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endo > w4 - adrenal physiology > Flashcards

w4 - adrenal physiology Flashcards

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

A

false

23
Q

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

A

false
reduction in ACTH

clin features

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

2ndary adrenal treated with fludrocortisone alone

A

false

hydrocortisone alone

25
Q 
17 year old female
3 year history of:
Central weight gain
Acne
Amenorrhoea
Hypertension
Severe osteoporosis
Proximal muscle weakness (myopathy)
what is disease
A

Cushings

26
Q

in males, what other clin feature in cushings

A

testicular atrophy

27
Q

cushings syndrome is due to high levels of __

A

cortisol

28
Q

cushings syndrome can be either ACTH dependent/independent, 3 causes for each

A

dependent

  • pituitary adenoma (CUSHINGS DISEASE)
  • ectopic ACTH (Carcinoid/carcinoma)
  • Ectopic CRH

independent

  • adrenlal adenoma
  • adrenal carcinoma
  • nodular hyperplasia
29
Q

3 screening tests for cushings syndrome

A

overnight dexamethasone suppression test

24hr urinary free cortisol

late night salivary cortisol

30
Q

test to diafgnose cushings syndrome

A

low dose dexamethasone suppression test

31
Q

commonest cause of cortisol excess

A

iatrogenic
prolonged high dose steroid therapy (asthma/RA/IBS/transplants)
(usually oral, but can occur in injections and inhaled)

32
Q 
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
A

too much mineralocorticoid (inap retention of Na)

conns syndrome
acromegaly

33
Q

primary aldosteronism (PA) is defined as

A

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

34
Q

spironolactone is a

A

mineralocorticoid receptor antagonist

35
Q

cardio actions of aldosterone (mineralocoritcoid)

A

incr sympa flow
incr cardiac collagen incr pressure response
na retention
cytokine and ROS synthesis

36
Q

clin featuress of PA

A

Significant hypertension
Hypokalaemia (in around 30%)
Alkalosis

37
Q

another name for adrenal adenoma

A

conns syndrome

bilateral adrenal hypperplasia is the commonest cause of PA

38
Q

diagnosis of PA

A

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
Q

management of PA

A

surgical

medical
-MR antagonists - spironolactone or eplerenone

40
Q

Adrenal cortex is major source

A

glucocort
mineralocorti
androgens

41
Q

Cortisol/androgen secretion regulated by __ ___ __ by a negative feedback mechanism

A

pit ACTh secretion

42
Q

Aldosterone secretion controlled by renin-angiotensin system and

A

plasma K+

43
Q

congenital adrenal hyperplasia is due to a deficiency of __ __, leading to a defiency in __and __V

A

21α hydroxylase
aldosterone
cortisol

44
Q

Principles of Treatment of CAH for a) paeds b) adult physicians

A 
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
Q

tests are looking for

A

17OH precursor

synACTHen test

46
Q

histology of adrenal, where iis mineralo, gluco, androgens and catecholamines produced

A

mineralo = glomerulosa (Aldo)

gluco = fasciculata (cortisol))

androgen = reticularis

catecholamines = medulla

47
Q

Clues to phaeochromocytoma

A

Labile hypertension

Postural hypotension

Paroxysmal sweating, headache, pallor,tachycardia

(can be none)

48
Q

`phaeochromocytoma

A

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
Q

classic triad of phaechrocytoma

A

hyperT (50% paroxysmal)
headache
sweating

50
Q

other symptoms of phaeoc

A 
Palpitations
Breathlessness
Constipation
Anxiety/Fear
Weight loss
Flushing – uncommon
Incidental finding on imaging
Family tracing
51
Q

signs involved in phaeoc

A 
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
Q

why is phaeoc callled 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%)
53
Q

diagnosis of phaeoc

A

Identify the source of catecholamine excess

MRI Scan
Abdomen
Whole body

MIBG – meta-iodobenzylguanidine
PET Scan
Difficulties with borderline cases

54
Q

therapy for phaeoc

A 
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

endo (21 decks)

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