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Medicine 3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the different types of intercellular messengers?

A 
Endocrine: hormone - blood - target cell
Autocrine: cell A - cell A
Paracrine: cell A - cell B
Neurodendocrine: neurotransmitter - blood - target cell
Neurotransmitter: nerve - nerve
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2
Q

Describe peptide hormones

A

Synthesised as a protein by the cell
Secreted by exocytosis
Travel free in the blood in active form
Short half life

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3
Q

Describe steroid hormones

A

Precursor molecule (e.g. cholesterol) and enzymes make the hormone
Released by simple diffusion
Hydrophobic so travel bound to protein (inactive)
Long half life

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4
Q

How do peptide hormones elicit a cell response?

A

Bind to membrane receptor (e.g. G-protein receptor) and lead to secondary messenger response inside cell

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5
Q

How do steroid hormones elicit a response?

A

Diffuse through target cell membrane and bind with either cytosolic receptor or to nuclear receptor (synthesis of required protein by cell)

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6
Q

How would you test for hyposecretion?

A

Stimulation test

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7
Q

How would you test for hypersecretion?

A

Suppression test

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8
Q

What is the embryological origin of the pituitary gland?

A

Ectodermal upgrowth from roof of primitive mouth (anterior lobe)
Neuroectodermal downgrowth of the brain (posterior lobe)

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9
Q

What is the blood supply to the pituitary?

A

Inferior and superior hypophyseal artery

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10
Q

What hormones does the hypothalamus secrete?

A

Releasing hormones - stimulate pituitary to release hormones e.g. corticotrophin releasing hormone (CRH), thyrotropin releasing hormone (TRH), gonadotrophin releasing hormone (GnRH), growth hormone releasing hormone (GHRH)

Somatostatin - stops pituitary releasing GH and TSH

Dopamine - prolactin inhibiting factor

Oxytocin and ADH - synthesised in hypothalamus but released in posterior pituitary

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11
Q

What hormones are secreted by the anterior pituitary?

A 
Thyrotropin (TH)
Luteinizing hormone (LH)
Follicle-stimulating hormone (FSH)
Growth hormone (GH)
Prolactin (PRL)
Adrenocorticotrophin (ACTH)
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12
Q

What hormones are secreted from the posterior pituitary?

A

ADH

Oxytocin

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13
Q

What hormones are secreted from the thyroid gland?

A

Thyroxine (T4)
Triiodothyronine (T3)
Calcitronin

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14
Q

What hormone is released from the parathyroid gland?

A

Parathyroid hormone (PTH)

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15
Q

What hormones are released from the adrenal medulla?

A

Adrenaline (epinephrine)

Noradrenaline (norepinephrine)

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16
Q

What hormones are released from the adrenal cortex?

A

Aldosterone
Cortisol
Androstenedione
Dehydroepiandosterone (DHEA)

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17
Q

What hormones are released from the pancreas?

A

Insulin
Glucagon
Somatostatin (SS)

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18
Q

How does the anterior pituitary (adenohypophysis) secrete hormones?

A

Releasing hormones from hypothalamic nerves secreted into capillary plexus
Hypophyseal portal vessels transport releasing hormones to secretory cells where pituitary hormones are secreted

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19
Q

How does the posterior pituitary (neurohypophysis) secrete hormones?

A

Supraoptic-hypothalamic nerve tract transports oxytocin and ADH from paraventricular and supraoptic nuclei in hypothalamus to inferior hypophyseal artery for secretion

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20
Q

What can an upward growth of a pituitary tumour cause?

A

Bitemporal hemianopia (loss of peripheral vision). Upwards compression of the optic chiasm by the pituitary

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21
Q

What can a lateral growth of a pituitary tumour into the cavernous sinus cause?

A

Opthalmoplegia (paralysis of eye movement) due to compression of CNIII, IV and VI, all involved in eye movement

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22
Q

What stimulates the hypothalamus to secrete growth hormone releasing hormone?

A

Stress, sleep, exercise

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23
Q

What are the direct metabolic effects of growth hormone (GH)?

A 
Lipolysis (increased [FFA])
Hepatic gluconeogenesis 
Inhibits glycogen synthesis
Increased BMR
Promotes long bone growth at epiphyseal plates
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24
Q

What hormone is growth hormone antagonistic to?

A

Insulin

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25
Q

What hormone is growth hormone synergistic with?

A

Cortisol

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26
Q

Describe stimulation and suppression of growth hormone release?

A

Stimulated by GHRH but suppressed by somatostatin and food intake (negative feedback from rise in FFA)

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27
Q

What is insulin-like growth factor 1 (IGF1)?

A

Released from the liver upon stimulation by GH. Negative feedback to hypothalamus and pituitary to regulate release of GH

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28
Q

What are the two types of growth hormone excess?

A

Gigantism - before bone epiphyseal plate fusion: increased linear bone growth leading to extremely tall final stature

Acromegaly - after epiphyseal plate fusion: no more linear growth so disproportionate growth

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29
Q

What are the clinical concerns with acromegaly?

A

Cardiac failure due to increased blood pressure

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30
Q

How would you test for GH excess?

A

Oral glucose administration. Would observe no reduction in GH levels

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31
Q

How would you treat growth hormone excess?

A

Somatostatin analogue drugs to suppress GH secretion
Dopamine agonists (if tumour secretes prolactin)
Radiotherapy to reduce tumour

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32
Q

What is caused by growth hormone deficiency?

A

In children - stunted growth

In adults - insidious presentation

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33
Q

How would you test for growth hormone deficiency?

A

Stimulation testing and identifying low serum IGF1

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34
Q

How would you treat GH deficiency?

A

Daily injection of hormone

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35
Q

What is the action of prolactin?

A

Support secretion of breast milk

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36
Q

How is prolactin secretion regulated?

A

Inhibited by dopamine

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37
Q

What stimulates prolactin secretion?

A

Thyrotropin releasing hormone (TRH)

Suckling, sleep, stress

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38
Q

What is the differential diagnosis for hyperprolactinaemia?

A

Pregnancy
Primary hypothyroidism (increased TRH due to fault in negative feedback from thyroid)
Stress
Drug treatment

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39
Q

How would you treat hyperprolactinaemia?

A

Dopamine agonists

Thyroxine (if due to hypothyroidism)

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40
Q

What are the effects of adrenocorticotrophic hormone (ACTH)?

A

Acts on adrenal cortex to stimulate conversion of cholesterol to cortisol or adrenal sex steroid precursors

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41
Q

How does ACTH elicit a response on its target cells?

A

Through G-protein coupled receptors to increase cellular cAMP

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42
Q

What stimulates the release of ACTH?

A

Corticotrophin releasing hormone (CRH) from hypothalamus.

Stress

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43
Q

What inhibits the release of ACTH?

A

Cortisol in a negative feedback loop from adrenal cortex

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44
Q

What is an excess of ACTH called?

A

Cushing syndrome

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45
Q

What happens in a patient with Cushing syndrome?

A

Overstimulation and enlargement of adrenal glands

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46
Q

What is Nelson syndrome?

A

After removal of the adrenal glands as a last resort to treat Cushing syndrome, there is no longer negative feedback to the pituitary by cortisol which leads to an enlargement of the pituitary adenoma

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47
Q

What are the effects of thyroid stimulating hormone (TSH)

A

Regulator of the thyroid gland. Act on thyroid follicular cell surface via G-protein receptor to increase intracellular cAMP

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48
Q

How is TSH production regulated?

A

By hypothalamic TRH levels

Secretion is inhibited by somatostatin

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49
Q

How does negative feedback of TSH work?

A

Decreased effectiveness of TRH by reducing receptor numbers

50
Q

What causes excess TSH levels?

A

Hypothyroidism (also causes increase TRH which increases FAH and PRL leading to increased testicular volume and galactorrhoea)

51
Q

What regulates LH and FSH secretion?

A 
Hypothalamic gonadotrophin releasing hormone (GnRH)
Stress and prolactin inhibit secretion
Negative feedback (and on GnRH) by hormones secreted by testis and ovaries
52
Q

What is the main cause of excess gonadotrophins?

A

Loss of negative feedback system

53
Q

What causes diabetes insipidus?

A

Decreased ADH secretion

54
Q

How would you distinguish between cranial diabetes insipidus and nephrogenic diabetes insipidus?

A

By giving the patient desmopressin (synthetic ADH analogue). If urine now concentrates, then it’s cranial but if not it’s nephrogenic.

55
Q

What are the effects of oxytocin?

A

Increases uterine contraction to expel fetus and placenta

Contracts mammary glands to expel milk

56
Q

How is oxytocin regulated?

A

Positive feedback by vaginal stretch. Further vaginal distension results in increased oxytocin secretion until birth

57
Q

What is the embryological origin of the adrenal cortex?

A

Epithelial cells lining the abdominal cavity of the developing embryo

58
Q

Which zones are different hormones synthesised in the adrenal cortex?

A

Zona glomerulosa - aldosterone
Zona fascialata - cortisol
Zona reticularis - sex steroid precursors

59
Q

How is cortisol transported in the blood?

A

Steroid hormone so bound to a protein: cortisol binding globulin (CBG)
Not stored, synthesised upon demand

60
Q

How does ACTH cause an increase in cortisol synthesis?

A

By increasing the flux of the cholesterol to cortisol pathway

61
Q

How is cortisol affect by circadian rhythm?

A

Sharp increase upon waking which slowly decreases throughout day until very low at night

62
Q

What is the function of cortisol?

A

To raise circulating FFA and glucose

Permissive action on adrenaline and glucagon which creates insulin resistance

63
Q

What is the effect of cortisol on muscle?

A

Catabolic effect reduce protein synthesis and result in atrophy

64
Q

What is the effect of cortisol on bone?

A

Shift cell type from osteoblasts (bone forming) to osteoclasts (bone reabsorbing). Predisposes osteoporosis

65
Q

What is the effect of cortisol on salt and water homeostasis and BP?

A

Increase Na+ reabsorption and K+ loss at DCT through mineralocorticoid receptors.
Increases GFR
Inhibits ADH
Increases BP by increasing sensitivity of vessels to catecholamines

66
Q

What is the effect of cortisol on growth and development?

A

Stimulates cell differentiation to mature phenotype
Stimulates lung surfactant production
Too much inhibits growth (Cushing syndrome)

67
Q

What are the effects of cortisol on the immune system?

A

Anti-inflammatory effect by suppressing T-lymphocytes and eosinophils (neutrophils rise)

68
Q

What type of hormones are produced in the innermost part of the adrenal cortex?

A

Sex precursor hormones - DHEA and androstenedione which are converted peripherally into androgens and oestrogens.

69
Q

What is the difference between primary and secondary hypoadrenalism?

A 
Primary = direct destruction of the adrenal gland
Secondary = loss of anterior pituitary corticotroph
70
Q

What is Addison disease?

A

Primary hypoadrenalism - autoimmune destruction of the adrenal cortex

71
Q

What are the common clinical signs of Addison disease?

A

Hyponatraemia and hyperkalaemia

72
Q

What is the treatment for Addison disease?

A

Pharmacological cortisol replacement (with caution not to give too much and cause hyperadrenalsim). Body loses ability to alter cortisol short term in response to stress

73
Q

How do you diagnose Cushing syndrome?

A

Dexamethasone suppression test - inhibits ACTH production (leading to reduced cortisol production). Cushing syndrome positive if 9am serum cortisol remains elevated

74
Q

How does the high dose dexamethasone suppression test localise glucocorticoid excess?

What would you do following this test?

A

If serum cortisol is suppressed >50% at 9am then anterior pituitary source
If serum cortisol is suppressed <50% at 9am then ectopic source or adrenal tumour

Scan either the pituitary or adrenal gland to visualise the tumour

75
Q

What is the treatment for Cushing syndrome?

A

Removal of tumour

76
Q

What can you expect following removal of tumours causing Cushing syndrome?

A

Signs of Addison disease as the body is not used to lower levels of cortisol and struggles to detect it. Cortisol therapy is needed post op

77
Q

What is Conn syndrome?

A

Tumours of zona glomerulosa of adrenal cortex resulting in excess aldosterone

78
Q

What are the signs of Conn syndrome?

A

Hypokalaemic hypertension

79
Q

How would you test for Conn syndrome?

A

Measure aldosterone levels but be aware of anti-hypertensives drugs such as ACE inhibitors as they will interfere with RAA system and will need to be stopped before testing

80
Q

How would you treat Conn syndrome?

A

Potassium soaring diuretic such as spironolactone which is an aldosterone receptor antagonist

81
Q

What is congenital adrenal hyperplasia and what does it cause?

A

Inherited condition causing mutation of genes that encode enzymes in pathway to cortisol. Causes reduced cortisol and high ACTH which leads to increased sex hormones

82
Q

How are glucocorticoids used therapeutically?

A

Premature labour to stimulate fetal lung surfactant production
Autoimmune and inflammatory disorders due to anti-inflammatory nature

83
Q

What is the embryological origin of the adrenal medulla?

A

Derived from neuroectoderm from vertebral column

84
Q

How doe adrenal medulla chromaffin cells respond to synaptic activation?

A

By releasing catecholamine hormones (noradrenaline and adrenaline)

85
Q

What is the process of catecholamine synthesis in the adrenal medulla?

A

Tyrosine is converted to dopamine which is then converted to noradrenaline. Noradrenaline is then either secreted or converted to adrenaline before excretion

86
Q

What is convention of noradrenaline to adrenaline dependent on?

A

Glucocorticoid, present in medulla due to centripetal drainage of venous blood from outer cortex

87
Q

How are catecholamine actions terminated?

A

Noradrenaline taken up by postganglionic sympathetic nerve terminals for metabolism by monoamine oxidase (MAO). Adrenaline taken up into platelets

88
Q

What are the actions of adrenaline?

A 
Increase systolic BP and heart rate
Circulation directed to limb muscle beds and away from gut
Decrease gut motility
Bronchodilation
Mydriasis (pupil dilation) 
Piloerection
89
Q

What are the actions of noradrenaline?

A

Increase systolic and diastolic BP

Decrease heart rate

90
Q

What are the synergistic actions of adrenaline and noradrenaline?

A

Fight or flight response. Raise BP, divert nutrients away from non essential organs, promote nutrient delivery to muscles active in fight or flight response, increase FFA, glycogenolysis and gluconeogenesis to increase blood glucose

91
Q

What is phaechromocytoma? How would you treat it?

A

Overactivity of the adrenal medulla due to tumour of the chromaffin cells. Treatment by blocking catecholamine receptors and surgical removal of the adrenal gland

92
Q

What is the blood supply to the thyroid?

A

Superior and inferior thyroid arteries (from external carotid and subclavian)

93
Q

Describe the histology of thyroid cells

A

Follicular cells with a colloid lumen

94
Q

What are the two thyroid hormones?

A

Thyroxine (T4)

Triiodothyronine (T3)

95
Q

What are the inactive forms of the thyroid hormones

A

Reverse T3

Diiodothyronine (T2)

96
Q

How does iodide enter the follicular cell if the thyroid?

A

By active transport via a I-/Na+ pump (both pumped in)

Na+ pumped out via Na+/K+ ATP pump

97
Q

What is thyroglobulin?

A

Glycoprotein substrate synthesised in the follicle cells of the thyroid. After synthesis, packaged into vesicles and released into colloid for synthesis of T3 and T4.

98
Q

How is thyroglobulin converted into thyroid hormones (T3 and T4)

A

Iodination catalysed by thyroid peroxidase (TPO)

99
Q

Which is the most active thyroid hormone?

A

T3

100
Q

How is TRH regulated?

A

Negative feedback from circulating T3

101
Q

How is T4 converted to the more active T3?

A

Via the deiodination selenodeiodinase enzymes (remove an iodine)

102
Q

What are the different types of selenodeiodinase?

A 
Type 1 (D1) - liver, kidney, muscle. Circulating T3
Type 2 (D2) - brain and pituitary. T3 negative feedback
Type 3 (D3) - T4 -> reverse T3
103
Q

What is the purpose of reverse T3?

A

When a cell has sufficient T3, switches to produce rT3 which is rapidly cleared

104
Q

How do thyroid hormones elicit a target cell response?

A

Bind to nuclear thyroid hormone receptor (TR), altering gene expression

105
Q

What effect does thyroid hormone have on the anterior pituitary?

A

Activate GH production and repress TSH production via negative feedback

106
Q

What other hormone is T3 synergistic with?

A

Catecholamines to increase heart rate

107
Q

What is a goitre?

A

Swelling of the thyroid gland

108
Q

What is primary hypothyroidism?

A

Underactivity of the thyroid gland - autoimmune destruction (Hashimoto’s thyroiditis)

109
Q

What is the function of thyroid hormones?

A

Increase metabolic rate

110
Q

What is the sign of primary hypothyroidism in a thyroid function test?

A

Elevated TSH and low T3 and T4

111
Q

How do you treat hypothyroidism?

A

Oral thyroxine with the goal to normalise TSH

112
Q

What should you consider before prescribing thyroxine to a patient with hypothyroidism?

A

Presence of Addison disease. If patient has Addison disease then increase of metabolic rate with thyroxine will increase demand for already inadequate cortisol supply

113
Q

What is secondary hypothyroidism?

A

Underactivity of anterior pituitary thyrotrophs with low TSH

114
Q

What is thyrotoxicosis?

A

Increased circulating thyroid hormones from hyperthyroidism

115
Q

What is Graves disease?

A

Autoimmune hyperthyroidism due to thyroid stimulating IgG antibodies activating TSH receptor

116
Q

What are the signs of hyperthyroidism in a thyroid function test?

A

Suppressed TSH and elevated T3 and T4. Elevated antithyroglobulin and antithyroid peroxidase

117
Q

How would you treat Graves’ disease?

A

Antithyroid drugs (carbimazole)
Surgery - thyroidectomy
Radioactive iodine (when no pregnancy or eye disease)
Beta-blockers (to reduce adrenergic excess)

118
Q

What is the concern for Graves disease in pregnancy?

A

Antithyroid drugs cross placenta and block fetal thyroid

Thyroid stimulating antibodies can cross placenta and cause fetal thyrotoxicosis

119
Q

What is thyroid eye disease (Graves orbitopathy)?

A

Swelling of the extraocular muscles of the orbit which leads to difficulty fully closing the eyes (staring appearance)

120
Q

What would you suspect in a patient with high T3 but no goitre?

A

Toxic adenoma of the thyroid gland (secretes T3)

121
Q

What is calitonin?

A

Hormone secreted from C-cells of thyroid gland with the action of reducing calcium

122
Q

What is parathyroid hormone (PTH)?

A

Hormone released from chief cells of parathyroid glands that increases calcium levels: increased calcium renal reabsorption, inhibits bone forming osteoblasts to release calcium into blood

Medicine 3 (8 decks)

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