- Head injury/ haemorrhage , subdural hematoma - Tumour (eg lung, prostate, pancreas, thymus, lymphoma, CNS) - Meningitis - Thrombosis - Lupus - Pulmonary lesions (TB, pneumonia, asthma, CF, lung abscess) - Alcohol withdrawal - Drugs: (SSRIs, sulfonylurea (DMT2) , cyclophosphamide (immunosuppressant), carbamazepine (anti-convulsant), some chemo )

- Low serum Na+, high urine Na+ - Low plasma osmolality, high urine osmolality - Euvolaemia - Need to distinguish between frail elderly patients’ hyponatraemia from salt and water depletion - -- Give 1-2L of 0.9%saline - -- If sodium depleted, will respond well as will fill in their defecit - -- SIADH will have no response, as the Na will be excreted in order to balance the low osmolality ``` No hypokalemia (low aldosterone! aldosterone ), No hypotension, no hypovolemia Normal adrenal, renal, thyroid function ```

endo middle tier Flashcards by David Sog

types of diabetes insipidus

cranial diabetes insipidus
nephrogenic diabetes insipidus

cranial - lack of vasopressin produced

nephrogenic - enough vasopressin is produced but resistance to vasopressin action

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symptoms for diabetes insipidus

both cranial and nephrogenic!

Similar appearance to diabetes mellitus (or primary polydipsia - has polydipsia and polyuria)

Polyuria 3L+/day
Polydipsia
Dehydration
Low BP
Lethargy, weakness

Distinct from diabetes mellitus

No glycosuria (sweet wee with sugar)
No elevated blood glucose levels

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diabetes insipidus osmolality

=high serum osmolality and low urine osmolality

lots of water lost and not reabsorbed in kidneys (no vasopressin action)

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diabetes insipidus diagnosis

1) to tell it is diabetes insipiud
2) to distinguish between cranial and nephrogenic diabetes insipidus

1) - Measure urine output - to confirm polyuria
- To distinguish it from DM, do plasma and urine glucose levels (no glycosuria/ elevated blood levels)
- Hyponatremia - due to water loss
- MRI hypothalamus - looking for masses

Water deprivation test
– 8h fasting with no fluids
– Measure urine and serum osmolality hourly
– Normal response: serum osmolality remains same and urine osmolality increases. Kidneys can concentrate urine.
– DI: serum osmolality rises, urine unable to be concentrated- remains low osmolality. Kidneys still produce dilute urine, despite dehydration.

2) Desmopressin given
No response over few hours = nephrogenic
Good response over few hours = cranial

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causes of cranial diabetes insipidus

Acquired

idiopathic
Tumours (rare)- metastases, posterior pituitary
Trauma
Infections (TB, encephalitis, meningitis)
Vascular (sickle cell, infection)
Inflammation
Sarcoidosis

Genetic (rare)
- Defect in ADH gene

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cranial diabetes management

Treat underlying condition (eg surgery for tumour, treat infection)

Give desmopressin (tablets, nasal spray, injection)
-- V2 receptor analogue (fits it, stimulates the action of vasopressin- that is not produced enough here)

Thiazide diureticsmild hypovolemia → kidneys will take up more Na+ and water in proximal tubule

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causes of nephrogenic diabetes insipidus

Acquired

Reduction in medullary concentrating gradient
– Hypokalaemia
– Hypercalcaemia
– Meant to be low NaCl and Ca in blood so more moves back to blood from urine. Meant to be high K in blood so more can be used in the Na/K pumps.
Antagonism to vasopressin effects
– Drugs (precipitating drugs? -Lithium chloride, gilbenclamide
– Renal impairment eg renal tubular acidosis
– Post obstructive uropathy
– Prolonged polyuria

Genetic (rare)

Sickle cell
Mutation of ADH receptor

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nephrogenic diabetes insipidus management

Difficult to treat

Access to water, to rehydrate

Give high dose desmopressin (tablets, nasal spray, injection) (V2 receptor analogue (fits it, stimulates the action of vasopressin))

Thiazide diuretics → mild hypovolemia → kidneys will take up more Na+ and water in proximal tubule

NSAIDs → lower urine volume and plasma Na as it inhibits prostaglandin synthase - and prostaglandins inhibit ADH action so it prevents that

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SIADH pathophysiology

too much vasopressin, inappropriate release (despite very dilute plasma)

Increased insertion of aquaporin 2 channels in the apical membrane of the collecting duct
(opposite to cranial diabetes insipidus)

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SIADH osmolality

low (lots of water)

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is SIADH hypo/eu/hypervolemic

retention of water –> intracellular volume increases (cells swell) but EUvolemic
- as volume rises, aldosterone is suppressed and ANP is released which increases renal excretion, so ps volume normal

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SIADH causes

Head injury/ haemorrhage , subdural hematoma
Tumour (eg lung, prostate, pancreas, thymus, lymphoma, CNS)
Meningitis
Thrombosis
Lupus
Pulmonary lesions (TB, pneumonia, asthma, CF, lung abscess)
Alcohol withdrawal
Drugs: (SSRIs, sulfonylurea (DMT2) , cyclophosphamide (immunosuppressant), carbamazepine (anti-convulsant), some chemo )

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SIADH signs and symptoms

why do u/ why do u not get oedema

concentrated urine
due to brain cell swelling:
– reduction in GCS
– fits, coma, confusion, drowsy, irritable
Weakness
Aches
Anorexia, Nausea
Malaise

NO !! Oedema !! – oedema is ECF increase whereas SIADH is euvolemic, only the intracellular fluid increases

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SIADH investigations

Low serum Na+, high urine Na+
Low plasma osmolality, high urine osmolality
Euvolaemia
Need to distinguish between frail elderly patients’ hyponatraemia from salt and water depletion
– Give 1-2L of 0.9%saline
– If sodium depleted, will respond well as will fill in their defecit
– SIADH will have no response, as the Na will be excreted in order to balance the low osmolality

No hypokalemia (low aldosterone! aldosterone ), No hypotension, 
no hypovolemia
Normal adrenal, renal, thyroid function

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SIADH treatment

Treat underlying condition (eg stop causative drug)

Increase Na in serum (hospital visits)

Restrict fluids (used for general low Na)

500-1000mL /day
This will increase Na+ concentration (less fluid excess so less excretion including Na excretion)

Vasopressin antagonist = tolvaptan (oral)
Blocks V2 receptor
Promotes water excretion (less absorbed), without affecting electrolytes

Demeclocycline
Inhibits the action of ADH on the kidneys - resistant to its action – induces nephrogenic DI

If severe and you are worried about circulatory overload – loop diuetic = furosemide

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tolvaptan vs desmopressin vs demeclocyclin

desmopressin = V2 receptor analogue - stimulates action of vasopressin (Agonist)

promotes water reabsorption
diabetes insipidus treatment

tolvaptan = vasopresssin antagonist - blocks V2 receptors

promotes water excretion, does not affect electrolytes
SIADH treatment

demeclocycline = vasopressin inhibitor at kidneys

induces nephrogenic DI
SIADH treatment

is hyponatraemia common?

salt deficiency or water excess?

yes

either- more commonly water excess

hyponatraemia symptoms

mild
severe

can be asymptomatic

Mild (often chronic)

Headache
nausea/ vomiting
Irritable
confusion/ disorientation/ mental slowing
Unstable gait
oedema?

Severe (often acute- eg marathon)

due to brain swelling (cerebral oedema) due to low osmolality. Then it adjusts to less swollen but often appears shrunk (chronic look)
coma/ stupor
Convulsions
Respiratory arrest

hyponatraemia causes/ treatment

find out underlying cause
find out serum volume levels (hypo /eu/ hypervolemic) - treatment depends on this!
find out serum and urine osmolality

is asymptomatic= fluid restriction

hypovolemic = saline replacement

bleeding
burns
pancreatitis
vom/diar

euvolemic = fluid restrict
- SIADH

hypervolemic = fluid restrict
- liver failure

addisons =

pathophysiology

autoimmune adrenalitis - loss of adrenal cortex
may also be caused by TB (commonest cause worldwide)

so primary adrenal insufficiency . this results in deficiciency of mineralocorticoid (aldosterone), glucocorticoid (coirtisol) and sex steroid (androgens, sex hormone precursors)

as a result there is no negative feedback on the anterior pituitary and hypothalamus so high levels of CRH and ACTH

addisons

gender
how common

female

- very rare

addisons causes

autoimmune adrenalitis = HIC
TB = LIC (commonest cause worldwide)
adrenal metastases
long term steroid use
oppertunistic HIV infection
adrenal haemorrhage/infarction

secondary adrenal insufficiency

pathophysiology
causes

lack of cortisol due to lack of ACTH
so cortisol levels are low , as well as ACTH

(but mineralocorticoid (aldosterone) and sex steroid (androgens, sex hormone precursors) are NOT lower!)

hypopituitarism

tumour
radiation
withdrawal from high dose steroid treatment (most common cause)

tertiary adrenal insufficiency

lack of CRH (hypothalamus) so suppression of HPA axis (hypothalamo- pituitary -adrenal)

due to withdrawal from high dose steroid treatment (most common cause)

effect of high ACTH and when is this seen

addisons (lack of cortisol negative feedback) causes skin pigmentation - bronzing (alpha melanocortin)

addisons signs and symptoms

- Skin pigmentation, bronzing - Vitiligo (white patches and loss of body hair due to loss of androgens) - Lean - hypotension/ Postural hypotension (Due to loss of aldosterone → hypovolaemia) - Dehydrated (Loss of Na+ due to loss of aldosterone, which also causes high K+ (less renal excretion)) - Tachycardia -To compensate for low BP and low volume - Lethargy, depression, low mood and self esteem - Dizzy - Anorexia, weight loss - Nausea /vomiting / diarrhea/ constipation /abdominal pain - hypogonadal (Amenorrhea Impotence, loss of libido )

secondary adrenal insufficiency symptoms

``` No pigmentation (low ACTH) Malaise may have similar things to addisons (no gonadal symptoms though, and not dehydrated/ hypertension as adolsterone unaffected) ```

investigations into adrenal insufficiency

Bloods - Low Na - High K - Hypoglycemia - due to low cortisol - Hypoaldosteronism (aldosterone) - Low cortisol - Uraemia (high urea) - Raised Ca2+ (due to low volume) - Anaemia (low volume) - Eosinophilia - high wbc as cortisol inhibits - anti-inflam - ACTH levels - high in addisons, low in secondary - Mineralocorticoid level- low in addisons, normal in secondary Short ACTH test = Synacthen test - Measure plasma cortisol - Give synACTHen (ACTH analogue = tetracosactide) - Measure plasma cortisol (30m) - Addisons: cortisol should be low- not raised by the stimulant - Secondary : cortisol rises Adrenal antibodies - 21 hydroxylase antibody -- high levels Abdom/CXR Looking for upper zone fibrosis or adrenal calcification → TB!

addisons managment

Immediate: - IV hydrocortisone - IV saline - Glucose if hypoglycaemic Later: - Steroids 3x a day - mimic circadian rhythm - glucocorticoids (hydrocortisone), AND mineralocorticoids (fludrocortisone) - Warn against abrupt steroid cessation - Steroid card/ bracelet given - steroid sick day rules: Mimic what the body would do. DOUBLE dose when infection/trauma/surgery and Increase dose in pregnancy/ before strenuous activity ``` Adrenal crisis (nausea, abdominal pain, muscle cramps, confusion) - IV hydrocortisone ```

secondary adrenal insufficiency treatment

If cause is long term steroid withdrawal: Adrenals will recover eventually Oral hydrocortisone

adrenal crisis symtpoms treatment

nausea, abdominal pain, muscle cramps, Confusion IV hydrocortisone

hyperkalemia causes

Renal impairment - Acute kidney injury Drugs: - Potassium sparing diuretic - spironolactone (common) - ACE i (decreases aldosterone so decreases K+ excretion) - (common) - NSAIDs - (common) - Heparin T1DM Redistribution of K+ - Intracellular → extracellular - Diabetic ketoacidosis - Metabolic acidosis - Tissue necrosis/lysis - -- Severe burns - -- Rhabdomyolysis (death of muscle fibres by traumatic crush injury, releasing K+ into blood stream) - --Tumour lysis syndrome Addison’s Increased load - Blood transfusion

artefactually high K+ result

- Could be due to haemolysis (vigorous venepuncutre, abnormal rbc) - FBC bottle anticoagulant contamination with k+ - Thrombocythaemia (increased platelets) - k+ leaks out during clotting - potassium spikes after vigorous exercise recheck if you get high K+

hyperkalemia pathophysiology

- Impaired neuromuscular transmission - Reduced difference between electrical potential of cardiac myocytes and outside of cells. - Threshold for action potentials is decreased, so more abnormal action potentials - -- Abnromal heart rhythyms - -- Muscle weakness,paralysis

hyperkalemia investigations

Blood test- serum potassium - recheck if unusual - >5.5 = hyperk - >6.5 = emergency ECG- - tall tented T waves - Widened QRS - Prolonged PR interval - Reduced P wave - Fast, irregular pulse

hyperkalemia symptoms

- Not many - Impaired neuromuscular transmission: Muscle weakness and paralysis - Fatigue - Light headed - Chest pain, heart racing, palpitations

hyperkalemia treatment - if urgent

IV calcium gluconate -- reduces excitability of cardiomyocytes Drive k+ into cells - Soluble insulin - IV actrapid (glucose takes K+ with it into the cell - Give gkucose too- otherwise patient will become hypoglycaemic! - IV salbutamol

hyperkalemia- if not urgent

Review medications : ACE i or NSAID or k+ sparing diuretic Restrict potassium in diet - Pinto beans, kidney beans - Leafy greens eg spinach - Dried fruit - Banana, oranges, Apricot, Grapefruit - Lentils - Some meats, sea food Polystyrene sulfonate resin binds to k+ in gut, reducing absorption Loop diuretic (not k+ sparing)

hyperkalemia complications

Arrhythmias MI Muscle weakness paralysis