Chempath ALM

  1. A 20-year-old female is found to have the following blood report taken as part of a routine assessment.
    Hb 114g/L (120 - 155)
    MCV 68 fL (78 - 100)
    WBC 7.2 x 109/L (4 - 11)
    Differential Normal
    Platelets 320 x 109/L (150 - 400)

    No abnormal cells seen on blood film.
    Select one:

    N. Thalassaemia
  2. A 62-year-old woman complains of slowly progressive tiredness. There is a past history of hypothyroidism. She eats an adequate diet and has no gastrointestinal tract symptoms.
    Hb 72g/L (120 - 155)
    MCV 110 fL (78 - 100)
    WBC 5.2 x 109/L (4 - 11)
    Neutrophils 2.1 x 109/L (2 - 7.5)
    Platelets 135 x 109/L (150 - 400)

    Blood film shows occasional hypersegmented neutrophil.

    Select one:

    N. Vitamin B12 deficiency
  3. A 60 year old man is receiving steroid and anti-inflammatory drug treatment for rheumatoid arthritis. He complains of continuing joint pain and stiffness and tiredness.
    Hb 102g/L (130 - 180) MCV 79 fL (78 - 100)
    WBC 10.2 x 109/L (4 - 11)
    Neutrophils 7.0 x 109/L (2 - 7.5)
    Platelets 421 x 109/L (150 - 400)
    No abnormal cells seen on blood film.
    Select one:

    L. Chronic disease
  4. A 60-year-old man with known alcoholism has the following blood film.
    Hb 110g/L (130 - 180)
    MCV 111 fL (78 - 100)
    WBC 5.3 x 109/L (4 - 11)
    Differential Normal
    Platelets 190 x 109/L (150 - 400)

    Blood film: oval macrocytes and hypersegmented neutrophils present.

    Select one:

    A. Folic acid deficiency
  5. A 24-year-old man has a one month history of slowly increasing tiredness. Over this period he has noted increased bruising on his legs.
    Hb 64g/L (130 - 180)
    MCV 82 fL (78 - 100)
    WBC 0.9 x 109/L (4 - 11)
    Neutrophils 0.4 x 109/L (2 - 7.5)
    Platelets 21 x 109/L (150 - 400)

    No abnormal cells seen on blood film.

    Select one:

    G. Aplastic anaemia
  6. A 22-year-old vegetarian woman complains of tiredness. She has two children aged 1yr and 3yrs. No abnormality is found on physical examination.
    Hb 92g/L (120 - 155)
    MCV 69fL (78 - 100)
    WBC 8.4 x 109/L (4 - 11)
    Differential Normal
    Platelets 490 x 109/L (150 - 400)

    Select one:

    G. Iron deficiency
  7. A 68-year-old man is found to have an abnormal blood film on a routine medical assessment.
    Hb 140 g/L (130 - 180)
    MCV 85fL (78 - 100)
    WBC 42 x 109/L (4 - 11)
    Neutrophils 4.8 x 109/L (2 - 7.5)
    Lymphocytes 36 x 109/L (0.9 - 3.6)
    Platelets 220 x 109/L (150 - 400)

    Blood film - smear cells noted
    Select one:

    L. Chronic lymphocytic leukaemia
  8. A 72-year-old man presents with an one month history of increasing back pain and sternal pain.
    Hb 115g/L (130 - 180)
    MCV 85fL (78 - 100)
    WBC 7.2 x 109/L (4 - 11)
    Differential Normal
    Platelets 110 x 109/L (150 - 400)

    Blood film: marked rouleaux
    Select one:

    K. Multiple myeloma
  9. A 60-year-old woman is loosing weight, tired and has a spleen 10cm below the costal margin. She is red cell transfusion dependent
    Hb 72g/L (125 - 155)
    MCV 90fL (78 - 100)
    WBC 4.0 x 109/L (4 - 11)
    Platelets 80 x 109/L (150 - 400)

    Blood film: marked leukoerythroblastic changes and tear-drop shaped red cells.
    Select one:

    M. Myelofibrosis
  10. A 65-year-old man has an enlarged spleen and complains of headache and skin itch.
    Hb 198g/L (130 - 180)
    MCV 74fL (78 - 100)
    WBC 12 x 109/L (4 - 11)
    Differential Mild neutrophilia
    Platelets 450 x 109/L (150 - 400)
    Select one:

    K. Polycythaemia vera
  11. A 7-year-old boy presented with tiredness and nose bleeds of one weeks duration. Examination revealed a palpable spleen and mildly enlarged lymph nodes in all areas.
    Hb 90g/L
    MCV 90fL (78 - 100)
    WBC 48 x 109/L (4 - 11)
    Neutrophils 0.7 x 109/L (2 - 7.5)
    Platelets 15 x 109/L (150 - 400)

    Blood film - A large population of blasts with no cytoplasmic granules. Auer rods not seen.
    Select one:

    E. Acute lymphoblastic leukaemia
  12. A 48-year-old man presented with a left sided transient ischaemic attack (now fully resolved). The spleen is palpable 2cm below the left costal margin.
    Hb 140g/L (130 - 180)
    MCV 90fL (78 - 100)
    WBC 13.2 x 109/L (4 - 11)
    Neutrophils 9.8 x 109/L (2 - 7.5)
    Lymphocytes 3.1 x 109/L (0.9 - 3.6)
    Platelets 1620 x 109/L (150 - 400)
    Select one:

    K. Essential thrombocythaemia
  13. A 19-year-old female presents with a sore throat and bilaterally enlarged and painful cervical lymph nodes. The spleen is palpable.
    Hb 130g/L (120 - 155)
    MCV 83fL (78 - 100)
    WBC 14.2 x 109/L (4 - 11)
    Neutrophils 5.2 x 109/L (2 - 7.5)
    Lymphocytes 9.0 x 109/L (0.9 - 3.6)
    Platelets 140 x 109/L (150 - 400)

    Blood film: many atypical lymphocytes.
    Select one:

    I. Glandular fever (infectious mononucleosis)
  14. A 32-year-old man is presents with tiredness and nose bleeds of one weeks duration. Examination revealed a palpable spleen. Petechiae were present.
    Hb 90 g/L (130 - 180)
    MCV 90fL (78 - 100)
    WBC 4.2 x 109/L (4 - 11)
    Neutrophils 0.7 x 109/L (2 - 7.5)
    Platelets 15 x 109/L (150 - 400)

    Blood film – Blood cells are seen with occasional Auer rods observed.
    Select one:

    M. Acute myeloblastic leukaemia
  15. A 72-year-old man is seen for a three monthly review. He is being treated for hypertension, type 2 diabetes and followed for known prostate cancer.
    Hb 105g/L (130 - 180)
    MCV 80fL (78 - 100)
    WBC 6.2 x 109/L (4 - 11)
    Neutrophils 3.1 x 109/L (2 - 7.5)
    Platelets 310 x 109/L (150 - 400)

    Occasional myelocyte and nucleated red cells seen (leukoerythroblastic changes).
    Select one:

    N. Metastatic carcinoma to bone marrow
  16. A 23-year-old woman is bleeding heavily (per vagina) after a traumatic delivery of a term infant. There is bleeding from an IV insertion site.
    Hb 82g/L (120 - 155)
    MCV 92fL (78 - 100)
    WBC 14.2 x 109/L (4 - 11)
    Neutrophils 11.4 x 109/L (2 - 7.5)
    Platelets 31 x 109/L (150 - 400)

    PT (INR) 2.1 (0.8 - 1.2)
    aPTT 72 sec (25 - 41)
    Fibrinogen 0.7g/L (2 - 4)

    Select one:

    B. Disseminated intravascular coagulation
  17. A 60-year-old man is admitted for coronary artery bypass surgery.
    Hb 138g/L (130 - 180)
    MCV 92fL (78 - 100)
    WBC 7.6 x 109/L (4 - 11)
    Differential: normal Platelets 320 x 109/L (150 – 400)
    PFA 100 190 sec (100 - 150)

    Select one:

    I. Aspirin therapy
  18. A 20-year-old female is referred from the gynaecologists (who find no abnormality) with menorrhagia.
    Hb 102g/L (120 - 155)
    MCV 71fL (78 - 100)
    WBC 6.2 x 109/L (4 - 11)
    Differential Normal
    Platelets 430 x 109/L (150 - 400)

    PT (INR) 1.1 (0.8 - 1.2)
    aPTT 53 sec (25 - 41)
    Fibrinogen 3.4g/L (2 - 4)
    PFA 100 (bleeding time) 240 sec (100 - 150)
    Select one:

    P. Von Willibrand's disease
  19. A 32-year-old man had an upper respiratory tract, viral type, illness two weeks before developing bruising and nose bleeds.
    Hb 138g/L (130 -180)
    MCV 92fL (78 - 100)
    WBC 9.3 x 109/L (4 - 11)
    Differential Normal
    Platelets 6 x 109/L (150 - 400)

    PT (INR) 1.0 (0.8 - 1.2)
    aPTT 36 sec (25 - 41)
    Fibrinogen 3.1g/L (2 - 4)
    Select one:

    Q. Immune thrombocytopenic purpura
  20. An 18-year-old male has been fit and well and with no provocation develops a painful swollen left calf. Doppler ultrasonograph demonstrates a proximal vein deep venous thrombosis.
    Hb 140g/L (130 - 180)
    MCV 87fL (78 - 100)
    WBC 8.4 x 109/L (4 - 11)
    Differential Normal
    Platelets 310 x 109/L (150 - 400)

    Pt (INR) 1.1 (0.8 - 1.2)
    aPTT 30 sec (25 - 41)
    Fibrinogen 3.1g/L (2 - 4)
    PFA 100 (bleeding time) 120 sec (100-150)
    Select one:

    C. Inherited thrombophilia eg antithrombin III deficiency
  21. A 50-year-old woman with known diabetes has a routine blood test which demonstrates the following:
    Na 130 (135–145 mmol/L)
    K 4.1 (3.5–5.0 mmol/L)
    Urea 4.2 (3.0–7.0 mmol/L)
    Glucose 3.1 (2.2–5.5 mmol/L)
    Osmolality 283 (275–295 mOsm/kg)

    F Hyperlipidaemia

    Pseudo-hyponatraemia can occur in patients with hyperlipidaemia or hyperproteinaemia. In such states, lipids and proteins will occupy a high proportion of the total serum volume. Although the sodium concentration in serum water is in fact normal, a lower sodium concentration will be detected due to dilution by increased lipids and protein molecules. As a consequence, there is an apparent hyponatraemia.

    A spurious result due to the sample being taken from the drip arm can also cause pseudo-hyponatraemia. A true hyponatraemic state occurs when the osmolality is simultaneously low.
  22. A 45-year-old man is seen by his specialist. His last blood and urine tests demonstrated the following:
    Na 129 (135–145 mmol/L)
    K 5.5 (3.5–5.0 mmol/L)
    Urea 8.2 (3.0–7.0 mmol/L)
    Glucose 4.2 (2.2–5.5 mmol/L)
    Osmolality 265 (275–295 mOsm/kg)
    Urine osmolality 26 mOsm/kg

    H Chronic kidney disease

    Chronic kidney disease results in urinary protein loss and hence oedema. A reduced circulating volume causes activation of the renin–angiotensin system, thereby raising blood sodium levels. This in turn causes release of antidiuretic hormone (ADH) from the posterior pituitary leading to water retention and hypervolaemic hyponatraemia.

    Water reabsorption in the renal tubules increases urine osmolality (>20 mmol/L indicates a renal cause of hyponatraemia). CKD is also associated with hyperkalaemia and azotaemia.
  23. A 30-year-old woman visits her GP due to pigmentation of her palmar creases. Two weeks later the following blood and urine tests are received:
    Na 128 (135–145 mmol/L)
    K 5.9 (3.5–5.0 mmol/L)
    Urea 5.2 (3.0–7.0 mmol/L)
    Glucose 1.8 (2.2–5.5 mmol/L)
    Osmolality 264 (275–295 mOsm/kg)
    Urine osmolality 24 mOsm/kg

    F Addison’s disease

    Addison’s disease is also known as primary adrenal insufficiency (reduced aldosterone and cortisol); consequently there is a rise in the production of adrenocorticotropic hormone (ACTH).

    An impaired synthesis of aldosterone reduces reabsorption of sodium and increases excretion of potassium in the distal convoluted tubule and collecting ducts of the kidney; this leads to a simultaneous hyponatraemia and hyperkalaemia.

    Reduced cortisol production causes hypoglycaemia due to impaired gluconeogenesis.

    Clinical features of Addison’s disease include hyperpigmentation, postural hypotension and weight loss.
  24. A 30-year old woman is seen by her GP after a 5-day episode of productive cough and lethargy. The GP notes dullness on percussion of the patient’s left lower lung. Blood and urine tests reveal the following:
    Na 128 (135–145 mmol/L)
    K 4.1 (3.5–5.0 mmol/L)
    Urea 3.5 (3.0–7.0 mmol/L)
    Glucose 3.2 (2.2–5.5 mmol/L)
    Osmolality 265 (275–295 mOsm/kg)
    Urine osmolality 285 mOsm/kg


    The syndrome of inappropriate ADH secretion results from the excess release of ADH. In this case the clinical features suggest pneumonia is the cause, but the aetiologies of SIADH are numerous, including malignancy, meningitis and drugs (carbamazepine).

    • Criteria to diagnose SIADH include the following:
    • - Hyponatraemia <135 mmol/L
    • - Plasma osmolality <270 mmol/L
    • - Urine osmolality >100 mmol/L
    • - High urine sodium >20 mmol/L
    • - Euvolaemia
    • - No adrenal, renal or thyroid dysfunction

    Characteristically the urine osmolality is inappropriately high; in normal circumstances if the plasma osmolality is low, the urine osmolality will stop rising as reduced ADH secretion prevents water retention. As a rule of thumb in SIADH, urine osmolality is greater than plasma osmolality.
  25. A 63-year-old man with chronic obstructive pulmonary disease (COPD) sees his GP due to oedematous ankles. His blood and urine tests show the following:
    Na 130 (135–145 mmol/L)
    K 4.4 (3.5–5.0 mmol/L)
    Urea 4.2 (3.0–7.0 mmol/L)
    Glucose 3.1 (2.2–5.5 mmol/L)
    Osmolality 268 (275–295 mOsm/kg)
    Urine osmolality 16–mmol/LmOsm/kg

    D Congestive cardiac failure

    Congestive cardiac failure may present with shortness of breath, pitting peripheral oedema and/or raised jugular venous pulse (JVP). In this scenario, shortness of breath may be masked by the patient’s COPD.

    The clinical picture together with the blood result demonstrating a low sodium and low osmolality suggest a hypervolaemic hyponatraemia. This scenario can be differentiated from hypervolaemia as a result of CKD by the urine osmolality, which is less than 20 mmol/L in this instance, thereby suggesting a non-renal cause for the hyponatraemia.
  26. More cards for sodium regulation?
    • Ethanol (A) may cause hyponatraemia in the context of a raised plasma osmolality (>295 mmol/L). Other low molecular weight solutes that can cause hyponatraemia (when osmolality is raised) include mannitol and glucose.
    • Frusemide (C) and other diuretics cause a hypovolaemic hyponatraemia. As well as a low plasma sodium and osmolality, the urine osmolality will be greater than 20 mmol/L, signifying a renal cause of hyponatraemia.
    • Conn’s syndrome (E), also known as primary aldosteronism, results from an aldosterone-producing adenoma producing excess aldosterone. Biochemical (and concurrent clinical) features include hypernatraemia (hypertension) and hypokalaemia (paraesthesia, tetany and weakness).
    • Diarrhoea (F) leads to a hypovolaemic hyponatraemia (as does vomiting). Plasma sodium and osmolality will be low and urine osmolality will be lower than 20 mmol/L indicating an extra-renal cause of hyponatraemia.
  27. A 15-year-old boy presents to accident and emergency with loss of consciousness. His blood sugars are found to be extremely low. Blood tests demonstrate the following:
    Na 138 (135–145 mmol/L)
    K 3.0 (3.5–5.0 mmol/L)
    Urea 4.2 (3.0–7.0 mmol/L)
    Creatinine 74 (60–120 mmol/L)
    pH 7.48 (7.35–7.45)
    HCO3 31 (22–28 mmol/L)

    A Insulin overdose

    Insulin overdose in a diabetic patient will cause a redistributive hypokalaemia and concurrent metabolic alkalosis.

    Insulin causes a shift of potassium ions from the extracellular space to the intracellular space, thereby lowering blood potassium levels. Metabolic alkalosis can also cause a redistributive hypokalaemia; a reduced hydrogen ion concentration in the blood causes increased intracellular hydrogen ion loss to increase extracellular levels via Na+/H+ ATPase; potassium ions therefore diffuse intracellularly to maintain the electrochemical potential.

    Adrenaline and re-feeding syndrome also cause redistributive hypokalaemia.
  28. A 64-year-old man who is an inpatient on the Care of the Elderly ward is found to have the following blood results:
    Na 136 (135–145 mmol/L)
    K 5.5 (3.5–5.0 mmol/L)
    Urea 14.4 (3.0–7.0 mmol/L)
    Creatinine 165 (60–120 mmol/L)
    pH 7.44 (7.35–7.45)
    HCO3 27 (22–28 mmol/L)

    D Renal failure

    Renal failure can lead to hyperkalaemia secondary to reduced distal renal delivery of sodium ions. As a consequence, there is reduced exchange of potassium ions via the Na/K ATPase pump in the collecting duct, which thereby leads to accumulation of potassium ions in the blood and hence hyperkalaemia.

    An increase in aldosterone release will initially cause a compensatory loss of potassium ions; as renal failure progresses, this homeostatic mechanism will become decompensated and hyperkalaemia will result.

    Renal failure will also be reflected in the deranged urea and creatinine levels due to reduced excretion.
  29. A 16-day-old baby girl is found to have low blood pressure. Urinary calcium levels are found to be elevated. Blood tests demonstrate the following results:
    Na 138 (135–145 mmol/L)
    K 2.8 (3.5–5.0 mmol/L)
    Urea 3.4 (3.0–7.0 mmol/L)
    Creatinine 62 (60–120 mmol/L)
    pH 7.51 (7.35–7.45)
    HCO3 33 (22–28mmol/L)

    E Bartter syndrome

    Bartter syndrome is an autosomal recessive condition due to a defect in the thick ascending limb of the loop of Henle. It is characterized by hypokalaemia, alkalosis and hypotension. The condition may also lead to increased calcium loss via the urine (hypercalcuria) and the kidneys (nephrocalcinosis). In the associated milder Gitelman syndrome, the potassium transporting defect is in the distal convoluted tubule of the kidney.
  30. A 32-year-old man presents to his GP for a check-up. His serum aldosterone is found to be low. Blood tests reveal the following:
    Na 140 (135–145 mmol/L)
    K 5.6 (3.5–5.0 mmol/L)
    Urea 5.3 (3.0–7.0 mmol/L)
    Creatinine 92 (60–120 mmol/L)
    pH 7.38 (7.35–7.45)
    HCO3 24 (22–28 mmol/L)

    D ACE inhibitors

    ACE inhibitors will lead to hyperkalaemia due to reduced potassium excretion. ACE inhibitors antagonize the effect of angiotensin converting enzyme, the enzyme which catalyzes the production of angiotensin II from angiotensin I.

    A decreased level of angiotensin II reduces the production of aldosterone in the adrenal glands, a key hormone causing the excretion of potassium. Other causes of reduced excretion of potassium include Addison’s disease, renal failure and potassium sparing diuretics.
  31. A 68-year-old woman on the Care of the Elderly ward is found to have the following blood results:
    Na 138 (135–145 mmol/L)
    K 3.0 (3.5–5.0 mmol/L)
    Urea 4.2 (3.0–7.0 mmol/L)
    Creatinine 74 (60–120 mmol/L)
    pH 7.31 (7.35–7.45)
    HCO3 28 (22–28 mmol/L)

    A Renal tubular acidosis

    Renal tubular acidosis occurs when there is a defect in hydrogen ion secretion into the renal tubules. Potassium secretion into the renal tubules therefore increases to balance sodium reabsorption. This results in hypokalaemia with acidosis.

    • Renal tubular acidosis is classified according to the location of the defect:
    • - type 1 (distal tubule and defective H+ secretion and urine pH > 5.5)
    • - type 2 (proximal tubule and defective HCO3 resorption and urine pH < 5.5)
    • Type 4 results from a defect in the adrenal glands (inadequate aldosterone) and is included in the classification as it results in a metabolic acidosis and hyperkalaemia. It is the most common type. Others produce hypokalemia
  32. Other cards;
    • Spurious sampling (A) of blood results in hyperkalaemia. Excessive vacuuming of blood or using too fine a needle can cause haemolysis, leading to a raised potassium.
    • Anorexia (B) will result in reduced potassium intake and hence hypokalaemia. Other causes of reduced potassium intake include dental problems, alcoholism and total parental nutrition deficient in potassium.
    • Diarrhoea (C) results in hypokalaemia due to increased gastrointestinal losses of potassium. Other causes of increased gastrointestinal loss of potassium include villous adenoma and VIPoma.
    • Frusemide (G) intake leads to hypokalaemia secondary to increased renal loss of potassium. This occurs due to increased collecting duct permeability and hence potassium loss.
  33. pH 7.31 (7.35–7.45)
    pO2 7.6 (10.6–13 kPa)
    pCO2 8.2 (4.7–6.0 kPa)
    HCO3 26 (22–28 mmol/L)

    I Respiratory acidosis

    Respiratory acidosis is defined by a low pH (acidosis) together with a high pCO2, due to carbon dioxide retention secondary to a pulmonary, neuromuscular or physical causes.

    There is no metabolic compensation in this case, suggesting this is an acute pathology; a compensatory metabolic rise in HCO3 from the kidneys can take hours or days.

    This patient is also hypoxic with a low pO2. Causes of an acute respiratory acidosis include an acute exacerbation of asthma, foreign body obstruction and cardiac arrest.
  34. pH 7.36 (7.35–7.45)
    pO2 14.2 (10.6–13 kPa)
    pCO2 4.1 (4.7–6.0 kPa)
    HCO3 14 (22–28 mmol/L)

    D Metabolic acidosis with respiratory compensation

    Metabolic acidosis with respiratory compensation occurs when pH is low (acidosis) and HCO3 is low with concurrent respiratory compensation by decreasing pCO2.

    • The anion gap can differentiate between causes of metabolic acidosis (anion gap = [Na+ + K+] – [Cl− + HCO3−]; normal range between 10 and 18 mmol/L). Causes of a raised anion gap can be remembered by the mnemonic MUDPILES:
    • - methanol/metformin,
    • - uraemia,
    • - diabetic ketoacidosis,
    • - paraldehyde,
    • - iron,
    • - lactate,
    • - ethanol
    • - salicylates.

    Causes of a normal anion gap include diarrhoea, Addison’s disease and renal tubular acidosis.
  35. pH 7.45 (7.35–7.45)
    pO2 10.2 (10.6–13 kPa)
    pCO2 7.2 (4.7–6.0 kPa)
    HCO3 32 (22–28 mmol/L)

    D Metabolic alkalosis with respiratory compensation

    Metabolic alkalosis with respiratory compensation occurs when pH is high (alkalosis) and HCO3 is high with a compensatory reduction in respiratory effort that increases pCO2. As respiratory effort is reduced there is the possibility of the patient becoming hypoxic.

    Causes of metabolic alkalosis include vomiting, potassium depletion secondary to diuretic use, burns and sodium bicarbonate ingestion. Respiratory compensation increase serum CO2 concentration, which reduces pH back towards normal.
  36. pH 7.30 (7.35–7.45)
    pO2 8.2 (10.6–13 kPa)
    pCO2 7.2 (4.7–6.0 kPa)
    HCO3 19 (22–28 mmol/L)

    D Mixed metabolic and respiratory acidosis

    Mixed metabolic and respiratory acidosis occurs when there is a low pH and a simultaneous high pCO2 and low HCO3.

    • In the case of a mixed metabolic and respiratory acidosis, the metabolic acidosis component may be due to conditions such as uraemia, ketones produced as a result of diabetes mellitus or renal tubular acidosis. The respiratory acidosis component may be due to any cause of respiratory failure.
    • Hence, this mixed picture may occur in a COPD patient with concurrent diabetes mellitus.
  37. pH 7.49 (7.35–7.45)
    pO2 13.6 (10.6–13 kPa)
    pCO2 4.1 (4.7–6.0 kPa)
    HCO3 23 (22–28 mmol/L)

    C Respiratory alkalosis

    Respiratory alkalosis is biochemically defined by a raised pH (alkalosis) and reduced pCO2. As previously mentioned, metabolic compensation can take hours or days to occur.

    The primary pathology causing respiratory alkalosis is hyperventilation which causes increased CO2 to be lost via the lungs. Causes of hyperventilation may be due to central nervous system disease, for example stroke. Other causes of hyperventilation include anxiety (panic attack), pulmonary embolism and drugs (salicylates).
  38. Other cards
    • Metabolic acidosis (A) occurs when pH is reduced due to low HCO3. If there is no respiratory compensation, pCO2 will be normal or elevated.
    • Metabolic alkalosis (C) occurs when pH is increased as a result of raised HCO3. If there is no respiratory compensation, pCO2will be normal or low.
    • Respiratory acidosis with metabolic compensation (F) is defined as a low pH as a consequence of high pCO2. There is a raised HCO3 concentration in order to raise pH back towards normal.
    • Respiratory alkalosis with metabolic compensation (H) is defined as a high pH due to low pCO2. There is a reduced HCO3 concentration in order to lower pH back towards normal.
  39. Ca 2.4 (2.2–2.6 mmol/L)
    PTH 4.2 (0.8–8.5 pmol/L)
    ALP 250 (30–150 u/L)
    PO4 1.1 (0.8–1.2 mmol/L)
    Vitamin D 76 (60–105 nmol/L)

    C Paget’s disease

    Paget’s disease is a condition associated with impaired bone remodelling. New bone is larger but weak and prone to fracture. The pathogenesis has been postulated to be linked to paramyxovirus.

    All calcium blood studies will be normal apart from ALP, which will be raised. Paget’s disease is associated with extreme bone pain, bowing and chalk-stick fractures.

    Bossing of the skull may lead to an eighth cranial nerve palsy and hence hearing loss. X-ray findings include lytic and sclerotic lesions.
  40. Ca 3.1 (2.2–2.6 mmol/L)
    PTH 10.5 (0.8–8.5 pmol/L)
    ALP 165 (30–150 u/L)
    PO4 0.6 (0.8–1.2 mmol/L)
    Vitamin D 78 (60–105 nmol/L)

    G Primary hyperparathyroidism

    Primary hyperparathyroidism is caused by a parathyroid adenoma or parathyroid chief cell hyperplasia that leads to increased PTH production.

    • Primary hyperparathyroidism leads to hypercalcaemia due to a raised PTH level. PTH achieves this by activating osteoclastic bone resorption (increasing blood ALP), stimulating calcium reabsorption in the kidney (with concurrent excretion of phosphate) and potentiating the action of the enzyme 1α-hydroxylase in the kidney.
    • - 1α-Hydroxylase acts on 25-hydroxyvitamin D3 to produce 1,25-dihydroxyvitamin D3 (calcitriol), which increases gut absorption of calcium.
  41. Ca 2.1 (2.2–2.6 mmol/L)
    PTH 10.4 (0.8–8.5 pmol/L)
    ALP 190 (30–150 u/L)
    PO4 0.69 (0.8–1.2 mmol/L)
    Vitamin D 41 (60–105 nmol/L)

    D Osteomalacia

    Osteomalacia (rickets in children) results from insufficient bone mineralization, secondary to vitamin D or phosphate deficiency. Low vitamin D causes hypocalcaemia, due to reduced 1,25-dihydoxyvitamin D3 production, and hence reduced reabsorption of calcium from the gut.

    Low blood calcium levels cause an increase in production of PTH in an attempt to normalize calcium. Therefore, calcium levels will either be low or inappropriately normal. Increased bone resorption will cause ALP levels to rise.
  42. Ca 1.8 (2.2–2.6 mmol/L)
    PTH 9.6 (0.8–8.5 pmol/L)
    ALP 50 (30–150 u/L)
    PO4 1.9 (0.8–1.2 mmol/L)
    Vitamin D 82 (60–105 nmol/L)

    G Pseudohypoparathyroidism

    Pseudohypoparathyroidism is a genetic condition in which there is resistance to PTH. As a result patients have high PTH and phosphate levels but are hypocalcaemic.
  43. Ca 1.8 (2.2–2.6 mmol/L)
    PTH 0.69 (0.8–8.5 pmol/L)
    ALP 89 (30–150 u/L)
    PO4 1.5 (0.8–1.2 mmol/L)
    Vitamin D 76 (60–105 nmol/L)

    E Primary hypoparathyroidism

    Primary hypoparathyroidism is defined as dysfunction of the parathyroid glands leading to reduced production of PTH. As a result, the actions of PTH are blunted leading to reduced bone resorption as well as renal and gut calcium reabsorption. As a consequence there is hypocalcaemia and hyperphosphataemia.

    Other causes of hypocalcaemia include pseudoparathyroidism, vitamin D deficiency, renal disease (unable to make 1,25-dihydroxyvitamin D3), magnesium deficiency (magnesium required for PTH rise) and post-surgical (neck surgery may damage parathyroid glands).
  44. Other cards;
    • Secondary hyperparathyroidism (B) is defined as the release of PTH as a consequence of hypocalcaemia that arises due to non-parathyroid pathology. The most common cause is chronic renal failure.
    • Tertiary hyperparathyroidism (C) results from hyperplasia of the parathyroid glands after a long period of secondary hyperparathyroidism. Autonomous production of PTH causes hypercalcaemia.
    • Osteoporosis (F) results in reduced bone density and all calcium studies are normal. Menopause, alcohol and drugs such as goserelin and steroids are risk factors.
    • Familial benign hypercalcaemia (I) is a genetic condition leading to raised blood calcium levels. The disease results from a mutation in the calcium receptor located on the parathyroid glands and kidneys. This receptor defect therefore leads to underestimation of calcium, causing an increased production of PTH, despite the raised calcium levels. It is important to distinguish these patients from hyperparathyroid patients as the management of these conditions differs. Receptor failure in the kidneys reduces calcium excretion, leading to a hypocalcuric state.
Card Set
Chempath ALM