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w4 - adrenal physiology Flashcards

(54 cards)

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1
Q

in males, most of the androgen is produced in the

A

testes

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2
Q

6 classes of steroid receptors

A 
Glucocorticoid
Mineralocorticoid
Progestin
Oestrogen
Androgen
Vitamin D
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3
Q

steroid hormones have an instantaneous effec

A

false

takes mins/hours/dyays

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4
Q

circulatory effects of glucocorticoids

A

incr CO
incr BP
incr renal flow and GFR

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5
Q

metabolic effects of glucocorticoids

A

incr blood sugar
inc lipolysis
incr proteolysis

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6
Q

cns effects of glucocorticoids

A

mood lability
reduced libido
euphoria

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7
Q

bone/connectiv tissue effects of glucocorticoids

A

accelerates osteoporosis
red calcium
red collagen formation
red wound healing

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8
Q

immune effects of glucocorticoids

A

red cap dilation
red leucocyte migration
red macrophage acitvity
red inflam cytokine

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9
Q

Clinical applications of corticosteroids

A

Suppress inflammation
Suppress immune system
Replacement treatment

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10
Q

purpose of mineralocorticoids

A

na/k pbalance
bp regulation
ECF volume

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11
Q

Mineralocorticoids receptors are found 4

A

kidneys
salivary glands
giut
sweat glands

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12
Q

until proven otherwise, Hyponatraemia + hyperkalaemia + hypotension =

A

Addisons disease

if suspected just treat it

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13
Q

addisons disease

A

primary adrenal insufficiency

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14
Q

causes of 2ndary insufficiency in adrenal glnad

A

lack of ACTH stimulation
iatrogenic (excess exogenous steroid)
pit/hypotha disorders

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15
Q

___ of adrenal cortex destroyed before symptomatic in addisons

A

90%

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16
Q

assoc autoimmune diseases of addisons

A

T1DM
autoimm thyroid
pernicious anaemia

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17
Q

features of addisons

A 
Anorexia, weight loss
Fatigue/lethargy
Dizziness and low BP
Abdominal pain, vomiting, diarrhoea
Skin pigmentation
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18
Q

hyperpigmentation occurs in addison bcoz

A

ACTH reacts with a skin receptor causing pigmentation

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19
Q

how is adrenal insufficiency diagnosed

A

suspicious bio

  • red Na, inc K
  • hypoglycaemia

synACTHen test
-measure plasma cortisol before/after ACTH inj
normal :>250nmol/L, post ACTH >550nmol/L

ACTH shd be hiiighh

renin hiiii + aldosterone low

adrenal autoantibodies

imaging

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20
Q

maanagement of adrenal insuff

A

hydrocortisone as cortisol replacement

  • if unwell = IV first
  • 15-30mg daily
  • try to mimic diurnal rhythm

fludrocortisone (aldosterone replacement)

education

  • sick day = DBL up dosage
  • vomiting = take it again or hospital for IV
  • ID
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21
Q

t/f 2ndary adrenal insufficiency will require glucocorticoid

A

true

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22
Q

t/f 2ndary adrenal insufficiency will require mineralocorticoid

23
Q

there is high levels of ACTH in 2ndary adrenal insufficiency t.fq

Study These Flashcards
A

false
reduction in ACTH

clin features

  • skin pale - no ACTH
  • aldosterone lvls nomal
24
Q

2ndary adrenal treated with fludrocortisone alone

Study These Flashcards
A

false

hydrocortisone alone

25
``` 17 year old female 3 year history of: Central weight gain Acne Amenorrhoea Hypertension Severe osteoporosis Proximal muscle weakness (myopathy) what is disease ```
Cushings
26
in males, what other clin feature in cushings
testicular atrophy
27
cushings syndrome is due to high levels of __
cortisol
28
cushings syndrome can be either ACTH dependent/independent, 3 causes for each
dependent - pituitary adenoma (CUSHINGS DISEASE) - ectopic ACTH (Carcinoid/carcinoma) - Ectopic CRH independent - adrenlal adenoma - adrenal carcinoma - nodular hyperplasia
29
3 screening tests for cushings syndrome
overnight dexamethasone suppression test 24hr urinary free cortisol late night salivary cortisol
30
test to diafgnose cushings syndrome
low dose dexamethasone suppression test
31
commonest cause of cortisol excess
iatrogenic prolonged high dose steroid therapy (asthma/RA/IBS/transplants) (usually oral, but can occur in injections and inhaled)
32
``` 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 what is the likely disorder ```
too much mineralocorticoid (inap retention of Na) conns syndrome acromegaly
33
primary aldosteronism (PA) is defined as
Autonomous production of aldosterone independent of its regulators (angiotensin II/potassium)
34
spironolactone is a
mineralocorticoid receptor antagonist
35
cardio actions of aldosterone (mineralocoritcoid)
incr sympa flow incr cardiac collagen incr pressure response na retention cytokine and ROS synthesis
36
clin featuress of PA
Significant hypertension Hypokalaemia (in around 30%) Alkalosis
37
another name for adrenal adenoma
conns syndrome bilateral adrenal hypperplasia is the commonest cause of PA
38
diagnosis of PA
Step 1: confirm aldosterone excess Measure plasma aldosterone and renin and express as ratio (ARR-aldosterone to renin ratio) (raised inveitgate further - saline suppression test -> confirmed if plasma aldo unable to suppress>50% with 2L of saline step 2: confirm subtype - Adrenal Ct - adeoma - mibby adrenal vein sampling (done more in oldr) - confirm adenoma, is true source of aldo excess
39
management of PA
surgical medical -MR antagonists - spironolactone or eplerenone
40
Adrenal cortex is major source
glucocort mineralocorti androgens
41
Cortisol/androgen secretion regulated by __ ___ __ by a negative feedback mechanism
pit ACTh secretion
42
Aldosterone secretion controlled by renin-angiotensin system and
plasma K+
43
congenital adrenal hyperplasia is due to a deficiency of __ __, leading to a defiency in __and __V
21α hydroxylase aldosterone cortisol
44
Principles of Treatment of CAH for a) paeds b) adult physicians
``` a)) Timely recognition Glucorticoid replacement Mineralocorticoid replacement in some Surgical correction Achieve maximal growth potential ``` b) Control androgen excess Restore fertility Avoid steroid over-replacement
45
tests are looking for
17OH precursor | synACTHen test
46
histology of adrenal, where iis mineralo, gluco, androgens and catecholamines produced
mineralo = glomerulosa (Aldo) gluco = fasciculata (cortisol)) androgen = reticularis catecholamines = medulla
47
Clues to phaeochromocytoma
Labile hypertension Postural hypotension Paroxysmal sweating, headache, pallor,tachycardia (can be none)
48
`phaeochromocytoma
neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue (paraganglioma) that failed to involute after birth, that secretes high amounts of catecholamines, mostly norepinephrine
49
classic triad of phaechrocytoma
hyperT (50% paroxysmal) headache sweating
50
other symptoms of phaeoc
``` Palpitations Breathlessness Constipation Anxiety/Fear Weight loss Flushing – uncommon Incidental finding on imaging Family tracing ```
51
signs involved in phaeoc
``` 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 ```
52
why is phaeoc callled the 10% tumour
``` 10% malignant 10% extra-adrenal [probably 20-30%] 10% bilateral 10% associated with hyperglycaemia 10% in children 10% familial (but probably 25%) ```
53
diagnosis of phaeoc
Identify the source of catecholamine excess MRI Scan Abdomen Whole body MIBG – meta-iodobenzylguanidine PET Scan Difficulties with borderline cases
54
therapy for phaeoc
``` Full α and β- blockade (A before B) Phenoxybenzamine (α-blocker) Propranolol, atenolol or metoprolol (β-blocker) Fluid and/or blood replacement Careful anaesthetic assessment ```

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