Rapid Review of Clinical Medicine for MRCP Part 2 by Sharma, Sanjay Kaushal, Rashmi (z-lib.org)

Clinical Cases 399

digestion and absorption. Failure to absorb fats results in The diagnosis of PBC is confirmed by the
failure to absorb fat-soluble vitamins, notably vitamins A, demonstration of IgM antimitochondrial antibodies
D, E and K. Vitamin D deficiency leads to osteomalacia (subtype M2), which are present in over 90% of the
and pathological fractures. This patient’s presentation is patients. A liver biopsy shows a dense infiltration of the
almost certainly due to a sternal fracture, which may be portal tract with lymphocytes and plasma cells. There is
detected on a lateral chest X-ray. The raised creatinine periportal fibrosis and cholestasis, and granulomas are
kinase is unlikely to represent an acute myocardial present around the small bile ducts.
infarction, given the chest tenderness. The most likely
explanation for the high creatinine kinase level is ANF antibodies and rheumatoid factor are present in
simvastatin-induced myositis. In liver and/or renal up to one-third of cases. Associations include CREST
failure, simvastatin may cause frank rhabdomyolysis. (calcinosis, Raynaud’s syndrome, oesophageal problems,
Patients also taking fibrates and ciclosporin with the scleroderma and telangiectasia) syndrome, membranous
statins are at risk of this complication. In this case, the glomerulonephritis, RTA and Sjögren’s syndrome.
best method of managing the hypercholesterolaemia is by
a low-fat diet and by therapy with cholestyramine, a resin There is no specific proven therapy, although
which binds bile and promotes its excretion. ursodeoxycholic acid does retard progression and time to
hepatic transplantation. Liver transplantation should be
considered when the serum bilirubin exceeds
100 μmol/l.

Question 394

A 35-year-old female with Crohn’s disease since the age
of 15 years presented with a six-month history of foul-
smelling diarrhoea and weight loss.

Investigations are shown.

Hb 10 g/dl 1. List two possible causes for this patient’s symptoms.
WCC 7 × 109/l 2. Which investigation would you perform next?
Platelets 199 × 109/l
MCV 106 fl
Serum folate
Serum B12 22 μg/l
Faecal fat 65 ng/l

Schilling test 50 mmol/l

(NR <20 mmol/l)

Pre-intrinsic factor 2% B12
isotope excreted

Post-intrinsic factor 2% B12
isotope excreted

400

Answer 394

1. i. Primary B12 malabsorption.
ii. Bacterial overgrowth.

2. Repeat Schilling test after a two-week course of antibiotics.

Table A The Schilling test

Part 1
• Give 1 mg 58Co-B12 orally to a patient who has fasted overnight, and also give 1 mg of non-radioactive B12 by

intramuscular injection to saturate B12 binding proteins. Collect urine for 24 hours
• Normal subjects excrete >10% of the radioactive dose

If part 1 is abnormal:

Part 2
• Repeat Schilling with oral intrinsic factor
• If excretion becomes normal, the primary abnormality is intrinsic factor deficiency
• If excretion remains abnormal, then the differential is between primary B12 malabsorption and bacterial

overgrowth

Table B Differentiation of primary B12 malabsorption from bacterial overgrowth

1° B12 malabsorption Bacterial overgrowth

1. Schilling test after antibiotics Abnormal Normal
2. Small bowel meal Terminal ileal stricture Fistulae, jejunal strictures
3. Jejunal aspirate Normal bacteria High concentration of

4. 14C-glycocholate breath test Positive Escherichia coli/Bacteroides
Positive

The patient has a history of Crohn’s disease and now Table C Causes of B12 deficiency
presents with steatorrhoea, B12 deficiency and an • Low dietary intake (vegans)
abnormal Schilling test (Table A), with and without
intrinsic factor. The two most likely causes for the B12 Intrinsic factor deficiency
deficiency in Crohn’s disease are primary B12 mal- • Congenital
absorption due to terminal ileal disease, or intestinal • Pernicious anaemia
destruction of dietary B12 by bacterial overgrowth within • Gastrectomy
small bowel strictures (394). Both conditions also cause • Chronic atrophic gastritis
steatorrhoea by impairing fat absorption due to
disturbances in bile salt absorption; the former by Primary B12 malabsorption
preventing absorption of bile salts which are required for • Terminal ileal disease
micelle formation, and the latter by deconjugation and • Bacterial overgrowth
dehydroxylation of bile salts. Repeating the Schilling test • Coeliac and tropical sprue (longstanding)
after a two-week course of metronidazole and tetracycline • Pancreatic insufficiency
may help to differentiate between terminal ileal disease
and bacterial overgrowth (Table B). Antibiotics destroy Miscellaneous
the large concentrations of Escherichia coli and/or • Fish tapeworm (Diphyllobothrium latum)
Bacteroides which are responsible for bacterial overgrowth, • Drug, e.g. colchicine, neomycin
and following this the Schilling test (without intrinsic
factor) becomes normal. In terminal ileal disease, the test overgrowth. Another method of differentiation is by
will remain abnormal. A small-bowel enema may also help jejunal aspiration and culture. Although E. coli and
in the differentiation by demonstrating a terminal stricture Bacteroides are found in the jejunum, it is unusual to find
responsible for primary B12 malabsorption, and any concentrations exceeding 106/ml unless there is
structural defects which will predispose to bacterial

Clinical Cases 401

Investigation of B12 deficiency 394

Schilling Normal Vegan
Abnormal Transcobalamin II deficiency
B12 <150 ng/l test Pregnancy
Thyrotoxicosis
part 1

Pernicious anaemia
Gastrectomy

Chronic atrophic gastritis

Congenital intrinsic factor Normal Repeat Schilling test
deficiency with intrinsic factor

part 2

Bacterial

overgrowth Normal Abnormal
Jejunal diverticuli
Blind loop Repeat part 1
syndrome after antibiotics*

Abnormal

Terminal ileal disease

Fish tapeworm

Drugs:
• colchicine

• neomycin *10 days of tetracycline and metronidazole
• para-amino-salicylic acid

overgrowth. A 14C-glycocholate breath test is into the colon where the concentration of E. coli is very
high, leading to deconjugation of bile salts and liberation
characteristically positive in bacterial overgrowth, as of 14C-glycine. In terminal ileal disease, faecal radioactivity
bacteria deconjugate bile salts to release 14C-glycine, is also high, whereas in bacterial overgrowth the radio-
which is metabolized to 14CO2. The radioactivity in the activity level is relatively low. Causes of B12 deficiency are
breath is easy to measure; however, it is important to tabulated (Table C).

realize that the test may also be positive in terminal ileal

disease because unabsorbed radiolabelled bile salts pass

Question 395

A 65-year-old male was seen in the out-patient’s clinic nystagmus. Examination of the fundi was normal. There
with a one-year history of dizziness which was worse on was a pill-rolling tremor affecting the right hand. There
getting out of bed, and occasionally associated with was increased tone in both legs, with the right leg being
collapse. The patient also complained of weakness affected more than the left. Power was slightly reduced
affecting both legs. On further questioning, he admitted (grade 4/5) in all limbs. The reflexes were generally brisk.
to urinary incontinence and his wife noted that he was The plantar response in the left foot was extensor, but was
generally slow and had an intermittent tremor affecting equivocal in the right foot. Sensation was normal. His gait
his right hand. was ataxic.

On examination, he appeared slightly withdrawn. His 1. What is the most likely diagnosis?
pulse was 84 beats/min, and blood pressure 2. List two further investigations you would pursue to
155/85 mmHg. The heart sounds were normal.
Examination of the respiratory and gastrointestinal confirm your diagnosis.
systems was normal. On examination of the central
nervous system he had sluggish pupillary reflexes and

402

Answer 395

1. Multi-system atrophy or Shy–Drager syndrome. Causes of autonomic failure
2. i. Lying and standing blood pressure.
1. Central (primary)
ii. Autonomic nervous system testing (loss of sinus Progressive autonomic failure (no obvious cause)
arrhythmias on ECG, loss of reflex bradycardia on Progressive autonomic failure with multi-system
carotid sinus massage, absence of a reflex
tachycardia after the Valsalva manoeuvre). atrophy (Shy–Drager syndrome)
Progressive autonomic failure with Parkinson’s
The patient has a pill-rolling tremor and increased
muscular tone, indicating an extrapyramidal syndrome disease
such as Parkinson’s disease. The presence of additional
neurological findings suggests that he has a Parkinson- 2. Central (secondary)
plus syndrome. There are several Parkinson-plus Central brain lesions: craniopharyngioma, vascular
syndromes in the literature, but the ones which are most
commonly tested include multi-system atrophy and the disease
SROS. Multi-system atrophy is the name given to a Encephalitis, tabes dorsalis, Chaga’s disease
sporadically occurring condition which begins in adult Spinal cord lesions
life, usually in the sixth decade. It is characterized by Familial dysautonomia
neuronal cell loss and gliosis changes in:
3. Distal autonomic neuropathies
• The substantia niagra pathways that cause Guillain–Barré syndrome, diabetes mellitus,
Parkinsonism.
amyloid, porphyria, rheumatoid arthritis,
• The olivopontocerebellar tract causing ataxia, myaesthenia gravis, Fabry’s disease
dysarthria, nystagmus and pyramidal signs.
4. Tricyclic antidepressants, MAOIs, ganglion-
• The intermediolateral cell column (pre-ganglionic blocking drugs
sympathetic neurones in the lateral horns of the spinal
cord) causing autonomic nervous system failure. Steele–Richardson–Olszewski syndrome
Other causes of autonomic failure are shown (Table). This is another multisystem degeneration syndrome. It is
characterized by cell loss and neurofibrillary tangles in the
These changes often overlap and may present as a brainstem, globus pallidus, subthalamic and dentate
mixture of neurological abnormalities. When features of nuclei, and causes the syndrome of progressive
Parkinson’s disease predominate, the disorder is called supranuclear palsy. It begins in the seventh decade.
striatonigral degeneration. When features of the Patients present with imbalance, particularly falling
autonomic failure predominate, the disorder is commonly backwards, a coarse dysarthria, involuntary groans and
known as Shy–Drager syndrome, and when cerebellar dysphagia. Perseverance may be obvious in speech with
features predominate it is called olivopontocerebellar repetition of syllables and words (palilalia) or even of
atrophy. When all three systems are involved the disorder whole phrases (palilogia). Involuntary eye closure is often
is known as multi-system atrophy. Unlike Parkinson’s seen. The brow may be furrowed and the eyebrows raised
disease, there is a shortened life expectancy, with a from frontalis hyperactivity in an attempt to keep the eyes
median survival of 9.3 years. open, resulting in a surprised expression. The
characteristic feature in SROS is a supranuclear palsy of
In Shy–Drager syndrome impotence is often the first voluntary gaze. Voluntary downgaze is slow and
symptom. Incontinence is common in both sexes. Speech incomplete, but when the patient’s neck is passively
differs from the hypophonic monotony of Parkinson’s extended while fixing his gaze on the examiner’s nose, a
disease, incorporating quivering, straining, slurring, and downward gaze is obtained. Patients may therefore have
dysarthric components. Patients may develop aphonia, problems with reading and eating. Patients with SROS
anarthria and dysphagia, which are the same as in can masquerade as having Parkinson’s disease because of
Parkinson’s disease. Respiratory stridor can occur in axial rigidity and gait disturbances, but lack features of
about 30% of patients. There is no specific treatment for distal Parkinsonism (distal limb akinesia or rigidity).
multi-system atrophy and the associated disorders. The Resting tremor is almost never seen. There is no effective
use of compression stockings, fludrocortisone, and treatment. Median survival is about 6–7 years.
pressor agents such as ephedrine have been used for the
postural symptoms. The response to L-dopa is usually
absent or poor.

Question 396 Clinical Cases 403

396a

A 31-year-old male was admitted to hospital with a two- Hb 13 g/dl
week history of progressive dyspnoea on exertion and
wheeze. He complained of aches and pains in his arms WCC 15.3 × 109/l
and legs. He had suffered from ulcerative colitis for four
years, and required several courses of high-dose (neutrophils 10.1 × 109/l,
prednisolone until the last two months, when his colitis
was relatively quiescent. He also had a past history of lymphocytes 1.0 × 109/l,
hyperthyroidism which was medically treated with
carbimazole. He was currently maintained on eosinophils 4.2 × 109/l)
sulphasalazine 1 g twice daily for the ulcerative colitis.
Platelets 308 × 109/l
On examination, he was dyspnoeic, had mild cervical
and axillary lymphadenopathy, and a generalized Sodium 126 mmol/l
maculopapular rash. He had a fever of 38.5°C (101.3°F).
The heart rate was 110 beats/min and regular. The Potassium 4.3 mmol/l
blood pressure was 140/80 mmHg. Heart sounds were
normal. Auscultation of the lung fields demonstrated Urea 7 mmol/l
widespread wheeze. His abdomen was very muscular and
difficult to examine. All other examinations were Creatinine 100 μmol/l
essentially normal.
ESR 98 mm/h
Investigations are shown.
Blood and sputum cultures: Negative

Arterial blood gases (on air):

pH 7.4

PaCO2 3.3 kPa
PaO2 8.7 kPa
Bicarbonate 21 mmol/l

O2 saturation 92%

Chest X-ray (396a)

What is the diagnosis?
a. Churg–Strauss syndrome.
b. Eosinophilic pneumonitis.
c. Allergic bronchopulmonary aspergillosis.
d. Pneumocystis jirovecii pneumonia.
e. Hodgkin’s lymphoma.

404

Answer 396

b. Eosinophilic pneumonitis. patients require a maintenance dose of 5 mg
prednisolone for several months to prevent recurrence.
The patient has a generalized illness consisting of a
widespread macular rash, generalized lymphadenopathy, The differential diagnosis here is the Churg–Strauss
and a very high eosinophil count. He has a wheeze, and syndrome, which is a small-vessel granulomatous
his chest X-ray reveals patchy consolidation, which is vasculitis characterized by skin rash, respiratory
worse in the right lung. He had been on prednisolone for involvement giving asthmatic symptoms, neuropathy and
ulcerative colitis but has recently commenced eosinophilia. It is a variant of Wegener’s granulomatosis,
sulphasalazine. The symptoms and signs appeared after but is a much milder disease and does not usually involve
the drug was commenced, and the most likely diagnosis the kidneys. Lymphoma is also associated with
for his respiratory problem is an eosinophilic pneumonia. eosinophilia; however, it would have to be fairly extensive
This question tests the reader’s knowledge of causes of to involve the cervical and axillary lymph nodes as well as
eosinophilia (396b) of which there are many; however, the chest. The normal Hb and lymphocyte count are not
the most common cause is allergy. An allergic reaction to consistent with extensive lymphoma.
drugs may precipitate a profound eosinophilia with multi-
system involvement, including eosinophilic infiltration Although the patient had been on steroids and is
into the lungs. Sulphonamides are a well-recognized currently taking carbimazole, his normal neutrophil
cause of eosinophilia and subsequent eosinophilic count is highly against the development of an
consolidation. Other drugs implicated include opportunistic infection such as TB or Pneumocystis
erythromycin, nitrofurantoin and imipramine. The most jirovecii pneumonia (previously known as Pneumocystis
obvious management of a drug-related eosinophilia is to carinii pneumonia).
stop the culprit agent. Pulmonary involvement responds
well to high-dose steroids, which may be tailed off over a Ulcerative colitis itself is a recognized cause of a mild
few weeks. However, relapse is not uncommon and some eosinophilia; however, an eosinophilia as high as in this
case and pulmonary involvement cannot be explained by
the disease.

396b Allergies Drugs:*
Addison’s disease Sulphonamides
Mild 0.5–2.0 Lymphoma (Hodgkin’s) Chlorpropamide
Eosinophilia Immunodeficiency Erythromycin
>0.5 × 109 (Wiskott–Aldrich) Nitrofurantoin
Severe >5 Vasculitidies
(Churg–Strauss syndrome) Asthma
Radiation Allergic rhinitis
Ulcerative colitis Allergic bronchopulmonary
aspergillosis
Chest X-ray Normal Parasites*
or Wucheria bancrofti
Abnormal Strongyloides
Blistering Other worms
skin disease
Pemphigus
Eosinophilic pneumonia Pemphigoid
Tropical pulmonary Erythema multiforme
eosinophilia
Eosinophilic leukaemia
Hypereosinophilic syndrome

*May be associated with severe eosinophilia and abnormal X-ray.

Clinical Cases 405

Question 397

A 16-year-old female is investigated for short stature. The 0.15 iu/kg of insulin, 100 μg of LHRH, and 200 μg of
results of a dynamic pituitary function tests following TRH are as follows:

Time Glucose GH Cortisol TSH LH FSH Oestradiol
(min) (mmol/l) mu/l (nmol/l) mu/l iu/l iu/l pmol/l

0 4.0 1.4 400 2.0 29 16 4
20 2.8 12.0 860 5.2 40 24 5
30 1.6 28 1270 - - -–
40 1.5 32 1450 - - -–
60 2.2 20 1120 8 34 20 6

1. The following statements are true with respect to a. Buccal smear for karyotyping.
the pituitary function tests above: b. CT scan of the pituitary gland.
a. There was an inadequate stimulus for GH c. Dexamethasone suppression test.
secretion. d. Investigation of other family members.
b. The GH response was abnormal. e. Thyroid antibodies.
c. The findings are consistent with pituitary
Cushing’s syndrome. 3. The following diagnoses are possible in this
d. The patient is hypothyroid. patient:
e. There is evidence of primary hypogonadism. a. Hypothyroidism.
b. Turner’s syndrome.
2. The following investigations would be useful in c. PCOS.
confirming the diagnosis: d. Testicular feminization syndrome.
e. Coeliac disease.

Question 398 398

A 70-year-old male on treatment for congestive cardiac
failure with an angiotensin-converting enzyme inhibitor,
spironolactone, digoxin and furosemide was admitted
with nausea. An ECG taken on admission is shown
(398).

Which investigation would you perform next?
a. Serum potassium.
b. Serum magnesium.
c. Cardiac troponin I.
d. Echocardiography.
e. 24-hour ECG.

406

Answer 397

1. e. There is evidence of primary hypogonadism. examined causes of short stature in the MRCP and
2. a. Buccal smear for karyotyping. similar examinations are listed (Table F).
3. b. Turner’s syndrome.
Testicular feminization syndrome is due to the
In order to answer this question correctly the reader absence of testosterone receptors on end organs. The
requires knowledge of the normal results of dynamic patient has male karyotype, but is phenotypically female
pituitary function tests and gonadotrophin and sex owing to the absence of the effect of testosterone in the
hormone levels (Tables A and B). normal development of male gonads. Testicles are
present but are usually intra-abdominal or in the hernial
In this case, there is an adequate stimulus to GH and orifices. Serum testosterone levels are very high. Lack of
cortisol secretion. The GH response is normal, and there testosterone receptors on the pituitary means that there is
is no evidence of hypothyroidism. The basal oestradiol is no negative feedback system to inhibit gonadotrophin
low and the basal LH and FSH are high, suggesting secretion, therefore both LH and FSH are very high.
primary hypogonadism. The LHRH test is normal (as is Excess stimulation of the testicular remnants leads to
the case) in primary hypogonadism. The most probable excess oestrogen production by the testes, which is
diagnosis is Turner’s syndrome. Turner’s syndrome is comparable with levels found in females. The oestrogen
characterized by a single X chromosome (karyotype 45 initiates breast development and maintains breasts. Lack
XO). It has an incidence of approximately 1 in 2,500. of the testosterone effect means that pubic hair may be
The main abnormality is gonadal dysgenesis, the absent or scanty. These patients are not particularly short.
consequences of which are primary amenorrhoea and They present with amenorrhoea. The diagnosis can be
infertility. Oestradiol levels are low, resulting in elevated confirmed by karyotyping.
gonadotrophin levels via the positive feedback on the
pituitary. The patients are typically short and have a Pituitary Cushing’s is unusual in this age group. It is
number of other morphological abnormalities (Table C). due to a basophil adenoma within the pituitary which
The diagnosis is confirmed by a buccal smear which secretes ACTH, causing adrenal hyperplasia and excess
reveals an absent Barr body. There are several other cortisol production. The serum cortisol is >900 nmol/l
causes of hypogonadism in females (Table D). and there is loss of diurnal variation, i.e. the midnight
cortisol is also >900 nmol/l (normally 150–750 nmol/l).
Polycystic ovary syndrome may also cause partial In the majority of cases high-dose dexamethasone (8 mg
hypogonadism, but in contrast with the other causes of per day) suppresses cortisol production (see Answer 173).
hypogonadism given in Table D, the oestradiol levels are In some cases the cortisol response to dexamethasone is
only slightly reduced and the FSH level is low (Table E). unaffected and in these instances the main definitive
Although coeliac disease is a recognized cause of short method of diagnosing pituitary Cushing’s is to perform
stature (and also delayed puberty), the gonadotrophin inferior petrosal sinus sampling for ACTH.
response to LHRH is entirely normal. The commonly

Table A Normal responses to dynamic pituitary function tests

• Following an insulin tolerance test, the GH level rises to >20 mu/l and the serum cortisol level should rise to
≥550 nmol/l and increase by 180 nmol/l from the basal level. The blood sugar should fall below 2.2 mmol/l
to ensure adequate metabolic stress for GH and cortisol secretion. Note: An insulin tolerance test should not
be performed if the basal cortisol level is below 180 nmol/l

• Following a TRH test, the TSH should increase by >2 mu/l from the basal level. Basal TSH levels are
between 0.5–5 mu/l

• Following an LHRH test, the LH and FSH should double from the basal level

Table B Normal gonadotrophin and sex hormone levels in males and females

Females Males
Follicular phase, FSH 1–10 iu/l and LH 2–20 iu/l FSH 1–7 iu/l and LH 1–10 iu/l
Oestradiol <110 pmol/l Testosterone 10–35 nmol/l
Testosterone 0.5–3 nmol/l

Clinical Cases 407

Table C Morphological features of Turner’s syndrome

Skeletal Renal anomalies
• Short stature • Horse-shoe kidneys
• Cubitus valgus
• Short fourth metacarpals Miscellaneous abnormalities
• High-arched palate* • Webbed neck (fused cervical vertebrae)
• Shield chest with widely spaced nipples • Lymphoedema
• Low hair line
Cardiac anomalies • Multiple naevi
• Septal defects • Increased incidence of auto-immune thyroiditis
• Coarctation of the aorta
and diabetes

* Also present in Marfan’s syndrome, homocystinuria and Friedreich’s ataxia.

Table D Causes of primary hypogonadism in females

• Turner’s syndrome • Ovariectomy
• Pure ovarian dysgenesis* • Chemotherapy
• Swyer’s syndrome** • Steroid biosynthetic defect
• Auto-immune oophoritis • (17-α-hydroxylase deficiency)

* The pathology is the same as Turner’s, but differs in that there is a normal complement of chromosomes and the
other morphological features of Turner’s syndrome are absent. Some patients may have sensorineuronal deafness.
** Swyer’s syndrome is characterized by the XY karyotype and gonadal dysgenesis. Affected individuals are
phenotypically female. It is associated with a high incidence of gonadoblastomas.

Table E Characteristics of PCOS (Stein–Levental syndrome)

• Irregular menstruation • Testosterone level slightly higher than 3.0 nmol/l
• Impaired fertility • High oestrone levels
• Hirsutism • Slightly elevated LH level
• Acne • Slightly depressed FSH level
• Obesity • LH/FSH ratio generally exceeds 2
• Low oestradiol levels

Table F Causes of short stature

• Constitutional delay* • Drugs, particularly steroids

• Familial • Emotional deprivation

• Systemic disorder, e.g. coeliac disease • Skeletal abnormalities (achondroplasia,

• Endocrine causes, e.g. hypothyroidism or GH deficiency vitamin D-resistant rickets)

* Slow growth from the beginning, spontaneous puberty, slight delay in bone maturity, normal LHRH test.

Answer 398 Tall tented T-waves ( >1.25 mV; 12 small squares) is an
ECG feature of hyperkalaemia. In this case, the cause of
a. Serum potassium. hyperkalaemia is a combination of potassium-sparing
drugs and obstructive uropathy. (See Table B, Answer
220.)

408

Question 399

A 65-year-old female was referred to a neurologist with a 1. What is the diagnosis?
six-month history of progressive weakness and clumsiness a. Motor neurone disease.
of her left hand. She mentioned having particular b. Syringomyelia.
difficulty in washing the dishes and using the gear stick c. Multiple sclerosis.
while driving her car. Her husband noticed that her gait d. Cervical myelopathy.
had been unsteady and she had suffered a few falls in the e. Subacute combined degeneration of the spinal
past year. On systemic enquiry there was no history of cord.
headaches, visual disturbance or weight loss, but she had
experienced dizziness on turning her head suddenly. 2. Which investigation would you perform to confirm
the diagnosis?
On examination she was thin and had marked a. Myelography.
kyphoscoliosis. There was evidence of wasting of the b. MRI scan cervical spine.
small muscles of the hands, which was more prominent c. Nerve conduction studies and electromyography.
on the left side than the right. There was reduced power d. CSF analysis for oligoclonal bands.
on flexion and abduction of the arms. The supinator and e. Serum B12 level.
biceps reflexes on the left side were absent but present on
the right. The triceps reflexes were brisk bilaterally. The
power in both lower limbs was grade 4 out of 5 in all
muscle groups. The tone was increased. The ankle and
knee reflexes were brisk bilaterally. The left plantar
response was upgoing but the right one was equivocal.
Sensation was normal with the exception of vibration
sense at both ankle joints.

Question 400

A young alcoholic who is well known to the local Accident 120 beats/min, and regular, with a weak pulse volume. The
and Emergency Department was admitted to hospital after blood pressure was 80/40 mmHg. The heart sounds were
being found collapsed. On examination, he was unrousable. normal. Auscultation of the lung fields revealed a few
His temperature was 36.5°C (97.7°F). His heart rate was crackles at both lung bases. The abdomen was rigid and
bowel sounds were absent. Rectal examination
Hb 7 g/dl demonstrated soft brown stool. Examination of the fundi
WCC 23 × 109/l was normal.
Platelets 50 × 109/l
MCV 102 fl Investigations are shown.
INR 1.9
Sodium 131 mmol/l 1. What is the diagnosis?
Potassium 5.6 mmol/l a. Diabetic ketoacidosis.
Urea 17 mmol/l b. Perforated duodenal ulcer.
Creatinine 200 μmol/l c. Gastrointestinal haemorrhage secondary to
Bicarbonate 16 mmol/l oesophageal varices.
Calcium 1.9 mmol/l d. Acute pancreatitis.
Phosphate 1.0 mmol/l e. Methanol poisoning.
Albumin 30 g/l
AST 64 iu/l 2. List five investigations that you would perform on
Bilirubin 53 μmol/l this patient immediately.
Alkaline phosphatase 204 iu/l
Gamma GT 190 iu/l
Glucose 21 mmol/l
Urinalysis Protein +1
Blood 0
Ketones +1

Question 401 Clinical Cases 409

401a 401b

A 44-year-old West Indian male presented with a three-week FEV1(l) Actual Predicted
history of polydipsia, polyuria and nocturia. He was passing FVC (l) 2.2 4.1
copious amounts of urine several times per day, and felt 2.5 5.4
excessively thirsty. According to his wife he was consuming TLC (l) 3.3 6.3
up to five 2-litre bottles of cola per day, and several large 0.9 1.40
(1-litre) flasks of water. His appetite and weight had been KCO (mmol/min/kPa)
normal. He was not taking any medication. For four years he
had been intermittently unwell, firstly with chest problems, Sodium 143 mmol/l
and then with arthritis affecting his hands and feet. The Potassium 4.5 mmol/l
respiratory problems – which were characterized by a dry Urea 6 mmol/l
cough and accompanied by night sweats, pains in his ankles Creatinine 90 μmol
and tender, raised lesions on his shins – were of relatively Calcium 2.3 mmol/l
sudden onset. The joint pains responded to pain killers Phosphate 1.1 mmol/l
prescribed by a doctor whom he saw in the West Indies, but Alkaline phosphatase 120 iu/l
the chest symptoms persisted for several months despite four Blood glucose 4.2 mmol/l
long courses of antibiotics. The skin lesions on the shins X-ray of hands (401b)
resolved about three months after the onset of his illness. He
was eventually referred to a chest physician with Fluid deprivation test:
breathlessness on exertion, and after respiratory function
tests (top panel of results) and a chest X-ray was told he had Time (min) PmOsm/l UmOsm/l
scarring on the lung, possibly due to several previous chest 0 303 120
infections, and was prescribed a steroid inhaler. 120
60 310 120
The patient’s breathing remained stable. He was able to 120
walk for over two miles on the flat, but experienced 120 318 120
breathlessness on negotiating inclines. After two years, he 800
developed pain and swelling in his hands and feet, which 180 328
were controlled to some extent with co-proxamol. His only
other complaint was of a gritty feeling in the eyes as the day 240 335
progressed, and dryness of the mouth for several months
before he developed polyuria. He worked as a bus 8 h after desmopressin
conductor. His brother, aged 58, had rheumatoid arthritis
which was complicated with lung fibrosis. 1. What were the painful lesions on the shins?
2. What do the patient’s respiratory function tests
On examination, the patient appeared well at rest, but
had mild bilateral parotid gland enlargement. The demonstrate?
appearance of the eyes is shown (401a). His eyes were red, 3. What does the X-ray of his hands reveal?
but the visual acuity, visual fields, pupils and fundi were 4. Why does he have gritty eyes?
normal. There was no focal neurological deficit. There was 5. What is the interpretation of the water deprivation
no evidence of a previous BCG scar. There was bone
swelling affecting several phalanges in the hands and feet. test?
There was no joint swelling. Cardiovascular examination was 6. What is the overall or underlying diagnosis?
normal. Auscultation of the lung fields revealed fine 7. What three investigations would you perform to
inspiratory crackles in the anterior chest, but auscultation of
the posterior aspect of the chest was normal. confirm your diagnosis?
8. Give three therapeutic steps in his management.
Investigations are shown (second panel of results).

410

Answer 399

1. d. Cervical myelopathy. has superseded myelography. In this case, the lesion
2. b. MRI scan cervical spine. appears to affect the C5 and C6 segments of the cervical
cord, hence the absent biceps and supinator reflexes on
The patient presents with progressive weakness affecting the left side. This would not explain the weakness and
her arms and hands. She has a combination of upper and wasting of the muscles of the hand as they are supplied
lower motor neurone signs in the upper limbs and purely by C8 and T1; however, small muscle wasting in cervical
upper motor neurone signs in the lower limbs. There is myelopathy appears to be due to reduced blood flow to
loss of vibration sense at the level of the ankles. This may the lower segments of the cord rather than to direct
be a normal finding in patients in their seventh decade compression of the C8 and T1 spinal nerves. It is worth
but may indicate pathology in the dorsal columns. noting that sensory disturbance in the upper limbs may
be absent or very mild in cervical myelopathy.
The differential diagnosis is between motor neurone
disease, cervical cord tumour and cervical myelopathy, Cervical myelopathy is due to bulging or extrusion of
and subacute combined degeneration of the spinal cord. the disc material into the cervical canal, which results in
pressure atrophy and ischaemia. The main cause is
Features against motor neurone disease include her osteoarthritis of the cervical spine. The posterior columns
gender (more common in males), the mid-cervical reflex (dorsal tracts carrying proprioception, vibration sense and
pattern (absent supinator and biceps reflex but light-touch fibres) and the lateral columns (pyramidal
exaggerated triceps reflex), which is more suggestive of tracts carrying upper motor neurones) are affected. The
cervical myelopathy, the association of her symptoms 5th–7th cervical segments are most commonly affected.
with rigidity in the neck and dizziness on turning The symptoms are those of lower motor neurone signs at
suddenly, which again suggests pathology in the cervical these levels and upper motor neurone signs below. Neck
cord, and the absence of weight loss, which is usually stiffness and upper limb pain may be present. Spasticity of
marked in motor neurone disease. the lower limbs is common and more pronounced than
physical examination would suggest. Ataxia may occur
Subacute combined degeneration of the spinal cord is owing to dorsal column involvement (sensory ataxia).
a remote possibility, but one would want more evidence Lhermitte’s sign (electrical shock feeling down the spinal
of a sensory neuropathy in this condition, for example, cord and into the legs) is recognized, but may also occur
absence of light touch and proprioception and absent with cervical cord tumours, multiple sclerosis and
knee or ankle jerks. subacute combined degeneration of the spinal cord.

Both cervical myelopathy and a cervical cord tumour The presence of lower motor neurone signs and the
may present with predominantly upper limb signs, which absence of cerebellar signs is against multiple sclerosis.
characteristically produce lower motor neurone
disturbances at the level of the lesion and upper motor The absence of dissociated sensory loss is against
signs below it. The best investigation to differentiate syringomyelia.
between the two is an MRI scan of the spinal cord, which

Answer 400

1. d. Acute pancreatitis. Diagnoses to consider in an unconscious
2. i. Serum amylase. alcoholic

ii. Arterial blood gases. • Hepatic encephalopathy
iii. Full clotting screen. • Wernicke’s encephalopathy
iv. Chest X-ray. • Methanol poisoning
v. Ultrasound of the abdomen. • Ethylene glycol poisoning
• Alcohol intoxication
The clinical scenario is of an alcohol abuser who presents • Subdural haemorrhage
with unconsciousness and a rigid abdomen. The • Haemorrhage from peptic ulcer or varices
differential diagnosis is between a perforated duodenal • Acute haemorrhagic pancreatitis
ulcer, acute pancreatitis, ethylene glycol poisoning and • Tuberculous meningitis
methanol poisoning, as all four are recognized causes of • Alcohol-induced hypoglycaemia
abdominal pain in alcoholism. The raised gamma GT
supports alcohol abuse. The low calcium favours either calcium). However, the diabetic state is more in keeping
acute pancreatitis or ethylene glycol poisoning (oxidation with acute pancreatitis, which results in damage to the
of ethylene glycol to oxalic acid results in chelation of

Clinical Cases 411

islets of Langerhans, which produce insulin. Methanol unconsciousness in this patient given the fact that the
poisoning may also cause hyperglycaemia, but bicarbonate is not very low and the ketonuria is mild. The
hypocalcaemia is unusual. Furthermore, the acidosis is mild ketonuria in this case is due to reduced dietary intake.
more severe in methanol poisoning and there is usually Rhabdomyolysis is unlikely because the creatinine is not
evidence of optic atrophy. The anaemia is quite severe, very high, and there is no evidence of blood in the urine
suggesting that there may be ongoing peritoneal bleeding on dipstick testing (remember that myoglobin gives a
from the pancreatitis. The MCV is high, indicating either positive dipstick test for blood).
alcohol-related marrow toxicity or alcohol-related liver
damage. The low platelets indicate either hypersplenism A very high serum amylase would confirm acute
secondary to portal hypertension or a DIC process pancreatitis in this case. The most common causes of death
complicating acute pancreatitis. The raised INR may be in acute pancreatitis are haemorrhage, renal failure and
due to hepatocellular dysfunction or it may be part of the respiratory failure; therefore an FBC, blood gases, chest X-
DIC. Diabetic ketoacidosis would not explain the ray and clotting would give important prognostic
information.

Answer 401

1. Erythema nodosum. Causes of erythema nodosum Sarcoidosis is a multisystem granulomatous disease of
are shown (Table A). unknown aetiology that usually affects females more
commonly than males. It is much more common in black
2. A restrictive lung defect with a low KCO. The people, and may present acutely with the Lofgren’s
differential diagnosis for conditions causing this syndrome, which is characterized by erythema nodosum,
picture is discussed in Answer 217.
Table A Causes of erythema nodosum
3. The X-ray of the hands demonstrates several lucent
lesions at the ends of most phalanges. Common conditions Other conditions
Streptococcal Behçet’s syndrome
4. Bilateral keratoconjunctivitis. TB
5. The fluid-deprivation test reveals an inability to infections, including Leprosy
rheumatic fever Histoplasmosis
concentrate urine until the administration of Sarcoidosis Yersinia
exogenous desmopressin (an ADH analogue), which Oral contraceptive pill Neisseria meningitidis
is indicative of cranial diabetes insipidus. and pregnancy
Interpretation of a fluid deprivation test is discussed Inflammatory bowel and gonococcal
below. Conditions causing cranial diabetes insipidus disease infections
and an abnormal chest X-ray include sarcoidosis, TB Sulphonamide drugs Pasteurella pestis
and histiocytosis X. In rare situations, bronchial
carcinoma may metastasize to the hypothalamus or Table B Causes of diabetes insipidus
pituitary and cause diabetes insipidus. Other causes of
diabetes insipidus are shown (Table B). Cranial Nephrogenic
6. The combination of erythema nodosum, ocular, lung,
bone, parotid and lachrymal gland involvement Familial X-linked (vasopressin
strongly suggests the diagnosis of sarcoidosis.
7. i. Transbronchial lung biopsy to demonstrate non- Autosomal dominant receptor-2 gene)

caseating granulomas. DIDMOAD syndrome Autosomal recessive
ii. MRI scan of the pituitary to demonstrate high-
Cerebral tumour (aquaporin receptor
intensity lesions in the mid-brain and hypothalamus.
iii. Serum ACE level. This is not specific for the Sarcoidosis gene)

diagnosis of sarcoidosis and may be elevated in TB, TB Hypokalaemia
histoplasmosis, berylliosis, silicosis, lymphoma,
diabetes mellitus, chronic liver disease, Histiocytosis X Hypercalcaemia
hyperthyroidism and Gaucher’s disease. Trauma Lithium
8. i. High-dose steroids. Indications for high-dose
steroids in sarcoidosis include cerebral Pituitary haemorrhage Post-obstructive
involvement, acute diffuse lung disease, uveitis
and hypercalcaemia. uropathy
ii. Desmopressin.
iii. Artificial tears. Sickle cell anaemia

Glibenclamide

Aminoglycosides

Amphotericin

412

arthralgia, dry cough, bilateral hilar lymphadenopathy on are referred to as lupus pernio. Arthralgia affecting the
the chest X-ray, and anterior uveitis. Patients with hands and feet is common; X-rays demonstrate small
sarcoidosis may have lacrimal and parotid gland lucent cysts in multiple phalanges. Cerebral involvement is
involvement, which is characterized by gland enlargement rare, but features include cranial nerve lesions, aseptic
and sometimes referred to as Mikulicz syndrome (causes of meningitis, psychosis and a multiple sclerosis-type
parotid gland enlargement are listed in Table C). Affected syndrome. Mononeuritis multiplex is a recognized
patients may complain of xerostomia and gritty eyes manifestation of the peripheral nervous system.
respectively, the latter being due to keratoconjunctivitis Hypercalcaemia occurs owing to the presence of excessive
resulting from impaired lacrimation. Mikulicz syndrome production of 1,25-DHCC by granulomatous cells. Other
may also complicate TB, lymphoma and leukaemia. conditions where a similar phenomenon occurs include TB
Mikulicz syndrome is relatively common and when it is and Candida infection.
associated with acute uveitis and facial nerve palsy it is
referred to as Heerfordt’s syndrome. In most patients the Water deprivation test
acute illness will resolve, although some will continue to In patients with polyuria and polydipsia and a normal
have respiratory symptoms for up to two years, and a small blood glucose, the differential diagnosis is between
percentage develop a chronic illness characterized by cranial diabetes insipidus, nephrogenic diabetes insipidus
relapses and remissions. and compulsive water deprivation. The water deprivation
test will help differentiate compulsive water drinking
In chronic cases lung parenchyma becomes involved, from both types of diabetes insipidus (Table D).
leading to fibrosis commonly affecting the apices. Ocular However, the differentiation of cranial diabetes insipidus
involvement is well recognized. Manifestations include from nephrogenic diabetes insipidus involves
anterior and posterior uveitis, which are characteristically measurement of plasma and urine osmolality following
associated with visual symptoms and pupillary administration of desmopressin. Patients with cranial
abnormalities, and episcleritis, scleritis, choroiditis, diabetes insipidus are deficient in ADH and respond
cataracts and glaucoma. Corneal calcification complicating dramatically to desmopressin with an increase in urine
hypercalcaemia may also occur in sarcoidosis. osmolality, whereas patients with nephrogenic diabetes
insipidus are resistant to the effects of ADH and therefore
Skin infiltration occurs in the chronic form of the illness the urine osmolality is not affected by desmopressin.
and comprises papules on the eyelids and around the
mouth. Papules affecting the nose may be disfiguring and

Table C Causes of parotid gland enlargement

• Mumps • Haemochromatosis
• Sarcoidosis • Amyloidosis
• Lymphoma • Acromegaly
• Leukaemia • Malabsorption syndromes
• Sjögren’s syndrome • Drugs; propylthiouracil
• Alcohol abuse • Toxins; lead
• Bulimia • Hyperlipidaemia
• Cystic fibrosis

Table D After a water deprivation test P mOsm/l U mOsm/l
300 Over 720 or double the plasma osmolality
Normal 300 Incomplete response, i.e. the U mOsm/l is not
Compulsive water drinking
quite 720 and does not exceed twice the value
Cranial diabetes inspidus >300 of the P mOsm/l. Typical value 600–700 mOsm/l
Nephrogenic diabetes insipidus >300 <150; over 720 mOsm/l after desmopressin
<150; remains <150 mOsm/l after desmopressin

Clinical Cases 413

Question 402 Hb 9.4 g/dl

A 26-year-old female presented with a six-month history WCC 8 × 109/l
of light-headedness on hanging the washing. She was
seen by her GP at the onset of her illness and he noted a Platelets 430 × 109/l
blood pressure of 80/50 mmHg in both arms but no
other abnormality. Over six months she had one episode ESR 112 mm/h
of weakness and numbness of the right arm and face for
almost an hour and two near syncopal episodes. She Sodium 135 mmol/l
developed increasing lethargy, night sweats, and aches
and pains in her upper limbs. Her appetite had reduced Potassium 4.5 mmol/l
and she had lost almost 3 kg in weight. There was no
other past medical history of note. She had smoked 10 Urea 6 mmol/l
cigarettes per day for three years from the age of 17.
Creatinine 84 μmol/l
On examination she had flushed cheeks but there was
no skin rash. The heart rate was 90 beats/min and Glucose 4.5 mmol/l
regular. The systolic blood pressure was 80 mmHg in
both upper limbs, but the diastolic blood pressure could Cholesterol 5.3 mmol/l
not be ascertained. On examination of the precordium,
the apex was heaving in nature but not displaced. On Autoantibody screen Rheumatoid factor absent
auscultation there was an audible fourth heart sound.
The radial pulses were absent bilaterally, the brachial Antinuclear antibodies
pulses were weak bilaterally, the right carotid pulse was
absent. The left carotid pulse was prominent. Both present in a titre of 1 in 16
femoral pulses were easily palpable. Neurological
examination was normal. Syphilis serology VDRL and TPHA absent

Investigations are shown. Chest X-ray Normal-sized heart

Clear lung fields

ECG Voltage criteria for left

ventricular hypertrophy

CT scan brain Normal

1. What is the diagnosis? 3. Which of the three below would best explain the
a. Giant cell arteritis. reason for left ventricular hypertrophy on the ECG?
b. Polyarteritis nodosa. a. Cardiac amyloid.
c. Buerger’s disease. b. Essential hypertension.
d. Takayasu’s arteritis. c. Hypertension secondary to renal artery stenosis.
e. Relapsing polychondritis. d. Chronic renal failure.
e. Fibromuscular dysplasia.
2. Which investigation would you request to confirm f. Renal vasculitis.
the diagnosis? g. Acquired co-arctation of the aorta.
a. Aortography. h. Reduced distensibility of the ascending aorta.
b. Invasive blood pressure monitoring.
c. Serum antineutrophil cytoplasmic antibody.
d. Fluorescent treponemal antibody.
e. Cardiac biopsy.

414

Answer 402

1. d. Takayasu’s arteritis. include pulseless vessels. Hypertension is present in 50%
2. a. Aortography. of cases, but was not detected in this case because of
3. c. Hypertension secondary to renal artery stenosis. disease in both subclavian arteries. The causes of
hypertension include renal artery stenosis, acquired co-
g. Acquired co-arctation of the aorta. arctation and reduced distensibility of the aortic arch.
h. Reduced distensibility of the ascending aorta. Complications are those of long-standing hypertension,
aortic regurgitation and congestive cardiac failure.
The absence of pulses in the arms and neck and the Inflammatory markers are usually raised and there may be
associated high ESR value in a young woman should raise an anaemia of chronic disease, but the diagnosis is a
the diagnosis of Takayasu’s arteritis. Takayasu’s arteritis is clinical one and can be confirmed with aortography. In
a rare disorder with a prevalence of 1.5–2 per million. It this case, the patient had an occluded brachiocephalic
has a strong female predisposition and is more common and left subclavian artery. The differential diagnosis is
in parts of Africa and Asia. The mean age of onset is 29 between other conditions which may produce an aortic
years, but it can occur from any age between infancy and arch syndrome, such as syphilitic aortitis and relapsing
middle age. It is very uncommon after middle age. The polychondritis; however, in this case syphilis serology is
condition is caused by granulomatous vasculitis of large negative and there are no clinical features of relapsing
vessels, particularly the aortic arch, which results in polychondritis. Treatment is with steroids and vascular
obliterative changes in the lumina of the vessels affected. stents.
Inflammation may be multi-segmental, interspersed with
normal segments. Symptoms comprise a systemic illness Aortography in this patient demonstrated occluded
(sweats, weight loss, anorexia and myalgia) as well as innominate and left subclavian arteries (402). Only the
vascular insufficiency in the limbs affected. Physical signs left common carotid artery is patent.

402

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Data Interpretations Tutorials

Calcium Biochemistry

Condition Ca PO4 Alkaline Additional

phosphatase

1° and 3° hyperparathyroidism ↑ ↓↑

2° hyperparathyroidism/CRF ↓/N ↑↑

Hypoparathyroidism ↓ ↑N PTH absent

Pseudohypoparathyroidism ↓ ↑N PTH elevated

Magnesium deficiency ↓ ↑↑ PTH normal

Pseudopseudohypoparathyroidism N NN

Osteomalacia/rickets ↓ ↓↑

Osteoporosis N NN

Myeloma ↑ N N*

Paget’s disease N** N↑ ↑ urinary hydroxyproline

Malignancy (bony metastases) ↑ N/↑ ↑

Sarcoidosis N/↑ NN

Vitamin D intoxication ↑ ↑N

* Increased with pathological fractures. ** Increased after prolonged immobilization.

Genetics

Patterns of inheritance X-linked dominant inheritance
• Males and females are both affected.
Autosomal dominant inheritance • No male-to-male transmission.
• Males and females are equally affected. • Affected males transmit the disease to 100% of their
• All individuals inheriting the abnormal gene are affected.
• Offspring of affected parents (irrespective of the parental daughters.
• An affected female will transmit the disease to 50% of all
sex) have a 50% chance of inheriting the disease.
• This is in contrast to X-linked conditions where male-to- offspring.

male transmission of disease does not occur. X-linked recessive inheritance
• Males are affected.
Autosomal recessive inheritance • Females are carriers.
• Males and females are equally affected, but are fewer in • No male-to-male transmission.
• Daughters of affected males will be carriers.
number than in autosomal dominant conditions. • Female carrier will have 50% affected sons and 50%
• Not all generations will be affected.
• If both parents are carriers for the recessive gene 25% of daughters who are carriers.

the offspring will be affected, 50% will become carriers, Inheritance of maternal mitochondrial genetic abnormalities
but will not have the disease and 25% will not have the • During conception, only mitochondria from the ovum
abnormal gene.
• If an affected individual marries a carrier, then 50% off- are passed on to the zygote.
spring will be affected and 50% offspring will be carriers. • Affected females will pass the disease to 100% offspring.
• If an affected individual marries another affected, then all • Affected males will not transmit disease to offspring.
offspring will be affected. • Examples include Leber’s optic atrophy, Kearnes–Sayer

syndrome, MELAS (mitochondrial encephalopathy,
lactic acidosis and stroke-like syndrome), MERF
(mitochondrial encephalopathy and red ragged fibres).

416

Audiograms

An audiogram of both ears may be presented on the same with high frequencies (2). Other causes of bilateral
graph, or there may be a separate audiogram for each ear. sensorineuronal deafness include congenital rubella infec-
A separate suffix will be given to differentiate between air tion, mumps infection and drugs such as high dose loop
conduction (AC) and bone conduction (BC). diuretics and aminoglycosides.

In sensorineuronal deafness, both air and bone conduc- Fluctuating low tone deafness (below 4,000 Hz) sug-
tion are diminished. The air–bone gap is usually narrow, gests Ménière’s disease. This is bilateral in 10% of cases
i.e. there is not much difference between air and bone (3) and may progress to sensorineuronal deafness in 25%
conduction. In conduction deafness, bone conduction is of patients (2).
superior to air conduction on the affected side.
Sudden and profound hearing loss at a frequency of
Normal hearing can detect sounds of a frequency 4,000 Hz is suggestive of noise-induced hearing loss (4).
between 250–8,000 Hz at a sound intensity of 0–10 dB
(1). The following audiograms are most commonly Unilateral sensorineuronal hearing loss (5) may be
tested in higher post-graduate examinations. degenerative or due to unilateral auditory nerve damage
as a result of a neuropathic process. It should also raise
Sensorineuronal deafness at progressively higher fre- the suspicion of lesion in the cerebello-pontine angle on
quencies. In degenerative sensorineuronal loss (presbycu- the affected side, for example, an acoustic neuroma.
sis), deafness is usually bilateral most profound at sounds

Hearing level (dB)1 AC Hearing level (dB) -10
Right 0
-10
0 Left 10
20
10 BC 30
20 Right 40
30 50
40 Left 60
50 70
60 Unmasked 80
70 90
80 500 1000 2000 4000 8000 100 500 1000 2000 4000 8000
90 Frequency HZ 110 Frequency HZ
100 120
110 130
120 140
130
140 125 250

125 250

Hearing level (dB)2 AC Hearing level (dB) -10
Right 0
-10 Left 500 1000 2000 4000 8000
0 10 Frequency HZ
BC 20
10 Right 30
20 Left 40
30 Unmasked 50
40 60
50 500 1000 2000 4000 8000 70
60 Frequency HZ 80
70 90
80 100
90 110
100 120
110 130
120 140
130
140 125 250

125 250

Data Interpretations Tutorials 417

Hearing level (dB) -10 AC Hearing level (dB) -10 3
0 Right 0
500 1000 2000 4000 8000
10 Left 10 Frequency HZ
20 20
30 BC 30
40 Right 40
50 50
60 Left 60
70 70
80 Unmasked 80
90 90
100 500 1000 2000 4000 8000 100 250
110 Frequency HZ 110
120 120
130 130
140 140

125 250 125

Hearing level (dB) -10 AC Hearing level (dB) -10 4
0 Right 0
500 1000 2000 4000 8000
10 Left 10 Frequency HZ
20 20
30 BC 30
40 Right 40
50 50
60 Left 60
70 70
80 Unmasked 80
90 90
100 500 1000 2000 4000 8000 100 250
110 Frequency HZ 110
120 120
130 130
140 140

125 250 125

Hearing level (dB) -10 AC Hearing level (dB) -10 5
0 Right 0
500 1000 2000 4000 8000
10 Left 10 Frequency HZ
20 20
30 BC 30
40 Right 40
50 50
60 Left 60
70 70
80 Unmasked 80
90 90
100 500 1000 2000 4000 8000 100 250
110 Frequency HZ 110
120 120
130 130
140 140

125 250 125

418

In the example below, bone conduction is superior to Causes of conduction deafness
air conduction suggesting conduction deafness (6).
Causes of conduction deafness are shown (Table). Ear wax
Chronic suppurative otitis media
Middle ear granuloma
Otosclerosis

6Hearing level (dB) AC -10
Hearing level (dB)Right0
-10
0 Left 10
20
10 BC 30
20 Right 40
30 50
40 Left 60
50 70
60 Unmasked 80
70 90
80 500 1000 2000 4000 8000 100 500 1000 2000 4000 8000
90 Frequency HZ 110 Frequency HZ
100 120
110 130
120 140
130
140 125 250

125 250

Guidelines for the Interpretation of Cardiac Catheter Data

• Right-heart saturations do not exceed 75%. Saturations more than this are suggestive of a left-to-right shunt.
• Left-heart saturations vary from 96–98%. Saturations less than this are suggestive of a right-to-left shunt.
• In right-to-left shunts, the arterial saturations do not change with inspired high-concentration oxygen.
• A VSD with a right-to-left shunt and pulmonary stenosis can be differentiated from Fallot’s tetralogy by

examining the oxygen saturation in the left ventricle and the ascending aorta. In the case of a VSD, the
saturations in the left ventricle and the aorta will both be low and very similar. In the case of Fallot’s tetralogy,
the aortic oxygen saturation will be much lower than the oxygen saturation in the left ventricle because the
right ventricle pumps most of the deoxygenated blood into the overriding aorta.
• A pulmonary artery pressure exceeding 35 mmHg is suggestive of pulmonary hypertension.
• A pressure drop of more than 10 mmHg across the aortic or pulmonary valve is suggestive of aortic or
pulmonary stenosis, respectively.
• The PCWP is equal to the LVEDP. When the PCWP exceeds the LVEDP, the diagnosis of mitral stenosis
should be considered.
• The diagnosis of mitral regurgitation cannot be made unless you are given the PCWP ‘v-wave’. A v-wave
higher than 20 mmHg is highly suggestive of mitral regurgitation.
• Aortic regurgitation is diagnosed by a wide pulse pressure in the aortic pressure.
• The right and LVEDP and the left and right atrial pressures are roughly equal in pericardial constriction.

Data Interpretations Tutorials 419

Respiratory Function Tests Restrictive lung defect

Obstructive lung defect Examples:
• Interstitial lung disease:
Examples:
• Chronic bronchitis. sarcoidosis,
• Emphysema. fibrotic lung disease
• Asthma. • Pulmonary emboli.
• Bronchiectasis. • Pulmonary oedema.
• Neuromuscular disease affecting respiratory muscles.
Spirometry • Pulmonary haemorrhage.
• Lymphangitis carcinomatosa.
FEV1 (l) ↓↓ • Thoracic cage defects.
FVC (l) ↓
FEV1/FVC <70% (normal Spirometry

TLC (l) 70–80%) FEV1 (l) ↓
RV ↑ (gas trapping) FVC (l) ↓↓
TLCO (l) ↑ FEV1/FVC >80%
KCO (mmol/min/kPa) ↓ TLC (l) ↓
↓* RV ↓
TLCO (l) ↓
*The KCO is always low in obstructive airways KCO** (mmol/min/kPa) ↓
disease, with the very rare exception of a limited
number of patients with asthma who may have a ** KCO is charcteristically reduced in most cases of
high KCO during an attack. The exact mechanism restrictive defect, with the exception of pulmonary
for this is not understood. The KCO is significantly haemorrhage, where it is increased, and thoracic
reduced in emphysema, and if a young patient or a cage deformities/neuromuscular defects and
non-smoker has a low KCO in the context of an pneumonectomy where it is unchanged or increased.
obstructive lung defect, always consider the
possibility of α-1 antitrypsin deficiency.

KCO Reduced KCO:
• Interstitial lung disease.
Increased KCO: • Primary pulmonary hypertension.
• Polycythaemia. • Multiple pulmonary emboli.
• Left-to-right shunts. • Pulmonary oedema.
• Pulmonary haemorrhage. • Lymphangitis carcinomatosa.
• Asthma (exceptionally rare). • Arteriovenous malformation.
• Thoracic cage deformities (may be normal). • Anaemia (spirometry normal).
• Obstructive airways disease (rare exception is asthma).

420

Interpretation of Respiratory Flow Loop Curves

The normal flow loop curve has a triangular expiratory Obstructive airways disease
flow limb and a semi-circular inspiratory flow limb (7). In obstructive airways disease the amount of elastic recoil
The explanation for this is as follows: following a full in- in the lung is reduced; therefore the onset of the expira-
spiration, the lung’s recoil is maximal, as is pleural pres- tory limb is not as explosive as in a normal individual and
sure. The onset of expiratory flow is therefore explosive reaches its peak later than usual. As expiration continues
and reaches its peak within 0.01 s. The expiratory curve the small airways collapse rapidly to produce a very early
decreases its flow gradually as the lung volume drops decline in flow which results in a ‘flat’ expiratory flow
from TLC to RV. This reflects the gradual drop in the loop curve after the initial peak (8).
lung’s elastic recoil as the lung gets smaller. In contrast
to expiration, inspiration does not reach an instant Extrathoracic airways disease obstruction
maximal flow. As the respiratory muscles contract, the Extrathoracic airways may be variable or fixed. In
power increases progressively from the start of the extrathoracic obstruction, the inspiratory loop is reduced
inspiration to achieve a maximal flow. This takes a significantly compared with the expiratory flow. Normally,
relatively long time, and the maximal inspiratory flow is during inspiration, the negative intrathoracic pressure
only achieved by the mid-point of the vital capacity. The pulls the intrathoracic airways open and promotes inspira-
flow then slows again as the maximum inspired volume is tory flow. In extrathoracic obstruction this does not
reached, giving the inspiratory limb a semi-circular happen; therefore the inspiratory flow rate is reduced. In
appearance. variable extrathoracic obstruction the expiratory flow limb
is preserved (9). Examples of variable obstruction include
Flow loops tested in the examination are those of tumour in the upper airways, fat, pharyngeal muscle
obstructive airways disease, extrathoracic airways obstruc- weakness, vocal cord paralysis or enlarged lymph nodes. In
tion, intrathoracic airways obstruction, and a restrictive fixed extrathoracic obstruction, such as tracheal stenosis,
lung defect. both expiratory flow and inspiratory flow limbs are
‘blunted’; however, the inspiratory limb is affected much
7 10 Expiration more than the expiratory limb (10).

Flow (l/sec) 8 Inspiration Intrathoracic airways obstruction
6 When obstruction is intrathoracic, inspiration is preserved
4 0 12 3 45 6 78 because the large extrathoracic airways are patent; however,
2 Change in lung volume (l) the expiratory flow is diminished because an increased
0 intrathoracic pressure is required to overcome the obstruc-
2 tion, which results in closure of the small airways (11).
4
6 Restrictive lung disease
8 The flow loop curve has the same shape as the normal
curve (7), but the lung volume is much smaller.
10

8 8 9 10
6
Flow (l/sec) Flow (l/sec) 8
6
4 4 Expiration
2
2 Expiration 0 Inspiration
2
0 Inspiration 4 0246
6 Change in lung volume (l)
2 012345 8
Change in lung volume (l)
4 10

6

Data Interpretations Tutorials 421

Flow (l/sec) 4 10 Flow (l/sec) 10 11
2 8
Expiration 6 Expiration
4 Inspiration
0 2
0 02 468
Inspiration 2 Change in lung volume (l)
2 4
6
4 8

012 10
Change in lung volume (l)
3

Echocardiography

Echocardiography has featured, and will continue to Normal values for cardiac dimensions
feature, in postgraduate examinations because it is widely
requested, and pictures from ‘still frames’ are relatively Chamber/structure Measurement
easy to interpret. Both M-mode and two-dimensional
(2-D) echocardiography are tested, although the latter is Left atrium <4.5 cm
being shown with an increasing frequency because it Left ventricular diastolic size <5.5 cm
allows the reader to have a better appreciation of cardiac Interventricular septum <1.2 cm
chambers. Posterior wall <1.2 cm

Normal values for cardiac dimensions are shown in the
table.

2-D echocardiography examination. Four-chamber views resemble what the
The view which is shown most often is the parasternal reader envisages the heart to look like, except that the
long-axis view (12). In this view it is not always easy to ventricles are at the top and the atria are at the bottom
study the right ventricle in detail, and therefore it is (13). Most echocardiograms are accompanied by a scale
unusual to be shown right-sided pathology in the where each square represents 1 cm.

12 13

1 6 72
2 84
3
5 4

Key: 3 Mitral valve 6 Aorta
1 Interventricular septum 4 Left atrium 7 Right ventricle
2 Left ventricle 5 Left ventricular posterior wall 8 Right atrium

422

Figures 14 and 15 are diagrammatic representations Common examples of conditions shown in examinations
of a common parasternal long axis and an apical four- using 2-D echocardiography:
chamber view respectively. • Pericardial effusion (16, effusion is arrowed).
• Left atrial myxoma (17, myxoma is arrowed).
• Mitral stenosis (18, stenosed mitral valve is arrowed).
• Vegetation on mitral valve (19, vegetation on the

anterior mitral valve leaflet is arrowed).

14 Right ventricular 15
outflow tract
Interventricular
septum

Right Left

Aorta ventricle ventricle

Aortic valve Left Interventricular
atrium septum
Left ventricle
Tricuspid
Mitral valve valve Mitral valve

Pericardium Right Left Interatrial
Left ventricular posteror wall atrium atrium septum

16 17

18 19

Data Interpretations Tutorials 423

• HCM (20, gross hypertrophy of the interventricular • Aortic stenosis (23, calcified aortic valve arrowed).
septum is arrowed). • Vegetation on aortic valve (24, echogenic mass on the

• Left ventricular thrombus (21 thrombus at the apex is aortic valve is arrowed).
arrowed; 22 thrombus is arrowed). • Aortic dissection (25, aortic dissection flap is arrowed).

20 21

22 23
24 25

424

Figure 26 is a diagrammatic representation of com- Examples commonly shown in M-mode echocardiography:
mon examples shown on parasternal long-axis view. • Pericardial effusion.
Figure 27 is a diagrammatic representation of common • Left atrial myxoma (29, echogenic mass prolapsing
examples shown in the four-chamber view.
through the mitral valve orifice in diastole is arrowed).
M-mode echocardiography • Mitral stenosis (30, thickened anterior mitral valve
The M-mode picture is derived by taking a cross-sectional
view from the 2-D parasternal long-axis view. The three leaflet is arrowed; reduced excursion of the mitral
main views include sections at the level of the aortic valve, valve in diastole is shown [1]).
at the level of the tips of the mitral valve, and at the level • Vegetation on mitral valve (31, echogenic mass on the
of the papillary muscle. The cross-sectional view at the posterior mitral valve leaflet is arrowed).
level of the mitral valve tips is by far the most common • Mitral valve prolapse (32, hammocking of the posterior
view which is shown in examinations because it allows the mitral valve leaflet in systole is arrowed).
examiners to test the readers on abnormalities on the • HCM (33, systolic anterior motion of the mitral valve
mitral valve and the left ventricle (28). is shown [1]).

26 Hypertrophic Vegetation on 27 Left ventricular
aortic valve thrombus
cardiomyopathy Hypertrophic
Calcific aortic cardiomyopathy Vegetation
Mitral stenosis stenosis (asymmetric on mitral
Vegetation septal valve
on mitral Atrial hypertrophy)
valve myxoma
Mitral stenosis

Left ventricular Pericardial effusion Atrial
thrombus myxoma

28 Chest wall Right ventricular wall 29

Right ventricular cavity Interventricular septum

Anterior mitral valve leaflet Left
ventricle

Posterior mitral valve leaflet Left ventricular
posterior wall

Pericardium 31

30

1

Data Interpretations Tutorials 425

32 33

1

Importance of carefully inspecting mitral valve leaflets appose. With the exception of pericardial effusion,
leaflets to diagnose cardiac abnormalities on the careful inspection of the mitral valve will enable the
M-mode echocardiogram reader to diagnose all the abnormalities which are com-
On an M-mode echocardiogram, the normal mitral valve monly tested (Table).
has an anterior leaflet which has a characteristic ‘M’-
shape and a posterior leaflet which has a semi ‘U’-shape. Figure 34 is a diagrammatic representation of the
In diastole, the anterior leaflet moves forward and the mitral valve in relation to cardiac lesions on the M-mode
posterior leaflet moves backward, and in systole both echocardiogram.

The mitral valve in relation to cardiac lesions on the M-mode echocardiogram

Abnormality Mitral valve abnormality
Mitral valve prolapse Normal appearance in diastole; however, in mid systole there is prolapse of
one or both leaflets

Mitral stenosis There is loss of the M-shape of the anterior leaflet
Mitral valve excursion is reduced and there is anterior movement of the
posterior leaflet in diastole

Atrial myxoma There is obliteration of the mitral valve cavity by an echogenic mass in diastole

Vegetation on mitral valve Echogenic mass on one or both leaflets

HCM The mitral valve moves forward towards the septum in systole (a phenomenon
termed systolic anterior motion of the mitral valve (SAM). In addition, the left
ventricular cavity is small and there is septal hypertrophy

Aortic regurgitation As the regurgitant jet flows back into the left ventricle it ‘tickles’ the anterior
leaflet, causing a fluttering appearance

Echo on AMVL Mitral stenosis Hypertrophic 34
cardiomyopathy
AMVL Normal systolic Vegetation on Loss of M-shape
appearance mitral valve Reduced excursion Systolic anterior
Forward movement of PMVL motion of MV

PMVL Normal Vegetation Myxoma Fluttering
diastolic on PMVL Echogenic mass in of AMVL
appearance mitral valve orifcie
Mitral valve prolapse Aortic
regurgitation
Hammocking of the leaflets in mid systole

AMVL: Anterior mitral valve leaflet
PMVL: Posterior mitral valve leaflet
MV: Mitral valve

426

Acid–base Disturbance

Acidosis agents. It is characterized by a high bicarbonate and a
The main source of acid (H+ ions) in the body is tissue high pH. Respiratory alkalosis is rare and is usually acute.
respiration. Carbon dioxide produced by cellular respira- Chronic cases, usually due to chronic hyperventilation,
tion is converted to carbonic acid, which dissociates to are compensated for by increasing bicarbonate excretion
generate H+ (acid) and HCO3– ions (buffering base). The by the kidneys. Metabolic alkalosis – which is much more
retention of CO2, increase in H+ or reduction in HCO3– common than respiratory alkalosis – is compensated for
may result in an acidosis. by respiratory hypoventilation, which results in an
increase in pCO2 and hence an increase in H+.
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3–
Causes of respiratory and metabolic acidosis
Three types of acidosis are recognized:
• Respiratory acidosis. Respiratory acidosis
• Metabolic acidosis with a high anion gap. • Hypoventilation from any cause, e.g. obesity,
• Metabolic acidosis with a normal anion gap.
thoracic cage deformities and neuromuscular
Respiratory acidosis is characterized by a fall in arterial disorders
pH (<7.35) due to CO2 retention. Metabolic acidosis • Obstructive airways disease
may result from the retention of fixed or organic acids • Acute asthma
causing a reduction in the bicarbonate level (which is the
main buffering agent for H+ in the blood) without any Metabolic acidosis (high anion gap)
change in the chloride situation. In these situations, it is • Diabetic ketoacidosis
termed metabolic acidosis with a high anion gap. Alterna- • Uraemic acidosis
tively, metabolic acidosis may occur as a consequence of • Salicylate poisoning
bicarbonate loss from the gastrointestinal tract or the • Lactic acidosis:
kidneys. In these situations, chloride is retained, resulting
in a hyperchloraemic acidosis or a metabolic acidosis with shock
a normal anion gap. The anion gap is calculated by sub- liver failure
tracting the sum of the sodium and potassium concen- metformin therapy
trations from the sum of the chloride and bicarbonate glucose-6-phosphate dehydrogenase deficiency
concentrations. The normal anion gap is between leukaemia
10–18 mmol/l. The hallmark of metabolic acidosis of • Methylene poisoning
either type is a low arterial pH and a low bicarbonate • Ethylene glycol poisoning
level.
Metabolic acidosis (normal anion gap)
Regulation of arterial pH is controlled by the kidneys • Severe diarrhoea
and the lungs. Acidosis can be compensated for either by • Pancreatic fistula
removing CO2 from the body (lungs) or by retaining • Ureterosigmoidostomy
bicarbonate ions (kidneys). Respiratory acidosis is • RTA
compensated for by the kidneys, which retain bicarbonate • Acetazolamide therapy
ions. In compensated respiratory acidosis the pH is
normal, or almost normal, and the bicarbonate level is Causes of respiratory and metabolic alkalosis
high. In compensated metabolic acidosis the arterial pH
is normal, or almost normal, and the pCO2 is low. Respiratory alkalosis:
Respiratory acidosis is compensated by the respiratory • Hyperventilation
system through a centrally mediated mechanism which • Hysteria
results in hyperventilation and a consequent reduction in • Encephalitis
the pCO2. Causes of respiratory and metabolic acidosis • Brainstem lesions
are given (Table). • Aspirin toxicity

Alkalosis Metabolic alkalosis:
Alkalosis may be respiratory or metabolic in origin. In • Vomiting
respiratory alkalosis, there is a high pH due to hyper- • Diuretics
ventilation, causing a low pCO2. Metabolic alkalosis is • Antacids
usually due to increased loss of H+ from the kidney or • Hypokalaemic states (these increase renal loss of
gastrointestinal tract, or to increased ingestion of alkaline
H+ by the distal convoluted tubule)

Normal Ranges 427

Normal Ranges

Haematology male SI units Traditional units
ESR female
Hb 0–10 mm in 1st h 0–10 mm in 1st h
male 130–180 g/l 13–18 g/dl
MCH female 115–150 g/l 11.5–15 g/dl
MCHC 27–32 pg –
MCV male 32–36 g/dl 32–36%
PCV (haematocrit) female 76–95 fl 76–95 x 106/mm3
0.40–0.54 l/l 40–54%
Platelet count total 0.35–0.47 l/l 35–47%
RBCs neutrophils 150–400 x 109/l 150–400 x 103/mm3
lymphocytes 4.5–6.5 x 1012/l 4.5–6.5 x 106/mm3
Reticulocyte count monocytes 3.9–5.6 x 1012/l 3.9–5.6 x 106/mm3
WCC eosinophils 0.2–2% 0.2–2%
basophils 4–11 x 109/l 4–11 x 103/mm3
2–7.5 x 109/l 2–7.5 x 103/mm3
Clotting 1.5–4.0 x 109/l 1.5–4.0 x 103/mm3
APTT 0.2–0.8 x 109/l 0.2–0.8 x 103/mm3
BT 0.04–0.4 x 109/l 0.04–0.4 x 103/mm3
Fibrinogen <0.1 x 109/l <0.1 x 103/mm3
PT
TT 30–46 s 30–46 s
2–8 min 2–8 min
Endocrinology 2–4 g/l 0.2–0.4 g/dl
12–14 s 12–14 s
Cortisol 09.00 h 15–19 s 15–19 s

24.00 h 170–700 nmol/l 6.1–25.2 ␮g/dl
<140 nmol/l 5.0 ␮g/dl
GH <10 ␮g/l <10 ng/ml
500–1,100 pmol/l 500–1,100 pmol/l
Oestradiol mid-cycle <360 mu/l <360 ␮u/ml
2–4 ␮g/l/h 2–4 ng/ml/h
Prolactin 5–14 ␮g/l/h 5–14 ng/ml/h
10–35 nmol/l 3–10 ng/ml
Renin lying 0.9–3.1 nmol/l 0.3–1.0 ng/ml
68–174 nmol/l 4.5–13.6 ␮g/dl
standing 0.4–3.6 mu/l 0.4–3.6 ␮u/ml

Testosterone male <10 ku/l <10 u/ml
5–30 iu/l 5–30 mu/ml
female 34–48 g/l 3.4–4.8 g/dl
25–100 iu/l 25–100 mu/ml
Thyroxine 10–40 iu/l 10–40 mu/ml
160–900 ng/l 160–900 pg/ml
TSH 22–30 mmol/l 22–30 mEq/l
2–17 ␮mol/l 0.12–1.0 mg/dl
Biochemistry
α-fetoprotein
ALT
Albumin
Alkaline phosphatase
AST
B12 (serum)
Bicarbonate
Bilirubin

428

Biochemistry (continued) SI units Traditional units

Calcium 2.2–2.7 mmol/l 8.8–10.8 mg/dl
3.6–7.8 mmol/l 139–302 mg/dl
Cholesterol 100–106 mmol/l 100–106 mEq/l
0–10 mg/l 0–1.0 mg/dl
Chloride 50–120 ␮mol/l 0.57–1.36 mg/dl
17–148 iu/l 17–148 mu/ml
C-reactive protein 10–79 iu/l 10–79 mu/ml
15–250 ␮g/l 1.5–25.0 ␮g/dl
Creatinine 3–20 ␮g/l 3–20 ng/ml
160–460 ␮g/l 160–460 ng/ml
Creatinine kinase males 5–30 u/l 5–30 u/l
2.5–7.5 mmol/l 45–135 mg/dl
females 14–32 ␮mol/l 78–180 ␮g/dl
10–30 ␮mol/l 56–168 ␮g/dl
Ferritin 280–296 mOsm/kg 280–296 mOsm/kg
0.8–1.5 mmol/l 2.5–4.65 mg/dl
Folate serum 3.5–5.0 mmol/l 3.5–5.0 mEq/l
62–80 g/l 6.2–8.0 g/dl
red cell 135–146 mmol/l 135–146 mEq/l
40–80 ␮mol/l 224–448 ␮g/dl
Gamma GT 0.12–0.42 2.0–7.0 mg/dl
2.5–6.7 mmol/l 15.0–40.2 mg/dl (BUN)
Glucose (blood)
0.8–4.0 g/l 80–400 mg/dl
Iron (serum) males 7.0–18.0 g/l 700–1,800 mg/dl
0.4–2.5 g/l 40–250 mg/dl
females
4.7–6.0 kPa 35–45 mmHg
Osmolality 11.2–14.0 kPa 84–105 mmHg
7.35–7.45 7.35–7.45
Phosphate
mmHg
Potassium 2–8
3–6
Protein 1–4
1–5
Sodium 20–30
2–7
TIBC 16–30
4–13
Urate 9–18
4.5–12
Urea 4–14
6–16
Immunology 6–11
IgA 90–140
IgG 6–12
IgM 90–140
70–90
Arterial Blood Gases 70–110

PaCO2
PaO2
pH

Cardiology mean
Venae cavae a-wave
Right atrium v-wave
mean
Right ventricle systolic
Pulmonary artery end diastolic
systolic
PCWP diastolic
Left atrium mean

Left ventricle a-wave
Aorta v-wave
mean
systolic
end diastolic
systolic
diastolic
mean

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