L

A
B

/e
M
14 E
S,
D
AM

I
O

C
R

I
N
E
 L 9.1 LABORATORY VALUES ƒƒ Suprapubic urine sample is best for culture sensitivity in
A infants for diagnosis of UTI. But it is associated with the
B Lab Values with age risk of needle injury to pelvic organs.
ƒƒ Most appropriate method for obtaining a urine specimen
Parameter Do not change Do change with age for culture in female infant is clean catch void sample.
M
with ↑ing age ƒƒ Thymol/ conc. HCl is used as preservative for transport of
E
1. LFT S bilirubin, AST, ALP ­ ↑ urine sample.
D
ALT, g -GT,
I
Coagulation tests Normal values
C
2. RFT Serum creatinine Cr-clearance ↓ (GFR) ƒƒ Normal composition of urine is:-
I
S.g. = 1.015-1.025 (but range is 1.008-1.030)
N 3. TFT T4 TSH ↑ T3 ↓
pH, reaction = 5.0-7.0 (average 6.0), acidic
E 4. CBC Hematocrit, Hb, WBC count ↓ Creatinine = 0.8-1.8 gm/L
RBC index, platelets
Urea = 25-30 gm/L
5. ABG pH, PaCO2 ↓ PaO2, ↓ VC, Systolic Uric acid = 0.5 gm/L

/e
BP, ­↑ PP, ↑
­ RV ƒƒ Normal urine output is 1-2 ml / kg / hr in children.
6. S.electrolytes Albumin, B12, HDL, (Volume =1200-1500ml/24 hr).
Biochemical Ca++, Phosphate, Mg++ in male↑ ƒƒ Polyuria is > 3000 ml /24 hr & oliguria is <500 ml/24h.

14
Total protein, folate ↑ Uric A., total
cholesterol, HDL in
Specific Gravity
female
Blood glucose ↑ ƒƒ Urine of low s.g. (< 1.007) is k/as hyposthenuria & urine
of fixed s.g. 1.010 is k/as isosthenuria (seen in late stages
Normal Serum Values of chronic GN) .
S,
ƒƒ Urinary s.g. after fluid restriction of 12 hrs. > 1.025
Serum substance Normal range Urinary s.g. after fluid restriction of 24 hrs. > 1.026
Na +
136- 145 mEq/L S.g. after deliberate water intake of 12 hrs. < 1.003\
K+ 3.5 - 5 mEq/L ƒƒ Causes of
AM

Ca++ 9-11 mg% High Specific gravity Low Specific gravity

2.2-2.6 mmol/L
1. Excess sweating 1. Excess water intake
Ionic Ca++ 4.5 - 5.1 mg% 2. Glycosuria 2. DI
Cl- 98 - 106 meq/L 3. Albuminuria 3. Chronic nephritis
4. Acute nephritis (All causes of polyuria except
Mg 1.6 - 2.1 mg% (Causes of oliguria/ DM)
O

P 2.5 - 3.1 mg% concentrated urine)

HCO3 -
21-24 mEq/L
Colour of Urine
R

Osmolality 285- 295 mmol/kg

Urea 15- 50 mg% Colour Cause (due to) Seen in
Dark yellow ↑ urochrome Fever,
thyrotoxicosis,
starvation
9.2 URINE ANALYSIS Pale , colourless ↑ fluid intake
Red Hb, Mb, porphyrin,
Urine Sample Collection RBCs (Rmp,
ƒƒ Early morning urine sample is used for phenindione, Beet)
°° Diagnosis of pregnancy (β-hCG based) Brownish black Homogentisic acid, Alkaptonuria
°° Nephrotic/nephritic syndrome. (dark brown on melanin met-Hb ochronosis
ƒƒ Culture of 3 morning urine samples is required for standing/O2­)
definitive diagnosis of genitourinary TB. Reddish purple Porphyrins Porphyria
ƒƒ Mid stream urine sample is reqiured for diagnosis of on standing/O2
328 UTI.
Pinkish brown on Bilirubin Hemolytic anemia
ƒƒ Freshly catheterized urine sample is required for standing (yellow
cytologic diagnostic purpose . brown)
 High-yield Points
Gross Microscopic L
•• Visible to naked eye Detected only A
44 Smoky (Cola Coloured) urine is d/ to RBCs in urine and is seen in •• If originates from by dipstick or B
acute glomerulonephritis. Kidney Lower UT and UB microscopic
44 Reddish brown urine is d/ to free Hb or Met-Hb and O-toluidine ↓ ↓ examination
test is +ve. defined as M
Brown/cola colored pink/red colored
Contains RBC casts contain clots > 5 RBCs/hpf E
(in 10 ml fresh D
centrifuged urine) I
Glomerular Extra glomerular or > 20 RBCs / hpf
diseases disease (In uncentrifuged
C
•• IgA nephropathy •• Tubulointerstitial urine) I
•• Alport syndrome nephritis N
•• Acute nephritic •• ATN
syndrome •• Papillary necrosis
E
•• GPS •• Hemoglobino­pathy
•• SLE nephritis •• Urolithiasis

/e
•• Post
streptococcal GN
•• Thin GBM
disease

14
ƒƒ Glomerular hematuria is ch/by dysmorphic RBCs in
urine when examined by phase contrast microscopy as the
RBC passes down through renal tubules it loses its shape
and size and becomes dysmorphic.
ƒƒ Non-glomerular hematuria is c/by isomorphic or
S,
Eumorphic RBCs (>85%) & RBCs clumps but no casts
in urine. Stones, hypercalciuria, tumours are imp. causes.

Hematuria in various settings

AM

Presentation Significance / Interpretation

Fig.: Approach to a patient with Red Urine •• Gross hematuria Post renal source (in urinary
tract)
•• Isolated hematuria Idiopathic congenital anomaly
BACTRIURIA (Alport Syndrome, PKD)
•• Isolated microscopic Glomerular d/s (IgA
ƒƒ Asymptomatic bacteriuria is defined as larger than normal
O

hematuria nephropathy, hereditary

numbers of bacteria are present in the urine but symptoms nephritis, thin GBM d/s)
do not result. •• Hematuria with dysmorphic Acute GN
ƒƒ Significant bacteriuria is defined as concentration of RBCs + RBCs casts,
R

pathogenic bacteria in the urine of 105 CFU of of a single proteinuria > 500 mg/d
uropathogen per ml. If bacterial count in midstream urine •• Hematuria + pulmonary Good Pasture syndrome
h'age (Anti-GBM d/s)
sample are:-
°° < 10 per ml → May be be due to contamination, not
4

significant
Recurrent Hematuria
°° 10 - 10 per ml → Equivocal, repeat culture advised.
4 5 Presentation Significance /
ƒƒ If bacterial counts are 102 per ml in catheterized sample Interpretation
→ UTI. •• Sensorineural deafness + Lenticonus Alport's
•• Pharyngitis f/b hematuria within 24 hr IgA nephropathy
•• Wt loss, fever, RVT in middle age RCC
HEMATURIA •• Chronic analgesic use + colicky pain Analgesic
nephropathy
There is a long list of causes of glomerular and extra
•• Renal failure ADPKD
glomerular hematuria. Summarized approach to hematuria
•• Colicky pain Stone
is given here. 329
[RVT = Renal vein thrombosis, RCC= Renal cell Ca]
 L High-yield Points
Cast Constituent Significance/Seen in
A Transparent/ Tom Horsfall protein Prerenal failure,
B 44 Alport syndrome can occur within 1st yr of life. IgA nephropathy Hyaline casts (THP) only Does not represent
after the age of 10 yrs & ADPKD after 3-4th decade. (Benign) any damage to
44 Electron microscopy is diagnostic in --- Alport's. tubules, Normally
M 44 Solid tissue tumours in which fever is seen --- Ewing's, RCC, HCC. seen after strenuous
E 44 In Good Pasture syndrome, antibodies are formed against a3 exercise
D component of collagen IV of GBM. Broad/waxy THP only Stasis in collecting
I 44 In Alport syndrome, a5 component of collagen IV is defective. casts (Size ↑) duct (CRF)
C Coarse granular/ THP + epithelial cell ATN (Intrinsic renal
Muddy brown debris tubular d/s)
I Recurrent gross hematuria is seen in WBC cast THP + WBCs Acute pyelonephritis
N
ƒƒ Alport's syndrome
E RBC casts THP + RBCs Acute GN
ƒƒ Berger’s disease (IgA nephropathy)
ƒƒ Idiopathic familial hypercalciuria Lipid casts THP + cholesterol Nephrotic syndrome
ƒƒ Thin GBM d/s Eosinophilic THP+ Eosinophils Acute interstitial

/e
ƒƒ Stones (Urolithiasis) casts nephritis,
Atheroembolism
Myoglobulinuria

14
ƒƒ Seen after vigorous exercise.
ƒƒ Pink/reddish urine, occasional amorphous debris 3-4 9.3 CSF ANALYSIS
granular casts but no RBCs
ƒƒ Myoglobin in urine is detected by orthotoludine reagent NORMAL CSF: FACTS
S,
Hemoglobinuria ƒƒ Normal pressure: 70-180 mm CSF or 70-180 mm of
water (10 mmHg). CSF pressure is mainly regulated by
ƒƒ Seen in mismatched blood transfusion, hemolytic anemias,
rate of CSF absorption at arachnoid villi.
snake bite, copper sulphate poisoning etc.
ƒƒ Production: CSF is produced by the choroid plexus in
AM

ƒƒ A/w hemoglobinemia or methemoglobinemia.

ventricles and is absorbed through the arachnoid villi into
veins, mainly the cerebral venous sinuses.
Albuminuria
°° Rate of production: is about 550ml/d (approximately
ƒƒ Excretion <30 mg/d → Normal 20 ml/hr).
ƒƒ 30- 300 mg/d → Microalbuminuria °° Turnover rate is 3.7 times per day.
ƒƒ 300mg - 3g/d → Sub nephrotic proteinuria (Macro- ƒƒ At CSF pressure 112 mm Hg, rate of formation and
O

albuminuria) absorption are equal. Below 68 mm Hg CSF absorption

ƒƒ >3 g /d → Nephrotic range (massive) proteinuria is nil.
ƒƒ Colour: Clear, colourless.
R

ƒƒ Volume: 150 ml in adults & 50 ml in infants (spinal CSF

URINARY CASTS
ƒƒ Casts are particles which precipitate in tubules in
ascending limb of Loop of Henle.
ƒƒ Tom Horsfall protein (THP) is a normal constituent of
urine. Dehydration results in precipitation of THP.
High-yield Points
44 If WBCs or pus cells (not casts) are seen in urine they indicate
urethritis, cystitis (not of renal origin).
44 Dysmorphic RBCs in urine indicate glomerular pathology.
44 Coarse granular casts in urine are always pathological.
330
volume is 50% of this).
ƒƒ Rate of CSF production 550 ml/d (20 ml/hr). Recycling
rate is 3.7 times/d.
ƒƒ Absorption: 112 mm CSF pressure, filtration & absorption
are equal. Absorption stops if CSF pressure is < 68 mm.
ƒƒ Absorbed by-arachnoid villi through their tight junctions
of their endothelium. Most CSF is extraventricular.
CSF is absorbed by lymphatics around CN 1, 2, 7, 8
ƒƒ pH :7.33 (cf plasma 7.40).
ƒƒ Specific gravity : 1.006- 1.007
ƒƒ In CSF there are high Mg++, HCO3—, Pco2, Creatinine,
Cl– (than blood) i.e. 4 “C” and magnesium. [ Remember
that all +ve ions are more in plasma except Mg++ (more in
CSF) & all negative ions are more in CSF]
ƒƒ Sugar: 40-70 mg%. L
ƒƒ CSF : plasma glucose ratio is 2:3. CSF Glucose is 2/3rd High-yield Points
A
( 66 % ) of blood glucose. 44 An ↑ level of IL-6 in CSF is seen in → CNS-Behcet's disease. B
44 Beta-2 transferrin is a CSF-specific and is used as an endogenous
marker of CSF leakage in CSF rhinorrhea.
ABNORMAL CSF M
44 CSF as well as serum IL-8 levels were found to be significantly
E
ƒƒ Low CSF proteins may be seen in : lower in Alzheimer's disease patients.
D
°° Pseudotumour cerebri I
°° Recurrent LP (lumbar puncture) ƒƒ Eosinophilic meningitis CSF shows predominance of C
°° Infants eosinophils and mononuclear cells. It is caused by I
°° Gnathostoma N
ƒƒ High CSF proteins may be seen in : °° Angiostrongylus cantonensis E
°° Infections °° Baylisascaris
°° GBS °° Coccidioidal meningitis
°° Multiple sclerosis °° Taenia solium [NOT seen with nocardia]

/e
°° Malignancies
°° ICH (Intracranial H'age) ƒƒ Froin syndrome is triad of CSF proteins > 500 mg% +
xanthochromia + spontaneous clotting. Usually there is

14
ƒƒ Albumino-cytological Dissociation : Proteins increased complete spinal block d/ to obstruction by tumour.
but cells are low. A disproportionate ↑ in proteins compared
to cells is seen in Pandy's Test
°° Spinal tumours ƒƒ Detects ↑ globulin in CSF (+ve in pyomeningitis) ,
°° GBS ƒƒ Disproportionately greater↑ in gammaglobulins is seen in
°° Cerebral arteriosclerosis, infarcts,
S,
multiple sclerosis and in neurosyphilis
°° Multiple sclerosis ƒƒ In meningococcal meningitis ↑ in IgM and in multiple-
ƒƒ Neighbourhood reaction sclerosis ↑ IgG
CSF shows variably ↑ed cells, normal glucose, N ƒƒ Very high CSF proteins (~ 10 g/L) are most likely d/to CSF
AM

to ↑ proteins and variable opening pressure. Seen in below a spinal block (usually d/ to spinal tumours)
mastoiditis, brain abscess, epidural abscess, sinusitis,
septic thrombus, brain tumour.

CSF FINDINGS IN IMPORTANT CNS DISORDERS

O

Type of Color Opening Cell/mL Predominant Protein Glucose Cl- Remark

meningitis pressure cells (mg%) (mg%) (mg%)
(mm water)
R

Normal Clear 70-180 0-5 Lympho 20-40 40-70 720-750

colourless Lympho
Pyogenic/ Turbid/ ↑↑ 200- PMNs ↑↑ ↓↓ ↓ , < 680
Acute bacterial purulent (>180) 20,000 > 95% (>50) (<45)
Aseptic/ Acute viral clear ↑ 25-2,000 Lympho ↑ N, ↓
(>250) (>50)
Meningo-encephalitis Clear Lympho
Tubercular/ TBM clear/ ↑ 100 -1,000 Lympho ↑ ↓ ↓↓↓ Cob web +ve
slight (>300) (>50) (<45)
turbid
Spirochetal clear/ N, ↑ 100-500 Lympho ↑ N ↓ , 650-
(Syphilitic, Lyme's d/s) turbid (25-60) 720
Meniningism in acute clear N Slight ↑ 15-50 N N
fever (lympho)
331
CSF = cerebrospinal fluid; CNS = central nervous system
 L Fibrin clots in CSF
A ƒƒ In pathological hemorrhagic CSF
B ƒƒ On standing when proteins ↑↑ (> 2g/L)
ƒƒ In TBM (Cob-web like coagulum on overnight standing)
M
E High-yield Points
D
I 44 In acute/early stage of TBM polymorphs may predominate.
C 44 CSF glucose must be considered in relation to blood glucose only
I normally CSF glucose is 2/3rd of blood glucose (or 20-30 mg%
N lower than blood glucose).
� ↓ in CSF chlorides is seen in TBM.
E HCO--3 = 24 + 2 mEq/L
44 For cryptococcal meningitis helpful diagnostic aid is antigen
detection in CSF and India ink/wet mount preparation showing
budding yeast.
ƒƒ In neurosyphilis and polio-meningitis.
Mollaret Meningitis
ƒƒ Also k/as recurrent lymphgocytic meningitis
ƒƒ HSV is the m/c cause.
ƒƒ D/g: HSV antibodies in CSF or persistence of HSV- DNA
in CSF
S,
Common Organisms in Meningitis
ƒƒ Neonatal → in India E.coli, Klebsiella spp.,Enterobacter
Listeria spp., Proteus spp. In west GBS are m/c
AM
ƒƒ In infants → Hib(in India), Streptococcus agalactiae,
ƒƒ In children → Hib(in India), N. menigitidis, S. pneumoniae.
ƒƒ Adolescents → Neisseria meningitidis
ƒƒ Adults → S. pneumoniae
ƒƒ Elderly → Gram-negative bacilli
ƒƒ In HIV → Cryptococcus
O
ƒƒ M/c cause of aseptic meningitis → ECHO viruses
High-yield Points
R
44 M/c cause of viral meningitis---Echovirus groups of enteroviruses
are the most common cause of viral meningitis.
44 M/c cause of viral encephalitis---HSV-1 , Arbovirus in epidemic
setting (Note:HSV-2 does not cause encephalitis)
Correction of hyponatremia in ARF
(when Na+ fall < 120 mEq/L it may be corrected using NS
or hypertonic 3% saline). Dose is calculated as
Na (mEq) = 0.6 × wt (kg) × (125 – S.Na+)
Partial pressure of oxygen in arterial blood (PaO2)
ƒƒ Partial pressure of oxygen in arterial blood by following
formula.
332
PaO2 = 104 - [patient’s age x 0.42 (in supine position)
or patient’s age x 0.27 (in sitting position)]
ƒƒ So in a 85 years old healthy male PaO2 will aprox.
80 mmHg.
ƒƒ PaO2 (in supine) - 90 mmHg (at age 20 year), 82 mmHg (at
60 year) & 72 mmHg (>60 year)
ƒƒ Calculation of intrinsic heart rate ( IHR)
IHR = 118.1– (Age × 0.57)
9.4 ACID-BASE DISTURBANCES
Normal Values
PCO2 = 40 + 5 mmHg
CO2 = 1.2 mEq/L
/e
Base acid ratio = 20 : 1
pH = 7.4 (range 7.38-7.44)
Base excess = + 2
Anion gap = 8-16 mEq/L
14
High-yield Points
44 Metabolic acidosis with fully compensated chronic respiratory
alkalosis occurs in single condition —very high altitude.
44 Met. alkalosis is most dangerous of all acid base disorders, as it
may induce cardiac arrhythmias.
44 Conditions where respiratory alkalosis and metabolic alkalosis
both exist together are --- Pulmonary embolism + diuretics
44 Conditions a/w metabolic acidosis with chronic respiratory
acidosis --- Very high altitude
44 In salicylate poisoning there is respiratory alkalosis first + ↑
salicylate anions f/b metabolic acidosis
Apply 3 simple & basic principles given below to solve any
acid base query
Simple disorder
In simple acid base disorder pCO2 and HCO3- levels change
in the same direction.
Simple disorder pH pCO2 HCO3
Metabolic acidosis ↓ ↓ ↓
Metobolic alkalosis ↑ ↑ ↑
Respiratory acidosis ↓ ↑ ↑
 (1 meq/ dL ↓ acute & 4 meq/ dL ↑ chronic)
Respiratory alkalosis ↑ ↓ ↓ 
 (2 meq/ dL ↓ chronic)
High-yield Points
44 pH, PO2 and PCO2 are measured values and HCO3 is calculated
value.
44 Change in HCO3– level < 15 meq/L is always associated with
mixed acid base disturbance
44 In fully compensated phase --- arterial pH is brought into the
normal range.
ABG decision tree L
A
B

M
E
D
I
C
I
N
E

THE MIXED DISTURBANCE ƒƒ Expected compensation

/e
ƒƒ For acute rise in PaCO2 over 40 mm Hg , HCO3 increases
ƒƒ If a patient with respiratory insufficiency develops
by 1 meq/L for each 10 mmHg PaCO2
metabolic acidosis, he loses his ability to compensate
and a mixed respiratory-metabolic acidosis supervenes. For each 10 mmHg PaCO2 elevation there is ↓ in pH by .08

14
Correspondingly, a mixed respiratory-metabolic alkalosis (example ---if PaCO2 becomes 60 mm Hg , HCO3 values
is also possible. are likely to be 26 meq/L and pH 7.24 )
ƒƒ In mixed disturbances, both metabolic (bicarbonate) and ƒƒ For acute fall in PaCO2 below 40 mm Hg , HCO-3 falls
respiratory (pCO2) factors pull in the opp. direction and by 2 meq/L for each 10 mmHg PaCO2fall
pH changes are exaggerated (double arrows). ƒƒ For chronic elevation in PaCO2 over 40 mm Hg, HCO-3
S,
increases by 4 meq/L for each 10 mmHg PaCO2fall
pH Bicarbonate PCO2 ƒƒ Anion gap (AG):
Mixed In certain mixed disorders pH, PaCO2 and HCO3 are
normal and the only clue to an acid base disorder may be
AM

Acidosis ↓↓ ↓ ↑
Alkalosis ↑↑ ↑ ↓ an increased anion gap. So AG is called “foot print” of
metabolic acidosis. Hyperchloremic metabolic acidosis
Compensation for Acid - Base imbalances leaves no “foot print”.
ƒƒ Compensation is done by an organ not primarily affected; (d) Compare fall in HCO3 with increase in plasma anion
for example, pulmonary disturbances resulting in gap.
O

respiratory acidosis or alkalosis will lead to compensation i. In high AG metabolic acidosis, rise in the
by the kidney. Conversely, primary disturbances of renal plasma AG (AG -12) matches with fall in serum
function or metabolism with acid-base imbalance lead to HCO3 (24 - HCO3– (24 - HCO3), (Rise in AG =
R

compensation by the lungs. Fall in HCO3).

ƒƒ Compensation will return the pH towards normal. ii. If increase in AG exceeds the fall in HCO3 (Rise
pH Bicarbonate PCO2 Compensation* in AG > Fall in HCO3), it suggests co-existing
Respiratory metabolic alkalosis.
Acidosis ↓ ↑↑ ↑ iii. If increase in AG is lesser than the fall of HCO3
Alkalosis ↑ ↓↓ ↓  Renal effect on
(Rise in AG < Fall in HCO3), it suggest loss of
 bicarbonate
HCO3– (diarrhoea) causing non-AG metabolic
Metabolic acidosis.
Acidosis ↓ ↓ ↓↓
Alkalosis ↑ ↑ ↑↑ Respiratory effect ABG Nomogram
 on CO2.
The steps in using the nomogram are:
ƒƒ Double arrows show direction of compensation. The 1. Is the pH normal or <7.36 or > 7.44?
pH change will be less pronounced in the presence of 2. Then is pCO2 normal or <36 or >44 mmHg? Depending
compensatory mechanism than in their absence. on the area it falls the interpretation is done as shown in 333
Figure.
 L
A 3. If the values fall in area 2,3,6 & 7 see if HCO3 is <24 or
9.6 ASCITIC FLUID ANALYSIS
B >24. If the HCO3 value is between 22 and 26 the results are
always isolated respiratory disturbance. ƒƒ Diagnosis of spontaneous bacterial peritonitis (SBP) is
M made when the ascitic fluid neutrophil count is >250/mm3
E ƒƒ Cirrhotic ascitis is char/by--- Straw color, albumin <2.5%,
D SG < 1016, WBC <200/mm3
I
ƒƒ SAAG = < 1.1 g/dL → Exudative.
C
SAAG = > 1.1 g/dL → Transudative
I
N
E
9.7 SYNOVIAL FLUID ANALYSIS
ƒƒ Normal synovial fluid is clear or pale straw and is viscous,

/e
primarily because of high levels of hyluronic acid
ƒƒ Non- inflammatory SF is ---clear , viscous, and amber
coloured with TLC < 2000/ µL and predominance of

14
mononuclear cells
ƒƒ Joint effusions in OA and trauma have normal viscocity
ƒƒ Inflammatory SF is ---turbid/ yellow,low viscocity, and
2 amber coloured with TLC >2000/ µL and predominance
of polymorphs.
S,
1. Metabolic acidosis ƒƒ Synovial fluid of low viscocity (thin) is seen in--
2. Metabolic and Respiratory acidosis Inflammatory arthritis (Gout, septic arthritis, TB, RA)
3. Respiratory acidosis ƒƒ Monosodium urate crystals are seen in gout & are long,
4. Respiratory acidosis and Metabolic alkalosis
AM

needle shaped, negatively birefringent, intracellular

5. Metabolic alkalosis
ƒƒ CPPD (Calcium pyrophosphate) crystals, seen in
6. Metabolic and Respiratory alkalosis
pseudogout and chondrocalcinosis are short, rhomboid-
7. Respiratory alkalosis
shaped, positively birefringent.
8. Respiratory alkalosis and Metabolic acidosis
9. Normal
(Courtesy --- Dr. So. Shivbalan, Dr. P. Rajkumar, Indian
O

Pediatrics, Vol. 42, 2005) 9.8 SPUTUM EXAMINATION

ƒƒ Sputum expectoration specimen is collected for
R

examination in
9.5 KFT (KIDNEY FUNCTION TEST)
°° Mycobacteria
Pre-renal azotemia °° Legionella
°° Pneumocystis.
ƒƒ Urinary Na+ is <10 m mol/L & SG is > 1.018 ƒƒ Sputum can NOT be disinfected by chlorhexidine.
ƒƒ Fe Na < 1%, Renal failure index <1 ƒƒ Charcot leyden crystals in sputum are seen in bronchial
ƒƒ Plasma BUN / Cr ratio = >20, U cr: Pl cr >40 asthma.

High-yield Points
44 A disproportionate elevation of blood urea as compared to 9.9 PLEURAL FLUID ANALYSIS
serum creatinine occurs in pre-renal azotemia
44 A definitive diagnosis of CRF can be established on the basis of ƒƒ Anchovy sauce appearance of pleural fluid may be seeen
bilaterally reduced renal size in Entamoeba histolytica infection.
334

ƒƒ Parapneumonic effusions are a/w bacterial pneumonia,
lung abscess, or bronchiectasis and are probably the m/c
cause of exudative pleural effussion.
ƒƒ Exudative pleural effusions meet at least one of the
following criteria
1. P/S protein > 0.5
2. P/S LDH > 0.6
3. Pleural fluid LDH > 2/3rds normal upper limit for serum
leading causes of exudative effusions are --- bacterial/
viral pneumonias, malignancy, pulmonary embolism
ƒƒ A pleural fluid NT-pro BNP >1500 pg/mL is virtually
diagnostic of an effusion secondary to CHF.
9.10 SEMINAL FLUID ANALYS
ƒƒ Normal quantity of seminal fluid in a single emission is 2-6
ml and contains about 60-150 million sperms per ml, of
which 90% are motile at the time of ejaculation. Analysis
should be performed within an hr of collection.
ƒƒ Fluid is alkaline with a pH of 7.4
S,
ƒƒ 3 Azoospermic or oligospermic results should be evaluated
by chromosomal study and testicular biopsy.
ƒƒ Sperm production per day - 120 million /day
AM
Interpretation of results: (2010 guidelines)
ƒƒ Normal:
Normal counts >15 million/ml
Quantity >1.5 ml
Motility >32% mobile
O
Morphology >4% normal morphology
WBCs <1million/ml
Immuno bead reaction test/mixed antiglobulin <50%
R
coated with antibody
ƒƒ Oligospermia:
Sperm counts <15 million/ mL (mild), 5-10 million/ mL
(moderate), below 5 million/ mL (severe) .
ƒƒ Aspermia: Means no semen
ƒƒ Azoospermia: Means no sperm in semen
ƒƒ Asthenospermia: No motile sperm or decreased motility
[For details see Infertility section in Obstetrics]
High-yield Points
44 A normal biopsy in an azoospermic man with a normal FSH level
suggests obstruction of the vas deferens.
44 Sertoli cell-only syndrome --- Absent germ cells on biopsy.
L
A
9.11 LIVER FUNCTION TEST (LFT)
B
SGOT : SGPT Ratio (AST : ALT) M
ƒƒ Normally 1:1, In alcoholic liver diseases it is >2:1 E
ƒƒ SGOT is elevated out of proportion to SGPT
D
or Very high SGOT is seen in
I
°° Alcoholic hepatitis
C
°° Fatty liver of pregnancy (ratio is > 2:1)
ƒƒ Aspartate aminotransferase, formerly called SGOT, I
is not as specific for liver disease as is ALT, which N
is increased in myocardial infarction, pancreatitis, E
muscle wasting diseases, and many other conditions.
However, differentiation of acute and chronic forms of
hepatocellular injury are aided by examining the ratio of
/e
ALT to AST, called the DeRitis ratio. In acute hepatitis,
Reye's syndrome, and infectious mononucleosis the ALT
predominates. However, in alcoholic liver disease, chronic
14
hepatitis, and cirrhosis the AST predominates.
ƒƒ In Dengue fever, elevation of SGOT > SGPT is found
usually.
ƒƒ In typhoid fever, elevation of SGPT > SGOT is found
usually.
GGT (Gama Glutamyl Transferase)
ƒƒ GGT is greatly ↑ed in obstructive jaundice, alcoholic
liver d/s, and hepatic cancer.
°° When the ↑ in GGT is >2 times greater than the ↑ in ALP,
the source of the ALP is considered to be from the liver.
°° When the ↑ in GGT is >5 times the ↑ in ALP, this
points to a diagnosis of alcoholic hepatitis. GGT,
but not AST and ALT, is elevated in the first stages
of liver inflammation d/ to alcohol consumption, and
GGT is useful as a marker for excessive drinking. GGT
has been shown to rise after acute persistent alcohol
ingestion and then fall when alcohol is avoided.
Alkaline Phosphatase (ALP)
ƒƒ Derived from 4 sources:- from placenta (PLAP), GI tract
liver and bone
ƒƒ From bone is heat liable while from liver is heat stable.
ƒƒ Increased in ↑osteoblast activity (bony conditions like
paget’s disease, rickets, osteomalasia, hyperparathyroidism
and Paget’s disease.
ƒƒ Also increase in liver disease, biliary obstruction, cirrhosis,
UC & CD.
ƒƒ ALP (Alkaline phosphatase) is elevated out of proportion to
serum transaminases (ALP >ALT)in diffuse intrahepatic
obstructive disease which may be caused by some drugs
or biliary cirrhosis, focal obstruction that may be caused
by malignancy, granuloma, or stones in the intrahepatic 335
bile ducts, or extrahepatic obstruction such as GB or
CBD stones, or pancreatic or bile duct cancer.
 L High-yield Points 9.12 TOXIC LEVELS
A
B 44 Presence of urobilinogen in urine rules out any obstructive cause ƒƒ Fluroide optimum concentration → 0.5 - 0.8 ppm. Fl-
of jaundice toxicity >1.5 ppm.
44 Gall stones can be explained by precipitation of bilirubinate
M ƒƒ MgSO4 therapeutic concentration → 4-7 mEq/L.
crystals in urine
E 44 ALP is produced from bone, liver, intestine, placenta. Hepatic  >8 → Knee jerk absent .
D isoenzyme of ALP is heat stable >10 → Urine output ↓ed.
I 44 Confirmation of elevation of ALP of hepatic origin is done by >13 → Respiratory paralysis.
-5' nucleotidase. 5' nucleotidase & glutathione transferase are ƒƒ Lithium therapeutic concentration → 0.8 - 1.2 mEq/L (in t/t
C more specific for liver diseases
I of acute mania) and 0.5- 0.8 mEq/L (in maintenance phase).
44 Prothrombin time is a good indices of hepatic synthetic function
N 44 GGT is a sensitive indicator of biliary tract disease
 >2 → toxicity starts .
E 44 SGOT is a mitochondrial enzyme released from heart, liver,
kidney,skeletal muscles
44 SGPT is a cytosolic enzyme released from liver. 9.13 RECENT POINTS
44 Direct bilirubin means conjugated fraction of total bilirubin.

/e
If direct bilirubin is >15% of total bilirubin,then it is called
ƒƒ The 3rd generation TSH detection methods can detect
conjugated or direct hyperbilirubinemia.
44 Initial investigation of choice in a case of obstructive jaundice is TSH levels as low as 0.004 mU/L.
---USG abdomen ƒƒ Steatorrhea is not a/w biliuria.

14
44 Low hemoglobin & elevated unconjugated bilirubin are typically ƒƒ Optimal plasma levels of lipids:
seen with hemolytic picture Total cholesterol < 200
44 In liver diseases colloidal oncotic pressure decreases TG <150
LDL-c <100
Three major types of Jaundice HDL-c > 40 (males) & >50 (females)
S,
Features Hemolytic Hepato- Obstructive ƒƒ Stain that distinguish early HCC (hepatocellular
cellular carcinoma) from dysplastic lesions: Glypican-3.
•• Hyper- Mainly un- Conjugated Conjugated ƒƒ NOT a marker of hepatocyte integrity- serum GGT.
bilirubinemia conjugated
ƒƒ Average serum ferritin value in males - 100 mg/dL.
•• Van den Bergh's
AM

Indirect Direct/Indirect Direct

reaction
•• Hb Low N N
•• Liver enzymes N Transaminases ALP is 9.14 EXFOLIATIVE CYTOLOGY
N are elevated elevated out
out of proporn of proporn ƒƒ Useful in diagnosis of tumours which shed off tumour cells
to ALP to transa­ in the lumen of vicinity.
O

ƒƒ SGOT,SGPT ↑↑↑ minases ƒƒ Useful in :

ƒƒ ALP Ν, ↑ ↑, Ν
↑↑↑ °° Ca cervix
•• Urine : °° Ca stomach
R

ƒƒ Colour Turmeric Dark yellow Dark yellow °° Ca lung/bronchus.

ƒƒ Urobillinogen +++ (turns ++ – °° Urothelial tumours
(bile dark on (acholuric) ƒƒ BAL (bronchoalveolar lavage) is a method of aspiration of
pigments) standing) exfoliated cells in case of ca lung.
ƒƒ Bilirubin – + (Bilirubinuria) ++
•• Stool
ƒƒ Colour N N in early phase Clay 9.15 HISTOPATHOLOGY
colored/
pale ƒƒ Fixatives most commonly used in histopathology is
ƒƒ Stercobilino- + + - formaldehyde (10% formalin).
gen
ƒƒ In a pap smear slide ethanol (95%) is used as a fixative to
•• Causes hemolytic •• Viral hepatitis Cholestasis
prevent air dying.
anemia •• Toxic/ drug
induced Ca pancreas ƒƒ Cytokeratin is the most important immunohistochemical
hepatitis stain to establish the diagnosis of poorly differentiated
336 •• Toxic/ drug carcinomas.
induce
Some basic stains in histopathology L
A
Stain Used for
B
Hemotoxylin Nuclei,nucleoli,bacterium,Ca++
Eosin Cytoplasm,collagen,fibrin,RBCs, M
thyroid colloid E
 
Oil red O Alveolar macrophages/ dust cells, fat D
I
Trichome Collagen
C
Reticulin Reticular fibres in loose conn.tissues I
Congo red Amyloid N
E
PAS Glycogen, glycoprotein,, mucin,mucoprotein
 
ƒƒ Heart failure cells are stained with hemosiderin > Prussian

/e
blue.
ƒƒ Inclusion bodies are stained with wright's stain.
ƒƒ Fat is stained by - sudan 4.
ƒƒ PTAH stain is used for staining muscle & glial filaments.

14
ƒƒ Stain is used for granulocytic sarcoma is → MPO
(Myeloperoxidase).
Fig.: Fibroadenoma
Other important immunohistochemical stains are
S,
Stain Used for
Cytokeratin Epithelial cells (Carcinomas)
Vimentin Connective tissue
AM

Desmin M/s ( mesenchymal tumours)

S100, NSE, Neurons (Neural crest derived tumours)
neurofilaments
GFAP Glial cells
Fig.: Squamous cell carcinoma

Some Important Histopathological Slides

O
R

 
Fig.: Benign prostatic hyperplasia
 
Fig.: Hydatid cyst

337
Fig.: Chronic pyelonephritis  
Fig.: Appendicitis
 L
A
B

M
E
D
I
C
I
N Fig.: Capillary hemangioma
E

Fig.: H. mole

/e
14
S,
AM

Fig.: Cholecystitis

 
O
R

Fig.: Cirrhosis-40x Fig.: Leiomyoma

338
 L
A
B

M
E
D
I
  C
I
N
Fig.: Mucinous adenocarcinoma
E

/e
14
 
S,
Fig.: Basal cell CA
AM

Fig.: Lipoma
O
R

Fig.: SqCC with Keratin pearls

339

Fig.: Rhinospondium Fig.: TB Lymphadenitis

 Exam Oriented Prototype IBQs (Including PGMEE 2016-17 IBQs)
L
A 1. Following instrument is used in histopathology for 2. True about the instrument given below:
B sectioning of parrafin blocks. Instrument is known
as:
M
E
D
I
C
I
N
E

/e
[ Image Courtesy: Dr. Suchita Modi]

a. It is used in histopathology

14
b. Known as automated tissue processor
[ Image Courtesy: Dr. Suchita Modi] c. Used for sectioning the paraffin blocks
d. Used for tissue processing of specimens fixed in
a. Automated tissue processor
10% formalin
b. Microwave processor
c. Rotary microtome
d. Cryostat
S,
AM

Ans.
O

1. c
2. c
R

340