DATA INTERPRETATION
FOR MEDICAL
STUDENTS
Third Edition
Paul K Hamilton
BSc(Hons), MB BCh BAO(Hons)
PGDip Toxicol, MD,
FRCP (Edin), FRCPath
Ian C Bickle
MB BCh BAO(Hons), FRCR
Data Interpretations 2017 00 prelims.indd 1 10/10/2017 3:38:48 PM
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DATA INTERPRETATION
FOR MEDICAL
STUDENTS
Third Edition
Paul K Hamilton
BSc(Hons), MB BCh BAO(Hons)
PGDip Toxicol, MD,
FRCP (Edin), FRCPath
Ian C Bickle
MB BCh BAO(Hons), FRCR
Contents
Preface to the Third Edition iv
Acknowledgements v
- Section 1. Interpreting Laboratory Results Reference ranges for adults vi
- Biochemistry
- Therapeutic Drug Monitoring and Toxicology
- Endocrinology
- Haematology
- Microbiology
- Immunology
- Cellular Pathology
- Genetics
- Interpreting Laboratory Results: Cases
- Interpreting Laboratory Results: Answers
- Genetics
- Section 2. Interpreting Medical Imaging
- Interpreting Chest and Abdominal Radiographs
- Cross-sectional Imaging
- Interpreting Medical Imaging: Cases
- Interpreting Medical Imaging: Answers
- Cross-sectional Imaging
- Section 3. At the Bedside and in the Clinic
- Observation Charts
- Investigations in Cardiology
- Respiratory Investigations
- Other Tests
- At the Bedside and in the Clinic: Cases
- At the Bedside and in the Clinic: Answers
- Other Tests
- Section 4. Complete Clinical Cases - Complete Clinical Cases: Answers
- Index
REFERENCE RANGES FOR ADULTS vii
Liver function tests
Albumin 35–50 g/l Alkaline phosphatase (ALP) 30–150 U/l Aspartate aminotransferase (AST) 5–35 U/l Alanine aminotransferase (ALT) 5–35 U/l γ-Glutamyl transpeptidase (GGT) Males 11–58 U/l Females 7–33 U/l Total bilirubin 3–17 μmol/l
Other
Amylase 25–125 U/l C-reactive protein (CRP) <10 mg/l Creatine kinase (CK) Male 25–195 U/l Female 25–170 U/l CK-MB <25 U/l Glucose (random) 4.0–8.0 mmol/l High sensitivity troponin T <14 ng/l Lactate dehydrogenase (LDH) 70–250 U/l Lactate 0.5–2.0 mmol/l N-terminal pro-brain natriuretic peptide (NT-proBNP) <125 ng/l Osmolality (serum) 280–300 mosmol/kg Total protein 60–80 g/l Urate 0.15–0.50 mmol/l
Tumour markers
α-Fetoprotein (AFP) <50 years <10 kU/l 50–70 years <15 kU/l 70–90 years <20 kU/l β Human chorionic gonadotrophin (β-hCG) <5 U/l CA-125 <35 U/ml CA-19-9 <37 U/ml Carcinoembryonic antigen (CEA) <10 ng/ml Prostate-specific antigen (PSA; males) 40–49 years <2.5 ng/ml 50–59 years <3.5 ng/ml 60–69 years <4.5 ng/ml 70–79 years <6.5 ng/ml
Urea and electrolytes (U+E)
Bicarbonate (HCO 3 −) 24–30 mmol/l Chloride (Cl−^ ) 95–105 mmol/l Creatinine 79–118 μmol/l (dependent on muscle mass) Magnesium (Mg2+) 0.7–1.0 mmol/l Potassium (K+) 3.5–5.0 mmol/l Sodium (Na+) 135–145 mmol/l Urea 2.5–6.7 mmol/l
Urine
Creatinine clearance Males 85–125 ml/min Females 75–115 ml/min
viii DATA iNTERpRETATiON FOR mEDiCAL STUDENTS
Haematology
Full blood picture
Erythrocyte sedimentation rate (ESR) (age-related range often quoted) Males 0–15 mm/h Females 0–22 mm/h Haemoglobin (Hb) Males 130–180 g/l Non-pregnant females 120–160 g/l HbA1c (glycated haemoglobin) 23.5–43.2 mmol/mol Mean cell volume (MCV) 76–96 fl Packed cell volume (PCV) Males 0.4–0. Females 0.37–0. Platelets 150–400 × 10^9 /l Red cell distribution width (RDW) 12–15% Reticulocytes 0.5–2.5% of red blood cells White cell count (WCC) 4.0–11.0 × 10 9 /l Basophils 0.0–0.1 × 10^9 /l Eosinophils 0.04–0.4 × 10^9 /l Lymphocytes 1.5–4.0 × 10^9 /l Monocytes 0.2–0.8 × 10^9 /l Neutrophils 2.0–7.5 × 10^9 /l
Tests of clotting
Activated partial thromboplastin time (APTT) 24–38 s Bleeding time 3–9 min D-dimer <0.5 mg/l Fibrinogen 2–4 g/l Prothrombin time (PT) 12–16 s
Endocrinology
Adrenal hormones
Aldosterone <46 ng/l Cortisol 9am 200–700 nmol/l 10pm 50–250 nmol/l Renin 3.2–32.6 pg/ml
Sex hormones
Young adult males Follicle stimulating hormone (FSH) 1.5–12.4 U/l Luteinising hormone (LH) 1.7–8.6 U/l Prolactin 86–324 mU/l Testosterone 11.4–27.9 nmol/l Females Follicle stimulating hormone (FSH) Depends on menstrual status Luteinising hormone (LH) Depends on menstrual status Mono-prolactin 102–496 mU/l Oestradiol Depends on menstrual status Progesterone Depends on menstrual status Prolactin 102–496 mU/l Testosterone 0.28–1.7 nmol/l
BiocHemiStrY 3
2. Assess the patient’s fluid status to decide if he or she is dehydrated
(hypovolaemic), fluid overloaded (hypervolaemic) or normally hydrated
(isovolaemic). The likely cause of the hyponatraemia varies depending
into which group the patient falls. The diagnosis and common causes of
hyponatraemia are illustrated in the flow diagram in Fig 1.1.
STEP 1: EVALUATE
- Assess patient for signs & symptoms of hyponatraemia. Monitor closely.
- Is patient on drugs that might lead to hyponatraemia, eg diuretics, antidepressants, (especially SSRIs), antiepileptics especially carbamazepine)?
- Review fluid balance, especially in postoperative patients.
Check serum osmolality
Normal (275–295) High (>295 mosmol/kg) Consider
- Hyperglycaemia
- Hypertonic infusions (glycerol/glycine/mannitol)
- Hyperlipidaemia
- Renal failure
- Hyperproteinaemia
- Alcohols
Low (<275 mosmol/kg)
Check BP and pulse for postural changes; JVP, oedema
STEP 2: ASSESS VOLUME STATUS
CHECK Extrarenal causes – urine [Na+] <15 mmol/l
- GI – vomiting
- GI – diarrhoea
- Fluid shifts Renal causes
- Diuretics
- Salt-wasting renal disease
- Nephropathy (analgesics, polycystic disease, pyelonephritis)
- Adrenal insufficiency
Urine [Na+] >15 mmol/l
- H 2 O intoxication (eg urine osmolality <100 mosmol/kg)
- SIADH (eg urine osmolality
100 mosmol/kg)
- Drugs
- Renal failure
- Hyperthyroidism
AT ALL STAGES ASK FOR SENIOR HELP IF UNCERTAIN
AT ALL STAGES ASK FOR SENIOR HELP IF UNCERTAIN
CHECK CHECK
- Liver failure
- Congestive cardiac failure
- Renal failure
- Nephrotic syndrome
In a patient with significant clinical symptoms believed to be due to hyponatraemia, 200 ml of 2.7% saline should be given immediately as an intravenous bolus over 30 minutes.
SYMPTOMATIC Restore volume with fluid challenge (1 litre 0.9% saline) over 2–4 hours. Repeat [Na+] in 1 hour and contInue fluids if [Na+] is rising.
SYMPTOMATIC SYMPTOMATIC/ Administration of ASYMPTOMATIC hypertonic saline Furosemide diuresis
ASYMPTOMATIC Water restriction
Treat underlying disorder Water and sodium restriction
[Na+^ ] should not increase by >12mmol/l in 24 hours
CHECK
ASYMPTOMATIC Restore volume with 0.9% saline
Hypovolaemic Isovolaemic Hypervolaemic
STEP 3: TREAT
Fig 1.1: The assessment of hyponatraemia in adult patients. From GAIN. Hyponatraemia in Adults (on or after 16th birthday). GAIN, 2010. Available at: http://www.gain-ni.org/Library/Guidelines/Hyponatraemia_guideline. pdf.
4 data interpretation for medical StUdentS
Sometimes it can be difficult to classify a patient’s volume status with
certainty. In this instance, measurement of the urinary sodium concentration
can be helpful.
USinG UrinarY SodiUm concentration to Help claSSifY VolUme StatUS
In hypovolaemic states, the kidney will attempt to hold on to sodium and water. The urinary sodium will be low (eg <15 mmol/l). Beware the following caveats:
- If a patient has taken a diuretic, the urinary sodium may be high due to the effects of the medication.
- In heart and liver failure, low effective circulating volume can also cause low urinary sodium.
Following the flow diagram in Fig 1.1, you can see that many more tests may
be necessary to get to the bottom of the cause of hyponatraemia. These
include:
- Assessment of renal function (page 8)
- Assessment of adrenal function (page 62)
- Assessment of thyroid function (page 60)
- Assessment of liver function (page 16)
- Assessment of cardiac function (page 36)
- Urine osmolality (pages 11 and 39).
GeneticS 103
autosomal conditions
Autosomal dominant inheritance
There are usually two copies of each chromosome in each cell, each carrying
copies of the same genes. In autosomal dominant conditions, inheritance
of one faulty gene is sufficient to give rise to the disorder. Thus one
chromosome in the pair will be normal; the other will carry the faulty gene.
In the following diagram, the letter ‘a’ is used to denote a normal
chromosome. The capital letter ‘A’ represents a chromosome with an
abnormal gene. Thus an individual with two ‘a’ chromosomes will be normal.
Someone with one ‘a’ chromosome and one ‘A’ chromosome will have
the disorder, since only one faulty gene is needed for the condition to be
manifest. If both parents are affected, it would also be possible for offspring
to have two ‘A’ chromosomes.
Since 50% of the offspring’s genetic code comes from one parent and 50%
from the other, there is a 50% chance that either chromosome will be passed
on.
mother
a a
father
a aa aa
A Aa Aa
In the example, the father has an autosomal dominant condition, and
therefore has one normal chromosome (a) and one abnormal chromosome
(A). The mother has two normal chromosomes. There are four possible ways
that the genes can be passed on to the offspring (aa, aa, Aa and Aa).
Thus for autosomal dominant conditions:
- both males and females can be affected
- if one parent is affected, there will be a 50% chance that a child will
also be affected.
Autosomal recessive inheritance
For an autosomal recessive disorder to be manifest, both chromosomes in a
pair must carry the abnormal gene. One abnormal gene must therefore be
passed on from each parent.
If a person has one normal and one abnormal chromosome, he or she is a
termed ‘a carrier’ and does not usually exhibit any features of the disorder,
and therefore will appear normal (ie normal phenotype).
104 data interpretation for medical StUdentS
The inheritance pattern for one carrier parent and one normal parent will be
as follows (remember ‘a’ is the normal chromosome, and ‘A’ the abnormal).
mother
a a
father
a aa aa
A Aa Aa
For autosomal recessive conditions with one carrier parent:
- both male and female offspring can be carriers
- 50% of the offspring will be carriers.
mother
a A
father
a aa aA
A Aa AA
For autosomal recessive conditions with two carrier parents:
- both male and female offspring can be carriers or be affected
- 50% of the offspring will be carriers
- 25% of the offspring will be normal (ie not carriers)
- 25% of the offspring will have the condition.
The inheritance pattern for one affected parent will be as follows.
mother
a a
father
A Aa Aa
A Aa Aa
For autosomal recessive conditions with an affected parent:
- both male and female offspring can be carriers
- all offspring will be carriers.
interpretinG laBoratorY reSUltS: caSeS 113
ca
S
e
S
case 1.
A 25-year-old woman is referred to her GP after having her BP measured at a
medical check-up arranged by her employer. She is asymptomatic, and there
is no significant family history. Her BP at the surgery is 162/104 mmHg.
On examination, she is of normal appearance with a body mass index of
23.2 kg/m^2. There are no cardiac murmurs, and peripheral pulses are normal.
She is on no prescribed medication. The following results are returned:
Na+^ 142 mmol/l (135–145 mmol/l) K+^ 2.8 mmol/l (3.5–5.0 mmol/l) Cl−^89 mmol/l (95–105 mmol/l) HCO 3 –^28 mmol/l (24–30 mmol/l) Urea 4.2 mmol/l (2.5–6.7 mmol/l) Creatinine 68 μmol/l (79–118 μmol/l) eGFR >60 ml/min per 1.73 m^2 (>60 ml/min per 1.73 m^2 ) Urinalysis: normal
1. What secondary cause for hypertension requires exclusion first?
2. What tests would you request to further investigate this situation?
3. What pathological abnormalities can underlie this condition?
answer on page 165
case 1.
A 48-year-old retired civil servant is concerned with her pale colour and
feelings of faintness that have occurred over the past 4 weeks. She had felt
well before this and enjoyed regular trips to southern France. Brief clinical
examination reveals pallor. Her blood tests come to your attention.
Hb 87 g/l (120–160 g/l females) MCV 64.5 fl (76–96 fl) Platelets 556 x 10 9 /l (150–400 × 10 9 /l) WCC 7.7 x 10 9 /l (4.0–11.0 × 10 9 /l) Iron 6 μmol/l (11–32 μmol/l) Ferritin 10 μg/l (12–200 μg/l) TIBC 90 μmol/l (42–80 μmol/l) Vitamin B 12 221 ng/l (191–663 ng/l) Folate 8.2 μg/l (>2 μg/l)
1. How would you interpret these results?
2. How would you investigate?
answer on page 165
164 data interpretation for medical StUdentS
answer 1.1 case on page 112
1. This man’s iron profile is highly abnormal, reflecting iron overload. Genetic
haemochromatosis could account for this, and may also explain the
diabetes mellitus.
2. It would be useful to repeat the iron studies in the fasted state, after the
patient had been abstaining from alcohol. Genetic tests for mutations in
the HFE gene would be helpful. MRI of the liver can be used to estimate
the degree of iron overload. The iron content of liver tissue can also be
measured in a biopsy specimen. Given that haemochromatosis is an
inherited condition, it is good practice for family members to have their
iron profiles checked.
3. Venesection is an effective means of depleting body iron stores, and can
help prevent some of the problems associated with iron overload.
answer 1.2 case on page 112
1. This patient has a macrocytic anaemia that does not appear to be due to
vitamin B 12 or folate deficiency. The serum free light chain analysis gives
the diagnosis – light chain myeloma. Most patients with multiple myeloma
have a monoclonal proliferation of plasma cells which produce IgG, IgM
or IgA. In these cases, the diagnosis is usually apparent on serum protein
electrophoresis. In a smaller percentage of patients, the abnormal plasma
cells secrete immunoglobulin light chains only. These can be detected in
the serum (as in this case, with an abnormal ratio of κ and λ light chains
pointing to the diagnosis) or the urine (where they are called Bence
Jones protein).
2. Other investigations that should be considered include: U+E, calcium,
β 2 -microglobulin, urinary Bence Jones protein and a bone marrow
examination.
INTERPRETING
CHEST AND ABDOMINAL
RADIOGRAPHS
Introduction to medical imaging
The interpretation of imaging investigations is a comprehensive
topic that forms a specialty in its own right. Its influence and remit in
contemporary medicine are vast, forming huge amounts of ‘digital data’
for interpretation.
X-ray images are technically known as ‘radiographs’, and it is essential that
medical students and trainee doctors have a sound basic understanding
of these, in particular chest and abdominal films. Likewise an appreciation
and insight into the more advanced imaging investigations at their
disposal are increasingly important, in particular the ever popular and
influential computed tomography (CT) imaging. A good professional
relationship with the radiology department, including thoughtful and
selective referral, can hugely aid patient care.
This chapter and the following chapter do not aim to be a concise
undergraduate textbook on radiology, nor an exhaustive description of
characteristic radiological findings in common diseases. They act as a
guide to approaching the interpretation of common radiographs and the
core cross-sectional imaging modalities. In the clinical cases featured,
the emphasis will be on inpatient films, ie radiographs that one might be
expected to interpret during work on general medical and surgical wards
or in an emergency department. No film will be viewed in isolation without
clinical information. As with all the data interpretation considered in this
book, investigations should be assessed in the light of the clinical scenario
and laboratory results. This should also be the gold standard to aspire to
in clinical practice.
9
InterpretInG chest and aBdomInal radIoGraphs 203
DON’T FORGET
Always interpret X-ray findings in their clinical context.
Compare images with old ones if possible.
Interpreting a chest x-ray
The chest X-ray (CXR) is the single most requested imaging investigation and
is also the most likely film to feature in daily practice or an undergraduate
exam. It provides a perfect prompt for questioning other aspects of a
patient’s condition and for exploring management strategies. To be able to
comment confidently on the film’s findings, and have an understanding of
how to approach interpretation, an appreciation of normality is required.
Don’t forget that a CXR is a two-dimensional representation of a three-
dimensional structure.
One may think of a CXR as a picture that contains five ‘shades’ on a black-
and-white scale. Four shades represent natural ‘tissues’ and one represents
artefacts.
The shades seen are:
1. Bone is WHITE
2. Gas is BLACK.
3. Soft tissue is GREY
4. Fat is DARKER GREY.
5. Most man-made things on the film are BRIGHT WHITE.
Posterior ribs
Anterior ribs
Carina
Lung apex Aortic knuckle
Hila
Right atrium Left ventricle
Costophrenic angle Breast shadow
Fig 9.1: CXR.
CROSS-SECTIONAL IMAGING 217
Check the review areas to finish:
- Is there anything in the ventricular system, eg blood in the occipital
horns?
- Are the visualised orbits normal?
- Is there any abnormality in the mastoid air cells or paranasal sinuses?
Normal anatomy as seen on other cross-sectional
imaging modalities
- CT of the neck
Fossa of Rosenmüller
Mandibles
Pterygoid plates
Maxillary sinus Nasal septum Zygoma
Fig 10.6: Axial CT of the neck (arterial phase): normal anatomy (a).
Mandible
Tongue
Vertebral artery in foramen transversum
Submandibular gland
Fig 10.7: Axial CT of the neck (arterial phase): normal anatomy (b).
220 data InterpretatIon for medIcal students
Lamina
Vertebral body
Foramen transversum
Hyoid bone
Spinous process
Vertebral foramen
Pedicle
10.12: Axial CT of the cervical spine (bone window): normal anatomy.
C
C C C C
C
Opisthion
Basion
Epiglottis
Intervertebral disc space
Spinous process
Spinal cord
Prevertebral soft tissue
10.13: Sagittal CT of the cervical spine (soft tissue window): normal anatomy.
Lamina
Vertebral body
Foramen transversum
Spinous process
Vertebral foramen
Pedicle
Trachea
Facet of articluar process
Thecal sac
10.14: Axial CT of the cervical spine (soft tissue window): normal anatomy.