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203 Endocrinology and Reproduction > Theme 1 - Endocrine System > Flashcards

Theme 1 - Endocrine System Flashcards

1
Q

Do the glands in the endocrine system have ducts?

A

No they are ductless

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2
Q

Do hormones act upon all cells?

A

No only those with target tissues

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3
Q

Draw or list the endocrine glands

A 
Hypothalamus
Pituitary (Anterior/Posterior)
Thyroid
ParaThyroid
Thymus
Kidney
Adrenal
Pancreas
Gonad
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4
Q

Draw and label the hypothalamus/pituitary gland.

A

Hypothalamus
Hypothalamico-hypophyseal vessel
Infindibulum
anterior/posterior

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5
Q

What is the main function of thyroid and parathyroid

A

Metabolic rate

calcium homeostasis

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6
Q

What hormone does the pancreas secrete

A

Insulin

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7
Q

Function of Adrenal medulla and cortex

A

Medulla -Stress response,

Cortex - Stress, Sodium and glucose

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8
Q

Function of gonads

A

Secondary sexual characteristics

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9
Q

What are the three main types of hormone receptor?

A

G protein coupled
Steriod
Tyrosine Kinase

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10
Q

Steroid hormone - Mechanism of action

A

Crosses membrane
binds to receptor in cytoplasm or nucleus
This complex then influences gene transcription

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11
Q

G protein mechanism of action

A

Binds to receptor
Synthesis of second messenger CAMP
Second messenger phosphorelates to cause …

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12
Q

Tyrosine mechanism of action

A

Sometimes dimerised
Hormone binds to receptor
recptor then acts as enzye to influence intracellular activity

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13
Q

What are the characteristics of peptide hormones?

A 
Water solvable
Not orally active
Rapid onset
Protease vulnerable
Unable to cross cell membrane without carrier protein
Short duration and plasma half life
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14
Q

Characteristics of steriod and thyroid hormones

A 
Lipid soluble
Orally active
Slow onset
Must be protein bound in blood
But unbound is biologically active
Can cross cell membrane
Long duration and half life
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15
Q

Is secretion usually controlled by the anterior or posterior pituitary

A

anterior

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16
Q

TSH stimulates?

A

Thyroid - Thyroxine

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17
Q

ACTH stimulates?

A

Adrenal cortex - cortisol

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18
Q

TRH, from/stimulates?

A

Hypothalamus/ant pit to relaese TSH

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19
Q

CRH from/stimualtes?

A

Hyopthalamus to ant pit to relaease ACTH

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20
Q

GnRH from/stimulates?

A

Hypothalamus to ant pit to release FSH

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21
Q

GHRH from stimulates?

A

Hypothalamus to ant pit to release growth hormone

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22
Q

How is hormone secretion typically regulated, give an example?

A

Negative feedback.
eg TRH, TSH, Thyroxine
CRH, ACTH, cortisol
GnRH, FSH, oestrodiol

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23
Q

What hormaones are secreted by the posterior pituitary ?

A

ADH/vasopressin and Oxytocin

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24
Q

What types of hormone are ADH and oxytocin, where are they synthesised?

A

Peptide

Synthesised in supraoptic and para-ventricular nuclei of the hypothalamus

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25
Q

What influences the secretion of ADH

A

Plasma osmolarity.

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26
Q

What affect does ADH have upon the kidney?

A

Stimulates v2 receptors which cause the translocation of aquaporins to membrane of tubule membrane that lead to water re absorption

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27
Q

How does vasopressin/ADH act upon the vascular system?

A

Stimulates v1 receptors to cause vasoconstriction.

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28
Q

What influences secretion of oxytocin?

A

Stimulation of genitals and nipples

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29
Q

What does oxytocin act upon?

A

Acts via IP3 channes to cause contraction of smooth muscle in breast and uterus.

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30
Q

During pregnancy there is an increase in oxytocin, explain why this dies not result in a premature birth?

A

Increase in oxytocin paralleled by an increase in oxytocinase. Inhibits the contraction of smooth muscle in uterus.

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31
Q

Explain how the childbirth an oxytocin constitutes a positive feedback loop.

A

oxytocin causes contraction of smooth muscle in uterus. Foetus pushes against cervix. Stimulation of cervix causes further release of oxytocin leading to further contraction of uterus.

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32
Q

What hormones are secreted by the anterior pituitary?

A 
Growth Hormone
Prolactin
TSH
ACTH
FSH
LH
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33
Q

What’s the difference between where hormones released from the ant and post pituitary gland are synthesised?

A

Hormones from post pituitary gland are synthesised in the hypothalamus (supraoptic and paraentricular).
Hormones secreted from ant pituitary gland are synthesised in the ant pituitary.

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34
Q

Where are the following hormones synthesised and by what cells? FSH, ACTH, TSH, proactin, growth hormone

A

In the ant pituitary by: gonadotrophe, corticotrophe, thyrotrophe and lactotrophe, somatotrophe cells respectively

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35
Q

What hormones inhibits/stimulates prolactin synthesis?

A

Dopamine inhibits. TRH stimulates.

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36
Q

What non hormonal factors can stimulate prolactin secretion?

A

Mild stress, nipple stimulation, coitus.

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37
Q

What is the role of prolactin?

A

Development of breast tissue and lactation.

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38
Q

Is prolactin secreted in males?

A

Yes

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39
Q

What inhibits and stimulates the release of growth hormone?

A

GHRH from hypothalamus

GHRIH /somatoststin

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40
Q

How do nutritional factors influence the secretion of growth hormone?

A

Stimulated by: Increased carbs and amino acids

Decreased amino acids.

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41
Q

In some tissues GH needs to act via second messengers, what are these and where are they produced?

A

INsulin like growth factor 1 &2. Made in the liver

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42
Q

What is the role of GH? Is

A

Increase linear growth in adolescence (foetal growth independent of this)

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43
Q

Which part of the adrenal/suprerenal gland is essential for life?

A

The cortex

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44
Q

What types of hormones are secreted from the adrenal cortex?

A

glutocorticoids

mineralcorticoids

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45
Q

What steriod hormones are synthesised from cholesterol?

A

Adosterone
Cortisol
Testerone to androsterone

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46
Q

It it significant that the adrenal glands secrete small amounts of male and female sex hormones?

A

No, this is only significant in adrenal disorders

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47
Q

When does ACTH secretion peak?

A

Morning (assuming non shift work)

Stress

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48
Q

What is the typical lad time of cortisol levels in relation to ACTH peak and nadir?

A

2hrs

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49
Q

What percentage of cortisol in the blood is free and what happens to the rest?

A

10% free the rest is protein bound.

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50
Q

In the plasma what is cortisol bound to?

A

10% free
15% albumin
75% corticosteroid binding globulin

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51
Q

What influence does pregnancy have on the levels of corticosteriod binding globulin?

A

CBG increses but cortisol increases to maintain some level of free cortisol.

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52
Q

Where does the metabolism of adrenal steroids take place?

A

Liver

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53
Q

How does cortisol influence carbohydrate metabolism?

A

Antagonises the effects of insulin on cellular uptake of glucose
Stimulates glycogenolysis
Stimulates hepatic gluconeogenesis

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54
Q

What influence does cortisol have on lipid metabolism?

A

Stimulates lipolysis and mobilisation of fatty acids.

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55
Q

In relation to fat synthesis and disposition, what can excessive levels of cortisol cause?

A

Increased fat synthesis.

fat deposited around face and inter scapula region and trunk.

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56
Q

What effect does cortisol have on amino protein metabolism?

A

Stimulates amino acid uptake in liver, leading to gluconeogenesis.
Inhibits amino acid uptake in periphery

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57
Q

How does cortisol influence blood pressure?

A

Enhances vasoconstrictor response to catechloamines, which then increases blood pressure.

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58
Q

What are the psycholgical effects of glutocosteroids ?

A

Elation and sedation

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59
Q

How do glutocorticoids affect immune response?

A

They suppress the lymphoid tissue, reduce the antibody production and inhibit the cellular immune system.
• They stabilize leucocyte membranes and reduce the release of proteolytic enzymes.
• They inhibit phospholipase A2 and reduce the synthesis of the inflammatory mediators.

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60
Q

Name 2 mineralocorticoid

A

Aldosterone and 11-deoxycorticosterone

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61
Q

What is the major controlling factor of aldosterone?

A

Renin angiotensin system

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62
Q

Other than renin-angiotensin, what other factors influence aldosterone?

A 
Stimulated by: 
Trauma
anxiety
Hyperkalemia
Hyponaturemia 
Inhibited by: atrial natriuric peptide
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63
Q

Within the circulation how much aldosterone is protein bound?

A

50%

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64
Q

Aldosterone mechanism of action?

A

intracellular receptors which cause expression of ion channels that transport sodium and potassium ions across the cell membrane

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65
Q

Upon what part of the kidey does aldosterone affect reabsorption?

A

distal tubule

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66
Q

To a lesser extent what tissues does aldersterone affect sodium reabsoption?

A 
Loop of Henle
collecting duct
proximal tubule
colon
sweat glands
salivary glands
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67
Q

Pharma uses of adrencorticosteroids (hydrocartisone)

A

Asthma, allergies, arthritis

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68
Q

What type of therapy are mineralocorticoids used for?

A

replacement therapy

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69
Q

What is used to replace aldersterone and why?

A

fludricortisol, because aldosteron has a short half life

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70
Q

What are the adverse affects of glucocortioids?

A

Steroid usage may suppress wound healing and may exacerbate infections due to their immunosuppresant effects.
Long term use in children may cause inhibition of growth, and in adults may result in osteoporosis.
The development of diabetes mellitus and other symptoms of Cushing’s syndrome also often accompanies steroid therapy.

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71
Q

Adverse chronic effect of glucocorticoid and explain this

A

Chronic administration of exogenous glucocorticoids results in suppression of ACTH secretion leading to atrophy of the adrenal cortex.

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72
Q

Why would it be a bad idea for a pt to suddenly stop long term steriod therapy?

A

If steroid therapy is then stopped abruptly, the adrenal cortex is unable to secrete endogenous hormones and the patient suffers an Addisonian crisis, which may be fatal. This consequence overcome by the gradual reduction of the dose of the exogenous steroid

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73
Q

Within the thyroid what is the function of the colliods

A

reserviour for thyroid hormone

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74
Q

Thyroid hormones are especially important for the development of the CNS, what aspect in particular

A

The mylenation of nerve fibres

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75
Q

By what primary mechanism do thyroid hormones increase metabolic rate?

A

Increase number and size of mitochondria, increase in metabolic enzymes

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76
Q

Thyroid hormones increase basal metabolic rate, and therefore oxygen consumption, in nearly every organ except?

A 
Brain
Uterus
Testes
Spleen
Thyroid gland
Anterior pituitary gland
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77
Q

What is levothyroxine used to treat and how is it administered?

A

treat thyroid deficiency. It can be used to suppress TSH secretion in the treatment of some thyroid tumours. It can be given by mouth or by injection.

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78
Q

Where is levothyroxine metabolised and what are the adverse effects associated with it?

A

Liver

palpitations, arrhythmias, diarrhoea, insomnia, tremor, weight loss

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79
Q

name two anti thyroid drugs

A

carbimazole
methimazole
potassium perchlorate

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80
Q

How can nuclear medicine be used to reduce thryroid hormaone secretion

A

Iodine 131 (raduioactive isotope) actively taken up by thyroid. This in turn will damage cells and reduce secretion.

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81
Q

What is carbimazole and its mechanism of action?

A

anti thyroid drug - used to treat hyperthyroidsim.

Converted into methimazole. Prevents synthesis if T3 and T4.

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82
Q

Adverse effects of carbimazole?

A

Rashes and pruritus are common which can often be treated with antihistamines. The most serious rare side effect is neutropenia and agranulocytosis. Teratogenic.

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83
Q

What is Propylthiouracil and its mechanism of action?

A

Used to treat hyperthyroidism. Inhibits thyroid hormone synthesis. can be used in first trimester

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84
Q

Adverse effects of Propythiouracil?

A

Rashes and pruritus are common which can often be treated with antihistamines. Its notable side effects include a risk of agranulocytosis and risk of serious liver injury, including liver failure and death

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85
Q

Goitre?

A

Enlargement of thyroid gland

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86
Q

Primary hypothyroidism

A

problem with thyroid

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87
Q

Secondary hypothyroidism

A

Problem with pituitary

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88
Q

Hypothyroidism Symptoms

A 
May be none
Lethargy
Mild weight gain
Cold intolerance 
Constipation
Facial puffiness
Dry skin
Hair loss
Hoarseness
Heavy menstrual periods
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89
Q

Severe hypothyroidism: signs

A 
Change in appearance eg face puffy and pale
Periorbital oedema
Dry flaking skin
Diffuse hair loss
Bradycardia
Signs of median nerve compression (carpal tunnel)
Effusions, eg ascites, pericardial
Delayed relaxation of reflexes
Croaky voice
Goitre
Rarely stupor or coma
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90
Q

Causes of Primary Hypothyroidism

A

Autoimmune
iatrogenic
Thyroiditis
Drugs (e.g. lithium

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91
Q

treatment for primary hypothyroidism?

A

Thyroxine

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92
Q

What is Hasimoto’s disease?

A

Chronic autoimmune thyroisitis

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93
Q

Symptoms of thyrotoxicosis?

A 
Weight loss
Lack of energy
Heat intolerance
Anxiety/irritability
Increased sweating
Increased appetite
Thirst
Palpitations
Pruritus
Weight gain
Loose bowels
Oligomenorrhoea
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94
Q

Signs of thyrotoxicosis

A 
Tremor
Warm, moist skin
Tachycardia
Brisk reflexes
Eye signs
Thyroid bruit
Muscle weakness
Atrial fibrillation
95
Q

Signs and symptoms of thyroid eye disease

A 
itchy eyes
bulging eyes
diplopia
loss of colour vision
inability to close eyes
reddening of conjunctiva
96
Q

what is the most common cause (75%) of hyperthyroidism?

A 
Graves Disease (autoimmune)
Autoantibody stimulates the 
TSH receptor, causing excess 
thyroid hormone production
and thyroid growth (goitre)
97
Q

Other causes of thyrotoxicosis

A

Toxic multinodular goitre
Toxic adenoma
Thyroiditis
Drugs (e.g. amiodarone)

98
Q

what is gestational thyrotoxicosis?

A

Placental β-human chorionic gonadotrophin is structurally similar to TSH and TSH-like action on the thyroid
 likely if hyperemesis / twin pregnancy
Settles after 1st trimester of pregnancy

99
Q

medical treatment of hyperthyroidism?

A

Carbimazole or propylthiouracil (PTU)

18 months – 2 years

100
Q

non medical treatment of hyperthyroidism?

A 
radioactive iodine
Sub-total thyroidectomy (“almost total”)
Patients must be euthyroid pre-operatively
Medical therapy first
Risks
Anaesthetic
Neck scar
Hypothyroidism
Hypoparathyroidism
Vocal cord palsy (recurrent laryngeal nerve damage)
101
Q

What are the features of thyroid storm/thyrotoxic crisis?

A 
Graves
Goitre, thyroid eye disease
Hyperpyrexia
CNS
Agitation, delirium
Cardiovascular
Tachycardia >140 bpm
Atrial dysrhythmias
Ventricular dysfunction
Heart failure
GI
Nausea & vomiting
Diarrhoea
Hepatocellular dysfunction
102
Q

Who gets thyroid storm?

A

Usually 2 degree Graves disease.
Unrecognised
Incompletely treated hyperthyroidism

103
Q

What percentage if cortisol is bound in plasma and what to?

A

90% to cortisol binding globulin

104
Q

Describe cortisol levels in relation to circadian rhythm

A

rise during the early morning
peak just prior to awakening
fall during the day
are low in the evening

105
Q

How does 11--HSD-2 relate to cortisol function in the kidney?q

A

inactivates cortisol, enabling aldosterone to bind the Mineralocorticoid receptor

106
Q

What syndrome is an excess of cortisol?

A

Cushings

107
Q

Signs of Cushings x4

A 
Weight gain
Central obesity
Hypertension
Insulin resistance
Neuropsychiatric problems
Osteoporosis
108
Q

Pathogenesis of Cushings? x4

A

Pituitary adenoma: ACTH-secreting cells (‘Cushing’s disease’)
Adrenal tumour: adenoma (or carcinoma)
‘Ectopic ACTH’: carcinoid, paraneoplastic

Iatrogenic: steroid treatment (‘Cushingoid’)

109
Q

Clinical features of Cushings in relation to appearance

A

Central obesity with thin arms & legs
Fat deposition over upper back (‘buffalo hump’)
Rounded ‘moon’ face
Thin skin with easy bruising, pigmented striae
Hirsutism

110
Q

Disease associated with lack of cortisol?

A

Addisons disease

111
Q

Pathogenesis of Addisons disease?

A

Primary adrenal insufficiency - usually autoimmune

iatrogentic - sudden withdrawl of steriods

112
Q

Clinical features of Addisons disease?

A 
Malaise, weakness, anorexia, weight loss
Increased skin pigmentation: 
knuckles, palmar creases, around / inside the mouth, pressure areas, scars
Hypotension / postural hypotension
Hypoglycaemia
113
Q

Differences between AUTOIMMUNE POLYENDOCRINE SYNDROMES type 1 and 2 in terms of epidemiology?

A

Rare/More common (still rare)

Infancy/Infancy to adulthood

114
Q

Differences between AUTOIMMUNE POLYENDOCRINE SYNDROMES type 1 and 2 in terms of genealogy?

A

AIRE gene/polygenic

115
Q

Common phenotype of AUTOIMMUNE POLYENDOCRINE SYNDROMES type 1

A

Addison’s disease
Hypoparathyroidism
Candidiasis

116
Q

Common phenotype of AUTOIMMUNE POLYENDOCRINE SYNDROMES type 2

A

Addison’s disease
T1 diabetes
Autoimmue thyroid disease

117
Q

In terms of AUTOIMMUNE POLYENDOCRINE SYNDROMES, what conditions can occur together?

A 
Type 1 diabetes
Autoimmune thyroid disease (hypo- or hyper-)
Also gestational / post-partum thyroiditis
Coeliac disease 
Addison’s disease
Pernicious anaemia
Alopecia
Vitiligo
Hepatitis
Premature ovarian failure
Myasthenia gravis
118
Q

Management of Cushings?

A

Surgical (depending on the cause)
Transphenoidal adenectomy
Adrenalectomy
Pituitary radiotherapy

119
Q

Managment of Addisons?

A

Steroid hormone replacement therapy (‘glucocorticoid’):
Usually hydrocortisone (sometimes prednisolone)
Patients with primary adrenal insufficiency also need mineralocorticoid replacement therapy (fludrocortisone).
Patients with secondary adrenal insufficiency will often be taking other hormone replacement therapy (do not need fludrocortisone).

120
Q

Considerations for patients on long term steroid replacement therapy?

A

They may not mount an adequate ‘stress response’.
Their steroid treatment should not be stopped suddenly.
If they need a major procedure / an operation, they require increased steroid cover as described.
They should be given a ‘Steroid Treatment Card’ to remind them (& their doctors) about this.

121
Q

Key hormone involved in fluid balance

A

ADH/vasopressin

122
Q

What stimulates ADH/vasopressin

A

Changes in plasma osmolality

123
Q

Osmoreceptors detect changes in plasma osmolality, where are these located?

A

Anterior wall of third ventricle

124
Q

How do osmorececeptors influence the fluid balance?

A

Their volume changes which in turn stimulates synthesis if ADH in the hypothalamus and signals cerebral cortex to generate feeling of thirst.

125
Q

Where is vasopressin synthesised and released from?

A

Synthesised in supraoptic and paraventricular nuclei of hypothalamus and secreted from posterior pituitary gland.

126
Q

What are the features of low plasma osmolality in terms of AVP, urine and thirst?

A

AVP undetectable
Dilute urine
High urine output
No thirst

127
Q

What are the features of high plasma osmolality in terms of AVP, urine and thirst?

A 
High AVP secretion
Concentrated urine
Low urine output
Increased thirst sensation
Drinking immediately transiently suppresses AVP secretion and thirst
Avoids ‘overshoot’
128
Q

Polydipsia

A

Excessive thirst

129
Q

Polyuria

A

Excessive urination

130
Q

Other than DM what are the 3 main causes of polydipsia and polyuria?

A

Cranial DI
Nephrogenic DI
Primary polydipsia

131
Q

Principle mechanism of cranial DI?

A

Decreased osmoregulated AVP recretion.

132
Q

Causes of cranial DI?

A

Genetic
Idiopathic
Secondary - post surgical/trauma

133
Q

How does cranial DI relate to polydipsia?

A

Excess solute free urine. So thirst stimulated to maintain plasma osmolality

134
Q

5 Symptoms of hypothalmic syndrome

A 
Disordered thirst and DI
Disordered appetite (hyperphagia)
Disordered temperature regulation
Disordered sleep rhythm
Hypopituitarism
135
Q

Mechanism of nephrogenic DI?

A

Renal tubules resistant to AVP

136
Q

causes of nephrogenic DI?

A 
Idiopathic
Genetic
Metabolic - High Ca/low K
Chronic Kidney Disease
Drugs - Lithium
137
Q

Wis primary polydipsia and how dies it relate to polyurea?

A

Psychogenic. Increased fluid intake leads to low plasma osmolality which in turn increases AVS secretion causing polyuria.

138
Q

What is the water deprivation test?

A 
Period of dehydration
Measure plasma and urine osmolalities & weight
Injection of synthetic vasopressin 
Desmopressin (DDAVP)
Measure plasma and urine osmolalities
139
Q

Following a water deprivation test what would the responses be for; normal, cranial DI and nephrogenic DI?

A

Normal response to dehydration
Normal plasma osmolality, high urine osmolality
Cranial diabetes insipidus
Poor urine concentration after dehydration
Rise in urine osmolality after desmopressin
Nephrogenic diabetes insipidus
Poor urine concentration after dehydration
No rise in urine osmolality after desmopressin

140
Q

Treatment for cranial DI?

A

DDAVP (desmopressin)

Over-treatment can cause hyponatraemia

141
Q

treatment for nephrogenic DI?

A

Correction of cause (metabolic / drug cause)

Thiazide diuretics / NSAIDs

142
Q

treatment for primary polydipsia?

A

Explanation, persuasion

Psychological therapy

143
Q

Definition and symptoms of hyponatraemia?

A 
[Sodium] <135 mmol/L
Severe [Na] <125 mmol/L
May be asymptomatic
Depends on rate of fall as well as absolute value
Brain adapts (chronic)
Non-specific
Headache, nausea, mood change, cramps, lethargy
Severe / sudden
Confusion, drowsiness, seizures, coma
144
Q

In terms of hyponatraemia, what factors need to be excluded?

A

Drug causes - thiazide

High glucose protein concentrations

145
Q

How is hyponatraemia classified?

A

Classify by extracellular fluid volume status
Hypovolaemia
Renal loss, non-renal loss (D&V, burns, sweating)
Normovolaemia (euvolaemia)
Hypoadrenalism, hypothyroidism
Syndrome of inappropriate ADH secretion (SIADH)
Hypervolaemia
Renal failure, cardiac failure, cirrhosis, excess IV dextrose

146
Q

What is SIADH?

A

syndrome of inappropriate ADH secretion

147
Q

Signs of SIADH?

A

Clinically euvolaemic patient
Low plasma sodium and low plasma osmolality
Inappropriately high urine sodium concentration and high urine osmolality

148
Q

treatment of SIADH

A 
Identify and treat the underlying cause
Fluid restriction (<1000 ml daily)
Induce negative fluid balance 500 ml
Aim ‘low normal’ sodium
Demeclocycline
Drug that induces mild nephrogenic DI
Vasopressin (V2 receptor) antagonists
“Vaptans” – induce a water diuresis
Expensive, variable responses, some attenuation 
Lack of clinically significant outcome data
149
Q

Risks of correcting hyponatraermi too rapidly?

A

oligodendrocyte degeneration and CNS myelinolysis (osmotic demyelination)
Severe neurological sequelae, may be permanent
Alcoholics & malnourished particularly at risk

150
Q

normal BMI range and calculation

A

18.5 - 24.9 kg/m2

151
Q

Ways of measuring body mass/obesity?

A 
BMI
Waist circumference
skin fold thickness
Bioelectrical impedance analysis
Ethnicity specific cut-offs
152
Q

8 Medical problems associated with obesity?

A 
Metabolic syndrome / type 2 diabetes
Cardiovascular disease
Respiratory disease
Liver disease
Cancer
Reproductive dysfunction
Joint problems
Psychological morbidity
153
Q

What is metabolic syndrome?

A

Constellation of closely associated CV risk factors’
Visceral obesity
Dyslipidaemia
Hyperglycaemia
Hypertension
INSULIN RESISTANCE is the underlying pathophysiological mechanism

154
Q

What is metabolic syndrom assocciated with in terms of BMI and body fat distribution?

A

central fat distribution and BMI above 30

155
Q

What is CV disease?

A 
Metabolic syndrome’ PLUS
 blood volume and blood viscosity
 vascular resistance
 hypertension
 left ventricular hypertrophy
 coronary artery disease
 stroke
156
Q

What respiratory related disorders are associated with obesity?

A 
Obstructive sleep apnoea
Hypoxia / hypercapnia
Pulmonary hypertension
Right heart failure
Accidents
Daytime somnolence
157
Q

What GI/liver disorders are associated with obesity?

A

Non-alcoholic fatty liver
Non-alcoholic steatohepatitis
May progress to cirrhosis, portal hypertension, hepatocellular cancer

Gallstones
Reflux

158
Q

Cancers associated with obesity?

A

Breast, endometrial, oesophagus,

colon, gall bladder, renal, thyroid

159
Q

Reproductive disorders associated with obesity

A 
Polycystic ovarian syndrome
Oligomenorrhoea, hirsutism, acne
Subfertility
Endometrial hyperplasia
Insulin resistance

Male hypogonadism

Adverse pregnancy outcomes

160
Q

What is the 1 licenced pharmacological treatment for obesity?

A

Orlistat

161
Q

Orlistat mechanism of action?

A

Binds & inhibits lipases in the lumen of the gut
Prevents the hydrolysis of dietary fat into absorbable free fatty acids / glycerol
Excrete ~ 1/3rd dietary fat

162
Q

Adverse affects of orlistat?

A

Flatulence
Oily faecal leakage
decreased absorptive of fat soluble vitamins

163
Q

2 surgical treatments for obesity?

A

Laparoscopic adjustable banding

Roux-en-Y gastric bypass

164
Q

Differences between Laparoscopic adjustable banding

Roux-en-Y gastric bypass

A

Restrictive
Malabsorptive
Alterations in gut hormones and bile acid flow contribute to weight loss
banding adjustable.

165
Q

Adverse affects of Roux-en-Y

A

Micronutrient deficiencies
Supplement with iron, B12, folate, calcium, vitamin D
Dumping syndrome
GI & vasomotor symptoms

166
Q

Advantages of surgical treatment for obesity?

A

Weight loss 25-30%
Resolve or improve co-morbidities
Brings cost savings

167
Q

Disadvantages of surgical treatment for obesity

A 
Perioperative mortality / morbidity
Depends on procedure and experience of surgeon
Long-term follow-up
Micronutrient deficiencies
Some weight re-gain
Patients will still be obese
Expense
168
Q

NICE guidelines for bariatric surgery

A

Recent onset T2DM:
Expedite bariatric surgery if BMI > 35
Consider surgery if BMI > 30
Must have been obese for at least 5 years
Must engage with non-surgical weight-loss programme for 12-24 months first

169
Q

Oestrogen, FSH and LH levels in pre and post menopausal women

A

Oestrogen levels
Pre-menopausal: cycling
Post-menopausal: very low constant levels
↓E2, ↑LH / FSH

170
Q

Age of menopause

A

50 +/-2

171
Q

Symptoms of menopause and median length of symptoms

A

Hot flushes and night sweats

7 years

172
Q

Morbidities associated with menopause

A

osteoporosis, CHD, sexual dysfunction

173
Q

Benefits of Hormone Replacement Therapy

A

Rx menopausal Sx
↓ osteoporosis / fracture risk
for duration Rx

174
Q

Adverse affects of Hormone Replacement Therapy?

A 
↑ venous thrombo-embolism
↑ breast Ca (small)
esp > 5 years 
↑ endometrial Ca
if use unopposed E2
175
Q

What are the effects of starvation/ anorexia nervosa upon hormones?

A 
↓ LH, ↓ FSH, 
↓ oestrogen / testosterone
↓ fertility, amenorrhoea
‘hypothalamic amenorrhoea’
makes ‘evolutionary sense’ in times of famine
Osteoporosis
Rx HRT / COCP
176
Q

Explain in terms of hyperglycaemia, how insulin deficiency can lead to CV collapse

A

Hyperglycaemia leads to hyper osmolality and glycusuria whcih in turn lead to severe dehyration, electrolyte loss, renal failure and CV collapse.

177
Q

Explain in terms of lypolysis, how insulin deficiency can lead to CV collapse

A

Increased rate of lypolysis and free fatty acids/ketone porduction. If supply is greater than demand from brain and muscle tissue ruslting affect will be acidosis that then causes CV collapse.

178
Q

How will the body ususally try to manage acidosis?

A

Intracellualr buffering via K/H ion pump
increased ventilation to breath off CO2 and lower pH
Incresed renal excretion of H+ ions

179
Q

In terms of electrolyte disturbances, what can the bodies managene t of ketoacidosis result in?

A

K+ depletion (possibly over 250mmol)
Sodium deplation
dehydration

180
Q

What pt group is most succeptable to diabetic ketoacidosis?

A

young T1DM

181
Q

name some precipitation factors of diabetic ketoacidisis x6

A 
Infections – pneumonia, urinary tract, viral illnesses, gastroenteritis
Error/ missed insulin administration
Myocardial infarction
Previously undiagnosed Type 1 diabetes
Drugs: steroids
Unidentified
182
Q

Symptoms of diabetic ketoacidosis caused by hypergycaemia and dehydration

A

Thirst and polyuria
Weakness and malaise
Drowsiness, confusion

183
Q

symptoms of diabetic ketoacidosis caused by acidosis

A

Nausea and vomiting
Abdominal pain
Breathlessness

184
Q

signs of diabetic ketoacidosis caused by hypergycaemia and dehydration

A

Dry mouth, Sunken eyes
Postural or supine hypotension
Hypothermia & Coma

185
Q

signs of diabetic ketoacidosis caused by acidosis

A

Facial flush
Hyperventilation
Smell of ketones on breath and ketonuria

186
Q

Clinical management of diabetic ketoacidosis 5 steps

A

Confirm diagnosis and check for precipitating causes
Rehydrate & monitor fluid balance
Iv fluids - saline with added potassium
Consider urinary catheter
Lower glucose
Intravenous insulin – fixed rate 0.1Unit/kg/hr
Monitor electrolytes
Potassium (and sodium)
Prevent clots
Prophylactic low molecular weight heparin

187
Q

What is most likely age group for Hyperosmolar Hyperglycaemic State?

A

40 plus

188
Q

What are the precipitation causes dor HHS?

A

previously undiagnosed,
steroids,
diuretics,
sugar

189
Q

Clinical managemt of HSS

A

Correct the profound dehydration

190
Q

4 Autonomic Symptoms of Hypoglycaemia

A

Sweating, feeling hot
Trembling or shakiness
Anxiety
palpitations

191
Q

Define hypoclycaemia

A

Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but is often used to describe a clinical state. The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopaenic’

192
Q

What are the 4 classifications of hypogycaemia?

A

Asymptomatic (Awake/sleeping)
Mild symptomatic (patient can treat himself)
Severe symptomatic (help needed by third party)
Coma and convulsions

193
Q

6 neuroglycopenic symptoms of hypoglycaemia

A 
Dizziness, light-headedness
Tiredness
Hunger, nausea
Headache
Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism
Coma and convulsions, hemiplegia
194
Q

Causes of hypoglycaemia

A

Insulin
Inappropriately excessive doses
Not eating, or insufficient carbohydrate
Sulfonylureas

195
Q

What factors help to counter regulate hypoglycaemia and how do they do this?

A

Glucagon stimulates glycogenolysis and gluconeogenesis ,

adrenaline increases glycogenolysis

cortisol and GH limit glucose disposal in peripheral tissues, but this effect takes several hours

196
Q

Treatment of hypoglycaemia (mild)

A

Minor episodes
20g carbohydrate as sugary drink, fruit juice, glucose tablets, glucose gels followed by something ‘starchy’ to eat
Glucose gels

197
Q

treatment of hypoglycaemic coma

A

im or iv Glucagon 1mg

iv dextrose 25g (150ml 10% glucose)

198
Q

What are the long term microvascular and macrovascular compliactions of diabeties mellitus?

A

Retinopathy
Neuropathy
Nephropathy

IHD
CVD
PVD

199
Q

What cells are related to the microvascular compliaction of DM?

A

Retinal endothelial cells
Mesangial cells of glomerulus
Schwann cells and peripheral nerve cells

200
Q

When are microvascular complications typically likely to presnt themselves in T1 and T2 DM?

A

May take years to develop so rare before 5 years of T1 DM and may be detected at presentation of T2 DM

201
Q

Why does DM affect the retina so acutely?

A

Low density of capillaries
Little functional reserve
Flow needs to respond to local needs

202
Q

What are the 4 Pathological Findings of Diabetic Retinopathy?

A

Loss of pericytes
Basement membrane thickening
Capillary closure
Ischaemia

203
Q

What are the 3 Clinical Stages of Retinopathy?

A

Non-proliferative
Proliferative
Macular Oedema

204
Q

What are the ways of managing and treating diabetic retinopathy?

A 
Diabetic control important
Blood pressure control important
Laser treatment (Pan retinal, Focal)
Intra-vitreal anti VEGF Ab
205
Q

What are the 3 types of neuropathy?

A

Peripheral neuropathy
Mononeuropathy
Autonomic neuropathy

206
Q

What 3 signs are indicative of peripheral neuropathy?

A

Muscle wasting in knuckles
Neuropathic ulcers on feet
Callus
Charcot foot

207
Q

5 signs of autonomic neuropathy?

A 
Gastroparesis
Postural hypotension
Erectile dysfunction
Gustatory sweating
Diarrhoea
208
Q

4 Pathological Findings of Diabetic Nephropathy?

A

Basement membrane thickening (Loss of negative charge )
Podocyte loss (Loss of integrity of filtration barrier)
Glomerular sclerosis
Mesangial expansion

209
Q

Management and treatment of diabetic nephropathy

A

Blood pressure control important
Blockers of RAS system preferred
Glucose control important but less so once overt proteinuria
Associated with increased CVD risk
Ultimately renal replacement / transplantation

210
Q

In plasma what % of testeron is bound and what to?

A

around 50% to albumin
44% sex hormone binding globulin
2% free

211
Q

What ate the two anatomical units within the testes?

A

Seminiferous tubules

Interstitium

212
Q

What do the seminiferour tubules produce?

A

inhibin B and anti-Müllerian hormone are synthesized by Sertoli cells and sperm

213
Q

What does the interstitium produce?

A

containing Leydig cells that produce androgens and peritubular myoid cells

214
Q

Describe/draw the The hypothalamic-pituitary-testicular axis

A

Pulsatile secretion of GnRH
Secretion of LH and FSH
LH and FSH are composed of two glycoprotein chains.
LH is involved in release of Testosterone
FSH is involved in spermatogenesis and Inhibin B secretion

215
Q

Describe testerone mechanism of action?

A

Steriod so passes through cell membrane where Androgen target cells generally convert testosterone to 5 α-dihydrotestosterone before it binds to the androgen receptor

216
Q

Give 5 functions of testerone?

A

Regulation of gonadotropin secretion by the hypothalamic-pituitary system
Initiation and maintenance of spermatogenesis
Formation of the male phenotype during embryogenesis
Promotion of sexual maturation at puberty and its maintenance thereafter
Increase in lean body mass and decrease in fat mass

217
Q

In terms of blood serum levels define primany and secondary hypoganadism

A

Primary hypogonadism: Testosterone below normal and the serum LHand/orFSH are above normal.
Secondary hypogonadism: Testosterone below normal and the serum LHand/orFSH are normal or low.

218
Q

7 causes of primary hypognoadism

A 
Klinefelter syndrome
Cryptorchidism
Infection-mump
Radiation
Trauma
Torsion
Idiopathic
219
Q

8 causes of secondary hypognoadism

A 
Congenital GnRH deficiency
Hyperprolactinemia
GnRH analog
Androgen
Opioids
Illness
Anorexia nervosa
Pituitary disorder
220
Q

Gestationl features of hypogonadism

A

First trimester – female genitalia to ambiguous genitalia to partial virilization
Third trimester – micropenis

221
Q

Symptoms/Signs of hypogonadism up tp 10

A

Incomplete sexual development, eunuchoidism
 Sexual desire & activity
 Spontaneous erections
Breast discomfort, gynecomastia
 Body hair (axillary & pubic),  shaving
Very small or shrinking testes (esp < 5 ml)
Inability to father children, low/zero sperm counts
 Height, low-trauma fracture, low BMD
 Muscle bulk & strength
Hot flushes, sweats

222
Q

Conditions with a High Prevalence of hypogonadism (Screening Suggested) up to 8.

A

Sellar mass, radiation to sella, other sellar disease
On meds that affect T production or metabolism
Glucocorticoids, ketoconazole, opioids
HIV-associated weight loss
ESRD and maintenance hemodialysis
Moderate to severe COPD
Osteoporosis or low trauma fracture (esp if young)
Type 2 diabetes mellitus
Infertility

223
Q

What signs should you look for upon examining someone with suspected hypogonadism?

A 
Amount of body hair
Breast exam for enlargement/tenderness
Size and consistency of testicles
Size of the penis
Signs of severe &amp; prolonged hypogonadism
Loss of body hair
Reduced muscle bulk and strength
Osteoporosis
Smaller testicles
Arm span
224
Q

what investigations would you carry out for suspected hypogonadism?

A 
Serum testosterone
LH/FSH
SHBG
LFT
Semen analysis
Karoyotyping
Pituitary function testing
MRI
DEXA scan
225
Q

What factors can lower SHBG?

A 
Moderate obesity
Nephrotic syndrome
Hypothyroidism
Use of
Glucocorticoids
Progestins
Androgenic steroids
226
Q

What can raise levels of SHBG?

A 
Aging
Hepatic cirrhosis
Hyperthyroidism
Anticonvulsants
Estrogens
HIV infection
227
Q

Treatment for hypoganaism and how can this be administered?

A

Testosterone
Gel
Injection
Buccal/Patch/Pellet

228
Q

WHat are the contraindiactions to testerone therapy?

A 
Breast or prostate cancer
Lump/hardness on prostate exam by DRE
PSA >3 ng/ml that has not been evaluated for prostate cancer
Severe untreated BPH (AUA/IPSS >19)
Erythrocytosis (hematocrit >50%)
Hyperviscosity
Untreated obstructive sleep apnea
Severe heart failure (class III or IV)
229
Q

Who does Gynecomastia affect?

A

Imbalance between androgen and estrogen
60% of boys during puberty – transient
30-70% in adult men

230
Q

Define Gynecomastia

A

Gynecomastia, a benign proliferation of the glandular tissue of the male breast
It may be unilateral or bilateral
diagnosed on exam as a palpable mass of tissue at least 0.5 cm in diameter (usually underlying the nipple).

231
Q

What can cause Gynecomastia?

A 
Persistent pubertal gynecomastia
Drugs
Idiopathic
Cirrhosis or malnutrition
Hypogonadism
Testicular tumour
Hyperthyroidism
Chronic renal insufficiency –Leydig cell dysfunction
232
Q

Investigations for gynaecomatia?

A 
Testosterone
LH/FSH
Prolactin
LFT/U&amp;Es
B-hCG
TFT
Estrogen
U/S-Mamogram
233
Q

Treatmet options for gynaecomatia

A

Conservative –Reassurance
Treatment of cause
Tamoxifen
Surgery

203 Endocrinology and Reproduction (3 decks)

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