WBUHHS

IMPORTANT TOPICS FOR

PRACTICAL EXAMINATIONN

1st Prof MBBS

By R G Kar Medical College Students Unity

KEY FEATURES
KEY FEATURES
KEYATURE
All important topics
are there which u must go
through before ur
practical exams..
"A ship in aharbour is safe, but that is not
what ships are built for."

First year medicOs, its time to face the storm

head on. The upcoming university exams may
be tough, but you are tougher. Concentrate
your efforts towards your goal, and make full
use of the limited time.Remember -"A good
plan, violently executed now, is better than a
perfect plan executed next week."

RGKSU wishes you best of luck for your ist

Professional MBBS examination.
Biochemistry Practicals

1. Charts
2. Urine Examination
3. Imp OSPE & Viva
Questions

STDENTS
KAR
UN
ROKSU

SpdfEdu
 INTERVAL/INTERPREI
BIOLOGICAL REFERENCE
ACCORDING TO CHARTS

Reference
Interval/Interpretation
Analyte Sample

Fasting 60-100 mg/dl

Plasma Glucose [Normal 60-100 mg/dl
Impaired/prediabetic: 101-125 mg/dl
Diabetic>=126 mg/dl
Random <200 mg/dl
[Diabetic >=200 mg/dl_
Postprandial 70-140 mg/dl
(2hr) [Normal:70-140mg/dl
Impaired/prediabetic: 141-199 mg/dl
Diabetic>=200 mg/d
CSF Infant/child-60-80mg/dl_
Adult-40-70 mg/dl

HbAIC-Glycated EDTA Non-diabetic: =5.6 %

Haemoglobin whole biood Pre-diabetic: 5.7-6.4 %
Diabetic:=6.5 %_
ACR U, spot <30 mg/gm of creatinine-Normal
30-300 mg/ gm of creatinine-
Aicroalbuminuria
>300 mg/ gm of creatinine - Macro
albuminuria
RFT
UREA Serum 13-43 mgdl
U,24 hrs 10-20 g/day
URIC ACID Serum M:3.5-7.2, F: 2.6-6.0 mg/dl
CREATININE Serum Adult:
M: 0.8-1.2:F: 0.6-1.1 mg/dl

Infant: 0.2-0.4 mg/dl

Child: 0.3-0.7 mg/dl
LIPID PROFILE
Total-Cholesterol Serum Desirable <200 mg/dl.
Borderline high 200-239 mg/dl.
High> 239 mg/dl.
HDL-C Serum
LDL-C 40to60 mg/dl
Serum Optimal: <100 mg/dl
Near/above optimal: 100-129
mg/dl
Borderline high: 130-159
mg/dl
High: 160-189 mg/dl
Very high: >=190
VLDL-C mg/dl
Chol;HDLc Ratio Serum 02-30 mg/dl
Serum <4.5

Low risk: upto 3.5

Moderate risk: 3.5-4.5
High risk:>4.5
[cardiovascular risk
evaluation interms
ratio of total-cholesterol of
Cholesterol to HDL

Scanned by CamScanner
 RG KAR MEDICAL COLLEGE& NOSPITAL
DEPARTMENT OF BIOCHEMISTRY
BIOLOGICAL REFERENCE INTERVAL/ INTERPIRETATION
ACCORDING TO CiIARTS

Triglyeceride Serum Desirable: <150 mg/hll

Borderline lliglh: 150.199 mg/dl
High: 200-199 my/ll
Very high: >199 mg/ll
Non-HDL Serum Optial: <I30 mg/dl
Cholesterol
LFT 02-1'0 /4UA.)
ull;)
Bilirubin Total Serum Upto f.0mg/dll.- (fo*
0-1 dlay(renature) I.0-8.0 mp/dl
0-2 day (ull terun) 2.0-6.0 mp/dl|
1-2 days (1premature) 6,0-12.0 mg/dl
1-2 days (ull term) 6.0-10.0 mg/d
3-5 days (pronaturo) 10.0-14,0 ng/dl
3-5 days (tull term) 4.0-8.0 mg/dl

Bilirubin Serum Upto 0.2 img/dl.

Conjugated
Bilirubin 0.2-0.8mg/dl
Unconjugated
Alanine Serum Male: up to 45 U/L
Aminotransferase Female: up to 34 U/LL
(SGPT)
Aspartate Serum Male: up to 35 U/L
Aminotransferase Female: up to 31 U/L
(SGOT)
Alkaline Serum MALE::
Phosphatase (ALP) Ito 12 yrs: 54-369 U/L
13 to 59 Yrs: 53-128 U/L
>=60 Yrs: 56-119 U/L

FEMALE::
I
to 15 Yrs: 54-369 U
16 to 59 Yrs: 42-98 U/L
yrs: 53-141 U/L
60
Total Protcin_ Serum 6.0-8.0 g/dl
Albumin Serum 3.5-5.0 g/dl
Globulin Serum 2.0-3.5 g/dl_
A/G ratio Serum 1.0 to 2,0
GGT Serum Male:<55 U/L at 37 C.
Female: <38 U/L at 37"C,
Urine urobilinogen Urine Normal: very low concentrations (0.2-1.0
mg/dl).positive.
Obstructive jaundicec: Nogative/decrensed.
Hepatic jaundice: ++
Hemolytic jaundice: +-e+
Urine for bile salt Urine Normal: Negative
Sinking sulphur in hay's sulphur surfiuce
tension test: positivc: presenco of bile salls-
obstructive jaundice,
Urine for bile Urine Normal: Negtive
Pigment [Obstructive jaundice: +-1t,
Hepatic jaundice: +/(-).
Hemolytic jaundice: Negative.]_

Scanned by CamScanner
 & HOSPITAL
RGKAR MEDICAL COLLEGE
BIOCHEMISTRY
DEPARTMENT OF
INTERVAL/INTERPRETATION
BIOLOGICAL REFERENCE
ACCORDING TO CHARTS
bilirubin reaches
Obstructive jaundice: no
Feces SBG Feces
small intestine,
meaning that there is no
stercobilinogen. The lack of
formation of
stercobilin and other bile
pigments causes

feces to become clay coloured.

ELECTROLYTES 136-145mmol/L. mEq/L

Sodium Serum

Potassiumn Serum 3.5-5.1 nmmol/L. mEq/L

Serum 98-107 mEq/L_

Chloride Total-8.6-10.2 mg/d
Calcium Serum -
Free (lonized) 4.6 to 5.3 mg/dl

Phosphorus Serum (Adult): 2.5-4.5 mg/dl.

(Children): 4.0-7.0 mg/dl.

ARTERIAL
BLOOD GAS_
pH Arterial 7.35-7.45s
blood
pCO Arterial 34-46 mmHg
blood
pO Arterial 90-110 mmHg
blood
HCO Arterial 22-26 mEq/L
blood
HCO Arterial 1.2 mEq/L
blood
HCO,7 H2cO Arterial 20:1
blood
Anion Gap Arterial 7-16 mmol/L
{[Na+K]-[ HCO blood
+CI}
Whole blood Whole At bed rest
(Heparinised) blood (Hep) Venous: 5-12 mg/dl
Lactate Arterial: 3-7 mg/dl

PANCREATIC
MARKER
AMYLASE Serum 28-100 U/L
LIPASE Serum K38 UL

THYROID
PROFILE
TSH Serum Adults
21-54 yr: 0.4-4.2 ulU/ml
55-87 yr; 0.5-8.9 ulU/ml
Children

Scanned by CamScanner
 & HOSPITAL
RG KAR MEDICAL COLLEGE
DEPARTMENT OF BIOCHEMISTRY
INTERPRETATION
BIOLOGICAL REFERENCE INTERVAL/
ACCORDING TO CHARTS

Birth-4 days: 1.0-39.0 ulU/ml

2-20 wk: 1.7-9.1 ulUml
ulU/ml
21 wk-20 yr: 0.7-64.0
Serum Adults (21-87 yr)
Free Thyroxine 0.8-2.7 ng/dl [10.3-34.7 pmol/L]
(FT4) [28.4-68.4
Newborn (1-4 days): 2.2-5.3 ng/dl
pmol/L]
[10.3-
Children (2 wk-20 yr): 0.8-2.0 ng/dl
25.8 pmol/L

CARDIAC
MARKER Male: 46-171 U/L at
37°C.
CPK Serum
Female: 34-145 U/L at 37'C.
Upto 24 U/L at 37"C.
CPK-MB Serum
230-460 U/L L at at 37 C.
LDH Serum
Body Body fluid:Upto-306
fluid(Asciti
c/pleural)
TROPONIN (T) EDTA Negative
Whole
blood

Urine Semi-quantitative test for reducing

Benedict's test
substances.
Green colour of solution: Reducing
substances upto 0.5 gm% (+)
Green precipitate: Reducing substances
0.5-1 gm%% (++)
Yellow precipitate: Reducing substancesl-
1.5 gm% (+++)
Yellow to orange precipitate: Reducing
substances 1.5-2 gm% (++++)
-

Brick red precipitate: Reducing substances

=>2.0 gm%

Rothera's test Urine Normal: Negative or no change in colour

(urine) Positive or presence of Ring: Ketone bodies
Urine blood Urine Negative

when sample examined under a

is

microscope, normal result is 4 red blood

cells per high power field or less]_
Urine for ferric Urine Blue-green color: Phenylketonuria.
chloride test Purple colour: Acetoacetate, salicylates,
Phenol, Antipyrine

Guthrie's test Positive: Phenylketonuria

Scanned by CamScanner
 KAR
MEDICAL COLLEGE & HOSPITAL
RG
DEPARTMENT OF BIOCHEMISTRY
BIOLOGICAL REFERENCE INTERVAL/ INTERPRETATION
ACCORDING TO CHARTS

Stool for Occult Stool Negative

Blood Test [Detect blood in the stool that is not visible
on gross gross inspection, usually less than
50 mg of haemoglobin per gram of stool.
Normal adults usually show less than 2 to 3
| mg/gm of stool]

HEMATOLOGICAL PARAMETERS
Blood hemoglobin EDTA 13-17gm/dl
blood
TLC EDTA 4000-11000/cumm
blood
Platelets EDTA 1.5-4.5 lac/cumm
blood
RBC count EDTA 4.5-5.5 million/cu.mm
blood
Reticulocyte count EDTA 0.5 to 1.5 %
blood
MCV EDTA 83-101 f1

blood
MCHC EDTA 31.5-34.5 %
blood
Ferritin Serum Newborn: 25-200 ng/ml
1-2 months; 200-600 ng/ml.
2-5 months: 50-200 ng/ml.
6 months-15 yrs: 7-140 ng/ml.
Adult Male: 20-250 ng/ml.
Adult female: 10-120 ng/ml.
Prothrombin time 11-13.5 seconds. INR of 0.8to 1.1

Scanned by CamScanner
 Binchomi/uy 5/12/20
JAUNDICg
CHART
year old pheAented medicw 0PD
UA 13
Srrumn Bitiuaiw 10 med .> Hiah
e
1) 0S
: Indruek)
( donsct)

ney 9 C hin
AST
28 -L uts/L Sallts C
32 u bile
ALT bile
60 A 10/L wobiliegem +tt)
ALP FLcal standobiUunopntt)
Lww Cqnting olility emaal
Excem etyugating Buurutoiw
Hemolytie Jaundice Maloua
TB
Deuaue
Henuditary Sphenootosis
CHART- Hemolrthe anewua
Snale Venom
A 27 Tean PHAen yeoL disce lowration Skim
Selona dan
PPer abdomimal pam fon 7 da
Anorenua Naupea, Occambual vomttm 1 das. He

tolen tthe meducation lout

exam blrdd & huea San
Lab
Sauwnn Biioin beA 10 /L
dhect G4 mg/
ALr 28 1u/L
AST 338 I/L www foru ile Soalt (
ALT 531 wwwe lile Pi
wrobiin0gen
Hepato collulau Jaundice
Hapatituo Bc, Vual Hepotit Lwez dfunetion Cat louund
alcoelic Hepottis AST, ALT o Cey abiuty
abnounel
CHART

$o yean ota 4tJo day hisoy Seloina

ectenus fovon ad uppe olodrmunA
ak
pain Lob exonnaion blobd and wune
neve al
Serum Biu 4 N wwwe fbn bile Sat
4.3 (++)
1093
ALP T/L-T sile (+)9
AST
23 IuL wobitinog0nNul
ALT TUL
178 0bstucthve Jaudsce
Bile duct stee .
At
Caneuma of Regungitation of
CHART V head o Paneneay ayugated
faccis
Jaachon) (No SB)
A mal
4 da 6l ugat a mecnatad ICU

Itenaive aundice wohiced dag before

amd t uas meeoALLN ut notma
dallvey fuul tuzm wtt oi tt
aanalL
LD
32 .by oaloy yelw

Selora. examulatuoa oesy all

Candiac tp fudimg
SRwmn 24
lL
Swrunm )
2 06 d
AST 38 L T

ALT
ALP S20
L
Neonatat Jaundiee neougoted

Hemo lysis
 Heme SYtess
metaboliom
RE 4SAn
8iuurubuw
Male a table
Co Iynthesis
wtabolim
Blirulpin
eiruu acts ontionisout (Asentbote,
unate)
661T differetiote bjuo olstuuetive
UNCONJUGATED Ogenal
Uncmyugaded Gitbert uglennata CONJ
UGnC
Dubn-Johwoon
Retet
TyreT Type Rotor
DIABETES

Fashing
0-140 mg dL (8 heuns Mo Calae Lwtake
ntake
p.P
PP hews)
140 mg/dt 2
Impained foating
9lueose
Impained Pediattic (101-125 Fenti
Gl olarnane (141 199 PP 2
)
Randm Blebd uonse diabetec
260
Polywr0a
PePolyphasia
lgdy Psea
Hb Ae Last 3-4 YS mantw ucose lavel

NORMAL
PREDIABETEC
DIABETEC
S4-64

A 43
2ass old Yam h
fon pumary cheel up . 0 Phsieal xam
BMI33-2
BP 140/90
mmm
e CLeumfernee
0tdentd
4 meh
His Phsiea
tbAC = 6*
For 10 Tug coude = 220
mg/
hou PP 180 m| d Total
PP IS6 LDL 109
HDL = 38 mg/d
18244
18.5 24.9 Noma L40 me malc)

25 29 w 35 (emal
303 Ty re T 0b
2 39.9 tyPe
HDL
40 40 60 male
30- 60 fenale)
T6 Is0Noumal)
PREDIABEC wH mpasred
SHOT ON MI A2
39 yea dlA lad 0PD, wiuld cheyt 0n èxand
Examuadimn, Palo NLL

130/8 m Eeherug-NiL

Palbe 8 mn Het-S 2
ínek
wot15 o12 1m
faat Plaome 6lu = 261 = (5x 36) + (2x 2.)
heletenal 25s d dia Cm
IS
Th BM 30
LDL 16S /d 160
HDL 39 d 40

HbAC 75
Diabctes,+ Dislpdomia
melutu5 chest Pan
due to Otunosclonosis

chart to Diabeue
old Knun dabetec male
oPD folmouup
houhnefolovd Palot

BP 16160 Pule =go m

em wetigaiom -
fontg 210 mya

Seruum Ura F
STma 1a 15-40) NOunal
7-13 (M)
Serum euatiune 2 m/ 7 .-12(
uuna albumm Cahnune
CCR)
4 30 NOmaL CcAhn
30-30D Miewalbumnuuia
300 ama Macroabumununa
, #perdewsirw
Diabetic Hypertenoive
Nepniopaty Dabehe witt eanly Nepwzapaty

wwa 13-40
CREATININE s 7-13 (M)
 CHART

Ketoaeidosis

tnceds6led Shanvahou
Dialees Malliu
Insun
nlucogom

48
tan old Lad
lady hua toe oAeity,
diabeles , dilipdama fmenygn
bougtt lto
Cemod2ed State. tomp911' F
eP /64 mut ER = 13
/m Rep nate
30
brtatts|mim
Lolb AG6 anayais PH 12
PCO
Amuem
=(34+-(2+12) 1n) Itmanty
1tmunby
HCD3
20
2 mL
PH Blaad ueose - SoF myld
12 7.4 acidocio
Seum Na 134 Ea/L
smetaualie K
HC3 = metabouc mEa)L
Diabettc (unetholled) C 2
wune analysis Rid PPt
Rotterna C) >ueloue body
Dubetie katoacidasi3
A 66 eara oldlad breu tComath lood
hrot Beuedict -ve
Byreiama Rot a tve)-Ketone
Stauahom mAaboue etoanidosts body
HCO3
12iitabeie
P 1 aoidoSiS
 Nepnalag
w
male PHAt Swelluing faes, us aua
www.aru 0utput. as karnt 4hat h
LeduceRd
itn tonsilit's days bacu
wos eated STREPTOCOecos (Tyre
Oedema ++
ho ytie) A

Puibial
BP 135/80 mme
wne
O
uport PHtem +
eruytreoy +
45
010od apese Stum wwa ld 40
Cruatinn 4
a/dt> o-s-1
0qunda Annwua ic ad mal
6:2
<46b m 100 ml wnineday
we daj3 tot protem s5 1 < 6-8
Rdema Albumin 2-4
BP
=
3]dtu 3-4-S
Na 134 mMal
NEPHROTIe SYN emauua X 44 mMol/
Be Same
Puteiwua +ttt
NEPHRITIC SYN
Aeutetemeulonghidi (Post strgtececcal)
Hematuia
yPoalbunuinemia cauais Edoma.
Potenurua t+
In hemolytic Stneptsceceus M PDteim
Secruted antibody agamat us

ASs gear od fmale ctila visitad eplealos'y

istoy o SeLuu anud s btth
fest amd s8 amd eenalised btdy uoetluiaNo
Jeva no ent iunes hematuua
BiLodera Piting oedema ++++) NEpwohie range Proten
M 3day +++
aAetis -dayalbuminuzia)
Hypenëholostene lmua
BP 100/60
HyPoallbmiueia
wunt tepot - albumun +++*) oedema
faohna- 122 m/a NEPHROTIC
AUbumum 11 SYNDROME
3/
Total Cuolestarol =4S1 mglat
Ta T 454 a
Senum wuA 52 mgl
 urvg Standun hstoty fdabeie
48
ea O1d male
Wpentenauow, Presemt wit Mausea Lossf apetite
eccasonal aleoholic and Cwnic
fatigua He
98.2°F HR 64/mw BP = 170 mm g
no k Temp
22 min, palou
Rasp node Markn
Lob westigation ;
Fostn plasma
cote = 204

wua 75 w/d
Suatinint 3.0 w1 d
Serum calewm 64 mald
Saruum phosphate =.s mgla
Na 130 mMl/L
4.9 mMoL/L

od 4
wwwe Ryaimatim
SAraD Coiouudat

Speic
aeans
av ity= I020
tubid
una{ voume 900 mL/ 24 hour
w ab albumn +tt
Sugan
Ps Cel =
I-3/ hu Pouen Held
RBC 1-2 hPf
oU
ektaUJumavPpitheual olls
A3irn.t
ng Chruc

wncndolted oetes , Hpentemirn9 CtMC Kldney disease

GFR 6uade I (90) ml/mn wwa
Cruati'nun t
6vnade u (60-89) CKD
4S-S
C446)
Gade u
Gnade )
4)IIL
Ma
( so-44)
&vrade -1V CE-30)
6uade (2Is) idney failure
CCK enoft 6ault forunula
wea uwumia A2otemua
Cuatine tJ
Kiduy dysguetiom enythuopoietine A Anenuc

D CCa- 7-11) scond ar pegePalo

Soum P dooneased exbretion ) [ 35-&s Pnaoidiom
Na Diutiomal hpenunocre mua
www vetum 1-S L) Chhonic Kidny disease
tinbid ( due to PuDteim)
bisl&
DA 34 yea OLd Lady fatigue Seuaitivity 09/12/20
+5 4
old
dny n Costipation, Slugasnes
wRgtt 1amPulse4) mu
amd wnex
plaun
BP
1/60 mm1
TSH 39 m I0/L 01S-)JG
TA
m/L (o2-4
cDuspondmg 39 Pienol! t)
Senun eholaenol =273 200
TSI
Pma
6s-
O
TSH
T4 Lo
Thyr
2 pentypoidim TSH L
TLow

31ea ld Lady nemen

ye eye quant dia Sewsih vity to heat
Aloe t02
BP

Blod TS 0-1 m IU
FTA
3.4 1t( Conpevds s0
piee
PAumary nypethynoLs m TSH dfect waly

AAd Yean 0d CwonicC aleoholie emtnqen dept

8 howns hasto o piaotnie
Spa
pain , antismahic au bue

wo 7eut, mauusia vemiting. hsto SHows

ean bacu
00/2
Pane tomM 8P

mm 1St haun AcuTE PANCRITITIS

ESR 2
TLC 2000
nun ouv
lae
Lupaoe
4rd T 2 xarsad du
dystuwcthon
to
6od Paneneatie
aeinas eet
 4 yean mal dinbetit yeons btugat Sudden
4)A
che pon
sha htwIS batt 3 An (Dyspnea)

addted o Smaeinq1 Cigenhates/

d
examnahion, 4emp 9F
Putne 120 Tachycandio

BP sD/a Hy penlensimn
Lab mum
Rep rate 30/
210 mg/d qa
Senum Cholesdenol 309
O Soduration e
93/
ahw mane 25( 28- 20)

Serum eKMB

LDH tst
Tupen T is enctusiely Candiac Specific
Fau a10 -14 daya)

AnemiaL
2/12/20
MCV
80 10o Fn t
MCHC

Micretic <20 Faatuus

Foctigue Shottues of buath
Mocroeyic
Noumocytie BitHte haunaulL
80- Joo
choilon@chea
Amemma due 4o blood oss Gitossitus

nututional A

acute
Cwonuc A
Haemolyie A

Aplasie A

Homaruneqic A
Megaloblashe A
Chand-
IS yeann yol OPD wit min Cplam
amd bttttw paim bm
faigue,brarthlone
wolwA
hinto Famy Ls Stuct Veqetaruam
0

aru lot

0M eam Palo+*+
Pulne
6/ m M
Tewnp notunoal

Lao iwestigahn 57m/dt

fouund m bladd
Plenby f maerocyte

Smean alng yperneamented tphul

TLE 30 2540 m
Platelt l04} tac MeH
CV116 E
MeHe 31-6 d
nmn Ferntin 464
Foue acid al
Vi B12
Macrecytic
MeV 71 amimLA
fervriin d
Macnoeyte NT)

MettotneMate
Penvucious animia

Fe desicouey
Hemoly-tiC eoeyhe annia

ThalaMamua
oww0HUNC
 o weman eooy fatigue mam mens
SA wa alo develmed taote of eotina
eoting la Pica)
she in mot pEAN
3nd Chila 8 ca She doRon't Soe auy 0hstuction
enam Palo ++
muld Spooi f mal (coilanechea )
(Cwnonic
pulne 86
BP
00$0 mm+j platelss 4S0 lae
Lab / TLe S400Me= 34S
bld ichn mete 29 m)a
MLCrUDehe pochnomie forritin=
SHool fon dccut blodd test -ve)

defieiene GTanofenrun Bmdug

Cowacquitwe puanan CapaetyTIBe)S
M damand o
fe uwmet

Inlbaun evos of motolbolom

those enetic @nnons a pertieulan Step of metabolue
blacued
Substnate dueto Parcticula e e/ pruotein
mtaloo ie pottnuoa due
todefeets of Hs enes.
Cotboydrote- 6epqen
Stog dweme
PRotein - Nieunauu's
F Peak diwase
Pe PKO
AULaptomuua
Maple 3yuup we dweaAe
Nucleoi de Less- Nyahan
diome
 ean OL mall Cud PHOsent it enataunt
uwgen C ing fond often). Gnao TUtandohun

amd blesding tendenc Palos +

Puloe 102 mum
BP
Ramd sd Gw = 3
84 46 wunta
mal
unic arid 8.S ei R= a.3
Lwen enlanged
LacHe acid = 19
-12)
T6 Loe 32 Diasnotis
Von Guanue diseane

| GuUucose 6P Cant Cvent Grlucose

HMP
foums ubose amd ibose puewrsD
Punine ucleddhde
mttesis whuch ncuaA)
wwoven aMd
wc acid Snthusus Lncncane
ATP cit+ate
lase Tn t
Clholestenol

6-Pt deposited n wen nlarzed

aloo in Newaus hssue, udmy, lwer

A mortiwo old male chld ubcoisk dineelaakim

SIm for last fe da
ectenus BP /44 mma
Palen +
Pulne
catanat
Lab Ramdm Blopd 6l = 39
Seum 4tal Eiui =2
6al- P
UDP Serum duuc 14
UDP
SUDe-P-undyl rawsfaraae
S6OT 9 IU/L
6alactese
Glu-1-P ShPT 42
3/L
Sal-1-P redueedto forun Salactitot Bad Pfect
UbP &kucose
8au, NT, Kduey
UDP 6lueoxamic acicd wer
 Thu layen chnomactogapig Sample

A old male cild VIAit OPD

pheAnuted
muend eephaly,
qtsal devolep omtal dlay, ke R foeal
P0 vouai pereeption popigmente d Seal
hain Sensnce
TLe F wun

Stama wtewi CoveApondm to Phe alanwe

LC of PlaomA= phwe atanue bond

feels ast of une Shoos3

Guetre's test is

Ph Ketonena
Ph alaune hydnox ylase
doiem h aclate
Ph Butynae
D
Ph alanna Tyosv Ph Pypuwode

evel 0es 20 Best mauesn o

morumai 1-2 /au) diagnasis

uuthue's taat- Baellu Suotin Lm

media f Phul alanine

Defcwey 8f THBP HeduckaAe d aloo Caune o

PLoduCm osu

phe alane accumulodes Banmuerndcuphaly,ohal...

1potophan to Senotou TUaurws hgdnoblose and THBP
THBP
defieut
yBexeAirh d (Cvalitdine&mi auHadntkalrr

5 ML nil moapw

sutio

yelrd-orn bitknad pht.

Tocti A the stant oduug
sa
C- O
li OH

Cwdial
Rmainu GPJ
Cus Eudiol
2eoH
tyata PP RA Ppi

mcble. o ns wdhel=

1 m nple Te) o mL dshullud nlezr

CCod )
piwe bulhur
Sulpur pandes áinks sulphupeveler fot

ci -A kilu énts uwer +h sur Henian

so slphar sinks,
ter
Dled
Bined To s ro prolein
m bumpl

2 mL 10'|, NoHoh salh

2 dmt a CuSoy

shapun

aih vieucalours

PAPHd bends

Piiniple
: 0-H

H
.

N
-N- TYedim

Paehae
ble N
O-14

Vial eolous cOmn.

a pesihw ust ini knnd gAnt im soy

w
 mple haned

e drt a Lacia ocete rid

Phole
inpa
Heatmg uils iserg anisrin
stetcla hains
wnAiug ekol
PPt
etie anil dsalu bhapnn
PRALt

Fuareid

les msisibu.yvAbneiA
aunb M
5-10 aldl (hnee)
tbe. idudiladlb-30ma
1L
Bnzine deg- A
r bloe d
m Aample

beild 2 mis

e ds Bunzi dim gsr odels.d

Blwsnamtn Bram alour

Pineipl- H a hlrd and nBts both hana RT dA
prodna- d tnbl

hasctLo

calours vealpur

bongler bailim ha pardaaa nehib a nes

Abnltis urnid od.
 5 mL AAnl
aedTsalud
brunt 0- onuum supuie

bodiunm wilooueide

wcnaded. amnouia oder nddss And

peo n brdy puA

Piweipls
bn brdinm witropmasida und kelo np aetuna bod
rs 4hing-thumidbodum-iso- nitrakro-pado
 ANALYSIS OF MILK
Introduction
Milk is a complote lood with all nutrients needed by
mammals.
Composition
1. Proteln: (a) Caseln A conjugated phosphoprotein, (b}
-

Lactalbumin. (c) Lactoglobulin

Carbohydrates: (a) Lactose -chiefty
Lipids: (a) Tngiycerides with short
and medium chain fatty acids, (b) Cholesteroi,
4. Vitamins & minerals : Calcium,
potassium, sodium, magnesium, phosphate, chloride. Foor
Iron. Rich in vitamin A, D, B2, B,, C (human n
milk) but human milk is p0or in vitamin K.
Physlcal characteristics
1.pH:6-7
2. Specific gravity: 1.028 1.034
3. Colour: White

Chemical analysis
Protein is precipitated by isoelectric precipitation method
of the precipitale is analysed for protein
at pH 4.55 by 1% glacial acetic acid. A. Ha
as described in chapter2. Remaining precipitate is mixed
concentrated sulphuric acid. All other
organic substances are charred only fat remains unarected.
win
That is measured. B. The fitrate is subjected to
analysis lor lactalbumin and lactglobulin by the testsS
for protein (described in chapter 2). Presence
of Lactose is tested with Benedict's test, & connrmed
with Osazone test etc.

ViVA QUESTIONS AND

-
ANSWERS
1. Percentage of carbohydrates In Indian diet?
A. 60-70%%
2. Which carbohydrates do not give positive
test with Molisch reagent?
A. Aminosugars
3. Why amino sugars do not give positlve
test with Molisch test? What are amino sugars?
A. Sugars containing-NH, group
in their structure are called armino sugars. 2 types
(a) Glycosylamine (AnomericOH group Is replaced by NH, group.)
-

(6) Glycosamine (Alcoholic 2-OH group is replaced by - NH, group.)

Presence of amine group prevents dehydration in Molisch test.
4. Other tests having same reaction principles like Molisch?
A. (a) Anthrone test, (D) Seliwanoff's test. (c) Bial orcinol
test
-

5. Which reagent can be used alternative to a-Napthol (5%) in alcohol

in Molisch test?
A. Thymol. Advantage of thymol is that, its solution do not deteriorates.
6. Whatare the substances other than carbohydrates can give posltive reactlon withn
u-Napthol (5%) In alcohol/ Alcohol1?
A. All aldehydes, all furfural yielding substances, acids like - formic, lactic, oxalic, citric acids and
Acelone,
7. Sensitivity of Molisch test?
A. Very sensitive,can give positive test with solution of 0.001% glucose and 0.0001% sucrose solution.
8. Benedict's test is called as sem-quantatlve lest. Why?
A. Green colour of solution after boiling indicates presence of
reducing sugar upto 0.5 gm% (+), Green
precipitate indicates-0.5-1 gm% (++), Yellow precipitate means 1-1.5 gm%
(+++), Yellow to
3
 means more than:2g
gm% (++++), and Brick red precipitate
Orange precipitate means 1.5-2 am%
determine the amount
present. So, by seeing the colour we can approximalely
reducing sugar is not accurale.
of reducing sugar in the samplo though
Fehling's test. Justify.
9. Benedict's test is more sensitlve than
A. See Table 8 for answer.
in Barfoed's test?
10. Why acidic medium is used med
reducing sugars are weakly reducing in nature. BesIdes in acidic
A. In acidic medium Hence within min boiling tim
1

monosaccharides can reduce more rapidly than disaccharides.

disaccharid
monOsaccharides reduce Cu". But il the reaction continues for longer time then des
only will reduce Cu".
Wi get acid hydrolysed and resulting
monosaccharide
11. Princlples of Benedict's test, Barfoed's
test and Fehling's test.
no. 3 & 4).
A. See text for answer (also see table
12. Principles of Seliwanoff's test and Molisch's test
are same. But in case of Molisch's test no
30 secs. Explaln.
bolling Is required but in case of Seliwanoff it ls requlred for
-

A. In Molisch's test conc. H,SO, is used to dehydrate

carbohydrates. But in case of Seliwanofs
It is the boiling wnich helps HCI to
test it is the dilute HCI having low dehydrating capacity.
group. But
dehydrate the sample. Keto group more actively atacks resorcinol than aldehyde
test because aldoses
if
the boiling Is continued longer then aldose will also give false positive
will get converted lo ketoses by the HCl.
13. Can sucrose give positive test with Seliwanoff's test?
A. Yes. If boiling is done for longer time the acid hydrolysis of sucrose gives glucose and fructose
The fructose then gives posifive test.
14. Why colour ot starch and dextrin are different after additlon of iodine in Kl to different solutions?
A. Dextrin is the partial break down product of starch. The colour of iodine (brown) is turmed bluein
starch and reddish-purple in case of dextrin. lodine gets adsorbed on the surface of the starch or
dextrin. As the length and branches dififer in dextrin from starch-also the visible colour also ditfers.
15. Composition of Benedict's qualitative and quantitative reagents, Seliwanoff's reagent, Barfoed
reagent, Fehling's reagent and Molisch's reagent.
A. See text (Table 3, 4, 8 etc.)
16. What is the role of sodium cltrate (Benedict's reagent) or Rochelle salt (Fehllng's reagent)?
A. They acts as stabilising agent, maintain pH of the solution, keep CusO, in solution and prevent
Surtace oxidation.
17. Amadori's rearrangement occurs in Osazone test. Name another test where Amadori's rear
rangement occurs7
A. In case of Glycation of N-terminal valine residue of f-chain or e-amino group of lysine of p-chain or
a-chain of Hb, Amadorn's rearrangement occurs. HbA (also called HbA,) is 97%, HbA2-2.5% and
HbF-0.56. After glycation HbA, is 3 types: HbAta-I is again 2 types. HbA1at-Combines with
Fructose 1, 6 bisphosphate, HbA1a2- Combines with glucose 6 phosphate. HbA-Combines
with pyruvate. HbAte Combines with Glucose (B0%). 1% glycated Hb represents 25-35 mg%
average blood glucose change.
Amadori's rearrangement in Glycation (Non enzymatic attachment):
HDA

NH2 +O=C-H H-C=N-HbA H2-C-NH-HbA

H-C-OH HC-OH
Amadon's
Rearrangement) R
N terminal
of beta chain Glucose Aldimine (Schiff base) Reurnine
 Amadori's earrangement in Osnzone test:
HC-O HC-N-NH- C.H, H-C-N-NHC,H,
HCOH C-OH 2 C N-NHC H,
HO-Ç-H HO-C-H
OHHN-NHC HO.H--OH-2H,N-NHC,H, H-C-OHNH, CHNH,
enyyd'azine)
H-O H-C-OH H-C-OH
CHOH CH,OH
CH,OH
(D-gcose) (D-glocose phenythydrazone) (D-glocose phenytosazone)
Intermediary Product End Product

NNH-CH, H-NH-NH-C,H, H-C-NH-NH-C,H C-NH-NH-C,H, CMNH,.cNH

H-OHJmadori C-O HH-NH-C.H,
Rearangement
R
c-M-C C-NH-NH-CH,
CN-NH-CH

HO-HO
3
HO -HN-N-C NH, O
H,C-HN-N- HC.-HN-N=C
(Phenylosazone)

18. Define Glycemic index.

A. It is the measure of the ability
of a food to raise the blood
with equivalent amount ot glucose or a concentration of glucose as compared
reference food ike boiled rice or white
19. Why glucose. fructose and mannose glve
bread.
Is Lobry de Bruyn Van Ekenstein
same needle shaped crystals in Osazone test? What
transtformation?
A. Glucose, fructose and mannose
ditter to each other in its first two carbon
are same. Now 2 molecules of phenyl hydrazine atoms. Remaining parts
attack the first two carbon atoms and forms same
crystals
Glucose, fructose and mannose are interconvertible
by intramolecular rearrangements in first two
carbon regions. This rearrangement is called Lobry
de Bruyn Van Ekenstein transtormation.

H-C-O H-C-OH CH,OH

H-C-OH
OH C-O
HO--H HO-6-H HO-C-H
H--OH H-C-OH H--OH
H-C-OH H-C-OH H-C-OH
CH-OH CH-OH CH-OH
Glocose Fructose
1,2 enediol form (intermediary)
Fig. 4.1: Lobry de Bruyn Van Ekenstein Transtormation
 VIVA QUESTIONS AND ANSWERSs

1. Conlirmatory test for protein identification?

A. Buret est.
2. Prlnciple of Biuret test?
A. See pninciple soction of this chapter.
3. Why this test is named as Biuret test?
A. Heating 2 molecules of urea at 180°C gives a compound called Biuret. This compound
On
reacting with alkaline Cuso, gives violet complex.
NH, HN

NH NH HN
*******

***.
Cu NH,
CU
== OH' NH,

NH,
NH

NH, H,N
Biurel-Formed by
heating 2 urea Violet complex with alkaline Cuso,
Similarly protein also gives same reaction positive as it has consecutive peptide bonds mimicking
Biuret (NH,CONHCONH,)
4. Can Biuret test be false positive?
A. any of the following bonds are present in a molecule in two or more consecutive positions
other than peptide bonds, the Biuret reaction will be false positive.
NH
-CH-NH,
-C-NH- -C-NA, -c-NH, -C-N,
5. Why Biuret test is called confirmatory test?
A. As this test identfies peptide linkages, positive for all kind of proteins whether primary or seconday
6. Principles of Esbach's test, Heler's test, MIllon's test, Heat and acetic acid test, Xanthoproteic test
A. See text of this chapter.
7. When the frothy white precipitate appeared at the top of the test tube in heat and acetic acid
test disappears on addition of acetic acld?
A. When the white precipitate is due to presence of phosphate in the sample instead of protein.
8. Denaturation of protein destroys which of following structures of protein?
A. Secondary, terliary and quaternary structures but primary structures are preserved.
Discuss the differences between Denaturation, Flocculation, Precipitation and Coagulation
A. See text of this chapter.
10. What is Complete Protein? What is Incomplete Protein?
a
A. a. Complele prolein is protein contains all 10 essential amino acids in necessary propori
by human body to promote growth. It is also called first cass protein. Their biological value s
high. Example Egg albumin (biological value = 95), Milk casein (biological value =
D. Incomplete or poor prolein lacks many essential amino /
acids. Plant proteins lack fe
essenlial amino acids. Example: Cereal proteins delicient in lysine, maize protein lac
tryptophan & ysine, wheal lacks lysine and threonine etc. But if cereals are taken w
 released on exposure to for
Y-globulins
antibodies Anlibodies are
:

precipitate the sneProte

() By specific type of antibody may bind to and
diseases lik anti
called antigens. Each clinicaly in treaing
produclion. This is ufilised anlibodies against the respeci.iphth
which induces Its containing Oacte
telanus wilh specific anlisera an inactivated toxin (toxoi
and
vaccination with an antigen hke antidodies which may
antigens. Similarly, production of specilIC recipitatethe
attenualed microbes induces the subsequent iniection. A protein may also be
a
same specific antigen in case of immuno-eleciropnoresIs,
containinodrate
Usinganisera containing
sample by specific
from a biological
particular protein.
antibodies which precipitate that
13. What is salting in of protein?
ot many proteins like gle
A. This is the increase insolubility (or
stability of the colloidal sol) ins
electrolyte ions. () In a dilute solution of a mineral
in presence of traces of small he
of its lons may lead to the prelerential adsorpion of only a particla icular ype
low concentration
ine ike cnarges on protein
of electrolyte ion on the protein particles; this increases es
the aqueous medium. (1) Adsorbed electrolyte ions may
and keeps them dispersed in

wilh surface counterionic groups of protein parlicles

to suppress anlagonistic surface chC
of the particles. But
lowering there by mutual elecirostatic altractions and aggregatons more
concentrated mineral salt solutions may precipitate a protein (saing out)

14. Name some denaturing agents.

A. (a) Acids or akalies change the pH and there by affect electrostatic and hydrogen bondt
belween polar groups of protein to uncoil and denature it.
) Urea decreases hydrophobic interactions between non-polar groups of protein to destabilza
its higher structures and denalure it.
(CWeakypolar solvents like acetone and alcohol also lower hydrophobic interactions between
non-polar groups of proteins to uncoil and denalure them. Moreover, such
solvents do not
have lower dielectric conslants than water; nor do they Torm as
water because they do not get hydrogen-bonded witn polar groups ot
efeciVe solvation layers as
proteins that easily
(d) Sufficiently high concentrations of electrolyte
ions, particularly the divalent and multivalent
metal ions, denature proteins by their salting out'
actions.
(e) Freezing may denature proteins in a solution
because the formation of pure ice-crystals
raises the electrolyte ion concentration in the remaining
solution, resulting in salting out
action; cold also weakens hydrophobic interactions
to destabilize their native contformations. between non-polar groups of proteins
() Heat denatures and coagulates proteins by
disrupting the electrostatic and hydrogen
that stabilize the higher orders of protein bonds
structure. Rate of rise in protein
heat amounts to hundred folds of that in denaturation by
however, requires heating far other chemical reactions. Thermal
above the body temperature of denaturation,
the relevant protein-protelns Irom the species normally carrying
a relatively low temperature.
a species with a low body temperature
Thermal denaturation depends are denatured at
and is often irreversible. also on the pH of the solution
15. Name the branched chain
amino acids.
A. Isoleucine, Leucine
and Valine.
16. Amino acid contains
thio-ether bond?
A. Methionine.
17. Heterocyclic amino
acids.
A. His and Trp.
18. Name some derived
amino acids.
A. Onithine, Citruline,
Homoserine, Homocysteine,
19. Guanidinium, Benzene Hydroxyproline, Hydroxylysine.
and Phenol groups
A. Arg. Phe, Tyr are present respectively
respectively. in?
20. Indole, Imidazole
and Pyrrolidine groups
A. Trp, His, Pro respectively. are present
respectively in?
54
 ABNORMAL CONSTTUENTS IN URINE
TESTS FOR
Observation Interence
Experlment
() Sinking sulphur
for bile salt: Hay's () Sulphur powder over test sence ol bile salts denolesoles
Test surface tension solution sinks to the bottom. as bile pre
Sulphur lower the surface tensionsalg s
test 10 sample
ml of
solution. So bile salt is preso
solution and distilled water distilled (i) Distilled waler acis
are taken in two different (i) Powder over the as cont
beakers. A pinch of sulphur Is water floals.
sprinkled over two beakers.

V
FIRST PROFESSIONAL & INTERNAL ASSESSMENT QUESTIONS FOR MBBS (10YEARS)

Write notes on 3x2=6

1. Proteinuria,
2. Bence-Jones proteinuria.
wwwwwwwweo eeedeNes0eeADASAAeAAeeeeck
wwwww ww ww w.a owwwwm
0O

VIVA QUEATIONS AND ANSWER

1 why Benzidine test the sample is bolled first?

In
In blood both Hb (in R8Cs) and WBCs have peroxidase like activity. Now in urine even
when
blood is not present, patient may pass some pus cells.or wBCs. Now this WBCs can give a
positive result with Benzidine reagent due to peroxidase ike activity of WECs. But the peroxi
acfivity of WBCs are heat labile and of Hb heat stable. So after boiling the peroxidase activt
WBCS will be lost. Now only Hb peroxidase will give positive result.
2. What are the other tests that can be performed to detect blood in urine or any other samples

A. Ortho-tolidine test, Guaiacum test, Gregersens test etc.

hat
AWhat is the risk of doing Benzidine test? Why glacial acetic acid is added?
Benzidine is çarcinogenic, So it has to be handled wearing gloves and mask. Glacial
acetic acd
& heat are likely responsible for hemolysis of RBCs and making
Hb free for peroxidase aclivity.
Which test is more sensltive - Benzidine or 0-tolidine or Guaiacum?
A. O-tolidine test is more Sensitivity to Benzidine test. Guaiacum test is a
less sensitive test in respec
of both Benzidine and O-tolidine. The sensitivity of Benzidine
test varies with the concentrao
used (10% or 5% or 3% or 1% in glacial acetic acid with different sensitivity). O-tolidine tes! ras
comparable results with 4%, 1.2% and 0.4% solutions.
sMost sensitive test for detecting blood in test sample?
MicroscopIc examination when intact RBCs are present.
Ls Why the positive test of Benzldine turns green to brown?
A. Due to oxidation in air O
7. What is Guaiacum test?
A. A presumptive test for blood, one of the first developed
but no longer used. It relied on gu Um
(a resin isolated from trees) in combination with
hydrogen peroxide. If a stain turned ou when a
treated with these reagents, it was considered a positive
126
result indicative of blood. o
 presumptive
nresumptive tests, tne resuils are not conclusive, nor
with Al do they prove that the d0a s
s
human
test and Guaiac test are same test? Other
acum te uses of this test.
Gu stools ol quaiac test or guaiac fecal occult
blood test (OBT) is one of several methoos
Yes he presence ot tecal OCcult blood
me which is blood in the feces that is
at de
eye
naked average
Though the Fl (recai inmunochemical
test) is prelerred here. even the
ivisiDe to
ge risk populations may have been guai
sufficient to reduce the mortalty associarE
testing of by about 25%.Vih this lower
wth
elficacy. t was not always cost effective to
Large population. ine term guaiac denotes the narme of the paper sutace USE
ree which has a phenolic compound, alpha-guaiaconic
acid, that is extracted trom ue
the e ot Guaiacum trees. Also t can be used to detect occult blood from other sES KE
etc.
causes of Hematurla? when there may be false positive
What are the hematuria?
divided into (a) Pre-renal, (b) Renal and (c) Post-Renal causes
A enal () Hemorrhagic diathesis (ldiopathic Thrombocytopenic Purpura Leukemia. Chronic
iseases. Vitamin K Oencency. Ant-epileptic drugs, Scunry. Dengue, Vasculotoxic snake
tc.),(i) Excessive anncoaguian tnerapy (with Warfarin, Dicourmarol etc). etc.
(0) AGN.
Fenal l (i) Rena fubercHosis, () Neoplasm (rv) Malignant hypertensIOn.
Nephrolithiasis. (v njuny. (Vin) Collagen vascular dsease etc
(Urinary tract intection). ) Urofithiass, ()Cysttis,
enal U
N) Carcinoma. (vi) irauma. (vin) of
() Pyetts
apiloma bladder. (vii) Benign Hypertrophy of prostate
Rupture of urethra. (x) Iraumatic cathetarisation.
Dunne menstruation in temale, there may be false positive henaturte tound. so atways in lema'e
menstrual history must be taken.

A lanat
are the causes of hemoglobinuria? (6) What are the causes of myogiobinuria?
E How to differentiate between hematuria and hemoglobinuria?
Blood transtusion. Black Yater fever (in falciparum malaria).
a) () Acute causes Mismatched
-

Rh incompatibility, Primaquine tntake tn G6PD deficiency, Favism, March hemoglobinuria,

Eciamptia. Burns, HUS (haemolytic uremic syndrome). Paroxysmal cold hemoglobinuria.
hemogobinuria). Cold
Snake bite etc. (i) Chronic causes PNH (parorysmal nocturnal
Hemagglutination diseases.
(b) 9 Acute myocardial intarction, (i)
Infarction of skeletal muscles, () uscde destructions due
(3) electric shock, (4) trauma.
to-(1) Crush injury. (2) heat stroke,
RECS will be found.
ey microscopy of the sample. In hematura intact
semiquantitative".
Explain: "Heat and acetic acid test is test
test or disappeared after addition of acetic acid suggests that the
No turbidity in the aboveappears after addition of aceticacid, then it place he test
tuDE
S (e). When turbidity and persist
on it the nsibitity ot the leters are considered
a
againsi white paper with some letters are written
as folliows
concentration:5- 10 mga (trace)
and can be read with
Leners are visible
identified: 10-30 mg'd (+)
LEters are seen but cannot be mga (+)
are blurred but the page is faintly Visible: 40-100
Leuers
mg/dt (+++)
Paper cannot be seen: 100 500 bottorm of test tube >
1gm'at (++++)
coming to the
EVY turbidity with precipitate amount of protein present by Seeng
the tuiroidity.
E can have an idea about
the
How to detect Bence Jones protein"? sampie o
Bence Jones prorein in the suppbed
detecting immunoglobulins excreted
methods are available for
erent multiple myeloma. Bence
Jones proteins are ighit chain
Ced
Ough urine multiple myeloma. sample is placed in a waterbath. The
temperature of the
in
(Confirmatory test): The start appearing and
increases gradualy 727
precipitates
est
aErbath is increased
gradually. At 40°C
 disappear when Ihe temperature
upto 60°C. After that the white precipitales
is
temperature below boC precipitale reappears and Crea
further. Again with decreasing
disappears below 40°C. These peculiar
characteristics only seen with Bence Janen
Bence Jones gan a
protein
globulin starts precipitating between 60°C 70°C.
Flasma albumin. to Heller s est. 5urne reagent is conc. HC.
(b) Bradshaw's test: This test is similar
of HNO3. A ring appears at the junction of two liquids. It can give positive result
Jono
in placo
dlbumin
in case of Bence Jones
But further dilutions of sample also give positive result prote
also.
what are the causes of Protelnurla"?
13 is Albumin except in case of multiple mnl.
A proteinuria main protein that usually excreted
In yeloma.
It
may be (a) Physiological and (b) Pathological
(on standing - orthostatic Orotot
Physiological causes of protelnurl () Postural (V) Massive exercise
einu
trimester of preghancy,
MExcessive cold water bathing. (i) Last
Pathologlcal causes of proteinuriá:
(i) CCF, (i) Fever, (ii) Severe anemia,
(v) High intra-abdominal
(a) Pre-renal
(V) Pre-eclampsia elc. (vi) Hyprtension, vil)Dehydration.
(D) Henal -WGlomerulonephritis, Nephrotic
syndrome, (1) Hypertensive nephropathy
(v) Pyelonephritis, (V) Diabetic nephropathy, (vi) Henal
cell carcinoma, (vii) Kidney i
(Vin) Analgesic and lead nephropathy, (ix) Multiple myeloma, (x) iereditary
nephropathy. (xiGOuty
nephropathy, (xi) Hypercalcemic and Hypokalemic
nephropathy etc.
UTT, (V) Urolithiasis, (v)
UoPost renal () Carcinoma of bladder, (i) Prostatitis, (i) Carcinn.
oma
of prostate, vi) Trauma etc.
M4. What is the normal maximum daily excretion of protein In urine?
A. Maximum 150 mg /day protein can be excreted.
15. What is Microalbumlnurla? What are the conditions in which this occurs?
A. When urinary albumin excretion is 20-200 ug min or 30-300 mg24 hours or 30- 300 mg' gm
of urinary creatinine the condition is called Microalbuminuria. True albuminuria occurs when
urinary albumin excretion is more than the above mentioned values. And normally urinary
protein level is « 20 ug/ min or 30 mg/day or 30 mg/gm of urine creatinine (Called absent urina
protein).
AJsually in early stage of Diabetes mellitus with nephropathy- microalbuminuria occurs.
V16. What ere the reducing sugars other than glucose abnormally excreted in urine?
A. Fructose, Lactose, Galactose, Pentoses etc.
17. What are the other redusiog substances.other than carbohydreates?
ASalisyluric acid, Salisylate, Uric acid, Glucuronate, Creatinine, Homogentisate etc.
r8. Causes of galactosuria?
A Occasionally during lactation, in Galactosemia.
TÍ. of Fructosuria?
Causes
A. Excess intake of fruits, honey, jam, syrup, in liver disease, Diabetes mellitus, in Essental
Fructosunia elc.

t20 Causes of Pentosurla?

A. Xylulose is excreted in Essential Pentosuria, in excess cherry, plums intake.
t1. What is sucrosurla? tonert
A. Sucrose may be excreted in urine in Pancreatitis, Sucrase deficiency in small intestine, Or n
gastrointestinal abnormalities in infants. Benedict's test remains negative till the urine is boi
with acid. After which it gives both Benedict's and Seliwanoff's
test positive. Specific gravuy
abgve 1.040.
,22/When lactosuria appears?
A. Last trimester gf nragnanGY and in lactatin0 thor A Io
 renal threshold for glucose?
Normal
180 mg'dl
tis uss the causes of glycosuria.
D ceS are broadly clasSmed into Iwo groups as follows-
Tne crtycemic Glycosuria (Gucosuria) -
(a Emotional Due o synpanec stirmulation
f Alimentary: Excessive intakeof carbohyarales
of nerve to liver, splanchnic nerve.
(0techolamine induced glycogernolysiS direc
)Endocne disorder Drabetes melitus,
Othroidism, Acromegaly. Cushing syndrome, Glucagonoma,
ytoma. Severe ver disese etc (w) Other causes Intection, Hyperpituttarism, PneocnrO
Glycosuria (Glucosurna) (0) Heredtary
-
anesthesia, asphyxia elc.
Due to absence of some carrier proteins.
)Acquired: Renal tubular disease, Heavy metal poisoning
threshold (Physiologjical in Fregnancy). (Pb, Cd, Hg), Decreased rena
Fanconi's Syndrome. Experimental in Phlondzin
glycoside administration.
one
Nameone condition where Benedict's test is positive
25. but the urine sample on standing turns
black?
tn
Alkaptonuria Homogenisic acio is excreted through urine which can
Benedict's test positive. And on standing reduce alkaline CuSO
and give turns black due to oxidation.
Aseslly 10% NaOH Is Used in Bluret reagent. But in
case of Urine examination we use 40%
NaOH. Why?
A To neutralise urinary organic and other acids.
27. eme the ketone bodies.
A Acetoacelic acid. Acelone, -hydroxy-butlyric acid.
28. What Is the normal level of ketone bodies present In urine
and blood of human being?
A. In 24 hours urine t IS less tnan 100 mg and usually
in most ol the times less than 1 mg. In blood
itis
usually less than 1mg/al but may be upto3 mg/dl.
29 6ntch ketone body ls present in highest
amoun1?
A. Usually B-hydroxy-butyric acid
is present about 78%-80%, Acetoacelic acid 20% and Acetone
1o-2%.
30. Deline Ketosis,
Ketonemia, Ketonuria and Keloacldosis.
A Ketosis :Accumulation of abnormal amount of ketone bodies in
tissues and body fluids. Uinary
excrelion of H-hydroxy-butyric acid may exceed 200 mg/day.
Ketonemla: Rise of ketone bodies in blood above normal level.
Ketonuria: When blood level of ketone bodies exceed renal threshold (70 mg/di).
they aree
excreled in urine and the condition is called as kelonuria.
:
Ketoacidosis As Acetoacetic acid and -hydroxy-butyric acid are acid in nature, they gradually
decrease alkali reserve of the blood and other tissue iuids and also pH level resulting in
ketoacídosis.
What are the causes of Ketoacidosis
&.
Starvation (ii) Diabetes mellitus (ii)
High fat diet (iv) After severe exercise (v) Toxemia in
ancy (vi) Alcoholic Ketoacidosis, (vi) Severe carbohydrate restriction, (vii) Anorexia
ervosa, (ix) Prolonged fast. (x) Salicylate ioOXICity.
Why Ketoacidosis occur in Diabetes and Starvation?

. ketone
A Explangidn is
available in Chapter 15
bodies are synthesised? Why ketone bodles are not metabollsed In liver
Ihough synthesised?
Bver. Dyeto deficiency of Thiophorase enzyme
A har ne tests to be performed to detect the presence of ketone bodles In urine?
ohera's test, Gerhardt's FeCl
test 129
 J5. What is the principle of Rothera's test?
chapter.
A. Seoinference section of Rothera's test of this
6Why (NH.):SO, Is added in Rothera's test? groups. any
A. Peptide bonds of proleins also have keto
I

prolein is present in urino

nonera s reagents, S the
keto group ol peptide bonds will also give taise postve
teSt wI
Sointaly
Saing Out done with (NH,):SO.
i
37. Can Rothera's test give an idea about the
amount of Kelone bodiles present?
ot ring we can develop an idea ah
Rothera's test is highly sensitive test. From the intensity boulhoa
much ketone bodies are present as follows -

No change in colour: Negative

Pinkish ring : (+)
RedDeepring: (+)
purple ring: (+++)

38 Drugs which can give false positive results in Rolhera's test?

A. Levg-dopa, Phenylpyruvic acid, Paraldehyde. Pyridium. Phathalein.

U3What type of toxiclty may occur if accidentally Nitroprusslde solution is swallowed by a

student?
A. There is chance of cyanide poisoning _and methemoglobinemia. As the Nitroprussideo c
cause
Cyanide and due to Oxidation of Fe of Hb, t can convert t to Fe torm. also can
It

Hypotension.
40Whlch test is avaliable for detecting B-hydroxy-butyrle acid?
ANo direct test is available for detecting p-hydroxy-butyric acid. B-hydroxy-butyric acid is negat
for both Rothera's test& Gerhardt's test. But if the urine solutton is boiled with H.0, - then
Rothera or Gerhardt's test is done then they will give positive result with ß-hydroxy-butyric acid
41. In what other conditlon FeCly is used as test reagent?
A. In phenylketonuria (PKU) FeCh is used as test reagent and Phenylpyruvate gives dark
gre
colour. Guthne's test can also be performed by heel prick in a newborn to detect PKU
42. When FeCl, test is posltive?
A. It gives purple colour with Acetoacetate, Salisylates, Phenol and Antipyrine. In PKU it gives
Gree
colour not Purple.
43. Name the dry chemistry methods to detect Ketone bodies.
A. Acetest (Dry Nitroprusside powder is used), Ketostix (Dry Nitroprusside powder
and glycine).
Direct method to detect -hydroxy-butyric acid?
A. Salicylaldehyde methods, Blacks reaction.
C 45 Name the bitle salts.
A. They are sodium and potassium salts of taurocholic and glycocholic acids. They are formed in te
Liverfrom cholesterol. They help in absorption and digestion of fat and reduce surface tension.
4Principles of Hay Sulphur test?
A. See the table. Urine preserved with thymol also
has reduced surface tension & may give tas
positive result.
47. Name another test which can detect Blle salts?
A. Pettenkofer's test. This test is less
sensitive than Hay's lest. Can give false positive resuis na
protein and other urinary pigments.
48. Causes of Pyurla?
A. () Urelhritis, (i) Pyelitis, (i) Prostatitis, (iv)
Pyelonephritis, (v) Kidney abscess.
tuberculosis ()
 of
presence urobilinogen In urine?
ol high

CAUSs ol liver, () Carcinoma O Iver, (n) Hemolytic Jaundico, (iv) Intoctive hepalitis (Preictoric
9 Cutto Feve
v) Fever. (vi) Constipation, etc.
pase).
Urobilinogen is sent?
ab
aWhen ma of the head ol pancreas. () Common
Cinoma bile duct stone / impacted in ampulla of vator.
rine
How spot
sample can be subject lo dry strip
test for detectlon of albumin7
used delect
to prolein in spot urine.
Atbys is
A in urine ls estimated
2
HO w 24 hours protein
Esba
in Esbach's AlDUminomeler by Esbach's
ured in
measured reagent.
A. M5
body and sugar in uine be measured by dry strip
test method?
elostix
Yes. K or acetest utilise Sodium nitroprusside powder, and glycine or aminoacetic acid and
*disodium phosphale to medsure kelone body.
Glucostix medsure giucose by Strip method
tests for determination or bile plgments (like bilirubin) In urlne.
niccUSS 1he
Foam test (shake the urine in a lest tube if the top is yellow bile pigments are present).
-

s
Gmelin's test. (c)Smitn test, (a) Foucher's test, (e) Diazo test, () Iodine ring test.
hGmelin's tes!: 10-20 mi ol uine med & acidilied with 1-2 drops of dil HCI. Then drop of conc. 1

HNO- green Due violel red- reddish yellow

ic)Smith's test: Dilute uncture 1Odine 9 lumes of its volume with Alcohol. Overlay the urine with
diuted lodine solution-Green ring at ihe junclion Bile pigment.
Fouchel's test (Harrison spol lest)-Fouchet's reagent: (a) Trichloroacetic acid -25 gms,
(b) 100 ml distilled waler, (c) 10% Fecl Solution - 10 ml. For test we need 10% Barium
Chloride Dissolve 10 gm. Barum chloride in 50 ml for dist. water and make the volume up
to 100 ml.
Procedure rake 3 m urine and add same quantity of 10% barium chloride in a test tube.
Mix and centrifuge. Discard the superannuate fluid and add 1 to 2 drops ofl Foucher's reagent
to the residue in the test lube. A greenish blue colour is obtained it ilinubin is present. Il the
bile pigment concentration is increased in the Urine we can report with the intensity of green
colour as trace,(+).(++).(+++).
Principle: Banum chloride precipilate phosphate, sulphate anions present in urine which
may interfere ith the test. FeClh oxidize bilirubin in presence ol trichloroacelic acid to green
biliverdin.
55. Discuss the tests for determination In urobilin or urobilinogen in urine.
A la) Schlesingers test, (b) Ehrlich's aldehyde test
56. Discuss the presence or absence of blirubin and uroblinogen In ditterent types of Jaundice
conditions.

Conditlons Urine blirubln Urine urobillinogen

Obstructive jaundice +++ Negative

Hepatic jaundice +/[ ++
Hmolytic jaundice Negative +

Kame one polysaccharide that may come in urine

A.
Inulin
me the bile acids. What are blte salts? Name two tests for bile salts. Fate
of bile salts?

Glycocholic, taurocholic, chenodeoxycholic acids. Secondary Deoxycholic and

hy: bile acids. Two tests are Hay's sulphur
oOcacids. Bile salts are sodium or potassium salt of
is excreled through stool (max. 400
mg/day).
Raetoeenkofer's test. Only 1% of total bile salt
**o s reabsorbed from intestine to liver by enterohepatic circulation
131
 is added 1o Duler solution
a there w
will
Thus if a small amount of base present. I
he addition of acita rise
the equivalent expense of amount ol weak acio of salls. Now it icie onvers ersey at
more weak acid at the
expense ol equivalent amount clear
D om valpre.
irom
or tne soluuon but the amount is ericallytheat
there will be a definite change
in pi added to the
concenlration ol H and OH ions Solulion. so Sman
In comparison to the range The
of pH for a bulfer extends
roughiy over a ph ol 1 around the
Dy Van SIyke's bufter
pka enectie
tat
acid nurtte.i
capacity of a bulter to resist p changes s
inoicare
or monoacidic base is roe hieh
of a strong monoDasic acid ich ar
the number of moles Dy 1. Hence a more concentrared to
1 litre of the bufler solution
to change ils pH butfer be
a smaler change in H concentration has
buffering capacity and sulfers
tiz
Anion Gap
Sum ot measured cations (Na 4 K
Anion gap is the difference between the 95%
cations) and the sum of measured antons
(HCOG+ U= 86% of the total anie
anions). o
is constituted by the unmeasurable anions presert
m ne Diood. Anion gap can sd
n can express
be
follows-
Anion gap (with K') = (Na* + K) - (HCO, + Ci)
Anion gap (without K) = Na' (HCo, +C)
Delta Anlon gap (without K) = [Na"
- (HCO, + C)] - 12
So, Delta anion gap = Calculated anion gap- expected anion gap
or Measured anion gap- Normal anion gap (12 mmoin
NolL)
WNomal anion gap = 8 12 mmolL
* 2)
ACauses of increased anion gap (>12
(a) Metabolic acidosis with increased unmeasurable anions: (PO, SO, Proteinr 24
() Ketoacidosis, (i) Lactic acidosis, (ii) Alcohol, (i) Salisylate, (v) Elhylene
(vi) Hyperalbuminemia. (vi) Uremia
(b) Deoreased unmeasurable cations (Ca*, Mg2* = 7 mmol/L):
)Hypomagnesemia, () Hypocalcemia
BDecreased Anion gap
mmoll: ) Decreased anions-Hypoalbuminemia, (i) Increased cations: Hypercaltema
8
Hyper-magnesemia, Hypergammaglobulinemia Muitiple myeloma), Li, Bromide toxicity
CNorma Anion gap
This occurs due to decrease in HCO,-level and compensatory increase in Ch level (to marer
electrical neutrality).
(i) Diarrhoea (loss of HCO,), (i) Cholestyramine therapy, (ii) Type I, Il, IV RTA (Rers
distal
tubular aCidosis).
D. Delta anion gapP
-
is useful in measuring HCO, > called HCO equivalent. So,
unit decrease in Hco, It is seen in mixed acid base disorder.
1 unit rise in anion gap

Expected anion gap = 2.5 x Serum Albumin level

Delta HCO (24 HCO,)
E. Delta ratio
Delta rano
Deltaanion gap
Delta [HCOi
(Measured anion gap
(Normal [HCO,] -
-Normal aníon gap)
Measured [HCo,])
(Anion gapP 12)
24 [HCO,
138
 1
mmoll decrease in [HCO,] = 1.3 mmHg decreas
Metabolic acidosis (Respira
ratory compensation DC
in
cannot be < 11.3 mmHg)

Metabolic alkalosis
1
mmolL increase in [HCO,J 0.75 mmHg increase
(Respiratorycompensalion)iin
(Uncompensated) 7.5 mmHg 5.5 nmol/L rise in
in |H
Respiratory acidosis
increase in puo <1 mmo/L iNCreas0 and
ed) 7.5 mmHg in[HCO
2.5 nmoll ise in [H]an
increse in pco 2-3 mmoL Inerease in [HCO,1
Respiratory Alkalosis (Uncompensaled) 7.5 mmHg= 5.5 nmol/L fall in H 1
fall in pCO,

Nomal average [H] = Normal average pH = 7.4 Change in pH by o.01=

Change
by 1 nmollL (Relation is invers in la
40 nmol/L

2. Discuss how compensatlon occurs in diflerent acid base disturbances.

A pH HCO
(0 Metabolic Acidosis Uncompensated
Norma
Partially compensated
Totally compensated Normal

i) Respiratory Acidosis Uncompensated Normal (may be

slight high)
Partially compensated
Totally compensated Normal
(ii) Metabolic Alkalosis Uncompensated Normal or
Partially compensated T
Totally compensated Normal
(V) Respiratory Alkalosis Uncompensated Normal (or mild
decreased)
Partially compensated T
Totally compensated Normal

3. Diseuss the causes of metabolic acidosis.

A High anion gap": (a) Increased Proton formation- Ketoacidosis (DKA, Alcoholism), LE

acidosis (tissue hypoxia, alcohol, phenformin, sorbitol, Von Gierke's disease etc.) PoisoningN
ethanol, methanol, ethylene glycol, salisylic acid, renal
failure. (b) Acid intake Hign pare
amino acid given, acid poisoning.
(i) Normal Anion gap" (a) Loss of HCO, Diarrhoea, Fistula in pancreas, intest
-

(b) Decreased proton excretion - Renal failure,

Carbonic anhydrase inhibitors, Hyper
renal tubular acidosis

4. Discus the causes of Resplratory acldosis.

A Obstructive (Airway): Bronchitis, Emphysema, Asthma, Aspiration. caus
(U
Fibrosis, Pneumonia, AHDS and IRDS (Adult and Infant Respiratory Distress ndore
(in) Obstruction (External,
chest wall): Kyphoscoliosis, Trauma (11ail cnes
(iv) Neuromuscular paralysis: ND M
Poliomyelitis, GB (Guillain Barre)
Neurone Disease), Sleep apnea, Bolulism, Bulbar tetanus, Neurotoxin,syndroatory
cen
(v) Resp
144 depression: Sedative, Hypnolic, CNS trauma, Brain tumors.
 auses of Metabollc alkalosis".
cause,
pcussiheprotons (a) Through Kidneys: in Cushing's syndrome, Conn's
of loop), (b) GI loSS: Severe vomiting. syndrome, Diuretic
Vomiting in pyloric stenosis.
LoHigh Akali
administration Mlk-alkali syndrome, Chronic Gastrnc
elc. (i). alkali ingestion.
Iaon
the causes of Hespiratory alkalos
oventilation, (i) Stimulation of respiratory centre :
hanicaate poisoning. Seplicemia, voluntary and Hysterical CNS trauma and tumor,
aNe, Salisy lmonary and Cardiac diseases: Pulmonary hyperventilation, Hepatic
Mening
. oedema and embolism,
Fevtiac failure. (v) Hypoxla . ign anmude syndrome, Lung diseases,
ongesive Severe anemia.
conditions where normal anion gap acidosls occurs.
answers3.
Se rincipal buffer of the exracellular fluld including plasma".
Naae
Rcarbonate buffer. It has 657o Dunering capacity in plasma and 40% of butfering capacity of

who body.
te most
huffer which is second imporlant lo bicarbonate buffer in extracellular fluld
the
Name
blood"
other Ihan
butfers (HPO,3 HPO,).
sic and monobasic phosphate
&

intracellular buffer other than erythrocytes.

the most Important
Lenhate buffers. In plasma its concentralion is only 8% of that of bicarbonate butfer. [HPO,*V
PO:] ratio in plasma normaly 4. This buftfer ralio coresponds to blood pH 7.4.
me
the different butfer systems of our body (or enumerate the ditferent physiological
burfers)
Phosphate buffer, (ii) Protein buffer (1% 2% of total butfering
Bicarbonate buffer, (ii)

capacity of plasma). (iv) Hemoglobin buffer.

What is reverse chloride shift?
2 What Is chloride shift"?
See text of this chapter, MCQ no. 6.
11 Discuss the causes of high anlon gap metabolic acidosis.
A See answer no. 3.

4What is anion gap? What its normal range?

See text of this chapter.
substances fill up the anion gap?
S.Whlich

Proteins, phosphates, sulfates and organic acids.

E What
renal ion-exchange mechanism?
Is
amount
actively by the tubular cells in exchange of equivalent
ions are reabsorbed
Na s secreted into the tubular filtrate. Out of the total amount
of tubular filtrates of H
from DCT& CD (distal
(proximal convoluted tubules) and 15% secreted
COnl m PCT
Tvoluted tubule & collecting duct).
conditions when
When it can be very high? What are the Osmolallty and
ts verv lasma osmolality?
calculated? What are the differences
between
Osmolarito" HOw it can be
blarity?
285-295 mOsm/Kg.

145
 TS
UDENT
KARS
UN
ROKSU

Edu
Sodf