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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define endocrinology

A

The study of hormones (and their gland of origin), their receptors, IC signalling pathways & associated diseases

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2
Q

Function of endocrine glands

A

Release hormones DIRECTLY into BLOOD

ductLESS

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3
Q

Why are endocrine glands useful?

A
  • allows rapid adaptive changes
  • integration of whole body physiology
  • maintenance of metabolic environment
  • communication for multi-cellular organisms
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4
Q

Examples of endocrine glands

A
  • thyroid
  • adrenal
  • beta cells of pancreas
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5
Q

Function of exocrine glands

A

Pour secretions through a duct to the site of action

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6
Q

Examples of exocrine glands

A
  • submandibular
  • parotid
  • pancreas
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7
Q

Endocrine hormone action

A
  • blood borne

- acting on distant sites

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8
Q

Paracrine hormone action

A

Acting on nearby adjacent cells

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9
Q

Autocrine hormone action

A

Feedback on same cell that secreted hormone - acts on itself

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10
Q

Characteristics of water-soluble hormones

A
  • transported unbound
  • bind to surface receptor
  • short half life
  • fast clearance
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11
Q

Examples of water-soluble hormones

A
  • peptides
  • monoamines
    (both stored in vesicles before secretion)
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12
Q

Characteristics of fat-soluble hormones

A
  • transported bound to protein
  • diffuse into cells
  • long half life
  • slow clearance
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13
Q

Examples of fat-soluble hormones

A
  • thyroid hormones
  • steroids
    (synthesised on demand)
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14
Q

Example of peptide hormone

A

Insulin (MAIN EXAMPLE)

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15
Q

Properties of insulin

A
  • hydrophilic
  • water soluble
  • stored in secretory granules
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16
Q

How is insulin released?

A

In pulses or bursts

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17
Q

How is insulin cleared?

A

By tissue or circulating enzymes

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18
Q

How is insulin activated?

A

1) Binds to insulin receptors
2) Phosphorylation of receptor
3) Secondary messenger activated - tyrosine kinase
4) Phosphorylation of signal molecules
5) Cascade effect
6) Glucose uptake

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19
Q

Examples of amines

A
  • dopamine
  • adrenaline
  • noradrenaline
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20
Q

Sequence of amines

A

Phenylalanine > L-tyrosine > L-dopa > Dopamine > Noradrenaline > Adrenaline

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21
Q

What is noradrenaline broken down by?

A

Catechol-O-methyl transferase (COMT)

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22
Q

What is noradrenaline broken down into?

A

Normetanephrin

norepinephrine go into normetanephrines

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23
Q

What is adrenaline broken down by?

A

COMT

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24
Q

What is adrenaline broken down into?

A

Metanephrin

epinephrine go into metanephrines

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25
Q

How can normetanephrin and metanephrin be measured?

A

In serum

- indicators of adrenaline and noradrenaline activity

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26
Q

What can amines bind to?

A

1) Alpha receptors

2) Beta receptors

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27
Q

What happens if amines bind to alpha receptors?

A
  • vasoconstriction
  • bowel muscle contraction
  • sweating
  • anxiety
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28
Q

What happens if amines bind to beta receptors?

A
  • vasodilation
  • increase in HR
  • increase in force of contractility
  • relaxation of bronchial smooth muscles
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29
Q

What are the iodothyronine hormones?

A

1) T3 - triiodothyronine

2) T4 - thyroxine

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30
Q

Which is more active: T3 or T4?

A

T3

but more T4 produced

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31
Q

Are iodothyronines protein bound?

A

Yes

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32
Q

What protein do iodothyronines bind to?

A

Thyroid-Binding Globulin (TBG)

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33
Q

What gives rise to T3 and T4?

A

Conjugation of iodothyrosines

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34
Q

How are T3 and T4 stored?

A

In colloid bound to thyroglobulin

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35
Q

How are iodothyrosines formed?

A

Incorporation of iodine on tyrosine molecule on thyroglobulin

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36
Q

Examples of cholesterol derivatives and steroid hormones

A

1) Vitamin D

2) Adrenocortical & gonadal steroids

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37
Q

Properties/ Functions of vitamin D

A
  • fat soluble
  • enters cell directly
  • binds to nucleus
  • stimulates mRNA production
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38
Q

How is vitamin D transported?

A

By vitamin D binding protein

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39
Q

Examples of Adrenocortical & Gonadal steroids

A

1) Cortisol
2) Aldosterone
3) Testosterone
4) Oestrogen
5) Progesterone

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40
Q

What % of adrenocortical and gonadal steroids are protein bound?

A

95%

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41
Q

How does a steroid hormone work?

cortisol/ aldosterone/ progesterone/ testosterone

A
  • diffuses through plasma membrane
  • binds to cytoplasm receptor
  • receptor-hormone complex enters nucleus
  • binds to glucocorticoid response element (GRE)
  • this initiates transcription of gene to mRNA
  • mRNA directs protein synthesis
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42
Q

What are the hormone receptor locations?

A

1) Cell membrane (peptides)
2) Cytoplasm (glucocorticoids, mineralocorticoids, androgens, progesterone)
3) Nucleus (thyroid hormones, oestrogen, vitamin D)

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43
Q

What are the different hormone secretion patterns?

A

1) Continuous release
2) Pulsatile
3) Circadian rhythms

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44
Q

Example of continuous release hormone

A

Prolactin

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45
Q

Example of pulsatile release hormone

A

Insulin

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46
Q

Examples of circadian rhythm release hormone

A

ACTH, prolactin, GH, TSH, cortisol

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47
Q

What are the different ways hormone action is controlled?

A

1) Hormone metabolism
2) Hormone receptor induction
3) Hormone receptor down regulation
4) Synergism
5) Antagonism

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48
Q

How does hormone metabolism work?

A

Increased metabolism = reduced function

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49
Q

Example of hormone receptor induction

A

Induction of LH receptors by FSH in follicle

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50
Q

How does hormone receptor down regulation work?

A

Hormone secreted in large quantities = down regulation of target receptor

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51
Q

How does synergism work?

A

Combined effects of 2 hormones amplified

e.g glucagon & adrenaline released together when hypoglycaemic - increase sugar levels

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52
Q

How does antagonism work?

A

One hormone opposes other hormone

e.g glucagon & insulin

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53
Q

What kind of hormones does the hypothalamus release?

A

Hypophysiotropic hormones

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54
Q

How do hypophysiotropic hormones reach the anterior pituitary?

A

Via the hypothalamo-hypophyseal portal vessel/vein

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55
Q

How many hormones in total does the anterior pituitary secrete?

A

6

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56
Q

What are the 5 hypophysiotropic hormones?

A

1) Corticotropin releasing hormone (CRH)
2) Growth hormone releasing hormone (GRHR)
3) Thyrotropin releasing hormone (TRH)
4) Gonadatropin releasing hormone (GnRH)
5) Dopamine

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57
Q

Function of CRH

A

Stimulates release of ACTH

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58
Q

Function of GRHR

A

Stimulates release of growth hormone

- somatostatin INHIBITS release of GHRH

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59
Q

Function of TRH

A

Stimulates release of TSH

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60
Q

Function of GnRH

A

Stimulates release of FSH and LH

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61
Q

Function of Dopamine

A 
Inhibits prolactin
(prolactin is under negative control by dopamine)
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62
Q

What are the 6 peptide hormone secreted by the anterior pituitary?
(FLATPIG)

A

1) FSH
2) LH
3) ACTH
4) TSH
5) Prolactin
I for ignore !!
6) Growth hormone

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63
Q

What is another name for the anterior pituitary?

And what is the blood supply?

A

Adenophysis

  • no arterial blood supply
  • blood through portal venous circulation from the hypothalamus
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64
Q

What is another name for the posterior pituitary?

A

Neurohypophysis

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65
Q

What 2 hormones are stored and released by the posterior pituitary?

A

1) Vasopressin/ADH - synthesised in cell body of supraoptic nucleus
2) Oxytocin - synthesised in cell body of paraventricular nucleus

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66
Q

What stimulates vasopressin/ADH to be released?

A
  • decreased blood volume
  • trauma
  • stress
  • increase blood CO2
  • decreased blood O2
  • increased osmotic pressure of blood
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67
Q

What receptors do ALL pituitary and hypothalamic hormones act on?

A

G-protein coupled receptors

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68
Q

What are the 3 vital presentation of pituitary tumour?

A

1) Pressure on local structures
2) Pressure on normal pituitary - hypopituitarism
3) Functioning tumour - hyperpituitarism

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69
Q

What can pressure on local structures cause?

A
  • optic chiasm pressrure = bitemporal hemianopia
  • hydrocephalus
  • can get CSF leak
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70
Q

What can hypopituitarism cause?

A
  • cortisol deficiency
    In males: pale, no body hair, central obesity, effeminate skin
    In females: lose body hair, jaundiced complexion
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71
Q

What can hyperpituitarism cause?

A
  • prolactinoma - increase prolactin
  • acromegaly - increased GH
  • Cushing’s - increased CTH
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72
Q

What is the HPA axis?

A

Hypothalamo-Pituitary-Adrenal axis

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73
Q

What is the pituitary-thyroid axis?

A
  • hypothalamus releases TRH
  • stimulates secretion of TSH from pituitary
  • stimulates release of T3 & T4 from thyroid
  • T3 & T4 have -ve feedback on hypothalamus & pituitary
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74
Q

What is the pituitary-gonadal axis?

A

hypothalamus > pituitary > gonads - release testosterone > -ve feedback on HT & pituitary

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75
Q

What are the diseases of the pituitary?

A
  • benign pituitary adenoma (pituitary produces less & presses on things e.g optic chiasm)
  • craniopharyngioma
  • trauma
  • Sheehan’s - pituitary infarction after labour
  • sarcoid/ TB
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76
Q

What happens in prolactinoma?

A
  • common in females
  • increased prolactin = increased milk production
  • galactorrhea - milk leaks
  • reduced fertility
  • menstruation stops = amenorrhea
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77
Q

How do you treat prolactinoma?

A
  • use dopamine agonist
  • inhibits prolactin production
    e. g CABERGOLINE
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78
Q

What happens in acromegaly?

A
  • increased GH
  • thick, greasy, sweaty skin
  • enlarged organs
    e. g large heart = high risk of heart attack/ disease
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79
Q

What happens in Cushing’s?

A
  • increased CTH
  • too much cortisol
  • central obesity
  • bruising, thin skin
  • osteoporosis
  • ulcers
  • purple stretch marks
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80
Q

Calcium homeostasis: What happens in response to decreased serum calcium?

A
  • increased parathyroid hormone
  • increased bone resorption
  • increased calcium reabsorption
  • increased calcium absorption
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81
Q

What are the actions of the parathyroid hormone?

A
  • increased Ca2+ reabsorption
  • decreased phosphate reabsorption
  • increased 1 α hydroxylation of 25-OH vit D
  • increased bone remodelling
    resorption>formation
  • increased Ca2+ absorption (because of increased 1,25 (OH)2 vit D
82
Q

Is calcium homeostasis +ve or -ve feedback?

A

Negative

83
Q

What is the set point of serum ionised calcium?

A

1.1mmol/L

84
Q

What percentage of total plasma calcium is ionised?

A

40% (only this is physiologically relevant)

- rest is bound to albumin (unavailable)

85
Q

What stimulates calcitriol release?

A
  • low plasma Ca2+
  • low plasma phosphate
  • PTH
86
Q

What are the roles of calcitriol?

A
  • increased Ca2+ and phosphate absorption in the gut
  • inhibits PTH release (-ve feedback)
  • increases no. of osteoclasts
  • increased Ca2+ & phosphate reabsorption in kidneys
87
Q

Where is calcitonin made?

A

C-cells of thyroid

88
Q

What does calcitonin do?

A

Decrease in plasma Ca2+ & phosphate

89
Q

Definition of Diabetes Mellitus

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both
(can be thought of as vascular disease)

90
Q

How much glucose is produced and utilised everyday?

A

200g

91
Q

What percentages of glucose are derived from where?

A
  • 90% from liver glycogen & hepatic gluconeogenesis

- 10% from renal gluconeogenesis

92
Q

Which organ is the main consumer of glucose?

A

The brain

93
Q

Why does the brain use the most glucose?

A
  • Cannot use free fatty acids to be converted to ketones (then acetal CoA & therefore Krebs)
  • fatty acids can’t cross BB barrier
94
Q

Is glucose uptake by the brain obligatory?

A

Yes

95
Q

Is glucose uptake in the brain dependent on insulin?

A

No

96
Q

What is glucose oxidised to in the brain?

A

CO2 and H2O

97
Q

What does fat use glucose for?

A

As a substrate for triglyceride synthesis

98
Q

What does insulin do?

A
  • suppresses hepatic glucose output
  • decreases glycogenolysis and gluconeogenesis
  • increases glucose uptake into muscle and fat
  • suppresses lipolysis and breakdown of muscle
99
Q

Biphasic insulin release

A 
- B cells sense rising glucose levels
Phase 1) RAPID RELEASE of stored insulin
Phase 2) initiated if glucose levels remain high
- longer than 1st phase
- more insulin has to be synthesised
100
Q

Which chromosome is insulin coded for on?

A

Chromosome 11

101
Q

What is insulin produced by and where?

A

B cells in the Islets of Langerhans in pancreas

102
Q

Function of FSH

A

Stimulates oestrogen release

103
Q

Function of LH

A

Stimulates release of egg = stimulates progesterone release = increased thickening of uterine wall

104
Q

Effect of LH in men

A

On Leydig cells = testosterone release

105
Q

Function of growth hormone (GH)

A
  • stimulates growth and protein synthesis
  • stimulates gluconeogenesis
  • inhibits insulin
    (inc. glucose)
  • lipolysis
  • inc. protein synthesis in liver = stimulates IGF-1
106
Q

What is measured to reflect GH levels?

A

Insulin-like growth factor 1 (IGF-1)

107
Q

Function of ACTH

A

Stimulates release of cortisol, androgen and adrenaline

108
Q

Where is cortisol secreted from?

A

Zona fasiculata

109
Q

Where are androgens released from?

A

Zona reticularis

110
Q

Where is adrenaline released from?

A

Adrenal medulla

111
Q

Effects of cortisol

A
  • regulates and breaks down proteins / fats / carbs
  • anti-inflammatory effect
  • lowered immune response
  • overcomes stress
112
Q

Name a disease where death would result from lack of cortisol

A

Addison’s

113
Q

Function of TSH

A
  • stimulates release of thyroid hormone

- prolactin release

114
Q

Functions of thyroid hormone

A
  • controls metabolic reactions
  • inc. food metabolism
  • inc. protein synthesis
  • stim. carb metabolism
  • inc. ventilation rate/ CO / HR
  • growth rate acceleration
  • brain development in foetus
115
Q

Effect of thyrotropic releasing hormone (TRH)

A

TRH -> TSH -> inc. release of T3 and T4 from thyroid -> inc. metabolism

116
Q

Effect of GnRH

A

GnRH -> LH & FSH -> targets gonads -> inc. oestrogen, progesterone and testosterone

117
Q

Effect of GRHR

A

GHRH -> GH -> stimulates growth and protein synthesis

118
Q

Effect of somatostatin

A

Somatostatin -> inhibits GH - > inhibits growth and protein synthesis

119
Q

Which hormone inhibits growth hormone?

A

Somatostatin

120
Q

Effect of CRH

A

CRH -> ACTH -> increases cortisol production in adrenal cortex from zone fasiculata

121
Q

Effect of dopamine

A

Inhibits prolactin -> inhibits growth and milk production

122
Q

What can hyperglycaemia result in?

A

Serious microvascular & microvascular problems

123
Q

3 microvascular problems of diabetes mellitus

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
124
Q

4 microvascular problems of diabetes mellitus

A
  1. Strokes
  2. Renovascular disease
  3. Limb ischaemia
  4. Heart disease
125
Q

Normal blood glucose levels

A

3.5-8.0mmol/L

126
Q

Effect of glucagon

A
  • increases hepatic glucose output
  • reduces peripheral glucose uptake
  • stim. peripheral release of gluconeogenic precursors
  • stim. lipolysis & ketogenesis
127
Q

Why is there a high level of C peptide in blood when insulin is released?

A

Because proinsulin is cleaved from C peptide

128
Q

Difference between synthetic insulin and natural

A

Synthetic insulin has no C peptide

- presence of it can determine whether insulin is natural or not

129
Q

Name of transporters that carry goose across membranes

A

GLUT proteins - specialised glucose transporter

130
Q

How many types of GLUT proteins are there?

A

4

131
Q

Function of GLUT 1

A

Enables basal non-insulin stimulates glucose uptake

132
Q

Characteristic and function of GLUT 2

A
  • low affinity transporter (allows glucose in when glucose conc. is high)
  • transports glucose into beta cells
133
Q

What can GLUT2 beta cells detect?

A

High glucose levels

- therefore release insulin in response

134
Q

Where is GLUT 2 found?

A

In beta cells of pancreas

- also found ion renal tubules and hepatocytes

135
Q

Function of GLUT 3

A

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

136
Q

Function of GLUT4

A
  • Mediates peripheral action of insulin
  • enables glucose uptake into muscle and adipose tissue
    (following stimulation of insulin receptor)
137
Q

What kind of protein is the insulin receptor?

A

Glycoprotein

138
Q

Where is insulin receptor coded for?

A

Short arm of Chromosome 19

139
Q

What results when insulin binds to receptor

A
  • activation of tyrosine kinase

- imitation of cascade response

140
Q

Consequence of cascade response

A

Migration of GLUT4 to cell surface

=increased transport of glucose into cell

141
Q

What might diabetes be secondary to?

A
  • pancreatic pathology
  • endocrine disease (acromegaly / Cushing’s)
  • drug induced
  • maturity onset diabetes of youth (MODY)
142
Q

Drugs that may cause secondary diabetes

A
  • thiazide diuretics

- corticosteroids

143
Q

Describe MODY

A
  • autosomal dominant form of type 2
  • single gene defect
  • alters beta cell function
  • presents <25 years with positive family history
144
Q

Define type 1 diabetes mellitus (DM1)

A

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

145
Q

What is insulitis?

A

Anti-bodies forming against insulin and islet beta cells

146
Q

Genetic susceptibility to DM1

A
  1. HLA-DR3-DQ2

2. HLA-DR4-DQ8

147
Q

Other autoimmune diseases associated with DM1

A
  • autoimmune thyroid
  • coeliac disease
  • Addison’s
  • pernicious anaemia
148
Q

Environmental risk factors for DM1

A
  • dietary constituents
  • enteroviruses (Coxsackie B4)
  • vit D deficiency
  • cleaner environment
149
Q

Symptoms of DM1

A
  • glycosuria
  • ketonuria
  • impaired glucose clearance in skeletal muscles/fats
  • polyuria
  • polydipsia (excess thirst)
  • thin
150
Q

Define diabetes mellitus type 2

A

Combination of increased insulin resistance and less severe decreased insulin deficiency

151
Q

Risk factors for DM2

A
  • obesity
  • family history
  • inc. age
  • ethnicity (Middle Eastern/ sE Asian)
  • environment
152
Q

What is DM2 associated with?

A
  • central obesity
  • hypertension
  • hypertriglycerideaemia
  • decreased HDL
  • inc. in number of pro-inflammatory markers
  • inc. CV risk
153
Q

Where does insulin resistance develop?

A

Post insulin receptor

- so DM2 is not a problem with insulin binding

154
Q

Beta cell mass at time of diagnosis of DM2

A

50% of the normal

155
Q

What do DM2 patients show at autopsy?

A

Amyloid deposition in islets of the pancreas

156
Q

Early sign of DM2

A

Loss of first phase of biphasic response to insulin

157
Q

Describe the Starling curve of the pancreas

A
  • circulating inulin levels are high
  • increase further
  • decline again after months / years (due to secretory failure)
158
Q

What does DM2 typically progress from?

A

Preliminary phase of impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)

159
Q

Fasting plasma glucose level in IGT

A

<7mmol/L

160
Q

Fasting plasma glucose level in IFG

A

> 6.1mmol/L
<7mmol/L
(6.1-7)

161
Q

Oral glucose tolerance of 2 hours glucose

A

> 7.8mmol/L

< 11 mmol/L

162
Q

Clinical presentation of DM2

A
  • overweight in abdomen
  • polydipsia
  • polyuria
  • weight loss
  • ketosis (v advanced DM2 with absolute insulin deficiency)
163
Q

Acute presentation of DM1 (2-6 weeks)

A
  1. Polyuria & nocturia
  2. Polydipsia
  3. Weight loss
164
Q

Reason for polyuria and nocturia in DM

A
  • kidneys are at renal max reabsorptive capacity
  • not enough glucose reabsorbed in kidneys
    = high levels of glucose in tubule urine
165
Q

Reason for polydipsia in DM

A

Loss of fluid and electrolytes from excess glucose & water in urine

166
Q

Reason for weight loss in DM

A

Fluid depletion & accelerated breakdown of fat and muscle
- secondary to insulin deficiency

167
Q

Subacute presentation of DM (months - years)

A
  • polyuria
  • polydipsia
  • weight loss
  • lack of energy
  • visual blurring
  • pruritus vulvae
168
Q

Complications of DM as a presenting feature

A
  • staphylococcal skin infection
  • retinopathy
  • polyneuropathy
  • erectile dysfunction
  • arterial disease (MI or peripheral gangrene)
169
Q

Physical examination of DM

A
  • weight loss / dehydration
  • breath smells of ketones
  • retinopathy
  • acanthosis nigricans (in patients with severe insulin resistance) - black pigmentation at nape of neck & axillae
170
Q

Diagnostic values for diabetes

A
  1. Random plasma glucose >11.1mmol/L
  2. Fasting plasma glucose >7mmol/L
  3. HbA1c > 48mmol/L (>6.5%)
171
Q

Is one abnormal test value diagnostic?

A

Yes - in symptomatic patients

No - in asymptomatic patients (two abnormal values needed)

172
Q

Diagnostic tests for diabetes

A
  1. Screen urine (microalbuminaemia)
  2. FBC / U&E / liver biochem / fasting blood for cholesterol /triglycerides
  3. Raised blood pH = metabolic acidosis
173
Q

Describe a good glycaemic control in a good diet

A
  • low in sugar
  • high in starchy carbs (low glycemic index - pasta)
  • high in fibre
  • low in fat
174
Q

Treatment of DM 1 and 2

A
  • maintain lean weight
  • stop smoking / alcohol
  • regular physical activity
  • ACEI to treat hypertension
  • statins to treat hyperlipidaemia
175
Q

Treatment of DM1

A
  • synthetic human insulin (SC injection)
  • change injection site (prevent lipohypertrophy)
  • finger pricking glucose before and after meal
176
Q

What is the legal requirement for someone on insulin?

A

Inform DVLA

- frequent hypoglycaemic events may be unfit to drive

177
Q

How many types of insulin are there for DM1? What are they?

A

3:

  • short acting (soluble) insulins
  • short acting insulin analogues
  • long acting insulins
178
Q

How long does it take for short acting insulins to start working?

A

30-60 minutes

179
Q

How long do short acting insulins last?

A

4-6 hours

180
Q

When are short acting insulins given?

A
  • 15-30 minutes before meals in patients on multiple dose regimens
  • continuous IV in labour / medical emergencies / surgery / using insulin pumps
181
Q

Examples of human insulin analogies

A
  • insulin aspart
  • insulin lispro
  • insulin glulisine
182
Q

Describe onset and duration of human insulin analogies

A
  • fast onset

- short duration

183
Q

What kind of patients are given human insulin analogies? Why?

A
  • those who are prone to nocturnal hypoglycaemia

- have reduced carry-over effect compared to soluble insulin

184
Q

What are longer acting insulins mixed with?

A

Retarding agents precipitate crystals

e.g protamine / zinc)

185
Q

How long do longer acting insulins work for?

A

Intermediate (12-24 hours)

Long-acting ( >24 hours)

186
Q

What are protamine insulins known as?

A

Isophane or NPH insulins

187
Q

What are zinc insulins known as?

A

Lente insulins

188
Q

What is insulin glargine? (long lasting insulins)

A

Structurally modified insulins that precipitates in tissues

- slowly released from injection site

189
Q

Complications of insulin treatment

A
  • hypoglycaemia
  • lipohypertrophy (injection site)
  • insulin resistance
  • weight gain (hunger)
190
Q

First line treatment of DM2

A
  • lifestyle & dietary changes
  • nutrient load spread through day (3 main meals)
  • BP control
  • hyperlipidaemia control
  • exercise / weight loss
  • orlistat
191
Q

What does orlistat do?

A

Intestinal lipase inhibitor

  • reduces absorption of fat from diet
  • promotes weight loss
192
Q

Second line treatment of DM2

A 
- oral metformin 
If HbA1c > 53mmol/L 16 weeks later: 
- add sulfonylurea (oral gliclazide)
If HbA1c > 57mmol/L after 6 months:
- insulin might be needed 
- GLITAZONE 
- glucagon like peptide analogues (GLP)
193
Q

Effects of metformin

A
  • reduces gluconeogensis in liver
  • increases sensitivity of cells to insulin
  • weight loss
  • reduces CVS risk
194
Q

Side effects of metformin

A
  • anorexia
  • diarrhoea
  • nausea
  • abdo pain
195
Q

Contraindications of metformin

A
  • heart failure
  • liver disease
  • renal disease
    (can induce lactic acidosis)
196
Q

Effects of gliclazide

A
  • promotes insulin secretion
  • avoided in pregnancy
  • used with care in people with liver disease
197
Q

When is gliclazide ineffective?

A

Without a functional beta-cell mass

effect wears off as beta cell mass declines

198
Q

Side effects of gliclazide

A
  • Hypoglycaemia
  • promote weight gain
    (avoided in overweight patients)
199
Q

Effect of glitazones

A

Replaces metformin and sulfonylurea

- increase insulin sensitivity

200
Q

Side effects of glitazone

A
  • hypoglycaemia
  • fractures
  • fluid retention
201
Q

Contraindications of glitazone

A
  • congestive heart failure

- osteoporosis

Phase 2a (7 decks)

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