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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3230_Библиотеки_им_академика_М_И_Перельмана
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CHAPTER 18 Laboratory tests
422
Hepatocellular jaundice
This condition is suggested by jaundice with dark stools and dark urine. It
is confirmed by raised serum bilirubin and raised urine urobilinogen. There
are highly abnormal liver function tests. Normal bile ducts appear on
ultrasound scan.
Some differential diagnoses and typical outline evidence
Acute (viral)
hepatitis A
Suggested by: tender hepatomegaly
Confirmed by: presence of hepatitis A IgM antibody
suggests acute infection
Acute
hepatitis B
Suggested by: history of IV drug use, blood transfusion,
needle punctures, tattoos, tender hepatomegaly
Confirmed by: presence of HBsAg in serum
Acute
hepatitis C
Suggested by: history of transfusion or other blood
products. Tender hepatomegaly
Confirmed by: presence of anti-HCV antibody and
antigen
Alcoholic
hepatitis
Suggested by: history of drinking, presence of spider
nevi and other signs of chronic liver disease
Confirmed by: AST:ALT ratio >2, liver biopsy
Drug-induced
hepatitis, e.g.,
acetaminophen
(dose depend-
ent), halothane
(independent)
Suggested by: drug history, recent surgery
Confirmed by: improvement after stopping the
offending drug
Primary
hepatoma
Suggested by: weight loss, abdominal pain, RUQ mass
Confirmed by: ultrasound/CT liver, liver biopsy,
iA-fetoprotein
Right heart
failure
Suggested by: iJVP, hepatomegaly, ankle edema
Confirmed by: CXR, echocardiogram
OBSTRUCTIVE JAUNDICE1
423
Obstructive jaundice
This condition is suggested by jaundice with pale stools and dark urine. It
is confirmed by raised urine and serum bilirubin but NO raised urobilino-
gen in urine. Markedly raised alkaline phosphatase occurs, with otherwise
slightly abnormal liver function tests. Dilated bile ducts appear on ultra-
sound scan.
Some differential diagnoses and typical outline evidence
Common bile
duct stones
Suggested by: pain in RUQ ± Murphy’s sign
Confirmed by: ultrasound liver/biliary ducts
Cancer of head
of pancreas
Suggested by: painless jaundice, palpable gallbladder
(Courvoisier’s law), weight loss
Confirmed by: CT pancreas, ERCP or MRCP
Sclerosing
cholangitis
Suggested by: progressive fatigue, pruritus
Confirmed by: serum alkaline phosphatase, no gall-
stones, ERCP (beading of the intra- and extrahepatic
biliary ducts)
Primary biliary
cirrhosis
Suggested by: scratch marks, non-tender hepa
t
omegaly,
± splenomegaly, xanthelasmata and xanthomas, ar-
thralgia
Confirmed by: positive antimitochondrial antibody,
iiserum IgM, liver biopsy
Drug induced,
e.g., oral
contraceptives,
phenothiazines,
anabolic steroids,
erythromycin
Suggested by: drug history
Confirmed by: symptoms recede when offending drug is
discontinued
Pregnancy
(last trimester)
Suggested by: jaundice during pregnancy and severe
itching
Confirmed by: resolution following delivery
Alcoholic
hepatitis or
cirrhosis
Suggested by: history of drinking, presence of spider
nevi and other signs of chronic liver disease
Confirmed by: liver biopsy
Dubin–Johnson
syndrome
Suggested by: intermittent jaundice and associated
RUQ pain. No hepatomegaly
Confirmed by: normal alkaline phosphatase, normal
liver function tests. Urinary bilirubin is raised. Pigment
granules on liver biopsy
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CHAPTER 18 Laboratory tests
424
Hypernatremia
Some differential diagnoses and typical outline evidence
Hypertonic
plasma with
hypervolemia
(e.g., excess IV
saline) or hypo-
volemia (e.g.,
diabetic polyuria
or diabetes
insipidus)
Suggested by: little hypotonic fluid orally or
intravenously and thirsty, high volume of urine with
low sodium content (e.g., in diabetic polyuria)
Confirmed by: plasma osmolality high and urine
osmolality higher (unless diabetes insipidus)
Diabetes
inspidus with
hypovolemia
Suggested by: drinking excessively and passing large
volumes of urine (polydipsia and polyuria). Thirst
Confirmed by: plasma osmolality high and urine
osmolality low
Primary hyper-
aldosteronism
due to adrenal
hyperplasia or
Conn’s syndrome
with adrenal
tumor
Suggested by: normal fluid intake, blood pressure
elevated. Serum potassium d
Confirmed by: plasma renin activity low and
aldosterone levels high. CT or MRI scan appearance
HYPONATREMIA1
425
Hyponatremia
This also usually indicates hypotonicity—low plasma osmolality.
Some differential diagnoses and typical outline evidence
Hypotonic with
hypovolemia
due to excess
renal or
nonrenal loss
Suggested by: excessive diuretic therapy, history of
renal tubular disease, diarrhea, vomit, fistula, burns,
small bowel obstruction, blood loss
Confirmed by: response to removal or treating of
cause, IV saline with careful monitoring of electrolytes
in severe cases
Hypotonic with
normovolemia
Suggested by: history of severe hypothyroidism or
glucocorticoid deficiency
Confirmed by: response to treating cause, balancing
fluid intake
Hypotonic with
hypervolemia
Suggested by: history of water overload, cardiac failure,
cirrhosis, renal failure, glucocorticoid deficiency, inap-
propriate antidiuretic hormone (ADH) secretion
Confirmed by: response to treating cause, reducing fluid
intake
Syndrome of
inappropriate
ADH
secretion
(SIADH)
Suggested by: serum sodium usually <120 mmol/L.
Confusion, progressing to coma, mild edema
Confirmed by: urine osmolality > serum osmolality
despite serum osmolality being low (<270 mmol/L).
Urine sodium >20 mmol/L usually
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CHAPTER 18 Laboratory tests
426
Hyperkalemia
Some differential diagnoses and typical outline evidence
Drug effect:
potassium
administration
or other drug
effect
Suggested by: potassium supplements, blood trans-
fusion, ACE inhibitor, spironolactone, amilioride,
triamterene, etc.
Confirmed by: normal potassium when drug reduced or
stopped
Metabolic
acidosis, renal
failure, diabetic
ketoacidosis
Suggested by: usually obvious illness and severe
metabolic disturbance, pHd and plasma HCO
3
d
Confirmed by: response to treatment of metabolic
disturbance
Addison’s
disease
Suggested by: fatigue, blood pressure low, pigmented
buccal mucosa and palmar creases, Nad, Ki
Confirmed by: random and 9
A.M. cortisol d, ACTHi,
and poor response to corticotropin stimulation.
Response to IV hydrocortisone and normal saline
Recent blood
transfusion
Suggested by: history
Confirmed by: fall in potassium after a few hours
Spurious result
due to hemolysis
in specimen
bottle
Suggested by: laboratory reporting hemolysis in
specimen bottle
Confirmed by: normal potassium when repeated
with no delay in delivery to lab
HYPOKALEMIA1
427
Hypokalemia
Some differential diagnoses and typical outline evidence
Diuretic therapy Suggested by: taking thiazide or loop diuretic
Confirmed by: normal potassium after stopping
diuretic
Beta-agonist
treatment
Suggested by: taking high doses of beta-agonist, usually
in nebulizer for acute asthmatic attack in hospital
Confirmed by: normal potassium after stopping drug
Vomiting, e.g.,
pyloric stenosis
Suggested by: history of severe vomiting with poor fluid
intake
Confirmed by: normal potassium without subsequent
need for replacement when cause of vomiting treated
Chronic diar-
rhea, purgative
abuse, intestinal
fistula, villous
adenoma of
rectum
Suggested by: history of severe diarrhea or mucous loss
Confirmed by: normal potassium without need for
further replacement when cause treated subsequently
Primary hyper-
aldosteronism
due to adrenal
hyperplasia or
Conn’s
syndrome with
adrenal tumor
Suggested by: normal fluid intake, blood pressure i.
Serum potassium d
Confirmed by: plasma renin activity low and
aldosterone levels high. CT or MRI scan
appearance
Renal tubular
defect
Suggested by: recovery phase from renal failure, recent
pyelonephritis, associated myeloma, heavy metal poi-
soning
Confirmed by: test for renal concentrating ability
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CHAPTER 18 Laboratory tests
428
Hypercalcemia
Present when specimen taken without a venous cuff and calcium result
was corrected for albumin concentration.
Some differential diagnoses and typical outline evidence
Bone metastases
from carcinoma of
breast, bronchus,
kidney, thyroid,
ovary, colon
Suggested by: normal phosphate and high alkaline
phosphatase
Confirmed by: metastases on X-rays, CT or nuclear
bone scan
Thiazide diuretics Suggested by: mild hypercalcemia, drug history,
normal phosphate and alkaline phosphatase.
Confirmed by: normal calcium when drug stopped
Primary (or tertiary)
hyperparathyroidism
Suggested by: low phosphate and high alkaline
phosphatase (tertiary after years of secondary
hyperparathyroidism)
Confirmed by: plasma parathyroid levels high with
high calcium
Myeloma Suggested by: normal phosphate and alkaline phos-
phatase
Confirmed by: Bence–Jones protein in urine. Pro-
tein electrophoresis. Lesions on X-ray, CT, or
bone scan
Sarcoidosis Suggested by: high phosphate and alkaline phos-
phatase. Bilateral hilar shadows on chest X-ray
Confirmed by: noncaseating granulomata on biopsy,
i vitamin D levels and i ACE levels
Vitamin D excess Suggested by: drug history and i phosphate
Confirmed by: normal calcium when drug stopped
Thyrotoxicosis Suggested by: mildly i calcium, T4 i or T3 i and
TSH very d. Normal phosphate and alkaline phos-
phatase
Confirmed by: response to treatment of
thyrotoxicosis
Ectopic parathyroid
hormone due to lung
cancer, usually
Suggested by: d phosphate and i alkaline
phosphatase
Confirmed by: plasma parathyroid levels i with
high calcium, presence of underlying neoplasm
HYPOCALCEMIA1
429
Hypocalcemia
Present when specimen taken without a venous cuff and corrected for
albumin concentration.
Some differential diagnoses and typical outline evidence
Vitamin D
deficiency—due
to dietary deficiency
or 1, 25(OH)2D
abnormality
Suggested by: diet history, d phosphate and
± ialkaline phosphatase
Confirmed by: decreased 1, 25(OH)
2
vitamin D,
normal calcium after adequate treatment with
vitamin D
Hypoparathyroidism
(transient or
permanent after
thyroid surgery,
autoimmune
disease, radiations)
Suggested by: recent neck surgery ± iphosphate
Confirmed by: parathyroid hormone d or normal in
presence of calcium d
Chronic renal
failure
Suggested by: ± iphosphate, ± icreatinine, ±
ialkaline phosphatase, normochromic anemia
Confirmed by: improvement with control of renal
failure and phosphate levels
Pseudohypo-
parathyroidism
Suggested by: short stature, obesity, round face,
short metacarpals, ± iphosphate
Confirmed by: plasma parathyroid levels i with
calcium d or normal
Pancreatitis Suggested by: abdominal pain and tenderness,
phosphate normal or d normal alkaline
phosphatase
Confirmed by: ii serum amylase and ultrasound
scan of abdomen
Fluid overload Suggested by: history and d phosphate and normal
alkaline phosphatase
Confirmed by: normalization with correction of fluid
balance
Rhabdomyolysis Suggested by: muscle pains, phosphate i
Confirmed by: CPKii, ± creatinine i
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CHAPTER 18 Laboratory tests
430
Raised alkaline phosphatase
Some differential diagnoses and typical outline evidence
Paget’s disease Suggested by: deformity of skull or tibia typically,
iialkaline phosphatase
Confirmed by: bone deformity, especially of skull
and tibia, and urinary hydroxyproline i
Vitamin D
deficiency due to
dietary deficiency
Suggested by: diet history, d phosphate and
ialkaline phosphatase
Confirmed by: 1,25 (OH)
2
vitamin D level d and
normal calcium after oral vitamin D and calcium
supplement
Bone metastases
from breast,
bronchus, kidney,
thyroid, ovary, colon
Suggested by: normal phosphate, i calcium, and
ialkaline phosphatase
Confirmed by: evidence of metastases on X-ray,
CT, or bone scan
Primary or tertiary
hyperparathyroidism
Suggested by: low phosphate and i alkaline
phosphatase after years of secondary
hyperparathyroidism
Confirmed by: plasma parathyroid levels high with
high calcium
Cholestasis Suggested by: jaundice with pale stools and dark
urine. Bilirubin conjugated and thus soluble in
urine
Confirmed by: i urine and serum bilirubin but NO
i urobilinogen in urine. ii alkaline phosphatase,
otherwise slightly abnormal liver function tests
RAISED BLOOD UREA NITROGEN & CREATININE (AZOTEMIA)1
431
Raised blood urea nitrogen & creatinine
(azotemia)
Raised blood urea nitrogen (BUN)
and creatinine (azotemia)
Some differential diagnoses and typical outline evidence
High protein load
due to GI bleed,
catabolism, sepsis,
etc.
Suggested by: iBUN and near-normal creatinine,
suggestive history and clinical signs
Confirmed by: recovery when catabolism or GI
bleeding stops
Prerenal azotemia
due to hypo-
volemia from low
fluid intake or high
fluid loss of any
cause
Suggested by: iBUN and creatinine with
BUN/creatinine ratio >20. Low urine Na (<20
mEq/L) or fractional excretion of Na (<1). History of
fluid imbalance with fluid loss exceeding intake.
Confirmed by: improvement with restoration of fluid
volume
Chronic renal
failure (CKD,
CRF) due to
pyelonephritis,
glomerulonephritis,
interstitial
nephritis,
diabetes mellitus,
renovascular
disease, analgesic
nephropathy,
hypertension
Suggested by: iBUN and creatinine and not rising
rapidly over days. dHb, small renal size on ultra-
sound scan, etc.
Confirmed by: renal biopsy appearance
Acute tubular
necrosis, severe
hypotension,
nephrotoxins
(NSAIDs
aminoglycosides,
amphoteracin B,
etc.)
Suggested by: raised BUN and creatinine and rising
rapidly over days. Hb normal. Recent acute illness
with hypotension and oliguria (fall in urine output <1
mL/kg/hr). iK
+
, etc. Ultrasound scan: normal kidney
size and no obstructive uropathy
Confirmed by: no improvement when euvolemic and
renal biopsy
Obstructive (or
“postobstructive”)
renal failure
Suggested by: raised BUN and creatinine and rising
further. Hb normal. Fall in urine output
Confirmed by: Ultrasound scan showing dilatation of
renal calyces or ureters. Improvement in renal
function with bladder or ureteral catheterization or
nephrostomy
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