HISTOPATH 1 Flashcards by LEDESMA, Anne Gelika

study of all changes in cells, tissues, and organs that underlie a disease

Pathology

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starting point in every disease process

Cells

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3 CLASSES
OF CELLS

Labile
Stable
Permanent

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Cells frequently dividing to replace lost body cells

LABILE CELL

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Replaces majority of body cells due to their limited lifespan

LABILE CELL

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example of LABILE cell

Epithelial cells of skin

Exception: cancer cells
(immortalized cells)

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Cells not frequently dividing; only divides to replace injured cells

STABLE CELL

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example of STABLE cell

Parenchymal cells of liver and kidneys

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Cells that do not undergo replication upon maturation

PERMANENT CELL

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example of PERMANENT cell

neurons (nerve cells)

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4 ABNORMALITIES IN CELL GROWTH

Aplasia
Agenesia
Hypoplasia
Atresia

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T/F

Young cells typically undergo maturation with interval in between. There could be abnormalities along the way before it reaches maturation

TRUE

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Incomplete/defective development of tissue/organ

Aplasia

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abnormalities in cell growth wherein the affected organ shows no resemblance to the normal mature structure

Aplasia

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abnormalities in cell growth that usually occur in PAIRED ORGANS (KIDNEYS, GONADS)

Aplasia

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Complete non-appearance of organ

Agenesia

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Failure of tissue/organ to reach normal mature adult size

Hypoplasia

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Failure of organ to form an opening

Atresia

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Imperforate anus and microtia (absence of ear canal) are both abnormalities in cell growth called as

Atresia

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T/F

Body cells may be exposed to stressful stimuli. Under normal condition, cells will able to adapt (through several adaptation mechanisms). If exposure to stressful stimuli is prolonged and the degree of stress is severe, cells will fail to adapt which can cause injury (reversible or irreversible).

TRUE

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6 CELLULAR ADAPTATION MECHANISMS

Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Anaplasia

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Acquired decrease in tissue/organ size

Atrophy

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Normal decrease in tissue/organ size as a consequence of maturation

Physiologic atrophy

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Decrease
in tissue/organ size is associated
with a disease

Pathologic atrophy

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State the cellular adaptation mechanism: Thymus at puberty

PHYSIOLOGIC atrophy

State the cellular adaptation mechanism: Decrease in uterus size after birth

PHYSIOLOGIC atrophy

TYPES OF PATHOLOGIC ATROPHY

"HE VAPE" Hunger/starvation atrophy Exhaustion atrophy Vascular atrophy Atrophy of disuse Pressure atrophy Endocrine atrophy

Decreased tissue/organ size if blood supply to an organ becomes reduced/below critical level

Vascular atrophy

Decreased tissue/organ size due to persistent pressure on the organ or tissue that may directly injure the cell or may secondarily promote diminution of blood supply (vascular atrophy)

Pressure atrophy

A correlated types of PATHOLOGIC ATROPHY

Pressure atrophy Vascular atrophy

Decreased tissue/organ size due to lack of hormones needed to maintain normal size and structure

Endocrine atrophy

Decreased tissue/organ size due to lack of nutritional supply to sustain normal growth

Hunger/starvation atrophy

Too much workload, causing general wasting of tissues -- leading to decreased tissue/organ size

Exhaustion atrophy

Inactivity/diminished activity or function causing decreased tissue/organ size

Atrophy of disuse

Increase in tissue/organ size due to increase in cell size making up the organ

Hypertrophy

Increase in tissue/organ size but NO NEW CELLS PRODUCED

Hypertrophy

Increase in tissue/organ size due to increase in cell number making up the organ

Hyperplasia

Increase in tissue/organ size; NEW CELLS PRODUCED

Hyperplasia

Reversible type of hypertrophy

Physiologic Hypertrophy

Normal increase in tissue/organ size due to increased cell size Reversible

Physiologic Hypertrophy

Increased tissue/organ size due to increased cell size caused by a disease

Pathologic Hypertrophy

Increased cell size as a response to a deficiency

Compensatory hypertrophy

Increase in tissue/organ size when one of the paired organs is removed

Compensatory hypertrophy

State the cellular adaptation mechanism: Bulging of skeletal muscles due to frequent exercise

Physiologic Hypertrophy

State the cellular adaptation mechanism; also state the reason for its occurrence: Increased size of myocardium (heart muscle)

Pathologic Hypertrophy due to HTN or aortic valve disease

cellular adaptation mechanism that may occur if a patient is experiencing hypertension or aortic valve dse

Pathologic Hypertrophy (inc. size of myocardium)

cellular adaptation mechanism that may occur if an individual is consistently exercising

Physiologic Hypertrophy (bulging of skeletal muscles)

State the cellular adaptation mechanism: Enlargement of one kidney (renal)

Compensatory hypertrophy (occur when one of the kidney is removed)

Normal increase in cell no. Happens in response to a need

Physiologic hyperplasia

Abnormal increase in cell no.

Pathologic hyperplasia

T/F If there is a compensatory hypertrophy, there is also compensatory hyperplasia.

TRUE!! Hypertrophy and hyperplasia are two different processes but usually occur together. Triggered by the same stimulus.

State the cellular adaptation mechanism: ↑ breast & uterus size during pregnancy

Physiologic hyperplasia

State the cellular adaptation mechanism: ↑ breast size during puberty due to glandular stimulation

Physiologic hyperplasia

State the cellular adaptation mechanism: Erythroid bone marrow hyperplasia (red cell precursor/immature RBCs in the bone marrow may undergo an ↑ in size, usually in individuals living in high altitude)

Physiologic hyperplasia

what cellular adaptation mechanism that usually occur in individuals living in high altitude

Physiologic hyperplasia (reversible if they transfer to low altitude)

State the cellular adaptation mechanism: Graves disease

Pathologic hyperplasia *Graves disease is also described as diffuse crowding of epithelial cells

State the cellular adaptation mechanism: Endometriosis due to inc. estrogen

Pathologic hyperplasia

State the cellular adaptation mechanism: TB of cervical lymph nodes (↑ no. of lymph nodules)

Pathologic hyperplasia

Involves transformation of adult cell type into another adult cell type REVERSIBLE

Metaplasia

2 types of metaplasia

Epithelial Metaplasia Mesenchymal Metaplasia

Cells involved in transformation from adult cell type to another adult cell type are epithelial cells

Epithelial Metaplasia

Cells involved in transformation from adult cell type to another adult cell type are connective tissue cells

Mesenchymal Metaplasia

Original tissue: Ciliated columnar epithelium of bronchi Stimulus: ? Metaplastic tissue: ?

Stimulus: Cigarette smoking Metaplastic tissue: Squamous epithelium

Original tissue: Transitional epithelium of bladder Stimulus: ? Metaplastic tissue: ?

Stimulus: Bladder trauma Metaplastic tissue: Squamous epithelium

Original tissue: Columnar glandular epithelium Stimulus: ? Metaplastic tissue: ?

Stimulus: Vit K deficiency Metaplastic tissue: Squamous epithelium

Original tissue: Esophageal squamous epithelium Stimulus: ? Metaplastic tissue: ?

Stimulus: Gastric acidity (triggered by excessive coffee Metaplastic tissue: Columnar epithelium

What is the affected tissue when a person is a persistent cigarette smoker? What will be the resulting metaplastic tissue?

Ciliated columnar epithelium of bronchi --> Squamous epithelium

What is the affected tissue when a person experienced a bladder trauma? What will be the resulting metaplastic tissue?

Transitional epithelium of bladder --> Squamous epithelium

What is the affected tissue when a person has Vit K deficiency? What will be the resulting metaplastic tissue?

Columnar glandular epithelium --> Squamous epithelium

What is the affected tissue when a person consumes excessive coffee causing gastric acidity? What will be the resulting metaplastic tissue?

Esophageal squamous epithelium --> Columnar epithelium

aka Dysplasia

Atypical metaplasia/ Pre-neoplastic lesion

aka Anaplasia

Dedifferentiation

No transformation; only change in cell size, shape, & orientation (cell arrangement) May lead to cancer, but not necessarily

Dysplasia

Dysplasia: reversible or irreversible?

Reversible

Anaplasia: reversible or irreversible?

Irreversible

With transformation of adult cells into embryonic or fetal cells (young)

Anaplasia

T/F Neoplasia is also considered as a cellular adaptation mechanism

FALSE

Causes of cell injury

Anoxia Infectious agents Mechanical agents Chemical agents

No. 1 cause of cell injury

Anoxia (O2 deprivation) - can also lead to cell death

Type of injury wherein the affected cell may recover

Reversible Injury

Type of injury wherein the affected cell will never recover (further undergo cell death); considered as a point of no return

Irreversible injury

Duration for a hypoxic injury to be IRREVERSIBLE in neurons

3-5 minutes

Duration for a hypoxic injury to be IRREVERSIBLE in myocardial cells and hepatocytes

1-2 hours

Duration for a hypoxic injury to be IRREVERSIBLE in skeletal muscles

many hours

Gross changes that can be observed to assume that the cell injury is still REVERSIBLE

1. Organ pallor/pale 2. Increased organ weight

Earliest microscopic changes to assume that the cell injury is still REVERSIBLE

1. Cellular swelling (reason for inc. wt) – 1st to occur 2. Fatty degeneration

IRREVERSIBLE INJURY changes are due to

Enzymatic digestion of cells Protein denaturation

To determine that the cell injury is IRREVERSIBLE, these cell parts are observed

Cytoplasm Nucleus

Cytoplasmic changes in irreversible injury

1. Larger cells “cloudy swelling” 2. ↑ eosinophilia (orange or bright pink cytoplasm)

Nuclear changes in irreversible injury

1. Pyknosis – nuclear condensation (small nucleus) 2. Karyorrhexis – nuclear fragmentation/segmentation 3. Karyolysis – dissolution of nucleus

ending of irreversible injury

CELL DEATH

PATTERNS OF CELL DEATH

Apoptosis Necrosis

Physiologic (programmed) cell death

Apoptosis

Normal cell death for all cells except for permanent cells (neuron)

Apoptosis

Death of single cell in a cluster of cells

Apoptosis

Course of events in APOPTOSIS

Cell shrinkage → Intact membrane integrity → No leakage of cellular components → NO INFLAMMATION

Course of events in NECROSIS

Cell swelling → Non-intact membrane → Leakage of cellular components → INFLAMMATION

Pathologic (accidental) cell death

Necrosis

5 Chief morphologic features in apoptosis

1. Chromatid condensation 2. Chromatid fragmentation 3. Cell shrinkage 4. Cytoplasmic bleb formation 5. Phagocytosis of apoptotic cells – removed by neighboring cells

TYPES OF NECROSIS

Coagulative Liquefactive Caseous Fibrinoid Fat Gangrenous

Necrosis due to sudden cut off of blood supply (O2)/ischemia

Coagulative necrosis

Hydrolytic enzymes’ action is blocked (lysozyme released upon cell death) in this type of necrosis

Coagulative necrosis

MICROSCOPIC APPEARANCE of coagulative necrosis

Preserved cell outline, empty (ghostly)

GROSS APPEARANCE of coagulative necrosis

Somewhat firm, boiled-like material

Coagulative necrosis is usually common in these organs

Solid organs (liver, kidneys, myocardial infarct)

Softening of organs due to action of hydrolytic enzymes

Liquefactive necrosis

Complete digestion of cells

Liquefactive necrosis

GROSS APPEARANCE of liquefactive necrosis

Soft, liquefied, creamy yellow

Liquefactive necrosis usually occur in these conditions

Brain infarct Suppurative bacterial infection

Coagulative + Liquefactive

Caseous necrosis

cheese-like

Caseous necrosis

MICROSCOPIC APPEARANCE of caseous necrosis

Amorphous granular debri surrounded by granulomatous inflammation

GROSS APPEARANCE of caseous necrosis

Greasy resembling “cheese”

Caseous necrosis is usually seen in these condition

Fibrin deposition in vessel wall

Fibrinoid Necrosis

MICROSCOPIC APPEARANCE of Fibrinoid Necrosis

Thickened blood vessels

GROSS APPEARANCE of Fibrinoid Necrosis

NO GROSS changes!!!

Fibrinoid necrosis usually occur in this condition

Immune reactions of the blood vessels

Destruction of fat cells due to release of pancreatic lipases Death of fat tissues (adipose cells) due to blood supply loss

Fat Necrosis

MICROSCOPIC APPEARANCE of Fat Necrosis

Infiltrates of foamy macrophage adjacent to adipose tissues

GROSS APPEARANCE of Fat Necrosis

Chalky white precipitates

Fat necrosis usually occur in these condition

pancreatitis

Fat necrosis usually affect this organ

breast

Necrosis secondary to ischemia

Gangrenous necrosis

NOT a specific pattern of necrosis

Gangrenous necrosis

usually refer to a limb/lower extremity that has interrupted blood supply

Gangrenous

GROSS APPEARANCE of gangrenous necrosis

Skin is dry, black, and observed in various stages of decomp.

gangrene due to venous occlusion

Wet gangrene

gangrene due to arterial occlusion

Dry gangrene

type of gangrene: foot embolism

DRY gangrene

type of gangrene: suppurative bacterial infection

WET gangrene

Immediate tissue reaction to injury

INFLAMMATION

Ultimate goal of INFLAMMATION

1. To remove the initial cause of injury 2. To remove consequences of injury

5 Cardinal signs

rubor (redness) calor (warmth/heat) tumor (swelling) dolor (pain) functio laesa (loss of function/destruction of functioning units of the cell)

cardinal sign: pain

DOLOR

cardinal sign: redness

RUBOR

cardinal sign: heat

CALOR

cardinal sign: swelling

TUMOR

cardinal sign: destruction of functioning units of the cell/loss of function

FUNCTIO LAESA

Rapid response to an injurious agent May progress to chronic inflammation if it fails to subside in several weeks

Acute Inflammation

Hallmark signs of an acute inflammation

Exudation Edema

escape of fluid, proteins, & blood cells from vascular system

Exudation

excess fluid in interstitial tissues and serous cavities

Edema

Cellular infiltrate in acute inflammation

NEUTROPHILS

Inflammation of prolonged duration Occur from nonresolution of acute inflammation

Chronic inflammation

Cellular infiltrate in chronic inflammation

MONONUCLEAR CELLS (macrophage, lymphocytes, plasma cells)

RESOLUTION OF INFLAMMATION

HEALING

TYPES OF HEALING

• Simple resolution • Regeneration • Replacement by a connective tissue scar

* No destruction of normal tissues * Offending agent is neutralized * Vessels return to their normal permeability state * Excess fluid (edema) is reabsorbed * Clearance of mediators and inflammatory cells

Simple resolution

Replacement of loss/necrotic tissues with a new tissue that is similar to those that were destroyed

Regeneration

Replacement of loss/necrotic tissues with a new tissue that is not that similar to those that were destroyed

Replacement by a connective tissue scar

Death of the entire body

SOMATIC DEATH

Changes that can be observed immediately after death

Primary changes

Primary changes in somatic death

1. CNS failure 2. Respiratory failure 3. Cardiac failure

Changes that can be observed few hours after death

Secondary changes

Secondary changes in somatic death

1. Algor mortis 2. Rigor mortis 3. Livor mortis 4. Post mortem clotting 5. Autolysis 6. Putrefaction 7. Desiccation

cooling of the body

Algor mortis

stiffening of the body

Rigor mortis

post mortem hemolysis

Livor mortis

Used to establish time of death

Algor mortis (cooling of the body)

Algor mortis (cooling of the body) happens at a rate of _____

70ºF/hour

Algor mortis (cooling of the body) is FASTER in:

cold weather lean malnourished individuals

Algor mortis (cooling of the body) is DELAYED in:

infectious diseases followed by ↑ temp.

Rigor mortis (stiffening of the body) STARTS ____ after death

2-3 hours

Rigor mortis (stiffening of the body) COMPLETES at ____ after death

6-8 hours

Rigor mortis (stiffening of the body) STIFFNESS REMAINS for ____ after death

12-36 hours, persist for 3-4 days

Hasten rigor mortis (stiffness):

warm environment in infants

Delays rigor mortis (stiffness):

cold temperature obese individuals

Purplish discoloration of the skin

Livor mortis (post mortem hemolysis)

Sinking of fluid blood into capillaries of dependent body part

Livor mortis (post mortem hemolysis)

Determine if body position has changed at the scene of death

Livor mortis (post mortem hemolysis)

Occur slowly or immediately after death Settling and separation of RBCs from the fluid phase

Post mortem clotting

Cell destruction due to the release of hydrolytic enzymes

Autolysis

Rotting and decomposition by bacterial action

Putrefaction

Drying and wrinkling of cornea and anterior chamber

Desiccation

examination of a dead body (NOT mandatory)

AUTOPSY/NECROPSY

aka AUTOPSY

NECROPSY

Main purpose of autopsy/necropsy

To determine cause of death

Most important requirement before performing autopsy/necropsy

Consent from the nearest kin

Autopsy types as to PURPOSE

Routine Hospital Autopsy – performed in hospital Medico Legal Autopsy – performed by government agencies

Autopsy types as to COMPLETENESS OF PROCEDURE

Complete autopsy – examine the body from head to foot Partial autopsy – examine only a few regions of the body

Autopsy types as to the MANNER OF INCISION

Y-shaped incision Straight cut incision

cadaver is opened from both shoulders down from xiphoid area and incised down to pubis

Y-shaped incision

manner of incision usually done in adult cadaver

Y-shaped incision

manner of incision usually done in children/infant cadaver

Straight cut incision

cadaver is opened from the midline of the body from the suprasternal notch down to the pubis

Straight cut incision

4 AUTOPSY TECHNIQUES by:

Rudolf Virchow Carl Rokitansky Anton Ghon Maurice Lettulle

Father of pathology

Rudolf Virchow

Organs are removed separately one by one, studied individually

technique by Rudolf Virchow

Cranial cavity → thoracic cavity → cervical region → abdominal cavity

technique by Rudolf Virchow

Autopsy technique is quick and suitable for beginners (advantage)

technique by Rudolf Virchow

Autopsy technique that causes loss of continuity (disadvantage)

technique by Rudolf Virchow

“In-situ” dissection (no removal, dissection in original place), combined with en bloc removal

technique by Carl Rokitansky

advantage: * Infected bodies (HIV, hepa B) * Good in children

technique by Carl Rokitansky

disadvantage: * Difficult to perform

technique by Carl Rokitansky

“En-bloc” removal of organs (removal of organs that belong to the same system)

technique by Anton Ghon

Cervico-thoracic, abdominal, pelvic organs are removed in 3 blocks Neuronal system is removed as another block

technique by Anton Ghon

Advantage: * Excellent preservation * Handling of organs easier

technique by Anton Ghon

Disadvantage: * Interrelationships are difficult to study; if disease is extending to all blocks

technique by Anton Ghon

“En masses” method All organs are removed en masse and dissected as organ block

technique by Maurice Lettulle

Advantage: * Organs interrelationships are preserved * Body can be handed over quickly

technique by Maurice Lettulle

Disadvantage: * Organs difficult to handle

technique by Maurice Lettulle

Process of tumor formation (abnormal proliferation of cells)

NEOPLASIA

New cells are produced but functionless and immortalized

NEOPLASIA

Practical remedy for NEOPLASIA

surgical removal of tumor → biopsy (to determine if benign or malignant)

PARTS OF TUMOR

1. Parenchyma 2. Stroma

neoplastic cells

Parenchyma

connective tissue framework; supplies blood supply to tumor → proliferation

Stroma

Types of tumor as to CAPACITY TO CAUSE DEATH

BENIGN TUMORS MALIGNANT TUMORS

Slowly growing mass

BENIGN TUMORS

Rapidly growing mass

MALIGNANT TUMORS

Regular surface, capsulated, not attached to deep structures

BENIGN TUMORS

type of tumor with irregular surface, non-capsulated, attached to deep surfaces

MALIGNANT TUMORS

Type of tumor noninvasive to another organ/tissues

BENIGN TUMORS

Invasive to other organs

MALIGNANT TUMORS

No spread or metastasis

BENIGN TUMORS

Spread and metastasis

MALIGNANT TUMORS

Well differentiated tumor

BENIGN TUMORS

Type of tumor that may be poorly differentiated, moderately or well differentiated

MALIGNANT TUMORS

tumor with NO recurrence after surgery

BENIGN TUMORS

Type of tumor with recurrence after surgery

MALIGNANT TUMORS

Tumor: No bleeding in cut surfaces

BENIGN TUMORS

Tumor: Bleeding from cut surfaces is common

MALIGNANT TUMORS

Named by adding suffix “-oma”

BENIGN TUMORS

Named by adding suffix “sarcoma” or “carcinoma”

MALIGNANT TUMORS

Type of tumor with slight pressure effect on the neighboring organ

BENIGN TUMORS

Type of tumor with remarkable pressure effect on neighboring tissue

MALIGNANT TUMORS

PURPOSE of grading tumor

To determine the percentage of differentiated and undifferentiated cells

Differentiated cells

Normal cells

Undifferentiated cells

Abnormal/neoplastic cells

Value of grading

1. Guide for treatment 2. Prognostic guide

Characteristics of cancerous cells:

1. Many cells continue to grow and divide 2. Variations in cell size and shape 3. Nucleus is larger and darker than normal 4. Abnormal no. of chromosomes arranged in a disorganized fashion 5. Cluster of cells without a boundary

Used to grade tumor

BRODER’S CLASSIFICATION

Differentiated cells: 100-75% Undifferentiated cells: 0-25%

GRADE I

Differentiated cells: 75-50% Undifferentiated cells: 25-50%

GRADE II

Differentiated cells: 50-25% Undifferentiated cells: 50-75%

GRADE III

Differentiated cells: 25-0% Undifferentiated cells: 75-100%

GRADE IV

prognosis of tumor with LOWER grades

GOOD prognosis amenable to surgery

prognosis of tumor with HIGHER grades

POOR prognosis requires radical tx (chemo, rad)

Purpose of staging tumors

To determine the spread of cancer Based on the size of primary lesions, extent of spread to regional lymph nodes and presence or absence of metastases

Used to STAGE tumors

TNM classification T = Size of tumor N = Number of lymph nodes involved M = Presence/absence of metastasis

Make use of antigen antibody reactions by directly labeling of the antibody or by means of a secondary labeling method

Immunohistochemistry

Purpose of IHC

Identification of tissue or cellular antigens or phenotypic markers

In IHC, detected in cells is ____.

Antigen

Used as detector in IHC

Antibodies

Most common form of antibody used in IHC

IgG

Antibodies produced by different cells

Polyclonal Ab

React with various epitopes (part of antigen that reacts with an antibody)

Polyclonal Ab

May be obtained from laboratory animal sources

Polyclonal Ab

Main source of Polyclonal Ab

Rabbits (immunized to produced Abs)

Other sources of Polyclonal Ab

Goat Pig Sheep

Produced from individual clone of plasma cells – MORE SPECIFIC

Monoclonal Ab

Produces only 1 type of antibody and reacts with 1 specific type of epitope

Monoclonal Ab

Animal source of Monoclonal Ab

Mice

Used in labeling antibodies

Enzymes Fluorochrome label Radioisotopes Colloidal metal/gold Lectins

most widely used enzyme for labeling Ab

Horse Radish Peroxidase (HRP)

requires the use of CHROMOGEN (color developer)

HRP

Chromogen used in HRP

DAB (3,3’-Diaminobenzidine) AEC (3-amino-9-ethylcarbazole)

Chromogen with BROWN as resulting color

DAB (3,3’-Diaminobenzidine)

Chromogen with BRICK-RED as resulting color

AEC (3-amino-9-ethylcarbazole)

alternative enzyme

Alkaline phosphatase

traditional counterstain used in labeling antibodies

hematoxylin

Optimum incubation time to link antibody with enzyme peroxidase

30-60 mins at RT

used in Fluorochrome label

FITC (Fluorescein Isothiocyanate)

Plant or animal proteins which can bind to tissue carbohydrate

lectin

Can also be used to detect antigens, can also be labelled like antibodies

lectin

specimens for IHC

Cryostat Frozen sections Processed specimens (formalin-fixed/paraffin-embedded)

Must be fixed in a few seconds using absolute methanol or acetone

Cryostat frozen sections

used to fix cryostat frozen sections

absolute methanol acetone

Purpose of fixation of Cryostat frozen sections

a) To prevent destruction of labile antigenic sites b) To preserve antigen position

IHC specimen that requires antigen retrieval

Processed specimens

Formalin-fixed Paraffin-embedded

Methods of antigen retrieval from processed tissues

Proteolytic enzyme retrieval (PIER) Microwave antigen retrieval/Heat Induced Epitope retrieval Pressure cooking antigen retrieval Autoclave heating Waterbath heating (90ºC or 95-98º) Steamer heating Decloaker heating Combination of microwave & enzyme digestion

most common method of antigen retrieval

Proteolytic enzyme retrieval (PIER)

commonly used in PIER

trypsin protease

Duration of Microwave antigen retrieval/Heat Induced Epitope retrieval

20 minutes

not preferred method of antigen retrieval

Pressure cooking antigen retrieval

Tissue section with the antigen being detected

Positive control

To prepare, primary antibody is omitted from staining sched

Negative control

Contains the target antigen, not only in the tissue but also in adjacent tissue elements

Internal tissue control (Built-in control)

necrosis due to fungal infections? what are the examples?

Caseous necrosis • Histoplasmosis • Blastomycosis • Coccidioidomycosis

site involved in DRY gangrene

limbs

site involved in WET gangrene

more common in bowel

mechanism of DRY gangrene

arterial occlusion

mechanism of WET gangrene

venous obstruction

Macroscopic appearance of DRY gangrene

dry shrunken black

Macroscopic appearance of WET gangrene

moist soft swollen rotten dark

Putrefaction in DRY gangrene

limited due to less blood supply

Putrefaction in WET gangrene

MARKED due to congestion of organ with blood

Line of demarcation: DRY gangrene

present

Line of demarcation: WET gangrene

no clear cut line

bacteria in DRY gangrene

fail to survive

bacteria in WET gangrene

numerous bacteria present

prognosis in DRY gangrene

better (due to septicemia)

prognosis in WET gangrene

POOR (due to toxemia)