HISTOPATH Flashcards
(150 cards)
1
Q
Father of Modern Pathology
A
Rudolf Ludwig Carl Virchow
2
Q
4 Aspects of Pathology
A
Etiology,Pathogenesis,Morphologic Changes,Functional derangements/Clinical manifestations
3
Q
Origin of the Disease
A
Etiology:
4
Q
Refers to the sequence of cellular, biochemical and molecular events that
follow the exposure of cells or tissues to an injurious agent
A
Pathogenesis:
5
Q
Refers to the structural alterations in cells or tissues that are either
characteristic of a disease or diagnostic of etiologic process.
A
Morphologic Changes:
6
Q
The end result of genetic, biochemical
and structural changes in cells and tissues are functional abnormalities which lead to the
clinical manifestations of disease, as well as its progress (Clinical course and outcome)
A
Functional derangements/Clinical manifestations:
7
Q
Causes of Necrosis
A
Ischemia/Hypoxia
Physical agents
Chemical agents
Biologic Products
8
Q
–is characterized by the formation of a gelatinous (gel-like)
substance in dead tissues in which the architecture of the tissue is maintained, and
can be observed by light microscopy. Coagulation occurs as a result of protein
denaturation, causing albumin to transform into a firm and opaque state.
A
1.Coagulative necrosis
9
Q
-Rapid coagulation of Cytoplasm due to intracellular enzymes
A
Myocardial infarction)
10
Q
Cells undergo lysis rapidly. in contrast to coagulative
necrosis, is characterized by the digestion of dead cells to form a viscous liquid mass
-fairly rapid total enzymatic dissolution of cells with complete destruction of the
entire cell.
A
2.Colliquative necrosis
11
Q
Mycobacterium tuberculosis interacts with macrophages. The
necrotic tissue appears as white and friable, like clumped cheese.
-The destroyed cells are converted into a granular, friable mass made up of a mixture
of coagulated protein and fat.
A
3.Caseous necrosis
12
Q
– refers to the massive death of tissue caused by combination
of ischemia and superimposed bacterial infection
- primary (bacterial toxins) or secondary (ischemia, infection)
A
Gangrenous necrosis
13
Q
is a special form of necrosis usually caused by
immune-mediated vascular damage
-smooth muscle necrosis, fibrin release (malignant hypertension)
A
5.Fibrinoid necrosis
14
Q
is specialized necrosis of fat tissue, resulting from the action of
activated lipases on fatty tissues such as the pancreas.
-Adipose are split into fatty acids and glycerol without affecting the cell membrane
A
6.Fat necrosis
15
Q
Nuclear Changes during Necrosis
A
Margination of chromatin
Pyknosis
Karyolysis
Karyorrhexis
16
Q
chromatin condensing around the
periphery of the nucleus
A
Margination of chromatin
17
Q
small and dense nuclei
A
Pyknosis
18
Q
complete lysis of the nuclei
A
Karyolysis
19
Q
fragmented nuclei (generally seen in apoptosis)
A
Karyorrhexis
20
Q
Irreversible cell injury is typically accompanied by:
Release of intracellular enzymes like:
A
- Cardiac muscle
- Hepatocytes
- Striated muscle
- Pancreas
21
Q
creatine kinase (MB isoform), aspartate transaminase, lactate dehydrogenase
A
*Cardiac muscle
22
Q
– alanine transaminase
A
*Hepatocytes
23
Q
– creatine kinase (MM isoform)
A
*Striated muscle
24
Q
amylase
A
*Pancreas
25
-From the Latin word “inflammare” (to set afire)
-Universal response to tissue damage by wide range of harmful stimuli including mechanical trauma, tissue necrosis and
infection.
Inflammation
26
```
To destroy (or contain) the damaging agent
To initiate repair processes
To return the damaged tissue to useful
function
```
Purpose of Inflammation
27
Causes of Inflammation
1. Living organisms
2. Chemicals
3. Mechanical & Thermal injuries
4. Immune reaction
28
causes inflammation due to Ag-Ab
reaction
ex. serum sickness
Immune reaction:
29
Changes during inflammation
```
I- Blood vessels changes
II-Changes in blood stream
III- Changes in rate of flow
IV- Leukocytic emigration
V- Diapedesis of WBCs
VI- Serum exudation
```
30
a. Momentary contraction of the Blood vessel
b. Vasodilation : causing more arterial blood
i. e. hyperemia
c. Increased permeability of venules & capillaries
- the effect is leakage of Plasma proteins, RBCs & WBCs.
Blood vessels changes
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a. Changes in Erythrocyte distribution
| b. Leukocytes margination (pavementing)
Changes in blood stream
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a. Acceleration of the rate: due to arteriolar dilation
Changes in rate of flow
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Ameboid movement.
| Cause : chemotactic forces
Leukocytic emigration
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process of attraction of leukocytes to certain
| area that has the chemotactic substances (ex.: C5a)
Chemotaxis
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Chemotactic substances are:
1- Products from pathogenic bacteria.
2- Substances from injured-cells. ex. mechanical or thermal injuries
3- Certain chemicals ex. turpentine.
complements ex. C3 (anaphylatoxin)
36
It is the movement of the WBC from the blood vessel to the site of inflammation
Diapedesis of WBCs
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1- It greatly dilutes toxic substances formed within the body especially bee-stings &
snake-bite.
2- It has blood serum that brings with it antibodies
i.e. it brings humoral immunity against specific infections.
3- Brings leukocytes to the area for phagocytosis.
4- Fibrinogen in the exudate forms fibrin. Fibrin may support ameboid movement of
leukocytes.
5- Has mechanical action by washing the irritant.
Serum exudation
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-The action of neutrophils is
phagocytic
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-Phagocytic power is shown toward
bacteria
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-It will produce pus & this process call
suppuration or purulent exudate
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This cell is present in parasitic infection and hypersensitivity
Eosinophils
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- The action of neutrophils is phagocytic
- Phagocytic power is shown toward bacteria
- It will produce pus & this process call suppuration or purulent exudate
Neutrophils
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-It is phagocytes cells inside the blood & when reach to the cells and tissue it will became
macrophage cells or called histiocytes
-The function of macrophage is phagocytosis of the foreign body
-Removes (scavengers) the debris
-They fuse to form multinucleated giant cells (Ex. Langhan's giant cell. )
Monocytes
44
-It is phagocytes cells inside the blood & when reach to the cells and tissue it will became
macrophage cells or called histiocytes
45
-Its similar to macrophage and similar o epithelial cells close to each other with no different
borders between its cytoplasm & they tend to have small nucleus
-These cells are no phagocytic cells but release lysosomal enzyme.
Epithelioid cells
46
Form by fused the cytoplasm of the macrophages ( 2 – 3 or reach to 20 ) .There are 4 types of
giant cells.
Giant cells
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.There are 4 types of
| giant cells.
1- Langhan's giant cell
2- Foreign body giant cells
3. Touton Giant cell
4. Warthin-Finkeldy
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-Wherein their nuclei can be located at the periphery
Langhan's giant cell
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Classification of the inflammation
1- Time
2- Type of exudate
3- Organ
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extend from hours to few days 🡪
* Infiltration of P.M.N.C.
* Edema
Acute Inflammation:
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extended from days to weeks -->presence of macrophages & lymphocytes
Subacute Inflammation:
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extended from weeks, months, years --> mononuclear cells (macrophages and giant cells)
Chronic Inflammation:
53
-sudden onset
-vascular dilatation
-increased vascular
permeability
-neutrophil activation and
migration
-predominantly PMNs
(Hallmark)
Polymorphonuclear cells ex:
Neutrophil
-when this fails to subside
within several weeks 🡪 chronic
inflammation
Acute Inflammation
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-lasts for weeks or
months/years
-predominantly mononuclears (macrophages,
lymphocytes, plasma cells) but PMNs mayalso be present
Chronic Inflammation
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-It is characterized by increase exudation of the clear albuminous fluid which accumulates in the
inflammation area showing the inflammatory edema
1-Serous inflammation (serous exudate)
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1- Watery fluid is seen in the cavity
2- Cloudy fluid & it has fibrin strands
3- Color could be red if there are RBC present
Microscopic App:
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1-Mechanical injury of tissue.
2- Chemical --> chloroform.
3- Biological --> virus
4- Insects --> bee sting
Causes:
58
- Characterized by too much fibrinogen clotting fibrin and precipitation of fibrin
masses
- Acute inflammatory exudates with a high plasma protein content
Fibrinous inflammation
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1- Mucus membrane ( digestive & respiratory system )
2- Serous surface .
3- Lungs and joints.
Occurrence of fibrinous inflammation
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1- Fibrin is present in network
2- Precipitated protein + WBC + RBC
3- There is hyperemia
Microscopic app of fibrinous inflammation
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1- The organs are firmer and tenser (ex. lungs ) because present of fibrin.
2- Fibrin appearance: string white or yellowish netlike material
Macroscopic app of fibrinous inflammation
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-It is the inflammation characterized by pus formation
-PUS is a liquid of creamy color & consistency but can be thin (watery) or (semi-solid).
The color is blue green when caused by Pseudomonas aeruginosa.
Purulent Inflammation
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implies that large amounts of pus is produced.
Suppurative inflammation:
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is inflammation when there is good amount of pus
| diffusely scattered through a tissue especially the subcutis.
Phlegmonous inflammation:
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is a circumscribed collection of pus with a capsule of Connective Tissue
Abscess:
66
Large number of degenerate neutrophils are seen.
Microscopic Appearance of Purulent Inflammation
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Characterized by large numbers or RBC's that leave by diapedesis .The blood may exudes from
body surface or nearby tissue.
Hemorrhagic Inflammation
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1- Septicemic diseases ex. Anthrax, Pasturellosis.
2- Hemorrhagic gastritis & enteritis.
3- Lungs.
Occurrence of Hemorrhagic Inflammation
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a. Free RBC
| b. Serum, fibrin and leukocytes
Microscopic Appearance of Hemorrhagic Inflammation
70
1. See blood-colored fluid or semi fluid usually clotted & gelatinous.
2. Streaked : vary in color &. consistency
3. Deep red inflamed surface
4. In hemorrhagic enteritis, feces colored black ( except when hemorrhagic inflammation is present in the last part of intestine),
5. In lungs: blood is foamy
Gross App of Hemorrhagic Inflammation
71
-Is inflammation in which the exudate is mucus
-The latter comes from the epithelial cells of mucous glands or from the goblet cells.-Inflammation of the mucous membranes
-It can result in a thick exudate of mucus and white blood cells
-caused by the swelling of the mucous membranes in the head in response to an infection.
Can be seen in:
-common colds
-sinus
-chesty cough
-tonsil
-adenoids
-middle ear
Catarrhal Inflammation
72
Cardinal Signs of Inflammation
```
Rubor – “redness”
Tumor – “swelling”
Calor – “heat”
Dolor – “pain”
Functio laesa – “diminished function”
```
73
-due to arteriolar and capillary dilatation with increased rate of blood flow towards the site of injury
Rubor – “redness”
74
due to increased capillary permeability causing extravasations of blood fluid
Tumor – “swelling”
75
-due to transfer of internal heat to the surface or site of injury, brought about by increased blood
content (hyperaemia)
Calor – “heat”
76
due to pressure upon the sensory nerve by the exudates/tumor
| -(resulting from release of bradykinin and PGE2)
Dolor – “pain”
77
-destruction of the functioning units of the tissue
Functio laesa – “diminished function”
78
arises following non-resolution of acute
| inflammation
Non-specific chronic inflammation
79
arises de novo in response to certain types of injurious agents
Specific (Primary) chronic inflammation
80
subset of specific inflammation characterized by
| the presence of granulomas
Granulomatous inflammation
81
SPECIFIC (PRIMARY)CHRONIC INFLAMMATION
| Types of agent
Immunological
| Non-immunological
82
presence of activated macrophages (Often with added T-Cells) and
multinucleate giant cells
GRANULOMATOUS INFLAMMATION
83
1. Change in the size of the cells
2. Change in the differentiation of cells
3. Change in the rate of cell division
Changes in cellular growth patterns
84
```
incomplete/defective
development of a tissue/organ
most commonly seen in one
paired structures (kidneys,
gonads) represented only by a
mass of fatty/fibrous tissue
-NO RESEMBLANCE TO ADULT
STRUCTURE
```
Aplasia –
85
– non-appearance of
| an organ
Agenesia
86
failure of an organ to reach its full, mature size
Hypoplasia
87
failure of an organ to form an opening
Atresia
88
decrease in size of a normally mature tissue/organ resulting from the reduction in cell size or decrease in the total number of cells
Atrophy
89
– occurs as a natural consequence of maturation
Examples: Atrophy of thymus during puberty
Atrophy of brain and sexual organ (at about 50 years old) – occurs as a natural consequence of maturation
*Physiologic
90
```
as a consequence of disease
Examples:
Endocrine Atrophy
Atrophy of disuse
Starvation/Hunger Atrophy
Pressure Atrophy
Vascular Atrophy
```
*Pathologic
91
increase in the size of existing cells (ex. exercise)
-Hypertrophy
92
due to increased workload or increase in endocrine stimulation
True Hypertrophy-
93
due to edema or connective tissue proliferation
False Hypertrophy
94
- Involved in Paired organs when the other organ is
removed
- One organ compensates for the entire workload
Compensatory Hypertrophy
95
```
increase in cell number as a consequence of
cell division (Cushing syndrome)
```
Hyperplasia
96
– tissues have abnormalities
Degenerative changes
97
usually used as a criterion toward malignancy
Anaplasia (dedifferentiation)
98
reversible change involving transformation in one
| type of adult cell to another
Metaplasia
99
(Atypical hyperplasia).This generally consists of
an expansion of immature cells, with a corresponding decrease in the number and location of mature cells.
-is often indicative of an early neoplastic process
Dysplasia
100
```
– continuous abnormal proliferation of cells
without control (no purpose or function)
```
Neoplasia (Tumor)
101
is an abnormal mass of tissue as a result of neoplasia.
| Neoplasia "new growth“ is the abnormal proliferation of cells
NEOPLASM
102
- Grow slowly and remain localized to the site of origin
| - suffix: -oma
*Benign neoplasms
103
- are collectively referred to as cancers
- grow rapidly and may spread widely
- Suffix: -Sarcoma (mesenchymal/connective tissue)
- Carcinoma (epithelial tissues)
*Malignant neoplasms
104
attempts to establish some
estimate of its aggressiveness or level of malignancy based on:
1. the cytologic differentiation of the tumor
3. the degree of variability of cellular shape and size
(pleomorphism)
2. the number of mitosis within tumor cells
“Grading”
105
is based on:
The size of the primary lesion
Extent of spread to regional lymph nodes
Presence or absence of metastases
“Staging”
106
breast free of tumors
T0
107
local lesion <2 cm in size
T1
108
lesion 2-5 cm in diameter
T2
109
lesion >5cm in diameter
T3
110
skin and/or chest wall involved
T4
111
no axillary nodes involved
NO
112
mobile nodes involved
N1
113
fixed nodes involved
N2
114
ipsilateral internal mammary node involved
N3
115
no metastases
MO
116
demonstrable metastases
M1
117
suspected metastases
MX
118
“Monster”is an encapsulated tumor with tissue or organ components resembling normal derivatives of all three germ layers
Type of neoplasm
Compound tumors
Greek: “Monstrous tumors”
Tumor with normal tissue or organ components that are
inappropriate to surrounding tissues
May contain hair, teeth, bones and very rarely eyeballs, torso and hands (tumors derived from germ cell)
Teratomas
119
-Relatively inexpensive
-May be performed regularly even in pregnant women
without undue risk
-Vaginal smears for such purpose are taken
from the upper lateral third of the vaginal wall
Vaginal Hormonal Cytology
120
- 45-50 um in diameter
- with dark pyknotic nuclei
- with “true acidophilia” (under estrogen)
Mature Superficial Cells/Superficial Cells
121
-medium sized
-polyhedral or elongated cells
-basophilic cytoplasm showing vacuoles
-Navicular Cells:- boat shaped intermediate cells
- folds or curls on edges
- found in the latter half of the menstrual cycle,
during pregnancy and
menopause
Intermediate Cells
122
-Round, oval or boat-shaped cells
-With translucent basophilic cytoplasm
-Nucleus pushed aside or towards the cells
membrane
-With double-walled boundary appearance
(deeper blue stain of
the cytoplasm at the
periphery)
Pregnancy Cells
123
-Thick, round to oval
-Smaller than intermediate cells
-Similar to fried fresh eggs with sunny-side up
-Have larger vesicular nucleus
-Normally found from two weeks of age to
puberty, after child birth, abortions and after
menopause
Parabasal Cells
124
-similar in appearance to parabasal cells
-slightly cylindrical with less basophilic
cytoplasm
-occurring in groups of 3 or more cells
-found during and 1-4 days after
menstruation
Endometrial Cells
125
```
-cytoplasm is usually stained pale blue/gray,
finely vacuolated
-nuclei with finely granular chromatin
-having a “honeycomb appearance” when
viewed on end
```
Endocervical Glandular Cells
126
-small, round to slightly oval cells
-with relatively large nuclei (occupying more than
half of the cell)
-strongly basophilic cytoplasm
-found before puberty and after menopause
Basal Cells
127
-Gram-positive, slender rod-shaped
-Most common organism of the normal vaginal
flora
-Pap’s stain – blue to lavender
-Numerous naked nuclei with many Doderlein’s
bacilli:
1. Last trimester of pregnancy
2. Infection
3. Estrogen deficiency
4. Diabetes mellitus
Doderlein Bacillus
128
technique used to determine the presence of estrogen in the uterine
cervical mucus. It is often used to test for ovulation. High levels of
estrogen cause the cervical mucus to dry in a fernlike pattern on a slide
Ferning
129
Cytologic Collection and Preparation
1. Conventional pap smear
2. endocervical brush
3. vaginal scrape
4. lateral vaginal scrape
5. four quadrant vaginal scrape
6. vulvar scrape
130
samples of endocervical canal
endocervical brush
131
for patients with hysterectomy
vaginal scrape
132
used for hormonal evaluation
lateral vaginal scrape
133
for localization of vaginal adenosis
four quadrant vaginal scrape
134
for detection of herpetic lesions or carcinoma
vulvar scrape
135
discovered by Drr. George Papanicolau
- the technique correlates patterns with the sexual cycle
developed a staining method which can identify stages in the maturation of exfoliated squamous epithelial cells
- formulate a method which malignant cell could be identified
pap smear
136
provides optimum nuclear detail information
modified papaniculau staining procedure
137
stain used for paps smear
1. harris hematoxylin
2. og-6 stain
3. ea 50
138
are the basic unit of tissues which form organs and systems in the human body
cells
139
defined as a variety of stresses a cell encounters as a result of changes in its internal and external environment
cell injury
140
the cells may be broadly injured by two major ways
a. by genetic causes
| b. by acquired causes
141
reduced supply of blood to cells due to interruption.
hypoxia
142
causation of disease are as under
- mechanical trauma
- thermal trauma
- electricity
- radiation
- rapid changes in atmospheric pressure
physical agents
143
an ever-increasing list of chemical agents and drugs may cause cell injury
chemical and drugs
144
injuries by microbes includes infections caused by bacteria, rickettsiae, viruses, fungi, protozoa, etc
microbial agents
145
is a double edged sword -- it protects the host against various injurious agents but it may also turn lethal and cause cell injury
immunologic agents
146
a deficiency or an excess of nutrients may result in nutritional imbalances
nutritional derangements
147
cellular aging or senescence leads to impaired ability of the cells to undergo replication and repair and ultimately lead to cell death culminating in death of the individual
aging
148
there are no specific biochemical or morphologic changes in common acquired mental diseases due to mental stress, strain, anxiety, overwork etc
psychogenic disease
149
physician is bound not to do or administer anything that causes harm to the patient
iatrogenic causes
150
means "of unknown cause"
idiopathic disease
