PATHOLOGY LABORATORY MANUAL I Modified 2017 (1) 4

TECHNOLOGICAL UNIVERSITY OF
SANTIAGO
“UTESA”
Medical career
Department of Microscopic Anatomy
PATHOLOGY LABORATORY MANUAL I
Prepared by: Víctor F. Liriano Rivas
Subject Name: Pathology Laboratory I
Clue : MED 305
No. Credits : 02
Practical Hours : 04 weekly
Pre : MED-860, MED-865

requirements
: MED-300
Corequisite
Teachers: Ana Portela Raquel Escoto

Josefina Madera Ornia Guzmán
Marianela Tactuk Anyolina Díaz
Milagros Garcia Arleny Morel
Ariana Cabrera Aracelis Ovalles
Jenny Puello Fiordaliza Castillo
Santiago de los Caballeros,

Dominican Republic
2014
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SANTIAGO
“UTESA” Medical career
PATHOLOGY LABORATORY MANUAL I
Medical career......................................................................................................................2
PATHOLOGY LABORATORY MANUAL I....................................................................2
2014 TECHNOLOGICAL UNIVERSITY OF SANTIAGO “UTESA”...........................5
Medical career......................................................................................................................5
PATHOLOGY I LABORATORY RULES.....................................................................6
GENERAL GUIDELINES FOR DEVELOPMENT OF EVALUATORY TESTS.......6
TECHNOLOGICAL UNIVERSITY OF SANTIAGO UTESA...................................13
PATHOLOGY I LABORATORY PROGRAM............................................................13
FIRST PARTIAL 30%...................................................................................................16
ADAPTATION, DAMAGE AND CELL DEATH.......................................................16
The type, state and adaptability of the affected cell also determine the consequences of
the damage (nutritional and hormonal status)................................................................19
Causes of necrosis..........................................................................................................20
a. Necrosis due to hypoxia..........................................................................................20
PLATE #1: Cardiac muscle hypertrophy.......................................................................20
Microscopic features:.....................................................................................................20
PLATE #2: Adenomatous hyperplasia of the prostate...................................................20
Microscopic features :....................................................................................................20
PLATE #3: Fibromuscular hyperplasia of the prostate..................................................20
Microscopic features :....................................................................................................20
PLATE #4: Simple Endometrial Hyperplasia................................................................21
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PLATE #5: Thyroid hyperplasia....................................................................................21
PLATE #6: Endometrial atrophy...................................................................................21
PLATE #7: Testicular atrophy.......................................................................................21
PLATE #8: Ovarian atrophy..........................................................................................21
PLATE #9: Squamous metaplasia of the endocervix.....................................................22
PLATE #10: Intestinal metaplasia.................................................................................22
QUIZ #1.........................................................................................................................25
Answer T or F as appropriate.........................................................................................25
PLATE #18: Colliquative necrosis................................................................................26
PLATE #19: Caseous necrosis.......................................................................................26
PLATE #20: Gangrenous necrosis.................................................................................26
PLATE #21: Hemorrhagic Necrosis..............................................................................27
PLATE #24: Tumor necrosis.........................................................................................27
QUIZ #2.........................................................................................................................28
Answer T or F as appropriate.........................................................................................29
QUIZ #3.........................................................................................................................34
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INFLAMMATION :......................................................................................................36
PLATE #39: Acute inflammation (Abscess).................................................................38
PLATE # 40: Chronic cervicitis.....................................................................................38
PLATE # 42: Chronic gastritis.......................................................................................39
PLATE # 43: Chronic prostatitis....................................................................................39
PLATE # 46: Chronic hepatitis......................................................................................41
Chronic Persistent Hepatitis:..........................................................................................42
Chronic Lobular Hepatitis:.............................................................................................42
Chronic Active Hepatitis:...............................................................................................42
CHRONIC HEPATITIS Final Diagnosis.............................................................................42
b......................................................................................................................................42
without............................................................................................................................42
QUIZ #4.........................................................................................................................45
PLATE #52: Hepatic congestion....................................................................................48
PLATE # 53: Splenic congestion (Spleen)....................................................................48
PLATE # 54: Hemorrhage (Soft tissues).......................................................................48
PLATE # 55: Arterial thrombosis..................................................................................48
PLATE #56: Recanalized thrombus...............................................................................49
PLATE # 57: Acute edema of the lung..........................................................................49
QUIZ #5.........................................................................................................................50
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THIRD PARTIAL 30%.................................................................................................50
CLASSIFICATION OF NEOPLASMS.........................................................................51
MALIGNITY CRITERIA..............................................................................................51
NUCLEAR AND NUCLEOLAR MALIGNITY CRITERIA.......................................52
PLATE # 58: Leiomyoma of the uterus.........................................................................52
PLATE #70: Hepatocarcinoma......................................................................................55
QUIZ #6.........................................................................................................................55
PLATE # 74: Systemic lupus erythematosus (Spleen)..................................................58
QUIZ #7.........................................................................................................................61
MORPHOLOGICAL DESCRIPTION CRITERIA TO APPLY IN THE
ASSESSMENT OF CASES...........................................................................................62
ELEMENTS IN THE DESCRIPTION OF MICROSCOPIC IMAGES.......................62
DIAGNOSTIC CASES..................................................................................................62
ELEMENTS FOR THE PRESENTATION OF A CLINICAL CASE, QUESTIONS,
ANSWERS AND BIBLIOGRAPHICAL QUOTES.....................................................62
SUGGESTED QUESTIONS.........................................................................................63
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SANTIAGO
“UTESA”
Santiago de los Caballeros,
Dominican Republic
2014
TECHNOLOGICAL UNIVERSITY OF SANTIAGO
“UTESA”
Medical career
Department of Microscopic Anatomy
PATHOLOGY I LABORATORY RULES
The objective of these standards is to maintain quality and biosafety in the

laboratory.
1. Entry to the laboratory requires that the professor be present, according to

the time indicated in the academic programs.
2. For protection, teachers, technicians and students must wear a long, clean
white coat during their stay in the laboratory.
3. Student attendance will be verified at the beginning of the practice.
4. The teacher must verify at the beginning of the practice that the students
have read the instructions in the manual of the practice to be carried out.
5. The teacher must verify the proper use of microscopes, slides and macro
pieces during the practices.
6. The student must attend 80% of the scheduled practices to be entitled to a

final grade. Otherwise, you must take all the practices again in the following
semester.
7. Hazardous (infectious) biological waste must be placed in specific bags for

storage, handling and final disposal.
8. The ingestion of food and drinks, as well as the use of cosmetics, is not
permitted.
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SANTIAGO
9. In the event“UTESA”
of accidents during practices, the particular specifications of
each case must be followed.
10. If a lamella is broken, the student will pay for its replacement.
11. The first violation of any of the previous points entails a verbal warning;
Subsequent violations will entail a written warning that will be filed in your
file.
GENERAL GUIDELINES FOR DEVELOPMENT

OF EVALUATORY TESTS
- For the exam, you should bring: 2 pencils, an eraser or correction fluid, a
clean white coat.
- Maintain silence and order at all times (before the exam, during the exam
and after the exam).
- The use of cell phones and/or electronic devices is prohibited in the exam
area.
- When starting your exam you must: write your name, registration number,
date and group number.
- You must continue on the first table from left to right.

-
You must follow your exam sequentially, without leaving any blank spaces.
-
You must attend your exam on time and at the scheduled time.
-
When you finish the last question, you must hand in your exam immediately,
since there is no additional time or opportunity to re-observe.
- It should not mobilize the microscopic fields.
- Violation of any of the above rules results in not being admitted or

suspension of your exam.
- Each question generally has two approaches.
- Please read the question carefully so you know what to answer.

SANTIAGO
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LOOK AT AN EVALUATION MODEL
PATHOLOGY I LABORATORY PARTIAL EXAM
Name Tuition____________
Cluster: Date: _________________
READ CAREFULLY AND ANSWER WHAT IS ASKED OF YOU
Medical career 2
PATHOLOGY LABORATORY MANUAL I 2
2014 TECHNOLOGICAL UNIVERSITY OF SANTIAGO “UTESA” 5
Medical career 5
PATHOLOGY I LABORATORY RULES 6
GENERAL GUIDELINES FOR DEVELOPMENT OF EVALUATORY TESTS 6
TECHNOLOGICAL UNIVERSITY OF SANTIAGO UTESA 13
PATHOLOGY I LABORATORY PROGRAM 13
FIRST PARTIAL 30% 16
ADAPTATION, DAMAGE AND CELL DEATH 16
The type, state and adaptability of the affected cell also determine the consequences of the
damage (nutritional and hormonal status). 19
Causes of necrosis 20
a. Necrosis due to hypoxia. 20
PLATE #1: Cardiac muscle hypertrophy 20
Microscopic features: 20
PLATE #2: Adenomatous hyperplasia of the prostate 20
Microscopic features : 20
SANTIAGO
“UTESA”
PLATE #3: Fibromuscular hyperplasia of the prostate 20

Microscopic features : 20
PLATE #4: Simple Endometrial Hyperplasia 21
PLATE #5: Thyroid hyperplasia 21
PLATE #6: Endometrial atrophy 21
PLATE #7: Testicular atrophy 21
PLATE #8: Ovarian atrophy 21
PLATE #9: Squamous metaplasia of the endocervix 22
PLATE #10: Intestinal metaplasia 22
QUIZ #1 25
Answer T or F as appropriate 25
PLATE #18: Colliquative necrosis 26
PLATE #19: Caseous necrosis 26
PLATE #20: Gangrenous necrosis 26
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PLATE #21: Hemorrhagic Necrosis 27
PLATE #24: Tumor necrosis 27
QUIZ #2 28
Answer T or F as appropriate 29
QUIZ #3 34
INFLAMMATION : 36
PLATE #39: Acute inflammation (Abscess) 38
PLATE # 40: Chronic cervicitis 38
PLATE # 42: Chronic gastritis 39
PLATE # 43: Chronic prostatitis 39
PLATE # 46: Chronic hepatitis 41
Chronic Persistent Hepatitis: 42
Chronic Lobular Hepatitis: 42
SANTIAGO
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Chronic Active Hepatitis: 42

CHRONIC HEPATITIS Final Diagnosis 42
b 42
without 42
QUIZ #4 45
PLATE #52: Hepatic congestion 48
PLATE # 53: Splenic congestion (Spleen) 48
PLATE # 54: Hemorrhage (Soft tissues) 48
PLATE # 55: Arterial thrombosis 48
PLATE #56: Recanalized thrombus 49
PLATE # 57: Acute edema of the lung 49
QUIZ #5 50
THIRD PARTIAL 30% 50
CLASSIFICATION OF NEOPLASMS 51
MALIGNITY CRITERIA 51
NUCLEAR AND NUCLEOLAR MALIGNITY CRITERIA 52
PLATE # 58: Leiomyoma of the uterus 52
PLATE #70: Hepatocarcinoma 55
SANTIAGO
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QUIZ #6 55
PLATE # 74: Systemic lupus erythematosus (Spleen) 58
QUIZ #7 61
MORPHOLOGICAL DESCRIPTION CRITERIA TO APPLY IN THE ASSESSMENT
OF CASES 62
ELEMENTS IN THE DESCRIPTION OF MICROSCOPIC IMAGES 62
DIAGNOSTIC CASES 62
ANSWERS AND BIBLIOGRAPHICAL QUOTES 62
SUGGESTED QUESTIONS 63
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TECHNOLOGICAL UNIVERSITY OF SANTIAGO

UTESA
“University of Knowledge for Life

“Year of Virtual Education”
PATHOLOGY I LABORATORY PROGRAM
Name of the subject: Year 2014
PATHOLOGY LABORATORY I
Key: MED-305 Credits: two (2) Pre-Req: MED-860, MED-865
Level: Eighth Semester (Basic Sciences) Co-Req: MED-300

Number of weekly practical hours: (4) Number of theoretical weekly hours: (6)
DESCRIPTION
The subject Pathology I has six theoretical hours, 4 practical hours and a total of 8
credits. It studies the basic processes that trigger pathologies and subsequently affect
microscopic structures.
It covers the study of the reactions of living organisms to injury and the combination of
mechanisms that end in the production of diseases that are observed in each of the
different organs and systems that make up the human organism.
JUSTIFICATION
The integration of knowledge of General Pathology is essential in the training of the

doctor. The purpose of the laboratory is to show the basic processes that give rise to a
pathology. Its programming or development aspires to increase the abilities, attitudes
and skills of each student when carrying out their observations and practices in the
laboratory and clinical work that the subsequent educational experiences demand.
With the aim that throughout his academic and professional career, he recognizes the
Pathological Anatomy of his patients to understand the various clinical manifestations
that he will face in his professional life and to be able to treat them with discipline,
ethics and respect.
GENERAL OBJECTIVE
The student will learn about the mechanisms of cellular adaptation, integrating
theoretical knowledge into the morphology of the different diseases that affect the
human organism, from a macroscopic and microscopic point of view.
SPECIFIC OBJECTIVES
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Upon completion of the course, the student will be able to:
- Identify adaptations, reversible and irreversible cell lesions, cell death and
neoplasias under the microscope.
- The student will have the necessary preparation to understand the intrinsic
mechanisms of diseases.
- Describe and adequately identify, using optical microscopy, the cellular
pathological changes that characterize a disease of tissue sections with
microscopic abnormalities.
- Understand the mechanisms of the disease and be able to apply their
knowledge to the study of individual clinical cases (for example: reconstructing
the natural history of a patient's disease with autopsy findings or with a case
study).
- Develop the art of describing clinical and morphological alterations with
appropriate terms.
- Develop the power of observation, either with the naked eye or with the help of
the microscope.
- Correctly answer the partial and final knowledge exams that will be made up of
questions related to macro, microscopic and clinical correlation aspects.
CONTENTS
FIRST PARTIAL
UNIT I: Cellular adaptation, cell injury and cell death

- Introduction to Pathology
- Cellular adaptation: hyperplasia, hypertrophy, atrophy and metaplasia
- Reversible and irreversible cellular injury and cellular aging
- Cell death: necrosis, apoptosis and autophagy
- intracellular accumulations
- Subcellular alterations
- Pathological calcification
- Cellular aging
SECOND PARTIAL
UNIT II: Acute and chronic inflammation. Cell renewal and repair
- Acute inflammation
- Morphological patterns of acute inflammation
- Chronic inflamation
- Systemic effects of inflammation
- Consequences of defective or excessive inflammation
- Tissue renewal, repair and regeneration

- Mechanisms of tissue and organ regeneration
- Extracellular matrix and cell-matrix interactions
- Healing by repair, scar formation and fibrosis
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THIRD PARTIAL
UNIT III: Hemodynamic Disorders. Thromboembolic disease, Shocks and Neoplasias

- Hemodynamic disorders
- Edema
- Hyperemia and congestion
- Hemorrhage
- Hemostasis and thrombosis.
- Embolism and heart attack
- Neoplasms: Nomenclature
- Characteristics of benign and malignant neoplasms
- Epidemiology
- Carcinogens and their cellular interactions
- Host defense against tumors: tumor immunity
- Clinical aspects of the neoplasia
- Systemic, infectious, genetic and immunological diseases
METHODOLOGY
Professor's presentations, accompanied by demonstration of the topics through the

observation of histological slides through the Optical Microscope. They are also
watched on television and explained to the students. Complementation of the topics by
the student, through research work, individual and collective exhibitions, seminars,
analysis, questionnaires and group discussion. Presentation and discussion of
previously assigned clinical cases.
EVALUATION SYSTEM
Three partial exams will be given on the dates established in the academic calendar,
with closed questions and some short ones. Each partial will be assigned a value of
30%, except for the Third, which will have a value of 20%. Participation in class,
seminars, questionnaires, discussion and resolution of clinical cases and presentation
10%. In addition to the assessment of the practice manual, which will have a value of
10%.
BIBLIOGRAPHY
Cotran Kumar Collins (2010). Structural and Functional Pathology. (8th Edition).
Elseiver-Saunder Publishing.
Rubín, Emmanuel (2000). Structural Pathology: Clinical-pathological foundations in

medicine. (4th Edition). McGraw Hill-Interamericana Publishing House.
Rosai, Juan Ackerman'sSurgical Pathology. (Ninth edition).

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CONTENTS OF EACH PRACTICE
FIRST PARTIAL 30%
ADAPTATION, DAMAGE AND CELL DEATH
1- Cardiac muscle hypertrophy

2- Adenomatous hyperplasia of the prostate
3- Fibromuscular hyperplasia of the prostate
4- Simple endometrial hyperplasia
5- Thyroid hyperplasia
6- Endometrial atrophy
7- testicular atrophy
8- Ovarian atrophy
9- Squamous metaplasia of the endocervix
10- intestinal metaplasia
11- Apocrine metaplasia of the mammary gland
12- Barrett's esophagus
13- Decidual metaplasia
14- Low Grade Squamous Intraepithelial Lesion-Mild dysplasia of the cervix.
15- High Grade Squamous Intraepithelial Lesion- Moderate and severe dysplasia of
the cervix.
16- Coagulation necrosis (Acute myocardial infarction)
17- Coagulation necrosis (Prostate infarction)
18- Colliquative necrosis
19- Caseous necrosis (Lymph node tuberculosis)
20- Gangrenous necrosis
21- Hemorrhagic necrosis
22- Enzymatic fat necrosis (acute pancreatitis)
23- Traumatic necrosis of fat (mammary gland)
24- Tumor necrosis (Breast Carcinoma)
SECOND PARTIAL 30%
INTRACELLULAR ACCUMULA, INFLAMMATION, REPAIR AND

HEMODYNAMIC AND FLUID DISORDERS
25- Lipid accumulation (liver fatty change)

26- Cholesterolosis (“Strawberry Gallbladder”)
27- Atherosclerosis
28- glycogen storage
29- Melanin deposit (Pigmented nevus)
30- Hepatic cholestasis (bile pigment deposition)
31- Hemosiderin depot
32- Melanosis coli
33- Carbon accumulation (pulmonary anthracosis)
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34- cholesterol needles
35- Dystrophic calcification (Mockemberg sclerosis)
36- Metastatic calcification (soft tissues)
37- Psammoma bodies
38- Acute inflammation (Acute appendicitis)
39- Acute inflammation (Abscess)
40- Chronic cervicitis
41- Chronic inflammation (Chronic Cholecystitis)
42- Chronic gastritis
43- chronic prostatitis
44- Focal chronic inflammation (Focal chronic mastitis)
45- Chronic follicular inflammation (Hashimoto's thyroiditis)
46- chronic hepatitis
47- Chronic granulomatous inflammation (Lymph Node Tuberculosis)
48- Chronic granulomatous inflammation due to a foreign body (surgical thread)
49- Normal scar
50- Keloid
51- Granulation tissue (Oral mucosa)
52- Liver congestion
53- Splenic congestion
54- Hemorrhage (soft tissues)
55- arterial thrombosis
56- recanalized thrombus
57- Acute lung edema
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THIRD PARTIAL 30%
NEOPLASMS, SYSTEMIC, INFECTIOUS, GENETIC AND IMMUNOLOGICAL

DISEASES
58- Leiomyoma of the uterus

59- Lipoma
60- Adenomatous polyp of the colon
61- Hyperplastic endometrial polyp
62- Breast fibroadenoma
63- Hemangioma
64- inclusion cyst
65- Giant cell tumor
66- Moderately differentiated invasive squamous cell carcinoma of the cervix
67- Adenocarcinoma metastatic to lymph node
68- Signet ring cell carcinoma
69- Infiltrating ductal carcinoma of the mammary gland
70- Hepatocarcinoma
71- Hemochromatosis (Liver cirrhosis) (Perls stain)
72- Amyloidosis (Kidney) (Congo Red Stain)
73- Acquired immunodeficiency syndrome (Kaposi's sarcoma)
74- Systemic lupus erythematosus
75- Scleroderma (Skin)
76- Fungi (Candida Albicans)
77- Trichomoniasis (Thricomonas vaginalis)
78- Gardnerella (Gardnerella Vaginalis)
79- Congenital megacolon (Hirschsprung's disease)
80- Multiple Neurofibromatosis (Von Recklinghausen Disease)
81- Gynecomastia (Klinefelter Syndrome)
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CELLULAR ADAPTATION
GOALS:
- Identify microscopic lesions in reversible cell injuries, cell death and

types of necrosis.
- Identify changes due to cellular adaptations.
- Understand the pathophysiology of the multiple mechanisms of cellular

injury; They can be correlated with the clinic if observed under the
microscope.
Cells are constantly exposed to changes in their environment: There are

homeostatic mechanisms that allow cells and tissues to successfully cope with
changes.
Cells adapt to tolerable changes in their environment by modifying their

metabolism or growth pattern: During periods of relative lack of calcium, calcium is
mobilized from the bone matrix through the activity of osteoclasts under the influence
of parathormone.
Intense changes in the environment surrounding the cell are called pathological
stimuli: Exposure to UV radiation while sunbathing produces skin responses that vary
from the induction of melanin production (physiological) to severe blistering and
shedding of cells. the epidermis (pathological).
THE REACTIONS OF THE CELL TO AN AGENT DEPEND ON THE TYPE OF

AGENT, ITS DURATION AND INTENSITY.
The type, state and adaptability of the affected cell also determine the
consequences of the damage (nutritional and hormonal status).
Cell damage can be:
ACUTE : Result of a very short action of a harmful agent. Ex.: Ischemia = Cellular
Necrosis.
CHRONIC : When the action of the harmful agent persists and there are two
possibilities: THE CELL DIES OR ADAPTS to the pathological situation. Ex.: Ischemia
^ Atrophy.
CELLULAR ADAPTATION translates into atrophy, hypertrophy, metaplasia,

hyperplasia, intracellular accumulation of various substances and also neoplasia.
Necrosis can be defined as pathological cell death recognizable by morphological

signs:
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Cytoplasm: hypereosinophilia and loss of normal structure.
Nucleus: Pycnosis: retraction of the nucleus with chromatin condensation.
Karyolysis: dissolution of the nucleus.
Karyorrhexis: fragmentation of the nucleus into pieces with condensed chromatin.
ALTERATIONS OF THE CYTOPLASM AND NUCLEUS ARE COEXISTENT.
Causes of necrosis
a. Necrosis due to hypoxia.
b. Radiation necrosis. Noxa corresponds to free radicals produced by ionizing
radiation.
c. Reperfusion necrosis: This is a prolonged but transient ischemia, lasting about
20 minutes, that produces flocculations of the mitochondrial matrix. When the tissue is
reperfused in this state, the phenomenon manifests itself with the production of high
amounts of free radicals, which prematurely alter the cell membrane and the
cytoskeleton with rapid mineralization of the mitochondria.
MICROSCOPIC PREPARATIONS TO OBSERVE (PLATE)
PLATE #1: Cardiac muscle hypertrophy
Microscopic features:
- Increase in the size and thickness of muscle fibers
- Fibers with sinuous contours
- Variation in the size of the nuclei
- Nuclear hyperchromasia
PLATE #2: Adenomatous hyperplasia of the prostate
Microscopic features :
- Increase in the number of glands
- Glands with variation in size
- Cylindrical glandular epithelium, with clear cytoplasm,
- granular and with basal nuclei that sometimes show papillary projections
- Presence of starchy bodies
PLATE #3: Fibromuscular hyperplasia of the prostate
- Few glands present
- Fibromuscular stromal hyperplasia
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- Bands of fibrous tissue
- Nodule formation
PLATE #4: Simple Endometrial Hyperplasia
- Increase in the number of glands
- Glands of variable size, from very small to cystic
- Glands lined by cubic to cylindrical epithelium, with a tendency to
Pseudostratification
- Hyperchromatic nuclei, with mitosis figures
- The stroma is hyperplastic and with the presence of mitosis
PLATE #5: Thyroid hyperplasia
- Increase in the number of acini
- Acini of variable size, from very small to cystic
- Large amount of colloid
- Acini covered by simple cuboidal epithelium
- The stroma is scarce and with the presence of hemorrhage
PLATE #6: Endometrial atrophy
- Decrease in the number of glands
- Small, straight tubular glands
- Cubic glandular epithelium
- Stromal fibrosis
- Some glands show cystic dilation
PLATE #7: Testicular atrophy
- Tubules with decreased thickness of the epithelium
- Peritubular fibrosis
- Decreased spermatogenesis
- Increase in interstitial stroma
- Decrease in Sertoli cells
- Leydig cell hyperplasia
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PLATE #8: Ovarian atrophy
- Absence of primordial follicles
- Absence of corpora lutea
- Presence of multiple corpora albicans
- Increase in interstitial stroma
- Bands of fibrous tissue
PLATE #9: Squamous metaplasia of the endocervix
- Replacement of the columnar epithelium by squamous epithelium, in the glands
and lining epithelium
- Identify the squamocylindrical junction
PLATE #10: Intestinal metaplasia
- Replacement of the columnar epithelium by goblet cells, in the glands and
lining epithelium of the stomach
- Identify the histological zone
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PLATE # 11 Apocrine metaplasia of the mammary gland
- Cells with extensive cytoplasm, eosinophilic and granular
- Duct dilation
- Resemblance to the lining epithelium of apocrine sweat glands
PLATE # 12 Barrett's esophagus
- Replacement of squamous epithelium by
epithelium
- Simple cylindrical, on the surface of
lining of the esophagus
PLATE # 15: High Grade Squamous Intraepithelial Lesion-Moderate and severe

dysplasia of the cervix.
- Disorganization in the pattern of maturation
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- Large, hyperchromatic nuclei, nucleus-cytoplasm disproportion
- Presence of suprabasal mitosis
- Note that these changes occupy 99% of the thickness of the epithelium
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QUIZ #1
1. List the four possible forms of cellular adaptation.
2. List the possible causes of cell injury.
3. Say which are the most vulnerable intracellular systems and determine
the main causes of irreversibility in cellular injury.
4. Define what hyperplasia is and determine the possible ways hyperplasia

occurs, its causes and examples
5. Define the concept of hypertrophy and give some examples that illustrate
the form of physiological and pathological hypertrophy.
6. Define the concept of metaplasia and describe some causes that produce it
and its different types.
7. Define the concept of atrophy and give some example(s) of physiological

and pathological atrophy .
Answer T or F as appropriate
8. ___Cellular injury can be produced by an aggressive stimulus and/or by

inability of cellular adaptation.
9. ___Hyperplasia is the same as Hypertrophy.
10. ___The cause of hypertrophy is the synthesis of structural components.
11. ___In hyperplasia, there must be the ability to synthesize DNA to perform
mitotic division.
12. ___Menopause is a pathological atrophy.
CELL DEATH (NECROSIS AND APOPTOSIS)
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PLATE #16: Coagulation necrosis (Acute myocardial infarction)
- Cellular boundaries are recognized
- Identify ghost or shadow cells
- Absence of nuclei
- Acidophilic cells
- Coagulation of intracellular proteins
PLATE # 17: Coagulation necrosis (Prostate infarction)
- Prostate glands with preserved margins
- Clotted cells
- Absence of core
- Eosinophilic cytoplasm
PLATE #18: Colliquative necrosis
- Total tissue destruction
- Cellular remains and detritus
- Edema and hemorrhage
- Fibrin areas
- Scattered leukocyte infiltrate
PLATE #19: Caseous necrosis
- Acellular, finely granular and amorphous area is recognized
- Surrounded by lymphoplasmacytic infiltrate
- Accompanied by granuloma formation
- Multinucleated giant cells type are observed
- Langhans and foreign body type
PLATE #20: Gangrenous necrosis
- Destruction of affected tissue
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- A modified coagulation pattern is observed due to the liquefactive action of
the bacteria and leukocytes attracted.
- Presence of bacterial colonies
- Extensive areas of hemorrhage and polymorphonuclear infiltrate
- Observe the surrounding blood vessels that show decreased lumen caliber
PLATE #21: Hemorrhagic Necrosis
- Cytoarchitecture is preserved
- Histological structures in shadow with preserved margins
- cellular eosinophilia
- anucleated cells
- Extensive hemorrhage
PLATE # 22: Enzymatic necrosis of fat (Acute pancreatitis)
- Destruction of surrounding adipose tissue
- Neutrophil infiltrate
- Note the deposit of calcium that adheres to the fatty acids (“fat
saponification”)
PLATE #23: Traumatic necrosis of fat (mammary gland)
- Destruction of adipose tissue
- Disintegration of adipocyte membranes with accumulation of fatty acids
- Neutrophil infiltrate
- Areas of edema and hemorrhage
PLATE #24: Tumor necrosis
- Coagulation effect of the affected tissue
- anucleated cells
- Cytoplasmic eosinophilia
- Neoplastic or tumor cells surrounding the necrotic area
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QUIZ #2
1- List the different forms of cell necrosis and give a brief description of each
of them.
2- What main differences do you find between necrosis and apoptosis ?
3- Briefly describe the terms pyknosis, karyolysis and karyorrhesis.
4- List some specific known form(s) of cellular apoptosis (apoptotic bodies)

according to their location.
5- Define what free radicals are and give some examples of the most
prominent molecules.
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6- How can free radicals form?
7- What physiological processes are free radicals known to be involved in?
8- What effects can free radicals cause on cells?
9- List three types of endogenous or exogenous antioxidant systems .
10-List the main antioxidant enzymes .
Answer T or F as appropriate
11- ___The cell has a high intracellular calcium content.

12- ___Ischemia produces a decrease in metabolic substrates.
13- ___An irreversible alteration caused by hypoxia can be the dispersion of
ribosomes.
14- ___ Therapeutic drugs are physical agents that cause cellular injury.
15- ___Intracellular calcium produces water accumulation causing the cell to swell.
16- ___Anaerobic glycolysis is an alternative pathway for obtaining ATP that is
activated when ATP levels are very low.
17- ___The increase in intracellular calcium and free radicals produces alterations
in the osmolarity of the cell.
SECOND PARTIAL 30%
INTRACELLULAR ACCUMULATIONS, INFLAMMATION, REPAIR, HEMODYNAMIC AND

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FLUID DISORDERS
GOALS:
- Identify the different types of intra and extracellular accumulations.
- Recognize the histopathological characteristics of acute and chronic
inflammation in different tissues.
- Recognize the granulation tissue characteristic of the healing process.
- Histological characteristics of healing.
- Observe the histopathological characteristics of edema, thrombosis and
hemorrhage in different tissues.
- Clinico-pathological correlation of the different pathological processes
exposed by the students.
PLATE # 25: Hepatic steatosis (Fatty change of the liver)
- Note the presence of vacuoles in the cytoplasm of hepatocytes
- Observe the different sizes of these vacuoles, some small, others moving the
nucleus towards the periphery
- Adjacent hepatocytes can rupture and release fat globules, which fuse and form
fatty cysts.
- Different stains to determine lipids in tissues
PLATE # 26: Cholesterolosis (“Strawberry Gallbladder”)
- Identify the gallbladder mucosa
- Observe in the lamina propria the presence of
- histiocytes (macrophages)
- Recognize the characteristics of these macrophages, observe the eosinophilic
cytoplasm, its foamy appearance. foam cells
- Cholesterol deposit in the cytoplasm of these cells
3
1
3
2
3
3
3
4
QUIZ #3
1. Define: intracytoplasmic accumulations and what are the main types of

intracytoplasmic accumulations?
2. What are the mechanisms by which intracellular accumulation can occur?
3. Define: what is steatosis or fatty degeneration? In what organs can it occur?

and list some causes
4. List some circumstances in which an accumulation of cholesterol and its esters

can occur.
5. List some circumstances in which an accumulation of cholesterol and its esters

can occur.
6. What special laboratory stains (histochemistry) can help us identify "fat" in

tissues?
7. List three types of endogenous and exogenous pigments that accumulate in

tissues.
8. What is the cause attributed to so-called melanosis coli?
3
5
9. What is Wilson's Disease and what molecule accumulates in it?
10. What is Saturnism? and mention the most common causes.
11. Defines the term thesaurismosis.
12. What is the normal calcium level in men?
13. Define what we mean by dystrophic calcification and give some examples in
which this process occurs.
14. It defines what we mean by metastatic calcification and lists some

circumstances in which it may occur.
15. Defines what we mean by idiopathic calcification and lists some examples in
which this process occurs.
3
6
INFLAMMATION :
It is one of the large categories of tissue response to disease. They are diseases
that end in -itis , such as appendicitis, cervicitis,…
Inflammation is divided into acute and chronic, although in reality both types often
form a continuous whole.
Acute inflammation has three main and interrelated components:
- vascular dilation
- Endothelial activation
- Neutrophil activation
Outcomes of acute inflammation If the patient survives, acute inflammation has four
main possibilities of evolution:
- Resolution
- Fibrosis healing
- Abscess formation, and
- Progression towards chronic inflammation
Chronic inflammation can be subdivided into the following types:
- Chronic nonspecific inflammation: follows unresolved acute

inflammation.
- Specific chronic inflammation: in response to certain types of causative
agents.
- Granulomatous inflammation: it is a variety of specific chronic
inflammation characterized by the presence of granulomas.
The chronic inflammatory infiltrate, in contrast to the marked predominance of

neutrophils that characterizes the acute inflammatory response, is dominated by:
- tissue macrophages
- Lymphocytes
- Plasma cells
Chronic inflammation usually heals by fibrosis.
Agents capable of causing chronic granulomatous inflammation include the

following:
- Low toxicity microorganisms such as Treponema Pallidum, the

causative agent of syphilis
3
7
- Infectious microorganisms that grow inside cells, for example
Mycobacterium Tuberculosis
- Infections due to fungi, protozoa and parasites
- Foreign body reaction
- Inert materials such as silica, talc, asbestos or beryllium.
The defining characteristic of granulomatous inflammation is the presence of:
Activated epithelioid macrophages and - multinucleated giant cells derived from

macrophages.
Epithelioid macrophages owe their name to their histological appearance, which is

reminiscent of epithelial (squamous) cells.
A special chronic granulomatous inflammation is tuberculous. Tuberculosis is a

contagious bacterial infection caused by Mycobacterium tuberculosis (TBC) that
primarily affects the lungs, but can then spread to other organs.
The characteristic histological lesion is tuberculous granuloma. In the center of it

there is an area of:
Caseous necrosis containing tubercle bacilli; These microorganisms can only be

shown using specific staining techniques for acid-fast bacilli. The caseous area is
surrounded by an area of epithelioid macrophages with abundant eosinophilic
cytoplasm. Some macrophages fuse with each other to produce multinucleated giant
cells called Langhans giant cells. At the periphery of the macrophages there is a rim
of lymphocytes.
BASOPHILE
MONOCYTE
HEATIES
EOSI-
NóEILO
LINEOCYTH
E
POLINUCLEAR
3
8
PLATE # 38: Acute inflammation (Acute
appendicitis)
- Mucosal ulceration
- Cellular remains, fibrin and intense infiltrate of
polymorphonuclear
- Areas of edema, necrosis and hemorrhage
PLATE #39: Acute inflammation (Abscess)
- Observe tissue destruction and replacement
- Due to cellular debris, fibrinoid material and a
- Dense inflammatory infiltrate of polymorphs
- Nuclear, which can be accompanied by
- bacterial colonies or other agents
- infectious
PLATE # 40: Chronic cervicitis
- Infiltrated lymphocytes and plasmacytes in the chorion
- There are some newly formed blood vessels
- There is epithelial spongiosis (intercellular edema), submucosal edema, and
epithelial and stromal alterations.
- It can be associated with trauma and specific microorganisms such as:
Chlamydia, gonococcus, mycoplasma, herpes virus (type 2), Trauma and other
infections
- Specifically: Spongiosis is associated with trichomonas, the formation of
lymphoid and plasma follicles with chlamydia infection, and ulcers with
intraepithelial inclusions with Herpes.
3
9
PLATE # 41: Chronic inflammation (Chronic cholecystitis)
- Epithelial sloughing
- Cellular remains, fibrin and intense infiltrate of lymphocytes, which cover the
entire wall
- There are areas of necrosis and hemorrhage
PLATE # 42: Chronic gastritis
- Infiltrate of lymphocytes, plasmacytes and some eosinophils in the lamina
propria which is widened
- Sometimes, if it goes on for a long time, it can
- lead to intestinal metaplasia and atrophy, and
- finally to peptic ulcers changes
- dysplastic and/or neoplastic.
- Chronic gastritis is an inflammation of the gastric mucosa, which can be
associated with: Helicobacter Pylori infections, anemia
pernicious, toxic substances (alcohol and cigarette abuse), distal
gastrectomy, radiation and granulomatous diseases.
- Stress and significant consumption of NSAIDs are more associated with the
acute phase of the disease.
- It produces few symptoms such as: Nausea,
- vomiting and discomfort in the upper abdomen)
PLATE # 43: Chronic prostatitis
- Note at the level of the stroma, the inflammatory
infiltrate
- at the expense of plasmacytes, some
macrophages
- and numerous lymphocytes primarily, which
- They are distributed diffusely and sometimes form
lymphoid follicles.
- It presents few symptoms: Lumbar pain, dysuria,
- perineal and suprapubic discomfort or be
- totally asymptomatic.
- The bacterial type can be associated with cystitis
and ureteritis, and the clinical diagnosis is made is
based on cultures of prostate secretions.
- The abacterial type is the most frequent and the clinical
- same as bacterial but no history of recurrent infection
4
0
PLATE # 44: Chronic Focal Inflammation (Chronic Mastitis)
- Note at the level of the fibroconnective stroma,
- the mononuclear inflammatory infiltrate,
- at the expense of lymphocytes and some
- macrophages, which can be seen
- focally, in small groups around
- of the mammary ducts.
- It presents the typical symptoms of inflammation,
- to a greater or lesser degree: pain, redness,
- heat, tumor.
- It is usually associated mainly with obstruction
- of the mammary ducts or infections that
- They penetrate through the cracked nipple, into the
- first weeks of breastfeeding
PLATE # 45: Chronic Follicular Inflammation (Hashimoto's Thyroiditis)
- Note around the thyroid follicles
- (many of them atrophic), with destruction
- of the stroma, which is fibrous, due to the
- dense mononuclear inflammatory infiltrate,
- at the expense of plasmacytes and numerous
- lymphocytes, which are arranged forming
- lymphoid follicles with germinal centers
- well developed.
- It is an autoimmune disease, but
- common in middle-aged women,
- with nonspecific, variable symptoms.
4
1
PLATE # 46: Chronic hepatitis
- Note the inflammatory infiltrate at the expense of lymphocytes and

plasmacytes, as well as occasional neutrophilic nuclear polymorphs, which
are distributed more notably around the portal spaces, accompanied by foci
of necrosis.
- The portal spaces present this inflammatory infiltrate limited to the space or
exceeding it towards the adjacent parenchyma, with necrosis of the
hepatocytes, inflammation and necrosis in bridging and fibrosis (portal, portal
and peri-portal or formation of fibrous septal bridges).
- The main causes are: HBV, which also presents the so-called “ground glass”
hepatocytes and “sandy” nuclei.
- HCV, in which proliferation of bile duct epithelial cells and formation of

lymphoid accumulations within the portal spaces and sublobular focal
regions of steatosis is observed.
- The deposit of fibrous tissue marks irreversible damage, since it leads to

Cirrhosis.
According to its histological alterations, chronic hepatitis is classified as: Chronic

persistent hepatitis.
Chronic lobular hepatitis
Chronic active hepatitis
This classification is important in the prognosis, since the first two histological
forms, in general, do not progress to cirrhosis, unlike chronic active hepatitis,
especially that with intense alterations, which very frequently evolves to liver
cirrhosis ( 80% of cases).
It must be taken into account, however, that the histological appearance may vary
from one sector of the liver to another and a small puncture biopsy may not reflect
the reality of all the liver tissue. These histological lesions are not static and usually
vary, in one direction or another, with the spontaneous evolution of the disease or
due to the effect of therapy. These observations emphasize the need to correlate
the clinical, biochemical, and serological history with the histopathological lesions at
the time of the diagnostic decision.
4
2
Chronic Persistent Hepatitis:
It is characterized by mild inflammatory infiltrate in the portal tracts, while the lobar
architecture and limiting plate are preserved.
Chronic Lobular Hepatitis:

It manifests itself with features of acute hepatitis with inflammation, extending into
the lobe, with isolated necrosis of hepatocytes; the limiting plate is intact.
Chronic Active Hepatitis:

In it there is a chronic inflammatory infiltrate, which expands the portal areas and
extends to the lobes, with erosion of the limiting plate and appearance of fibrosis.
The symptoms are variable.
I | LIVER BIOPSY ]
■ Hepatitis? ___________ _
CHRONIC HEPATITIS
Final Diagnosis
Hepatocellular necrosis + Inflammation
Inflammatory activity?
necrointlamatorla activity indices: Degrees

portal / periportal and lobulliar injury
Chronic Hepatitis
Chronic process?__________________________ Chronic Hepatitis Hepatitis Hepatitis
Hepa Hepatitis chronicle chronicle
chronicle
Chronicle Car-
Fibrosis index: Staging
titis ByD by r xiptocga
c immune
b fariracos
c
Moderate
Injury pattern (HE)
Activity Activity Activity Activity
Histochemical markers (HQ)
serious serious serious activity
Immunohistochemical markers (IHC) Genomic Moderate mild
sequences (HIS, PCR) activity
Moderate Fibrosis Cirrhosis Without with
■ Does it evolve
Fibrosis fibrosis cam fibrosis out
। Comparison with your previous liver biopsies
serious
4
3
PLATE # 47: Chronic granulomatous inflammation (Tuberculosis in lymph node)
- Clearly delimited and typically transmural involvement of the intestine due to an
inflammatory process with mucosal damage:
- There is destruction of the crypts, progressive atrophy and ulceration of the
mucosa
- Widening of the lamina propria due to inflammatory infiltrate of lymphocytes,
plasmacytes, eosinophils, and multinucleated giant cells, which affects all
layers, which can form lymphoid follicles and sometimes abscesses at the level
of the crypts.
- Formation of non-caseated granulomas, in approximately half of the cases
- Fissure with formation of fistulas or sinusoidal tracts. Free perforations or
localized abscesses may develop
- It can occur at any age, with a predilection in the 2nd and 3rd decades, more
frequent in Caucasians and slightly more frequent in women.
- In 40% it affects only the small intestine, in 30% only the colon and in the
remaining 30% both are affected. Although it is known that it can affect any
location in the digestive tract, including the mouth.
PLATE # 48: Chronic granulomatous inflammation due to a foreign body

(Surgical thread)
- Granuloma formation
- Infiltrate of lymphocytes and plasmacytes and multinucleated giant cells
- Note within some giant cells the presence of the foreign body
4
4
4
5
QUIZ #4
16. Define and say characteristics of acute inflammation.
17. Define and say characteristics of chronic inflammation.
18. What are the cardinal signs of inflammation?
19. Mention some of the general (systemic) symptoms of inflammation or its

clinical manifestations?
20. How does it manifest and what are the different phases of the acute
inflammatory response?
21. What components can we find in an inflammatory exudate?
22. List the elements that intervene in the inflammatory response.
23. What is the main effector cell of acute inflammation?
24. Make a morphological classification of acute inflammation.
25. What do we understand by neutrophil marginalization and what stages can

we distinguish in it?
26. What molecules do we know that intervene in the adhesion of neutrophils to

the endothelium?
4
6
27. Define what we mean by chemotaxis:
28. List what substances we know as the main agents of chemotaxis.
29. In phagocytosis, it explains the role that opsonins play and lists two of the
main known opsonins.
30. List some defect(s) of leukocyte function (phagocytosis) in which the acute
inflammatory response is altered.
31. What are the effector cells of chronic inflammation?
32. List some organ-specific macrophages belonging to the mononuclear

phagocytic system.
33. In a peripheral blood smear, tell the different normal percentage (%) of the
types of leukocytes.
34. What are the main characteristics of so-called chronic granulomatous

inflammation?
35. Lists the types of multinucleated giant cells that are characteristic of different
types of granulomatous inflammation.
36. Lists the different varieties of granulomas classified according to their
etiology.
4
7
37. In inflammation which molecules can cause pain and fever.
38. Tell the differences between healing by first intention and healing by second
intention.
39. What factors favor or disfavor wound healing?

4
8
HEMODYNAMIC DISORDERS:
PLATE #52: Hepatic congestion
- The sinusoids are distended and filled with erythrocytes
- The central veins are dilated
PLATE # 53: Splenic congestion (Spleen)

- The sinusoids are filled with blood
- Malphigi follicles are atrophic and small
- There are areas of hemorrhage and the capsule is thickened.
PLATE # 54: Hemorrhage (Soft tissues)

- Note the large number of erythrocytes scattered in the tissue, as well as
congested vessels.
PLATE # 55: Arterial thrombosis
- The thrombus is adhered to the intimal layer and is made up of fibrin,
platelets, erythrocytes and leukocytes.
4
9
PLATE #56: Recanalized thrombus
- Observe the endothelial cells that cover the external surface of the
thrombus, which is invaded and organized by capillaries.
PLATE # 57: Acute edema of the lung

- Note the presence of acellular, eosinophilic, granular and amorphous
material inside the alveoli.
5
0
QUIZ #5
40. What are the hemodynamic disorders recognized in pathology?
41. Explain the process of edema formation.
42. Define exudate, transudate, edema and pus.
43. What is the difference between hyperemia and congestion?
44. Regarding the type of hemorrhage according to its distribution and diameter.
Define: Petechia. Purpura and Ecchymosis.
45. Define: Thrombus. Clot and Embolus.
46. What is the preferred location where thrombosis occurs?
47. List the possible causes of anaphylactic, septic, and neurogenic shock.
THIRD PARTIAL 30%
NEOPLASMS, SYSTEMIC, INFECTIOUS, GENETIC AND IMMUNOLOGICAL

5
1
DISEASES
CLINICAL CHARACTERISTICS OF NEOPLASTIC LESIONS
CLASSIFICATION OF NEOPLASMS
a) Epithelial . The samples in these cases are usually quite cellular. These cells
are distinguished by being polyhedral, they are angular when well
differentiated and can be found individually or in sheets or both. They can be
epithelial: papillomas, if they are benign, or carcinomas, if they are malignant;
or glandular: adenomas or adenocarcinomas, if they are benign or malignant,
respectively. Glandular cells in general show a greater fragility of the
cytoplasm than other cells, the cytoplasm is found in moderate to abundant
amounts and naked nuclei are frequently observed. Sometimes secretion
material is seen in the cytoplasm. Likewise, cells can be found with the
nucleus eccentric and oppressed by the large amount of secretion material.
b) Mesenchymal . In general, cellularity is usually very scarce, therefore,

making evaluation more difficult. The cells commonly occur individually and
are characterized by being fusiform, in general, and having an inapparent
cytoplasmic membrane. The nucleus is mainly centric oval or fusiform.
Examples of these tumors are benign ones, with the suffix OMA , and
malignant ones with the suffix SARCOMA (osteoma, osteosarcoma;
chondroma, chondrosarcoma; fibroma, fibrosarcoma; hemangioma,
hemangiosarcoma).
c) Round cells . This type of tumor generally presents samples with high
cellularity, the shape is round as its classification indicates. This type of cell is
characterized by having an evident cytoplasmic membrane, cytoplasm in
moderate quantity and a generally centric round nucleus. Examples of round
cell tumors are histiocytomas, melanomas, transmissible venereal tumors,
mastocytomas, lymphosarcomas, and plasma cell sarcomas (multiple
myelomas).
MALIGNITY CRITERIA
There are general malignancy criteria such as anisocytosis, macrocytosis,

hypercellularity and pleomorphism, which do not have great weight in the final
interpretation, as well as cytoplasmic malignancy criteria such as basophilia,
vacuolation and the densest cytoplasmic membrane.
The criteria of capital importance in the interpretation are nuclear and nucleolar, the
latter having greater weight in the final designation.
5
2
NUCLEAR AND NUCLEOLAR MALIGNITY CRITERIA
a) Macrokaryosis . It is the presence of larger nuclei than those of the normal

cell line.
b) Anisokaryosis. Cores of different sizes.
c) Nucleus/cytoplasm ratio . Increased by increase in nuclear size.
d) Multinucleation . Cells that have two or more nuclei. Most important criterion
if the same cell also presents anisokaryosis.
e) High mitotic index . In general, cells in mitosis are not observed.
f) Abnormal mitoses . Very important criterion for the designation of
malignancy .
g) Coarse granular chromatin , in cords or clumps. Indicates high activity or
mitotic capacity of cells.
h) Anisonucleolosis . Nucleoli of different sizes.
i) Macronucleolosis . When the nucleoli are larger than an erythrocyte.
j) Different number of nucleoli.
k) Angular nucleoli.
PLATE # 58: Leiomyoma of the uterus
- Benign mesenchymal neoplasm, consisting of well-differentiated smooth
muscle cells intertwined in a swirling pattern
- Note that there is no capsule
5
3
5
4
PLATE # 67: Adenocarcinoma metastatic to Lymph Node

5
5
- Observe the lymphoid tissue
- Note the nests of atypical epithelial cells arranged to form glandular lumens.
PLATE #68: Ring cell carcinoma

stamp
- Malignant neoplasm of epithelial origin,
- made up of sheets of cells with nuclei
- flattened and eccentric with ample cytoplasm
- of course, with mucus, which is positive for
- PAS staining
- Note the presence of abundant mitoses.
PLATE #69: Infiltrating ductal carcinoma

of the mammary gland
- Malignant neoplasm of epithelial origin, consisting of ducts of variable size
and shape, lined with cells of variable pleomorphism.
- Note the presence of invasion of fibro-adipose tissue by malignant cells
PLATE #70: Hepatocarcinoma
- Malignant neoplasm of epithelial origin, where the cells of the liver
parenchyma (hepatocytes) show disorganization (loss of the usual
architecture), in addition to variable pleomorphism
- Figures of atypical mitosis, binucleation, as well as areas of necrosis stand
out.
QUIZ #6
1. Definehe term: Desmoplasia.
2. Definehe term: Papilloma.

5
6
3. Definehe term: Teratoma.
4. Define the term: Choristoma.
5. Define the term: Hamartoma.
6. What is the classification of neoplasms?
7. What is Hodgkin's Disease? What is your characteristic cell? And List the four
types into which it is classified.
8. What is Ewing's Tumor? And Mention histological characteristics.
9. What is Brenner Tumor?
10. Define the term: Pleomorphism.
11. Define the term: Anaplasia.

12. What is the contribution of immunohistochemical techniques to
hististopathological diagnosis? Cite some example.
13. What are the most common malignant neoplasms in men and which are the most
common in women in the Dominican Republic?
14. What neoplasms are known to be related to tobacco consumption?
15. What neoplasms are known to be related to alcohol consumption?

5
7
16. What types of genes are involved in malignant transformation?
17. List some of the known tumor suppressor genes or oncogenes.
18. What chemical carcinogen has been linked to the development of gastric
adenocarcinoma in humans?
19. What neoplasm(s) is/are known to be primarily related to radiation exposure?
20. What neoplasm(s) can occur most frequently due to exposure to ultraviolet
radiation?
5
8
SYSTEMIC DISEASES
PLATE # 71: Hemochromatosis (Liver cirrhosis) (Perls stain)
- The liver tissue is divided by fibrous tissue into small nodules
- Note the deposition of iron pigment (blue) in fibrous tissue and liver cells.
PLATE # 72: Amyloidosis (Kidney) (Congo Red Stain)
- Note the presence of deposition of Amyloid material between the cells
and in the Glomeruli.
- It is amorphous, acellular, and colored
“apple green” when viewed with polarized light lenses
PLATE # 73: Acquired immunodeficiency syndrome (Kaposi's sarcoma)
- Proliferation of multiple small vessels, lined with endothelial cells,
containing hyperchromatic nuclei
- Proliferation of clusters of spindle cells with nuclear atypia
- Infiltrate of lymphocytes, macrophages
PLATE # 74: Systemic lupus erythematosus (Spleen)
- Concentric periarterial fibrosis (in penicillated arteries), giving an “onion
web” appearance
5
9
PLATE #75: Scleroderma (skin)
Diffuse atrophy of the skin Compact sclerosis
Atrophy of the adnexa
INFECTIOUS AND PARASITIC DISEASES

6
0
GENETIC DISORDERS
6
1
QUIZ #7
21. What are the general characteristics of Systemic Autoimmune Diseases?
22. What are the risk groups in the Acquired Immune Deficiency Syndrome
(AIDS) pandemic?
23. What infections are recognized as most prevalent in patients with AIDS?
24. Regarding neoplasms, which ones occur more frequently in patients with
immune depression?
25. What is the so-called amyloid substance and what injury causes its deposit
in tissues?
26. What special histochemistry stain identifies amyloid substance in histology?

6
2
MORPHOLOGICAL DESCRIPTION
CRITERIA TO APPLY IN THE ASSESSMENT OF CASES
ELEMENTS IN THE DESCRIPTION OF MICROSCOPIC IMAGES
- Identify the organ

- Identify normal tissues in the section to take them as a reference
- Describe the types of inflammatory cells infiltrated
- Describe the microscopic alterations
- Issues differential diagnosis
- Provides possible diagnosis
DIAGNOSTIC CASES
- Provide the review, anamnesis and clinical history of your patient

- Describe the physical examination of the patient
- Analyze the macroscopic and microscopic findings
- Analyzes the elements used to discriminate in differential diagnosis
- Provides the bibliographic references used

ANSWERS AND BIBLIOGRAPHICAL QUOTES
- Look for a possible association between:

- The age, sex and clinical symptoms of the patient.
- The clinical history (signology and clinical course) and the injuries found.
- The probable diagnosis and the auxiliary diagnostic tools used.
6
3
SUGGESTED QUESTIONS
1. What is the typical clinical picture of the disease?

2. What is the frequency of the disease?
3. What are the differential diagnoses?
4. What are the disease prevention measures?
5. What is the most appropriate diagnostic aid?
6. What are the possible complications of the disease?
7. Other questions can you ask and correlate?
Student: __________________________________Practice Number:___________

Date: ______________________________ Cluster:_________________________
The final and fundamental objective of the General Pathological Anatomy subject is
to provide the student with a global knowledge of the morphological and molecular
bases of Pathological Anatomy, as well as to provide basic knowledge of the
functioning of the Pathological Anatomy Services and their integration in the
context. hospitable. At the end of this course, the student will have to be able to
recognize the basic morphological alterations in the different tissues of the body
and interpret them appropriately. Likewise, the student will have to become familiar
with the histopathology of the most common non-tumor diseases, their diagnosis,
classification and prognosis.
CONTINUE LEARNING AND STUDYING ALWAYS DON'T STOP

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TECHNOLOGICAL UNIVERSITY OF

PATHOLOGY LABORATORY MANUAL I

Prepared by: Víctor F. Liriano Rivas

Subject Name: Pathology Laboratory I

Clue : MED 305

Practical Hours : 04 weekly

Pre : MED-860, MED-865

Teachers: Ana Portela Raquel Escoto

Santiago de los Caballeros,

PATHOLOGY LABORATORY MANUAL I

PATHOLOGY I LABORATORY RULES

The objective of these standards is to maintain quality and biosafety in the

1. Entry to the laboratory requires that the professor be present, according to

3. Student attendance will be verified at the beginning of the practice.

6. The student must attend 80% of the scheduled practices to be entitled to a

7. Hazardous (infectious) biological waste must be placed in specific bags for

GENERAL GUIDELINES FOR DEVELOPMENT

- You must continue on the first table from left to right.

- It should not mobilize the microscopic fields.

- Violation of any of the above rules results in not being admitted or

- Each question generally has two approaches.

- Please read the question carefully so you know what to answer.

LOOK AT AN EVALUATION MODEL

PATHOLOGY I LABORATORY PARTIAL EXAM

READ CAREFULLY AND ANSWER WHAT IS ASKED OF YOU

PLATE #3: Fibromuscular hyperplasia of the prostate 20

Chronic Active Hepatitis: 42

TECHNOLOGICAL UNIVERSITY OF SANTIAGO

“University of Knowledge for Life

Key: MED-305 Credits: two (2) Pre-Req: MED-860, MED-865

Level: Eighth Semester (Basic Sciences) Co-Req: MED-300

The integration of knowledge of General Pathology is essential in the training of the

UNIT I: Cellular adaptation, cell injury and cell death

- Tissue renewal, repair and regeneration

UNIT III: Hemodynamic Disorders. Thromboembolic disease, Shocks and Neoplasias

Professor's presentations, accompanied by demonstration of the topics through the

Rubín, Emmanuel (2000). Structural Pathology: Clinical-pathological foundations in

Rosai, Juan Ackerman'sSurgical Pathology. (Ninth edition).

FIRST PARTIAL 30%

ADAPTATION, DAMAGE AND CELL DEATH

1- Cardiac muscle hypertrophy

SECOND PARTIAL 30%

INTRACELLULAR ACCUMULA, INFLAMMATION, REPAIR AND

25- Lipid accumulation (liver fatty change)

THIRD PARTIAL 30%

NEOPLASMS, SYSTEMIC, INFECTIOUS, GENETIC AND IMMUNOLOGICAL

58- Leiomyoma of the uterus

- Identify microscopic lesions in reversible cell injuries, cell death and

- Identify changes due to cellular adaptations.

- Understand the pathophysiology of the multiple mechanisms of cellular

Cells are constantly exposed to changes in their environment: There are

Cells adapt to tolerable changes in their environment by modifying their

THE REACTIONS OF THE CELL TO AN AGENT DEPEND ON THE TYPE OF

CELLULAR ADAPTATION translates into atrophy, hypertrophy, metaplasia,

Necrosis can be defined as pathological cell death recognizable by morphological

ALTERATIONS OF THE CYTOPLASM AND NUCLEUS ARE COEXISTENT.

MICROSCOPIC PREPARATIONS TO OBSERVE (PLATE)

PLATE #1: Cardiac muscle hypertrophy

PLATE #2: Adenomatous hyperplasia of the prostate

PLATE #4: Simple Endometrial Hyperplasia

PLATE #5: Thyroid hyperplasia

PLATE #6: Endometrial atrophy

PLATE #7: Testicular atrophy