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Jaundice
Liver
T
e bowel
Faecal excretionUrinary excretion
Kidney
14
INTRODUCTION
Jaundice (icterus) is the yellow discoloration of the skin,
sclera and mucosae that is detectable when serum bilirubin
concentrations exceed approximately 35 μmol/L. Normal
bilirubin metabolism is summarized in Fig.14.1. Jaundice
can arise because of increased red blood cell breakdown, disordered bilirubin metabolism or reduced bilirubin excretion.
Erythrocyte breakdown
in the reticuloendothelial
system
Biliverdin
Unconjugated bilirubin (water insoluble)
transported to liver bound to albumin
Hepatic conjugation with glucuronic acid
Conjugated bilirubin
Excreted into bile
and passed to
terminal ileum
Enterohepatic
circulation
erminal ileum
Urobilinogen
Systemic circulation Oxidation in larg
Fig.14.1 Normal bilirubin metabolism.
Bacterial action in
terminal ileum
Stercobilinogen
The causes of jaundice are outlined in Table 14.1.
Prehepatic jaundice (unconjugated hyperbilirubinaemia)
usually results from the excessive production of bilirubin
by haemolysis (see Fig. 14.1), in haemolytic anaemia for
instance, but it can also result from inherited metabolic defects, the commonest of which is Gilbert syndrome. Hepatic
jaundice results from hepatocyte dysfunction causing disordered bilirubin metabolism. Hepatocellular dysfunction
usually causes some cholestasis and may cause ‘pale stools/
dark urine’ (see later). Posthepatic jaundice (cholestasis) is
caused by reduced bilirubin excretion due to intrahepatic or
extrahepatic biliary obstruction.
HISTORY AND EXAMINATION
History
Ask about:
• Pruritus, dark urine and pale stools: underlying
cholestasis.
• Abdominal pain: the episodic, colicky, right
hypochondrial pain of biliary colic will commonly be
due to gallstones. A dull, persistent epigastric or central
pain radiating to the back may suggest a pancreatic
origin.
• Fevers or rigors: cholangitis.
• Weight loss: underlying malignancy, particularly
pancreatic cancer.
• Duration of illness: a short history of malaise, anorexia
and myalgia is suggestive of viral hepatitis.
• Drug history: particularly paracetamol, oral
contraceptive pill.
• Alcohol consumption: acute alcoholic hepatitis,
cirrhosis.
• Infectious contacts: hepatitis A.
• Recent foreign travel to areas of high hepatitis risk.
• Recent surgery: surgery for known malignancy, biliary
stricture due to previous endoscopic retrograde
cholangiopancreatography (if the patient had a
sphincterotomy).
• Intravenous drug abuse, tattoos, unprotected sex:
increased risk of hepatitis B and hepatitis C.
• Occupation: sewage workers and people who
participate in open water sports and activities are at
increased risk of leptospirosis.
• Family history of recurrent jaundice: inherited
haemolytic anaemias and Gilbert syndrome.
89
Jaundice
Head
— Y
— Anaemi
— Fetor hepaticus
— Xanthelasmata
— Kayser–Fleischer rings
— Drowsiness
— Constructional
Abdomen
— Hepatomegaly
— Splenomegal
— Palpable gallbladder
— Caput medusae
— Ascite
Chest and arms
— Scratch marks
— Spider naevi
— Gynaecomastia
— Loss of body hai
— Bruising
— Needle marks
— T
Hands
— Leuconychia
— Palmar erythema
— Clubbing
— Dupuytren contracture
— Asterixi
Table14.1 The differential diagnosis of jaundice
Prehepatic (see
Chapter36) Hepatic (see Chapter29) Posthepatic (see Chapter29)
Acute hepatocellular
damage
Haemolysis Viral infection (e.g.
hepatitis A, B, C, E;
EBV; CMV)
CMV, Cytomegalovirus; EBV, Epstein-Barr virus.
Chronic hepatocellular
damage
Inherited defects (e.g.
primary haemochromatosis,
Wilson disease, α1-antitrypsin
deficiency)
Extrahepatic
obstruction
Intrahepatic
obstruction
Gallstones Primary biliary cirrhosis
Examination
The causes of jaundice are multiple and may therefore
indicate underlying disease in one of many organ systems. There are three important groups of abnormalities
that should specifically be looked for in the jaundiced
patient:
• How severe is the jaundice? Is there any evidence of
encephalopathy?
• Is this an acute or a chronic problem? Are there any
signs of chronic liver disease?
• Are there any signs of specific disorders?
This approach is summarized in Fig.14.2.
CLINICAL NOTE
ENCEPHALOPATHY
Encephalopathy is defined as disordered brain
function. The following suggest encephalopathy:
• Drowsiness: this will eventually progress through
stupor to coma.
• Slurred speech.
• Asterixis: flapping tremor of outstretched
hands.
• Seizures.
• Constructional apraxia: test for this by asking
the patient to copy a five-pointed star.
• Hepatic fetor: mercaptans pass directly into the
lungs because of portal hypertension, causing
a characteristic odour of the patient’s exhaled
breath.
ellow sclera and mucosae
a
apraxia
r
attoos
y
s
s
Testicular atrophy
Peripheral oedema
Fig.14.2 Examining the patient with jaundice.
CLINICAL NOTES
SIGNS OF CHRONIC LIVER DISEASE
Hepatic encephalopathy can arise because of fulminating
acute liver failure or when chronic disease decompensates.
Precipitating factors, grading and management are described in Chapter29.
90
• Palmar erythema.
• Leuconychia and oedema: hypoalbuminaemia.
• Clubbing.
Investigations
1414
• Dupuytren contractures: particularly in alcoholic
cirrhosis.
• Spider naevi: more than five in the distribution of
the superior vena cava.
• Scratch marks: cholestasis.
• Gynaecomastia, loss of body hair and testicular
atrophy: elevated oestrogen level.
• Bruising: disordered coagulation.
• Hepatomegaly: not in well-established cirrhosis.
• Splenomegaly, ascites and caput medusae:
portal hypertension.
Signs of specific diseases:
• Xanthelasmata: primary biliary cirrhosis.
• Kayser–Fleischer rings: Wilson disease.
• Slate-grey pigmentation: haemochromatosis.
• Hard, irregular hepatomegaly: malignant
metastases.
• Nontender, palpable gallbladder: jaundice is unlikely
to be caused by gallstones (Courvoisier's law).
• Parotid gland enlargement: alcohol.
• Needle marks or tattoos: hepatitis B, hepatitis C.
INVESTIGATIONS
The investigation of jaundiced patients falls into two stages.
First the type of jaundice must be determined (prehepatic,
hepatic or posthepatic); then more detailed tests should be
performed to determine the specific cause. Fig.14.3 summarizes this approach.
Table14.2 describes biochemical abnormalities in differ-
ent types of jaundice.
• Blood tests: Conjugated bilirubin, alanine transaminase,
aspartate transaminase, alkaline phosphatase, γ-
glutamyltransferase: will give a reasonable indication as
to the type of abnormality present. Alkaline phosphatase
level is commonly raised in biliary disorders but is also
elevated in pregnancy. Raised alanine transaminase and
aspartate transaminase levels indicate hepatocellular
dysfunction. γ-Glutamyltranspeptidase level is raised in
the case of alcohol excess.
• Urinary bilirubin and urobilinogen: urine is
normally free of bilirubin. Dark urine indicates the
presence of conjugated bilirubin. Low urobilinogen
level suggests obstructive jaundice, whereas
raised urobilinogen level suggests haemolysis or
intrahepatic damage.
Jaundice
Specific clues in
history or examination
No
Urine dipstick
Serum liver enzymes and bilirubin
Abdominal ultrasound scan
Haemolysis
Appropriate
confirmatory tests
Fig.14.3 Investigation of the patient with jaundice. Computed tomography (CT) and magnetic resonance
cholangiopancreatography (MRCP) are usually performed before endoscopic retrograde cholangiopancreatography
(ERCP) or percutaneous transhepatic cholangiography (PTC). EUS, Endoscopic ultrasonography.
Biliary
dilatation
ERCP/PTC/
CT pancreas/
MRCP/EUS
Yes
Appropriate
confirmatory tests
Normal
biliary tree
Viral serology
Autoantibodies
Immunoglobulins
Ferritin
Caeruloplasmin
-antitrypsin
a
1
Liver biopsy
91
Jaundice
Table14.2 Biochemical abnormalities in different types of jaundice
Specimen Test Haemolysis Hepatocellular Cholestasis
Urine Urobilinogen
Conjugated bilirubin
Faeces Stercobilinogen Raised level Normal or decreased
Blood Bilirubin
Liver enzymes
ALT, alanine transaminase; AST, aspartate transaminase; GCT, γ-glutamyltransferase.
Raised level
Absent
Unconjugated
Normal levels
Normal or raised level
Present
level
Unconjugated and
conjugated
AST, ALT
Decreased level or
absent
Raised
Decreased level or
absent
Conjugated
Alkaline phosphatase,
GGT
• Abdominal ultrasound scan, CT scan, magnetic
resonance cholangiopancreatography (MRCP),
endoscopic retrograde cholangiopancreatography
(ERCP): to investigate the cause.
• Serum caeruloplasmin: Wilson disease.
• α1-Antitrypsin.
• Liver biopsy: definitive diagnostic test for intrinsic liver
disease.
• Fasting lipid profile: triglycerides for steatosis.
Haemolysis screen
The haemolysis screen is detailed in Chapter29.
HINTS AND TIPS
Hepatocellular screen
• Viral serology: hepatitis A, B and C; EBV, CMV.
• Autoantibody screen: antimitochondrial antibodies
(levels raised in primary biliary cirrhosis), anti-smooth
muscle antibodies, antinuclear antibodies.
• Ferritin: haemochromatosis.
Chapter Summary
• Bilirubin is the breakdown product of haemoglobin.
• Jaundice becomes apparent if bilirubin level is greater than 35 μmol/L.
• Jaundice can be of prehepatic, hepatic or posthepatic origin.
• The history and examination, together with investigations, will point towards the cause.
• Management depends on the underlying disease.
Liver dysfunction affects the synthesis of clotting
factors, and therefore the prothrombin time must
be checked and corrected before an invasive
procedure (e.g. liver biopsy).
92
Urinary symptoms and
INTRODUCTION
The volume of water in the circulation is under constant
physiological control. Water is normally reabsorbed from
the loop of Henle as it passes through the hyperosmolar
renal medulla, and is also reabsorbed from the collecting
ducts under the control of antidiuretic hormone (ADH),
also called ‘vasopressin’ (Fig. 15.1). ADH is synthesized by
the hypothalamus and released from the posterior pituitary
in response to a rise in serum osmolality or fall in plasma
volume. Conversely, a fall in osmolality or rise in plasma
volume leads to a decrease in ADH secretion.
Polyuria is defined as the passage of excessive volumes
of urine (>3 L in 24 h). Urine output depends on fluid intake and loss via other routes (e.g. respiration, sweat, faeces), and typically ranges from 1 to 3 L/day. Polydipsia is
defined as excessive thirst, often manifested as the ingestion
of excessive volumes of fluid, and is usually a consequence
of polyuria.
haematuria
15
Frequency is the frequent passage of small volumes of
urine, and dysuria is pain on passing urine. Symptoms of bladder outflow obstruction, such as those caused by an enlarged
prostate gland, include hesitancy (difficulty initiating micturition), terminal dribbling and poor stream. Nocturia, the
passage of urine at night, may be associated with frequency
or polyuria. Urinary incontinence is common, and is broadly
divided into stress incontinence and urge incontinence.
Oliguria and anuria, the passage of small volumes or no
urine, respectively, may be due to renal impairment or urinary tract obstruction (see Chapter30).
HINTS AND TIPS
There are many causes of polyuria, but those
seen most commonly in clinical practice are
hyperglycaemia and hypercalcaemia.
Distal
tubule
Hypo-
osmolar
+
Na
+
K
–
2Cl
Thin
+
Na
–
Cl
ascending
limb
Loop of Henle
H
O
2
Thick
ascending
limb
+
Na
–
Cl
H
2
Impermeable
O
to H
2
O
Collecting
+
O
2
H
Thin
limb
2
Proximal
tubule
O
Hyperosmolar
Cortex
Na
H
Iso-osmolar
Outer
medulla
descending
Inner
medulla
Fig.15.1 Water and electrolyte balance in the loop of Henle. ADH, antidiuretic hormone.
ADH
duct
93
Urinary symptoms and haematuria
The differential diagnosis of polyuria/polydipsia is summarized in Table15.1.
Frequency is commonly due to bladder irritation, which
is often due to infection but can also be caused by chemical
irritation, tumours or calculi in the bladder.
CLINICAL NOTES
Symptoms of prostatic hypertrophy include poor
stream, hesitancy, postmicturition dribbling and
incomplete emptying. Nocturia is a troubling
symptom. Ask the patient about sleep disturbance.
Dysuria is most commonly due to infection, but can also
be caused by chemical irritation. When accompanied by
frequency, it may indicate cystitis, and in men may also be
caused by prostatitis.
Stress incontinence is common in women and is often
due to weakened pelvic floor muscles resulting from physical changes following pregnancy and childbirth. Urge
incontinence is associated with detrusor instability and inappropriate contraction, which may be a consequence of local factors such as infection or inflammation, or may be due
to damage to the nerve supply. Innervation is mainly from
the autonomic nervous system, although there is voluntary
control of the external urinary sphincter, and higher control
of urination in the micturition centre of the pons.
Micturition disturbances
History and examination findings
For many urinary symptoms, there will be a simple explanation, for instance infection or prostatic hypertrophy. The
history should focus on the following points:
• Frequency: is there coexistent fever, dysuria or
cloudy urine (pyuria) which may indicate infection?
If so, is there a history of recurrent infection that
might indicate a predisposition (e.g. diabetes,
urinary stasis, immunosuppression)? In men, are
there associated symptoms of prostatic hypertrophy;
is there urinary stasis from incomplete bladder
emptying?
• Does the patient have loin pain, or a history of renal
calculi?
• Is there associated haematuria? In the presence of other
lower urinary tract symptoms this could be due to
infection, calculus or bladder tumour.
• If incontinence is present, be careful to determine the
circumstances in which it occurs and the effect it is
having on the patient's everyday activities.
• The patient's current medication may provide clues as
to the cause (e.g. is the patient taking diuretics?).
Table15.1 Differential diagnosis of polyuria
Causes Examples/notes
Cranial DI (insufficient ADH secretion) Idiopathic (often familial and commonest form)
Nephrogenic DI (inability of kidney to
respond to ADH)
Chronic renal failure Can result in depressed kidney concentrating ability and therefore higher urine
Acute renal failure Diuretic phase of ATN
Osmotic diuresis Glucose (diabetes mellitus)
ANP release Arrhythmia (e.g. after SVT)
Psychogenic polydipsia Relatively common psychiatric disturbance characterized by excessive water
ADH, Antidiuretic hormone; ANP, atrial natriuretic peptide; ATN, acute tubular necrosis; DI, diabetes insipidus; SVT, supraventricular
tachycardia.
After pituitary surgery/irradiation
After head trauma
Malignancy (e.g. craniopharyngioma, pinealoma, glioma, metastases)
Infections (e.g. meningitis)
Infiltrations (e.g. sarcoid and histiocytosis X)
Drugs (e.g. alcohol)
Congenital (primary renal tubular defect)
Electrolyte imbalance (hypokalaemia and hypercalcaemia)
Lithium toxicity
Long-standing pyelonephritis or hydronephrosis
volume to excrete a given solute load
Following relief of obstructive uropathy
Early stages of analgesic nephropathy
Calcium (hypercalcaemia)
intake (if prolonged can cause temporary ‘renal medullary washout’ with
reduction of kidney’s concentrating ability)
94
Introduction
Heart
—Cardiac examination
—Tachycardia
→
—Hypertensive nephropathy
(chronic renal failure)
1515
Polyuria and polydipsia may pose a more difficult diagnostic challenge, and after general questions the enquiry
should focus on the following:
• Differentiation between polyuria (an increase in the
volume of urine production) and frequency (the
frequent passage of small amounts of urine).
• Weight loss: associated with malignancy which may
result in hypercalcaemia (e.g. bone metastases of bone
infiltration in myeloma may cause hypercalcaemia).
• Headache: primary or secondary brain tumours can
cause diabetes insipidus.
• Family history: this is relevant in diabetes mellitus,
both forms of diabetes insipidus (cranial and
nephrogenic) and renal stone disease.
• Medical history: consider previous neurosurgery
or radiotherapy, head injuries and meningitis in
particular.
Eyes
—Papilloedema (raised intracranial
pressure)
—Diabetic or hypertensive fundi
—Visual field defects
—Anaemia (carcinoma or
chronic renal failue)
• Drug history: lithium may cause nephrogenic diabetes
insipidus; vitamin D or milk–alkali syndrome may lead
to hypercalcaemia.
• Recurrent infections: may be due to diabetes mellitus.
• Features of hypercalcaemia (see Chapter 31).
• Brief psychiatric history: especially if thirst is
predominant. These patients may drink surreptitiously,
resist investigation, have other neurotic symptoms and
lack nocturnal symptoms.
Examination
The examination approach in the patient with urinary
symptoms is summarized in Fig.15.2.
General appearance
• Wasting/cachexia (malignancy and initial presentation
of type 1 diabetes mellitus) and hydration status.
Lymph nodes/liver/spleen
—Malignancy
—Infiltrative disorder
Blood pressure
Fig.15.2 Examining the patient with polyuria or polydipsia. ANP, atrial natriuretic peptide.
elevated
ANP → polyuria
Kidneys
—Enlarged (polycystic
kidney disease,
hydronephrosis)
Bladder
—Obstruction
Reflexes
—Reduced in hypokalaemia
Skin
—Yellow-brown skin (uraemia)
—Signs of infection (diabetes)
—Signs of malignancy
Extremities
—Peripheral neuropathy (diabetes)
—Pulses (diabetes)
Hands
—Clubbing (bronchial
carcinoma)
—Brown arcs on nails
General appearance
—Cushingoid facies
—Wasting (malignancy,
diabetes)
—Hydration status
95
Urinary symptoms and haematuria
• Skin manifestations: diabetes mellitus and malignancy
(see Chapter35).
• Nails: clubbing—associated with bronchogenic
carcinoma, which may produce parathyroid hormone
(and result in hypercalcaemia), or may metastasize to
the brain.
• Anaemia: malignancy or chronic renal failure.
• Lymphadenopathy: malignancy or infiltrative disorder.
• Optic signs: fundal changes of hypertension or
diabetes.
Cardiovascular system
Check the blood pressure for hypertensive nephropathy.
Abdominal examination
Palpate the kidneys carefully as they may be enlarged in
polycystic kidney disease or with a hydronephrosis. A large
bladder may indicate urinary tract obstruction. The liver
and spleen may be enlarged in malignancy and infiltrative
disorders. An enlarged or craggy prostate can often be palpated on rectal examination.
Neurological examination
The neurological examination should assess:
• peripheral neuropathy (caused by diabetes or
infiltrative disorders);
• hypotonia and areflexia with hypokalaemia;
• wasting in malignancy;
• visual fields (classically bitemporal hemianopia with
pituitary disease) and papilloedema (raised intracranial
pressure);
• in idiopathic urge incontinence if there is evidence of
any underlying neurological abnormality.
Investigations
The following investigations should be carried out.
Urine tests
• Simple urinalysis (urine dip) will give a pH, and
detect protein, blood, glucose and ketones, as well as
leucocytes and nitrites, the presence of which may
indicate infection.
• Laboratory urine analysis can measure urine
osmolality. Quantify protein loss, with protein/
creatinine or albumin/creatinine ratios. Urinary
electrolytes, including sodium, potassium, phosphate,
calcium and oxalate, can be measured. Urine
microscopy may reveal the presence of blood cells,
bacteria or casts, and culture may reveal a pathogenic
organism.
Blood tests
• Biochemistry: renal failure (see Chapter30),
hypercalcaemia, hypokalaemia (see Chapter31) and
hyperglycaemia.
• Full blood count: anaemia with chronic renal failure or
malignancy (e.g. leukaemia, myeloma). Raised white
cell count suggests infection.
Imaging
• Chest X-ray: if any suspicion of sarcoidosis, primary or
secondary malignancy.
• Renal tract ultrasound scan can detect abnormal
kidney size, cysts and masses, congenital defects of the
renal tract, hydronephrosis or hydroureter.
• CT of the kidneys/ureters/bladder if there is suspicion of
renal tract calculi (this can be a noncontrast CT scan).
• CT or MRI of brain to investigate intracranial disease
(e.g. if you are considering a space-occupying lesion).
Further investigations
• Renal concentration tests in polyuria: if either a
hypothalamic or a pituitary cause or renal tubular
dysfunction is suspected. It is mandatory to exclude
other potential causes of polyuria, as renal concentration
tests may be dangerous. The patient is asked to drink
nothing from 16:00 the day before attending the
outpatient department. If the urine osmolality the next
morning is not greater than 800 mmol/kg, inpatient tests
are required (Box 15.1 and Table 15.2).
• Urodynamic tests: these commonly measure the
prevoid and postvoid bladder volume and flow rate to
assess bladder emptying.
• Nuclear renography: radioisotope uptake scans
(e.g. dimercaptosuccinic acid (DMSA) or
mercaptoacetyltriglycine (MAG3) scans) can provide
detailed information about asymmetric kidney
function and can evaluate kidney scarring.
Haematuria
This should be classified as visible or nonvisible, painful
or painless and whether it is associated with proteinuria.
Haematuria and proteinuria together is suggestive of intrinsic renal damage, and is discussed in Chapter30. Painful
BOX15.1 PROCEDURE FOR TESTING
PATIENTS WITH POLYURIA AND POLYDIPSIA
• Weigh the patient.
• Deprive the patient of all fluids the night before
the tests.
• The next morning, weigh the patient every
2 h (a decrease in weight by >3% indicates
dehydration, so stop the test).
• Collect urine and blood for osmolality
measurement.
• If the urine osmolality fails to reach 800 mmol/
kg, intramuscularly administer desmopressin
(which is synthetic vasopressin), which acts in
the same way as ADH.
• Collect blood and urine for osmolality
measurement.
96
Introduction
Table15.2 Interpretation of patient test results
Fluid deprivation
Pituitary DI ↑ → ↑ ↑
Psychogenic
polydipsia
Nephrogenic DI ↑ → ↑ →
a
Urine is concentrated, but less than in normal response
DI, diabetes insipidus; ↑, increase in osmolality; →, no significant change in osmolality.
Plasma osmolality Urine osmolality Plasma osmolality Urine osmolality
↑ ↑
a
After intramuscular administration of
desmopressin
↑ ↑
1515
haematuria may suggest renal calculus or urinary tract infection; painless haematuria suggests the possibility of renal
tract malignancy. Remember that red urine may also be due
to haemoglobinuria, myoglobinuria, porphyria, drugs (e.g.
rifampicin) or even the ingestion of beetroot.
Haematuria can come from anywhere in the urogenital tract. It can be classified by the site of disease (see
Table 15.3). Systemic conditions (e.g. thrombocytopenia)
or anticoagulants can predispose to bleeding.
CLINICAL NOTES
If haematuria is present in a young woman, it
is important to ask about the menstrual cycle
and whether she was menstruating when the
haematuria was noticed.
Table15.3 Causes of haematuria from the urinary tract
Site Causes
Kidney Infections (pyelonephritis, tuberculosis)
Tumours (renal cell carcinoma)
Trauma (spontaneous or after renal
biopsy)
Papillary necrosis (associated with
diabetes)
Ureters Renal calculi
Tumours; transitional cell
Trauma
Bladder Cystitis; infection, postradiation cystitis
Tumours; transitional cell carcinoma
Trauma
Bladder calculi
Infections; tuberculosis and
schistosomiasis
Prostate Prostate carcinoma
Benign prostatic hypertrophy
Infection; prostatitis
Urethra Calculi
Trauma
Tumours
Foreign bodies
History and examination findings
• Ask about the appearance of the urine. Is there frank
blood (malignancy)?
• Ask about associated urinary symptoms.
• Is the haematuria worse with exercise?
• Ask about loin pain (present with pyelonephritis or
renal calculi).
• Ask about colicky pain. This suggests a ureteric
calculus.
• Is there a history of trauma?
• Does the patient have a vaginal or penile discharge?
CLINICAL NOTES
Ask when in the urinary stream the patient
notices the blood. Patients may not volunteer
this information because they do not think it is
important.
• If the urine is bloodstained at the start of
micturition and clears later, the site of disease is
likely to be the urethra or prostate.
• If the urine is more bloodstained towards the
end of micturition, the site of disease is likely to
be the bladder.
• If the urine is evenly bloodstained throughout
micturition, the site of disease is likely to be the
kidney or ureter.
Initial tests
• Gross appearance: visible asymptomatic haematuria in
patients older than 45years should always make you
consider malignancy (Fig 15.3).
• Urinary dipstick: provides initial information about the
presence or absence and degree of protein and haematuria.
It also tests for nitrites/leucocytes/ketones/pH and glucose.
• Microscopy and culture (midstream urine): infection.
• Early morning urine: acid-fast bacilli if tuberculosis is
suspected.
• Cytology: malignancy.
97