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HISTOPATH > HISTOPATH > Flashcards

HISTOPATH Flashcards

1
Q

Father of Modern Pathology

A

Rudolf Ludwig Carl Virchow

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2
Q

4 Aspects of Pathology

A

Etiology,Pathogenesis,Morphologic Changes,Functional derangements/Clinical manifestations

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3
Q

Origin of the Disease

A

Etiology:

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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:

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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:

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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:

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7
Q

Causes of Necrosis

A

Ischemia/Hypoxia
Physical agents
Chemical agents
Biologic Products

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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

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9
Q

-Rapid coagulation of Cytoplasm due to intracellular enzymes

A

Myocardial infarction)

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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

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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

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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

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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

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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

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15
Q

Nuclear Changes during Necrosis

A

Margination of chromatin
Pyknosis
Karyolysis
Karyorrhexis

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16
Q

chromatin condensing around the

periphery of the nucleus

A

Margination of chromatin

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17
Q

small and dense nuclei

A

Pyknosis

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18
Q

complete lysis of the nuclei

A

Karyolysis

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19
Q

fragmented nuclei (generally seen in apoptosis)

A

Karyorrhexis

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20
Q

Irreversible cell injury is typically accompanied by:

Release of intracellular enzymes like:

A
  • Cardiac muscle
  • Hepatocytes
  • Striated muscle
  • Pancreas
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21
Q 
creatine kinase (MB isoform), aspartate transaminase,
lactate dehydrogenase
A

*Cardiac muscle

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22
Q

– alanine transaminase

A

*Hepatocytes

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23
Q

– creatine kinase (MM isoform)

A

*Striated muscle

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24
Q

amylase

A

*Pancreas

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25
Q

-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.

A

Inflammation

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26
Q 
To destroy (or contain) the damaging agent
To initiate repair processes
To return the damaged tissue to useful
function
A

Purpose of Inflammation

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27
Q

Causes of Inflammation

A
  1. Living organisms
  2. Chemicals
  3. Mechanical & Thermal injuries
  4. Immune reaction
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28
Q

causes inflammation due to Ag-Ab
reaction
ex. serum sickness

A

Immune reaction:

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29
Q

Changes during inflammation

A 
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
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30
Q

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.

A

Blood vessels changes

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31
Q

a. Changes in Erythrocyte distribution

b. Leukocytes margination (pavementing)

A

Changes in blood stream

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32
Q

a. Acceleration of the rate: due to arteriolar dilation

A

Changes in rate of flow

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33
Q

Ameboid movement.

Cause : chemotactic forces

A

Leukocytic emigration

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34
Q

process of attraction of leukocytes to certain

area that has the chemotactic substances (ex.: C5a)

A

Chemotaxis

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35
Q

Chemotactic substances are:

A

1- Products from pathogenic bacteria.
2- Substances from injured-cells. ex. mechanical or thermal injuries
3- Certain chemicals ex. turpentine.
complements ex. C3 (anaphylatoxin)

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36
Q

It is the movement of the WBC from the blood vessel to the site of inflammation

A

Diapedesis of WBCs

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37
Q

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.

A

Serum exudation

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38
Q

-The action of neutrophils is

A

phagocytic

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39
Q

-Phagocytic power is shown toward

A

bacteria

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40
Q

-It will produce pus & this process call

A

suppuration or purulent exudate

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41
Q

This cell is present in parasitic infection and hypersensitivity

A

Eosinophils

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42
Q
  • The action of neutrophils is phagocytic
  • Phagocytic power is shown toward bacteria
  • It will produce pus & this process call suppuration or purulent exudate
A

Neutrophils

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43
Q

-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. )

A

Monocytes

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44
Q

-It is phagocytes cells inside the blood & when reach to the cells and tissue it will became

A

macrophage cells or called histiocytes

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45
Q

-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.

A

Epithelioid cells

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46
Q

Form by fused the cytoplasm of the macrophages ( 2 – 3 or reach to 20 ) .There are 4 types of
giant cells.

A

Giant cells

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47
Q

.There are 4 types of

giant cells.

A

1- Langhan’s giant cell
2- Foreign body giant cells
3. Touton Giant cell
4. Warthin-Finkeldy

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48
Q

-Wherein their nuclei can be located at the periphery

A

Langhan’s giant cell

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49
Q

Classification of the inflammation

A

1- Time
2- Type of exudate
3- Organ

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50
Q

extend from hours to few days 🡪

  • Infiltration of P.M.N.C.
  • Edema
A

Acute Inflammation:

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51
Q

extended from days to weeks –>presence of macrophages & lymphocytes

A

Subacute Inflammation:

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52
Q

extended from weeks, months, years –> mononuclear cells (macrophages and giant cells)

A

Chronic Inflammation:

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53
Q

-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

A

Acute Inflammation

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54
Q

-lasts for weeks or
months/years
-predominantly mononuclears (macrophages,
lymphocytes, plasma cells) but PMNs mayalso be present

A

Chronic Inflammation

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55
Q

-It is characterized by increase exudation of the clear albuminous fluid which accumulates in the
inflammation area showing the inflammatory edema

A

1-Serous inflammation (serous exudate)

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56
Q

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

A

Microscopic App:

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57
Q

1-Mechanical injury of tissue.
2- Chemical –> chloroform.
3- Biological –> virus
4- Insects –> bee sting

A

Causes:

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58
Q
  • Characterized by too much fibrinogen clotting fibrin and precipitation of fibrin
    masses
  • Acute inflammatory exudates with a high plasma protein content
A

Fibrinous inflammation

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59
Q

1- Mucus membrane ( digestive & respiratory system )
2- Serous surface .
3- Lungs and joints.

A

Occurrence of fibrinous inflammation

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60
Q

1- Fibrin is present in network
2- Precipitated protein + WBC + RBC
3- There is hyperemia

A

Microscopic app of fibrinous inflammation

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61
Q

1- The organs are firmer and tenser (ex. lungs ) because present of fibrin.
2- Fibrin appearance: string white or yellowish netlike material

A

Macroscopic app of fibrinous inflammation

62
Q

-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.

A

Purulent Inflammation

63
Q

implies that large amounts of pus is produced.

A

Suppurative inflammation:

64
Q

is inflammation when there is good amount of pus

diffusely scattered through a tissue especially the subcutis.

A

Phlegmonous inflammation:

65
Q

is a circumscribed collection of pus with a capsule of Connective Tissue

A

Abscess:

66
Q

Large number of degenerate neutrophils are seen.

A

Microscopic Appearance of Purulent Inflammation

67
Q

Characterized by large numbers or RBC’s that leave by diapedesis .The blood may exudes from
body surface or nearby tissue.

A

Hemorrhagic Inflammation

68
Q

1- Septicemic diseases ex. Anthrax, Pasturellosis.
2- Hemorrhagic gastritis & enteritis.
3- Lungs.

A

Occurrence of Hemorrhagic Inflammation

69
Q

a. Free RBC

b. Serum, fibrin and leukocytes

A

Microscopic Appearance of Hemorrhagic Inflammation

70
Q
  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
A

Gross App of Hemorrhagic Inflammation

71
Q

-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

A

Catarrhal Inflammation

72
Q

Cardinal Signs of Inflammation

A 
Rubor – “redness”
Tumor – “swelling”
Calor – “heat”
Dolor – “pain”
Functio laesa – “diminished function”
73
Q

-due to arteriolar and capillary dilatation with increased rate of blood flow towards the site of injury

A

Rubor – “redness”

74
Q

due to increased capillary permeability causing extravasations of blood fluid

A

Tumor – “swelling”

75
Q

-due to transfer of internal heat to the surface or site of injury, brought about by increased blood
content (hyperaemia)

A

Calor – “heat”

76
Q

due to pressure upon the sensory nerve by the exudates/tumor

-(resulting from release of bradykinin and PGE2)

A

Dolor – “pain”

77
Q

-destruction of the functioning units of the tissue

A

Functio laesa – “diminished function”

78
Q

arises following non-resolution of acute

inflammation

A

Non-specific chronic inflammation

79
Q

arises de novo in response to certain types of injurious agents

A

Specific (Primary) chronic inflammation

80
Q

subset of specific inflammation characterized by

the presence of granulomas

A

Granulomatous inflammation

81
Q

SPECIFIC (PRIMARY)CHRONIC INFLAMMATION

Types of agent

A

Immunological

Non-immunological

82
Q

presence of activated macrophages (Often with added T-Cells) and
multinucleate giant cells

A

GRANULOMATOUS INFLAMMATION

83
Q
  1. Change in the size of the cells
  2. Change in the differentiation of cells
  3. Change in the rate of cell division
A

Changes in cellular growth patterns

84
Q 
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
A

Aplasia –

85
Q

– non-appearance of

an organ

A

Agenesia

86
Q

failure of an organ to reach its full, mature size

A

Hypoplasia

87
Q

failure of an organ to form an opening

A

Atresia

88
Q

decrease in size of a normally mature tissue/organ resulting from the reduction in cell size or decrease in the total number of cells

A

Atrophy

89
Q

– 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

A

*Physiologic

90
Q 
as a consequence of disease
Examples:
Endocrine Atrophy
Atrophy of disuse
Starvation/Hunger Atrophy
Pressure Atrophy
Vascular Atrophy
A

*Pathologic

91
Q

increase in the size of existing cells (ex. exercise)

A

-Hypertrophy

92
Q

due to increased workload or increase in endocrine stimulation

A

True Hypertrophy-

93
Q

due to edema or connective tissue proliferation

A

False Hypertrophy

94
Q
  • Involved in Paired organs when the other organ is
    removed
  • One organ compensates for the entire workload
A

Compensatory Hypertrophy

95
Q 
increase in cell number as a consequence of
cell division (Cushing syndrome)
A

Hyperplasia

96
Q

– tissues have abnormalities

A

Degenerative changes

97
Q

usually used as a criterion toward malignancy

A

Anaplasia (dedifferentiation)

98
Q

reversible change involving transformation in one

type of adult cell to another

A

Metaplasia

99
Q

(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

A

Dysplasia

100
Q 
– continuous abnormal proliferation of cells
without control (no purpose or function)
A

Neoplasia (Tumor)

101
Q

is an abnormal mass of tissue as a result of neoplasia.

Neoplasia “new growth“ is the abnormal proliferation of cells

A

NEOPLASM

102
Q
  • Grow slowly and remain localized to the site of origin

- suffix: -oma

A

*Benign neoplasms

103
Q
  • are collectively referred to as cancers
  • grow rapidly and may spread widely
  • Suffix: -Sarcoma (mesenchymal/connective tissue)
  • Carcinoma (epithelial tissues)
A

*Malignant neoplasms

104
Q

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

A

“Grading”

105
Q

is based on:
The size of the primary lesion
Extent of spread to regional lymph nodes
Presence or absence of metastases

A

“Staging”

106
Q

breast free of tumors

A

T0

107
Q

local lesion <2 cm in size

A

T1

108
Q

lesion 2-5 cm in diameter

A

T2

109
Q

lesion >5cm in diameter

A

T3

110
Q

skin and/or chest wall involved

A

T4

111
Q

no axillary nodes involved

A

NO

112
Q

mobile nodes involved

A

N1

113
Q

fixed nodes involved

A

N2

114
Q

ipsilateral internal mammary node involved

A

N3

115
Q

no metastases

A

MO

116
Q

demonstrable metastases

A

M1

117
Q

suspected metastases

A

MX

118
Q

“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)

A

Teratomas

119
Q

-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

A

Vaginal Hormonal Cytology

120
Q
  • 45-50 um in diameter
  • with dark pyknotic nuclei
  • with “true acidophilia” (under estrogen)
A

Mature Superficial Cells/Superficial Cells

121
Q

-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

A

Intermediate Cells

122
Q

-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)

A

Pregnancy Cells

123
Q

-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

A

Parabasal Cells

124
Q

-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

A

Endometrial Cells

125
Q 
-cytoplasm is usually stained pale blue/gray,
finely vacuolated
-nuclei with finely granular chromatin
-having a “honeycomb appearance” when
viewed on end
A

Endocervical Glandular Cells

126
Q

-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

A

Basal Cells

127
Q

-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

A

Doderlein Bacillus

128
Q

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

A

Ferning

129
Q

Cytologic Collection and Preparation

A
  1. Conventional pap smear
  2. endocervical brush
  3. vaginal scrape
  4. lateral vaginal scrape
  5. four quadrant vaginal scrape
  6. vulvar scrape
130
Q

samples of endocervical canal

A

endocervical brush

131
Q

for patients with hysterectomy

A

vaginal scrape

132
Q

used for hormonal evaluation

A

lateral vaginal scrape

133
Q

for localization of vaginal adenosis

A

four quadrant vaginal scrape

134
Q

for detection of herpetic lesions or carcinoma

A

vulvar scrape

135
Q

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

A

pap smear

136
Q

provides optimum nuclear detail information

A

modified papaniculau staining procedure

137
Q

stain used for paps smear

A
  1. harris hematoxylin
  2. og-6 stain
  3. ea 50
138
Q

are the basic unit of tissues which form organs and systems in the human body

A

cells

139
Q

defined as a variety of stresses a cell encounters as a result of changes in its internal and external environment

A

cell injury

140
Q

the cells may be broadly injured by two major ways

A

a. by genetic causes

b. by acquired causes

141
Q

reduced supply of blood to cells due to interruption.

A

hypoxia

142
Q

causation of disease are as under

  • mechanical trauma
  • thermal trauma
  • electricity
  • radiation
  • rapid changes in atmospheric pressure
A

physical agents

143
Q

an ever-increasing list of chemical agents and drugs may cause cell injury

A

chemical and drugs

144
Q

injuries by microbes includes infections caused by bacteria, rickettsiae, viruses, fungi, protozoa, etc

A

microbial agents

145
Q

is a double edged sword – it protects the host against various injurious agents but it may also turn lethal and cause cell injury

A

immunologic agents

146
Q

a deficiency or an excess of nutrients may result in nutritional imbalances

A

nutritional derangements

147
Q

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

A

aging

148
Q

there are no specific biochemical or morphologic changes in common acquired mental diseases due to mental stress, strain, anxiety, overwork etc

A

psychogenic disease

149
Q

physician is bound not to do or administer anything that causes harm to the patient

A

iatrogenic causes

150
Q

means “of unknown cause”

A

idiopathic disease

HISTOPATH (3 decks)

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