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MBChB - year 2 > Week 2 Endocrine Lectures > Flashcards

Week 2 Endocrine Lectures Flashcards

1
Q

What are the dietary lipids?

A
  • Triglycerides
  • Cholesterol - capable of making it yourself not required in the diet
  • Phospholipids
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2
Q

Where does lipid digestion take place?

A

In the small intestine

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3
Q

What are the main enzymes involved in lipid digestion?

A

Pancreatic lipase and colipase

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4
Q

What do pancreatic lipase and colipase do?

A

Bread down TAG into 2 fatty acids and MAG

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5
Q

What are bile salts synthesized from?

A

Cholesterol

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6
Q

Where are bile salts secreted from?

A

The liver through the bile duct

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7
Q

What do bile salts do?

A

Emulsify fats to micelles

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8
Q

What happens to TAG in intestinal cells?

A

Packaged with cholesterol, lipoproteins and other lipids to form chylomicrons

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9
Q

What happens once TAG has been packaged into chylomicrons?

A

Released into the lymphatic system by exocytosis

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10
Q

what are used to transport fatty acids in the blood?

A

Lipoproteins

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11
Q

What is beta-oxidation of fatty acids?

A

Generation of energy from fatty acids

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12
Q

What is required for fatty acids to cross the inner mitochondrial membrane?

A

Requires a carrier molecule - carnitine - derived from lysine and methionine

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13
Q

What are the steps of beta oxidation?

A
  1. Fatty acids + acetyl CoA = Fatty acyl-CoA
  2. fatty acyl CoA are degraded by oxidation at the β carbon
    - produces 1 FADH2 NADH and acetyl CoA (2 carbons) per turn
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14
Q

How is ATP produced from beta oxidation?

A

Acetyl CoA can be further oxidised to yield ATP (TCA cycle/oxidative phosphorylation)

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15
Q

How are triglycerides formed?

A

Esterification of 3 fatty acids and glycerol

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16
Q

What is responsible for the breakdown of triglycerides?

A

Hormone sensitive lipase in adipose tissue

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17
Q

What activates hormone sensitive lipase?

A

cAMP

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18
Q

How are fatty acids synthesised?

A

2 carbons at a time

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19
Q

What are the key regulatory enzymes in fatty acid synthesis?

A
  • Acetyl CoA carboxylase

- Fatty acid synthase

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20
Q

What does Acetyl CoA carboxylase do?

A

Forms malonyl CoA

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21
Q

What is biotin?

A

A B vitamin involved in the formation of malonyl CoA in fatty acid synthesis

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22
Q

What inhibits FA oxidation?

A

Malonyl CoA

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23
Q

Why are ketone bodies formed?

A

It is an “overflow” pathway for acetyl CoA

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24
Q

What are essential fatty acids?

A

Fatty acids that cannot be synthesised and are obtained from the diet

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25
Q

What are the functions of essential fatty acids?

A
  • Cell membrane formation
  • required for proper growth and development
  • required for brain and nerve function
  • precursors for eicosanoids - prostanoids & leukotrienes - inflammatory response
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26
Q

What are the key hormonal regulators of lipid metabolism?

A

Insulin and (nor) adrenaline

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27
Q

What does insulin do in regards to lipid metabolism?

A
  • Stimulates FA synthesis and TAG synthesis

- Suppresses lipolysis

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28
Q

What does (nor)adrenaline do in regards to lipid metabolism?

A

Stimulates lipolysis

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29
Q

What does noradrenaline stimulate?

A
  • cAMP synthesis
  • cAMP-dependent protein kinase (PKA) activation
  • PKA-mediated phosphorylation and activation of HSL
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30
Q

What is diabetic ketoacidosis?

A

Metabolic acidosis (pH<7.3) with bicarbonate <15mmol/l

  • Hyperglycaemia
  • ketosis

Characterised by uncontrolled catabolism

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31
Q

What is the normal response to hyperglycaemia?

A

Increase in insulin

Decrease in glucagon

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32
Q

What happens in the kidney in diabetic ketoacidosis?

A
  • Osmotic diuresis
    • Glucose (and ketones) freely filtered at glomerulus
    • Maximal reabsorption threshold of glucose exceeded
    • Increased solute concentration in tubular lumen causes osmotic gradient
    • Increased water loss in urine
  • Potassium
    • Hyperaldosteronism exacerbates renal K+ loss
    • Lack of insulin prevents K+ from moving into cells
    • Plasma K+ levels may be elevated but total body K+ depleted
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33
Q

Why is there metabolic acidosis in diabetic ketoacidosis?

A

Increased production of acidic ketone bodies reduces the plasma pH

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34
Q

What is the treatment for diabetic ketoacidosis?

A

IV fluid, IV insulin, IV potassium

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35
Q

Why is insulin essential in diabetic ketoacidosis?

A

Essential for switching off ketogenesis and uncontrolled catabolism

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36
Q

What happens to the ECG in hypokalaemia?

A
  • Depressed ST segment
  • Biphasic T wave
  • Prominent U wave
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37
Q

What happens to the ECG in hyperkalaemia?

A
  • Long PR interval
  • Prolonged QRS
  • Tall T wave
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38
Q

What is HHS?

A

A complication of diabetes when a person is in a hyperglycaemic state which results in high osmolarity with no significant ketoacidosis

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39
Q

what is the differences in the length of the presenting complaints in DKA and HHS?

A

DKA comes on quickly HHS takes longer

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40
Q

Is HHS more common in type 1 or type 2 diabetes?

A

Type 2

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41
Q

Is DKA more common in type 1 or type 2 diabetes?

42
Q

What are the signs of DKA?

A
  • Hyperglycaemia
  • Dehydration
  • Acidosis
  • Patient usually alert
43
Q

What are the signs of HHS?

A
  • Profound hyperglycaemia
  • Significant dehydration and hypernatremia
  • no acidosis
  • Patient often drowsy
44
Q

What is the normal response to hypoglycaemia?

A

Decreased insulin

Increased Glucagon

45
Q

What are the counter regulatory hormones for hypoglycaemia?

A

increases in:

  • Glucagon
  • Adrenaline
  • Noradrenaline
  • Ach
  • cortisol
  • Growth hormone
46
Q

What are the early symptoms of hypoglycaemia?

A
  • Sweating
  • Tremor
  • Palpitations
  • Hunger
  • Anxiety
47
Q

What are the later symptoms of hypoglycaemia?

A

These are neurological as the brain doesn’t have sufficient energy

  • Confusion
  • Impaired conscious level
48
Q

What is hypoglycaemia unawareness?

A

Associated with frequent episodes of hypoglycaemia the mechanism is not clear.
Can result in significant mortality rates and driving restrictions

49
Q

How is mild hypoglycaemia treated?

A

15-20g of fast acting carbohydrate

50
Q

How is severe hypoglycaemia treated?

A
  • 15-20g of fast acting carbohydrate

- If there is reduced conscious level then IM glucagon and/or IV dextrose

51
Q

What are the acute complications of diabetes?

A
  • Ketoacidosis

- Hypoglycaemia

52
Q

What are the two categories of chronic diabetes complication?

A

Microvascular and macrovascular

53
Q

What are the microvascular complications of diabetes?

A

Retinopathy
Neuropathy
Nephropathy

54
Q

What are the macrovascular complications of diabetes?

A

Ischaemic heart disease
Peripheral vascular disease
Cerebrovascular disease

55
Q

What is the basal bolus regime for treating diabetes?

A

Take long acting insulin in the morning then a bit of insulin with every meal

56
Q

What causes microvascular disease?

A
  • capillary damage

- Metabolic damage

57
Q

How does capillary damage happen in microvascular disease? (in diabetes)

A
  • Hyperglycaemia
  • Increased blood flow
  • Increased capillary pressure
  • Thickened and damaged vessel walls
  • Endothelial damage - leakage of albumin and other proteins
58
Q

How does metabolic damage happen in microvascular disease? (in diabetes)

A
  • Most tissues need insulin to take up glucose
    • Retina/ kidney/ nerves don’t
  • Glucose metabolised to sorbitol by aldose reductase
59
Q

What happens when glucose concentration rises?

A
  • Excessive glucose enters polyol pathway
  • sorbitol accumulates
  • Less NADPH is available
  • Build up of ROS and oxidative stress

Cell damage

60
Q

Why is microvascular disease less of an issue in T2DM?

A

Patients usually die of CV complications/disease first

61
Q

What is the leading cause of impaired vision in 20-74?

A

Diabetic retinopathy

62
Q

When will nearly all diabetic patients acquire some degree of retinopathy?

A

> 20years of diabetes

63
Q

What happens in the early stages (non-proliferative) of retinopathy?

A 
- Hyperglycaemia 
      •	Damage to small vessel wall 
      •	Microaneurysms
- When vessel wall is breached
      •	Dot haemorrhages
- Protein and fluid left behind 
      •	Hard exudates 
- Micro-infarcts
      •	Cotton wool spots
64
Q

What happens in the later stages of retinopathy?

A 
- Damage to veins:
      •	Venous budding 
      •	Blockage of blood supply
- Ischaemia  VEGF and other growth factors 
      •	Neovascularisation 
      •	Proliferative retinopathy 
      •	Vitreous haemorrhage
- Fluid not cleared from macular area
      •	Macular oedema
65
Q

What happens in proliferative retinopathy?

A

New vessels form to try and bypass the haemorrhages

66
Q

How can retinopathy be prevented?

A
  • Good glycaemic control
  • stop smoking
  • Good blood pressure control
67
Q

How can retinopathy be treated?

A
  • Address risk factors
  • Ophthalmic review
    o laser
    o VEGF inhibitors (bevacizumab)
    o Vitrectomy
68
Q

What are the stages of nephropathy?

A
  • renal enlargement and hyperfiltration
  • Microalbuminuria
  • Macroalbuminuria
  • End stage renal failure
69
Q

What is Microalbuminuria?

A

Tiny traces of albumin that are too small to be detected on dipstick

70
Q

What are the first steps in Nephropathy?

A
  • Renal hypertrophy
  • Increase in GFR
  • Afferent arteriole vasodilates
71
Q

What is the result of the afferent arteriole of the kidney vasodilating in nephropathy?

A
  • glomerular pressure
  • thickened GBM
  • capillary damage
  • shear stress on endothelial cells
  • End result – leakage of protein into urine
72
Q

What are the later stages of nephropathy?

A
  • Progressive glomerulosclerosis
  • Glomeruli destroyed
  • Progressive proteinuria
  • Renal failure
73
Q

What can be done for nephropathy?

A
  • Screen for microalbuminuria - every year from diagnosis
  • ACE inhibitors / Angiotensin receptor blockers
  • Improve glycaemic control
74
Q

What do SGLT2 inhibitors do?

A

Inhibit the reabsorption of glucose in the PCT meaning the glucose can be peed out

75
Q

What is diabetic neuropathy?

A

Reduced blood supply to the neural tissue results in impairments in nerve signalling that affect both sensory and motor function

76
Q

How does glucose lead to inability to transmit signals through nerves?

A
  • Metabolic changes - sorbitol accumulation
  • Vascular changes - capillary damage
  • Structural changes
77
Q

What are the symptoms of diabetic neuropathy?

A
  • Numbness or loss of feeling (asleep or bunched up sock under toes)
  • Prickling or tingling
  • Burning pain
  • Lancinating pain
  • Unusual sensitivity or tenderness when feet are touched
78
Q

What are the signs of diabetic neuropathy?

A
  • Diminished vibratory perception
  • Decreased knee and ankle reflexes
  • Reduced protective sensation such as pressure, hot and cold, pain
  • Diminished ability to sense position of toes and feet
79
Q

What is the diabetic foot?

A

A combinations of neuropathy and peripheral vascular disease

80
Q

What are the NICE classifications for diabetic foot?

A
  • low risk - Normal sensation and pulses - annual review
  • Medium risk - Neuropathy or absent pulses - review by podiatrist every 3-6/12 months
  • High risk - Deformities or ulceration - review by podiatrist every 1-3 months
81
Q

What is Charcot foot?

A
  • Numb foot - Repetitive microtrauma - stress fractures

- Dysregulated blood flow - Increased bone turnover - fragile bone

82
Q

What are the effects of autonomic neuropathy?

A
  • CV - Postural hypotension
  • GU - Erectile dysfunction
  • GI - Gustatory sweating and gastroparesis
83
Q

What is diabetic amyotrophy?

A

Painful proximal neuropathy usually in the thigh/ buttock

84
Q

What reduces the risk of all complications diabetes?

A

Good glycaemic control

85
Q

What is the definition of diabetes mellitus?

A

a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, protein and fat metabolism, resulting from defects in insulin secretion, insulin action, or both.

86
Q

What percentage of women with gestational diabetes will develop T2DM?

87
Q

What are the greatest triggers for T2DM?

A

Weight gain and genetic predisposition?

88
Q

What is the significance of insulin resistance in T2DM?

A
  • May be the best predictor of T2DM
  • Gets worse as patients get older and heavier
  • Can be present for years before the onset of T2DM
  • Hyperinsulinemia can be found often in prediabetes and early stages
89
Q

What does leptin do?

T2DM

A

Tells the hypothalamus about the amount of stored fat

90
Q

What does adiponectin do?

T2DM

A

reduces levels of free fatty acids

91
Q

What does TNFa(alpha) do?

A

Insulin receptor signalling interference

92
Q

What does resistin do?

A

Enhances hypothalamic stimulation of glucose production

93
Q

What happens when there is mutations to the insulin receptor gene?

A

Severe hyperinsulinemia, associated with acanthosis nigricans and hyperandrogenism

94
Q

What is acanthosis nigricans?

A

a skin condition characterized by areas of dark, velvety discoloration in body folds and creases. The affected skin can become thickened.

95
Q

What drug affects glucose absorption?

96
Q

What drugs decrease glucose uptake?

A

Metformin
Pioglitazone
Conc. Insulin
Insulin/GLP 1 combinations

97
Q

What drug decreases glucose reabsorption?

A

SGLT2 inhibitors

98
Q

What drugs are used to treat impaired insulin secretion?

A 
Insulin
Sulphonylureas
Meglitinides
GLP-1 receptor agonists
DPP-4 inhibitors
99
Q

What drugs are used to treat increased glucose production?

A

Metformin
GLP-1 receptor agonists
DPP-4 inhibitors
Insulin

100
Q

What are the effects of GLP-1 on the body?

A
  1. Beta cells -Enhances glucose dependent secretion in the pancreas
  2. Alpha cells - supresses postprandial glucagon secretion
  3. Liver- Reduces hepatic glucose output
  4. Stomach - Slows the rate of gastric emptying
  5. Brain - Promotes satiety and reduces appetite
101
Q

In normal renal glucose handling, how much glucose is reabsorbed by SGLT2?

MBChB - year 2 (25 decks)

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