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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is endocrinology?

A

Study of hormones, their gland of origin, their receptors, the intracellular signalling pathways and their associated diseases

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2
Q

Describe endocrine glands

A
  • ductless

- release hormones directly into blood

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3
Q

main purpose of endocrine system?

A

To release hormones directly into blood, allowing for rapid adaptive changes, integration of whole body physiology, chronic maintenance of metabolic environment and the communication for multi-cellular organisms.

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4
Q

Definition of endocrine:

A

These glands ‘pour’ secretions directly into the blood stream without ducts.
E.g. thyroid, adrenal and beta cells of pancreas

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5
Q

Definition of exocrine:

A

These glands ‘pour’ secretions through a duct to site of action.
E.g. submandibular, parotid, pancreas - amylase & lipase

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6
Q

Definition of hormone action:

A

Endocrine - blood-bourne, acting on distant sites
Paracrine - acting on nearby adjacent cells
Autocrine - feedback on same cell that secreted the hormone (acts on itself)

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7
Q

features of water-soluble hormones?

A
  • transported unbound
  • bind to surface receptor on cells
  • have a short half-life
  • are cleared fast
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8
Q

give examples of water soluble hormones

A

peptides and monoamines - both stored in vesicles before secretion

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9
Q

features of fat-soluble hormones?

A
  • transported bound to proteins
  • diffuse into cells
  • have a long half-life
  • are cleared slowly
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10
Q

Give examples of fat-soluble hormones

A

Thyroid hormone and steroids (synthesised on demand)

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11
Q

Describe the features of hormone class; peptides (e.g. insulin)

A
  • stored in secretory granules
  • hydrophilic and water soluble
  • released in pulses of bursts
  • cleared by tissue or circulating enzymes
  • Synthesis: preprohormone –> prohormone
  • Packaging: prohormone –> hormone
  • Storage - hormone
  • Secretion - hormone
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12
Q

Describe the process of insulin activation:

A
  • Binds to insulin receptors
  • resulting in phosphorylation of the receptor and the activation of secondary messenger (Tyrosine Kinase)
  • Phosphorylation of signal molecules
  • cascade of effect
  • glucose uptake
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13
Q

Give examples of Amine hormones

A

Dopamine, adrenaline, noradrenaline

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14
Q

What are the intermediates created when converting Phenylalanine into Adrenaline?

A

Phenylalanine –> L-Tyrosine –> L-Dopa –> Dopamine –> Noradrenaline –> Adrenaline

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15
Q

What breaks down noradrenaline?

A
  • Catechol-O-mehtyl transferase breaks down noradrenaline into normetanephrine

Noradrenaline – CMT –> Normetanephrine

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16
Q

What is adrenaline broken down by?

A

Adrenaline – CMT –> Metanephrine

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17
Q

What can normetanephrine and metanephrine used for?

A
  • Can be used as indicators of adrenaline and noradrenaline

- Measured in serum

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18
Q

What do amine hormones bind to?

A
  • Alpha receptors

- Beta receptors

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19
Q

What does amine binding to alpha receptors cause?

A
  • Vasoconstriction
  • Bowel muscle contraction
  • Sweating
  • Anxiety
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20
Q

What does amine binding to beta receptors cause?

A
  • Vasodilation
  • Increase in heart rate
  • Increases force of contractility
  • Relaxation of bronchial smooth muscles
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21
Q

Features of Iodothyronine hormones:

A
  • Have to be bound to protein (as are not water soluble on their own)
  • 99% is protein bound to thyroid - binding globulin (TBG)
    T3 - Triiodothyronine - more active
    T4 - Thyroxine - less active but more produced
  • incorporation of Iodine + Tyrosine molecule + Thyroglobulin form iodothyrosines
  • Conjugation of iodothyrosines gives rise to T3 and T4
  • Stored in colloid bound to thyroglobulin
  • TSH stimulates the movement of colloid into secretory cell, T4 and T3 cleaved from thyroglobulin
  • T4 = reservoir for additional T3
  • Majority of T3 comes from the breakdown of T4 (converted outside the thyroid gland)
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22
Q

What are the features of vitamin D and what hormone class does it belong to?

A
  • Cholesterol derivatives
  • fat soluble
  • enters cell directly to bind to nucleus and stimulate mRNA production
  • transported by vitamin D binding protein
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23
Q

What are the features of adrenocortical & gonadal steroids

A
  • 95% are protein bound
  • After entering cell they can pass to nucleus to induce response (oestrogen)
    or act like steroid hormones
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24
Q

What are the features of steroid hormones

A
  • diffuse through plasma membrane and bind to cytoplasm receptor
  • receptor-hormone complex then enters the nucleus
  • where it binds to glucocorticoid response element (GRE)
  • binding initiates transcription of gene to mRNA
  • mRNA directs protein synthesis
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25
Q

Where are hormone receptors located?

A

Cell membrane - peptides (i.e. insulin)
Cytoplasm - steroids, glucocorticoids (i.e. cortisol), mineralocorticoids (i.e. aldosterone), androgens (i.e. testosterone), progesterone
Nucleus - thyroid hormones, oestrogen, vitamin D

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26
Q

Where are receptors for fat soluble hormones?

steroid hormones

A

Receptors can either be in the cytoplasm or nucleus

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27
Q

What are the different types of hormone secretion patterns

example for each

A
  • Continuous release (prolactin- inhibited by dopamine)
  • Pulsatile; multiple pulses throughout the day (insulin)
  • Circadian rhythm (ACTH, prolactin, GH, TSH and cortisol)
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28
Q

How is hormone action controlled?

A
  • Hormone metabolism (increased metabolism = decreased function)
  • Hormone receptor induction
  • Hormone receptor down regulation (hormone secreted in large quantities causes down regulation of its target receptor)
  • Synergism; combined effect of 2 hormones amplified
  • Antagonism
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29
Q

Give an example of hormone receptor induction

A

Induction of LH receptors by FSH in follicle

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30
Q

Give an example of synergism in the context of control of hormone action

A

Glucagon with adrenaline - both released when hypoglycaemic to increase sugar levels

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31
Q

Give an example of antagonism in the context of control of hormone action

A

Glucagon (raises glucose levels) antagonises insulin (reduces glucose levels)

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32
Q

What is called the hypophysis?

A

The pituitary gland.

Refers to the glands position on the underside of the brain.

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33
Q

Describe the positioning of the pituitary gland

A

Sits in the pituitary fossa - inferior to the optic chiasm.
In a pocket of the sphenoid bone at the base of the brain, below the hypothalamus to which it is connected to by the infundibulum (contains axons and small blood vessels).
Two cavernous sinuses either side of it.

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34
Q

What else can pathology in the pituitary affect?

A
  • Vision problems, if pituitary places pressure on the chiasm
  • Cavernous sinus structures if it applies pressure to them
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35
Q

What makes up the pituitary?

A

2 glands;

  • Anterior pituitary gland; adenophysis
  • Posterior pituitary gland; neurohypophysis
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36
Q

What are hypophysiotropic hormones?

A
  • released by the hypothalamus to reach the anterior pituitary via the Hypathalamo-hypophyseal portal vessels/veins
  • Stimulate the anterior pituitary to release 6 hormones
  • Corticotropin releasing hormone (CRH); stimulates release of ACTH
  • Growth hormone-releasing hormone (GHRH)(; is inhibited by somatostatin)
  • Thyrotropin-releasing hormone (TRH); stimulates release of TSH
  • Gonadatropin-releasing hormone (GnRH); stimulates release of LH and FSH
  • Dopamine (DA); inhibits release of prolactin
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37
Q

Describe the relationship between dopamine and prolactin

A

Prolactin is under negative control by dopamine.
If pituitary was destroyed, would result in an increase in the secretion of prolactin as its negative pressure would not be able to reach it.

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38
Q

What is the blood supply to the anterior pituitary?

A
  • No arterial blood supply
  • Receives blood via portal venous circulation (hypothalamo-hypophyseal portal vessels/veins)
  • local blood system; mechanism for hormones of the hypothalamus to directly affect the anterior pituitary
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39
Q

What is the three hormone sequence that all hypophysiotropic hormones go through (bar Dopmaine)?

A
  1. A hypophysiotropic hormone controls the secretion…
  2. Of a anterior pituitary gland hormone which controls the secretion of…
  3. A hormone from some other endocrine gland. this last hormone is the one that acts on target cells.
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40
Q

Advantages of the 3 step sequence of hypophysiotropic hormones?

A
  • Permit a variety of hormonal feedback, most importantly, negative feedback
  • Allow for amplification of a response of a small number of hypothalamic neurones into a large peripheral hormone signal
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41
Q

What are the 6 peptide hormones of the anterior pituitary and where are they produced?
(FLATPIG)

A
  1. Follicle-stimulating hormone (FSH); gonadotrophs
  2. Lutenizing hormone (LH); gonadotrophs
  3. Adrenocotricotropic homone (ACTH); corticotrophs
  4. Thyroid-stimulating hormone (TSH); thyrotophs
  5. Prolactin; lactotrophs
  6. Growth hormone (- somtotropin, GH); somatotrophs
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42
Q

Describe actions of FSH and LH…

A
  • target the gonads
  • stimulate germ cell development (females = ovum, males = sperm)
    FSH: oestrogen release
    Positive feedback: release of oestrogen and stimulation of LH
    LH; release of the egg; stimulates progesterone release = thickening of the uterine wall
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43
Q

What is the effect of LH in men?

A

Effect leydig cells and result in testosterone release.

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44
Q

Describe the action of GH

A
  • stimulates growth and protein synthesis
  • effects on the whole body;
  • stimulates glucogenesis + inhibits insulin = increase in glucose
  • adipose tissue; breaks down fat
  • liver; increases protein synthesis stimulates IGF-1 (increases cartilage proliferation)
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45
Q

Describe the action of ACTH

A
  • stimulates adrenal cortex to secrete cortisol from zona fasiculata
  • stimulates androgen release from zona reticularis
  • stimulate adrenaline release from adrenal medulla
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46
Q

Describe the effect of TSH

A
  • stimulates the release of thyroid hormone:
  • controls rate of metabolic reactions
  • accelerate food metabolism
  • increases protein synthesis
  • stimulation of carbohydrate metabolism
  • enhance fat metabolism
  • increase ventilation rate
  • increases CO and HR
  • Brain development during foetal life and postnatal development
  • growth rate acceleration
    T3 half life = 1 day
    T4 half life = 5 to 7 days
    too little = everything is slow
    too much = everything is fast
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47
Q

Describe the effect of prolactin

A

Stimulates breasts to produce milk.
Helps with breast development.
Inhibited by dopamine.

48
Q

Effects of TRH on pituitary and further

A

TRH –> TSH –> increased release of T3 and T4 from thyroid –> increased metabolism

49
Q

Effects of GnRH on pituitary and further

A

GnRH –> FSH and LH –> target gonads –> increase oestorgen, progesterone and testosterone

50
Q

Effects of GHRH on pituitary and further

A

GHRH –> GH –> stimulates growth and protein synthesis

51
Q

Effects of somatostatin on pituitary and further

A

SST –> inhibits GH –> inhibits growth and protein synthesis

52
Q

Effects of corticotropin-releasing hormone on pituitary and further

A

CRH –> ACTH –> increased cortisol production (in adrenal cortex from zona fasiculata)

53
Q

Effects of dopamine on pituitary and further

A

DA –> inhibits prolactin –> inhibits growth and milk production

54
Q

Where is the negative feedback produced by the hypophysiotropic hormone exerted?

A

Both the hypothalamus and anterior pituitary

55
Q

What is the point of the negative feedback?

A

It is effective in dampening hormonal responses thereby limiting the extremes of hormone secretory rates.

56
Q

What hormones elicit long-loop feedback?

A
  • Plasma cortisol (CRH)
  • FSH
  • LH
  • TSH
57
Q

Why can the long-loop feedback mechanism not work for prolactin?

A

Prolactin is anterior pituitary hormone that does not have major control over another endocrine gland - so does not participate in a 3 step hormone sequence.

58
Q

Explain the process of prolactin (as it does not go through the expected 3 step process)…

A
  • Still goes through negative feedback
  • Prolactin acts on hypothalamus to stimulate the secretion of dopamine which inhibits the secretion of prolactin
  • Process known as short-loop feedback
59
Q

What hormones adopt the short-loop feedback mechanism?

A
  • Prolactin

- Growth hormone

60
Q

What is the difference between the anterior and posterior pituitary glands?

A

Hormone production occurs in ONLY the hypothalamus.

The posterior pituitary is just simply used to store hormones.

61
Q

What is the posterior pituitary?

A

An extension of the hypothalamus, which stores and releases 2 peptide hormones produced by the hypothalamus.
Originates from neuronal tissue with large numbers of glial cells present.

62
Q

What 2 peptide hormones are produced by the hypothalamus then stored and released by the posterior pituitary?

A
  • Vasopressin/ADH - in the cell body of the supraoptic nucleus
  • Oxytocin - in the cell body of the paraventricular nucleus
63
Q

Explain the structure of the posterior pituitary and how the hormones pass into it:

A

Axons of both the supraoptic and paraventricular nuclei pass down the infundibulum/pituitary stalk ad terminate in the posterior pituitary.
The hormones move down the axons enclosed in vesicles and accumulate at the axon terminal in the posterior pituitary.

64
Q

What are the effects of Vasopressin/ADH?

A
  • Decrease water secretion in the urine, so retaining fluid in body and helping in maintaining blood volume
  • Acts on smooth muscle cells surrounding vessels to constrict –> vasoconstriction, to increase blood pressure (will occur in response to a decrease in blood pressure - i.e. from loss of blood due to injury)
  • Stimulates ACTH release from the anterior pituitary to increase aldosterone release (further fluid retention)
65
Q

What is vasopressin released in response to?

A
  • Decreased blood volume
  • Trauma
  • Stress
  • Increase blood CO2
  • Decreased blood O2
  • Increased osmotic pressure of blood
66
Q

What are the 2 main functions of oxytocin?

A
  • Important for ejection of milk during breast feeding; stimulation of mammary glands stimulates release of oxytocin and release of milk
  • Pregnancy; stimulates contraction of uterine smooth muscle until birth, promotes the onset of labour (contractions!)
67
Q

What do all pituitary and hypothalamic hormones act on?

A

All act on G-protein coupled receptors.

68
Q

List the diseases of the pituitary:

A
  • Benign pituitary adenoma (pituitary produces less and presses on things)
  • Craniopharyngioma
  • Trauma
  • Sheehans (pituitary infarction after labour)
  • Sacroid/TB
69
Q

What are the 3 vital presentation points of pituitary tumour?

A
  • tumours cause
  • pressure on normal pituitary - hypopituitarism
  • functioning tumour - hyperpituitarism
70
Q

What to consider for the cause of a pituitary tumour?

A
  • Pressure on local structures;
  • Optic chiasm - resulting in bitemporal hemianopia
  • can cause hydrocephalus
  • can get CSF leak
71
Q

What to consider with hypopituitarism (pressure on normal pituitary) with a tumour?

A 
- Can be fatal (cortisol deficiency) 
Males:
- pale, no body hair, central obesity 
- effeminate skin 
Females: 
- loose body hair 
- sallow complexion
72
Q

What to consider with hyperpituitarism (functioning tumour)?

A

Prolactinoma - increased prolactin:
- common in young women
- results in increased milk production in breast and reduced fertility
- Amenorrhea (menstruation stops)
Treated using dopamine agonist, to inhibit prolactin release (i.e. Cabergoline)

Acromegaly - increased GH:

  • thick, greasy, sweaty skin
  • Enlarged organs

Cushing’s - increased CTH:

  • Too much cortisol
  • central obesity
  • bruising, thin skin, osteoporosis, ulcers, purply stretch marks
73
Q

What is the definition of Diabetes Mellitus?

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both.
Hyperglycaemia can result in serious microvascular or macrovascular problems.

74
Q

Give examples of microvascular problems

A
  • retinopathy
  • nephropathy
  • neuropathy
75
Q

Give examples of macrovascular problems

A
  • strokes
  • renovascular disease
  • limb ischaemia
  • heart disease
76
Q

What should be the level of blood glucose levels under all conditions?

A

3.5 - 8.0 mmol/L

77
Q

What is the role of the liver in glucose homeostasis?

A
  • Stores and absorbs glucose as glycogen (in post-absorptive state)
  • performs gluconeogenesis from fat, protein and glycogen
  • High blood glucose levels, liver will make glycogen via glycogenolysis
  • in longer term the liver will make glucose from amino acids and lactate via gluconeogenesis
78
Q

How much glucose is utilised each day?

A

About 200g

79
Q

Where is the glucose that is utilised each day derived from?

A

90% derived from liver glycogen and hepatic gluconeogenesis.
Remainder form renal gluconeogenesis.

80
Q

Where is glucose utilised in the body?

A
  • The brain = major consumer, relays on it to function
  • Tissues such as muscle and fat have insulin-responsive glucose transporters, absorb glucose in response to postprandial peaks in glucose and insulin
  • Glucose taken up by muscle if stored asa glycogen, or metabolised into lactate or CO2 and H2O
  • Lipolysis of triglyceride releases fatty acids + glycerol; glycerol is then used as a substrate for hepatic gluconeogenesis
81
Q

Why does the brain relay on glucose so heavily?

A
  • Glucose uptake in brain is not dependent on insulin, glucose is oxidised to CO2 and H2O
  • The brain cannot use free fatty acids to be converted to ketones to then be converted into acetyl-coA to be used in the Kreb’s cycle for energy production
  • This is because free fatty acids cannot pass through the blood brain barrier
82
Q

What are the key hormonal regulators of carbohydrate metabolism?

A
  • Insulin

- Glucagon

83
Q

Describe the actions of insulin:

A
  • suppresses hepatic glucose output (decreases glycogenolysis and gluconeogenesis)
  • Increases glucose uptake into insulin sensitive tissues: muscle - glycogen and protein synthesis, fat - fatty acid synthesis
  • suppresses lipolysis and breakdown of muscles (decreased ketogenesis)
84
Q

Explain the process of biphasic insulin release

A

B-cells can sense the rising glucose levels and aim to metabolise it by releasing insulin.
First phase = rapid release of stored insulin
If glucose levels remain high then the second phase is initiated; takes longer than the first phase as more insulin needs to be synthesised.

85
Q

Describe the effects of glucagon:

A
  • increases hepatic glucose output - increases glycogenolysis and gluconeogenesis
  • reduces peripheral glucose uptake
  • stimulates peripheral resistance of gluconeogenic precursors (glycerol and amino acids)
  • stimulates lipolysis and muscle glycogenolysis and breakdown (increased ketogenesis)
86
Q

What other counter-regulatory hormones are involved in control of blood glucose levels?

A
  • Adrenaline
  • Cortisol
  • Growth hormone
    These all increase glucose production in the liver and reduce its utilisation in fat and muscle.
87
Q

Where is insulin coded for and produced?

A

Coded for: on chromosome 11

Produced: in the Beta cells of the Islets of Langerhans of the Pancreas

88
Q

What is the precursor of insulin?

A

Proinsulin

89
Q

Explain the process of insulin production?

A

Proinsulin contains the Alpha and Beta chains of insulin which are joined together by a C peptide.
Proinsulin is cleaved from its C peptide and is then used to make insulin which is then packaged into insulin secretory granules.
With insulin release comes high level os C peptide in the blood (can be used to determine whether the release is natural) or synthetic (no C peptide will be present).

90
Q

What happens to insulin after secretion?

A
  • Insulin enters the portal circulation and is carried to the liver, its prime target organ
  • Around 50% of secreted insulin is extracted and degraded in the liver
91
Q

What is the main action of the liver in the fasting state and post-prandial state?

A

Fasting state: regulate glucose release

Post-prandial state: promote glucose uptake by fat and muscle

92
Q

How to tell the difference between natural and synthetic insulin release?

A

Synthetic insulin does not have C peptide.

Presence of C peptide indicates natural release.

93
Q

What is the purpose of GLUT proteins?

A

Specialised glucose-transporter proteins.

They carry glucose through membranes and into cells, as cell membranes are not inherently permeable to glucose.

94
Q

What is the specific action of GLUT-1?

A

Enables basal non-insulin-stimulated glucose uptake into many cells.

95
Q

What is the specific action of GLUT-2?

A
  • found in beta cells of pancreas, renal tubules and hepatocytes
  • transport glucose into the beta cell - allows them to sense glucose levels
  • it is a low affinity transporter - will only allow glucose in when there is a high concentration of glucose
  • GLUT-2 beta cells are able to detect high glucose levels and release insulin in response
96
Q

What is the specific action of GLUT-3?

A

Enables non-insulin-mediated glucose uptake into brain, neurones and placenta.

97
Q

What is the specific action of GLUT-4?

A
  • A glycoprotein, coded for on short arm of chromosome 19
  • Straddles the cell membranes of many cells
  • When insulin binds to the receptor, tyrosine kinase is activated and the cascade response is initiated
  • This causes the migration of the GLUT-4 transporter to the cell surface and increased transport of glucose into the cells
98
Q

What stimulates the release of glucagon?

A

Low blood glucose (hypoglycaemia)

99
Q

What effects does glucagon have on the liver?

A
  • Convert glycogen into glucose

- Form glucose from lactic acid and amino acids

100
Q

What happens in hyperglycaemia?

A

The release of glucagon is inhibited.

The release of insulin is stimulated.

101
Q

What is the affect of insulin on various cells?

A
  • Accelerate diffusion of glucose into cells
  • Speed up the conversion of glucose into glycogen
  • Increase the uptake of amino acids and increase protein synthesis
  • Speed up the synthesis of fatty acids
  • Slow glycogenolysis
  • Slow gluconeogensis
102
Q

What happens in hypoglycaemia?

A

Release of insulin is inhibited.

Release of glucagon is stimulated.

103
Q

What other conditions may be the cause of secondary diabetes?

A
  • Pancreatic pathology (chronic pancreatitis, haemochromatosis, total pancreatectomy)
  • Endocrine disease (acromegaly, Cushing’s disease)
  • Drug induced (commonly by thiazide diuretics and corticosteroids
  • Maturity onset diabetes of youth (MODY); autosomal dominant form of type 2 diabetes, a single gene defect altering beta cell function
104
Q

Describe the epidemic of type 1 diabetes:

A
  • The type 1 diabetic is young, has insulin deficiency with no resistance and immunogenic markers
  • Most prevalent in Northern European countries, i.e. Finland,
  • Incidence is increasing in most populations - particularly in young children
  • Typically manifests in childhood, peak incidence is around the time of puberty (but can present at any age)
  • Usually young, <30
  • Patient is usually lean
105
Q

What is the definition of Type 1 Diabetes Mellitus?

A

Disease of insulin deficiency usually caused by autoimmune destruction of beta-cells of the pancreas.

106
Q

What is the latent autoimmune disease in adults (LADA)?

A
  • A ‘slow burning’ variant with slower progression to insulin deficiency that occurs in later life.
  • May be difficult to differentiate from type 2 diabetes.
    Clinical clues:
  • leaner build
  • rapid progression to insulin therapy following an initial response to other therapies
  • The presence of circulating islet antibodies
107
Q

What is the aetiology of T1DM?

A
  • Autoimmune; auto-antibodies forming against insulin and islet beta cells - insulitis
  • Idiopathic
  • Genetic susceptibility; HLA-DR3-DQ2 or HLA-DR4-DQ8
108
Q

What are the risk factors of T1DM?

A
  • Northern European (especially Finnish)
  • Family history; HLA-DR3-DQ2 0r HLA-DR4-DQ8 in >90%
  • associated with other autoimmune disease: autoimmune thyroid, coeliac disease, Addison’s disease (excess cortisol), Pernicious anaemia
109
Q

What are the environmental factors of T1DM?

A
  • Dietary constituents
  • Enteroviruses such as Coxsackle B4
  • Vitamin D deficiency
  • Cleaner environment may increase type 1 susceptibility
110
Q

What is the pathophysiology of T1DM?

A
  • Due to autoimmune destruction by autoantibodies of the pancreatic insulin-secreting beta cells in the islets of Langerhans
  • insulin deficiency, so continued breakdown of liver glycogen, leading to glycosuria and ketonuria (more glucose in blood)
  • Impaired glucose clearance in skeletal muscle and fats
  • Increased blood glucose, at 10 mmol/L, body can no longer absorb any, resulting in thirst and polyuria
  • Insulin MUST be administered as patient is at risk of diabetic ketoacidosis (caused by reduced supply of glucose and increase in fatty acid oxidation)
  • increased production of acetyl-coA –> ketone body production that exceeds peripheral tissue ability to oxidise them –> pH of blood lowered
  • Acidification of blood leads to impaired ability of haemoglobin to bind to oxygen
    (diabetic ketoacidosis, patients breath will smell of pear drops due to excess ketones)
  • excess fat breakdown can lead to; patient becoming acidotic, anorexic, dehydrated leading to AKI and hyperglycaemia and eventual death
111
Q

What happens to serum C-peptide in T1DM?

A

Eventual complete Beta cell destruction results in the absence of serum C-peptide
Often T1DM presents very late with only 10% of beta cells remaining.

112
Q

What is the definition of Type 2 Diabetes Mellitus?

A

Disease resulting from a combination of insulin resistance and less severe insulin deficiency.

113
Q

Describe the epidemiology of T2DM:

A
  • Common in all populations enjoying an affluent lifestyle
  • Is increasing in frequency, particularly in adolescents
  • Increased in incidence due to ageing population and increasing obesity in the western world
  • Older, usually >30 y.o.
  • Often overweight around the abdomen
  • More prevalent in South Asian, African and Caribbean ancestry
  • Middle easter and Hispanic Americans are also more at risk
114
Q

Describe the aetiology of T2DM

A
  • Decreased insulin secretion +/- increased insulin resistance
  • Associated with obesity, lack of exercise, calorie and alcohol excess
  • No immune disturbance
  • No HLA disturbance but there is a stronger genetic link
  • Polygenic disorder
  • More common in males
115
Q

What are the risk factors for T2DM?

A
  • family history (genetics)
  • increasing age
  • obesity and poor exercise
  • ethnicity; middle eastern, south-east asian, western pacific
  • environment; low weight at birth, poor-nutrition early in life impairs beta-cell development and function (predisposing to diabetes)

Phase 2a (8 decks)

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