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Endocrinology > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Where are mineralocorticoids produced?

A

Zona glomerulosa

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2
Q

Where are glucocorticoids produced?

A

Zona fasciculata

regulated by ACTH

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3
Q

Where are androgens produced?

A

Zona reticularis

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4
Q

Wehere are catecholamines produced?

A

Medulla

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5
Q

What regulates aldosterone?

A

Renin-angiotensin system and plasma potassium

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6
Q

What does angiotensin II do?

A

Causes vasoconstriction and stimulates release of aldosterone from adrenals

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7
Q

Name a vitamin which is a steroid?

A

Vitamin D is a steroid

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8
Q

Immunological effects of cortisol?

A

Increases capillary permeability
Increases macrophage activity
Increases inflammatory cytokine production
Increases leucocyte migration

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9
Q

Metabolic effects of cortisol?

A

Increases lipolysis, central redistribution
Increases break down of carbohydrate (increases blood sugar)
Increases proteolysis

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10
Q

Circulatory/renal effects of cortisol

A

Increases cardiac output
Increases blood pressure
Increases renal blood flow and GFR

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11
Q

Cortisol effects on bone/connective tissue

A

Accelerates osteoporosis
Decreases serum calcium
Decreases collagen formation
Decreases wound healing

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12
Q

Aldosterone and Na+?

A

Aldosterone increases reabsorption of Na+

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13
Q 
21 year old female
‘unwell’ for few months
Weight loss
Amenorrhoea
Acutely unwell over past 48 hours with vomiting and diarrhoea
On examination:
Dark skin
Dehydrated
Hypotensive
Decreased Na Increased K
A

Addisons

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14
Q

Commonest cause of secondary adrenal insufficiency?

A

Exogenous steroid use
e.g. high dose prednisolone
inhaled corticosteroid
dexamethasone

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15
Q

Aldosterone replacement?

A

Fludrocortisone

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16
Q

Cortisol replacement

A

Hydrocortisone

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17
Q

Might you see acne amenhorrea and hypertension in Cushing’s?

A

Yes

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18
Q

Main cause of Cushing’s?

A

-Taking too much steroid (= chronic suppression of pituitary ACTH and adrenal atrophy)
Pituitary adenoma
(then ectopic ACTH e.g. in carcinoid/carcinoma)

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19
Q

Types of cancer that produced ACTH?

A

Carcinoid/carcinoma

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20
Q

Possible complications of long term steroid and ACTH suppression?

A

Body is unable to respond to stress (illness/surgery)

Need extra doses of steroid when ill/surgery

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21
Q

Hypertension and hypokalaemia?

A

Could be primary aldosteronism

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22
Q

Difference between primary and secondary hyperaldosteronism

A

Primary hyperaldosteronism = excessive levels of aldosterone independent of renin-angiotensin system
Secondary hyperaldosteronism = excessive levels of aldosteronism because of high renin levels

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23
Q

Cardiovascular effects of aldosterone

A 
Altered endothelial function
Increase in ROS and cytokine synthesis
Increased cardiac collagen
Increased blood pressure
Sodium retention
Increased sympathetic outflow
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24
Q

Commonest secondary cause of hypertension?

A

Primary aldosteronism (essential hypertension is most common primary cause)

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25
Q

Somebosy presents with hypertension, hypokalaemia and cramps (because of alkalosis) what might they have?

A

Hyperaldosteronism

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26
Q

Con’s syndrome

A

Adrenal adenoma (produces aldosterone)

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27
Q

Causes of hyperaldosteronism?

A 
Conns syndrome (adrenal adenoma)
Bilateral adrenal hyperplasia --> MOST COMMON CAUSE (unilateral is rare)
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28
Q

KCNJ5 mutations?

A

May lead to primary aldosteronism

=allows more sodium into cell and depolarisation etc

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29
Q

Management of primary aldosteronism?

A 
Surgical
Unilateral laparoscopic adrenalectomy
Only if adrenal adenoma (and excess confirmed in adrenal vein sampling)
Cure of hypokalaemia
Cures hypertension in 30-70% cases
Medical
In bilateral adrenal hyperplasia
Use MR antagonists (spironolactone or eplerenone)
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30
Q

CAH

A

Congenital adrenal hyperplasia
21 a hydroxylase
Autosomal recessive

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31
Q

Management of hypercalcemia?

A

Fluids
Frusemide
Bisphosphonates

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32
Q

Where do papillary thyroid cancers occur?

A

In iodine rich areas

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33
Q

Do follicular adenoma and carcinoma share the same architecture?

A

Yes, difficult to distinguish

Excisional biopsy may be required

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34
Q

Which type of thyroid cancer are related with MEN?

A

Medullary carcinomas are related with MEN

They originate from parathyroid follicular C cells and secrete calcitonin

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35
Q

Which type of thyroid cancers originate from parathyroid follicular C cells and secrete calcitonin?

A

Medullary

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36
Q

How do follicular thyroid cancers spread

A

Via blood

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37
Q

Can phaechromoctyoma lead to diabetes?

A

Yes

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38
Q

Most common cause of death in acromegalics?

A

Cardiovascular disease

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39
Q

Is acne common in acromegaly?

A

Yes

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40
Q

Cardiovascular disease seen in acromegaly?

A

Fibrosis, hypertrophy, carditis

VALVE DISEASE IS NOT COMMON

41
Q

Growth in children with Cushing’s?

A

Growth is often arrested due to excess steroid

42
Q

Causes of SIADH?

A

C, C, C
Chest: pneumonia, TB, carcinoma, abscess
Cranial causes: head injury, intracranial bleed, meningoencephalitis, space occupying lesions
CHLORPROPRAMIDE and other drugs

43
Q

Drugs which could cause gynaecomastia?

A

Sprionolactone

Methyldopa

44
Q

Visual field loss, sweaty greasy skin, large tongue, difficulty with dentures (because of jaw or something), spade shaped hands. Who am I

A

Acromegaly

45
Q

Congenital heart disease can cause growth retardation?

A

Pastest says yes

46
Q

Diabetic nephropathy and death?

A

Responsible for 25% of diabetic deaths under the age of 30

47
Q

Is diabetic nephropathy commonly associated with coronary artery disease?

A

yes

48
Q

Drug which you should give to diabetics, can help slow down proteinuria etc

A

ACE INHIBITOR OMG

49
Q

Amylase levels in diabetic ketoacidosis

A

Usually raised

50
Q

Hypothyroidism and Down Syndrome?

A

Hypothyroidism is common in people with Down Syndrome

51
Q

Salt wasting form of CAH

A

Weight loss, extreme tiredness, dehydration, vomitting

52
Q

Virilising form of CAH

A

-Recognised at 2-4 years
Early virilisation
Penis enlargement
Growth of hair

53
Q

Non-classical form of CAH

A 
Less severe
Develop sexually at an early age
-Hirsutis
-Acne
-Oligomenorrhea
-Precocious puberty
-Infertility or subfertility
54
Q

Diagnosis of CAH?

A

Basal or stimulated 17-OH-Progeseterone

Genetic being used more

55
Q

Sources of phaeochromocytoma

A

Phaechromocytoma in adrenal medulla

rarely = sympathetic chain –> paraganglioma

56
Q

Chromaffin cell reaction colour

A

Chromaffin cells reduce chrome salts to metal chromium resulting in a brown colour reaction

57
Q

Phaechromocytoma symptoms?

A 
Classic triad: sweating, hypertension, headache
Labile hypertension
Postural hypotension
Paroxsymal sweating, headache, pallor, tachycardia
(chromaffin cells reduce chrome salts to metal chromium resulting in a brown colour reaction)
-Try to diagnose Phaechromocytoma! Risks in pregnancy and other risks for everyone relating to arrythmia and ischemia --> could cause death etc
Palpitations
Breathlessness
Constipation
Anxiety/Fear
Weight loss
Hypertension
Postural hypotension in 50% cases
Pallor
Bradycardia and Tachycardia
Pyrexia
Signs of complications
Left ventricular failure
Myocardial necrosis
Stroke
Shock
Paralytic ileus of bowel
58
Q

Differentials for Phaeochromocytoma

A 
Angina
Anxiety
Carcinoid
Thyrotoxicosis
Insulinoma
Menopause
Arrhythmia( eg. SVT)
Migraine
Drug toxicity
Alcohol withdrawal
Pregnancy
Hypoglycaemia
Mastocytosis
Autonomic neuropathy
Factitious
59
Q

Biochemical Abnormalities in Phaeochromocytoma

A

Hyperglycaemia – adrenaline secreting tumours
May have low potassium level
High haematocrit – i.e. raised Hb concentration
Mild hypercalcaemia
Lactic acidosis – in absence of shock

60
Q

The 10% tumour

A 
Phaeochromocytoma
10% malignant
10% extra-adrenal [probably 20-30%]
10% bilateral
10% associated with hyperglycaemia
10% in children
10% familial (but probably 25%)
61
Q

Hypertension and hyperglycemia?

A

Consider phaeochromocytoma

62
Q

Diagnosis of Phaeochromocytoma/catecholamine excess

A

-2 x 24 hour urine catecholamine/metanephrine
-Plasma: ideally at time of symptoms
Identify source of catecholamines:
-MRI
-MIBG
-PET

63
Q

Clinical Syndrome Associations (phaechromocytoma)

A 
Multiple Endocrine Neoplasia II
Von-Hippel-Lindau syndrome
Succinate dehydrogenase mutations
Neurofibromatosis
Tuberose sclerosis
64
Q

MEN II

A 
Autosomal dominant
 Activating mutation in tyrosine kinase receptor 	(RET proto-oncogene)
 Associations:
	Medullary thyroid cancer
	Parathyroid hyperplasia
	Bilateral phaeochromocytomas
65
Q

What is MENII associated with?

A

Medullary thyroid carcinoma
Bilateral phaeochromocytoma
Parathyroid carcinoma

66
Q

Von Hippel Lindau Syndrome

A

Mutation in HIF 1-a
Autosomal dominant
Range of vascular tumours
Family screening vital

67
Q

Succinate Dehydrogenase

A

SDH – B, C & D
Inactivating mutations – stabilise HIF-1a
50% extra-adrenal
SDH-D = head & neck PGL; > 70% penetrance
SDH-B = malignant PGL; < 50% penetrance

68
Q

Pitfalls in Phaeochromocytoma

A

catecholamines raised in heart failure

episodic catecholamine secretion - levels in plasma + urine may be normal

malignant and extra-adrenal tumours less efficient at catecholamine synthesis  Dopamine > Norepinephrine >Adrenaline

remember genetic syndromes

69
Q

Permanent agranulocytosis is a serious side effects of which drugs?

A

Agranulocytosis - big decrease in WBC, particularly neutrophils
Carbimazole and propylthiouracil (drugs for hyperthyroidism)

70
Q

Someone presents insidiously with diastolic hypertension…

A

Phaeochromocytoma

71
Q

What is a dermoid cyst?

A

Contains mature material like skin, hair follicles and sweat glands

(i. e. material usually found on the outside)
- usually present in teenage years

72
Q

Cystic hygroma

A 
Posterior triangle swelling
Contains lots of watery fluid
ALMOST ALWAYS FOUND IN CHILDREN
-present from birth
-often large and disfiguring
-just below angle of mandible
-lymph fluid
-transilluminate
73
Q

congenital epithelial cysts, which arise on the lateral part of the neck from a failure of obliteration of the second branchial cleft in embryonic development

A

Branchial cysts

74
Q

Level of carotid bifurcation?

A

Level of the superior border of the thyroid cartilage

vertebral body C4

75
Q

What does a branchial cyst contain on fine needle aspiration?

A

Cholesterol crystals

76
Q

“half filled hot water bottle”

A

Branchial cyst

77
Q

Branchial cyst and cystic hygroma, anterior or posterior swellings?

A

Branchial cyst : anterior triangle

Cystic hygroma: posterior swelling

78
Q

FNA thyroid and when you should re do aspiration?

A

inadequate Thy 1- repeat FNA
benign Thy 2 – repeat FNA 6/12
suspicious Thy 3 – thyroid lobectomy
malignant Thy 4-5 – total thyroidectomy

79
Q

How is ADH assessed?

A

Urine osmolarity

80
Q

Low sodium but volume stats unremarkable, what should you think about?

A

SIADH

-diagnosis of water excess as the cause is often done as diagnosis of exclusion

81
Q

Talk to me about hypovolemia

A

Hypovolaemia implies water deficit. If it is present when [Na] is low, then there must be an even bigger sodium deficit. This is important:
hypovolaemia in hyponatraemia → too little sodium.

Hypervolaemia is most often seen as oedema. This too is useful as it gives useful information about sodium and water balanc

82
Q

What does hypovolemia in hyponatremia mean?

A

Too little sodium

83
Q

What is derived from Rathke’s pouch?

A

Anterior pituitary

84
Q

Acidophils

A

Somatotrophs
Mammotrophs
(GH and PRL)
anterior pituitary

85
Q

Basophils

A

Corticotrophs
Thyrotrophys
Gonadotrophs

86
Q

Location of mineralocorticoid receptors?

A

Kidneys
Salivary glands
Gut
Sweat glands

  • sodium/potassium balance
  • blood pressure regulation
  • control of extracellular volume
87
Q

Loosers zones

A

Osteomalacia

88
Q

Adrenal crisis

A 
Extreme fatigue
V v. low serum sodium, high serum K
Dehydration
Vascular collapse (because of low BP)
Renal shut down
89
Q

Which autoimmune diseases are associated with Addisons?

A

T1Dm
Pernicious anemia
Autoimmune thyroid disorders

90
Q

Normal results of short SynACTHen test?

A

Normal: cortisol = baseline >250nmol/L, post : >480

91
Q

Hydrocortisone as cortisol replacement

A

If unwell, give intravenously first
Usually 15-30mg daily in divided doses
Try to mimic diurnal rhythm

92
Q

Which kind of tumour will take up MIBG?

A

Phaechromocytoma

93
Q

What might someone with a phaeochromocytoma die from?

A

Arrhythmia

Ischemia

94
Q

Carcinoid syndrome

A

Abdominal pain that comes and goes
Bright red flushing of the face, neck, or upper chest
Diarrhea
Heart palpitations
Low blood pressure
Skin lesions on the face called telangiectasias
Wheezing

95
Q

Advice you should give patients if they are taking long term steroids?

A
  • Know how to increase steroid replacement dose for intercurrent illness
  • Carry a ‘steroid’ card
  • Wear a Medic-Alert bracelet (gives details of their condition so tat emergency replacement therapy can be given if found unconscious)
96
Q

Hirsutism developing before puberty is suggestive of what?

A

CAH

97
Q

Biochemistry classical of Addisons?

A

Classically hyponatremia, hyperkalaemia, high urea (although biochem may be normal)

98
Q

Severe hypotension and dehydration precipitated by intercurrent illness, accident or operation?

A

ADDISONIAN CRISIS

99
Q

Most common cause of ambiguous genitalia?

A

CAH

Endocrinology (30 decks)

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