Robbins and Cotran Review of Pathology ( PDFDrive ) (1)

4 8 8 U N I T I I   Diseases of Organ Systems

result from autosomal recessive mutation in a­ denosine de- 60  D  The figure shows a mass that is typical of adenocar-
aminase with accumulation of ­purine metabolites toxic to T cinoma of the ascending colon. Such cancers are unlikely to
cells. In SCID, although T cells are primarily involved, there obstruct, but they can bleed a small amount over months to
is secondary impairment of B-cell function, so that affected years, causing iron deficiency anemia. This relatively young
individuals have diminished IgG levels and no IgA or IgM, woman has evidence for an additional cancer, an endometrial
and decreased T-cell function, resulting in increased suscep- cancer, and this combination is most likely due to an inherit-
tibility to virtually all infectious organisms. ed mutation in one of the DNA mismatch-repair genes, such
as MSH2 and MLH1. Homozygous loss of these genes can
PBD9 241–242  BP9 141  PBD8 233  BP8 152–153 give rise to right-sided colon cancer and endometrial cancer.
Such a mutation is typically associated with microsatellite
57  F  Myotonic dystrophy is a form of muscular dystro- instability. In contrast the APC gene, a negative regulator of
phy in which there are increased CTG trinucleotide repeat β-catenin in the WNT signaling pathway, is associated with
sequences in the gene. Weakness in skeletal, cardiac, and familial adenomatous polyposis syndrome and most spo-
smooth muscle develops, along with cataracts, dementia, radic colon cancers. This latter pathway also is known as the
gonadal atrophy, and hypogammaglobulinemia. Deficiency adenoma-carcinoma sequence, because the carcinomas develop
of α-1,4-glucosidase leads to Pompe disease in infancy. Ab- through an identifiable series of molecular and morphologic
sence of dystrophin characterizes Duchenne muscular dys- steps. Loss of the PTEN tumor-suppressor gene is seen in en-
trophy, which affects young boys. The FGFR3 mutation is dometrial carcinomas not associated with colon carcinoma
seen in achondroplasia, a form of short-limbed dwarfism. and with some hamartomatous polyps of the colon. Infec-
Mutations in the mitochondrial oxidative phosphorylase tion with some strains of human papillomavirus leads to Rb
genes (mitochondrial myopathies) can produce neurodegen- protein inactivation and development of cervical carcinoma.
erative disorders and hearing loss, in addition to myopathy. Mutation with activation of c-KIT tyrosine kinase activity oc-
Myophosphorylase is diminished in McArdle disease, which curs in gastrointestinal stromal tumors, which respond well
causes muscle pain on strenuous exercise. to treatment with imatinib mesylate, a tyrosine kinase inhibi-
tor also used to treat chronic myelogenous leukemia.
PBD9 1244  BP9 804  PBD8 1269–1270  BP8 828–829
PBD9 810–814  BP9 597–600  PBD8 822–825  BP8 622–624
5 8  E  Both the ethanol and the immobilization with re-
duced local blood flow predispose to rhabdomyolysis from 6 1  A  Was the death of Napoleon Bonaparte the result of
skeletal muscle injury. Myoglobin is released from the in- arsenic poisoning perpetrated by former enemies? The FBI
jured muscle cells, and it is toxic to renal tubules and can analyzed a hair sample in 1995 and found increased arsenic
lead to toxic acute tubular necrosis. Cystine crystals are rare levels, but the amount was equivocal. Another hypothesis
and may represent cystinuria or severe liver disease. Glu- is that the wallpaper at Longwood House, where he lived,
cosuria is indicative of diabetes mellitus. Hyaline casts can contained copper arsenate and became moldy, releasing ar-
be found in healthy persons, and large numbers suggest re- sine vapor. A third hypothesis suggests that he died of the
duced urine output. Ketonuria occurs when intake or use of effects of gastric cancer, not related to arsenic ingestion, sub-
carbohydrates is reduced. stantiated by an observation at autopsy of lymphadenopathy
­adjacent to the stomach. Chronic arsenic exposure has been
PBD9 927–929  BP9 806  BPD8 936–938  BP8 564–566 associated with a greatly elevated risk of skin cancer and pos-
sibly of cancers of the lung, liver (angiosarcoma), bladder,
59  D  These findings strongly suggest a ruptured ectopic kidney, and colon. Beryllium acutely produces a pneumoni-
pregnancy—hence human chorionic gonadotropin levels tis, and long-term exposure leads to nonnecrotizing granu-
would be increased. Gonococcal and chlamydial infections are lomas, similar to sarcoidosis. Chromium or nickel exposure
risk factors for pelvic inflammatory disease, which increases may lead to respiratory tract cancers. Cobalt poisoning can
the risk of ectopic pregnancy. A ruptured ectopic pregnancy produce pulmonary interstitial fibrosis. Lead poisoning can
may lead to disseminated intravascular coagulation with in- produce abdominal pain, anemia, neuropathy, and decreased
creased partial thromboplastin time and prothrombin time, mental sharpness, but it is not associated with malignancies.
but the normal platelet count in this patient suggests that this
has not yet occurred. Factor XIII, which stabilizes fibrin clots, PBD9 412–413, 1155  BP9 275–276, 863  PBD8 408  BP8 285
can be deficient, but this is extremely rare. Bleeding is first ob-
served in the neonatal period; older patients may have poor 6 2  E  This woman has features seen in individuals who
wound healing, intracerebral hemorrhage, infertility (men), are bedridden for extended periods. There is a large saddle
and abortion (women). Decreased follicle-stimulating hor- thromboembolus in the pulmonary arterial trunk. Antiphos-
mone is typical of pituitary failure, which does not explain pholipid syndrome can include thromboembolic events, but
the bleeding. An increase in carcinoembryonic antigen is seen osteoporosis, decubitus ulcers, and muscle wasting are not
in some gastrointestinal tract neoplasms, but this patient is features. Aplastic anemia leads to high-output congestive
young to have such malignancies. Amebiasis would produce heart failure, bleeding diathesis from thrombocytopenia, and
a bloody diarrhea, and perforation of the colon is uncommon. risk of infections. Chronic alcoholism produces chronic liver
Schistosomiasis resulting from Schistosoma haematobium can disease that predisposes to bleeding problems, not throm-
produce hematuria, but the bladder is not perforated. bosis. Blunt trauma is marked by contusions and fractures.
Malnutrition could account for decreased bone density from
PBD9 368, 383, 1036  BP9 701  PBD8 1053–1054  BP8 734–735 osteomalacia, poor wound healing with skin ulceration, and

C H A P T E R 3 0   Final Review and Assessment 4 8 9

muscle wasting, but coagulopathy with bleeding is more 66  B  Pneumocystis jiroveci pneumonia is shown with Go-
likely to occur than thromboembolism. mori methenamine silver stain. The spectrum of opportunis-
tic infections, wasting syndrome, and lymphopenia suggest
PBD9 127, 697–699  BP9 90, 484–485  PBD8 706–707  BP8 98–99 AIDS complicating HIV infection. This spectrum of findings
is not typical of patients with systemic lupus erythemato-
63  C  The combination of nongonococcal urethritis, ar- sus (SLE), who have a positive ANA test result. When SLE
thritis, and conjunctivitis suggests reactive arthritis, one of is treated with immunosuppressive therapy, opportunistic
the spondyloarthropathies; the changes in the spine can re- infections are common. SLE-like disease is seen in C2 defi-
semble ankylosing spondylitis and can be equally debilitat- ciency. B-cell function tends to be preserved in HIV infection,
ing. ANCA is indicative of various forms of vasculitis, such so marked hypogammaglobulinemia is unlikely to be pres-
as granulomatous vasculitis and microscopic polyangiitis. ent. The neutrophil oxidative burst assay is used to test for
The ANA test result is positive in many autoimmune dis- chronic granulomatous disease, an immunodeficiency condi-
eases, such as systemic lupus erythematosus (SLE), but it is tion in which bacterial infections are more likely to appear in
not a feature of spondyloarthropathies. Lyme disease can in- children. Rapid plasma reagin (RPR) is a screening test for
clude large joint arthritis, but not urethritis or conjunctivitis. syphilis, which is a sexually transmitted disease that is not
Rapid plasma reagin (RPR) is a screening test for syphilis, accompanied by immunodeficiency.
which can include arthritis of large joints (Charcot joint) in
the tertiary form, but it takes decades to develop. Rheuma- PBD9 348, 711  BP9 501–502  PBD8 246, 720  BP8 525–526
toid factor is a feature of rheumatoid arthritis, which initially
manifests more commonly in small joints of the hands and 6 7  A  Metabolic acidosis, tinnitus, platelet function abnor-
feet. U1-RNP is a marker for mixed connective tissue disease, malities, and gastritis with ulceration are typical effects of
which has features of rheumatoid arthritis, scleroderma, excessive aspirin ingestion. Acetaminophen in large quanti-
polymyositis, and SLE; arthralgias are not accompanied by ties may produce hepatotoxicity. Adalimumab, a monoclonal
joint destruction or deformity. antibody directed against tumor necrosis factor, and metho-
trexate are drugs used to treat rheumatoid arthritis and do
PBD9 1213  BP9 786  PBD8 1241  BP8 147–148 not have antiplatelet effects. Oxycodone is an opiate, and pro-
poxyphene is a nonnarcotic analgesic; these drugs do not have
6 4  E  Von Hippel–Lindau disease is rare and results from significant effects on the gastrointestinal tract or on platelets.
acquired or inherited mutation in a tumor suppressor gene.
The neoplasms in this case include, in order, retinal angio- PBD9 422–423  BP9 284  PBD8 417  BP8 294
mas, adrenal pheochromocytoma, cerebellar hemangioblas-
tomas, and renal cell carcinomas producing erythropoietin. 68  B  Choriocarcinoma is the most aggressive, and the
Gardner syndrome has the same mutation in the adenoma- least common, form of gestational trophoblastic disease. It
tous polyposis coli (APC) gene as familial polyposis, but also can metastasize widely, particularly to the lungs and vagina,
has osteomas, epidermal cysts, and fibromatoses. The MET and also to the brain, liver, and kidney. The neoplasm is com-
oncogene is mutated in papillary renal carcinomas (not as- posed of a malignant-appearing syncytiotrophoblast and
sociated with other tumors elsewhere) and in Denys-Drash forms a soft, hemorrhagic mass that can rupture and bleed.
syndrome, which also includes Wilms tumor plus gonadal In addition, the amount of human chorionic gonadotropin
dysgenesis and nephropathy. Neurofibromatosis type 2 in- (hCG) produced by a choriocarcinoma is marked; hCG shares
cludes schwannomas, meningiomas, gliomas, and ependy- the same α-subunit as other glycoprotein hormones, such as
momas. Tuberous sclerosis is one of the phakomatoses with thyroid-stimulating hormone (TSH), and may enhance the
cortical hamartomas called tubers, renal angiomyolipomas, effect of TSH, leading to features of hyperthyroidism. Many
cardiac rhabdomyomas, and subungual fibromas. Beckwith- choriocarcinomas respond to chemotherapy. Endometrial
Wiedemann syndrome includes Wilms tumor, hemihyper- adenocarcinoma is most often seen in postmenopausal wom-
trophy, and adrenal cytomegaly. en. Clear cell carcinomas of the vagina most often appear in
young women whose mothers were given diethylstilbestrol
PBD9 299, 1317  BP9 847  PBD8 295, 964, 1343  BP8 201, 574, 797, 901 (DES) during pregnancy. A leiomyosarcoma is an uncom-
mon lesion in women and usually produces a large uterine
6 5  A  Limited scleroderma (former CREST syndrome), a mass. Likewise, a malignant mixed müllerian tumor is a rare
form of systemic sclerosis, does not progress to include se- neoplasm seen in women. Sarcoma botryoides is a neoplasm
rious pulmonary fibrosis or renal disease. Therefore she is found in girls younger than 5 years.
less likely to have diffuse scleroderma, which is associated
with the anti–DNA topoisomerase antibody. Antimicro- PBD9 1041  BP9 703  PBD8 1059–1060  BP8 736–737
somal (anti–thyroid peroxidase) antibodies are seen in au-
toimmune thyroid diseases, such as Hashimoto thyroiditis 69  C  She has rheumatoid arthritis with anemia of chronic
and Graves disease. Antimitochondrial antibody appears disease. Despite abundant stored iron stores, such anemias
most frequently in primary biliary cirrhosis. ANCA can be are caused by impaired transfer of iron from macrophages
a marker for various forms of vasculitis. Anti-transglutamin- to developing erythroid cells. Hepcidin is synthesized in the
ase antibodies are seen in celiac disease, which is marked by liver and normally released in response to increased intra-
malabsorption, not esophageal dysmotility. hepatic iron levels. Hepcidin inhibits ferroportin function in
macrophages and thus prevents transfer of iron. Hepcidin
PBD9 228–230  BP9 132–134  PBD8 223–225  BP8 149–151

4 9 0 U N I T I I   Diseases of Organ Systems

production in the liver is increased in chronic inflammatory where the primary defect is in the hematopoietic cells, or the
states by the action of inflammatory mediators such as IL-6. marrow cells can deliver normal genes to the affected tissues.
Rheumatoid factor is likely present but does not affect hep- Even if one could transduce the fibrillin-1 gene into T cells,
cidin levels. TNF plays a role in the joint inflammation. GM- the protein cannot be delivered to the extracellular matrix.
CSF can cause increased production of normal macrophages. Marfan syndrome does not have abnormal lysosomes, and
the vascular disorders are not the result of atherosclerosis ac-
PBD9 651–653  BP9 421  PBD8 661–662, 1237–1240  BP8 437 celerated by dietary factors.

70  B  Rickets in children (and osteomalacia in adults) results PBD9 144–145, 502–504  BP9 220–221, 344–345 
from vitamin D deficiency. The left figure panel shows a costo- PBD8 144–145, 508–510  BP8 230–232, 359–361
chondral junction in which the palisade of cartilage is lost, with
widened irregular trabeculae with uncalcified osteoid. Com- 73  E  Vitamin A deficiency leads to epithelial disorders af-
pare with a normal costochondral junction in the right panel fecting the cornea, skin, respiratory tract, and urinary tract.
with orderly transition from cartilage to new bone. Exposure It is the leading cause for preventable blindness worldwide.
to sunlight is essential for synthesis of vitamin D from endog- Squamous metaplasia (shown) in the respiratory tract in-
enous sources. Sufficient vitamin D reduces the risk for cancer, creases the risk of infection; desquamation of keratin de-
inflammatory conditions, and atherosclerosis. Thus the sage bris forms the nidus of urinary tract calculi. Hyperkeratosis
advice for children: go outside and be active. Lack of dietary and follicular plugging affect the epidermis. Cystic fibrosis
fresh fruits and vegetables can lead to scurvy from vitamin C leads to an increased risk of respiratory tract infections, par-
deficiency, with poor osteoid formation, but other connective ticularly infections caused by Pseudomonas, from widespread
tissues would also be affected. Hypopituitarism could lead to bronchiectasis; the skin and eye are not affected. Congenital
reduced growth hormone with reduced stature but no defor- syphilis can produce bone deformities and gummas. HIV
mities. Mutations affecting collagen genes could lead to os- infection can be complicated by opportunistic infections, in-
teogenesis imperfecta with risk for fractures. Trauma leads to cluding infections of the respiratory tract, but keratomala-
fractures, and the callus of healing fractures has an orderly cia is not a feature of HIV infection. Kartagener syndrome
process of ossification. Polymorphisms of vitamin D receptor can lead to bronchiectasis from an altered respiratory tract
affect can be involved in the pathogenesis of osteoporosis. epithelium in which the ciliary dynein arms are absent; situs
inversus is present, but not eye and skin changes.
PBD9 438–442  BP9 298–301   PBD8 433–437  BP8 309–312
PBD9 436–438  BP9 296–298  PBD8 430–433  BP8 306–309
7 1  D  The sudden nature of the death requires investiga-
tion by the medical examiner (coroner), who would notify the 74  E  The pattern of metastases with seeding of the peri-
local law enforcement agency on discovery of the findings in toneal cavity along with the microscopic and serum tumor
this case. The pattern of injuries is consistent with vigorous markers are most characteristic for an ovarian serous cystad-
shaking of the infant. Because an infant’s head is larger in pro- enocarcinoma, the most common malignant neoplasm aris-
portion to its body compared with an adult, it cannot counter ing in the ovary. Ileal adenocarcinomas are rare and would
the shaking with neck musculature. Grasping the arms of the probably lead to bowel obstruction. Carcinoid tumors are
infant strongly and pressing or hitting the head against a hard unlikely to be widely metastatic. Choriocarcinomas are as-
surface increases the risk of internal injuries, including frac- sociated with high hCG levels and hemorrhagic metastases.
tures. Another feature of trauma with shaking of the infant’s A malignant mesothelioma is a rare complication of asbesto-
head is diffuse axonal injury with axonal retraction balls from sis. It is unlikely that a cystadenocarcinoma would recur 10
marked stretching and tearing with acceleration-deceleration years later. Cystadenomas are benign.
forces. Congenital syphilis produces osteochondritis with
skeletal deformities, not fractures, and without a bleeding PBD9 1024–1026  BP9 697  PBD8 1044  BP8 730
tendency. Hemophilia A could account for hemorrhages in a
child or adult, but not fractures. Osteogenesis imperfecta can 75  D  We go back to the future in the thirteenth century
account for fractures, but not hemorrhages. In sudden infant for this answer from Rumi of Balkh, and it is applicable for
death syndrome, there would be no signs of trauma. Thana- any time and place. The art of medicine is more than science,
tophoric dysplasia is a lethal form of short-limbed dwarfism. and relies upon human interaction. The concept of empathy
is part of this. The authors have enough medical conditions
PBD9 471–473, 1259–1262  BP9 252–254, 820–822  to know its importance and are passing that understanding
PBD8 471–473, 1289  BP8 259–261, 869 on to you. Do not let it go. You need it for your family, your
friends, and your patients.
72  A  He has features of Marfan syndrome, and although
the primary defect is mutation in the fibrillin-1 gene and PBD, BP inclusive
hence poor formation of microfibrils, there is an important
secondary effect on transforming growth factor beta (TGF-β) 7 6 (All are correct) We hope that you have advanced
bioavailability. Normally microfibrils sequester TGF-β, but your knowledge and are now better able to help others in
in Marfan syndrome, abnormal microfibrils allow excessive your health science career. Go make the world a better place
TGF-β signaling, which is responsible for the cardiac symp- for everyone!
toms. Bone marrow transplants are useful in those diseases
PBD, BP inclusive

Figure Credits

Chapter 5 Chapter 13

FIGURE 5-11: From Nussbaum RL, McInnes RR, Willard HF: Thompson FIGURE 13-53: Courtesy Dr. George Murphy, University of Pennsylvania
and Thompson Genetics in Medicine, ed 6, Philadelphia, Saunders, 2001, Perelman School of Medicine, Philadelphia.
p 212.
Chapter 15
FIGURE 5-18: Courtesy Department of Pathology, University of Pittsburgh
Medical Center, Pittsburgh. FIGURE 15-41: From the teaching collection of the Department of Pathology,
The University of Texas Southwestern Medical School, Dallas.
FIGURE 5-26: Courtesy Dr. Vijay Tonk, Department of Pathology, The
University of Texas Southwestern Medical Center, Dallas. Chapter 16

FIGURE 5-28: Courtesy Dr. Nancy R. Schneider and Jeff Doolittle, FIGURE 16-10: Courtesy Drs. E.E. Vokes, S. Lippman, et-al, Department
Cytogenetics Laboratory, The University of Texas Southwestern Medical of Thoracic/Head and Neck Oncology, Texas Medical Center, Houston.
Center, Dallas. Reprinted with permission from N Engl J Med 328:184, 1993.

Chapter 6 Chapter 17

FIGURE 6-21: Courtesy Dr. Richard Sontheimer, Department of FIGURE 17-64: Courtesy Dr. Tad Wieczorek, Brigham and Women’s
Dermatology, The University of Texas Southwestern Medical School, Dallas. Hospital, Boston.

FIGURE 6-31: Courtesy Dr. Trace Worrell, Department of Pathology, The Chapter 20
University of Texas Southwestern Medical School, Dallas.
FIGURE 20-7: Courtesy Dr. M.A. Ventkatachalam, Department of Pathology,
Chapter 8 The University of Texas Health Sciences Center, San Antonio.

FIGURE 8-16: Courtesy Dr. Arlene Sharpe, Brigham and Women’s Hospital, FIGURE 20-15: Courtesy Dr. Helmut Rennke, Department of Pathology,
Boston. Brigham and Women’s Hospital, Boston.

FIGURE 8-60: Courtesy Dr. Willy Pressens, Harvard School of Public Health, FIGURE 20-40: Courtesy Dr. M.A. Ventkatachalam, Department of
Boston. Pathology, The University of Texas Health Sciences Center, San Antonio.

Chapter 9 Chapter 21

FIGURE 9-25: Courtesy George Katsas, MD, forensic pathologist, Boston. FIGURE 21-8: Courtesy Dr. Christopher Corless, University of Oregon,
Eugene.
FIGURE 9-27: From the teaching collection of the Department of Pathology,
The University of Texas Southwestern Medical School, Dallas. Chapter 22

Chapter 11 FIGURE 22-7: Courtesy Dr. Jag Bhawan, Boston University School of
Medicine, Boston.
FIGURE 11-20: From the teaching collection of the Department of Pathology,
The University of Texas Southwestern Medical School, Dallas. FIGURE 22-41: Courtesy Dr. Christopher Crum, Brigham and Women’s
Hospital, Boston.
FIGURE 11-22: Courtesy Tom Rogers, MD, Department of Pathology, The
University of Texas Southwestern Medical School, Dallas. Chapter 23

FIGURE 11-47: Courtesy Tom Rogers, MD, Department of Pathology, The FIGURE 23-26: Courtesy Dr. Jack G. Meyer, Brigham and Women’s
University of Texas Southwestern Medical School, Dallas. Hospital, Boston.

Chapter 12

FIGURE 12-10: Courtesy Arthur Weinberg, MD, Department of Pathology,
The University of Texas Southwestern Medical School, Dallas.

491

492 Figure Credits Chapter 30

Chapter 28 FIGURE 30-62: Courtesy Dr. Linda Margraf, Department of Pathology, The
University of Texas Southwestern Medical School, Dallas.
FIGURE 28-55: Courtesy Eileen Bigio, MD, Department of Pathology, The
University of Texas Southwestern Medical School, Dallas.
FIGURE 28-59: Courtesy Eileen Bigio, MD, Department of Pathology, The
University of Texas Southwestern Medical School, Dallas.

NORMAL VALUES Reference Range

BLOOD: PLASMA, SERUM <30 U/L

Alanine aminotransferase (ALT), serum 3.5-5.5 g/dL
30-130 U/L
Albumin 30-110 U/L
Alkaline phosphatase, serum (adult) <40 U/L
Amylase, serum (adult) 0.1-1.0 mg/dL // 0.0-0.3 mg/dL
Aspartate aminotransferase (AST), serum 8.4-10.2 mg/dL
Bilirubin, serum (adult) total // direct <200 mg/dL // >35 mg/dL
Calcium, serum (Ca++) 0.5-1.2 mg/dL
Cholesterol, total // HDL <0.5 μg/mL
Creatinine, serum
D-dimer 135-145 mEq/L
Electrolytes, serum 3.5-5.0 mEq/L
  Sodium (Na+) 95-105 mEq/L
  Potassium (K+) 22-28 mEq/L
  Chloride (Cl–) 9-14 mEq/L
 HCO3
  Anion gap 7.35-7.45
Gases, arterial blood (room air) 35-45 mm Hg
 pH 80-100 mm Hg
 PCO2 22-28 mEq/L
 PO2 2.3-3.5 g/dL
 HCO3 70-110 mg/dL (fasting)
Globulin 16-200 mg/dL
Glucose, serum <6%
Haptoglobin 50-160 μg/dL
Hemoglobin A1c 250-450 μg/dL
Iron, serum 45-90 U/L
Iron binding capacity, total (TIBC) 16-63 U/L
Lactate dehydrogenase (LDH), serum 275-295 mOsmol/kg H2O
Lipase, serum 3.0-4.5 mg/dL
Osmolality, serum 6.0-7.8 g/dL
Phosphorus (inorganic), serum 0.5-5.0 μU/mL
Proteins, serum, total 5-12 μg/dL
Thyroid stimulating hormone (TSH) <150 mg/dL
Thyroxine (T4), serum 7-20 mg/dL
Triglycerides, serum 3.0-8.2 mg/dL
Urea nitrogen, serum
Uric acid, serum Male: 4.1-5.9 million/mm3
HEMATOLOGIC Female: 3.6-5.5 million/mm3
Erythrocyte (RBC) count Male: 0-15 mm/hr
Female: 0-20 mm/hr
Erythrocyte sedimentation rate (ESR) Male: 41%-50%
Female: 36%-46%
Hematocrit Male: 13.5-16.5 g/dL
Female: 12.0-15.0 g/dL
Hemoglobin, blood 4500-11,000/mm3
54%-62%
Leukocyte (WBC) count, total 3%-5%
  Segmented neutrophils 1%-3%
 Bands 0%-1%
 Eosinophils 25%-33%
 Basophils 3%-7%
 Lymphocytes 26-34 pg/cell
 Monocytes 80-100 μm3
Mean corpuscular hemoglobin (MCH) 25-40 sec
Mean corpuscular volume (MCV) 150,000-400,000/mm3
Partial thromboplastin time, activated (aPTT) 11-15 sec
Platelet count Adult: 19-25 kg/m2
Prothrombin time (PT)
BODY MASS INDEX (BMI)