Normal Lab Values

Week 14: Renal & Hematopoietic Disease

Suggested readings from
Robbins 8th ed.
Anemias: pp.639-676
 
Hematologic Malignancies: pp. 589-638
 
Non-glomerular renal diseases: 935-967
 
Glomerular renal diseases: 907-935
 
Non-glomerular renal diseases: 935-967

Cases for Week 14

Review Items for Week 14: Renal Pathology

Review Items for Week 14: Hematologic Pathology

 

Pathology Case Descriptions

CASE NUMBER 413
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Clinical History: This 57-year-old male presented with back pain, lytic lesions in many bones, Bence-Jones proteinurea and marked plasmacytosis of the marrow. Some therapeutic response was obtained with chemical agents and X-radiation. Death followed pneumonia and sepsis.

Image Gallery:

(Summary of Gross Findings - click here)
Many of the bones contained poorly delineated, soft gelatinous red tumor masses of various dimensions. Plain film of the skull shows sharply punched out bone lesions.
(Summary of Microscopic Findings - click here)
The marrow is heavily infiltrated with plasma cells which vary in degree of maturation. Islets of normoblasts are present, but granulocytes and megakaryocytes are markedly decreased. There is considerable loss of trabecular and cortical bone.
(Review Normal Histology - click here)
Specimen No. 67. Bone marrow, human, H&E
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A thin layer of compact/dense bone borders this section, with internal cancellous/spongy bone. The spaces between bony spicules are filled with hematopoietic cells. Not the large numbers of (round, empty) fat cells present within the marrow space. The fat is lost during processing into paraffin sections. Megakaryocytes can be readily identified, since they are approximately 5-fold larger than most bone marrow cells and contain strongly eosinophilic cytoplasm and multiple nuclei.

(slide and description courtesy of Dr. Laura Hale, Duke PATHOL725 course director)

 

413-1. This following is a common feature of this neoplasm:

  1. Presents with Waldenstrom macroglobulinaemia
  2. Proliferation and survival of neoplastic cells are dependent on IL-1
  3. Most common site of bone involvement is the epiphyses of long bones
  4. May be associated with excretion of Bence-Jones proteins

ANSWER

 

413-2. What is the diagnosis?

  1. Lymphoplasmacytic lymphoma
  2. Plasmacytoma
  3. Castleman’s disease, plasma cell variant
  4. Multiple myeloma
  5. Plasmablastic lymphoma

ANSWER

 

413-3. Which of the following cytogenetic alterations is associated with multiple myeloma?

  1. t (11; 18) translocation
  2. t (14; 18) translocation
  3. t (11; 14) translocation
  4. t (8; 14) translocation
  5. t (9; 22) translocation

ANSWER

 

 

 

CASE NUMBER 295
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Clinical History: A 16-year-old boy presented with cervical lymphadenopathy and was found to have a mediastinal mass. The neck node was biopsied.

Image Gallery:

(Summary of Gross Findings - click here)
The lymph node was enlarged, and remarkable for fibrous bands separating areas of firm, fleshy material.
(Summary of Microscopic Findings - click here)
The normal lymph node architecture is completely destroyed. In its place are thick bands of collagen, separating islands of lymphoid tissue. In some of these nodules, there is a mixed infiltrate consisting of lymphocytes, eosinophils, some neutrophils and plasma cells, and numerous large cells with highly pleomorphic nuclei. Nuclei are frequently multi lobulated but classic binucleate Reed-Stemberg cells are uncommon. Many cells are so-called "lacunar variants", with nuclei which have artefactually shrunken away from their cytoplasmic borders, leaving a clear space than can often easily be appreciated at low power.
(Review Normal Histology - click here)
Norm No. 29 Lymph node
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The lymph node contains a cortex which includes the lymphoid follicles and a medulla which is looser tissue containing the lymphatic channels and blood vessels.

 

295-1. What is the BEST diagnosis?

  1. Nodular sclerosis Hodgkin lymphoma
  2. Lymphocyte predominant Hodgkin lymphoma
  3. Lymphocyte depleted Hodgkin lymphoma
  4. Mixed cellularity Hodgkin lymphoma

ANSWER

 

295-2. The following may represent the phenotype of neoplastic cells EXCEPT:

  1. CD20+ CD79a+ CD30+ CD15-
  2. CD20- CD79a- CD30+ CD15+
  3. CD20- CD79a- CD30- CD15+
  4. CD20+ CD79a- CD30+ CD15+
  5. CD20- CD79a- CD30+ CD15-

ANSWER

 

 

 

CASE NUMBER 9 (Micro Case 7)
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Clinical History: A 51-year-old male had a "neurogenic bladder", caused by a spinal cord tumor. He had multiple bladder infections which were treated with antibiotics. He had surgery to remove the tumor. Postoperatively, he developed fever and costovertebral angle tenderness which did not respond to antibiotics. He expired and an autopsy was performed.

Image Gallery:

(Summary of Lab & Gross Findings - click here)
The organism grew on blood agar and on MacConkey agar. Gram stain of a blood culture showed gram negative rods. A catheterized urine specimen was obtained before death. Greater than 100,000 colonies of E. Coli were cultured. The bladder was distended, with a thickened, trabeculated wall. There was a bilateral hydroureter and hydronephrosis. The left kidney was swollen, and the cut surface showed soft foci of yellow streaks extending toward the pelvis.
(Summary of Microscopic Findings - click here)
Naked eye examination of the slide reveals dark streaks extending from the outer cortex to the inner medulla. Microscopically these are foci of acute inflammation, including necrosis and hemorrhage, with masses of polymorphonuclear leukocytes that are also found in many tubules.
(Review Normal Histology - click here)
Norm No. 2 Kidney
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The kidney excretes soluble waste from the body and controls electrolyte balance. It consists of the cortex and the medulla. Within the outer cortex, glomeruli with delicate capillary loops are seen.  The basement membrane is thin and without inflammation or thickening. Bowman’s capsule that surrounds the glomerulus is thin. The interstitium demonstrates no evidence of inflammation or fibrosis.  In the areas between the glomeruli, tubules and arterioles are seen. The tubules are intact.  The vessels exhibit no narrowing or wall thickening. The inner medulla of the kidney contains only tubules and blood vessels. Larger arteries and veins are located at the interface between cortex and medulla.

 

9-1. What is your diagnosis?

  1. Acute pyelonephritis
  2. Acute glomerulonephritis
  3. Chronic pyelonephritis
  4. Chronic glomerulonephritis

ANSWER

 

9-2. ALL of the following are risk factors for this condition EXCEPT:

  1. Reflux nephropathy
  2. Congenital vesicoureteral reflux
  3. Posterior urethral valves
  4. Acetaminophen (Paracetamol)overdose
  5. Urolithiasis

ANSWER

 

 

 

CASE NUMBER 12
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Clinical History: A 65-year-old woman had experienced increasing malaise with nocturia and polyuria for the past year. Her blood pressure was 170/95. Urinalysis showed 1+ proteinuria. Serum BUN and creatinine were elevated. She developed worsening renal failure and died of pneumonia.

Image Gallery:

(Summary of Gross Findings - click here)
The kidneys are small with irregular and coarse U-shaped corticomedullary scars overlying dilated, blunt, deformed calyces. Extensive scarring is noted at the hilum of each kidney. Evidence of hydronephrosis and cortical thinning is also observed.
(Summary of Microscopic Findings - click here)
Interstitial tissue shows prominent infiltration by lymphocytes and plasma cells, and occasional polymorphonuclear neutrophils; irregular fibrous scars and peri-glomerular fibrosis. Tubules are dilated, many filled with eosinophilic casts giving the region a "thyroid-like" appearance. A few tubules contain polymorphonuclear neutrophils, indicating that this is an active exacerbation of a chronic pyelonephritis. Arteries are markedly thickened, with intimal proliferation resulting in narrowing of the lumen. Many arterioles show hyaline changes in their walls. Most glomeruli are replaced by fibrous tissue. A few are surprisingly normal in appearance with intact capillaries. There is a prominent peri-glomerular fibrosis in many regions with a thick rim of fibrous tissue circling the outside of Bowman's capsule.
(Review Normal Histology - click here)
Norm No. 2 Kidney
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The kidney excretes soluble waste from the body and controls electrolyte balance. It consists of the cortex and the medulla. Within the outer cortex, glomeruli with delicate capillary loops are seen.  The basement membrane is thin and without inflammation or thickening. Bowman’s capsule that surrounds the glomerulus is thin. The interstitium demonstrates no evidence of inflammation or fibrosis.  In the areas between the glomeruli, tubules and arterioles are seen. The tubules are intact.  The vessels exhibit no narrowing or wall thickening. The inner medulla of the kidney contains only tubules and blood vessels. Larger arteries and veins are located at the interface between cortex and medulla.

 

12-1. What is the BEST diagnosis?

  1. Chronic glomerulonephritis
  2. Chronic pyelonephritis
  3. Arteriolonephrosclerosis
  4. Nodular glomerulosclerosis
  5. Analgesic nephropathy

ANSWER

 

12-2. A child with hypertension should be studied to rule out:

  1. Chronic glomerulonephritis
  2. Arteriolonephrosclerosis
  3. Reflux nephropathy
  4. Renal artery dilatation
  5. Wilm’s tumor

ANSWER

 

 

 

 

CASE NUMBER 20
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Clinical History: This 55 year old female first came to medical attention when she complained of frequent urination, increased thirst and weight loss at age 15. Insulin dependent diabetes was diagnosed. She developed proteinuria at age 20. Her disease progressed until she became dialysis dependent at age 45. She expired due to pneumonia after a below knee amputation

Image Gallery:

(Summary of Gross Findings - click here)
The kidneys were small and each weighed 100 grams. The surface was irregular with pits and small cysts. (image courtesy of VA Commonwealth University)
(Summary of Microscopic Findings - click here)
There are glomerular lesions consisting of diffuse and nodular glomeroslerosis. Nodular glomerulosclerosis or Kimmelstiel-Wilson lesions are ball-like deposits of PAS positive material which contain trapped mesangial cells. These occur in 15-30% of long time diabetics and are virtually pathognomonic of the disease. Diffuse glomeruloslerosis usually appears as global sclerosis of the glomerular tuft. Chronic pyelonephritis, arterio and arteriolo nephrosclerosis as seen here are also typical findings in diabetic kidneys.
(Review Normal Histology - click here)
Norm No. 2 Kidney
[ImageScope] [WebScope]

The kidney excretes soluble waste from the body and controls electrolyte balance. It consists of the cortex and the medulla. Within the outer cortex, glomeruli with delicate capillary loops are seen.  The basement membrane is thin and without inflammation or thickening. Bowman’s capsule that surrounds the glomerulus is thin. The interstitium demonstrates no evidence of inflammation or fibrosis.  In the areas between the glomeruli, tubules and arterioles are seen. The tubules are intact.  The vessels exhibit no narrowing or wall thickening. The inner medulla of the kidney contains only tubules and blood vessels. Larger arteries and veins are located at the interface between cortex and medulla.

 

What is the MOST LIKELY diagnosis?

ANSWER

 

20-1. What is the most prominent glomerular lesion in this patient?

  1. Basement membrane thickening
  2. Nodular glomerulosclerosis
  3. Capsular drop
  4. Fibrin cap

ANSWER

 

20-2. Non-enzymatic glycosylation is fundamental to basement membrane thickening in the eye and kidney through:

  1. B-cell response to protein neoantigens
  2. T-cell response to protein neoantigens
  3. Protein cross linking
  4. Protein denaturation

ANSWER

 

20-3. The most common cause of end stage renal disease is:

  1. Hypertension
  2. Polycystic kidney
  3. Diabetes mellitus
  4. Glomerulonephritis

ANSWER

 

20-4. What type of glomerular lesion is seen characteristically in diabetic nephropathy?

  1. Basement membrane thickening
  2. Nodular glomerulosclerosis
  3. Capsular drop
  4. Fibrin cap
  5. ALL of the above

ANSWER

 

 

RENAL PATHOLOGY Review Items

Key Vocabulary Terms (click here to search any additional terms on Stedman's Online Medical Dictionary)

anuria nephrolithiasis
azotemia nephrosclerosis
bacteriuria nocturia
Bence Jones protein oliguria
cast proteinuria
dysuria pyelonephritis
glomerulonephritis pyuria
hematuria uremia
hepatorenal syndrome urolithiasis
hydronephrosis von Hippel-Lindau (VHL) syndrome    
Kimmelstiel-Wilson disease wire-loop lesion

LEARNING OBJECTIVES

Absolutely critical information you must know to practice medicine is in bold font.
Important information that will be needed for routine patient care is in regular font.
Information about less common diseases that you may encounter in clinical practice and that will probably appear on examinations is in italics

  1. List the clinical criteria for diagnosis and pathology
  2. Discuss the proper use of the following laboratory tests in the evaluation of urinary tract disease and interpret abnormalities of these parameters in clinical context:
    • creatinine
    • urea (blood urea nitrogen, BUN)
    • urinalysis

  3. Discuss the clinical and pathologic features of the following congenital renal anomalies:
  4. Compare and contrast the clinical and pathologic features of  cystic diseases of the kidney:
  5. Define the following terms as they apply to glomerular histopathology:
    • focal
    • diffuse
    • segmental

  6. Discuss clinical and pathologic features of the following glomerular diseases:
  7. Describe the major clinical and histopathologic findings associated with renal involvement by the following systemic diseases:
  8. Discuss lupus nephritis in terms of:
    • etiology and pathogenesis
    • clinical presentation
    • nomenclature, morphologic features, and prognosis of each of the five classes

  9. Discuss the clinical and pathologic features of renal tubular diseases:
  10. Discuss the significance of unilateral renal artery disease, including:
    • usual causes
    • mechanism(s) of clinical effects
    • morphologic changes in contralateral kidney
    • tests used for detection and localization

  11. Describe the pathophysiology of hypertension induced by renal artery constriction

  12. Compare and contrast benign and malignant nephrosclerosis with regard to:
    • pathogenesis
    • morphologic (gross and microscopic) appearance
    • clinical presentation, course, and prognosis

  13. List the three major thrombotic microangiopathies; describe the renal effects and pathogenesis in terms of:
    • microscopic appearance
    • clinical presentation, course, and prognosis

  14. Discuss renal vein thrombosis in terms of:
    • etiology/pathogenesis
    • morphology
    • method(s) of diagnosis
    • clinical and laboratory features

  15. Discuss urolithiasis in terms of:
    • composition and relative incidence of various types of stones
    • pathophysiologic abnormalities associated with the common types of stones
    • etiology and pathogenesis of stone formation
    • effect of location of stones on clinical and anatomic findings
    • clinical course and complications

  16. Discuss hydronephrosis in terms of:
    • etiologic factors and their relative frequencies
    • pathogenesis
    • morphology (gross and microscopic)
    • clinical course and prognosis

  17. Discuss the following renal neoplasms:

 

HEMATOPATHOLOGY Review Items

Key Vocabulary Terms (click here to search any additional terms on Stedman's Online Medical Dictionary)

achlorhydria leukemia
acute leukemia  leukemoid reaction
agnogenic (idiopathic) myeloid metaplasia leukocytosis
aleukemic leukemia leukoerythroblastosis
amyloidosis leukopenia
anemia lymphoma
anisocytosis  macrocytosis
autosplenectomy marginating pool
basophilic stippling maturation/storage pool
Bence Jones protein mean cell hemoglobin (MCH)
Birbeck granule (HX body) mean cell hemoglobin concentration (MCHC)
bronchus-associated lymphoid tissue (BALT) mean cell volume (MCV)
chronic leukemia microcytosis
circulating pool mucosa-associated lymphoid tissue (MALT)
coagulation myelodysplastic syndrome
complete blood count (CBC) myelophthisic syndrome
cryoglobulinemia myeloproliferative disorder
direct antiglobulin (Coombs) test nuclear-cytoplasmic asynchrony
dyserythropoiesis pancytopenia
dysmegakaryocytopoiesis petechiae
ecchymoses Philadelphia chromosome
erythropoiesis Plummer-Vinson syndrome
erythropoietin poikilocytosis
extramedullary hematopoiesis polychromasia
extravascular hemolysis proliferating pool
ferritin purpura
G6PD screen red cell distribution width (RDW)
granulocytopenia reticulocyte count
granulopoiesis Schilling test
haptoglobin sickle cell disease
hematocrit sickle cell prep
hematoma sickle cell trait
hemoglobin electrophoresis stem cell
hemostasis thalassemia 
hyperviscosity syndrome thrombocytopenia
hypochromia thrombocytosis
idiopathic thrombocytopenic purpura (ITP) thrombopoiesis
indirect antiglobulin (Coombs) test thrombopoietin
ineffective hematopoiesis thrombotic thromocytopenic purpura (TTP)
intravascular hemolysis total iron binding capacity (TIBC)
intrinsic factor transferrin

LEARNING OBJECTIVES

Absolutely critical information you must know to practice medicine is in bold font.
Important information that will be needed for routine patient care is in regular font.
Information about less common diseases that you may encounter in clinical practice and that will probably appear on examinations is in italics

  1. Define and state the significance of each of these peripheral blood smear findings:

  2. Define and state the significance of each of the following cells on a bone marrow smear:

  3. Explain:
    • the concept of reference (normal) range
    • the theory of the automated cell counter
    • the components of the complete blood count (CBC)
    • CBC application in patient evaluation

  4. Compare and contrast the reporting of leukocyte differential counts as relative percentages vs. absolute numbers, in terms of the advantages and disadvantages of each system.

  5. Discuss the stages of erythropoiesis in terms of:
    • morphology of each stage
    • stages in which hemoglobin is produced
    • lifespan of reticulocytes and mature red blood cells
    • mechanisms of degradation of senescent erythrocytes
    • factors (vitamin, minerals and hormones) which influence erythropoiesis

  6. Discuss the stages of granulopoiesis in terms of:
    • morphology of each stage
    • time to form and life span of mature granulocytes
    • basic functions of the different types of maturing granulocytes
    • factors which influence granulopoiesis.

  7. Discuss the stages of development of lymphocytes, plasma cells, and monocytes, in terms of:
    • morphology
    • life span of mature forms
    • functions of mature forms
    • factors which influence production.

  8. Discuss thrombocytopoiesis in terms of:
    • morphology of megakaryocytes
    • fate of megakaryocytes
    • life span of platelets
    • factors which influence thrombocytopoiesis
    • abnormal morphologic forms of platelets and megakaryocytes

  9. Discuss the following classification of anemia in terms of rationale for its use, and specific examples in each category:
  10. Categorize and discuss laboratory test procedures used in the diagnosis of anemia, outlining the basic workup of a patient who presents with anemia.

  11. Assess bone marrow function in the diagnosis of the anemic patient, on the basis of:
    • reticulocyte count (relative, absolute, and corrected)
    • serum bilirubin
    • urobilinogen concentration

  12. Discuss the clinical and pathologic features of the following types of anemia:
  13. Utilize peripheral blood and bone marrow smears to assess the deviations from normal marrow response which occur in:
    • hemolytic anemias
    • nuclear maturation defects
    • cytoplasmic maturation defects
    • hypoproliferative anemias

  14. Compare and contrast anemia secondary to acute vs. chronic blood loss
    • etiology
    • pathophysiologic changes
    • clinicopathologic diagnosis

  15. Discuss the clinical and pathologic features of these types of anemia:
  16. Compare and contrast warm vs. cold antibody immunohemolytic anemias in terms of:
    • etiology
    • pathogenesis
    • associated risks-diseases
    • laboratory diagnosis
    • clinical features and course

  17. Compare and contrast intravascular vs. extravascular hemolysis, in terms of:
    • etiology
    • pathogenesis
    • laboratory diagnosis
    • clinical findings and course

  18. Compare and contrast clinical and pathologic features of :
  19. Describe the WHO classification of acute myeloblastic leukemias in  terms of:
    • nomenclature
    • incidence of each type
    • general features of each type

  20. List the major etiology and pathogenesis of the following:

  21. Distinguish between leukemia and leukemoid reaction on the basis of:
    • etiology
    • pathogenesis
    • laboratory data

  22. Morphologically differentiate a blast from a monocyte and lymphocyte.

  23. Discuss the clinical and pathologic features of these myelodysplastic syndromes:
  24. Define and classify the myeloproliferative disorders.

  25. Discuss the clinical and pathologic features of these myeloproliferative disorders:
  26. Compare and contrast the clinical and pathologic features of:
  27. Describe the proper mode of submission of a lymph node biopsy to the surgical pathology laboratory for workup of a suspected lymphoproliferative disorder.

  28. Define, state the significance of, and identify in a microscopic section of a lymph node or extranodal site of involvement each of the following:
  29. Compare and contrast the clinical and pathologic features of follicular hyperplasia and follicular lymphoma.

  30. Discuss general features of non-Hodgkin lymphoma in terms of:
    • incidence
    • immunophenotyping (T vs B cells)
    • morphologic patterns (diffuse vs. follicular)
    • principles of:
    • classification (WHO)
    • grading
    • staging
    • laboratory methods of diagnosis
    • clinical features
    • prognosis
    • extra lymphatic organs involved
    • likelihood of a leukemic phase

  31. Compare and contrast the clinical and pathologic features of :
  32. Compare and contrast clinical and pathologic features of:
  33. Discuss Hodgkin lymphoma in terms of:
    • classification
    • morphology of each type
    • incidence of each type
    • laboratory diagnosis
    • etiology
    • clinical features
    • pathogenesis
    • prognosis

  34. Compare and contrast the clinical and pathologic features of :
  35. Discuss clinical and pathologic features of:
  36. List benign and malignant etiologies of lymphadenopathy and splenomegaly.

  37. Categorize and discuss the different types of plasma cell dyscrasias in terms of definitions and clinical presentation.

  38. Discuss clinical and pathologic features of multiple myeloma.

  39. Discuss clinical and pathologic features of Waldenström macroglobulinemia.

  40. Compare and contrast the clinical and pathologic features of:
  41. Discuss the different laboratory procedures used in the clinicopathologic diagnosis of the different plasma cell dyscrasias.

  42. List benign and malignant etiologies of monoclonal gammopathies.

  43. Discuss the clinical and pathologic features of Langerhans cell histiocytosis.

  44. Classify major causes of changes in size of the spleen, either increasing OR decreasing.

  45. Discuss Hodgkin lymphoma in terms of:
    • infarcts
    • amyloid
    • sickle cell disease
    • leukemia
    • extramedullary hematopoiesis
    • lymphoma
    • passive congestion
    • rupture

  46. List the major complications of splenomegaly.

  47. Briefly describe the morphologic features and clinical findings in:
  48. Discuss thrombocytopenia in terms of:
    • differential diagnosis
    • clinical features
    • bone marrow morphology and
    • laboratory features

  49. Discuss thrombocytosis in terms of diagnosis and differential diagnosis.

  50. Outline the role of platelets in normal hemostasis.

  51. Outline the process for stepwise evaluation of a patient with suspected platelet disorder.

  52. Compare and contrast the following disorders of platelets the clinical and pathologic:
     

  53. Categorize and discuss acquired disorders of platelet function.

  54. Compare and contrast clinical and pathologic features of:
  55. List and discuss the laboratory diagnostic procedures used to approach patients with:
    • bleeding disorders
    • thrombotic disorders

  56. Discuss the pathophysiology of disseminated intravascular coagulopathy (DIC).

 

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