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Medicine Year 2 > Scenario 16 > Flashcards

Scenario 16 Flashcards

1
Q

Defeciency of TRH is a …. Deficiency of thyroid axis?

A

3

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2
Q

A deficiency in TSH is a …. Deficiency of the thyroid axis

A

2

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3
Q

A deficiency in t3/4 is a …. Deficiency of the thyroid axis

A

1

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4
Q

A person with low T4 and high or low TSH is…

A

Hypothyroid

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5
Q

A person with high T4 and low/ normal TSH is

A

Hyperthyroid

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6
Q

A person with thyrotoxicosis has …

A

High T4 and low TSH

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7
Q

Hashimotos affects …% of the population?

A

3

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8
Q

Hashimoto’s thyroiditis is a disease resulting from….

A

Autoimmune Ig against thyroglobulin or thyroid peroxidase

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9
Q

What level of iodine leads to non-toxic goitre?

A

Less than 50 micrograms per day

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10
Q

2 drugs to treat hypothyroidism

A

Thyroxine and liothyronine

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11
Q

What is a goitrogen?

A

A substance that suppresses the function of the thyroid by interfering with iodine uptake

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12
Q

How long does it take for a person taking anti thyroid drugs to become euthyroid?

A

4-8 weeks

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13
Q

How long is treatment for graves with anti thyroid drugs maintained?

A

12-18 months

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14
Q

2 anti thyroid drugs

A

Carbimazole and propylthiouracil (prevent conversion from T4–>T3)
Side effects- neutropenia and agranulocytosis

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15
Q

What is used to treat hyperthyroidism by radiation and what is its half life?

A

Radio iodine and 8 days

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16
Q

When do you use radio iodine to treat hyperthyroidism?

A

Failed drug treatment, need for urgent treatment, toxic nodules

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17
Q

What sequence of events leads from iodine deficiency to hyperthyroidism?

A

Iron deficiency leads to decreased T4,thyroid cell hyperplasia, mutation of TSH receptor to constitutively active form

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18
Q

What cytokine induces bystander activation in autoimmune thyroid disease?

A

TNF alpha

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19
Q

What causes Graves?

A

Autoimmune Ig acting as TSH receptor agonist

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20
Q

What are the effects of cortisol?

A

Increase blood glucose levels, increase gluconeogenesis, increase the use of fatty acids for energy and decrease the use of glucose for energy

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21
Q

What does the zone glomerulosa secrete?

A

Aldosterone

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22
Q

What does the zone fasciculata secrete?

A

Cortisol

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23
Q

What does the zone reticularis secrete?

A

Weak androgens

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24
Q

What input does the adrenal medulla receive?

A

Cholinergic pre ganglionic sympathetic input

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25
Q

What does cortisol down regulate?

A

Release of ACTH from ant pit and CRH from hypothalamus

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26
Q

Which 2 factors up regulate CRH release from the hypothalamus and therefore cortisol?

A

Circadian rhythm and stress

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27
Q

In the adrenal gland which second messenger is activated by ACTH to stimulate the production of cortisol?

A

cAMP

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28
Q

What hormones are produced in the adrenal cortex?

A

Cortisol and aldosterone

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29
Q

What are the role of glucocorticoids?

A

Increase gluconeogenesis, protein breakdoen, increase osteoclasts activity and decrease glucose uptake into the cell, protein synthesis, osteoblasts activity, COX2 expression, cytokine production, nitric oxide production, histamine release, IgG production

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30
Q

Does cortisol or aldosterone have greater affinity for a mineralocorticoid receptor?

A

Equal

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31
Q

Which enzyme coverts cortisol into cortisone?

A

11betaHSD

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32
Q

When steroids enter the cell and bing to receptor what dissociated from the receptor?

A

Hsp90

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33
Q

Which element and amino acid are used to make T3 and T4?

A

Iodine and tyrosine

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34
Q

Thyroid epithelial cells secrete

A

Thyroglobulin

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35
Q

The thyroglobulin that accumulates is called

A

Colloid

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36
Q

When the thyroid is stimulated what do the follicular calls do to the iodinated thyroglobulin?

A

Endocrine them and break them down in lysosomes

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37
Q

Where in the thyroid is the iodinated thyroglobulin stored?

A

Lumen of the follicles

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38
Q

Which enzyme oxidises iodide to iodine in the thyroid?

A

Thyroid peroxidase

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39
Q

What effect to high iodine levels have on thyroid hormone synthesis?

A

Inhibition by inhibition of the iodide pump

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40
Q

What chemical class to the posterior pit hormones belong to?

A

Peptide

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41
Q

Release of GH is controlled by which hormones?

A

GHRH and somatostatin

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42
Q

What four physiological stimuli stimulate GH secretion?

A

Stress, exercise, sleep, post prandial glucose decline

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43
Q

When are GH levels at the peak?

A

Sleep stages 3-4

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44
Q

When are PRL levels at their peak

A

2 hours after sleep begins

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45
Q

When do ACTH levels reach their peak?

A

Before waking up

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46
Q

Which second messenger does the V1a and b (3) ADH receptor activate?

A

IP3 and DAG

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47
Q

Which second messenger does the V2 receptor activate?

A

cAMP

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48
Q

Where in the body are V1a

A

Blood vessels (vasoconstriction)

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49
Q

Where are V1b (3)?

A

Corticotrophs in the ant pit (increase ADH release)

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50
Q

Where are V2 receptors?

A

DCT and collecting tubule and duct of the nephron (increase h2O permeability)

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51
Q

Through which 2 mechanisms does ADH increase blood pressure?

A

Vasoconstriction and reabsorption of h2O in the nephron

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52
Q

What general effect do T3/4 have on the body?

A

Increase BMR

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53
Q

Is t3 or 4 more active

A

T3

54
Q

Which arteries supply the thyroid?

A

Superior and inferior thyroid

55
Q

What effects do thyroid hormone have?

A

Increase transcription, protein synthesis, na/k atpase, atp turnover, oxygen consumption, heat production, cardiac muscle contractility, gut motility, erythropoiesis, bone turnover, protein turnover

56
Q

What is the dietary iodine requirement?

A

150 micrograms/day

57
Q

What is the thyroid derived from?

A

Endoderm

58
Q

What is the half life of T3 and T4

A

1 day, 6 days

59
Q

Aldosterone is a…

A

Mineralocorticoid

60
Q

What tissue does aldosterone target?

A

DCT of the nephron

61
Q

What is the action of aldosterone?

A

Increases Na and Cl reabsorption in the kidneys and increased K and H secretion. also increases bp

62
Q

What effect do pregnancy, progesterone and prostaglandins have on aldosterone secretion?

A

Increase it

63
Q

What are 2 main causes of primary hyperaldosteronism?

A

Aldosterone producing adrenal adenoma, bilateral adrenal hyperplasia

64
Q

What does primary hyperaldosteronism present with classically?

A

Hypertension, hypernatraemia, hypokalaemia, alkalosis

65
Q

Which drugs are used to treat primary hyperaldosteronism?

A

Aldosterone receptor antagonist- spironolactone or eplerenone and K sparing diuretic (Amiloride)

66
Q

Primary aldosteronism is also called?

A

Conns syndrome (>30 aldosterone:plasma renin activity ratio)

67
Q

What chemical class does PTH belong to?

A

Peptide

68
Q

How are chief cells organised

A

Irregular cords around blood vessels

69
Q

…. Levels of calcium in the plasma up regulate PTH secretion

A

Low

70
Q

What GH producing tumour causes what?

A

Acromegaly

71
Q

Abnormally high levels of plasma PRL is caused by

A

Hyperprolactinaemia

72
Q

3 symptoms of hyperprolactinaemis in males and females?

A

Gynaecomastia, erectile dysfunction, infertility and for females galactorrhoea and infertility

73
Q

2 drugs to treat hyperprolactinaemia

A

Cabergoline, bromocriptine (D2 receptor agonists)

74
Q

4 pharmacological stimuli stimulate GH secretion?

A

Drug induced hypoglycaemia, amino acid infusion, small peptide hormones, monoamines

75
Q

Hypersecretion of GH before the fusion of long bone epiphyses results in

A

Gigantism

76
Q

Hypersecretion of GH after the fusion of long bone epiphyses results in

A

Acromegaly

77
Q

Hyposecretion of GH before the fusion of long bone epiphyses results in

A

Short stature

78
Q

Hyposecretion of GH after the fusion of long bone epiphyses results in

A

adult GH deficiency

79
Q

3 drugs to treat acromegaly

A

D2 receptor agonist- bromocriptine, cabergoline or somatostatin analogue (octreotride)

80
Q

2 drugs to treat small stature

A

recomninant human GH- somatotropin, recombinant human IGF-1- mecasermin

81
Q

Procedure for a GH stimulation test

A

Fast for 12 hours then give insulin/ arginine- should cause an increase in GH

82
Q

Procedure for a GH suppression test and normal result

A

Fast for 12 hours then give insulin/ arginine- should cause increase in GH

83
Q

2 other treatments to treat acromegaly

A

Surgery and radiotherapy

84
Q

Hypersecretion of ADH results in

A

SIADH

85
Q

Hyposecretion of ADH results in

A

Diabetes Insipidus

86
Q

What condition is SIADH related to?

A

Small cell carcinoma of the lung

87
Q

What does SIADH present with (3)

A

Fluid retention, hyponatraemia, urine osmolarity>serum osmolarity

88
Q

3 drugs to treat SIADH

A

Impairment of ADH signalling- demeclocycline, ADH receptor antagonists- Conivaptan (V1a/V2), Tolvaptan (V2)

89
Q

What is diabetes insipidus?

A

Polydipsia and poly uria with severely dilute urine and reduction in fluid intake having no effect on urine concentation. No glucose in the urine

90
Q

Drugs to treat central DI?

A

Desmopressin

91
Q

What does GH act on to stimulate bone growth?

A

Chondrocytes

92
Q

How is DI diagnosed?

A

Water deprivation test- no increase in urine osmolality

93
Q

What is the serum and urine osmolality in DI?

A

Serum >290m specific gravity

94
Q

What is nephrogenic ADH?

A

Lack of renal response to ADH

95
Q

Characteristics of peptide hormone secreting cell

A

Lots of rER, golgi and secretory vesicles

96
Q

Characteristics of steroid secreting cells

A

Lots of sER, mitochondria, lipid droplets

97
Q

Anatomy of the pituitary

A

Round 1cm diameter, connected to the floor of III ventricle by infundibulum just post to optic chiasma, lies in depression of the body of the sphenoid and is covered by dura

98
Q

What are the parts of the ant pit (adenohypophysis)

A

Pars distalis, pars tuberalis and pars intermedia

99
Q

What are the parts of the posterior pit (neurohypophysis)

A

Pars nervosa and infundibulum

100
Q

What class of hormones are ADH and oxytocin

A

Peptides

101
Q

How are ADH and oxytocin released?

A

Made in cell bodies of neurons in hypothalamus (supraoptic and paraventricular nuclei) and transported down axons to terminals where they are released into fenestrated capillaries on stimulation of the cell bodies. Accumulations of hormones within the axons are called Herring bodies

102
Q

Which ant pit pars distalis cells are acidophils?

A

Somatotrophs and Mammatrophs

103
Q

Which ant pit pars distalis cells are basophils?

A

Thryrotrophs, corticotrophs and gonadotrophs

104
Q

Which cells are in pars tuberalis of ant pit?

A

Gonadotrophs

105
Q

What does the pars intermedia secrete?

A

Melanocyte stim hormone

106
Q

How is the secretion of the ant pituitary regulated?

A

Neuroendocrine cells of hypothalamus whose axons project to the median eminence discharging into capillaries of pit portal vessels which bathe the cells of the ant pit

107
Q

What are the advantages of a portal system?

A

Need less releasing hormone, more immediate response, can use same hormones again somewhere else

108
Q

Which hormones are tyrosine derivatives?

A

Dopamine, adrenaline and thyroxine

109
Q

Which hormones are peptide hormones?

A

TRH, ACTH, PRL, insulin

Glycoprotein hormones- LH, FSH, TSH, hCG (alpha chain species specific, beta hormone specific)

110
Q

Which hormones are steroid hormones?

A

Mineralocorticoid- Aldosterone
Glucocorticoid- Cortisol
Sex- oestrogen, progesterone, testosterone

111
Q

What is bioassay

A

Good for determining biologically active hormone (intact animal, isolated tissues BUT problems

112
Q

What is radioimmunoassay

A

Antibody radioactively labelled hormone but too much RA waste

113
Q

What is ELISA

A

Antibody with associated enzyme- colour change

114
Q

What is ultradian release

A

period less than 24 hours

115
Q

What is circadian release

A

24 hours (eg cortisol)

116
Q

Infradian

A

Longer than 24 hours

117
Q

Seasonal

A

Prolactin

118
Q

What are adverse effects of glucocorticoids?

A

Suppression of response to infection, suppression of endogenous glucocorticoid production, metabolic effects, osteoporosis, iatrogenic Cushing’s syndrome

119
Q

What is Cushing’s?

A

Disease due to pit tumour, syndrome due to other reasons but both high cortisol

120
Q

What are the symptoms of Cushing’s

A

Easy bruiding, poor wound healing, muscle wasting, thinning of skin, increased abdominal fat, buffalo hump, moon face, osteoporosis, obesity, increased appetite, increased susceptibility to infection, infertility in women

121
Q

What are the treatments for Cushing’s disease?

A

Metyrapone- 11 beta hydroxylase inhbitor, Ketoclonazone, pasireotide, mifeprestone

122
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

123
Q

What are the symptoms of Addisons disease?

A

Muscular weakness (low BP, depression), anorexia, hypoglycaemia

124
Q

What is thryotoxicosis?

A

State of increased circulating thyroid hormone without knowing the source

125
Q

What are the signs and symptoms of thyrotoxicosis/ hyperthyroidism?

A

Hyperactivity, heat intolerance, sweating, palpitations, fatigue, weight loss, increased appetite, diarrhoea, polyuria, tachycardia, goiter, fine hair

126
Q

What are the s and s of hypothryroidism

A

cold intolerance, weight gain, constipation, dry skin, coarse hair, slow reflexes

127
Q

What is phaeochrocytoma?

A

tumour of adr medulla secreting NA,Adr- headaches, palpitations, chest pain, weight loss, hypertension

128
Q

What are the s and s of Graves disease?

A

weight loss, sweating, tremor, tachycarida, diarrhoea, goitre, exophthalmos and upper lid retraction

129
Q

What is goitre?

A

Abnormal swelling of the thryoid gland

130
Q

How do you define a disease as autoimmune?

A

Evidence of loss of immunological tolerance to self, clinical responsiveness to immune suppression and passive transfer of disease by immune effectors

Medicine Year 2 (19 decks)

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