History Of Presenting Complaint Biology Essay

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Last year MM had been suffering from painful aching joints with swelling of the fingers, feet, knees, elbows and ankles as well as decreased energy levels. A blood test conducted by her GP revealed hypercalcemia, and she was referred to nuclear medicine for thyroid scans; the results of which proved as indicators for a parathyroidectomy. The surgery was successful; removing 3 of the 4 glands (due to difficulty locating the 4th). MM states that she saw a big improvement in her general well-being; feeling more full of energy and reduced aches and pain in her joints.

MM is a 58 year old female who is currently unemployed due to the pain in her joints. She is a non-smoker, seldom drinks and has no known allergies. Current co-morbidities include osteoporosis; her last dexa scan was in 2008. She lives at home with her husband (49), and has no children. Her mother suffers from type II insulin controlled diabetes, pernicious anaemia, hypothyroidism, has had a previous "heart attack", cardiomegaly and had a cholecystectomy. Her grandmother (70) died from a cerebral haemorrhage and also had type II diabetes. Her father died before she was born, and she knows nothing about her grandfather.

Systemic Enquiry

No breathlessness/cough, or sore throat. She is however recovering from a recent throat infection/cold.

No chest pain/palpitations.

No nausea/vomiting, passing stools ok, normal appetite, no abdominal pain.

No past history of headaches, seizures or syncope.

Some joint pain, stiffness, of the fingers, feet, knees, elbows and ankles. No weakness of the limbs.

Asthma and diabetes mellitus is absent.

Previous Medical/Surgical History

2009 - Cholecystectomy

2009 - Parathyroidectomy

1994 - Hysterectomy due to ovarian cyst

1991 - Splenectomy - Reported a noticeable decrease in her immune system since

1984 - Identified an autoimmune condition causing a decrease in RBC lifespan. Received immunoglobulin treatment which helped. Splenomegaly identified.

1971 - Appendectomy

Fractures of her left scaphoid, right distal radius and both ankles was also noted in her history.


Not currently taking any medications.

NSAIDs for joint pain when required.


On general examination AE appeared well orientated and well kempt. She appeared to look appropriate for her age. She expressed that she felt well in herself, reporting that some days she has more "energy" than others. There was only minor pain and stiffness in her joints.

On examination of her wrists and arms, a marked deviation of the scaphoid bone on the left arm and slight depression of the distal radius was noted on the right. These were noted to be artefacts of previous fractures.

Examinations of the abdomen revealed a longitudinal paramedian scar in the left umbilical region; gridiron scar in the right iliac fossa; small scars were noted in the epigastrium and right iliac fossa where a cholecystectomy had been conducted.

No signs of clubbing, peripheral oedema, splinter haemorrhaging, osler's nodes, dupuytren's contracture; blood pressure 144/77, pulse 77 with regular rate, rhythm, character and volume; no signs of jaundice, lips and tongue did not appear anaemic, no irregularity in the buccal mucosa, JVP appeared not to be raised, no deviation of the trachea and thyroid was not enlarged.


AE is a 58 year-old female who last year had a parathyroidectomy which removed 3 of the 4 glands. She is currently in hospital for venous sampling to locate the 4th gland. She reports some pain the stiffness in her fingers, feet, knees, elbows and ankles as well as varying "energy levels".

Differential Diagnosis (Hypercalcemia)

Primary hyperparathyroidism

Familial benign hypercalcemia

Squamous cell carcinoma

Adverse drug reaction to lithium

Adverse reaction to parenteral nutrition

Adverse drug reaction to thiazide diuretics

Cancers producing parathyroid hormone-related protein

Cancers producing ectopic production of 1,25-dihydroxyvitamin D

Milk-alkali syndrome

Reflective Commentary

Hypercalcemia is a disorder that most commonly results from malignancy or primary hyperparathyroidism1. Other causes of elevated calcium are less common and usually are not considered until malignancy and parathyroid disease are ruled out.

Hypercalcemic crisis does not have an exact definition, although marked elevation of serum calcium, usually more than 14 mg/dL, is associated with acute signs and symptoms of hypercalcemia. The reference range of serum calcium levels is 8.7-10.4 mg/dL.

This lady complained of painful aching joints with swelling of the fingers, feet, knees, elbows and ankles as well as lethargy; all of which can be associated with hypercalcemia (assuming the joint swelling if due to inflammation). However, she did not present with more typical signs such as nausea, vomiting, headaches, constipation and polyuria. I my opinion it would seem the hypercalcemia was the cause of her joint discomfort, a point reinforced due to the improvement in her condition after a parathyroidectomy.


The parathyroid glands regulate serum calcium and phosphorus levels through the secretion of parathyroid hormone (PTH), which raises serum calcium levels while lowering the serum phosphorus concentration. The regulation of PTH secretion occurs through a negative feedback loop in which calcium-sensing receptors on the membranes of parathyroid cells trigger decreased PTH production as serum calcium concentrations rise.

Hyperparathyroidism is often incidentally discovered during routine laboratory testing when hypercalcemia is noted. In 80% of patients with hyperparathyroidism, the symptoms of hypercalcemia are mild or are not notable at the time of discovery.


Primary hyperparathyroidism is one of the most common causes of hypercalcemia and should be considered in any individual with an elevated calcium level2. Primary hyperparathyroidism is usually the result of a single benign adenoma; a minority of patients have hyperplasia in all 4 parathyroid glands.

In the setting of asymptomatic primary hyperparathyroidism, the parathyroid hormone (PTH) level is typically 1.5-2 times the upper limit of the reference range. Hypophosphatemia and hyperchloremia are typically seen only in patients who are highly symptomatic patients and have advanced hyperparathyroidism.

Secondary hyperparathyroidism occurs when the parathyroid glands become hyperplastic after long-term hyperstimulation and release of PTH. In secondary hyperparathyroidism, elevated PTH levels do not result in hypercalcemia. This has been classically attributed to an underlying state of hypocalcemia in those with chronic renal failure (CRF). However, hypocalcemia is not necessary for the development of secondary hyperparathyroidism in this setting. Eventually, nearly all patients on maintenance dialysis will develop secondary hyperparathyroidism3.

When hyperparathyroidism manifests with hyperplasia in all 4 glands, familial-genetic syndromes should be considered within the differential diagnosis.

With long-term hyperstimulation, the glands function autonomously and produce high levels of PTH even after correction of chronic hypocalcemia.

Clinical History

Most patients with primary hyperparathyroidism are asymptomatic or minimally symptomatic.

Symptomatic hyperparathyroidism is characterized by vague, nonspecific symptoms including generalized weakness, fatigue, poor concentration, and depression.

A helpful mnemonic, "painful bones, renal stones, abdominal groans, and psychic moans," can be used to recall the typical symptoms of hypercalcemia. Painful bones are the result of abnormal bone remodeling due to overproduction of parathyroid hormone (PTH). Nephrolithiasis occurs secondary to hyperparathyroid disease-induced hypercalcemia and resultant hypercalciuria. Abdominal groans refers to hypercalcemia-induced ileus. Psychic moans or depression may occur in the presence of persistently elevated serum calcium levels.

Investigatory Workup

Elevated parathyroid hormone (PTH) levels in the setting of hypercalcemia establish the diagnosis of hyperparathyroidism. The most common other cause of hypercalcemia in older individuals, hypercalcemia of malignancy, is associated with suppressed PTH levels.

The normal range for the PTH-intact assay is generally 10-65 pg/mL.

Serum calcium

In cases of primary hyperparathyroidism or tertiary hyperparathyroidism heightened PTH leads to increased serum calcium (hypercalcemia) due to:

1. Increased bone resorption, allowing flow of calcium from bone to blood

2. Reduced renal clearance of calcium

3. Increased intestinal calcium absorption

By contrast, in secondary hyperparathyroidism effectiveness of PTH is reduced.

Serum phosphate

In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate reabsorption. However, this is only present in about 50% of cases. This contrasts with secondary hyperparathyroidism, in which serum phosphate levels are generally elevated because of renal disease.

Alkaline phosphatase

Kumar and Clark 6th edition states that alkaline phosphatase levels do not increase in primary hyperparathyroidism but may increase in secondary hyperparathyroidism.

Venous Sampling4

The role of pre-operative localisation of abnormal parathyroid glands remains controversial but is particularly relevant to the management of patients with recurrent or uncured hyperparathyroidism and familial syndromes.

Transfemoral venous catheterisation is performed and serum parathormone measured in samples from high and low internal jugular, thyroid, inferior thyroid, thymic mediastinal, subclavian, innominate, azygos, left superior intercostal veins, superior vena cava and right atrium. A gradient of >2 vs. peripheral parathormone concentration was considered positive for localisation and absence of a mediastinal gradient as negative for the presence of intrathoracic parathyroid pathology.



Only in the most severe acute manifestation of hyperparathyroidism, hypercalcemia-induced altered mental status, does management need to begin in the prehospital setting. In such cases, prehospital care should focus on the stabilization of airway, breathing, and circulation. In the field and the emergency department, hydration is the principal primary therapy directed at hypercalcemia.

Emergency Department Care

The emergency department (ED) management of hyperparathyroidism is focused on the treatment of hypercalcemia. Specifically, the goal of treatment is to reduce the calcium level to below 11.5 mg/dL; most patients have resolution of hypercalcemia-induced symptoms when calcium levels are below this level.

Intravenous administration of isotonic saline is the first and most vital step in the management of severe hypercalcemia. Severe hypercalcemia is nearly always accompanied by severe dehydration. When the depleted intravascular volume is restored to the reference range, the serum calcium concentration declines by the degree to which dehydration raised it. Subsequent hydration serves to enhance renal excretion of excess calcium.

Loop diuretics may facilitate the urinary excretion of calcium and may prevent the volume overload that may accompany the administration of large volumes of saline.

In postmenopausal women with mild hyperparathyroidism, oestrogen therapy has been advocated because it may inhibit demineralization of the skeleton and may reduce blood calcium levels.

Calcimimetic agents - Calcium regulators are also used in hypercalcemia of malignancy. These agents bind to and modulate the parathyroid calcium-sensing receptor, increase sensitivity to extracellular calcium, and reduce PTH secretion.

Successful parathyroidectomy induces normocalcemia.

Indications for surgery

Patients with overt clinical manifestations of disease

Age younger than 50 years

Serum calcium concentration more than 1 mg/dL above upper limit of reference range

Urinary calcium excretion greater than 400 mg/d

Low or declining bone mineral density

Uncertain prospect for successful medical monitoring

Patient requests surgery

Poor or uncertain follow-up

Coexistent disease that may confound or contribute to disease progression

Reduction in creatinine clearance of 30% or more

Reduction of bone mineral density greater than 2.5 standard deviations below the reference range for bone density in terms of age, gender, and race (T score <2.5)

Further Outpatient Care

Calcium levels must be periodically monitored for several months postparathyroidectomy. If calcium levels begin to rise postoperatively, the patient needs to be evaluated for possible accessory parathyroid glands.

If the serum calcium concentration falls below 8 mg/dL postparathyroidectomy with a concomitant rise in serum phosphate level, consider the possibility of postsurgical hypoparathyroidism.


Ariyan CE, Sosa JA. Assessment and management of patients with abnormal calcium. Crit Care Med. Apr 2004;32(4 Suppl):S146-54.

Boonen S, Vanderschueren D, Pelemans W, Bouillon R. Primary hyperthyroidism: diagnosis and management in the older individual. Eur J Endocrinol. Sept 2004;151(3):297-304.

Brommage D, Gallgano C. The role of cinacalcet in treating secondary hyperparathyroidism. Nephrol Nurs J. Mar-Apr 2005;32(2):229-31

Selective parathyroid venous sampling in patients with complicated primary hyperparathyroidism. CM Ogilvie, PL Brown, M Matson, R Carpenter, WM Drake, PJ Jenkins, SL Chew & JP Monson. Department of Endocrinology, St Bartholomew's Hospital, London; 2Department of Radiology, St Bartholomew's Hospital, London, UK; 3Department of Surgery, St Bartholomew's Hospital, London, UK.