You are on page 1of 10

WEEK #16&17: LIVER FUNCTION

LIVER FUNCTION o small areas wherein body fluids also (may


sinabi si sir pero di ko maintindihan)
LIVER LOBES AND LIGAMENTS
• Canaliculi
• Portal Vein
o had a thin basement membrane
o it has RBC
• Hepatic Artery
o had a thick basement membrane
o doesn’t have any RBC
• Hepatic Vein

o right and left lobe which is separated by falciform


ligament, this recieves blood from hepatic artery
(?). also, it transfer blood to inferior vena cava
o gallbladder – storage of bile, which is produced
by the liver
MICROSTRUCTURE OF THE LIVER

o bile duct – doesn’t contain any RBC


o hepa
CELLS FOUND INSIDE THE LIVER
KUPFFER CELLS

• Derived from monocytes


• Contains lysosomes with hydrolytic enzymes,
immunoglobulin and complement receptors
• Secretes interleukins, TNF, collagenase,
prostaglandins
o microstructure of the liver is the hepatocytes, o which contribute to inflammation, when the
wherein you can see it as hexagonal formed organ is beings invaded by a pathogen.
o it has the main blood supply, the hepatic artery HEPATOCYTES
(?)
o branch of portal vein – simple circulation of the • major functioning cells; performs most of the
liver metabolic and synthetic functions of the liver
o within hepatocytes, the bile is transmitted to o main cell of the liver
other parts of the body such as gallbladder to be o production of the bile
stored we have the bile duct o detoxifying of blood
o bile duct is one of the portal triad
STELLATE CELLS (ITO CELLS)
o portal triad composed of branch of bile duct,
branch of hepatic portal vein, and branch of • site of storage for fat-soluble vitamins
hepatic artery o Vitamin A,P,E,K
MICROSTRUCTURE OF THE LIVER • Synthesize collagen → fibrosis → cirrhosis
• Synthesize nitric oxide → regulate intrahepatic blood
• Hepatocytes
flow
• Kupffer Cells
o macrophages found in the liver
• Sinusoids

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


OVAL CELLS • Protein metabolism
• Hormone metabolism
• liver stem cells involved in the regeneration of o parts of erythropoietin
hepatocytes and bile ducts after liver injury
o mainly responsible for regeneration of the SECRETION OF BILE
liver
o kaya pwedeng magdonate ng liver sa ibang • Metabolism (conjugation) and excretion of bilirubin
tao kasi kaya magregenerate ng liver. • Synthesis of bile salts or bile acids
o liver is the only organ that can regenerate
itself and dahil yun sa oval cells STORAGE

LIVER SYSTEMS • Glycogen


• Vitamin A
BIOCHEMICAL HEPATOCYTIC SYSTEM
• Vitamin B12
• responsible for the vast majority of all metabolic • Iron
activities
BILE
o such as the detoxification
o detoxification is mostly by the blood o main component of the liver
circulation, those substances (harmful to o main secretion of the liver
our body) that are found in the blood it can • Components: bile acids, lecithin, cholesterol,
be detoxified by the liver or eliminated by bilirubin, urobilinogen, and electrolytes
the liver. • Important in lipid digestion: formation of micelles
o some of drugs can also be detoxified by the o if ever na hindi sapat yung bile sa body
liver kaya meron tayong tinatawag na “first natin, magaaccumulate ang body natin ng
pass metabolism” na ginagawa ni liver sa lipids
drugs. Kaya hindi fully naaabsorbed ng o bile is a emulsifying agent, it will degrade
katawan natin ang dosage ng gamot kasi lipids into simpler molecules to be used up
nagkakaroon ng first pass metabolism by the body
• Cholic acid and chenodeoxycholic acid
HEPATOBILIARY SYSTEM
BILIRUBIN
• concerned with the metabolism of bilirubin
o production of bile and degradation of • Bile pigment that results from the catabolism of the
bilirubin from other metabolic processes heme moiety of the hemoglobin molecule due to old
age or trauma
RETICULOENDOTHELIAL SYSTEM • Degradation occurs in the spleen, bone marrow and
liver
• involved with the immune system o not only found in the liver but also in spleen
o liver is an area for detoxification and also and bone morrow
fighting for microorganisms o place an important role in heme or RBC
o tinatry ni kupffer cells and other immune production
inflammatory cells to fight the pathogens o if ever na RBC died, it will release bile. Also,
within the liver hemolysis in blood can cause releasing of
bilirubin in blood. Kaya hindi gumagamit ng
FUNCTION OF THE LIVER hemolyzed sample sa bilirubin
DETOXIFICATION OF BLOOD (EXCRETION) determination kasi bilirubin is within RBC

• Phagocytosis by Kupffer cells


• Metabolism and excretion of steroid hormones,
drugs and foreign compounds
• Production of urea, uric acid and other molecules
that are less toxic than their parent compound
o being a toxic compound dinidegrade nila
ang mga molecules into a simpler form that
can be secreted to the urine such as urea,
uric acid

METABOLIC FUNCTIONS

• Carbohydrate metabolism
o degrade (?) carbohydrates to form smaller
molecules to be used for energy production
• Lipid metabolism
o degrade the lipids as to be need in the body
o produce lipids to excess carbohydrate

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


o we have different types of bilirubin: B1 and ➢ Neonatal Jaundice (Rapid turnover of
B2 hemoglobin after birth)
o B1 – it is non water soluble, not soluble in o normal phenomenon but if the infant
water but soluble in alcohol doesn’t normalize within 4 days, then there
o B2 – soluble in both water and alcohol is something wrong with regards to the liver
o B1 – high affinity with serum albumin o kaya pinapaarawan yung bata since
o B2 – no affinity in serum albumin bilirubin is sensitive sa light
o Lipid membrane permeability B1 is the most
applicable POST-HEPATIC JAUNDICE
o Renal excretion, B1 cannot be excreted by
o not related to liver but related to the tract (?)
the kidney, while B2 can be excreted by the
of bilirubin after being formed in liver,
kidney
possible sa gallbladder, kidney etc.
o B1 (synonyms) – correlated with regards of
the function of bilirubin • Regurgitative, obstructive or cholestatic jaundice.
• Due to obstruction of the biliary flow
DELTA BILIRUBIN o in the bile duct of gallbladder
➢ Intra-hepatic cholestasis
• Bilirubin tightly bound to albumin
• Obstruction in the extra-hepatic biliary tree
o B1
➢ Gallstone (cholelithiasis)
• Has longer half-life than other forms of bilirubin
➢ Strictures
• Formed due to prolonged elevation of conjugated ➢ Spasms
bilirubin ➢ Atresia
o B2 ➢ Parasite or bacteria
• Helps in monitoring the decline of serum bilirubin ➢ Cancer of the pancreas
following gallstones formation o biliary tree is the area wherein the liver is
o if may gallstone, hindi enough yung bilirubin connected to gallbladder. In gallbladder is
na ineexcrete ng gallbladder then the delta also connected to pancreas. The tail of the
bilirubin is maactivated pancreas touches the area of biliary tree.

JAUNDICE CHOLESTASIS
• Also known as “icterus”
• Hyperbilirubinemia with bilirubinuria
• Yellowish pigmentation of the skin, mucous
o hyperbilirubinemia – increase bilirubin
membrane and sclera of the eyes
o bilirubinuria – presence of bilirubin in the
• Due to accumulation of abnormal amounts of either
urine
free or conjugated bilirubin or both
• Elevation of ALP, GGT, 5’-nucleotidase and LAP
• Normal concentration: 0.5-1.0 mg/dL
o part of liver function test – assess your liver
• Jaundice: 2 mg/dL
function
• Hypercholesterolemia
o hindi nakakaproduce ng sapat na bile kaya
no emulsification of liver, no degradation of
lipids kaya tumataas ang cholesterol natin
• High serum bile salts (cholate and
chenodeoxycholate)

DIFFERENTIAL DIAGNOSIS OF PRE-HEPATIC AND


POST-HEPATIC JAUNDICE

CLASSES OF JAUNDICE
PRE-HEPATIC JAUNDICE

o occurs before liver function, it doesn’t have


correlation with regards of liver function
• Hemolytic/retention jaundice
• Due to excessive destruction of RBCs
• Free bilirubin is increased
➢ EF/Malaria o Elevated urine urobilinogen – degragation
o destruction of RBC of bilirubin that can be found in urine. The
➢ Prolonged fasting, drug intake

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


intestine and kidneys degrade the bilirubin • obstruction of the hepatobiliary tree (?)
to form urobilinogen • Drugs (Methyltestosterone)
o Darkly-colored stool – correlated with • Inherited disorders of bilirubin metabolism (Dubin-
bilirubin Johnson Syndrome)
o Kernicterus – the liver blood (?) into the
heart and then the heart delivers it into the INTRAHEPATIC OBSTRUCTION
body. After the increase bilirubin in the
blood before the liver, the liver will degrade • the sinusoids, bile ducts are being
it then the liver will transport the excess obstructed
bilirubin through the blood being degraded • Hepatitis
into other parts of the body.The brain is not • inflammation of the cells within liver
excluded to that because of the blood • Cirrhosis
contains increase bilirubin will result • causing fibrosis of the liver, nagbubuhol na
kernicterus. Kaya nagkakaroon ng elevated ang liver
na urobilinogen and darkly colored stool • Infiltrations (Lymphoma, amyloidosis)
because of that. • these are agents that can occlude (?) bile
o Clay-colored – decreased urobilinogen. duct
Buo si bilirubin na naeexcrete kaya walang • Biliary atresia
pigment to give the stool color. • Tumors
o Steatorrhea – presence of fats / lipids within • Extrahepatic sepsis
the stool. The bilirubin is not degraded by
liver, not formed as to the bile kaya yung INHERITED DISORDERS OF BILIRUBIN METABOLISM
bilirubin is nagcacause ng decrease
GILBERT’S DISEASE
emulsification of the fats in the intestine and
the fats is being excreted in the stool.
• Characterized by a mild unconjugated
hyperbilirubinemia
HEPATIC JAUNDICE
• Characterized by decreased conjugation and
• Hepatocellular or infectious jaundice decreased uptake of bilirubin
• Due to severe damage to hepatocytes • Pre-conjugation failure
• Both free and conjugated bilirubin is elevated • Increased B1
• Due to alcohol or microorganisms • insertion of two bases into the promoter region of the
o destroys hepatocytes UGT1A1 gene resulting in lower transcriptional rates
• Neonatal Jaundice (Decreased activity of UDPGT and an overall lower enzymatic activity
after birth)
CRIGLER-NAJJAR SYNDROME
PRE-MICROSOMAL
TYPE 1: AUTOSOMAL RECESSIVE
• Drugs (Rifampicin) → interferes with bilirubin uptake
• Absence of UDPGT
o the rifampicin a TB drug which inhibits the
• Severe increase of B1 – death
uptake of bilirubin by the liver
• since b1 is increase, it can cause
MICROSOMAL kernicterus or accumulation of bilirubin in
the brain which impedes the function of the
o the detect is found within the hepatocytes brain
within the liver.
o the liver has a defect TYPE 2: AUTOSOMAL DOMINANT
o liver itself
• Partial defect of the conjugating enzyme
• Prematurity
o the liver / hepatocytes are not matured • meron kang enzyme pero may defect
enough to do its metabolic function • Increased B1 – survival to adulthood
• Hepatitis
DUBIN-JOHNSON SYNDROME
o inflammation of liver / hepatocytes
• Inherited disorders of bilirubin metabolism (Gilbert’s • Characterized by a decreased hepatic excretion of
Syndrome, Crigler-Najjar Syndrome) bilirubin
• Increased B2 with hepatic pigmentation (melanin)
POST-MICROSOMAL
• Bilirubin Excretion Deficit
o majority of the cases are not related to the • mababa ang excretion ng bilirubin
liver
o within the factors affecting the function of
the liver
• Impaired excretion
• obstruction of the biliary tree (?)
• Hepatitis

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


• +++ gray or clay-colored stools
• relates to the gallbladder, so if the
gallbladder is defective the production of
urobilinogen which causes the stool to be
gray colored

TWO BROAD CATEGORIES

• some diseases include one or both types


• clinical features within type may be similar
irrespective of the specific disorder
• sometimes the hepatocellular disease can
cause cholestatic and vice versa

SIGNS OF LIVER DISEASE


• no abnormalities
• hepatic enlargement
• tender liver due to capsule distention
• nodular liver
• may bukol-bukol
ROTOR SYNDROME • shrunken liver
• pagliit ng liver due to cirrhosis
• Cause is still unknown
• jaundice
• Similar to Dubin-Johnson but without hepatic
• edema
pigmentation
• relative hypotension and tachycardia
• Increased B2
• can be afebrile, hypo or hyperthermic
LUCEY-DRISCOLL SYNDROME • spider angiomata

• A familial form of unconjugated hyperbilirubinemia


caused by a circulating inhibitor of bilirubin
conjugation
• merong nagcicirculate na inhibitor of
conjugation of bilirubin, kaya nagkakaroon
ng b1 hyperbilirubinemia

LIVER DISEASE
HEPATOCELLULAR DISEASE

• Diseases of the liver cells

SYMPTOMS:
• spider angiomata parang nagkakaroon ng
• patient may have no symptoms
maliit na mga tuldok and nagkakaroon ng
• fatigue, malaise
pigment (?) and yung mga rashes is parang
• anorexia, nausea galamay
• jaundice • palmar erythema
• pruritus • nail clubbing
• easy bruising and bleeding
• hematemesis
• abdominal pain, swelling
• day night reversal, confusion, coma

CHOLESTATIC DISEASE

• Diseases of the biliary tree

SYMPTOMS:

• patient may have no symptoms


• fatigue, malaise
• anorexia, nausea
• jaundice
• +++ pruritus
• +++ abdominal pain and pancreatitis

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


• Dupuytren's contracture ALCOHOL
• hindi na magalaw ang finger, nagkaroon na
ng paninigas. hindi na nabebend ng normal
HEPATITIS
VIRAL HEPATITIS- HISTORICAL PERSPECTIVES

• testicular atrophy
• splenomegaly

ADD. NOTES
o A – is infectious
• Ascites
o B and D – found in the serum which is also
o nagkakaroon ng accumulation of fluids
infectious
within the peritoneal cavity. Ascites can be
o E – the enterically transmitted
formed of edema (?)
o C – parenterally transmitted
o F, G, and TTV and others is unknown

TYPE OF HEPATITIS

DIFFERENTIAL DIAGNOSIS

COMMON HEPATOCELLULAR DISEASE


o the patient having hepatitis A, their feces
HEPATITIS can be infective. Kaya it can be found
sometimes in foods. In the Philippines, we
• autoimmune hepatitis are endemic in Hepa A, lalo na sa mga
• Acute and chronic hepatitis street foods it can cause hepa because of
• granulomatous hepatitis hepa A
o percutaneous – needle prick injury,
METABOLIC breakage of the skin
o permucosal – via sex transmission
• hemochromatosis
o if may hepa B, need magpatest sa HIV +
• Wilson's disease
other STI’s since sa PH combo combo sila.
• Amyloidosis
(practice safe sex guys advice ni sir use
SHOCK LIVER condom if marami kayong partner because
di kayo mapoprotektahan ng pills sa STI’s)
o hepa B – lifelong disease, walang treatment
sa hepa B but the treatment is based on a
FATTY LIVER OF PREGNANCY supportive treatment.
o hepa C – doesn’t have immunization
o (pabasa na lang po yung table)

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


CIRRHOSIS DRUG AND ALCOHOL RELATED DISORDERS
• clinical condition in which scar tissue replaces • immune-mediated injury to the hepatocytes
normal, healthy liver tissue • drug induces an adverse immune response directed
o liver has a normal tissue then there is against the liver itself and results in hepatic and/or
scarring, scarring nagkakaroon ng fibrosis cholestatic disease
ang tissue which is parang bato • Ethanol - causes very mild, transient, and unnoticed
• blocks the flow of blood through the organ and injury to the liver; however, with heavier and
prevents the liver from functioning properly prolonged consumption, it can lead to alcoholic
o nawawalan na ng normal function ang liver cirrhosis
if ever na may cirrhosis because the blood
cannot flow within the vessels of the liver COMMON CHOLESTATIC DISEASES
kasi nagiging scarred tissue na siya. EXTRAHEPATIC BILIARY TREE OBSTRUCTION
naninigas na siya wala ng contraction (?) na
nabubuo • choledocholithiasis
• signs and symptoms appear, including fatigue, • choloangiocarcinoma
nausea, unintended weight loss, jaundice, bleeding • pancreatic cancer
from the gastrointestinal tract, intense itching, and
swelling in the legs and abdomen INTRA-HEPATIC BILIARY TREE OBSTRUCTION

CAUSES OF CIRRHOSIS • hepatocellular carcinoma


• metastatic carcinoma
• Chronic alcoholism
• sclerosing cholangitis
o the alcohol is intaking (?) agent with regard
to liver. if heavy drinker prone sa cirrhosis • primary biliary cirrhosis
kasi liver is irritated sa alcohol then the liver
CHOLESTATIC DISEASES
will response to be scarred
• Chronic hepatitis C virus infection INTRA-HEPATIC CHOLESTASIS
• Chronic hepatitis B and D virus infection
• abscess: bacteria, fungi, protozoa, helminth
o hepa D can only be occurred if may hepa B
na, this is coinfection. • statins and just about any drug
• Autoimmune hepatitis
LIVER DISEASE PATHOGENESIS
o the liver itself is being destroyed by the
body’s immune system
• Inherited disorders (e.g., 1-antitrypsin deficiency,
Wilson disease, hemachromatosis, and
galactosemia
• Non-alcoholic steatohepatitis, blocked bile ducts,
drugs, toxins, and infections

TUMOR
• Primary liver cancer - cancer that begins in the liver
cells
• Metastatic cancer occurs when tumors from other
parts of the body spread (metastasize) to the liver
o ang possible na mag metastasize sa liver is
almost all because of hepatic portal
circulation specially those organs below the
liver. o Liver is normal if magintroduce ng irritant
o Gastrointestinal cancer can cause liver (for example alcohol) maglelead yun sa
cancer if mamemetastasize kasi yung fatty liver or alcohol hepatitis.
hepatobiliary tract is travelling to liver o Alcohol hepatitis can lead to cirrhosis which
• Benign – hepatocellular adenoma and hemangiomas eventually result to liver failure
• Malignant - hepatocellular carcinoma (HCC), o lahat ng agents na pwedeng maging toxic
hepatocarcinoma, and hepatoma to liver can result to liver failure

REYE SYNDROME HOW MUCH ALCOHOL?

• preceded by a viral syndrome such as varicella, THRESHOLD CONSUMPTION


gastroenteritis, or an upper respiratory tract infection
such as influenza • 80 gm/day for 10-20 years
• Characterized by noninflammatory encephalopathy ➢ 1 liter wine
and fatty degeneration of the liver ➢ 8 std sized beers
➢ 1/2-pint hard liquor
• mild hyperbilirubinemia and threefold increases in
ammonia and the aminotranferases (AST and ALT)

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


o excess consumption can lead to
possible signs and symptoms of
alcoholism and liver damage

AMONG HEAVY DRINKERS

• 230 gm / day x > 20 years


➢ 80 % mod to severe fatty liver
➢ 50 % cirrhosis or "precirrhotic" lesions

LIVER DISEASE PATHOGENESIS

o healthy liver – shiny reddish organ


o Fatty – yellowish
o Fibrotic – white yellowish
o Cirrhosis – darkening of liver, progression of fats

o Fast days – some individuals don’t


have a (may sinabi si sir di ko magets)
with regards to toxins na iniintroduce
sa liver na nagcacause ng liver failure.
The liver cannot metabolize kaya
nagkakaroon ng liver failure
o Slow years – the liver can still degrade
it but merong limitations.

CLINICAL STATUS IN LIVER DISEASE

o slow progressions

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


MODIFIED CHILD-PUGH SCORE ENZYMES HAVE ALTERNATE SOURCES

• ALP (placenta, bone)

ENZYMES AS MARKERS OF HEPATIC DISORDERS


HEPATIC DISORDERS

• Acute injury (Acute hepatitis) and Necrosis

• Cirrhosis

o (pabasa po binasa ni sir)


o parameter 2: signs, nagkakaroon ng
controlled medically. Ascites, dinidrain yung
fluid within peritoneum. Encephalopathy,
dinidrain yung fluid within the membrane
o parameter 3: serum albumin : <2.3 (?)

PROGNOSIS
• 1 Year Survival
• Biliary Tract Obstruction
o their liver is defective
➢ Child Pugh A 80 - 100%
➢ Child Pugh B 60 - 80%
➢ Child Pugh C 35 - 45%

LABORATORY TEST RELATED TO LIVER FUNCTION METHODS USE IN EVALUATION OF LIVER FUNCTION
AND DISEASES • 1883 → Ehrlich (Urine samples)
NON-SPECIFIC LABORATORY FINDINGS • 1913 → Van den Bergh
• 1937 → Malloy and Evelyn
• Anemia • 1938 → Jendrassik and Grof
• Low platelets
BILIRUBINOMETRY
• Hyponatremia
• Hyperbilirubinemia • useful in the neonatal population because of the
• Low albumin presence of carotenoid compounds in adult serum
• Elevated liver enzymes that causes strong positive interference in the adult
• Elevated ammonia population
• Elevated creatinine (hepato-renal) • involves the measurement of reflected light from the
skin using two wavelengths that provide a numerical
LIVER ENZYMES index based on spectral reflectance
• Microspectrophotometers → that determine the
SUGGESTS HEPATOCELLULAR DISEASE
optical densities of bilirubin, hemoglobin, and
• ALT Alanine amino transferase (SGPT) melanin in the subcutaneous layers of the
o formerly known as serum glutamate infant’s skin
phosphatase (SGPT) o mas okay siya sa babies kasi manipis pa
yung skin nila, walang interference na
• AST Aspartyl amino transferase (SGOT)
nakikita sa subcutaneous layers unlike sa
o formerly known as serum glutamate oxalate
adults.
transaminase (SGOT)
o kapag may AST may SGOT SPECIMEN COLLECTION AND STORAGE

SUGGESTS CHOLESTATIC DISEASE • fasting sample is preferred as the presence of


lipemia will increase measured bilirubin
• ALP Alkaline Phosphatase concentrations
o hindi nirerequired ng fasting pero if yung
GGT GAMMA GLUTAMYL TRANSFERASE sample is lipemic nirerequired ng fasting
o lipemia – caused turbidity which results to
• non-specific test
increase bilirubin content
o non-specific test sa liver pero significant
• Hemolyzed samples should be avoided as they may
rise in GPT sa liver pero hindi always
decrease the reaction of bilirubin with the diazo
reagent

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales


• Bilirubin is very sensitive to and is destroyed by
light; therefore, specimens should be protected from
light (bilirubin values may reduce by 30%–50% per
hour)
o kaya meron tayong amber bottle tubes or
amber tubes. Also, if walang amber tubes
pwedeng gumamit ng aluminum foil para
macover yung tube and yung blue na
paper.
• 2 days at room temperature, 1 week at 4°C, and
indefinitely at -20°C

MALLOY-EVELYN PROCEDURE
• pH 1.2 – acidic environment
• Methanol – reagent being used
• red-purple in color with a maximal absorption of 560
nm

JENDRASSIK-GROF METHOD
• caffeine-benzoate – reagent being used
• Ascorbic acid = terminates the initial reaction and
destroys the excess diazo reagent.
• alkaline tartrate solution → which shifts the
absorbance spectrum of the azobilirubin to a more
intense blue color
• final blue product is measured at 600 nm

ADVANTAGE OF JENDRASSIK-GROF OVER MALLOY-


EVELYN

• Not affected by pH changes


• Insensitive to a 50-fold variation in protein
concentration of the sample
• Maintains optical sensitivity even at low bilirubin
concentrations
➢ Has minimal turbidity and a relatively
constant serum blank
➢ Is not affected by hemoglobin up to 750
mg/dL
o hemolysis cannot affect jendrassik-grof

UROBILINOGEN DETERMINATION
• p-dimethylaminobenzaldehyde (Ehrlich’s reagent)
• red color
• Ascorbic acid → reducing agent to maintain
urobilinogen in the reduced state
• saturated sodium acetate → stops the reaction and
minimizes the combination of other chromogens
with the Ehrlich’s reagent

-------- END OF CCHM LECTURE --------

goodluck sa exam mga lods <33 ipasa niyo na lang ako


HAHAHAHA charz goodluck!

Bachelor of Science in Medical Laboratory Science | Finals | Ge and Gonzales

You might also like