HEMATLOGY 2 RMT

Clinical Hematology
Midterm Topic 1- ADDITIONAL NOTE – Introduction to
2022
Anemia

[TRANS] TOPIC 1: INTRODUCTION TO ANEMIA

 Common in infants, children, pregnant women
OUTLINE
1) ANEMIA  Number of circulating RBC are not affected—the
A. Microcytic, Hypochromic problem is, you lack Hemoglobin
B. Normocytic, Normochromic  DUE TO:
C. Macrocytic o Dietary inadequancy
o Malabsorption
ANEMIA o Increased Iron loss
 ↓ levels of RBC & Hemoglobin, resulting to ↓ levels of o Increased Iron requirement
Oxygen delivery to the tissues  LAB FINDINGS:
 Can be classified morphologically using RBC Indices o Presence of Ovalocytes
such as MCV, MCH, MCHC or based on o ↓ Hemoglobin & Hematocrit
Etiology/Cause o ↓ Iron & Ferritin
 Hemoglobin is <12g/dL in men: < 11 g/dL in women o Nor. or ↓ Reticulocyte count
 Signs and Symptoms: o ↓ Percent Saturation
o Headache o ↓ OFT
o Faintness, & Vertigo o ↓ RBC indices including RDW 
o Easy fatigue o ↑ TIBC
o Pallor ANEMIA OF CHRONIC INFLAMMATION
o Dyspnea on exertion  Second to most common cause of Anemia
o ↓ Blood Pressure  There is normal supplies of iron but its delivery is
o Bounding pulse blocked because of Inflammation
o Systolic murmur  Due to inability to use the available iron for production
o Spoon nails of Hemoglobin
TYPES OF ANEMIA  Associated with persistent infections & chronic
RELATIVE ANEMIA inflammatory disorders such as SLE, RA, Hodgkin’s
 -RBC mass is normal; Blood volume is ↓ Lymphoma, Cancer
 Transient, Secondary to unrelated condition  Immpaired released of storage iron (Ferritin) is
 include conditions that result in Hemodilution such as associated with ↑ levels of Hepcidin
Pregnancy or Volume overload o Hepcidin is a liver hormone, and a positive
 LAB FINDINGS: Acute-phase reactant which plays a major role
o Nor. Reticulocyte count in body iron regulation by influencing intestinal
o Normo-Normo Anemia iron absorption & release of storage iron from
ABSOLUTE ANEMIA Macrophages
 RBC mass ↓; Blood volume is normal o Inflammation & Infection causes Hepcidin
 indicative of a true ↓ in RBC & Hemoglobin levels to ↑, which ↓ release of stored iron
 LAB FINDINGS:
 DUE TO:  ↓
o ↑ ESR
o RBC delivery into circulation
o Nor. or ↑ Ferritin
o impaired or defective production -
o ↓ Iron
o RETICULOCYTOPENIA: ↓ levels of
o ↑ TIBC
reticulocytes
SIDEROBLASTIC ANEMIA
o ↑ loss of RBC from the circulation
o Acute Bleeding  Iron was able to enter the cell but it was not able to
o HEMOLYSIS: accelerated rupture of RBC use in Heme synthesis because of lack in
CLASSIFICATION OF ANEMIA  Protoporphyrin resulting to defective Hemoglobin
MORPHOLOGY OF RED CELLS synthesis & Iron overload
 Size of RBC  Excess iron accumulates in the mitochondrial region
 Diameter of central pallor of the immature RBC in the Bone marrow & encircles
MICROCYTIC—HYPOCHROMIC: the Nucleus → “Ringed Sideroblast”
 Thalassemia  Excess iron accumulates in the mitochondrial region
 Iron Deficiency Anemia of the mature RBC in circulation → “Siderocytes” with
 Chronic Disease siderotic granules such as Papenheimer bodies
 Sideroblastic Anemia o Pearl’s Prussian Blue: stain for Sideroblasts
IRON DEFICIENCY ANEMIA (IDA) o WGram’s Stain: stain for Papenheimer bodies
 PRIMARY
 Most common & easiest to manage
o - irreversible
PADAYHAG, RIGIDOR S. | MLS-3D 1
 HEMATLOGY 2
Clinical Hematology
RMT
Midterm Topic 1- ADDITIONAL NOTE – Introduction to 2022
Anemia
o Cause of the blocks are unknown 
Radiation or Chemotherapy
o 2 RBC populations (dimorphic) are seen Idiopathic → about 50-70% have no known
o
o This is one of the Myelodysplastic cause
Syndromes— Refractory Anemia w/ Ringed  LAB FINDINGS: (severe if ¾ of the criteria are
Sideroblast (RARS) present)
 SECONDARY - reversible; causes include Alcohol, o ↓ Hemoglobin, Hematocrit, or Reticulocytes
Chloramphenicol, Anti-TB drugs o No response to Erythropoietin
 LAB FINDINGS: o Markedly Hypocellular bone marrow
o Nor. Reticulocyte count o Neutrophil: <500/uL
o ↑ Iron & Ferritin o Platelet: <20,000/uL
o ↑ Lactate Dehydrogenase (LDH) o Reticulocytes: <10,000/uL
o ↑ RDW  TREATMENT:
o ↑ TIBC o Blood transfusion
THALASSEMIA o BM transplant/Stem cell transplant
 Inherited disorders caused by genetic alterations that o Counteract the complications
reduce or preclude the synthesis of the globin chains  DIAMOND-BLACKFAN ANEMIA
of hemoglobin tetramer. o Autosomal inheritance
 Predominant in Mediterranean, African and Asian o True Red Cell Aplasia (WBC & PLT are in
ancestry. normal #)
 Describe by Cooley and Lee in 1925. o Will lead to Severe Anemia with
 Types of Thalassemia Reticulocytopenia
o Beta () Thalassemia – Chromosome 11  MYELOPHTHISIC ANEMIA
o Alpha () Thalassemia – Chromosome 6 o Hypoproliferative Anemia caused by
o Hereditary Persistence of Hb F (HPHF) – replacement of Bone marrow Hematopoietic
inactivation of delta/beta cells by Malignant cells or Fibrotic tissue
o Hemoglobin Lepore – crossing over of beta and o Associated with Cancer with Bone metastasis
delta. HEMOLYTIC ANEMIA
o Hemoglobinopathy + Thalassemia ̵  Immediate RBC rapture/destruction
o Hemoglobin S – Thalassemia ̵  LAB FINDINGS:
o Hemoglobin C – Thalassemia o ↑ Reticulocyte count
o Hemoglobin E – Thalassemia o ↑ Lactate Dehydrogenase (LDH)
NORMOCYTIC—NORMOCHROMIC o ↓ Bilirubin, Urobilinogen
 Often checked using Blood indices o ↓ Haptoglobin
 The morphology is normal but the number of  CLASSIFICATION:
distribution is affected o INTRINSIC
o APLASTIC ANEMIA o EXTRINSIC
o HEMOLYTIC ANEMIA o INTRAVASCULAR
o ACUTE BLOOD LOSS o EXTRAVASCULAR
o RENAL DISEASE  INTRINSIC HEMOLYTIC ANEMIA :
APLASTIC ANEMIA o HEREDITARY DEFECTS:
 Due to bone marrow’s failure to produce blood cells o RBC MEMBRANE DEFECTS
leading to Pancytopenia INTRINSIC HEMOLYTIC ANEMIA: HEREDITARY
 Can be genetic, acquired, or idiopathic DEFECTS
 Mostly occurs in children & elderly (>50 y/o)
 Patients have poor prognosis with complications that RBC MEMBRANE DEFECTS
include bleeding HEREDITARY SPHEROCYTOSIS
 DUE TO:  Most common RBC membrane defect
o Genetics/Congenital → FANCONI ANEMIA  Autosomal dominant trait in whites
o Autosomal, recessive trait  DUE TO:
o Dwarfism, Renal disease, Mental retardation  o Loss of RBC membrane resulting in ↓ Surface
o Acquired Area-to-Volume ratio
 about 30% are due to Drug exposure o ↑ permeability of the membrane to Sodium
 Antibiotics: Chlorampenicol, Sulfonamides, o No Spectrin & Actin (susceptible to lysis)
o Anti-TB drugs  LAB FINDINGS:
 Chemicals: Benzene & Herbicides o MCHC > 37 g/dL
 Viruses: Parvovirus B19 secondary to o ↑ OFT
Hepatitis, o ↑ Lactate Dehydrogenase (LDH)

PADAYHAG, RIGIDOR S. | MLS-3D 2

 HEMATLOGY 2
Clinical Hematology
RMT
Midterm Topic 1- ADDITIONAL NOTE – Introduction to 2022
Anemia
o ↑Vitamin B1 o Congenital Hemolytic Anemia
o ↑Serum Bilirubin, Urobilinogen o Drug-induced: Primaquine (for malaria)
o ↓ Haptoglobin o Fava Beans & Legiums (can deplete G6-PD)
 CLINICAL FINDINGS: PYRUVATE KINASE DEFICIENCY
o Variable degree of Anemia  Failure to generate ATP in Embden Meyer Pathway
o Presence of Spherocytes & Stomatocytes which results in defective control of Cation Pump
o Splenomegaly  If RBC has no energy, it becomes permeable to
o Gall stones Sodium causing it to swell & burst
o Jaundice o PK ASSAY: confirmatory test for PK deficiency
o Skeletal abnormalities  LAB FINDINGS:
o Chronic leg ulcers o Reticulocytosis
HEREDITARY ELLIPTOCYTOSIS/OVALOCYTOSIS o Presence of Echinocytes
 Autosomal dominant  CLINICAL FINDINGS:
 Most patients are asymptomatic due to normal RBC o Jaundice
life span but it has presence of >25% Ovalocytes o Splenomegaly
 DUE TO: INTRINSIC HEMOLYTIC ANEMIA: ACQUIRED
o Defect Protein membrane skeleton structure DEFECTS
o Membrane defect is caused by Polarization of
Cholesterol at the ends of the cell rather than HEMOGLOBIN PRODUCTION DEFECTS
around the pallor area PAROXYSMAL NOCTURNAL HEMOGLOBINURIA
HEREDITARY STOMATOCYTOSIS  RBC membrane has ↑ sensitivity to Complement
 Autosomal dominant binding leading to lysis
 up to 50% Stomatocytes in the blood smear  RBC lacks Decay Accelerating Factor (DAF)
 DUE TO:  Deficient in Acetylcholinesterase activity &
o Membrane defect is due to abnormal abnormally constituted Glycoproteins
permeability to both Sodium & Potassium  Etiology are unknown
causes RBC swelling  LAB TESTS:
HEREDITARY ACANTHOCYTOSIS / o SUCROSE LYSIS TEST - non-cofirmatory test
ABETALIPOPROTEINEMIA for PNH
 Autosomal recessive o excessive hemolysis when exposed to ↓ Ionic
 Mild Anemia with Steatorrhea, Neurological & Retinal strength solution
abnormalities o HAM’S ACID HEMOLYSIS TEST - excessive
 50-100% Acathocytes in the blood smear hemolysis when exposed to Complement
 DUE TO: containing Serum @ low pH
o ↑ Cholesterol  LAB FINDINGS:
o Lecithin ratio in the membrane due to Abnormal o Pancytopenia
Plasma lipid concentrations o Risk factor for Acute Leukemia
o Absence of Serum B-Lipoprotein needed for o Chronic Intravascular Hemolysis causing
lipid transport Hemoglobinuria & Hemosiderinuria
RBC ENZYME DEFECTS o Acid pH @ night
G6-PD DEFICIENCY o Protuberances on the RBC surface
o ↓ Leukocyte Alkaline Phopshatase (LAP) score
 An X-linked disorder
EXTRINSIC HEMOLYTIC ANEMIA: IMMUNE
 Lack of NADP in Hexose Monophosphate Shunt
resulting to ↓ levels of Glutathione resulting to
AUTOANTIBODIES
Oxidation of Hemoglobin to Methemoglobin; dentures
COLD AUTOIMMUNE HEMOLYTIC ANEMIA / COLD
to Heinz bodies
HEMAGGLUTININ DISEASE
 Screening Test for G6PD
o ASCORBATE CYANIDE TEST  RBCs are coated with IgM and Complement @
o FLUORESCENCE TEST temperatures below 37°c
 Classification  RBCs are lysed by Complement of Phagocytised by
o Class I and II- Severe Deficiency Macrophages
o Class III- Mild Deficiency  Can be idiopathic, or secondary to Mycoplasma
o Class IV and V- Non-deficiency (Normal G6- pneumoniae, Lymphoma, or Infectious
PD) Mononucleosis
 CLINICAL PATTERN: o ANTI-I: if you have Infectious Mononucleosis
o Neonatal Jaundice o ANTI-i: Primary Atypical Anemia (PAP)
 LAB FINDINGS:
PADAYHAG, RIGIDOR S. | MLS-3D 3
 HEMATLOGY 2
Clinical Hematology
RMT
Midterm Topic 1- ADDITIONAL NOTE – Introduction to 2022
Anemia
o MCHC > 37 g/dL o
Exchange transfusions in Utero or shortly after
o (+) DAT birth - no longer a common problem because of
o ↑ Cold Agglutinin titer Rh immunoglobulin (RhoGam)
o ↑ Reticulocyte count o LAB FINDINGS:
o ↑ Bilirubin o Presence of nRBC
o In the blood smear: Polychromatophilia, o Severe Anemia
Spherocytosis, Agglutination of RBC o ↑ Bilirubin causing Kernicterus
WARM AUTOIMMUNE HEMOLYTIC ANEMIA / WARM o (+) DAT
HEMAGGLUTININ DISEASE  Due to ABO incompatibility - Group “O” woman
 RBCs are coated with IgG and Complement @ develops IgG Antibody that crosses placenta & coats
temperatures above 37°c the fetal RBC when the fetus is Group “A” or “B”
 60% of the cases are Idiopathic or Secondary to  LAB FINDINGS:
diseases that alter the immune response such as o Presence of Spherocytes
Chronic Lymphocytic Leukemia, or Lymphoma; it can o Mild or totally no Anemia
also be drug-induced. o Weakly (+) DAT
 LAB FINDINGS: o ↑ Bilirubin
o MCHC > 37 g/dL EXTRINSIC HEMOLYTIC ANEMIA: NONIMMUNE
o (+) DAT differentiates to Hereditary MARCH HEMOGLOBINURIA
Spherocytosis  Transient Hemolytic Anemia that occurs after forceful
o ↑ OFT contact of the body with hard surfaces
o ↑ Reticulocyte count MICRO-ANGIOPATHIC HEMOLYTIC ANEMIA
o ↑ Bilirubin  There are unwanted substances in your blood, and as
PAROXYSYMAL COLD HEMOGLOBINURIA RBC pass through, it becomes Schistocytes
 An IgG biphasic Donath-Landsteiner Antibody with P-  DISSEMINATED INTRAVASCULAR
specificity fixes Antibody or Complement to RBC COAGULOPATHY (DIC)
when cold ( 20C) then lysis will occur when warm o Systemic clotting that is initiated by activation
(37C) of the Coagulation cascade due to toxins or
 Can be idiopathic, or secondary to viral infections conditions that trigger release of Tissue
such as Measles or Mumps; or Lymphoma factor/Procoagulants
 LAB FINDINGS: o Multiple Organ Failure can occur due to clotting
o ↑ Reticulocyte count o Fibrin is deposited in small vessels, causing
o ↑ Indirect BIlirubin RBC fragmentation
o ↑ Hemoglobin  HEMOLYTIC UREMIC SYNDROME (HUS)
o ↓ Haptoglobin o occurs most often in children following a GI
o (+)DAT infection - the clots formed causes Renal
o (+) ANTI-P: Donut Lansteiner of Rosenbach damage
o Ehrlich test or Sanford test  THROMBOTIC THROMBOCYTOPENIC PURPURA
ALLOANTIBODIES o Occurs most often in adults
TRANSFUSION REACTIONS o Deficiency of enzyme ADAMST 13 which is
 Recipient has Antibodies to donor’s RBC Antigen responsible for breaking down large VWF
 Due to ABO incompatibility causes immediate multimers
reaction with Massive Intravascular Hemolysis that is o When multimers are not broken down, clots will
induced by Complement form, causing RBC fragmentation & CNS
 Usually IgM Antibodies impairment
 Can trigger Disseminated Intravascular OTHER CAUSES
Coagulopathy (DIC) due to release of Tissue factor  INFECTIOUS AGENTS
from the lysed RBCs o Ex: P. falciparum, C. perfigens which damages
 LAB FINDINGS: RBC
o (+) DAT  Presence of Schistocytes & Spherocytes in the
o ↑ Hemoglobin blood smear

HEMOLYTIC DISEASE OF THE NEWBORN (HDN)  MECHANICAL TRAUMA

 Due to Rh incompatibility (Erythroblastosis Fetalis) – o Caused by Chemicals & Drugs, Snake venom,
o Rh(-) woman is exposed to fetus’ Rh Ag & form or Prosthetic heart valves (Waring Blender
IgG Antibody which will cost the placenta & Syndrome) which also damages the RBC
destroy RBCs of the next fetus that is Rh(+) membrane
 THERMAL BURNS (3rd degree)
PADAYHAG, RIGIDOR S. | MLS-3D 4
 HEMATLOGY 2
Clinical Hematology
RMT
Midterm Topic 1- ADDITIONAL NOTE – Introduction to 2022
Anemia
o Causes direct damage to the RBC membrane, o Veganism
producing Acute Hemolysis, which is o D. latum infection- increased utilization of vit
characterized by Severe Anemia with B12
Schistocytes & Spherocytes o Failure to Separate Vitamin B12 from Food Proteins:
HEMORRHAGIC ANEMIA condition known as food-cobalamin malabsorption is
 The body adjusts; ↑ heart rate to pump more blood in characterized by hypochlorhydria due to atrophic
gastritis or atrophy of the stomach lining that often
order to compensate to the blood lost
occurs with increasing age.
 Expanding circulatory volume o Failure to Separate Vitamin B12 from Haptocorrin:
 LAB FINDINGS: lack of gastric acidity or lack of trypsin because of
o ↑ Platelet count chronic pancreatic disease can prevent vitamin B12
o ↑ circulating Granulocytes absorption because the vitamin remains bound to
o ↑ Erythropoeitin levels (6hrs) haptocorrin in the intestine and unavailable to
o Reticulocytosis (24hrs) intrinsic factor.
INTERNAL BLEEDING o Lack of Intrinsic Factor: pernicious anemia, but can
also result from the loss of parietal cells with
 Chronic; Gradual, long term blood loss Helicobacter pylori infection, total or partial
 Often caused by GI bleeding gastrectomy. D. Malabsorption: celiac disease,
 LAB FINDINGS: tropical sprue, and inflammatory bowel disease.
o ↓ Hemoglobin & Hematocrit  Peptic digestion of pepsin and HCl releases dietary
o ↓ Iron Vit B12 to bind to protein bound in food. Vitamin B12/
EXTERNAL BLEEDING Cobalamin binds to haptocorrin released from
 Acute; characterized by sudden loss of blood salivary glands.
resulting from trauma or other severe injuries such as  On entering duodenum, haptocorrin-B12 complexes
stab wound or gunshot cleaved by pancreatic proteases which releases B12
 LAB FINDINGS: Initially.. to bind to intrinsic factor from parietal cells.
o Normal Reticulocyte count  In distal ileum, it binds to cubulin/amnionless/megalin
o Normal Hemoglobin & Hematocrit to be taken by enterocytes
 In a few hours..  Transfer to liver or pronormoblast by Transcobalamin
o ↓ Hemoglobin & Hematocrit  PERNICIOUS ANEMIA
o ↑ Platelet count o Vitamin B12 deficiency resulting from an
o Leukocytosis with a Left shift autoimmune disease that causes atrophic
o Reticulocytosis in 3-5 days destruction of gastric parietal cells. H+ and intrinsic
factor secretion are lost. Antibodies to parietal cells
MACROCYTIC
or intrinsic factor or both are detectable in the serum.
MEGALOBLASTIC ANEMIA A sign of lemon yellow appearance of the skin.
 Defective DNA synthesis causes abnormal Nuclear o Deficiency in Intrinsic factor, Ab to Intrinsic factor, or
maturation Ab to Parietal cells
 However, RNA synthesis is normal, therefore o They are needed to absorb Vit.B12 in Terminal Ileum
Cytoplasm is not affected o It takes 3-6 years to develop because of high storage
 The Nucleus matures slower than Cytoplasm in the body
(Asynchronism) o Prevalent in older adults of English, Irish, &
 Caused by either Vit. B12 or Folic Acid deficiency Scandinavian descent
o Characterized by Achlorhydria – seen in pernicious
 LAB FINDINGS:
anemia due to atrophy of parietal cells which
o Pancytopenia produces hydrochloric acid
o ↑ LDH, Bilirubin, Iron  CLINICAL FINDINGS:
o Hypersegmented Neutrophils o Weaknes & Numbness
o Oval Macrocytes & Dacryocytes o Jaundice
 Inclusions: o Sore tongue
o Nucleated RBC o other CNS disease
o Howell-Jolly bodies  Imerslun-Grasbeck Syndrome – mutations for cubilin
o Pappenheimer boides and amnionless that decreased endocytosis of the
o Basophilic Stipplings intrinsic factor–vitamin B12 complex by ileal
o Cabot rings enterocytes.
VITAMIN B12 DEFICIENCY / COBALAMIN  Schilling Test: Obsolete test in which was done to
 DUE TO: establish the cause of vitamin B12 deficiency in a
o Malabsorption states patient with undetectable IF antibody and now
o Total Gastrectomy- – malabsorption of vitamin replaces by anti-IF assay (anti-parietal cell
B12 antibodies).
o Atophic Gastritis
PADAYHAG, RIGIDOR S. | MLS-3D 5
 HEMATLOGY 2
Clinical Hematology
RMT
Midterm Topic 1- ADDITIONAL NOTE – Introduction to 2022
Anemia
o However, because the test requires a 24-hour  CLINICAL FINDINGS:
urine collection and the use of radioactive o Photosensitivity
cobalt in vitamin B12. o Abdominal pain
FOLATE DEFICIENCY o CNS disorders
IRON OVERLOAD
 Has a blood picture & Clinical symptoms similar to Vit.  HEMOCHROMATOSIS - ↑ absorption of Iron & systemic
B12 deficiency except there’s no CNS involvement iron overload
 DUE TO:  Iron deposits in the Liver
o Poor diet or Malabsorption states HEMOSIDEROSIS
o Pregnancy  Failure to use Iron as Heme
o ↑ demand of Folate or ↑loss of Folate  Secondary iron accumulation
o Chemotherapeutic Anti-Folic Acid drugs such  Iron deposits in Parenchymal cells & Kupffer cells in the
as Methotrexate portal tract
 LAB FINDINGS: LEAD POISONING
o Macro-Ovalocytes  Multiple blocks in the Protoporphyrin pathway affect Heme
o Hypersegmented Neutrophils synthesis
o Presence of Witch Inclusion Bodies  In children, it’s because of “PICA” or finger food
o Bone marrow: Erythroid Hyperplasia  In Adult, it’s usually occupational
o ↑ B1, Iron, & LDH  ↓ enzyme DELTA-AMINO LEVULINIC DEHYDRATASE
 LAB FINDINGS:
o ↓ Platelet count
o Blood usually >40 ug/mL
o ↓ WBC count o Ringed sideroblast
o ↓ Reticulocyte count o Bone marrow: Erythroid Hyperplasia
o ↑ Reticulocyte count
o ↓ OFT
 CLINICAL FINDINGS:
o Abdominal pain
o Muscle weakness
o Gum lead line that forms blue/black deposits of Lead
NON-MEGALOBLASTIC ANEMIA Sulfate
 Problem is within the RBC membrane due to ↓
Cholesterol synthesis which allows it to expand but
susceptible to Lysis
 Connected with Alcoholism, Liver diseases, &
conditions that cause Accelerated Erythropoiesis
 LAB FINDINGS:
o Presence of Spurr cells & Acanthocytes
OTHERS
ERYTHROCYTOSIS
 Excess production of RBC
 Transient, body will produce more RBC to compensate with
Hypoxia
o PRIMARY ERYTHROCYTOSIS - uncontrolled
growth of cells for no apparent prupose
REFRACTORY ANEMIA
 Deals with Myelodysplasia
 Once you have abnormal cells, it will produce Dacryocytes
 The precursors are Megaloblastic
PORPHYRIAS
 Genetically-Acquired inborn error of metabolism
 Deficiency of enzymes involved in Protoporphyrin Pathway
of Heme synthesis
 Heme precursors before the block accumulate in the
tissues, & large amounts are excreted in urine or feces
 What’s affected is the level of D-ALA
 Partners with Sideroblastic Anemia
 GENETIC PORPHYRIAS- manifestations may be “To everyone with a dream, know that your
Neurologic (excruciating pain & other neurologic dreams are valid. And on your path you are
symptoms) or Cutaneous never denied, only redirected.”
 LAB FINDINGS:
o ↑Urine Phorphobilonogen -Catriona Gray

PADAYHAG, RIGIDOR S. | MLS-3D 6