COMP PATHOLOGY REVIEW
Cecil W. Cone II, M.D.
Professor and Emeritus Chair of Pathology
Asst. Dean of Diversity, Equity, and Inclusion
AUC School of Medicine
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CELL ADAPTATION AND INJURY
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Cellular Response to Stress and Injury
Types of Cellular Adaptation
•Hyperplasia
•Hypertrophy
•Atrophy
•Metaplasia
Hypertrophy
UAB Dept. of Pathology
Metaplasia
SITES OF DAMAGE IN CELL INJURY
HYPOXIC INJURY
INCREASED CALCIUM IN CELL INJURY
IRREVERSIBLE INJURY
Hydropic change
Hydropic and fatty change
COAGULATIVE NECROSIS
UAB Dept. Pathology
MECHANISMS OF APOPTOSIS
COUNCILMAN/ACIDOPHILIC BODY
Apoptosis
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NECROSIS VS APOPTOSIS
MALLORY-DENK BODY
LIPOFUSCIN PIGMENT
HEMOSIDERIN AND PRUSSIAN BLUE STAIN
DYSTROPHIC CALCIFICATION
CAUSES OF HYPERCALCEMIA
(CHIMPS)
•C – Cancer
•H – Hyperparathyroidism
•I – Intoxication of vit D
•M – Multiple myeloma/Milk alkali syndrome
•P – Paget disease of the bone
•S - Sarcoidosis
ACUTE INFLAMMATION
Cecil W. Cone II, M.D.
Professor and Emeritus Chair of Pathology
Asst. Dean of Diversity, Equity, and Inclusion
AUC School of Medicine
Neutrophils
Precursor Neutrophil (Band Cell)
UAB Dept. of Pathology
Adhesion and Migration
Oxygen-Dependent Killing
Acute Phase Response
Fibrinous Inflammation
Purulent Inflammation
UAB Dept. of Pathology
Purulent Inflammation (Abscess)
Acute Inflammation Outcome
CHRONIC INFLAMMATION
Cecil W. Cone II, M.D.
Professor and Emeritus Chair of Pathology
Asst. Dean of Diversity, Equity, and Inclusion
AUC School of Medicine
Monocyte
Eosinophil
Basophil
Lymphocytes
UAB Dept. of Pathology
Plasma Cells
Granuloma Formation
Caseating Granuloma
Non-caseating Granuloma
UAB Dept. of Pathology
Non-caseating Granuloma
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Interstitial Inflammation
UAB Dept. of Pathology
TISSUE REPAIR
Cecil W. Cone II, M.D.
Professor and Emeritus Chair of Pathology
Asst. Dean of Diversity, Equity, and Inclusion
AUC School of Medicine
Regeneration and Healing
Granulation Tissue
UAB Dept. of Pathology
Granulation Tissue
UAB Dept. of Pathology
Healed MI
UAB Dept. of Pathology
Healed MI
UAB Dept. of Pathology
Trichrome stain
Keloid
FLUID AND HEMODYNAMIC
DISORDERS
Cecil W. Cone II, M.D.
Professor and Chair Emeritus
Department of Pathology
Third Semester Lead
AUC School of Medicine
Key Definitions
•Tumor (mass lesion)
–A growth or enlargement (may be neoplastic or non-neoplastic)
•Hamartoma
–A localized mass-like lesion of haphazard growth of tissues
normally found at a given site
•Choristoma (heterotopia, ectopia)
–A mass-like growth consisting of tissue that is not normal to the
site of origin
•Neoplasia
–New, uncontrolled growth
Key Definitions
•Benign neoplasia
–Non-infiltrative growth with a low fatality potential
•Malignant neoplasia
–An infiltrative growth with high fatality potential
•Cancer
–Implies a malignant neoplasm
•Metastasis
–A distant spread of a malignant lesion
BENIGN NEOPLASMS
•Clinical Features
▪Usually solitary
▪May cause problem through mass effect or secretion of
substances (hormones, etc.)
•Nomenclature
▪Word usually ends with –oma (adenoma); exceptions: lymphoma,
glioma, melanoma, seminoma
Malignant Neoplasms
•Cytologic features
–Increased nuclear size (increased nuclear, cytoplasmic ratio)
–Variation in nuclear size and shape (pleomorphism)
–Lack of differentiation (anaplasia)
–Increased nuclear DNA content
–Prominent nucleoli with the nuclei
–Increased mitosis (irregular or bizarre mitosis)
HISTIOGENESIS OF CARCINOMA
•Epithelial surfaces
▪Squamous, columnar, transitional cells
•Organs with epithelia-lined ducts
▪Breast, pancreas
•Endocrine glands
▪Thyroid
HISTIOGENESIS OF SARCOMAS
•Arise from soft tissue (connective tissue)
▪Nerve, muscle, fat, bone, cartilage, fibroblasts, blood
vessels
•Generally big and fleshy
•Composed of cells that are:
▪Very pleomorphic
▪Spindle-shaped
BENIGN VS MALIGNANT NEOPLASMS
Age-related tumors
AGE GROUPS TUMORS
Children Leukemia, Brain tumors, blastomas
Young Adults Gonadal tumor, lymphomas
Elderly Carcinoma, prostate and endometrium
Commonly associated oncogenes
Oncogenes
Tumor suppressor genes
RB gene
P53
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Chemical carcinogenesis
Radiation-associated tumors
Etiology of neoplasia
CLASS EXAMPLE RELATED TUMOR
Chemicals
man-made
drugs
natural occurring
compounds
Aniline dyes
Cigarette smoke
Aflatoxins
Urinary bladder
Lung
Liver
Oncogenic viruses
Human papilloma virus (HPV)
Epstein-Barr virus (EBV)
Hepatitis B virus (HBV)
•Tetralogy of Fallot
•Transposition of the great vessels
•Truncus arteriosus
•Tricuspid atresia
•Total anomalous pulmonary venous return
Right-to-Left Shunts (5 Ts)
Tetralogy of Fallot
Transposition
(PREDUCTAL VS POSTDUCTAL)
Causes of High Output Cardiac Failure
•Beri beri (wet)
•Grave disease (high metabolic rate)
•Paget disease of the bone (a/v shunts)
•Pregnancy (twin, triplet, etc.)
•Severe anemia
Atherosclerotic Plaque Rupture
Thrombosis and Atherosclerotic Plaque with Rupture
•Left anterior descending branch
▪Anterior wall of the left ventricle
▪Anterior 2/3 of the interventricular septum
•Left circumflex branch
▪Lateral border of the left heart
•Right coronary artery
-Inferior/posterior wall of the left ventricle
▪Posterior 1/3 of the interventricular septum
▪Inferior/posterior right ventricular free wall
Distribution of Coronary Blood Flow
•MAJOR CAUSES OF DEATH
▪Cardiac arrhythmia
▪Cardiogenic shock
▪Congestive heart failure
▪Thromboembolization
Disorders which mimic acute appendicitis
•Mesenteric lymphadenitis (often secondary to unrecognized
Yersinia infection or viral enterocolitis)
•Acute salpingitis
•Ectopic pregnancy
•Ovarian cyst or torsion
•Mittelschmerz pain (caused by minor pelvic bleeding at the time of
ovulation)
•Meckel diverticulitis
•Crohn disease
Peptic Ulcer Disease: Etiology and Complications
•Acid and pepsin are
thought to be crucial to
ulcer development, but
the great majority of
peptic ulcers are directly
commonly related to
infection with
Helicobacter pylori or
NSAID use.
•Vomiting of bright red blood
or coffee-ground material
and/or passage of dark tarry
stool (melena) or
hematochezia may indicate
bleeding from a peptic ulcer.
Chromosomal instability pathway
Modified from: Lynch JP et al. Hematol Oncol Clin North Am 2002;16:775.
Main point: It’s the accumulation of multiple genetic mutations (oncogene
activation with loss of tumor suppressor genes) which results in cancer.
Robbins & Cotran Pathologic Basis of Disease, 9
th
ed.
Test taking strats
•RTFQ!
▪Understand what the question is asking you
•Read the last line again
•Skip it!
•Slice it up!
▪Cut the test block time and number of questions in half
•Read back!
▪Read the line before the last line
•The biopsy or autopsy is the answer!
•Click and move!
▪Study long, study wrong!
▪Be confident!
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