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Exam 1 PNP > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

what does the adrenal cortex produce

A

glucocorticoids (cortisol)
mineralocorticoids (aldosterone)
androgens

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2
Q

what regulates cortisol/ androgen secretion

A

pituitary ACTH (which is regulated by hormones made in the hypothalamus)

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3
Q

what controls aldosterone secretion

A

renin-angiotensin system
and
plasma K+

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4
Q

what is the role of aldosterone (mineralocorticoid)

A

regulates blood pressure and electrolyte excretion

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5
Q

what long term treatment does adrenal insufficiency need

A

lifelong replacement of cortisol and aldosterone

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6
Q

what can cause cortisol excess

A

iatrogenic
due to disorders of pituitary (ACTH dependent)
or adrenal gland (non ACTH dependent)

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7
Q

what can cause aldosterone excess

A

bilateral adrenal hyperplasia

adrenal adenoma

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8
Q

how is adrenal adenoma treated

A

surgically

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9
Q

what does aldosterone excess cause

A

hypertension

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10
Q

how much does a healthy adrenal gland weigh

A

4 grams in adults

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11
Q

what does the medulla of the adrenal gland produce

A

catecholamines- adrenalin and noradrenaline

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12
Q

what is corticosterone

A

a glucocorticoid

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13
Q

what are the zones of the adrenal gland and what do they produce

A

(from capsule to medulla)

zona glomerulosa (mineralocorticoids)

zona fasciculata (glucocorticoids)

zona reticularis (adrenal androgens)

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14
Q

what is released by the hypothalamus which stimulates the anterior pituitary to produce

A

corticotropin releasing hormone

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15
Q

what does the hypothalamus release corticotropin releasing hormone in response to

A

illness, stress, time of day

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16
Q

what does ACTH do

A

acts on adrenal cortex to release cortisol

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17
Q

what is the HPA axis

A

hypothalamus - (anterior) pituitary - adrenal cortex

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18
Q

what does cortisol have a negative feedback effect on

A

both the hypothalamus and the anterior pituitary

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19
Q

what activates the renin-angiotensin system

A

decreased blood pressure

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20
Q

describe the pathway of the renin angiotensin system (its not that bad chill)

A 
blood pressure falls 
- 
kidney produces renin
- 
renin acts on angiotensinogen...
-
...forms angiotensin I
-
angiotensin-converting enzyme turns it into...
-
angiotensin II which has two actions...
-
1. stimulates adrenal gland to secrete aldosterone which....
-
causes the kidneys to retain salt (indirectly increases BP)
-
2. causes direction vasoconstriction (directly increased BP)
=
increased blood pressure
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21
Q

what do corticosteroids do

A

bind to intracellular receptors

receptor ligand complex binds DNA to alter transcription

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22
Q

what are mineralocorticoids and glucocorticoids

A

corticosteroids

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23
Q

what are the 6 different types of steroid receptors

A 
glucocorticoid
mineralocorticoid
progestin 
oestrogen 
androgen 
vitamin D
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24
Q

what are the CNS effects of cortisol

A

mood lability
euphoria/psychosis
decreased libido

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25
Q

what are the effects of cortisol on bone/ connective tissue

A

accelerates osteoporosis

decreased: serum calcium, collagen formation, wound healing

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26
Q

what are the immunological actions of cortisol

A

decreased:

  • capillary dilation, permeability
  • leucocyte migration
  • macrophage activity
  • inflammatory cytokine production

(reduces immune response)

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27
Q

what are the metabolic effects of cortisol

A

increased blood sugar
increased lipolysis, central redistribution of lipids
increased proteolysis

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28
Q

what are the circulatory/ renal effects of cortisol

A

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

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29
Q

what are the clinical uses of corticosteroids

A

suppress inflammation
suppress immune system (both supraphysiological levels)
replacement treatment (physiological levels)

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30
Q

what diseases are corticosteroids used to treat

A

allergic diseases: asthma/ anaphylaxis
inflammatory disease: RA, UC, crohns
malignant disease

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31
Q

how can you administer corticosteroids

A

IV, IM orally

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32
Q

where are mineralocorticoid receptors

A

kidneys, salivary glands, gut, sweat glands

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33
Q

how does aldosterone affect mineral balance

A

causes excretion of K+/H+

causes reabsorption of sodium

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34
Q 
what is this: 
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 disease going into addisonian crisis

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35
Q

what should you worry about with hyperkalaemia and hyponatraemia

A

ADDISONS - IF YOU SUSPECT THIS TREAT IT IMMEDIATELY

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36
Q

what can cause primary adrenal insufficiency

A

addisons disease
congential adrenal hyperplasia (CAH)
adrenal TB, HIV, malignancy

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37
Q

what are the causes of secondary adrenal insufficiency

A

lack of ATCH stimulation:
iatrogenic (excess exogenous steroid)
pituitary/ hypothalamic disorder

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38
Q

what is CAH

A

congenital adrenal hyperplasia- block in production of adrenal corticosteroid, present in neonates or early childhood

milder forms can present in adulthood

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39
Q

what is addisons disease

A

autoimmune condition causing destruction of the adrenal cortex resulting in adrenal insufficiency

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40
Q

what is the commonest cause of primary adrenal insuffiency

A

addisons disease

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41
Q

does addisons present early or late in the disease

A

more than 90% of adrenal cortex destroyed before symptoms start

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42
Q

what other conditions are associated with addisons

A

autoimmune conditions:

  • T1DM
  • autoimmune thyroid disease
  • pernicious anaemia
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43
Q

what are the clinical features of addisons disease

A 
anorexia, weight loss 
fatigue. lethargy 
dizziness and low BP
abdo pain, vomiting, diarrhoea 
increased skin pigmentation
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44
Q

what tests can be done to diagnose adrenal insufficiency

A

biochem: decreased Na, increased k, hypoglycaemia

short synacthen test: see if cortisol is produced

ACTH levels: increased (causes skin pigementation)

renin/aldosterone levels: increased renin, decreased aldosterone (loss in water and sodium)

adrenal autoantibodies

imaging

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45
Q

what antibodies can be used to investigate pimary adrenal insufficiency

A

17-OH-progesterone (infants and some childre/adults)

21-OH antibody (all > 6 months old)

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46
Q

what happens to CRH and ACTH if cortisol not produced

A

increase as loose negative feedback

47
Q

how do you manage adrenal insufficiency

A

do not wait for diagnosis
hydrocortisone as cortisol replacement (if unwell IV) try to mimic diurnal rhythm to avoid sleep disturbance

fludrocortisone as aldosterone replacement (monitor BP and K)

fluids (saline as sodium deficiency)

need to wear identification

48
Q

what are the sick day rules for adrenal insufficiency

A

double the dose of oral hydro-cortisone at time of inter current illness
if vomit it up admit to hospital (to get IV)

49
Q

what is the treatment for an acute adrenal illness

A

rapid IV saline

hydrocortisone IV

50
Q

what hormones are lacking in secondary adrenal insufficiency

A

either CRH or ACTH

51
Q

what is the treatment for pituitary/ hypothalamic disease tumours

A

surgery/ radiotherapy

52
Q

do you need to replace mineralocorticoid in secondary adrenal insufficiency (fludrocortisone)

A

no

53
Q

what are the clinical features of secondary adrenal insufficiency

A

lack of CRH or ACTH

similar to addisons but- skin pale (no increased ATCH), aldosterone production intake

54
Q

how do you treat secondary adrenal insufficiency

A

hydrocortisone replacement

55
Q

how do exogenous steroids cause secondary adrenal insufficiency

A

have negative affect on ACTH and CRH

56
Q

what are the normal levels for cortisol after a synthacthen test

A

baseline >250 nmol/L
post ACTH > 550 nmol/L

if below this think adrenal insufficiency

57
Q 
what is this:
17 year old female
3 year history of:
Central weight gain
Acne
Amenorrhoea
Hypertension
Severe osteoporosis
Proximal muscle weakness (myopathy)
A

cushings

58
Q

what is cushings syndrome

A

prolonged exposure to excess cortisol - has high mortality

59
Q

who is cushings common in

A

women, ages 20-40

60
Q

what are the clinical features of cortisol excess

A 
easy bruising 
facial plethora 
striae 
proximal myopathy and muscle wasting 
moon face 
red (plethoric) cheeks 
centripetal obesity 
intrascapular fat pad
61
Q

what are the ACT dependent causes of cushings

A

(all driven by high levels of ACTH)

  • pituitary adenoma
  • ectopic ACTH (carcinoid/ carcinoma)
  • ectopic CRH

(in order of most to least common)

62
Q

what are the ACTH independent causes of cushings

A

adrenal adenoma
adrenal carcinoma
nodular hyperplasia

or exogenous glucocorticoids

63
Q

ACTH dependent cushings originated from a pathology affecting where

A

the pituitary gland (or ectopic)- causes too much ACTH production

64
Q

ACTH independent cushings originated from a pathology affecting where

A

adrenal glands (or exogenous steriods)- causes too much cortisol production

65
Q

how do establish the cause of cushings

A

overnight dexamthasone suppression test (giving exogenous steroid should suppress production of cortisol)

24 hours urinary free cortisol

late night salivary cortisol

66
Q

what is the commonest cause or cortisol excess

A

iatrogenic - due to prolonged high dose steroid therapy causing chronic suppression of pituitary ACTH and adrenal atrophy

‘Cushing’s syndrome is caused by prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids’

cortisol is a glucocorticoid

67
Q

what does long term steroid treatment do to ACTH production

A

suppresses it (negative feedback)

68
Q

what does long term steroid treatment do to the adrenal glands

A

causes atrophy of adrenal cortex

69
Q

what are the implications of adrenal suppression (e.g. due to long term steroid treatment)

A

unable to respond to stress (illness surgery)
need extra doses of steroid when ill/ surgical procedure
cannot stop steroids suddenly

70
Q

how long should long term steroid therapy be withdrawn for

A

> 4-6 weeks

71
Q 
what is this:
34 year old male
1 year history of hypertension
No other past medical history
No regular medications
On examination:
BP 168/98 mm Hg
Renal function normal but plasma potassium low
A

endocrine cause of hypertension:

-hypertension + hypokalaemia = primary aldosteronism

72
Q

what are the endocrine causes of hypertension

A

cushings - too much glucocorticoid
pheochromocytoma- secretes high amounts of catecholamines
acromegaly- too much growth hormone

73
Q

what is a pheochromocytoma

A

neuroendocrine tumour of the medulla of the adrenal glands

74
Q

what are the biochemical signs of conns

A

hypokalaemia

75
Q

what causes conns

A

an adrenal adenoma

76
Q

what is primary aldosteronism

A

autonomous production of aldosterone independent of its regulators (angiotensin II/ potassium)

77
Q

what can cause primary aldosteronism

A

a benign growth in adrenal gland- (adrenal adenoma)= conns syndrome

bilateral adrenal hyperplasia

rarer: adrenal cortical carcinoma, genetic mutations, unilateral hyperplasia

78
Q

what is the action of aldosterone

A

blocks the action of sprionolactone

79
Q

what are the cardiovascular effects of aldosterone

A

increased cardiac collagen
increased BP
left ventricular hypertrophy
atheroma

80
Q

what are the CNS effects of aldosterone

A

increases sympathetic outflow

81
Q

what are the cellular effects of aldosterone

A

increases cytokine and reactive oxygen species synthesis

alters endothelial function (increased pressure response)

82
Q

what is the commonest cause of secondary hypertension

A

primary aldosteronism

83
Q

what are the clinical features of primary aldosteronism

A

hypertension
hypokalaemia
alkalosis

84
Q

mutations in what drives conns adenomas and hereditary hypertension

A

potassium channel mutations

85
Q

how do you diagnose primary aldosteronism

A

step 1- confirm aldosterone excess: measure plasma aldosterone and renin ratio, if raised do saline suppression test. failure of plasma aldosterone to suppress by >50% with 2 litres of saline confirms PA

step 2 - Confirm cause: adrenal CT to demonstrate adenoma, sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess

86
Q

what is the treatment for conns

A

unliateral laparoscopic adrenalectomy

87
Q

what is the treatment for bilateral adrenal hyperplasia

A

MR antagonists (spironolactone, eplerenone)

88
Q

what is congenital adrenal hyperplasia

A

group of conditions associated with enzyme defects in the steroid pathway

89
Q

what is the most common enzyme deficiency causes CAH

A

21alpha hydroxylase deficiency

90
Q

what inheritance pattern does 21alpha hydroylase deficiency follow

A

autosomal recessive inheritance

91
Q

what are the variants of 21alpha hydroxylase deficiency

A

classical: salt wasting, simple virilising

non classical: hyperadrongenaemia

92
Q

how do you diagnose CAH

A

basal (or stimulates) 17-OH progesterone (in excess as ant be converted into cortisol)

can stimulate 17-OH progesterone with synacthen (measure that it rather than cortisol)

93
Q

what is the presentation of congential adrenal hyperplasia

A

males:

  • adrenal insufficiency (2-3 weeks)
  • poor weight gain
  • biochemical pattern (similar to addisons)

females:
-genital ambiguity

non classical:

  • hirsute
  • acne
  • oligomenorrhoea
  • precocious puberty
  • infertility or sub fertility
94
Q

what is the paediatric treatment for congential adrenal hyperplasia

A

glucocorticoid replacement
mineralocorticoid replacement (in some)
surgical correction

achieve maximal growth potential

95
Q

what is the treatment for CAH in adults

A

give mineralocorticoids and glucocorticoids (cortisol and aldosterone) to suppress androgen production (gives negative feedback to stop ACTH being produced)

96
Q

what other forms does adrenaline as it is being made

A

dopamine and noradrenaline

97
Q

what is adrenaline synthesised from

A

tyrosine

98
Q

why might tumours of the adrenal medulla secrete dopamine

A

as unable to convert it to noradrenaline or adrenaline

99
Q 
what is this:
28y/o female 
1998 - dyspnoea, palpitations
 echocardiogram = poor LV function
 ? viral cardiomyopathy

1999 - pregnancy
deterioration in cardiac function
BP - 154/110 at 26 weeks

noradrenaline = 1200nmol/24 hr (900)
adrenaline = 150 nmol/24 hr (200)
dopamine = 31,140 nmol/24hr (2800)

noradrenaline = 4.9nmol/l (<4)
adrenaline = 0.6nmol/l (<1)

CT shows extra adrenal mass

A

paraganglioma

100
Q

are the majority of pheochromocytomas benign or malignant

A

benign

101
Q

what are the symptoms of a pheochromocytoma

A

labile hypertension
postural hypotension
paroxysmal sweating, headache, pallor, tachycardia, pyrexia

Palpitations
Breathlessness
Constipation
Anxiety/Fear
Weight loss
Flushing – uncommon
Incidental finding on imaging
Family tracing
102
Q

what is the difference between a pheochromocytoma and a paraganglioma

A

pheochromocytoma are in the adrenal medulla

paragangliomas are extra adrenal

103
Q

what is the 10% percent tumour

A

a pheochromocytoma

104
Q

when do pheochromocytomas pose greater risks

A

in surgery and pregnancy

105
Q

what are the signs of complications of a pheochromocytoma

A

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

106
Q

what are the biochemical abnormalities of pheochromocytomas

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

107
Q

how is the pheochromocytoms the 10% tumour

A 
10% malignant
10% extra-adrenal [probably 20-30%]
10% bilateral
10% associated with hyperglycaemia
10% in children
10% familial (but probably 25%)
108
Q

when should you think pheochromocytomas

A 
Family members with syndromes
Resistant hypertension
The young [<50] with hypertension
Classical symptoms
Consider with hypertension and hyperglycaemia
109
Q

how do you diagnose pheochromocytomas

A

confirm catecholamine excess: urine, plasma

identify source: MRI of abdomen/ whole body

MIBG scan
PET scan

110
Q

how do you treat pheochromocytoma

A

full alpha and beta blockade (A before B as other way around will cause profuse vasoconstriction)
alpha- phenoxybenzamin
beta- propranolol, atenolol, metoprolol

-fluid and/or blood replacement (as blockade will cause vasodilatation)

surgery

chemo if malignant

long term follow up

genetic testing

111
Q

what syndromes are associated with pheochromocytomas

A

MEN2, von-hippel-lindau syndrome, SDH B (B for bad), SDH D (D for get it from Dad)

112
Q

what happens to catecholamines in heart failure

A

are raised (as stress put on the heart)

113
Q

what ‘pheochromocytoma’ or adrenal tumours are less efficient at producing catecholamines

A

malignant or extra adrenal tumours

Exam 1 PNP (21 decks)

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