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From Flashcardlet > Endocrinology > Flashcards

Endocrinology Flashcards

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0
Q

Hormones secreted from the anterior pituitary.

A

LH, FSH, GH, ACTH, TSH, Prl.

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1
Q

Major morphological feature of endocrine glands..

A

They are ductless - they release hormones directly into the blood stream.

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2
Q

Hormones secreted from the posterior pituitary.

A

Vasopressin / ADH, Oxytocin.

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3
Q

Non-classical endocrine glands includes..

A

production of hormones in tissues whose primary function is not Endocrine.

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4
Q

Examples of non-classical endocrine glands

A

Heart, liver, kidney, fat, brain, blood.

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5
Q

ACTH is produced in which cells and as what?

A

Pituitary corticotroph cells as the pro-hormone - Pro-opiomelanocortin (POMC)

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6
Q

POMC is processing in the …. to form the active form ACTH.

A

Golgi

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7
Q

Hormones are secreted directly into the systemic circulation except..

A

Hormones produced by the hypothalamus - released into hypophyseal portal system to bath anterior pituitary.

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8
Q

Major classes of membrane receptors for protein hormones

A

GPCRs and receptor Tyrosine kinases

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9
Q

StAR protein does what?

A

mediates transfer of cholesterol from outer to inner mitochondrial membrane

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10
Q

Distinguishing characteristic of endocrine system is…

A

Feedback control of hormonal production.

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11
Q

In order to assess endocrine status, need measurement of…

A

Simultaneous measurement of stimulatory and peripheral hormone to indicate where problem lies.

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12
Q

Primary gland hypofunction

A

Peripheral gland failure -> low peripheral hormone, high stimulatory hormone.

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13
Q

Secondary gland hypofunction

A

Stimulatory gland failure e.g. Pituitary -> low peripheral hormone, low stimulatory hormone.

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14
Q

The adenohypophysis is derived from…

A

(Anterior pituitary) derived from ectodermal tissue of pharynx.

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15
Q

Neurohypophysis is derived from…

A

(Posterior pituitary) derived from evagination of neural tissue from hypothalamus.

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16
Q

(anterior) Pituitary gland is covered superiorly by..

A

Diaphragma sellae

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17
Q

What hypothalamic hormones regulate Growth Hormone (somatotrophin) secretion?

A

Growth hormone releasing hormone (GHRH) positively acts on GH secretion, somatostatin has a negative effect.

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18
Q

What hypothalamic hormones regulate Prolactin secretion?

A

Dopamine negatively regulates secretion. Thyrotrophin releasing hormone has a minor positive effect on prolactin secretion, but mainly effects TSH secretion.

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19
Q

What hypothalamic hormones regulate Corticotrophin (ACTH) secretion?

A

Corticotrophin releasing hormone (CRH) and Vasopressin (AVP/ADH) both have a stimulatory effect on ACTH secretion.

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20
Q

What hypothalamic hormones regulate luteinising hormone (LH) and follicular stimulating hormone (FSH) secretion?

A

Gonadotrophin releasing hormone (GnRH / LHRH) positively regulates both their secretion.

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21
Q

5 main secretory cell types in anterior pituitary:

A 
Somatotrophs,
Lactotrophs,
Thyrotrophs,
Gonadotrophs,
Corticotrophs.
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22
Q

Which adenohypophysial hormones share a common alpha subunit?

A

TSH, LH and FSH. All are glycoproteins also.

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23
Q

Effects of GH on the periphery

A

Acts in the liver to stimulate production of somatomedins (IGF-1+2) which then cause metabolic changes throughout the body.

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24
Q

Effects of prolactin on the periphery.

A

Breast lactogenesis,

Increases no. LH receptors in testes/ovaries whilst inhibiting LH release from pituitary.

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25
Q

Tertiary endocrine glad disease…

A

Results from failure of hypothalamus to stimulate / inhibit pituitary

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26
Q

A single hormone measurement is inadequate for…

A

Pulsatile hormones, but adequate for hormones with long half lives e.g. T4

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27
Q

Which types of dynamic tests are used if hypo- or hyper-function is suspected?

A

Hypofunction - stimulation test.

Hyperfunction - suppression test.

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28
Q

Stimulation tests involve…

A

Administration of trophic hormone exogenously and/or stimulation of endogenous hormone.

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29
Q

Synacthen test assesses…

A

Cortisol reserve.

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30
Q

Insulin tolerance tests (ITT) assesses

A

GH and ACTH (cortisol) reserve.

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31
Q

Suppression tests involve…

A

Administration of exogenous hormone

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32
Q

Dexamethasone suppression test used if..

A

Cortisol hyper secretion suspected.

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33
Q

Oral glucose tolerance test used if…

A

Acromegaly suspected (GH hypersecretion)

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34
Q

What visual field defect do you often get with pituitary tumours?

A

Bitemporal hemianopia.

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35
Q

Excess corticotrophin causes…

A

Cushing’s disease

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36
Q

Excess thyrotrophin (TSH) causes..

A

Thyrotoxicosis.

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37
Q

Excess gonadotrophins cause..

A

Precocious puberty in children.

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38
Q

Excess prolactin causes..

A

Hyperprolactinaemia.

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39
Q

Excess somatotrophin causes…

A

Gigantism, acromegaly.

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40
Q

Commonest presenting feature of prolactinomas?

A

Galactorrhoa - 80%

Hypogonadism secondary to gonadotrophin suppression.

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41
Q

First line treatment for prolactinomas

A

Dopamine agonists - Bromocriptine, cabergoline

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42
Q

Cabergoline

A

DA2 receptor antagonist used to treat prolactinomas. Long half-life, orally admin 1-2 x week.

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43
Q

Unwanted effects of bromocriptine

A 
Nausea/vomiting/abdo cramps,
Psychomotor excitation,
Dyskinesias,
Postural hypotension,
Vasospasm in fingers and toes.
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44
Q

Untreated GH excess is associated with increased morbidity and mortality due to..

A

Cardiovascular (majority) and respiratory complications

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45
Q

First line treatment for GH secreting pituitary adenoma.

A

Surgery! Curative 75%

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46
Q

Medical treatments for GH secreting pituitary adenoma

A

Somatostatin analogues (octreotide), dopamine agonists in high doses (bromocriptine)

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47
Q

Clinical features of Cushing’s disease

A 
Truncal obesity,
Moon face,
Thin skin, easy bruising, straie,
Hirsuitism and acne,
Depression and psychosis,
Insomnia,
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48
Q

ACTH independent causes of Cushing’s syndrome

A

Primary adrenal adenoma or carcinoma,

Iatrogenic Cushing’s syndrome.

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49
Q

ACTH dependent Cushing’s syndrome

A

Cushing’s disease (ACTH pituitary adenoma)
Ectopic ACTH - oat cell tumour, carcinoid tumours, pheochromocytoma,
Ectopic CRH syndrome.

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50
Q

High dose dexamethasone suppression test can differentiate between…

A

Pituitary and adrenal/ectopic source of excess ACTH (pituitary adenoma usually suppresses)

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51
Q

Inferior petrosal sinus sampling (IPSS)

A

Confirms pituitary source of excess ACTH and lateralises tumour.

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52
Q

First line treatment for ACTH pituitary adenoma

A

Transphenoidal surgery - 70-80% cure/remission.
Total or hemi-hypophysectomy if tumour not visible.
Bilateral adrenelactomy if relapses after hypophysectomy.

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53
Q

Nelson’s syndrome

A

Aggressive expansion of ACTH secreting tumour due to loss of negative feedback of high cortisol level.

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54
Q

30% of pituitary tumours are…

A

Non-functioning. Present with hypopituitarism and visual disturbances.

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55
Q

Least common pituitary adenoma

A

Thyrotrope adenoma

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56
Q

Progressive loss of pituitary secretion in Panhypopituitarism often in which order?

A 
Gonadotrophins,
GH,
Thyrotrophin,
ACTH,
(Prolactin).
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57
Q

Sheehan’s syndrome

A

Panhypopituitarism developing acutely following post-partum haemorrage resulting in pituitary infarction.

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58
Q

Pituitary apoplexy

A

Panhypopituitarism due to intra-pituitary haemorrhage in patients with pre-existing pituitary tumours which suddenly infarct.

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59
Q

Lack of somatotrophin (GH) in children results in…

A

Pituitary dwarfism

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60
Q

Hormone replacement therapies for hypopituitism

A 
ACTH - hydrocortisone,
TSH - thyroxine,
Women LH/FSH - ethinyloestradiol + medroxyprogesterone,
Men LH/FSH - testosterone + undecanoate,
GH - GH,
Vasopressin - desmopressin.
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61
Q

The posterior pituitary mainly contains axons projecting from…

A

Supraoptic and paraventricular nuclei of the hypothalamus.

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62
Q

What type of neuron mainly terminate in the neurohypophysis?

A

Magnocellular neurons. Some parvocellular neurons terminate in the median eminence.

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63
Q

Supraoptic and paraventricular neurons are either…

A

Vasopressinergic or oxytocinergic.

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64
Q

Magonocellular neurons have…. along their axons.

A

Herring bodies

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65
Q

Steps of Vasopressin synthesis.

A

Pre-prohormone -> prohormone -> hormone.

Pre-provasopressin -> pro-vasopressin -> vasopressin + neurophysin + glycopeptide.

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66
Q

Vasopressin and oxytocin structure.

A

Nonapeptides that differ from each other by two amino acids.

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67
Q

Principle physiological action of vasopressin

A

Acts in the renal collecting ducts to stimulate water reabsorption -> antidiuretic.

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68
Q

Secondary actions of vasopressin

A

Vasoconstriction, corticotrophin release, CNS effects, neurotransmitter effects, synthesis of factor VIII and Von Willbrandt factor, hepatic glycogenolysis.

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69
Q

Vasopressin receptor types in kidney and vasculature

A

V1a -> arterial smooth muscle

V2 -> collecting duct cells

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70
Q

Different vasopressin receptors are linked to..

A

V1 -> phospholipase C

V2 -> adenyl cyclase

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71
Q

Vasopressin effects on collecting duct cells

A

Stimulates (via V2 R) synthesis and insertion of AQP2 channels.

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72
Q

Controls of vasopressin secretion

A

Plasma osmolarity and arterial blood pressure. Also influences from higher centres.

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73
Q

Actions of oxytocin

A

Stimulates myoepithelial cells of breast and myometrial cells of uterus to contract at appropriate times (lactation and parturition)

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74
Q

Uterine actions of oxytocin are suppressed and enhance by…

A

Suppressed by progesterone, enhanced by oestrogen. Most marked in late stages of pregnancy.

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75
Q

Secondary effects of oxytocin

A

Cardiovascular - transient vasodilation and tachycardia, constriction of umbilical arteries and veins.
Renal - anti-diuresis and secondary hyponatraemia.
CNS - maternal behaviour, social recognition.

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76
Q

Clinical uses of oxytocin

A

Induction of labour at term,
Prevention of post-partum haemorrhage,
Facilitation of milk let-down.

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77
Q

Lack of vasopressin causes

A

Diabetes insipidus

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78
Q

Types of diabetes insipidus

A

Central (lack of circulating vasopressin.

Nephrogenic (kidney vasopressin resistance.

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79
Q

With diabetes insipidus, plasma osmolarity is always…

A

On the high end of normal or high. With psychogenic polydipsia, it is on the low end of normal / low.

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80
Q

Excess vasopressin causes…

A

Syndrome of inappropriate ADH (SIADH)

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81
Q

Signs of SIADH

A

Increased urine osmolarity, decreased volume (initially),

Hyponatraemia.

82
Q

Administration of what drug can distinguish between central and nephrogenic diabetes insipidus?

A

Desmopressin (DDAVP)

83
Q

Selective V1 and V2 receptor agonists?

A

V1 - terlipressin

V2 - desmopressin (DDAVP)

84
Q

Drugs affecting vasopressin secretion

A

Nicotine increases secretion,

Alcohol and glucocorticoids decrease secretion.

85
Q

Clinical uses of V1 receptor agonists

A

Oesophageal varacies,

To prolong action of local anaesthetics.

86
Q

Treatment for nephrogenic diabetes insipidus

A

Thiazide diuretics - unknown mechanism!

87
Q

What happens to leptin levels with prolonged fasting?

A

Levels decline, more so in obese people

88
Q

Orexigenic neuropeptides

A

NPY, AgRP, MCH, Orexin.

89
Q

Anorexigenic neuropeptides

A

AlphaMSH, CART, BDNF, CRH, TRH.

90
Q

In the hypothalamus, leptin inhibits which cell population?

A

NPY/AgRP orexigenic neurons.
Leptin stimulates POMC/CART a orexigenic neurons.
Ghrelin has the opposite effect.

91
Q

Brainstem raphe nuclei affect food intake how?

A

Inhibit food intake by simultaneously inhibiting and stimulating NPY/AgRP and POMC neurons with serotonin, respectively. Serotonin reuptaken inhibitors reduces food intake.

92
Q

BMI ranges

A 
15-20 underweight
20-25 normal
25-30 overweight
30-40 obese
>40 morbidly obese
93
Q

Metabolic syndrome characteristic

A

Abdominal obesity, hyperinsulinemia, high fasting plasma glucose, impaired glucose tolerance, hypertriglyceridemia, low LDL-cholesterol, hypertension.

94
Q

Endocrine causes of obesity

A 
Hypothyroidism,
PCOS,
Cushing's syndrome,
GH deficiency,
Hypogonadism.
95
Q

Sibutramine

A

5HT/Na re-uptake inhibitor, appetite suppressant, increased HR/BP. (anti-obesity drug)

96
Q

How does roux-en-Y gastric bypass reduce appetite?

A

Increases anorexigenic hormones

97
Q

Half-life of insulin it the circulation

A

6 minutes

98
Q

How is mature insulin produced?

A

Preproinsulin has C-peptide cleaved off, then carboxypeptidase E produces mature insulin (all within secretory vesicle)

99
Q

Glucose sensor in beta cells

A

Glucose transported into cell via Glut2 receptor, increased in ATP depolarised cell leading to Ca influx which stimulates insulin release.

100
Q

Glucagon-like peptide 1 (GLP-1)

A

Stimulates insulin secretion and inhibits appetite and gastric emptying.

101
Q

Cellular effects of insulin

A

Stimulates MAPK pathway - cellular growth,
Stimulates PI3K pathway leading to insertion of GLUT4 receptors into membrane - glucose uptake into muscle and fat mainly.

102
Q

Other than insulin and glucagon, islet secrete…

A 
Pancreatic polypeptide,
Vasoactive intestinal polypeptide,
Ghrelin,
Gastrin,
Somatostatin.
103
Q

Hyperglycaemic crisis in diabetes mellitus type 2

A

Hyperosmolar hyperglycaemic state (HHS).

Diabetic ketoacidosis is seen with type I (but can occur with type II)

104
Q

Which type of diabetes mellitus has a stronger genetic component?

A

Type 2 DM

105
Q

Diabetic ketoacidosis occurs because…

A

Of a shortage of insulin, no inhibition to Hormone sensitive lipase -> increases ketogenesis. Vomiting and osmotic diuresis causes dehydration.

106
Q

Hyperglycaemic hyperosmolar state occurs because..

A

High plasma glucose causes osmotic diuretic leading to profound dehydration.

107
Q

Microvascular complications of T2DM

A

Retinopathy, nephropathy, neuropathy.

108
Q

What is HbA1c?

A

Non-enzymatic glycosylated product of Hb that can be used as a measure of average glycaemia over past 2-4 weeks.

109
Q

Which is the predominant collagen type in bone?

A

Type 1

110
Q

Two types of bone formation.

A

Endochondral ossification - long bones.

Intramembranous ossification - craniofacial bones.

111
Q

Bone resorption and bone formation are by which cells?

A

Resorption - osteoclasts

Formation - osteoblasts

112
Q

How do osteoclasts reabsorb bone?

A

Secrete hydrogen ions to dissolve bone mineral and secrete MMPs and cathepsin K to degrade collagen matrix.

113
Q

Bone mineral

A

Hydroxyapatite.

114
Q

Regulation of PTH synthesis

A

Extracellular Ca inhibits transcription and secretion via CaSR.
1,25(OH)2D increases CaSR expression.
Magnesium inhibits PTH release (including prolonged hypomagnesemia).
Catecholamines and hyperphosphatemia stimulate PTH.

115
Q

PRH regulation of Ca in the kidney

A

PTHR1 in kidney

  • inhibits phosphate resorption
  • stimulates 1,25(OH)2D
  • stimulates calbindin -> ca resorption
116
Q

Which bone cells express PTHR1?

A

Osteoblasts and osteocytes, NOT osteoclasts.

117
Q

PTH action in the bone.

A

Continuous PTH -> net cortical resorption
Intermittent PTH -> net trabecular formation
Increases osteoclast differentiation via increase RANKL expression in osteoblasts.

118
Q

Active form of vitamin D

A

1,25(OH)2D

119
Q

Livers roles in active vitD formation

A

Turns VitD into 25(OH)D, which the kidney then turns into 1,25(OH)2D.

120
Q

1,25(OH)2D action in the gut

A

Enhances Ca and phosphate absorption.

121
Q

1,25(OH)2D effect in kidney

A

Increases Ca reabsorption and PTH sensitivity via PTHR1 expression.

122
Q

1,25(OH)2D inhibits…

A

PTH synthesis and release.

It’s own synthesis.

123
Q

FGF23 regulation of phosphate

A

Inhibits phosphate reabsorption from kidney,
Inhibits synthesis of 1,25(OH)2D,
Enhances 1,25(OH)2D inactivation.

124
Q

Physiological response to high Ca

A

Reduced PTH secretion, and inhibition of VitD activation. This decreased Ca absorption in gut and kidney and bone resorption.

125
Q

Defect in familial hypocalciuric hypercalcaemia

A

Loss of function of CaSR. Autosomal dominant.

126
Q

80% of humeral hypercalcaemia of malignancy is due to…

A

Ectopic secretion of PTHrP. Frequently life threatening Ca level.

127
Q

Mechanisms of hypocalcaemia

A

PTH or vitD deficiency or resistance.

128
Q

DiGeorge syndrome

A

Failure of parathyroid development

129
Q

Difference between hypoparathyroidism and pseudohypoparathyroidism

A

PTH deficiency versus PTH resistance.

130
Q

Mutations in pseudohypoparathyroidism affect…

A

GNAS locus - G-alpha-s protein.

131
Q

Risk factors for vitD deficiency

A

South asian and Afro-Caribbean ethnic origin,
Diet,
UV exposure.

132
Q

VitD deficiency during growth causes

A

Rickets - hypocalcaemia and hypophosphataemia during growth.

133
Q

VitD deficiency in adults causes…

A

Osteomalacia - reduced osteoid mineralisation (soft bones)

134
Q

Which populations of cells response to LH and FSH in the testes?

A

Sertoli cells respond to FSH by producing inhibin.

Leydig cells respond to LH by producing testicular androgens.

135
Q

Which enzymes convert circulating testosterone to active hormones?

A

5-alpha-reductase converts to dihydrotestosterone (DHT).

Aromatase converts to 17-beta-oestradiol (E2).

136
Q

Estriol

A

Principle estrogen during pregnancy

137
Q

Major estrogen in non-pregnant women?

A

17-beta-oestradiol (E2)

138
Q

SERMs are…

A

Selective oestrogen receptor modulating drugs. Don’t have classical steroid structure, tissue specific actions.

139
Q

Clomiphene

A

Fertility drug - binds to oestrogen receptors in hypothalamus blocking -ve feedback.

140
Q

Raloxifene

A

Used for treatment and prevention of postmenopausal osteoporosis.

141
Q

Activation and capacitation of spermatozoa occur…where?

A

Activation occurs in the vas deferens (mobility and limited capacity to fertilisation)
Capacitation occurs within the oviduct (full activity and fertilisation capacity)

142
Q

Zygote divides to form the initial 2 cell….

A

Conceptus

143
Q

Decidualisation reaction is where…

A

Trophoblast cells of the blastocyst invade the underlying uterine stromal tissue. Requires progesterone domination + oestrogen.

144
Q

Infertility defined as…

A

The inability to conceive after 1 year of regular unprotected sex.

145
Q

Clinical features of male hypogonadism

A

Loss of libido, impotence, small testes, decreased muscle bulk, osteoporosis.

146
Q

Kallmans syndrome

A

Genetic disorder characterised by hypogonadism and anosmia (no sense of smell)

147
Q

Azoospermia

A

Absence of sperm in ejaculate. Oligospermia is reduced numbers

148
Q

Primary amenorrhoea definition

A

Failure to begin spontaneous menstruation by age 16

149
Q

Secondary amenorrhoea definition

A

Absence of menstruation for 3 months in a women who has previously had cycles.

150
Q

PCOS diagnostic criteria

A

2 of;
Polycystic ovaries on ultrasound,
Oligo- / anovulation
Clinical / biochemical androgen excess

151
Q

Clinical features of PCOS

A

Hirsuitism,
Menstrual cycle disturbance,
Increased BMI.

152
Q

Premature menopause / ovarian failure occurs before the age of..

A
  1. It occurs in 1% of women.
153
Q

Oestrogen only HrT is for…

A

Women who have had a hysterectomy - no risk of endometrial cancer. If haven’t, combined HRT (oestrogen + progesterone)

154
Q

Tibolone

A

Synthetic prohormone. Oestrogenic, progesterogenic and weak androgenic actions.

155
Q

Where does the thyroid gland originate from?

A

As an outpouching of pharyngeal floor, from where it then descends to the trachea.

156
Q

The two lateral lobes of the thymus gland are connected by the…

A

Isthmus

157
Q

What cell type secretes calcitonin?

A

Parafollicular C-cell in the thyroid gland.

158
Q

Which enzyme couples 2 pairs of tyrosyl residues together?

A

TPO (thyroid peroxidise)

159
Q

T3 and T4 are respectively formed from…

A

Coupling of MIT and DIT.

Coupling of DIT and DIT.

160
Q

How is T3 generated in periphery?

A

From T4 by 5’-deiodination

161
Q

Respective half lives of T4 and T3

A

7 days

1 day

162
Q

Which plasma protein is the majority of thyroid hormones bound to?

A

Thyroid binding globulin

163
Q

What kind of molecules are deiodinases?

A

Selenoproteins with selenocyctine in the active site.

164
Q

How are deiodinases controlled by thyroid hormone?

A

D1 + D3 activity increased by thyroid hormone.

D2 activity is inhibited.

165
Q

Which deiodinase Inactivates T4/T3?

A

Type 3 (D3)

166
Q

Intracellular supply of active thyroid hormone is controlled by…

A

Local expression of D2 (activating) and D3 (inactivating).

167
Q

Major tissue effects of thyroid hormones

A

Promote differentiation and inhibit proliferation. Increased basal metabolic rate also.

168
Q

Which thyroid hormone is the key regulator of TRH (thyrotrophin releasing hormone)?

A

T4 as it can access the TRH neurons via the CSF.

169
Q

Autoimmune thyroid destruction aka

A

Hashimoto’s thyroiditis

170
Q

Neonatal hypothyroidism

A

Failure of thyroid development, inborn errors of thyroid hormone synthesis.

171
Q

Cretinism results from…

A

Severe iodine deficiency in childhood. Causes growth arrest, deaf mutism, mental retardation

172
Q

Guthrie test

A

Newborn screen for elevated TSH

173
Q

Commonest form of thyrotoxicosis

A

Graves Disease - TSHR antibodies

174
Q

De Quervain’s thyroiditis caused by..

A

Acute viral inflammation. Initial symptoms oh thyrotoxicosis followed by hypothyroidism.

175
Q

Plummer’s disease aka..

A

Toxic multinodular goitre (MNG).

176
Q

Gestational thyrotoxicosis (GTT) results from…

A

Promiscuous activation of TSHR by hCG during first trimester pregnancy (4% - twins)

177
Q

Treatment for hyperthyroidism

A

Thionamides/thioureylene -> inhibit thyroperoxidase (TPO)

All patients must be given advice regarding agranulocytosis side effects.

178
Q

Most frequent type of thyroid cancer…

A

Papillary thyroid cancer (80%), followed by follicular thyroid cancer (10%)

179
Q

The adrenal cortex can be divided into..

A 
From the outside in...
Zona glomerulosa,
Zona fasciculata
Zona reticularia.
At the centre is the adrenal medulla.
180
Q

What do the adrenal medulla and cortex secrete?

A

Adrenal medulla -> catecholamines

Adrenal cortex -> corticosteroids

181
Q

Which section of the adrenals secretes mineralocorticoids?

A

Zona Glomerulosa secretes aldosterone.

182
Q

What plasma protein does the majority of cortisol bind to?

A

Cortisol binding globulin (CBG) also binds aldosterone.

183
Q

Where does aldosterone have it’s main effect?

A

In the distal convoluted tubule and cortical collecting duct where it stimulates Na reabsorption and K + H secretion.

184
Q

What stimulates aldosterone production?

A

Angiotensin II, raised plasma K, decreased plasma Na and ACTH.

185
Q

Effects of large amounts of cortisol

A

Anti-inflammatory, Immunosuppressive, Anti-allergic.

All due to inhibition of migration of inflammatory cells, cytokine release and leukocyte production.

186
Q

Cortisol blocks the production of…

A

Prostaglandins from arachidonic acid -> anti inflammatory effects

187
Q

Adrenal androgens are synthesised in the…

A

Zona reticularis.

188
Q

Adrenal medulla is derived from…

A

Ectodermal neural crest.

189
Q

Catecholamines are degraded by which hepatic enzymes?

A

Monoamine oxidase and catechol-O-methyl transferase.

190
Q

Which zone of the adrenals predominantly produces cortisol?

A

Zona fasciculata

191
Q

Commonest causes of Adrenocortical failure

A

Tuberculous Addison’s disease (worldwide)
Autoimmune Addison’s disease (UK)
Congenital adrenal hyperplasia.

192
Q

Consequences of Adrenocortical failure

A

Fall in BP, increased plasma K, fall in glucose, high ACTH (causing increased pigmentation), death due to severe hypotension.

193
Q

How does Adrenocortical failure result in increased pigmentation?

A

ACTH produced by breakdown pro-opio melanocortin (POMC) in pituitary. Increased ACTH secretion results in more breakdown of POMC, and hence production of melanocyte stimulating hormone also (MSH) which increases pigmentation.

194
Q

Short synACTHen test

A

Intramuscular injection of 250 mcg synacthen. Cortisol response should exceed 550nmol/L

195
Q

Treatment for Addison’s disease.

A

Hydrocortisone to replace cortisol,

Fludrocortisone to replace aldosterone.

196
Q

Commonest cause of congenital adrenal hyperplasia

A

21-hydroxylase deficiency, complete or partial.

197
Q

With 21-hydroxylase deficiency, which hormones are deficient?

A

Lack of aldosterone and cortisol, and an excess of sex steroids.

198
Q

Clinical features of Cushings

A 
Centripetal obesity,
Moon face and buffalo hump,
Proximal myopathy,
Hypertension and hypokalaemia,
Red striae, thin skin and bruising,
Osteoporosis and diabetes.
199
Q

Failure to suppress low dose dexamethasone test =

A

Any cause of Cushing’s syndrome

200
Q

Medical inhibitors of cortisol synthesis

A

Metyrapone and ketoconazole.

201
Q

Conn’s syndrome

A

Tumour of adrenal cortex (z.glomerulosa) -> primary hyperaldosteronism. Hypertension and hypokalaemia.

202
Q

Management of pheochromocytoma

A

Alpha blockade to reduce arterial constriction, then beta blockage to prevent tachycardia. Prepare for surgery.

From Flashcardlet (6 decks)

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