 1 - Semester 2 - Part 1 (51 decks)

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