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Example of case Conns SyndromeExample of case Conns Syndrome

CSIM 2.25 - ELECTROLYTE

ABNORMALITIES
SODIUM PROBLEMS
HYPONATRAEMIA
1. Determine by plasma Na+ concentration: 135-144mmol/L
2. Clinical features
Symptoms
none.
headache
nausea
vomiting
muscle cramps
lethargy

Signs
disorientation
seizure
coma
cerebral oedema
death

3. Aetiology
a. Pseudohyponatraemia; Hyperglycemia, Hyperlipidaemia, Non-physiological osmolyte
b. Sodium depletion; renal loss, diuretics, salt wasting nephropathy, hypoadrenalism, salt
wasting, gut loss
c. Excess water intake; dipsogenic DI, sodium-free, hypoosmolar, irrigant solutions, IV fluid
therapy
d. reduced renal free water clearance; cardiac failure, Nephrotic syndrome,
hypothyroidism, hypoadrenalism, SIAD, NSIAD, hypovolaemia
e. reduced renal free water clearance; hypovalaemia
4. CNS consequence of rapid Na+ correction
a. Clinical features
i. 1-4d post change plasma Na+
ii. neurology
quadriplegia
opthalmoplegia
pseudo-bulbar palsy
coma
b. Pathology
i. de-myelination
pontine
extra-pontine
ii. necrosis
HYPERNATREMIA
1. Too little water or too much salt.
2. Dehydration: the elderly, terminal illness, water loss > water intake.
3. Excess Na+ in IV therapy.

Example of case Conns SyndromeExample of case Conns Syndrome

POTASSIUM PROBLEMS
Distal tubule is main control point
HYPOKAL AEMIA
1. Presentation
Cardiovascular

abnormal electrocardiogram
predisposition to digoxin toxicity
atrial ventricular arrhythmias

Endocrine & metabolic

decreased insulin secretion

carbohydrate intolerance
growth retardation

Neuromuscular

constipation/ileus
bladder dysfunction
weakness, cramps
tetany
paralysis
myalgias
rhabdomyolysis

Renal & electrolyte

decreased GFR
decreased renal blood flow
renal concentrating defect
chloride wasting
metabolic alkalosis
hypercalciuria
phosphaturia
dilation & vacuolization of proximal tubules
medullary cyst formation
interstitial nephritis

2. Causes

GI
o
o

Deficient intake
GI losses; vomiting, diarrhoea,
fistula, uretero-sigmoidostomy

Renal
o Tubular disorders
Renal tubular acidosis
Laekaemia

Liddles syndrome
Varrters syndrome
Gitelmans syndrome
antibiotics
o Metabolic alkalosis
o Diuretics
o Mineralocorticoid/GC effects
Cell shifts w/o depletion

1. HYPERKAL AEMIA
Presentation
Cardiovascular

abnormal electrocardiogram
atrial/ventricular arrhythmias
pacemaker dysfunction

Neuromuscular

Endocrine & metabolic

increased insulin secretion

parasthesias
weakness
paralysis
Renal & electrolyte

decreased renal NH4 production

EXAMPLE OF CASE CONNS SYNDROME

Personal details; 34
History: tetany, paraesthesia & periodic weakness polyuria/dipsia
Examination: mild hypertension
Investigations:
a. hypokalemic alkalosis, hypernatraemia,
b. suppressed renin
c. reduced free water excretion
d. increased urine aldosterone
Intervention
Progress
o symptoms
o biochemistry; 10 days
o hypertension; 18 days

EXAMPLE OF CASE BARRTERS SYNDROME

1. Increased Na+ delivery to distal control point
2. Features
a. metabolic alkalosis
b. hypokalaemia
c. hypercalciuria
d. elevated renin
e. elevated aldosterone
f. normal BP
3. Mechanism
a. loss of function
b. NKCC2
c. Clc Cl- channel
4. Diagnosis
a. high urine K+
b. high urine Clc. high renin
d. hypercalciuria