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Endocrine > Adrenal Pathology + Fluid Balance > Flashcards

Adrenal Pathology + Fluid Balance Flashcards

1
Q

What is the pathology behind Congenital adrenal hyperplasia ?

A

Autosomal recessive disorder
Reduced corticoids due to deficiency in 21-hydroxylase. Causes increase in ACTH to increase in androgens. Salt losing crisis causes hyperkalaemia + hyponatraemia

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2
Q

Why do you get hypovolaemic hyponatraemia?

A

mild dehydration

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3
Q

S+S Addisons

A 
Fatigue 
Weakness 
N+V
Weight loss 
Abdo pain 
Diarrhoea/ constipation 
Muscle cramps 
Hyperpigmentation 
Cravings for salt 
Hypotension 
Crisis brought on by infection of stress
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4
Q

Primary + secondary Addisons

A 
Primary = inability to produce enough steroids in adrenal glands 
Secondary = inadequate stimulation by pituitary glands
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5
Q

Blood results for Addisons

A 
Hyponatraemia 
Hyperkalaemia 
Hypercalcaemia 
Raised LFTs 
Reduced cortisol 
ACTH = high in primary, low in secondary
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6
Q

Management of addisons

A

Glucocorticoids (hydrocortisone) + mineralcorticoids (fludracortisone)

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7
Q

Steroids + chickenpox

A

At risk of severe chicken pox when on steroids

Cause pneumonia, hepatitis + shingles

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8
Q

When should addisons be suspected in hypothyroidism + diabetes?

A 
Hypothyroidism = when symptoms worsen with thyroxine 
T1DM = unexplained hypos
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9
Q

How is Addisons diagnosed?

A

Adrenocorticotrophic hormone stimulation test

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10
Q

Management of adrenal crisis

A

IM or IV hydrocortisone

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11
Q

Mechanism of familial hypercholesterolaemia

A

Inherited defected gene

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12
Q

What blood results indicate FH may be present?

A

<30 y/o with total cholesterol >7.5

>30 y/o with total cholesterol >9

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13
Q

What is the primary care management of FH?

A

Lifestyle advice
High intensity statin or ezetimibe
Anti HTN drugs
Aspirin as primary prevention of CVD

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14
Q

What is the pathology of Cushings?

A

Prolonged exposure to high levels of steroids

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15
Q

What are the causes of Cushings?

A

ACTH dependant:
Cushings disease, ACTH producing tumours or excess ACTH meds
Non-ACTH dependant:
excess steroids, adrenal adenoma or carcinoma

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16
Q

What is Cushings disease?

A

Excessive ACTH from pituitary (pituitary adenoma)

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17
Q

RF for Cushings

A

Females

25-40

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18
Q

S+S of Cushings

A 
Truncal obesity, buffalo hump, supraclavicular fat pads 
Facial fullness/ moon face
Proximal muscle wasting + weakness 
Diabetes 
Gonadal dysfunction 
HTN
Skin atrophy, easy bruising, hirsuitism, acne 
Depression 
Osteoporosis 
Thirst, polyuria/dipsia
19
Q

Investigations for ?Cushings

A 
24hr urine cortisol 
Overnight dexamethasone suppression test
Late night salivary cortisol 
RBC - raised WCC 
Hypokalaemia, metabolic alkalosis 
Plasma ACTH (high + elevated cortisol = ACTH dependant Cushings)
20
Q

What is inferior petrosal sinus sampling?

A

Performed with CRH stimulation to aid in diagnosing source of excess ACTH

21
Q

Management of Cushings

A

Surgery or RT

Metyrapone, ketoconazole, and mitotane can all be used to lower cortisol

22
Q

Complications of Cushings

A 
Metabolic syndrome 
HTN 
Diabetes 
Obesity
Hyperlipidemia 
Osteoporosis 
Thrombophilia 
Nelson's syndrome 
Primary pituitary tumour
23
Q

Presentation of congenital adrenal hyperplasia

A

Females = ambiguous genitalia
Boys with classic form = no signs at birth, possible penis enlargement. Early virilisation at 2-4 y/o
Boys with salt-losing form = present at 7-14 days with vomiting, weight loss, lethargy, dehydration
Non classic = hyperandrogenism in later childhood (early puberty, infertility, hirsutism, acne, PCOS)

24
Q

Investigations for ?congenital adrenal hyperplasia

A 
Hyponatraemia 
Hyperkalaemia 
Hypoglycaemia 
High serum 17-hydroxyprogesterone 
Corticotropin stimulation test 
Pelvic US for ambiguous genitalia
25
Q

Management of classic congenital adrenal hyperplasia

A

Hydrocortisone (kids) + prednisolone (adults)
Fludrocortisone
Additional salt intake in hot weather + exercise

26
Q

Management of non-classic congenital adrenal hyperplasia

A

Treatment only for symptomatic

Hydrocortisone + hormones (female)

27
Q

Complications of congenital adrenal hyperplasia

A 
Poor growth
Obesity 
Insulin resistance 
HTN 
CVD 
Central precocious puberty 
Infertility 
PCOS
Testicular adrenal rest tumours
28
Q

What is hyperaldosteronism?

A

Excess levels of aldosterone due to high renin levels (secondary) or independant of renin-angiotensin axis (primary)

29
Q

What does excess aldosterone do in the kidneys?

A

Acts at distal renal tubule, promoting sodium retention
causes water retention + HTN
Excretion of potassium

30
Q

Causes of primary hyperaldosteronism

A

Adrenal adenoma (Conn’s syndrome)
Adrenal hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

31
Q

S+S of hyperaldosteronism

A

HTN
Polyuria/ dipsia
Weakness
Headaches + lethargy

32
Q

Blood results for hyperaldosteronism

A

Hypokalaemia
Metabolic alkalosis
Hypernatraemia
Spot renin + aldosterone levels (low renin + high aldosterone for primary)

33
Q

Diagnosis of hyperaldosteronism

A

Selective adrenal venous sampling
CT/ MRI
Salt loading test

34
Q

What is the key differential of hyperaldosteronism + how is it different?

A

Renal artery stenosis due to HTN + hypokalaemia

Renal arteriogram

35
Q

Management of Conn’s syndrome + hyperaldosteronism

A 
Aldosterone antagonists (spironolactone or amiloride)
Surgery - adrenalectomy
36
Q

Causes of secondary hyperaldosteronism

A

Diuretics, HF, hepatic failure, nephrotic syndrome, RAS, malignant HTN

37
Q

Investigation results for hypoaldosteronism

A

Hyperkalaemia

Metabolic acidosis

38
Q

What is hypoaldosteronism also known as?

A

Type 4 renal tubular acidosis

39
Q

Causes of hypoaldosteronism

A

Reduced aldosterone: hyporeninemic hypoaldosteronism, pharmacologic inhibition of renin or angiotensin II, heparin therapy, and primary adrenal insufficiency
Aldosterone resistance: pharmacologic inhibition of the epithelial sodium channel in the collecting tubule, due either to potassium-sparing diuretics or antibiotics

40
Q

Management of hypoaldosteronism

A

Fludrocortisone

41
Q

Pathology of SIADH

A

Ingestion of water does not suppress ADH
Concentrated urine leads to water retention
This lowers plasma sodium by dilution
High total body water triggers increased urinary sodium excretion

42
Q

Causes of SIADH

A

CNS disorders (stroke, hemorrhage, infection, trauma)
SCC of lung producing ADH
Some drugs increase ADH release
Surgery
Pulmonary disease eg pneumonia, asthma, acute resp failure

43
Q

Management of SIADH

A

Fluid restriction

NaCl (oral or IV)

Endocrine (6 decks)

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