Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > Adrenal > Flashcards

Adrenal Flashcards

1
Q

<p>Where do the adrenal glands sit?</p>

A

<p>Superior and medial to upper pole of kidneys</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

<p>What zones is the adrenal cortex organised into?</p>

A

<p>Zona : glomerulosa, fasciculata, reticularis </p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

<p>What is the function of the zona glomerulosa?</p>

A

<p>Production and secretion of mineralocorticoids and aldosterone</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

<p>What is the function of the zona fasciculata?</p>

A

<p>Production and secretion of glucocorticoids and cortisol</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

<p>What is the function of the zona reticularis?</p>

A

<p>Production and secretion of glucocorticoids and sex steroids</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

<p>What is the adrenal medulla innervated by?</p>

A

<p>Pre-synaptic fibres from sympathetic nervous system</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

<p>What is the medulla mainly composed of, and what do they secrete?</p>

A

<p>Chromaffin cells-secrete catecholamines</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

<p>What can cause adrenal hyperfunction?</p>

A

<p>Hyperplasia, adenoma, carcinoma</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

<p>What can cause adrenal hypofunction?</p>

A

<p>Acute: Waterhouse-Friderichsen, Chronic: Addison's disease</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

<p>What causes congenital adrenocortical hyperplasia?</p>

A

<p>Deficiency or lack of enzyme required for steroid biosynthesis</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

<p>What does the altered biosynthesis in congenital adrenocortical hyperplasia result in?</p>

A

<p>Increased androgen production-reduced cortisol stimulates ACTH release and cortical hyperplasia (10-15x weight)-leads to masculinisation and precocious puberty</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

<p>What causes acquired adrenocortical hyperplasia?</p>

A

<p>Endogenous ACTH production-pituitary adenoma (cushings), ectopic ACTH (paraneoplastic (SCLC)), bilateral adrenal enlargement, diffuse or nodular: diffuse ACTH driven, nodular usually ACTH independent</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

<p>In what population do adrenocortical tumours usually occur?</p>

A

<p>Adults (can be young (Li-Fraumeni syndrome), M=F</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

<p>How will someone with an adrenocortical tumour usually present?</p>

A

<p>Incidental finding, hormonal effects, mass lesion, carcinomas with necrosis can cause fever</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

<p>How do adrenocortical adenomas appear?</p>

A

<p>Well circumscribed, encapsulated lesions. Usually small:2-3cm. Yellow/brown surface. Cells resemble adrenocortical cells. Well differentiated, small nuclei, rare mitoses</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

<p>Are adrenocortical carcinomas more likely to be functional or non functional? </p>

A

<p>Functional </p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

<p>What can adrenocortical carcinoma resemble?</p>

A

<p>Adenoma- form a spectrum</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

<p>What is the spread of adrenocortical carcinoma?</p>

A

<p>Local-retroperitoneum, kidney. Metastasis-usually vascular (Liver, lung, bone), peritoneum and pleura, RLN</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

<p>What features suggest adrenocortical carcinoma?</p>

A

<p>Large size (>50g, often >20cm), haemorrhage and necrosis, frequent mitoses, atypical mitoses, lack of clear cells, capsular or vascular invasion</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

<p>What is primary hyperaldosteronism also known as?</p>

A

<p>Conn's syndrome</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

<p>Primary hyperaldosteronism is usually associated with what?</p>

A

<p>Diffuse of nodular hyperplasia of both adrenal glands (60%)</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

<p>What percentage of primary hyperaldosteronism cases are due to adenoma?</p>

A

<p>35%</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

<p>Describe adenomas causing primary hyperaldosteronism </p>

A

<p>Solitary, small, bright yellow and buried in gland-do not cause mass lesion. Spironolactone bodies. Do not suppress ACTH so adjacent and contralateral adrenal tissue is not atrophic. </p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

<p>What is secondary hyperaldosteronism ?</p>

A

<p>Increased renin-decreased renal perfusion, hypovolaemia, pregnancy</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

<p>What are the ACTH dependent endogenous causes of hypercortisolism?</p>

A

<p>ACTH secreting pituitary adenoma, ectopic ACTH (SCLC). (gives ruse to adrenal hyperplasia)</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

<p>What are the ACTH independent endogenous causes of hypercortisolism?</p>

A

<p>Adrenal adenoma (10%) or carcinoma (5%), non-lesional adrenal gland atrophies</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

<p>What are some causes of acute Primary Adrenocortical Insufficiency?</p>

A

<p>Rapid withdrawal of steroid treatment, crisis in patient's with chronic adrenocortical insufficiency due to stress e.g. infection or not increase steroid dose. Massive adrenal haemorrhage- newborn, anticoagulant treatment, DIC, septicaemic infection-Waterhouse Friderichsen</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

<p>What are the causes of chronic Primary Adrenocortical Insufficiency (Addison's)?</p>

A

<p>AI adrenalitis, Infections-TB, fungal (histoplasma), HIV e.g. MAI, Kaposi's, Metastatic malignancy-lung, breast. Unusual-amyloid, sarcoidosis, haemochromatosis </p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

<p>When do signs and symptoms of chronic Primary Adrenocortical Insufficiency present?</p>

A

<p>Once >90% of gland destroyed</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

<p>What are the symptoms/signs of Addison's?</p>

A

<p>Vague-weakness, fatigue, anorexia, nausea, vomiting, weight loss, diarrhoea. Pigmentation (raised POMC- not seen in hypopituitarism), low BP, abdo pain</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

<p>What are the biochemical changes in Addison's?</p>

A

<p>Decreased mineralocorticoids-K+ retention, Na+ loss, hyperkalaemia, hyponatraemia, volume depletion and hypotention. Decreased glucocorticoids-hypoglycaemia. </p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

<p>What are the adrenal medullary tumours?</p>

A

<p>Phaeochromocytoma, neuroblastoma</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

<p>When is neuroblastoma usually diagnosed?</p>

A

<p>18 months, 40% in infancy</p>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

<p>What are neuroblastomas composed of?</p>

A

<p>Primitive appearing cells but can show maturation and differentiation towards ganglion cells</p>

35
Q

<p>What are predictors of a poor outcome in neuroblastoma patients?</p>

A

<p>Amplification of N-myc and expression of telomerase </p>

36
Q

<p>What are phaeochromocytomas derived from and what d they secrete?</p>

A

<p>Chromaffin cells-secrete catecholamines</p>

37
Q

<p>What are phaeochromocytomas a cause of?</p>

A

<p>Hypertension (up to 90%)</p>

38
Q

<p>What complications are associated with phaeochromocytoma?</p>

A

<p>Cardiac failure, infarction, arrhythmias, CVA. </p>

39
Q

<p>How is phaeochromocytoma diagnosed?</p>

A

<p>Lab-detection of urinary excretion of catecholamines and metabolites</p>

40
Q

<p>If the phaeochromocytoma arises in the bladder, what is it associated with?</p>

A

<p>Micturition</p>

41
Q

<p>Why are phaeochromocytomas known as the 10% tumour?</p>

A

<p>10% extra adrenal (paragangliomas), 10% bilateral (up to 50 in familial cases), 10% biologically malignant, 10% not associated with HT, and 25% familial </p>

42
Q

<p>Where will a phaeochromocytoma likely metastasise too?</p>

A

<p>Skeletal metastasis-also RLN, liver and lung</p>

43
Q

<p>What do phaeochromocytoma cells characteristically form?</p>

A

<p>Nests (zellballen)</p>

44
Q

<p>What are the primary adrenal insufficiencies?</p>

A

<p>Addison's, congenital adrenal hyperplasia (CAH), adrenal TB/malignancy</p>

45
Q

<p>What are the secondary adrenal insufficiencies?</p>

A

<p>Due to lack of ACTH stimulation, Iatrogenic (excess exogenous steroid), pituitary/hypothalamic disorders </p>

46
Q

<p>What is Addison's disease?</p>

A

<p>AI destruction of adrenal cortext </p>

47
Q

<p>How is adrenal insufficiency diagnosed?</p>

A

<p>Biochemistry-decreased Na, increased K, hypoglycaemia. Short syncthen test, ACTH levels (should be increased), renin/aldosterone levels (increased renin, decreased aldosterone), adrenal autoantibodies</p>

48
Q

<p>How is a short synacthen test performed?</p>

A

<p>Measure plasma cortisol before and 30 mins after IV/IM ACTH injection. Normal: baseline >250nmol/l, post ACTH >550nmol/l</p>

49
Q

<p>How is adrenal insufficiency managed?</p>

A

<p>Hydrocortisone (cortisol replacement), fludrocortisone (aldosterone replacement)-education</p>

50
Q

<p>What is the commonest cause of secondary adrenal insufficiency?</p>

A

<p>Exogenous steroid use</p>

51
Q

<p>What are some examples of exogenous steroids that may lead to 2' adrenal insufficiency?</p>

A

<p>High dose prednisolone, dexamethasone, inhaled corticosteroid</p>

52
Q

<p>What are the differences in 2' adrenal insufficiency compared to Addison's?</p>

A

<p>Features similar except: skin pale (no increased ACTH), aldosterone production intact (RAAS)</p>

53
Q

<p>How is 2' adrenal insufficiency treated?</p>

A

<p>Hydrocortisone (replacement)</p>

54
Q

<p>What are the ACTH dependent causes of Cushing's?</p>

A

<p>Pituitary adenoma (cushings disease)68%, ectopic ACTH (carcinoid/carcinoma) 12%, ectopic CRH (</p>

55
Q

<p>What are the ACTH independent causes of cushing's syndrome?</p>

A

<p>Adrenal adenoma 10%, adrenal carcinoma 8%, nnodular hyperplasia 1%</p>

56
Q

<p>How is cushing's syndrome diagnosed?</p>

A

<p>Establish cortisol excess: overnight dexamethasone suppression test, 24 hr urinary free cortisol, late night salivary control, low dose dexa test, repeat</p>

57
Q

<p>What is the commonest cause of cortisol excess?</p>

A

<p>Prolonged high dose steroid therapy</p>

58
Q

<p>What does prolonged high dose steroid therapy lead to?</p>

A

<p>Iatrogenic cushing's syndrome-chronic suppression of pituitary ACTH production and adrenal atrophy</p>

59
Q

<p>What is primary aldosteronism?</p>

A

<p>Autonomous production of aldosterone independent of its regulators (AT2, K)</p>

60
Q

<p>What are the CV actions of aldosterone?</p>

A

<p>Increase cardiac collagen, cytokine and ROS synthesis, sodium retention, altered endothelial function, increased pressor response, increased sympathetic outflow</p>

61
Q

<p>What are the clinical features of primary aldosteronism?</p>

A

<p>Significant hypertension, hypokalaemia (in around 30%), alkalosis</p>

62
Q

<p>What is step 1 in PA diagnosis?</p>

A

<p>Confirm aldosterone excess (measure plasma aldosterone and renin and express as ratio (ARR), if raised investigate further with saline suppression test, failure of aldosterone to suppress by >50% with 2l of normal saline:confirms PA)</p>

63
Q

<p>What is step 2 in PA diagnosis?</p>

A

<p>Confirm subtype- adrenal CT to demonstrate adenoma, sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess</p>

64
Q

<p>What is the surgical management of PA?</p>

A

<p>Unilateral laparoscopic adrenalectomy (only if adrenal adenoma, and vein sampling confirmed), cure of hypokalaemia and HT in 30-70%</p>

65
Q

<p>What is the medical management of PA?</p>

A

<p>In bilateral adrenal hyperplasia- use MR antagonists (spironolactone or eplerenone)</p>

66
Q

What are the congenital adrenal hyperplasias?

A

Rare conditions associated with enzyme defects in the steroid pathway

67
Q

What is the commonest CAH?

A

21alpha hydroxylase deficiency (95%)

68
Q

How is 21a hydroxylase deficiency diagnosed?

A

Basal (or stimulated) 17-OH progesterone-supported by genetic analysis

69
Q

What is the presentation of classical CAH?

A

Males-adrenal insufficiency (2/3wks), poor wt gain, biochemical pattern (Addison’s). Females-genital ambiguity

70
Q

What is the presentation of non-classical CAH?

A

Hirsute, acne, oligomenorrhoea, precocious puberty, infertility or sub-fertility

71
Q

What are the principles of treatment of CAH?

A

Glucocorticoid replacement, mineralocorticoid replacement in some, surgical correction, control androgen excess, restore fertility

72
Q

What are some clinical features that can be indicative of a phaeochromocytoma?

A

Labile HT, postural hypotension, paroxysmal sweating, headache, pallor, tachycardia, or none of above!

73
Q

What is the classical triad of features in phaeochromocytoma?

A

HT (50% paroxysmal), headache, swelling

74
Q

What are the symptoms of phaeochromocytoma other than the classical triad?

A

Palpitations, breathlessness, constipation, anxiety/fear, wt loss, flushing-uncommon, incidental finding on imaging, family tracing

75
Q

What are the signs of phaeochromocytoma?

A

HT, postural HT in 50%, pallor, bradycardia, tachycardia, pyrexia

76
Q

What are the signs of complications in phaeochromocytoma?

A

LVF, myocardial necrosis, stroke, shock, paralytic ileus of bowel

77
Q

What biochemical abnormalities may you see in phaeochromocytoma?

A

Hyperglycaemia (adrenaline secreting tumours), low K, high haematocrit (i.e. raised Hb concentration), mild hypercalcaemia, lactic acidosis

78
Q

How is phaeochromocytoma diagnosed initially?

A

Confirm Catecholamine excess-urine :2x24hr catecholamine/metanephrins, plasma: ideally at time of symptoms

79
Q

How do you identify the source of catecholamine excess in phaeochromocytoma?

A

MRI scan-abdo, whole body. MIBG (meta-iodobenzylguanidine), PET scan

80
Q

How is phaeochromocytoma managed medically?

A

Full alpha/beta blockade (A before B)-phenoxybenzamine (alpha blocker), beta blocker. Fluid and/or blood replacement, anaesthetic assessment

81
Q

How is phaeochromocytoma managed surgically?

A

Laparoscopic-total excision where possible

82
Q

How is phaeochromocytoma managed if malignant?

A

Chemotherapy- radio-labelled MIBG

83
Q

What clinical syndromes are phaeochromocytoma associated with?

A

MEN2, VHL syndrome, succinate dehydrogenase mutations, NF, tuberose sclerosis

Endocrine (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions