Metabolic acidosis occurs when an acid other than carbonic acid (due to CO₂ retention) accumulates in the body, resulting in a fall in the plasma bicarbonate.

 

* Davidson’s Principles and Practice of Medicine, 22nd edition Page 445

Causes of metabolic acidosis

Disorder	Mechanism
A. Normal anion gap**
Ingestion or infusion of inorganic acid	Therapeutic infusion of or poisoning with NH4Cl, HCl
Gastrointestinal HCO3 loss	Loss of HCO3 in diarrhoea, small bowel fistula, urinary diversion procedure
Renal tubular acidosis (RTA)	Urinary loss of HCO3 in proximal RTA; impaired tubular acid secretion in distal RTA
B. Increased anion gap
Endogenous acid load
Diabetic ketoacidosis	Accumulation of ketones1 with hyperglycaemia
Starvation ketosis	Accumulation of ketones without hyperglycaemia
Lactic acidosis	Shock, liver disease, drugs
Renal failure	Accumulation of organic acids
Exogenous acid load
Aspirin poisoning	Accumulation of salicylate2
Methanol poisoning	Accumulation of formate
Ethylene glycol poisoning	Accumulation of glycolate, oxalate
1Ketones include acid anions acetoacetate and β-hydroxybutyrate 2Salicylate poisoning is also associated with respiratory alkalosis due to direct ventilatory stimulation.

**Anion gap = Difference between the main measured cations (Na⁺ + K⁺) and the anions (Cl⁻ + HCO3⁻). This ‘gap’ is normally around 12–16 mmol/L (12–16 meq/L)

* Davidson’s Principles and Practice of Medicine, 22nd edition Page 445

*  Macleod’s Clinical Examination, 13th Edition

Many illnesses are associated with a positive family history. Such as –

• Cardiovascular and cerebrovascular: Hypertension, IHD, CVD
• Respiratory system: Atopic asthma, emphysema, TB
• Gastrointestinal system: Irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), peptic ulcer disease, polyps, colorectal cancer
• Genitourinary system: Prostate carcinoma
• Breast: Breast cancer

*  Macleod’s Clinical Examination, 13th Edition; Oxford Handbook of Clinical Medicine, 9th Edition

The dangers of cigarette smoking

1. General
   • Lung cancer
   • Chronic obstructive pulmonary disease (COPD)
   • Carcinoma of the oesophagus
   • Ischaemic heart disease
   • Peripheral vascular disease
   • Bladder cancer
   • An increase in abnormal spermatozoa
   • Memory problems
2. Maternal smoking
   • A decrease in birth weight of the infant
   • An increase in fetal and neonatal mortality
   • An increase in asthma
3. Passive smoking
   • Risk of asthma, pneumonia and bronchitis in infants of smoking parents
   • An increase in cough and breathlessness in smokers and non-smokers with COPD and asthma
   • An increase in cancer risk

* Kumar and Clark’s Clinical Medicine, 9th Edition

Disorder	Appearance
Acromegaly	Coarsening with enlarged features, e.g. nose, lips, orbital ridges and jaw (prognathism)
Hypothyroidism	Pale, puffy skin with loss of lateral third of eyebrows
Hyperthyroidism	Startled appearance with lid retraction
Cushing’s disease	‘Moon face’, plethoric complexion and buffalo hump over lower cervical—upper thoracic spine
Parkinsonism	Expressionless facies and drooling
Myasthenia gravis	Expressionless facies with bilateral ptosis
Myotonia dystrophica	Frontal baldness and bilateral ptosis
Superior vena caval obstruction	Plethoric, oedematous face and neck, chemosis of conjunctivae, prominent veins and venules
Malar flush	Dusky redness of cheeks seen in low cardiac output, e.g. mitral stenosis; also seen in myxoedema
Systemic lupus erythematosus	Rash over nose and cheeks — ‘butterfly rash’
Progressive systemic sclerosis	Taut skin around mouth with ‘beaking’ of nose

*  Macleod’s Clinical Diagnosis, 1st Edition

1. Dry or moist
   • Dry: Dehydration, mouth breathing xerostomia (in Sjogren syndrome), anticholinergic drug therapy.
   • Moist: Sialorrhoea in postencephalitic Parkinsonism, local mouth infection, gastroesophageal reflux disease (GERD), heavy metal poisoning.
2. Colour
   • Pale: Anaemia.
   • Yellow: Jaundice (mainly in undersurface of tongue).
   • Bluish: Central cyanosis, methaemoglobinaemia, sulphaemoglobinaemia (mainly involves the sides of the tongue), blue coloured food material.
   • Bluish red: Polycythaemia.
   • Black tongue (lingua nigra): Ingestion of bismuth, liquorice, charcoal, etc., Addison disease (pigmented).
   • Brownish: CKD.
   • Magenta coloured: Riboflavin (vitamin B₂) deficiency.
   • Raw beefy tongue (red, swollen and painful): Vitamin B₁₂ deficiency, niacin deficiency (pellagra).
   • White patches over tongue: Candidiasis, leukoplakia, chronic superficial glossitis.
   • Black hairy tongue: Smoking, fungal infection, tetracycline, penicillins.
   • White or greyish coating or”furred tongue’: Smoking, chronic debilitating disease.
   • White and red strawberry tongue: Scarlet fever.
   • Geographical tongue (there are irregular red and white patches on the tongue. These lesions look like a geographic map. Slowly changing red rings and lines that occur on the surface of the tongue). It has no clinical significance, but, can be a sign of riboflavin deficiency.
   • Scrotal tongue (deep horizontal fissure): No clinical significance.
   • Mushroom-like tongue (sore tongue with white slough): Corrosive poisoning.
   • Blotting paper-like pallor with black pigmentation in the margin: Hook worm infestation.
   • Angry looking tongue (central coating with red tip and margins): Enteric fever.
   • Glossitis or bald tongue (total loss or atrophy of papillae, smooth tongue): Vitamin B₁₂ deficiency, iron-deficiency anaemia, coeliac disease, pellagra, tropical sprue.
3. Mass or ulcers
   • Ulcers: Aphthous, malignant, tuberculous, snail track ulcer in secondary syphilis, denture, Crohn disease.
   • Bite mark: Convulsion.
   • Growth in tongue: Squamous cell carcinoma.
   • Hairy leukoplakia (painless white corrugated lesion on sides): Found in AIDS due to EBV infection.
   • Papilloma (viral wart)
   • Median rhomboid glossitis (lozenge shaped area with loss of papillae and fissuring in the midline of the tongue, anterior to the foramen caecum). It is a congenital anomaly.
   • Cysts in the floor of the mouth: Ranula, sublingual dermoid cyst.
4. Size and shape
   • Macroglossia: Found in Down syndrome, acromegaly, cretinism, myxoedema, primary amyloidosis, mucopolysaccharidosis (e. g., Flurler syndrome), lymphangioma, tumour infiltration.
   • Microglossia (atrophy or hemiatrophy): Found in bulbar and pseudobulbar palsy, lower motor neuron (LMN) lesion of Xllth cranial nerve.
   • Tongue-tie (ankyloglossia).
   • Acute swelling: Infection, angioneurotic oedema.
5. Neurological disease
   • Flaccid wasted tongue with fasciculation: Bulbar palsy.
   • Spastic tongue without fasciculation: Pseudobulbar palsy.
   • Jack in the box sign: Rheumatic chorea.
   • Tremor: Aruciety neurosis, thyrotoxicosis, chronic alcoholism, Parkinsonism.
   • Deviation of the tongue: Deviated to the opposite side is due to upper motor lesion of the 12th cranial nerve. Deviated to the same side is due to lower motor lesion of the 12th nerve.
   • Loss of taste sensation: Anterior 2/3rd by facial nerve, posterior 1/3rd by glossopharyngeal nerve. (Site of taste sensation –sweet at the tip, sour at the margin, bitter at the back and salty at any part of the tongue).
   • Fasciculation: Bulbar palsy, LMN palsy of Xllth cranial nerve.
   • Trombone tongue: Rapid forward and backward movement of the tongue, found in general paresis of insane (GPI).
   • Chewing tongue: Found in athetosis

* Short Cases in Clinical Medicine, ABM Abdullah

1. Warm and sweaty hands: Hyperthyroidism
2. Cold and sweaty hands: Anxiety
3. Cold and dry hand: Peripheral vascular disease
4. Large, fleshy and sweaty hand: Acromegaly
5. Dry hands with coarse skin: Hypothyroidism
6. Delayed relaxation of grip: myotonic dystrophy (diagnosed by handshake or asking the patient to close and open the hands)
7. Deformities in the hands and fingures: Myotonic dystrophy, rheumatoid arthritis
8. Wrist drop: Radial nerve palsy
9. Claw hand: Ulnar nerve palsy
10. Carpal spasm: Tetany
11. Palm
    • Palor: Anaemia
    • Yellowish: Anaemia
    • Palmar erythema: Chronic liver disease
    • Single palmar crease (Simian crease): Down syndrome
    • Wasting of palmar muscles: Median and ulnar nerve palsies
12. Tremor
    • Fine tremor: Anxiety, thyrotoxicosis.
    • Resting tremor: Parkinson’s disease.
    • Flapping tremor: Liver failure, renal failure, respiratory failure
13. Bluish discoloration of the fingers: Cyanosis
14. Nail and nail beds
    • Clubbing: Suppurative lung disease, bronchial carcinoma, interstitial lung disease, congenital
      cyanotic heart diseases, liver cirrhosis, inflammatory bowel disease, familial etc.
    • Brittle and spoon chaped nail (koilonychia): Iron deficiency anaemia
    • Leuconychia: CLD, nephrotic syndrome, PEM
    • Splinter haemorrhage: Infective endocarditis
    • Brown line pigmentatign: Chronic kidney disease
    • Mees line: Arsenic poisoning
    • Thickening, crumbing and discoloration: Fungal infection (onychomycosis)
    • Onycholysis: Psoriasis
    • Beau’s line: Fever, cachexia, malnutriotion

As follows

1. Osler nodes (small painful violaceous raised nodule, 0. 5–1. 5 cm, present on the tip of the fingers and toes, also palmar aspect, probably due to development of vasculitis or septic emboli).
2. Splinter haemorrhage
3. Clubbing
4. Janeway lesion (large painless erythematous macule containing bacteria on palm, pulp of the fingers. It may be found in the sole)
5. Petechial haemorrhage
6. Infarction on the tip of the fingers

*Short Cases in Clinical Medicine, ABM Abdullah

As follows

1. Palmar erythema
2. Dupuytren contracture
3. Clubbing
4. Leukonychia
5. Flapping tremor
6. Spider angioma
7. Pigmentation
8. Jaundice
9. Scratch mark
10. Xanthoma
11. Cyanosis

*Short Cases in Clinical Medicine, ABM Abdullah

Nail abnormality may occur in many local, systemic and dermatological diseases. These are described below.

1. Clubbing, koilonychias, leukonychia
2. Pale nail: Anemia
3. Nail fold infarction: (usually vasculities due to any cause)
   • SLE
   • Dermatomyositis
   • Systemic sclerosis
   • Rheumatoid arthritis (RA)
   • Polyarteritis nodosa
4. Splinter haemorrhage: Linear dark brown, longitudinal flecks, parallel to long axis of nail.
   • Trauma (the commonest).
   • SBE
   • Septicaemia
   • Collagen disease (vasculitis) : SLE, RA and polyarteritis nodosa
   • Others : Haematological malignancy, severe anaemia, psoriasis. Rarely in trichinosis (usually transverse haemorrhage).
5. Half-and-half nail: Proximal part of nail is white-to-pink and distal part is red or brown. Causes are
   • CRF (the commonest cause)
   • Cirrhosis of liver
   • Occasionally, in normal person
   • Red half moon occurs in congestive cardiac failure (CCF).
6. Nail fold telangiectasia: Causes are
   • SLE
   • Systemic sclerosis.
   • Dermatomyositis
   • Mixed connective tissue disease (MCRD).
   • Raynaud phenomenon.
7. Beau line: Nonpigmented transverse line or grooves in nail due to transient arrest of nail growth. This appears at the same time, on all the nails, a few weeks after an acute illness. Causes are
   • Chronic illness (chronic infection, malignancy and collagen disease).
   • Prolonged fever.
   • Pneumonia
   • Coronary artery disease.
   • Others : Cachexia, malnutrition, psychiatric illness, use of cytotoxic drugs.
8. Onycholysis: Separation of distal nail plate from the nail bed (free edge looks white). Causes are
   • Psoriasis (the commonest).
   • Fungal infection.
   • Thyrotoxicosis (Plummer sign).
   • Idiopathic
   • Occasionally drugs (tetracycline and psoralen).
   • Porphyria
   • Trauma or faulty manicure.
9. Mee line: Single transverse white band in nail. Causes are
   • Chronic arsenic poisoning
   • CRF
   • Also, after chemotherapy and severe illness.
10. Yellow nail: Found in yellow nail syndrome, an inherited disease in which the nails are thick, yellow or pigmented with separation of distal part of nail bed due to hypoplasia of lymphatic system. It is associated with Iymphoedema of legs, bronchiectasis and pleurai effusion.
11. Loss of nail (or dystrophy): Causes are
    • Severe lichen planus.
    • Epidermolysis bullosa.
    • Trauma (tooth biting)
12. Nail pitting (depression in nail): Causes are
    • Psoriasis
    • Alopecia areata.
    • Atopic eczema (when involves proximal nail bed).
    • Pityriasis rosacea.
13. Brittle nail (easily broken): Causes are
    • Iron-deficiency anaemia.
    • Peripheral vascular disease.
    • Fungal infection.
    • Hypocalcaemia
    • Psoriasis
    • Injury (nail biting).
    • Idiopathic
14. Blue nail: Normal white Iunulae become blue, found in Wilson disease due to deposition of copper (normally, half-moon Iunulae at the proximal end of nail is white-blue half moon). Also found in cyanosis and ochronosis.
15. Red nail: May be normal finding. Also in polycythaemia, carbon monoxide poisoning (cherry red).
16. Brown nail: Usually present in chronic kidney disease (CKD).
17. Periungual or subungual fibroma: Suggests tuberous sclerosis (epiloia).
18. Fungal nail: Nail has thick, white, green, black, discolouration and crust formation.
19. Absent or small, dysplastic nail: Its causes are
    • Nail patella syndrome [autosomal dominant (AD), associated with no or hypoplastic patella and glomerulonephritis, abnormalities in eye].
    • Others : Congenital, traumatic and vasculitis.
20. Nail hyperpigmentation: May occur due to some drugs (such as zidovudine, doxorubicin, bleomycin, cyclophosphamide, fluorouracil, melphalan and nitrosoureas).
21. Terry nail: Proximal part is white or pink, but nail tip is red or brown. It is due to decrease in vascularity and an increase in connective tissue within the nail bed. Causes are
    • Old age (normally present in elderly).
    • Cirrhosis of liver.
    • CCF
    • Hyperthyroidism
    • Malnutrition
    • Renal failure.
22. Dark nail: May be a normal finding mostly in black people. Sometimes may be due to subungual melanoma.

Remember the following points

• Normal nail growth is 0.1 mm/day; finger nails grow quickly than toe nails.
• Nail plate grows continuously and slowly at the rate of 1 cm every 3 months. Hence, renewal of finger nails takes about 3-6 months, and toe nails that grow more slowly take 1 year.
• Rapid growth of nail plate occurs in psoriasis.
• Nail growth is arrested by acute illness and ischaemia (Beau line).

*Short Cases in Clinical Medicine, ABM Abdullah

Fat-soluble vitamins are vitamins A, D, E, and K.

Vitamins	Deficiency symptoms
Vitamin A	Night blindness Xerophthalmia Bitot’s spots Keratomalacia Blindness
Vitamin D	Rickets and osteomalacia
Vitamin E	Mild hemolytic anemia, ataxia and visual scotomas
Vitamin K	Delayed coagulation and bleeding

* Pre-exam preparation for medicine, HN Sarker

Water-soluble vitamins are:

• Thiamin (vitamin B₁)
• Riboflavin (vitamin B₂)
• Niacin (vitamin B₃)
• Pyridoxine (vitamin B₆)
• Biotin (vitamin B₇)
• Vitamin B₁₂ and folate
• Vitamin C (ascorbic acid).

* Pre-exam preparation for medicine, HN Sarker

1. Skin: Vitamin D
2. Intestine (by intestinal flora): Vitamin B₁₂, vitamin K, vitamin B₇

Vitamin	Major clinical features of deficiency	Dietary sources
Fat-soluble
A (retinol)	Xerophthalmia, night blindness, keratomalacia, follicular hyperkeratosis	Oily fish, liver, dairy products (provitamin A carotenoids – carrots, dark green leafy vegetables, corn, tomatoes)
D (cholecalciferol)	Rickets, osteomalacia	Oily fish, fortified breakfast cereals and margarine, eggs, milk
K	Coagulation defects	Green leafy vegetables, liver cheese, certain fruit (kiwi fruit, rhubarb)
E (α-tocopherol)	Neurological disorders, e.g. ataxia	Plant oils (soya, palm oil), animal fats, nuts, seeds, vegetables, wheatgerm
Water-soluble
B1 (thiamin)	Beriberi, Wernicke– Korsakoff syndrome	Wide range of animal and vegetable products. Fortified cereals, flour, and bread, unrefined cereals, grain, nuts, legumes, organ meats
B2 (riboflavin)	Angular stomatitis	Dairy products (major source) cereals grains, meat, fish, broccoli, spinach
Niacin	Pellagra	Meat, cereals
B6 (pyridoxine)	Polyneuropathy	Meat, cereals
B12 (cobalamin)	Megaloblastic anaemia, neurologicaln disorders	Meat, fortified breakfast cereals, eggs
Folate	Megaloblastic anaemia	Widely distributed in animal (especially liver) and plant foods (e.g. vegetables)
C (ascorbic acid)	Scurvy	Fresh vegetables, citrus fruits, strawberries, spinach, tomatoes

* Kumar and Clark’s Clinical Medicine, 9th Edition Box: 10.13 

Ocular manifestations of xeropthalmia:

• XN – Night blindness
• X1A – Conjunctival xerosis
• X1B – Bitot’s spot
• X2 – Corneal xerosis
• X3A – Corneal ulceration / keratomalacia involving < 1/3 of corneal surface
• X3B – Corneal ulceration/keratomalacia involving ≥ 1/3 of corneal surface
• XS – Corneal scar
• XF – Xerophthalmic fundi (white retinal lesion)

Extra-ocular manifestations:

• Skin chances: Dry scaly skin specially over the outer aspect of the limbs called follicular hyperkeratosis (phrynoderma).
• Susceptibility to infection: Increased.
• Sqamous metaplasia: Involving respiratory, urinary and vaginal epithelium.
• Urinary problem: Renal and vesical calculi, pyuria, haematuria.
• CNS problems: Raised intracranial pressure, rarely optic or cranial nerve palsy, mental retardation, apathy.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 80

All the stages of xerophthalmia should be treated immediately with vitamin A.

Dose recommendation:

Age	Dose	Day
<6 months	50,000 IU	0, 1, 14
6 – <12 months	1,00,000 IU	0, 1, 14
≥12 months	2,00,000 IU	0, 1, 14

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 80

Giving oral vitamin A supplement –

1. 100000 IU first day
2. 100000 IU second day
3. 100000 IU eighth day

* Pre-exam preparation for medicine, HN Sarker

The eye lesions are completely reversible at the stage of conjunctival or corneal xerosis, but once keratomalacia develops blindness is inevitable.

Prevention of xerophthalmia / vitamin A deficiency:

• Exclusive breast feeding.
• Routine vitamin A supplementation (every 6 months upto 5 years).
• Vitamin A supplementation in special situations e.g. diarrhoea and measles.
• Regular intake of vitamin A rich foods e.g. dark green, leafy vegetables, coloured fruits, egg, liver, fat of fish, meat, cod liver oil, mola-dhela fish etc.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 80

Acute overdose leads to nausea and headache, increased intracranial pressure and skin desquamation.

* Pre-exam preparation for medicine, HN Sarker

It can cause liver damage, hyperostosis, and teratogenicity.

* Pre-exam preparation for medicine, HN Sarker

Deficiency features are:

Beriberi—

1. Dry (or neurological) beriberi—manifests with chronic peripheral neuropathy and with wrist and/or foot drop and may cause Korsakoff’s psychosis and Wernicke’s encephalopathy.
2. Wet (or cardiac) beriberi—Generalized edema due to biventricular heart failure with pulmonary congestion.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 128; Pre-exam preparation for medicine, HN Sarker

Pellagra (the disease of the three Ds)— Dermatitis, diarrhea, and dementia.

* Pre-exam preparation for medicine, HN Sarker

The haematological disorders –

• Macrocytic or megaloblastic anaemias.

Neurological findings in B₁₂ deficiency –

1. Peripheral nerves
   • Glove and stocking paraesthesiae
   • Loss of ankle reflexes
2. Spinal cord
   • Subacute combined degeneration of the cord
     • Posterior columns – diminished vibration sensation and proprioception
     • Corticospinal tracts – upper motor neuron signs
3. Cerebrum
   • Dementia
   • Optic atrophy
4. Autonomic neuropathy

Davidson’s Principles and Practice of Medicine, 22nd edition Page: 129, 1024

Folic acid deficiency is more common. Because –

1. Folic acid is more destroyed by heating (60-90%) during cooking.
2. Requirement of folic acid is more.
3. Vitamin B₁₂ is less destroyed (10-30%) by heating during cooking.
4. Daily requirement of vit-B₁₂ is less (only 3 μg).
5. Vit-B₁₂ can be stored in liver for long time (3 years).

Scurvy is the deficiency features of vitamin C deficiency.

* Pre-exam preparation for medicine, HN Sarker

Pathogenesis –
Vitamin C is essential for hydroxylation of lysine and proline for the formation of collagen. Its deficiency leads to faulty collagen tissue synthesis in bones, cartilage and teeth. In addition, the intercellular substance of capillaries also become defective often leading to bleeding.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 80

Clinical features are—

1. Swollen gums which bleed easily
2. Petechial and perifollicular hemorrhages giving rise to corkscrew hair
3. Ecchymosis
4. Hemarthrosis
5. Gastrointestinal bleeding
6. Anemia
7. Poor wound healing.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 130; Pre-exam preparation for medicine, HN Sarker

Clinical manifestations: 

Peak incidence is around 6-24 months of age. Presenting symptoms include-

• Vague irritability and loss of appetite.
• The baby cries on handling e. g. dressing, bathing etc.
• Generalized tenderness especially in legs resulting in pseudo-paralysis and legs assume typical frog position.
• Bluish purple, spongy swelling of gum mucosa is seen when tmth are erupted.
• Sharp painful scorbutic rosary is palpable at costochondral junction and depression of sternum.
• Peri-follicular haemorrhage, petechial haemorrhage, ecchymosis of extremities, haematuria, melaena, orbital haemorrhage may be found.
• Delay in wound healing.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 80

X-findings are:

1. Epiphysis is ring-shaped, sclerotic and sharply demarcated (Wimberger’s sign).
2. Metaphysis is dense resembling a white line (white line of Frankle).
3. Beneath metaphysic, a lucent zone (Trumerfeld zone) is present.
4. There is spur at the corner (Pelkan’s spur).

* Pre-exam preparation for medicine, HN Sarker

• For rapid recovery oral Vit C 200 mg daily for several weeks. The administration of 3-4 ounces of tomato or orangejuice are equally effective.
  • Clinical recovery occurs within 24-48 hours.
  • Radiological improvement takes a week or two; disappearance of sub-periosteal haemonhage takes months.
• After scurvy has been cured, 35-50 mg of  vitamin C should be given daily as drug or in diet.
• Dietary supplements especially fresh fruits (orange, mango, pineapple, guava, etc.) and liver extract.
• Bottle-fed infants should be given fruit juice. Nursing mother should take sufficient vitamin C, which is secreted in the breast milk.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 81; Short Cases in Clinical Medicine, ABM Abdullah Page: 563

Deficiency features of vitamin D are:

– In children—Rickets

– In adult—Osteomalacia.

* Pre-exam preparation for medicine, HN Sarker

The main source of vitamin D in the body is synthesis of cholecalciferol from 7-dehydrocholesterol in the skin by the action of ultraviolet sunlight, a minor portion comes from diet. Cholecalciferol is inactive, which is converted first in the liver to 25-hydroxycholecalciferol (25(OH)D₃) and subsequently in the kidney (by the enzyme 1 hydroxylase) to 1,25-dihydroxycholecalciferol (1,25(OH)₂D₃) which is active form of vitamin D.

* Pre-exam preparation for medicine, HN Sarker

Functions of vitamin D on—

• Intestine—Vitamin D increases Ca²⁺ absorption from the gut.
• Bone—Vitamin D increases calcification of osteoid tissue and also bone resorption.
• Kidney—Vitamin D increases calcium reabsorption and phosphate excretion.

* Pre-exam preparation for medicine, HN Sarker

Rickets is a disease of growing bone which occurs in children before fusion of epiphysis and is due to
inadequate mineralization of growing bones leading to an excess of unmineralized matrix at the growing plate.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 81

1. General features
   • Short stature, listlessness, protruded abdomen, nutscle weakness.
2. Head
   • Box-like square head, hot-cross-bun appeafance of skull, craniotabes.
3. Teeth
   • Delayed dentition, dental caries and impaired enamel formation.
4. Chest
   • Pigeon chest deformity, painless rachitic rosary at costochondral junction, Harrison sulcus.
5. Spine
   • Deformities like scoliosis, kyphosis lordosis etc. These may lead to recurrent respiratory infections.
6. Extremities
   • Widening of wrist and ankle, vulgus and varus detbrmity, amerior bowing of leg, coxa vara, fractures and pain, gait deformity
7. Symptoms of ypercalcaemiah
   • Tetany, seizure, stridor due to laryngeal spasm.

* Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 82

1. X-ray upper and lower limbs including knee, ankle, elbows and wrist joints.
2. Serum calcium and phosphate (both are low).
3. Serum alkaline phosphatase (high).
4. Seium 25-hydroxy proline (low or absent).

* Short Cases in Clinical Medicine, ABM Abdullah Page: 562; Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 84

1. X-ray knee & wrist shows:
   • Widening, splaying, cupping, and irregularities of metaphysis
   • Distance between epiphysis and metaphysis is increased (zone of provisional calcification is lost)
   • Density of shaft of bone is reduced (ostmpenia)
   • Deformity of long bone may be present
   • Green stick fracture may be present
2. Chest X-ray shows:
   • Chondral ends of ribs are expanded, cupped and indistinct
   • Rachitic rosary may be identified radiologically.

* Pre-exam preparation for medicine, HN Sarker; Short Cases in Clinical Medicine, ABM Abdullah Page: 562; Step on to Paediatrics, Md Abid Hossain Mollah, 3rd Edition Page: 84

• 25-Hydroxycholecalciferol, 50 µg daily or active vitamin D metabolite ( 1-α-hydroxycholecalciferol ), 1- 2 µg daily or 1,25 di-hydroxycholecalciferol, 0.25 to 1.5 µg daily.
• Plus calcium-500-1000 mg daily. Higher dose may be required in patients with malabsorption.
• Adequate exposure to sunlight.
• Dietary supplement.

* Short Cases in Clinical Medicine, ABM Abdullah Page: 562

Common nutritional disorders are:

• Kwashiorkor
• Marasmus
• Iodine deficiency
• Night blindness due to vitamin A deficiency
• Iron deficiency anemia.

* Pre-exam preparation for medicine, HN Sarker

Vitamin B1 deficiency	Peripheral neuropathy Korsakoff’s psychosis Wernicke’s encephalopathy
Vitamin B6 deficiency	Peripheral neuropathy
Niacin deficiency	Dementia
Vitamin B12 deficiency	Peripheral neuropathy Subacute combined degeneration of spinal cord Optic atrophy Dementia

* Pre-exam preparation for medicine, HN Sarker

1. Abnormal micronutrient status is commonly manifest in clinical signs in the skin and mucous membranes, or in other systems.
2. Anthropometric measurements
   • Body mass index (BMI)
   • Waist circumference (measured at the level of the umbilicus)
   • Hip circumference (measured at the level of the greater trochanters)
   • Waist : hip ratios (show whether the distribution of fat is android or gynoid)
   • Skinfold measurements (can be used to calculate body fat content)
   • Mid-arm circumference (at the middle of the humerus) (muscle mass is estimated by subtracting triceps skinfold thickness from mid-arm circumference)
3. Measurement of body fat by bio-impedance or dual energy X-ray absorptiometry (DEXA) scanning.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 114

Systemic radiation effects

1. Acute effects
   • Haemopoietic syndrome
     • Severe lymphopenia
     • Thrombocytopenia
     • No new cells are formed in the marrow
   • Gastrointestinal syndrome
     • Vomiting
     • Intractable bloody diarrhoea follows, with dehydration, secondary infection and sometimes death
   • CNS syndrome
     • Nausea, vomiting, disorientation and coma.
     • Death due to cerebral oedema can follow
   • Radiation dermatitis
     • Skin erythema, purpura, blistering and secondary infection occur.
     • Total loss of body hair is a bad prognostic sign

2. Delayed effects
   • Infertility
   • Teratogenesis
   • Cataract
   • Neoplasia:
     • Acute myeloid leukaemia
     • Thyroid
     • Salivary glands
     • Skin
     • Others

* Kumar and Clark’s Clinical Medicine, 9th Edition Box 5.5

Temperature-related disorders are:

• Hypothermia
• Heat cramps
• Heat syncope
• Heat exhaustion
• Heat stroke.

* Pre-exam preparation for medicine, HN Sarker

Figure: Clinical features of abnormal core temperature. The hypothalamus normally maintains core temperature at 37°C.

* Figure: Davidson’s Principles and Practice of Medicine, 22nd edition Page: 104

 

When core temperature falls below 35°C, it is called hypothermia.

* Pre-exam preparation for medicine, HN Sarker

Common causes are:

• Immersion in cold water
• Exposure to extreme climates such as during hill walking
• Hypothyroidism
• Glucocorticoid insufficiency
• Stroke
• Hepatic failure

* Pre-exam preparation for medicine, HN Sarker

Clinical features are:

• Depressed conscious level
• Dehydration
• Confusion
• Muscle stiffness
• Ice cold and pale
• Bradycardia

* Pre-exam preparation for medicine, HN Sarker

ECG may show characteristic J waves, which occur at the junction of the QRS complex and the ST segment.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 104

Treatments are:

1. Resuscitation-maintain ABC
2. Rewarming the patient in a controlled manner
3. Treatment of associated hypoxia (by oxygenation and ventilation if necessary), fluid and electrolyte disturbance and dysrhythmias if present.

 * Pre-exam preparation for medicine, HN Sarker

Heat-related illnesses are:

• Heat cramps
• Heat syncope
• Heat exhaustion
• Heat stroke.

* Pre-exam preparation for medicine, HN Sarker

Heat stroke occurs when the core body temperature rises above 40°C and is a life-threatening condition.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 106

 

• The symptoms of heat exhaustion (dehydration, tachycardia, irritability, fatigue, headache, weakness) progress to include headache, nausea and vomiting.
• Neurological manifestations include –
  • a coarse muscle tremor and confusion,
  • aggression or loss of consciousness.
• The patient’s skin feels very hot, and sweating is often absent due to failure of thermoregulatory mechanisms.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 106

Treatments are:

1. The patient should be resuscitated with rapid cooling by spraying with water, fanning, and ice packs in the axillae and groins.
2. Cold crystalloid intravenous fluids are given but solutions containing potassium should be avoided.
3. Over-aggressive fluid replacement must be avoided, as it may precipitate pulmonary oedema or further metabolic disturbance.
4. Appropriate monitoring of fluid balance, including central venous pressure, is important.
5. Once emergency treatment is established, heat stroke patients are best managed in intensive care.
6. Clear advice to avoid heat and heavy exercise during recovery is important.

 * Davidson’s Principles and Practice of Medicine, 22nd edition Page: 106

Complications include –

• hypovolaemic shock,
• lactic acidosis,
• disseminated intravascular coagulation,
• rhabdomyolysis,
• hepatic and renal failure, and
• pulmonary and cerebral oedema.

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 106

Investigations for complications include –

• routine haematology and biochemistry,
• coagulation screen,
• hepatic transaminases (aspartate aminotransferase and alanine aminotransferase),
• creatine kinase and
• chest X-ray

* Davidson’s Principles and Practice of Medicine, 22nd edition Page: 106

In heat stroke, core temperature is >40°C and sweating is absent but in heat exhaustion, core temperature is > 37–40°C and sweating is present.

* Pre-exam preparation for medicine, HN Sarker

Hyperthermia is an increase in body temperature over the body’s thermoregulatory set-point, due to excessive heat production and/or insufficient thermoregulation. It is not a fever.

Hyperpyrexia is a fever with an extreme elevation of body temperature greater than or equal to 41.5°C (106.7°F).

* Pre-exam preparation for medicine, HN Sarker

Hyperpyrexia	Hyperthermia
Hyperpyrexia is a fever	It is not a fever
Temperature is above the normal temperature but within thermoregulatory set-point	The body temperature rises above its set-point
Body generates heat to achieve this temperature	The body temperature rises due to an outside source

* Pre-exam preparation for medicine, HN Sarker

 

In a typical adult male, total body water (TBW) is approximately 60% of body weight (somewhat more for infants and less for women).

Figure: Normal distribution of body water and electrolytes. Schematic representation of volume (L = litres) and composition (dominant ionic species only shown) of the ICF and ECF in a 70 kg male. The main difference in composition between the plasma and ISF is the presence of appreciable concentrations of protein in the plasma but not the ISF. ECF = extracellular fluid; ICF = intracellular fluid; ISF = interstitial fluid; IVF = intravascular fluid; TBW = total body water.

* Davidson’s Principles and Practice of Medicine, 22nd edition; Goldman’s Cecil Medicine 24th edition

Name	Average normal value* (mOsm/L H2O)	Reference Ranges**
Na+	142	135 – 145 mmol/L
K+	4.2	3.5 – 5 mmol/L
Ca++	1.3	8.4­ – 10.2 mg/dl
Mg++	0.8	1.5 – 2.4 mg/dL
Cl–	106	98 – 106 mmol/L
HCO3–	24	22 – 30 mmol/L
PO4– –	2	2.9 – 5.4 mg/dL
SO4– –	0.5	2.4 – 4.1 mg/dL

* Guyton and Hall Textbook of Medical Physiology 13th Edition; ** Step on to Paediatrics, Md Abid Hossain Mollah

Normal Na level: 135–145 mmol/L

Normal plasma concentration 3.5–5 mmol/L

When plasma sodium

Classifications—
According to severity—

1. Mild hyponatremia: When sodium level is 130–135 mmol/L (S/S:Malaise, nausea)
2. Moderate hyponatremia: When sodium level is 120– 130 mmol/L (S/S: Headache, vomiting, lethargy)
3. Severe hyponatremia: When sodium level is
4. Very severe hyponatremia: When Na level is

*Pre-exam preparation for medicine, HN Sarker

Neurological dysfunction showing:

• Anorexia
• Nausea and vomiting
• Apathy
• Dizziness
• Confusion
• Convulsion
• Coma.

*Pre-exam preparation for medicine, HN Sarker

Volume status	Examples
Hypovolaemic (sodium deficit with a relatively smaller water deficit)	Renal sodium losses Diuretic therapy (especially thiazides) Adrenocortical failure Gastrointestinal sodium losses Vomiting Diarrhoea Skin sodium losses Burns
Euvolaemic (water retention alone)	Primary polydipsia Excessive electrolyte-free water infusion SIADH Hypothyroidism
Hypervolaemic (sodium retention with relatively greater water retention)	Congestive cardiac failure Cirrhosis Nephrotic syndrome Chronic renal failure (during free water intake)
SIADH = syndrome of inappropriate antidiuretic hormone secretion

* Davidson’s Principles and Practice of Medicine, 22nd edition

Figure: The diagnostic approach to hyponatremia. U_Na = Urinary sodium (mmol/L).

* Harrison’s Principles of Internal Medicine, 19th Edition

The cause of hyponatraemia with apparently normal extracellular volume requires investigation:

1. Plasma and urine electrolytes and osmolalities.
   • The plasma plasma concentrations of sodium, chloride and urea are low, giving a low osmolality.
   • The urine sodium concentration is usually high and the urine osmolality is typically higher than the plasma osmolality. However, maximal dilution (
2. Further investigations. These are needed to exclude –
   • Addison’s disease,
   • hypothyroidism,
   • syndrome of inappropriate ADH secretion (SIADH) and
   • water retention induced by drugs, e.g. chlorpropamide.

* Kumar and Clark’s Clinical Medicine, 9th Edition

The treatment of hyponatraemia is critically dependent on its rate of development, severity and underlying cause. Treatments are:

1. If hyponatremia has developed rapidly (over hours to days), severe (
2. Treatment of underlying cause.
   • For hypovolaemic patients, controlling the source of sodium loss, and administering intravenous saline if clinically warranted.
   • Patients with dilutional hyponatraemia (euvolaemic) generally respond to fluid restriction in the range of 600–1000 mL/day, accompanied where possible by withdrawal of the precipitating stimulus (such as drugs causing SIADH).
   • Hypervolaemic patients with hyponatraemia need treatment of the underlying condition, accompanied by cautious use of diuretics in conjunction with strict fluid restriction.

*Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition

Note: Key points in the management of hyponatraemia

1. Always treat the underlying cause
2. What is the volume status of the patient?
   • If hypovolaemic: rehydrate with 0.9% saline
   • If euvolaemic (SIADH): restrict fluid to 500–700 mL/day
   • If hypervolaemic (chronic kidney disease/heart failure): restrict fluid and salt
3. Does the patient have symptomatic hyponatraemia (seizures/coma)?
   • Yes: involve critical care input early; 3% saline 1 mL/kg over 1 h
4. Is the hyponatraemia acute or chronic?
   • If acute: more likely to develop symptomatic hyponatraemia
   • If chronic: increased risk of osmotic demyelination due to rapid correction
   • If unsure: give 3% saline very slowly
5. Check sodium levels frequently: may need to check Na every 1–2 h
6. Correction must not exceed 10 mmol in first 24 h and 18 mmol in 48 h

* Kumar and Clark’s Clinical Medicine, 9th Edition

Rapid correction may lead to central pontine mylinolysis (osmotic demyelinating syndrome).

Note:

In hyponatraemia that has developed slowly (over weeks to months), brain cells adapt to slowly developing hypo-osmolality by reducing the intracellular osmolality, thus maintaining normal cell volume. Under these conditions, an abrupt increase in extracellular osmolality can lead to water shifting out of neurons, abruptly reducing their volume and causing them to detach from their myelin sheaths. The resulting ‘myelinolysis’ can produce permanent structural and functional damage to mid-brain structures, and is generally fatal. The rate of correction of the plasma Na concentration in chronic asymptomatic hyponatraemia should not exceed 10 mmol/L/day, and an even slower rate is generally safer.

Figure: Hyponatraemia and the brain. Numbers represent osmolality (osmo) in mmol/kg.

*Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition

Points to know:

1. Daily maximum Na⁺ sodium correction limit:
   • Acute case: 0.5 mmol/L/hours e.g. (weight in kg × 12) mmol/day
   • Chronic case: 10 mmol/L/day e.g. (weight in kg × 10) mmol/day
2. Total sodium deficit: 0.6 × weight in kg × (Desired Na⁺ – Observed Na⁺) mmol
3. In case of children, daily maintenance Na⁺ 2–3 mmol/kg/day for next 2 days needs to be added.
4. Total fluid requirement:
   • (Daily limit or requirement/154) L for normal saline (0.9% NaCl)
   • (Daily limit or requirement/514) L for 3% NaCl
5. Choice of fluid:
   • 0.9% NaCl in asymptomatic patient or Na⁺ >110 mmol/L
   • 3% NaCl in rapidly developed hyponatremia (over hours to days), severe hyponatremia (

Case 1: Patient asymptomatic or Na⁺ >110 mmol/L

Scenario: Patient weight 50 kg, serum Na+ 125mmol/L Calculation: 1.     In case of this patient, daily maximum sodium correction limit: 50 × 10 = 500 mmol 2.     His total sodium deficit: 0.6 × 50 × (135 – 125) = 300 mmol, that should be corrected within 1 day. 3.     Total fluid requirement: (300/154) = 1.9 ≈ 2 L normal saline

Case 2: Symptomatic rapidly developed hyponatremic patient or Na⁺

Scenario: Patient weight 50 kg, serum Na+ 105mmol/L Calculation: 1.     In case of this patient, daily maximum sodium correction limit: 50 × 12 = 600 mmol 2.     His total sodium deficit: 0.6 × 50 × (135 – 105) = 900 mmol, that should be corrected in 2 days. 3.     Total fluid requirement: a.     Day 1: (600/514) ≈ 1 L 3% NaCl b.     Day 2: correction of rest of the 300 mmol

Case 3: 7 days old baby

Scenario: Patient weight 1.5 kg, serum Na+ 122mmol/L Calculation: 1.     In case of this patient, daily maximum sodium correction limit: 1.5 × 10 = 15 mmol 2.     Sodium requirement a.     His sodium deficit: 0.6 × 1.5 × (135 – 122) = 11.7 mmol, b.     Maintenance Na+: 3 × 1.5 × 2 = 9 mmol c.     Total: 11.7 + 9 = 20.7 ≈ 21 mmol, that should be corrected in 2 days.

Excess DA administration or sample collected from hand used for IV line.

*Pre-exam preparation for medicine, HN Sarker

Pseudohyponatremia is the spurious low value seen if a high proportion of the serum volume is free of water. For example severe hyperlipidemia.

*Pre-exam preparation for medicine, HN Sarker

When K⁺ level > 5 mmol/L, then its called hyperkalemia.

Types are:

1. Mild hyperkalemia: 5–6 mmol/L
2. Moderate hyperkalemia: 6–7 mmol/L
3. Severe hyperkalemia: >7 mmol/L

*Pre-exam preparation for medicine, HN Sarker

Common causes are:

1. Renal impairment
   • Acute renal failure
   • Chronic renal failure
2. Adrenocortical insufficiency (Addison’s disease)
3. Excess intake or load—
   • Exogenous—Dietary and IV therapy.
   • Endogenous—Hemolysis and rhabdomyolysis.
4. Transcellular shift—Acidosis (diabetic ketoacidosis), insulin deficiency, hyperkalemic periodic paralysis.
5. Drugs—ACE inhibitor and potassium sparing diuretics.

Figure: Diagnostic decision tree for hyperkalaemia. Creatinine of 500 μmol/L = 5.67 mg/dL.

*Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition

Clinical features –

1. Hyperkalaemia typically presents with progressive muscular weakness (unless (as is commonly the case) the hyperkalaemia is associated with metabolic acidosis, causing Kussmaul respiration).
2. Sometimes there are no symptoms until cardiac arrest (in diastole) occurs. Hyperkalaemia causes depolarization of cell membranes, leading to decreased cardiac excitability, hypotension, bradycardia and eventual asystole.

*Davidson’s Essentials of Medicine, 2nd Edition Page 147; Kumar and Clark’s Clinical Medicine, 9th Edition

ECG changes are:

1. Tall peaked T-waves
2. Wide QRS complexes
3. Loss of P-wave
4. Sine wave.

*Pre-exam preparation for medicine, HN Sarker; Figure: Davidson’s Principles and Practice of Medicine, 22nd edition

Management—

Treatment of hyperkalaemia depends on its severity and the rate of development.

1. In the absence of neuromuscular symptoms or ECG changes –
   • Reduction of potassium intake and correction of underlying abnormalities may be sufficient.
2. However, in acute and/or severe hyperkalaemia (plasma K > 6.5–7.0 mmol/L) more urgent measures must be taken.
   • Intravenous calcium gluconate (10 mL of 10% solution)— To stabilize conductive tissue membranes.
   • Inhaled β2 agonist, e.g. salbutamol. or, Intravenous glucose (50 mL of 50% solution) and insulin (5 U Actrapid).
   • Intravenous sodium bicarbonate (100 mL of 8.4% solution), if acidosis present.
   • Remove K⁺ from body, intravenous furosemide, and normal saline.
   • Ion-exchange resin (e.g. resonium) orally or rectally.
   • Dialysis.

*Pre-exam preparation for medicine, HN Sarker; Davidson’s Principles and Practice of Medicine, 22nd edition Page 443

During venepuncture for blood sample collection, due to incorrect/repeated handling there may be—

• Tissue damage
• RBC damage
• Endothelial cell damage
• Delayed processing.
  This results in release of potassium and show hyperkalemia in blood sample, although patient’s K⁺ is normal.

*Pre-exam preparation for medicine, HN Sarker

Figure:  Causes and diagnostic decision tree for hypokalaemia. (ACTH = adrenocorticotrophic hormone)

* Davidson’s Principles and Practice of Medicine, 22nd edition

Causes of hypokalaemia:

1. Increased renal excretion (Urinary K⁺ >20 mmol/day)
   • Diuretics: – Thiazides, loop diuretics
2. Increased aldosterone secretion
   • Liver failure
   • Heart failure
   • Nephrotic syndrome
   • Cushing syndrome
   • Conn syndrome
   • ACTH-producing tumours
3. Exogenous mineralocorticoid
   • Corticosteroids
   • Liquorice (potentiates renal actions of cortisol)
4. Renal disease
   • Renal tubular acidosis types 1 and 2
   • Renal tubular damage (diuretic phase)
   • Acute leukaemia
   • Nephrotoxicity: Amphotericin, Aminoglycosides, Cytotoxic drugs
   • Release of urinary tract obstruction
   • Bartter syndrome
   • Liddle syndrome
   • Gitelman syndrome
5. Reduced intake of K⁺
   • Intravenous fluids without K⁺
   • Dietary deficiency
6. Redistribution into cells
   • β-Adrenergic stimulation
   • Acute myocardial infarction
   • Beta-agonists, e.g. fenoterol, salbutamol
   • Insulin treatment, e.g. treatment of diabetic ketoacidosis
   • Correction of megaloblastic anaemia, e.g. B12 deficiency
   • Alkalosis
   • Hypokalaemic periodic paralysis
7. Gastrointestinal losses (Urinary K⁺ 
   • Vomiting
   • Severe diarrhoea
   • Purgative abuse
   • Villous adenoma
   • Ileostomy or uterosigmoidostomy
   • Fistulae
   • Ileus/intestinal obstruction

* Kumar and Clark’s Clinical Medicine, 9th Edition Box 9.15

ECG changes are:

1. Small or inverted T waves,
2. Prominent U waves (after T wave), a
3. A long PR interval, and
4. Depressed ST segments.

** Oxford Handbook of Clinical Medicine, 9th Edition Page: 688; Figure: Davidson’s Principles and Practice of Medicine, 22nd edition

Treatments are:

1. The underlying cause should be identified and treated if possible.
2. Acute hypokalemia may correct spontaneously.
3. In most cases, the oral administration of potassium supplements in the form of slow-release potassium or effervescent potassium, is sufficient.
4. Intravenous potassium replacement is required only in conditions such as cardiac arrhythmias, muscle weakness or severe diabetic ketoacidosis.

*Pre-exam preparation for medicine, HN Sarker

Treatment

1. If mild: (>2.5mmol/L, no symptoms) give oral K+supplement. Review K+ after 3 days. If taking a thiazide diuretic, and K+ >3.0 consider repeating and/or K+ sparing diuretic.
2. If severe: (<2.5mmol/L, and/or dangerous symptoms) give IV potassium cautiously, not more than 20mmol/h, and not more concentrated than 40mmol/L. Do not give K+ if oliguric.

Note:

• Never give K+ as a fast stat bolus dose. *
• The rate of administration depends on the severity of hypokalaemia and the presence of cardiac or neuromuscular complications, but should generally not exceed 10 mmol of potassium per hour. **

* Oxford Handbook of Clinical Medicine, 9th Edition, Page: 688; ** Davidson’s Principles and Practice of Medicine, 22nd edition, Page: 442

Clinical assessment –

Mild hypocalcaemia is often asymptomatic but, with more profound reductions in serum calcium, tetany can occur.

Hypocalcaemia tetany

• This is characterised by muscle spasms due to increased excitability of peripheral nerves.
• Children are more liable to develop tetany than adults.
• In childern:
  • A characteristic triad of –
    1. carpopedal spasm,
       • flexion of the metacarpophalangeal joints of the fingers and
       • adduction of the thumb (‘main d’accoucheur’)
    2. stridor (caused by spasm of the glottis) and
    3. convulsions, although one or more of these may be found independently of the others.
  • Pedal spasm can also occur but is less frequent.
• In adult:
  • Adults can also develop carpopedal spasm in association with tingling of the hands and feet and around the mouth,
  • Stridor and fits are rare.

Signs:

Latent tetany may be detected by eliciting –

1. Trousseau’s sign; inflation of a sphygmomanometer cuff on the upper arm to more than the systolic blood pressure is followed by carpal spasm (tetanic spasm of the singers and wrist) within 3 minutes.
2. Less specific is Chvostek’s sign, in which tapping over the branches of the facial nerve as they emerge from the parotid gland produces twitching of the ipsilateral facial muscles.

Other features:

• Hypocalcaemia can cause papilloedema and prolongation of the ECG QT interval, which may predispose to ventricular arrhythmias.
• Prolonged hypocalcaemia and hyperphosphataemia (as in hypoparathyroidism) may cause calcification of the basal ganglia, grand mal epilepsy, psychosis and cataracts.
• Hypocalcaemia associated with hypophosphataemia, as in vitamin D deficiency, causes rickets in children and osteomalacia in adults.

*Davidson’s Principles and Practice of Medicine, 22nd edition Page 768, 769; Kumar and Clark’s Clinical Medicine, 9th Edition; Figure: Oxford Handbook of Clinical Medicine, 9th Edition Page: 692

 

The approach to treatment depends on –

• the severity of the hypocalcemia,
• the rapidity with which it develops, and
• the accompanying complications (e.g., seizures, laryngospasm).

Mild symptoms:

• Oral calcium 5mmol/6 hourly, with daily plasma Ca²⁺ levels.**

Acute, symptomatic hypocalcemia

• It is initially managed with 10–20 mL 10% calcium gluconate (diluted in 50 mL of 5% dextrose or 0.9% sodium chloride) given intravenously over 10-20 minutes.
• Continuing hypocalcemia often requires a constant intravenous infusion (equivalent of 10 mL 10% calcium gluconate/hr, typically 10 ampules of calcium gluconate or 900 mg of calcium in 1 L of 5% dextrose or 0.9% sodium chloride administered over 24 h).
• Cardiac monitoring is recommended.
• Accompanying hypomagnesemia, if present, should be treated with appropriate magnesium supplementation.

Chronic hypocalcemia due to hypoparathyroidism

• It is treated with calcium supplements and either vitamin D2 or D3 (25,000–100,000 U daily) or calcitriol [1,25(OH)₂D, 0.25–2 μg/d].

 

*Harrison’s Principles of Internal Medicine, 19th Edition Page: 315; Davidson’s Principles and Practice of Medicine, 22nd edition Page 790; ** Oxford Handbook of Clinical Medicine, 9th Edition Page: 692

 

 

Symptoms and signs of hypercalcaemia include –

• polyuria and polydipsia,
• renal colic,
• lethargy,
• anorexia,
• nausea,
• dyspepsia and peptic ulceration,
• constipation,
• depression,
• drowsiness and impaired cognition.

Patients with malignant hypercalcaemia can have a rapid onset of symptoms and may have clinical features that help to localise the tumour. The classic symptoms of primary hyperparathyroidism are described by the adage ‘bones, stones and abdominal groans’, but few patients present in this way nowadays and the disorder is most often picked up as an incidental finding on biochemical testing. A family history of hypercalcaemia raises the possibility of FHH or MEN**.

**FHH = Familial hypocalciuric hypercalcemia, MEN = Multiple endocrine neoplasia.

 

*Davidson’s Principles and Practice of Medicine, 22nd edition Page 767