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Y1B2 (PPMIP & PPP) 📗 > Pathology 🩺 > Flashcards

Pathology 🩺 Flashcards

1
Q

What is the definition of pathology?

A

Is the science which deals with the study of diseases.

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2
Q

What does the study of pathology include?

A

ENCF PPPP

1) Etiology.
2) Nature of the disease.
3) Pathogenesis.
4) Pathological examination of lesions.
5) Prognosis.
6) Complications.
7) Fate.
8) Pathological investigations.

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3
Q

What is etiology?

A

This means the cause of the disease.

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4
Q

What does etiology include?

A

-Predisposing factors
-Exciting factors

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5
Q

Predisposing factors

A

-Factors that help the development of the disease.

-This occurs in one of two ways:
1) Decreased body defense (favors infection).
2) Increased susceptibility (suggested to be hereditary) as Bronchial asthma.

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6
Q

Exciting factors

A

-Is the direct cause of the disease (i.e. cause lesion).

-It includes:
1) Defective fetal development in the uterus:
 Congenital.
 Hereditary (genetic). “Like Trisomy 21”

2) Acquired factors (after birth):
 Exogenous (environmental) factors as microbes, nutritional deficiency (protein, vitamins, etc.)
 Endogenous (internal factors) as endocrine disturbance, hypertension, peptic ulcer.

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7
Q

What can the nature of the disease be?

A

-Congenital & Hereditary diseases.

-Acquired diseases:
 Inflammation.
 Degeneration. “Diseased but not dead”
 Circulatory disturbance. “Disturbance in CVS”
 Tumors.

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8
Q

What is pathogenesis?

A

The mechanisms by which the causative agent produces the pathological changes in the tissues (i.e. mechanism of formation of the lesion.).

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9
Q

Pathological examination of the lesions

A

Structural changes in the diseased tissues include:

 Gross picture (macroscopic picture): A naked eye description of the pathological changes.

 Microscopic picture (histological): These are the changes in the tissues of organs detected on microscopic examination by Light microscope, Electron microscope, and Immunohistological techniques

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10
Q

What is an example of an immunohistological technique?

A

as immunofluorescence technique by the use of antibodies to various constituents of human cells and their products.

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11
Q

What is the prognosis?

A

Is the forecast of the course & termination of a disease.

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12
Q

What are “complications”?

A

-Are additional pathological changes which may occur during or after the termination of the usual course of the disease.

-They affect or modify the prognosis of the disease.

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13
Q

What is the definition of “fate”?

A

It includes prognosis & complications of the disease.

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14
Q

What do the pathological investigations include?

A

-Biopsy: This is the study of a specimen from the lesion during life.

-Autopsy: This is a post-mortem examination of the cadaver.

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15
Q

What is the difference between congenital and hereditary diseases?

A

-Congenital disease: normally fertilized ovum is affected in the uterus by microbes, drugs, X-rays, etc.

-Hereditary (genetic disease): inherited from parents.

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16
Q

What are lesions?

A

The structural changes occurring in the tissue as the result of the disease are called lesions.

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17
Q

How are the material obtained for pathological investigation preserved?

A

The materials obtained are put immediately in a fixative fluid to prevent autolysis, mainly 10% formalin.

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18
Q

What does surgical pathology involve?

A

Surgical pathology involves gross and microscopic examination of surgical specimens, as well as biopsies submitted by clinicians.

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19
Q

What does the practice of surgical pathology allow us for?

A

definitive diagnosis of disease in removed tissue.

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20
Q

How is surgical pathology performed?

A

This is usually performed by a combination of:
 Gross (Macroscopic) examination of the tissue.
 Histopathologic (Microscopic) examination.
 Molecular studies (immunohistochemistry).

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21
Q

What are the types of spicemens?

A

-Excision biopsy
-Incision biopsy
-True-cut Biopsy
-Fine Needle Biopsy
-Aspiration of body fluids

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22
Q

Excision Biopsy

A

Therapeutic surgical resection (TSR) of the entire lesion

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23
Q

Incision biopsy

A

Surgical resection of part of the lesion for diagnosis.

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24
Q

TRUE-CUT BIOPSY

A

The core of tissue is obtained by the use of large-bore needles, sometimes under the guidance of radiological techniques.

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25
Q

FINE NEEDLE ASPIRATION

A

Fluid aspiration from the lesion tissue by a fine needle for cytologic smear preparation and examination of aspirated cells.

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26
Q

Aspiration of body fluids

A

For cytologic smear preparation & examination (as urine, ascites…)

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27
Q

Fixation

A

-Immediate specimen fixation is mandatory.

-The widely used fixative is 10% formaldehyde (Formalin) buffered to a neutral ph.

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28
Q

What is the importance of fixation?

A

1) Fixation will preserve the morphology.
2) Prevent decomposition and autolysis.
3) Minimize microbial/fungal growth.
4) Minimize the loss of molecular components.

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29
Q

Gross examination

A

LG COLR

1) Recognition of the anatomic landmarks for proper anatomic orientation and measuring specimen.

2) Localization of the lesion.

3) Opening and examination of the whole Specimen.

4) Cutting proper Sections needed for diagnosis (sampling).

5) Labeling sections.

6) Gross description which represents a permanent record of the specimen’s macroscopic features and enables the pathologist to correlate each slide to a precise location on the specimen.

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30
Q

Microscopic examinations

A

-All samples cut grossly from the specimen should be processed and sectioned on glass slides.

-Sections should be stained by Hematoxylin and Eosin (H&E) for microscopic examination.

-Other special stains could be used.

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31
Q

Immunohistochemistry

A

-Specific monoclonal antibodies help to identify cell products or surface markers

-Determination of the origin of the cell population.

-Detection of prognostic and therapeutic markers

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32
Q

Intraoperative Consultation

A

-Rapid microscopic examination of fresh tissue is done for intraoperative consultation which is needed for important decisions during operation.

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33
Q

What are the methods of intraoperative consultation?

A

Methods:
 Preparation of histologic slides using the frozen section technique.
 Preparation of cytologic slides.

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34
Q

Developmental abnormalities of cell growth

A

 Occurs due to defective fetal development in uterus.
 They manifest at birth or shortly after.
 Either hereditary or congenital.

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35
Q

What are the causes of developmental abdnormalities of cell growth?

A

Hereditary abnormalities:• Inherited from the parents. e.g. Genetic disease

Congenital abnormalities:• Due to affection of the normal fertilized ovum by adverse factors as infection, chemicals, irradiation or an increased maternal age.

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36
Q

What are the congenital disorders of cell growth?

A

Agenesis
Aplasia
Hypoplasia
Atresia
Heterotobia(choristoma)
Hamartoma

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37
Q

What is agenesis?

A

Congenital absence of an organ e.g. solitary kidney.

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38
Q

What is aplasia?

A

The organ is represented by a rudimentary structure

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39
Q

What is hypoplasia?

A

The organ is a normal structure but fails to reach adult size e.g. kidney.

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40
Q

What is atresia?

A

• Absence of a normal opening
• Failure of canalization of hollow organ e.g. intestine

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41
Q

What is Heterotobia(choristoma)?

A

• Presence of normal tissue in abnormal sites
• e.g pancreatic tissue in stomach or thyroid tissue in
the base of the tongue.

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42
Q

What is hamartoma?

A

• Formation of a mass of mature tissue of the locality, but in abnormal arrangement or quantity as pigmented nevi.

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43
Q

What are the cellular adaptations to stress?

A

Reversible changes in the number, size, phenotype, metabolic activity, or functions of cells.

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44
Q

What are the types of cellular adaptations to stress?

A

Physiologic adaptations:-
 In response to normal stimulation e.g. by hormones

Pathologic adaptations:-
 In responses to stress

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45
Q

What are acquired disorders of growth?

A

1- Atrophy
2- Hypertrophy
3- Hyperplasia
4- Metaplasia
5- Dysplasia

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46
Q

What is the definition of atrophy?

A

Decrease in organ size by decrease in size and/or the number of its cells.

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47
Q

What is the classification of atrophy?

A

Physiological and pathological

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48
Q

What are the types of physiological atrophy?

A

-General (Senile): It is an aging process.

-Local: Involution of an organ due to loss of its physiologic function. and its causes are (After labor: ↓ uterus, After child weaning: ↓ breast size)

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49
Q

What are the types and causes of pathological atrophy?

A

-General (Senile)

-Causes
 Starvation.
 Toxic.
 Hormonal.

Local

-Causes
 Disuse Atrophy.
 Neurogenic atrophy.
 Ischemic atrophy.
 Pressure atrophy.
 Thermal.

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50
Q

What is the gross morphology of atrophy?

A

General Atrophy
 All organs are affected to a variable extent:
1. Skin is wrinkled
2. Loss of fat of adipose tissue
3. Wasting especially of liver, muscles
4. Brown atrophy of heart.

Local Atrophy
 The organ is decreased in size and weight.

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51
Q

What is the microscopic morphology of atrophy?

A

1- Reduction of cytoplasmic mass.
2- The nucleus is apparently normal.
3- Spaces created by atrophied cells are occupied by fibrous tissue or fat.

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52
Q

What is hypertrophy?

A

Increase in organ size due to increase in the size of its constituent cells.

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53
Q

What is the classification of hypertrophy?

A

Pathological and physiological

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54
Q

What are examples of physiological hypertrophy?

A

➢ In response to hormones: Smooth muscles of the pregnant uterus.

➢ Excess functional demand: skeletal muscles in manual workers and
athletes.

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55
Q

What are examples of pathological hypertrophy?

A

Hormonal:
- Occurs with an excess growth hormone of the anterior pituitary, leading to gigantism and acromegaly.

Excess functional demand:
1- To overcome distal resistance: in hollow organs
2- Compensatory hypertrophy: in paired organs.

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56
Q

What is the term “neoplasia”?

A

The term “Neoplasia”:-
Neo = new
plasia = creation (growth)

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57
Q

What is the term “Tumor”?

A

tumor = swelling

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58
Q

What is the definition of neoplasia?

A

An abnormal mass of tissue which:

1- Grows more rapidly than the normal tissue.
2- Its growth is uncontrolled by the normal growth control mechanisms (autonomous).
3- Competes with the normal tissue for metabolic needs.

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59
Q

What is any tumor composed of?

A

Cells:
**Which is neoplastic
**May be benign or malignant
**Tumor is named according to it.

Supporting stroma: which is non-neoplastic

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60
Q

What are tumors classified according to?

A

Tumors can be classified according to:
The cell of origin into:
1- of epithelial origin
2- of mesenchymal origin

Behavior into:
1-benign
2-malignant
3-locally malignant

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61
Q

What are tumors of epithelial origin?

A

Benign tumors

Papilloma:
From surface epithelium e.g. squamous cell papilloma
And transitional cell papilloma

Adenoma:
From secretory epithelium e.g. tubular adenoma and liver cell adenoma

Malignant tumors

The name of epithelium + carcinoma e.g. squamous cell carcinoma and transitional cell carcinoma and hepatocellular carcinoma

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62
Q

What is papilloma?

A

Papilloma = benign tumor of surface epithelium.

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63
Q

What is adenoma?

A

Adenoma = benign tumor of secretory epithelium.

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64
Q

What is carcinoma?

A

Carcinoma = malignant tumor of epithelium.

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65
Q

What are tumors of mesenchymal origin?

A

Benign tumors

-The name of mesenchymal tissue + oma

*from fibrous tissue — fibroma
*from cartilage ——— chondroma
*from bone ————- osteoma
*from fat —————- lipoma

Malignant tumors

-The name of mesenchymal tissue + sarcoma

*from fibrous tissue — fibrosarcoma
*from cartilage ——– chondrosarcoma
*from bone ————- osteosarcoma
*from fat —————- liposarcoma

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66
Q

What is fibroma?

A

benign tumor of fibrous tissue.

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67
Q

What is fibrosarcoma?

A

malignant tumor of fibrous tissue.

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68
Q

What Is liposarcoma?

A

malignant tumor of fat cells.

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69
Q

Compare between benign and malignant tumors

A

Origin
Growth
N/E
M/E
Prognosis

1- Arise from normal cells.

1- Arise from either normal cells or premalignant lesions.

2- Grow slowly by expansion (i.e. push the surrounding normal tissue without tissue damage).

2- Grow rapidly by both expansion & infiltration (i.e. infiltrate & damage the surrounding normal tissue).

3- N/E:- *single.
*small.
*capsulated.
*no hemorrhage or necrosis.

3- N/E:-
*begin single then spread.
*reach a large size in a short time.
*non-capsulated
*hemorrhage or necrosis

4- M/E:-
**cells: similar to cell of origin, no criteria of malignancy.
**Pattern of arrangement: similar to tissue of origin.
**stroma:
few blood vessels,
no hemorrhage or necrosis.

4- M/E:-
**cells: show criteria of malignancy.
**Pattern of arrangement: depends on tumor grade.
**stroma:
prominent bl. Vs.,
with hemorrhage & necrosis.

5- Prognosis:- **No spread
**No recurrence
**Not harmful except if: *In vital organ
*Obstruct hollow organ *Produce hormone *Turn malignant

5- Prognosis:-
- spread occurs either:
*direct (in surrounding tissue)
*distant metastasis [by blood, lymphatic vessels or through serous sacs (transcoelomic)]
- recurrence occurs (due to infiltrating borders with the absence of capsule)
-harmful due to:
*Organ destruction (infiltration) *Obstruction of hollow organ *Clinical syndromes related to tumor

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70
Q

What is the origin of benign tumors?

A

Arise from normal cells.

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71
Q

What is the origin of malignant tumors?

A

1- Arise from either normal cells or premalignant lesions.

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72
Q

How do begin tumors grow?

A

Grow slowly by expansion (i.e. push the surrounding normal tissue without tissue damage).

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73
Q

How do malignant tumors grow?

A

Grow rapidly by both expansion & infiltration (i.e. infiltrate & damage the surrounding normal tissue).

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74
Q

What is the N/E of benign tumors?

A

*single.
*small.
*capsulated.
*no hemorrhage or necrosis.

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75
Q

What is the N/E of Malignant tumors?

A

*begin single then spread.
*reach a large size in a short time.
*non-capsulated
*hemorrhage or necrosis

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76
Q

What is the M/E of the benign
tumors?

A

cells: similar to cell of origin, no criteria of malignancy.
**Pattern of arrangement: similar to tissue of origin.

**stroma:
few blood vessels,
no hemorrhage or necrosis.

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77
Q

What is the M/E of malignant tumors?

A

**cells: show criteria of malignancy.
**Pattern of arrangement: depends on tumor grade.

**stroma:
prominent bl. Vs.,
with hemorrhage & necrosis.

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78
Q

What is the prognosis of benign tumors?

A

5- Prognosis:-
**No spread
**No recurrence
**Not harmful except if:
*In vital organ
*Obstruct hollow organ
*Produce hormone
*Turn malignant

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79
Q

What is the prognosis of malignant tumors?

A
  • spread occurs either:
    *direct (in surrounding tissue)
    *distant metastasis[by blood, lymphatic vessels or through serous sacs(transcoelomic)]
  • recurrence occurs (due to infiltrating borders with the absence of capsule)
    -harmful due to:
    *Organ destruction (infiltration)
    *Obstruction of a hollow organ
    *Clinical syndromes related to tumor
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80
Q

What are the Microscopic Criteria of malignancy (not present in benign tumors)?

A

1- Pleomorphism (variability in size & shape of cells & nuclei).
2- Hyperchromatism (dense chromatin inside the nuclei).
3- increased N/C ratio to 1:2 (instead of 1:4 in normal cells).
4- Tumor giant cells.
5- Atypical (abnormal) mitoses.
6- Prominent nucleoli.

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81
Q

What is a Tumor grade?

A

It means the degree of similarity of tumor tissue to the tissue of origin regarding morphology & function (i.e. how much the tumor resembles the normal tissue).

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82
Q

What are the grades for any tumor?

A

1- Grade I (well-differentiated tumors).
2- Grade II (moderately differentiated tumors).
3- Grade III (poorly differentiated tumors).
4- Grade IV (undifferentiated tumors = anaplastic tumors)

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83
Q

What is the definition of locally malignant tumors?

A

These are tumors characterized by:
1- Grow by local infiltration.
2- No blood or lymphatic spread.
3- Microscopically show criteria of malignancy.
4- Recur after incomplete removal
5- May turn malignant.

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84
Q

What are the examples of Locally malignant tumors?

A

1- Adamantinoma of mandible.
2- Basal cell carcinoma of the skin.
3- Craniopharyngioma of the pituitary gland.
4- Carcinoid tumor.
5- Giant cell tumor of bone.

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85
Q

What does the tumor grade estimate?

A

It estimates the tumor aggressiveness.

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86
Q

What is the tumor stage?

A

It is based on 3 items: [TNM staging system]
1- the size of the primary tumor.
2- presence or absence of lymph node spread.
3- presence or absence of metastasis (distant spread).

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87
Q

What is the definition of hyalinosis (hyaline degeneration)?

A

Glassy Refractile Homogenous Structurless Transparent material with unknown nature that stains Red with Eosin.

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88
Q

What are the types of hyalinosis?

A

Intracellular hyalinosis
1. Corpora Amylacia: Prostate
2. Russell bodies: Plasma cells in Rhinoscleroma
3. Old thrombi
4. Mallory body “Apoptotic bodies”: in Alcoholic
hepatitis
5. Councilman body: in Viral hepatitis (Yellow fever)

Extracellular hyalinosis
A. Vascular:-
1. Artery: Atherosclerosis
2. Arteriole: Spleen in Old age, Hypertension

B. Extra-vascular:-
1. Old scar
2. Spleen capsule & trabeculae

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89
Q

What are the sites, examples, and M/E of mucinous & myxomatus degeneration?

A

Sites:-

-Epithelial “Mucinous - Mucoid”
-Connective tissue “Myxomatous”

Examples

-Catarrhal inflammation, Mucoid adenocarcinoma
-Myxoma “CT tumor”, Myxedema

M/E
-none
-Star-shaped cells separated by pale blue mucin

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90
Q

What is the definition of amyloidosis?

A

Abnormal deposition of protein substance in between cells and in blood vessels in different tissues and organs.

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91
Q

What is the morphology of amyloidosis?

A

N/E: Waxy Translucent

M/E: Homogenous Structurless Red material (Like Hyalinosis & Fibrinoid necrosis)

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92
Q

What are the stains of amyloidosis?

A

Gross stains
1) lodine: Brown
2) lodine with sulphoric acid: Blue

Microscopic stains
1) Congo red: When viewed under polarized light it gives Apple Green birefringence

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93
Q

What are the types of systemic amyloidosis?

A

1) Immunocyte dyscrasias with amyloidosis “Primary amyloidosis
2) Reactive systemic amyloidosis “Secondary amyloidosis”
3) Heredofamilial amyloidosis

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94
Q

Where is Immunocyte dyscrasias with amyloidosis “Primary amyloidosis” seen in and what is its site, and cause of diseases?

A

-Seen in:
Multiple Myeloma (Plasma cell tumor).

-Site:
a) Early in Muscle - Heart - GIT “Alimentary tract”.
b) Late in: Solid organs.

-Cause of Death:
Heart failure - Renal failure

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95
Q

Where is Reactive systemic amyloidosis “Secondary amyloidosis” seen in and what is its site, and cause of diseases?

A

-Seen in Chronic inflammatory lesions with continuous breakdown (TB - Rheumatoid arthritis).

-Site: Early in Solid organs.

  • Cause of Death: Renal failure.
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96
Q

Describe Heredofamilial amyloidosis

A

Familial Mediterranean Fever “FMF” characterized
by recurrent inflammations of Joints & Serous sacs.

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97
Q

What are examples of localized amyloidosis?

A

1) Senile Cardiac Amyloidosis
2) Senile Cerebral Amyloidosis “Alzheimer disease”
3) Medullary Thyroid Carcinoma MTC
4) Nodules in Skin - Tongue - Larynx - Lung - Urinary bladder

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98
Q

What is the N/E of any organ with amyloidosis?

A

V Size: Enlarged
V Shape: Preserved
V Surface: Smooth
V Consistency: Firm
V Color: Pale Greyish-brown
V Edges: Sharp edges

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99
Q

What is Gout “Hyperuricemia”?

A

Disturbance of Purines in nucleoprotein metabolism.

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100
Q

What is the pathology of Gout “Hyperuricemia”?

A

In joints:-
1. Recurrent attacks of acute arthritis.
2. Chronic gouty Tophi: Joints - Eyelid - Cartilage of ear.

In kidney:-
1. Urate stones
2. Chronic renal failure

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101
Q

What is pathological calcification?

A

Deposition of Ca salts in tissues other than bone & teeth.

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102
Q

What is the N/E of pathological calcification?

A

Dull opaque - White - Hard - Finely granular surface.

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103
Q

What is the M/E of pathological calcification?

A

Dark blue with Hematoxylin.

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104
Q

What is the classification of calcification?

A
  1. Dystrophic calcification
  2. Metastatic calcification
  3. Stone formation (Urinary tract - Biliary tract - Duct of the salivary gland - Appendix).
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105
Q

Dystrophic calcification

Ca level:
Type of tissues:
Sites:

A

-Ca level: Blood Ca is normal
-Damaged tissues are more liable to Ca deposition (Hyalinosis & Necrosis).
-Sites:- Degenerated tissue: Old scar - Wall of chronic abscess and necrotic tissues

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106
Q

Metastatic Calcification

Ca level:
Type of tissues:
Pathogenesis (causes of hypercalcemia)

A
  • Blood Ca is elevated
  • Deposition in normal tissues

-1. Excess mobilization of Ca from bone:-
a) Bone destruction (Multiple myeloma - Secondary Bone tumors)
b) Hyperparathyroidism
c) Prolonged immobilization

  1. Excess absorption of Ca from intestine:-
    a) Hypervitaminosis D
    b) Increased Milk intake
  2. Sarcoidosis
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107
Q

What is hemosiderosis?

A

Pathological accumulation of Hemosiderin (Localized - Generalized)

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108
Q

How does hemosiderosis take place?

A

Fe is absorbed from duodenum - Carried in plasma trans-ferritin, Stored as Fe or Apo-ferritin in macrophages in Liver - Spleen - BM.

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109
Q

What is the definition of localized hemosiderosis?

A

Local accumulation of hemosiderin.

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110
Q

What are the causes of localized hemosiderosis?

A

Occurs around areas of hemorrhage as in:-
a) Interstitial hemorrhage.
b) Chronic venous congestion of the lung.

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111
Q

What is the def of generalized hemosiderosis (hemochromatosis)?

A

Generalized increase of hemosiderin.

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112
Q

What are the causes of generalized hemosiderosis (hemochromatosis)?

A

Iron overload due to:-
1) Over-dose of iron intake.
2) Prolonged iron therapy.
3) Increased iron absorption.
4) Repeated blood transfusions.
5) Hemolytic anemias

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113
Q

What is the pathology of Generalized Hemosiderosis(Hemochromatosis)?

A

The pigment is deposited in Liver cells - Pancreas - Skin - Heart - Other organs:-
1) Skin: Bronzed color.
2) Pancreas: Diabetes mellitus.
3) Liver: Develops Pigmentary cirrhosis.
4) Heart: Fibrosis - Arrhythmia - Cardiomyópathy - Heart failure.

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114
Q

What is the N/E of Generalized Hemosiderosis(Hemochromatosis)?

A

The affected organs are Enlarged - Brown - Hard.

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115
Q

What are the types of pigments?

A

Types of pigments:-
1. Exogenous:-
a) Inhalation: Pneumoconiosis due to Silica.
b) Ingestion: Melanosis coli - Chronic lead poisoning.
c) Inoculation: Tattooing

  1. Endogenous:-
    a) Melanin
    b) Hemoglobin derived pigments
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116
Q

What are increased melanin pigments?

A
  1. Prolonged exposure to the sun: Stimulation of MSH (Melanocyte Stimulating Hormone)
  2. Addison’s disease.
  3. Chloasma of pregnancy: Pigmentation around Nipple - Face - Vulva during pregnancy.
  4. Tumors; Melanoma.
  5. Chronic irritation
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117
Q

What are decreased melanin pigments?

A
  1. Albinism: Partial or Complete absence of tyrosinase.
  2. Leukoderma (Congenital).
  3. Vitiligo (Acquired).
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118
Q

What is the definition of inflammation?

A

-Inflammation is a complex reaction of a tissue and its microcirculation to a pathogenic insult.

-It is characterized by the generation of inflammatory mediators and movement of fluid & leukocytes from the blood into extravascular tissues.

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119
Q

What is the aim of inflammation?

A
  • Neutralization of irritant
  • Elimination of injurious agent
  • Engulfment/entrapment
  • To get rid of the attacking agent and to prepare tissue for repair
120
Q

What are the types of inflammation? And what are their characters in brief?

A

1) Acute inflammation:
- Elimination of injurious agent
- Lasting for a few minutes up to a few days (7 max)
- Fluid and plasma protein exudation.
- Neutrophils (then monocytes)are the main inflammatory cells.

(2) Chronic inflammation: (tissue damage and repair happen simuantansouely)
- Lasting for a longer duration (days to years). (Up to 25 years).
- Vascular proliferation and scarring.
- Lymphocytes and macrophages are the predominant cells

121
Q

What are the cardinal signs of acute inflammation?

A
  • Redness (rubor) - Swelling ( tumor) - Heat ( calor)
  • Pain (dolor) - Loss of function ( functio laesa), the fifth cardinal sign added by Virchow
122
Q

What are the major components (changes - mechanism - pathogenesis )of acute inflammation?

A

1- Vascular changes: - Vasodilation and increased blood flow - Increased vascular permeability

2- Cellular events: - Leucocyte transmigration - Phagocytosis

3- Chemical mediators (acute & chronic).

123
Q

What are the vasoactive changes that occur in acute inflammation?

A
  • Change in diameter
  • Increased capillary permeability
124
Q

Change in diameter process in acute inflammation

A

Transient VC then permanent VD of arterioles, capillaries, and postcapillary venules. This results in a marked increase in the blood flow to the area which is manifested clinically by local redness and hotness of the affected area.

125
Q

Increased capillary permeability in acute inflammation.

A

It is due to endothelial changes in the form of either:

  • Endothelial swelling with the widening of Intra endothelial gaps of postcapillary venules. OR Major endothelial damage involving arterioles, capillaries, and venule
    This results in leakage of proteinaceous fluid (Exudate) which causes inflammatory edema.
126
Q

Compare between transudate and exudate

A

Transudate:
▪ Due to increased hydrostatic pressure.
▪ Low protein content. (clear)
▪ Does not coagulate on standing.
▪ Low specific gravity ( less than 1012)
▪ Can occur early in inflammation

Exudate:
▪ Due to increased vascular permeability.
▪ Rich in protein esp. fibrin (turbid)
▪ Coagulates on standing.
▪ High specific gravity ( more than 1018
▪ Contains inflammatory cells Exudate.
▪ Occurs late in inflammation

127
Q

What are the cellular events that happen in acute inflammation?

A

1- Leucocyte movement and functions.
2- Chemotaxis
3- Phagocytosis

128
Q

Leucocyte movement and functions in acute inflammation

A

Inside the area of inflammation, leukocytes move out of the blood vessels (Emigration)…….Includes margination, pave mentation, rolling, adhesion and transmigration.

129
Q

What is emigration?

A

It is the passage of inflammatory leukocytes between the endothelial cells into the adjacent interstitial tissue.

130
Q

Margination in acute inflammation

A

Occurs as leukocytes localize to the outer margin of blood flow adjacent to the vascular endothelium.

131
Q

pavementation in acute inflammation

A

leukocytes line the endothelial surface.

132
Q

Describe rolling in acute inflammation and what it is mediated by.

A

Is mediated by the action of E selectins which bind endothelial cells loosely to leukocytes ( Through sialyl Lewis X modified glycoprotein) producing a characteristic rolling movement of leukocytes along the endothelial surface.

133
Q

Adhesion in acute inflammation

A

Leukocytes adhere to the endothelial surface through the interaction of integrins (leukocytes) and the immunoglobulin family adhesion proteins (endothelium)

134
Q

Transmigration In acute inflammation

A

It is the movement of leukocytes across the endothelium.

135
Q

What is chemotaxis?

A

It is the directional movement of leucocytes towards the irritant within the area of inflammation

136
Q

What is phagocytosis?

A

It is the ingestion and destruction of particulate material (tissue debris, living or dead bacteria, and other foreign cells) by phagocytic cells mainly neutrophils and monocytes macrophages.

137
Q

What are the steps of phagocytosis?

A

1.Recognition and attachment
2.Engulfment
3.Degradation (killing)

138
Q

What are the types of Chemical mediators?

A

• Exogenous of microbial origin (E.coli chemotactic).
• Endogenous mediators from cells or plasma.

139
Q

What are the chemical mediators responsible for vascular dilatation?

A

histamine

140
Q

What are the chemical mediators responsible for vascular permeability?

A

histamine and kinins

141
Q

What are the chemical mediators responsible for chemotaxis?

A

Leukotrienes, lysosomal components and C5a.

142
Q

What are the chemical mediators responsible for pain?

A

Bradykinin (from plasma), prostaglandins (fro necrotic cells)

143
Q

What are the systemic effects of acute inflammation? And what are they caused by?

A
  1. Fever: caused by pyrogens (i.e. fever producing substances):
    ▪ • Exogenous: released from bacteria and fungi.
    ▪ • Endogenous: cytokines as interleukin 1 (IL-1) and
    tumor necrosis factor (TNF).
  2. Leucocytosis: caused by IL-1 and TNF that stimulate the release of leukocytes from bone marrow.
144
Q

What are the types of acute inflammation?

A

According to the presence or absence of pus, acute inflammation is either suppurative or non-suppurative

145
Q

What is suppurative (purulent) inflammation? And what is it caused by?

A
  • Severe acute inflammation with pus formation
    -It is caused by pyogenic bacteria e.g. staph aureus, strept. Pyogenes, E.coli …..
146
Q

What is pus?

A

Pus is semi-fluid, viscous material formed of dead and dying neutrophils, microorganisms, plasma proteins, fluid exudate, and necrotic liquefied tissue.

147
Q

What are the types of suppurative inflammation?

A

A. Localized (Abcess or furuncle or carbuncle)
B. Diffuse

148
Q

What is abscess?

A

It is a localized suppurative inflammation characterized by the formation of an irregular cavity containing pus

149
Q

What is found in the irregular cavity of the abscess?

A
  • It is formed of 3 zones.
    a. Central zone of necrotic tissue and dead neutrophils.
    b. Midzone of pus
    c.Peripheral zone of inflamed tissue (pyogenic membrane).
150
Q

What is the fate of abscess?

A

▪ If not evacuated:
a. Change to a chronic abscess.
b. Blood or lymphatic spread.

▪ If evacuated:
a. Healing by granulation tissue.
b. Sinus formation. (Sinus = blind-ended tract opening to the surface)
c. Fistula formation. (Fistula = tract joining two Surfaces)
d. Ulcer formation (Ulcer = defect in the surface lining of the skin or mucous Membrane) e.g peptic ulcer

151
Q

What is a boil?

A

Small abscess related to hair follicles, sweat, or sebaceous glands.

152
Q

What is carbuncle?

A

Multiple communicating suppurative foci in the subcutaneous tissue opening to the surface by multiple sinuses. It is common in diabetic patients

153
Q

What is the cause of cellulitis and what are its sites?

A

▪ Due to streptococcal infection which produce enzymes that facilitate the spread of infection e.g
(Fibrinolysin - Hyalourinidase - Leucocidin)

▪ Sites:
Loose connective e.g orbit, wall of the appendix

154
Q

What are the types of non-suppurative inflammation?

A

1- Serous and serofibrinous inflammation…

2- Catarrhal inflammation…e.g common cold

3- Pseudomembranous inflammation…e.g diphtheria & bacillary dysentery.

4- Hemorrhagic inflammation ….Vascular damage and hemorrhage

5- Necrotizing inflammation …. Excess tissue necrosis

6- Allergic inflammation… From Antigen/Antibody reaction

155
Q

What is serous inflammation? And where does it occur?

A

Excess watery fluid Exudate - Occurs in burns and some viral infections where (blisters) are formed.

156
Q

What is serofibrionous inflammation and what are its sites?

A

-Exudation of serous fluid rich in fibrin.

-Occurs in serous sacs and lung alveoli in lobar pneumonia.

157
Q

What are the types of sirofibrionous inflammation?

A

▪ Wet type = excess serous than fibrin.
▪ Dry-type = excess fibrin Than serous fluid.

158
Q

What is catarrhal inflammation and its sites and what is an example for it?

A

▪ Mild acute inflammation of the mucous membranes with excess watery mucous secretion.
▪ Sites
- Mucous membranes of respiratory and GIT.
Ex:- common cold

159
Q

What is Pseudomembranous inflammation?

A

▪ A severe form of non-suppurative inflammation caused by toxin-producing strains as:-

a. Diphtheria
b. Shigella (bacillary dysentery) and Clostridium difficile.

160
Q

What is the fate of acute inflammation?

A

▪ Resolution
(the hoped-for result)

▪ Abscess
(via liquefactive necrosis)

▪ Scar (sometimes occurs even if the pathogen is eliminated)

▪ Persistent inflammation
(chronic inflammation) due to a failure to completely eliminate the pathological insult (injury)

161
Q

What is the definition of chronic inflammation?

A
  • inflammation of prolonged duration (weeks or months) in which inflammation, tissue injury, and attempts at repair coexist, in varying combinations.
  • It may follow acute inflammation or start as chronic specific inflammation (Granuloma).
162
Q

What are the causes of chronic inflammation?

A

1- Persistent infections by microorganisms
2- Immune-mediated inflammatory diseases
3- Prolonged exposure to potentially toxic agents
4- unregulated immune responses

163
Q

What are the microorganisms that cause persistent infection? And what type of reaction do they cause?

A

-such as mycobacteria, and certain viruses, fungi,
and parasites, they difficult to eradicate

-These organisms often evoke an immune reaction called delayed-type hypersensitivity. (DTH)

164
Q

Immune-mediated inflammatory diseases (IMID) (Auto-immune diseases)

A
  • Under certain conditions immune reactions develop against the individual’s own tissues.
  • auto-antigens produce a self-perpetuating immune reaction that results in chronic tissue damage and inflammation

examples: rheumatoid arthritis and multiple sclerosis.

165
Q

What are the potentially toxic agents that cause chronic inflammation?

A
  • either exogenous or endogenous.
  • example of an exogenous agent: is particulate silica, a non-degradable inanimate material that, when inhaled for prolonged periods, results in an inflammatory lung disease called silicosis
166
Q

What are examples of unregulated immune responses?

A
  • against microbes, as in inflammatory bowel disease.
  • Immune responses against common environmental substances are the cause of allergic diseases, such as bronchial asthma.
167
Q

What are the morphological features of chronic inflammation?

A
  1. Infiltration with mononuclear cells, which include macrophages, lymphocytes, and plasma cells.
  2. Tissue destruction induced by the persistent offending agent or by the inflammatory cells.
  3. Attempts at healing by connective tissue are accomplished by the proliferation of small blood vessels (angiogenesis) (for blood supply needed for repair) and fibrosis.
168
Q

What is hyperplasia?

A

Enlargement of the organ due to an increase in the number of its component cells.

169
Q

What are the types of hyperplasia?

A

a. Physiological Hyperplasia
b. Pathologic Hyperplasia

170
Q

What are the types of physiological hyperplasia?

A

Hormonal:
-Hyperplasia of female breast at puberty and lactation.
-Smooth muscles of gravid uterus

Excess demand:
- Thyroid gland in girls at puberty and pregnancy.

171
Q

What are the types of pathological hyperplasia?

A

Hormonal: Due to excessive hormonal stimulation (Cushing syndrome)

Compensatory hyperplasia: Liver cells proliferation after partial surgical excision or destruction

Irritative hyperplasia: Occurs in response to local irritation e.g. lymphoid tissue.

172
Q

What is metaplasia?

A

Transformation of a differentiated tissue into another differentiated tissue of the same category i.e. epithelial to epithelial and connective tissue to connective tissue.

173
Q

What are the types of metaplasia?

A
  1. Epithelial metaplasia.
  2. Connective tissue metaplasia.
  3. Mesothelial metaplasia.
174
Q

What are the causes of epithelial metaplasia?

A

The adaptive mechanism by which the cells which are more sensitive to stress are replaced by another cell type with better ability to withstand the adverse environment as occurs in Chronic irritation.

175
Q

What are the forms of epithelial metaplasia?

A

Squamous metaplasia:

➢ in response to chronic irritation:
➢ E.g. trachea, gall bladder, and uterine cervix

Glandular metaplasia

➢ Barret’s Esophagus.
➢ Metaplasia of the gastric mucosa to
the intestinal epithelium.

176
Q

What is connective tissue metaplasia?

A

Connective tissue as fibrous, myxomatous, cartilage, bone, or fat can be changed to each other.

177
Q

What is mesothelioma metaplasia?

A

 Affects flattened cells that line the serous sacs.
 Chronic irritation may change them to cubical, columnar, glandular, or stratified squamous.

178
Q

What is the definition of symposia?

A

It is disordered but nonneoplastic cellular proliferation Characterized by :
1. loss of individual cell uniformity
2. loss of normal arrangement within the tissue.

179
Q

What are the sites of dysplasia?

A

a. Skin
b. Mucous membranes
c. Liver

180
Q

What are the causes of reversible cell injury?

A

1- Oxygen deprivation (hypoxia, ischemia)
2- Oxygen free radicals.
3- Physical agents (heat, cold, radiation, trauma).
4- Chemical agents e.g. drugs, toxins
5- Infectious organisms.
6- Immunologic reactions.
7- Genetic derangements.
8- Nutritional imbalances e.g. starvation, obesity

181
Q

What is the role of mitochondria in cell injury?

A

• Mitochondria is concerned with cell respiration and the production of ATP which is responsible for important vital functions of cell:-
1- Cellular osmolarity (Na/K )
2- membrane transport process.
3- Protein synthesis.

182
Q

What is the pathogenesis of cell injury?

A

➢ Mitochondrial oxidative phosphorylation is disrupted first → Decreased ATP →
1. Decreased Na/K pump → gain of intracellular Na → cell swelling

  1. Altered metabolism → depletion of glycogen (anaerobic respiration with glycogenolysis).
  2. Lactic acid accumulation → ↓ pH & ↑ intracellular osmotic pressure → ↑intracellular H2O → cell swelling.
  3. Release of mitochondrial protein →↑ cytoplasmic osmotic pressure and helps intra-cellular water accumulation
183
Q

What is the morphology of cloudy selling?

A

LM
➢ Occurs in organs rich in mitochondria e.g. renal tubules, cardiac muscles, and hepatocytes.

Grossly
➢ The organ is enlarged, soft, pale with tense capsules and rounded borders.
➢ C/S is bulging.

M/E
➢ Swollen cells
➢ Granular cytoplasm.
➢ Nucleus is NORMAL

184
Q

What is hydronic degeneration?

A

 A severe form of cloudy swelling.
 Cytoplasm accumulates vacuoles of water.
 The nucleus is still normal

185
Q

What is the definition of fatty change(stenosis)?

A

Abnormal accumulation of intracellular neutral fat that occurs in parenchymatous organs most commonly liver, kidney, and heart.

186
Q

What are the causes of fatty change?

A

As other causes of cell injury

187
Q

What is the mitochondrial theory?

A

Mild prolonged or severe short injury leads to injury of mitochondria with the release of its fat that accumulates in the cytoplasm (fatty degeneration).

188
Q

What are the causes of fatty change in the liver?

A
  1. Increased fatty acids entry to the liver (Obesity, starvation & cortisone therapy).
  2. Increased Fatty acid synthesis in the liver from acetate (alcoholism).
  3. Decreased oxidation of fatty acids (hypoxia, anemia, respiratory failure).
  4. Increased esterification of fatty acids to TGs (DM, alcoholism)
  5. Decreased formation of apoprotein (protein malnutrition, alcoholism, and CCL4 toxicity)
189
Q

What is the gross morphology of fatty change?

A

Grossly:

Size: enlarged

Shape: Preserved

Surface: Smooth

Capsule: Tense

Consistency: Soft, greasy

Cut surface: Bulging

Color: Pale yellow

Borders: Rounded

190
Q

What is the M/E of fatty change?

A

a. liver cells accumulate fat which appears in H&E stained section as clear vacuoles.

b. These vacuoles are first small (microsteatosis).

c. Later on the vacuoles fuse to form one large vacuole which pushes the nucleus to one side of the cell.

d. The nucleus becomes flattened (signet ring cell).

191
Q

What are the fat stains for fatty change?

A

➢ During routine staining of sections by Hx and E fat is dissolved during preparation by the organic solvents.

➢ For a demonstration of fat, frozen sections are used and stained by
- Sudan III & oil red O →Orange-red
- Osmic acid →Black

192
Q

What are the patterns of fatty change in the liver?

A

Focal
Zonal
Massive or diffuse

193
Q

What is focal fatty change?

A

➢ Random single or small clusters
➢ e.g. in viral hepatitis C.

194
Q

What is zonal fatty change?

A

➢ Centrizonal (zone 3) →hypoxic injury →away from the blood supply.
➢ Peripheral zonal ( zone 1) →toxic injury →first area to meet blood.

195
Q

What is massive or diffuse fatty change?

A

➢ Reye syndrome

196
Q

What are the types of fatty changes in the heart?

A

Localized
Diffuse

197
Q

What are examples of localized fatty change in the heart?

A

In moderate cases Mostly due to anemia

198
Q

What is the morphology of localized fatty change in the heart?

A

Gives yellow streaks alternating with dark brown fibers (tigroid or tabby cat appearance).

199
Q

What is the examples of diffuse fatty change in the heart?

A

In severe toxicity e.g. diphtheria.

200
Q

What is the morphology of diffuse fatty change in the heart?

A
  • leads to toxic myocarditis & acute heart failure.
  • If the patient survives, myocytes are replaced by fibrous tissue.
201
Q

What are the cells that become active in chronic inflammation?

A

1- Macrophages
2- Lymphocytes and plasma cells
3- dendritic cells
4- acute inflammatory cells
5- fibroblasts

202
Q

What are macrophages derived from?

A

They are derived from blood monocytes. Various levels of ‘activation’.

203
Q

What are the functions of macrophage?

A
  1. Phagocytosis and destruction of debris & bacteria.
  2. Processing and presentation of antigen to immune system.
  3. Control of other cells by cytokine release
  4. Synthesis; Cytokines, complement components, blood clotting factors, proteases.
204
Q

What is the definition of tissue repair?

A

replacement of damaged tissue by a healthy one.

205
Q

What are the types of tissue repair?

A

1- Repair by regeneration
2- repair by fibrosis
3- repair by organization

206
Q

What is the definition of healing by regeneration?

A

replacement of the damaged tissue by a healthy tissue of the same kind.

207
Q

What are the cells of the body classified according to?

A
  • Cells of the body are divided according to the power of regeneration into three groups:

(1) Labile cells: cells proliferate continuously throughout life e.g:

a- Cells of all epithelial surfaces: epidermis of the skin, gastrointestinal tract respiratory tract, and genitourinary tract.

b- Cells of bone marrow and lymphoid tissue.

(2) Stable cells: Do not proliferate under normal conditions, but proliferate in need.
E.g
a- Parenchymal cells of all glands.
b- Mesenchymal cells: fibroblast, chondroblast, and osteoblast.

(3)Permanent cells: cannot proliferate at all and include nerve cells.

208
Q

What are examples of regeneration?

A

I- Regeneration of skin: The epidermal cells are labile cells, which regenerate easily
II- Regeneration of liver cells.
III- Repair of bone fracture:

209
Q

Repair of bone fracture:

A

1- site of fracture is the seat of hemorrhage and necrotic bone cells. These products irritate the area leading to mild acute inflammation.

2- Macrophages and osteoclasts clean the area.

3- Provisional callus formation: woven bone produced by osteoblasts (External, intermediate, and internal callus).

4- Permanent bone The external and internal callus is removed by osteoclasts.
- Woven bone of intermediate callus is replaced by lamellar bone

210
Q

What is the definition of healing by fibrosis?

A

Replacement of damaged tissue by granulation tissue which matures to fibrous tissue.

211
Q

What is the granulation tissue?

A

It is a transitory tissue formed during the repair.

212
Q

What is the the N/E of granulation tissue?

A

“RBG VMR”

red granular, velvety, moist, bleeds easily, and resistant to infection.

213
Q

What is the M/E of granulation tissue?

A

capillaries and fibroblasts infiltrated by inflammatory cells.

214
Q

What is the mechanism of the formation of fibrosis (granulation tissue)?

A

1- The new capillaries arise as solid endothelial buds from the capillaries at the edges of the damaged area and form capillary loops.

2- Newly formed capillaries are highly permeable

3- Fibroblasts proliferate

4- Fibroblasts produce collagen fibers.

5- The collagen compresses and obliterates the capillaries.

6- Fibroblasts contract

7- Fibroblasts change to fibrocytes.

8- Fibrocytes and collagen fibers are remodeled to give a full tensile strength

9- Finally avascular strong fibrous tissue ( scar) is produced.

215
Q

What are the types of healing of wounds?

A

1- Primary union of wound (Healing by first intention)
2- Secondary union

216
Q

Where does Primary union of wound (Healing by first intention) take pale?

A

Occurs in:
1- clean incised wound
2- minimal tissue destruction
3- Approximated edges

e.g: Surgical wounds.

217
Q

What are the steps of the Primary union of wounds?

A

1- Blood is clotted between the wound edges and on the surface.

2- The incision causes mild acute inflammation in the edges of the wound. Then products of inflammation are rapidly removed by macrophages.

3- The basal cell layer of the epidermis on both edges of the wound proliferates across the clot to meet in the center.

4 -The gap of the wound under the new epithelium gets filled by granulation tissue

218
Q

What are the characters of the primary union?

A

1- occurs in clean incised wounds
e.g. surgical wounds.
2- minimal tissue destruction and gaping
3- less inflammatory reaction
4- a small amount of granulation tissue
5- rapid healing
6- small scar (thin and linear)
7- complications rare

219
Q

What are the characters of the secondary union?

A

1- occurs in septic wounds.
2- tissue destruction and gaping are present
3- more inflammatory reaction
4- a large amount of granulation tissue
5- slow healing
6- large scar (irregular)
7- complications as ulcer and keloid are more common

220
Q

What is the definition of repair by organization?

A

replacement of solid nonliving material as dead tissue, blood clots, or fibrin by fibrous tissue.

221
Q

What are the examples of repair by organization?

A

E.g; Serofibrinous inflammation, thrombus, hematoma, and infract heal by organization.

222
Q

What are the complications of repair?

A

A- Too less cellular proliferation resulting in:
1- Ulcer
2- Sinus
3- Fistula
4- Stretching of a weak scar and formation of incisional hernia.

B- Too much cellular proliferation and scar formation
1- Excessive granulation tissue (Proud flesh)
2- Excessive scaring forming keloid
4- Scar may be painful as in stump neuroma.
5-Squamous cell carcinoma rarely develops in a scar.

223
Q

What are the factors that impair repair?

A

Local and general

224
Q

What are the local factors that impair the repair process?

A

1- Infection
2- foreign body
3- ischemia
4- Severe damage

225
Q

What are the general factors that Impair repair process?

A

1- Age: repair is more rapid and adequate at a young age.

2- Nutrition
a- protein deficiency delays repair.
b- vitamin deficiency: Vit C deficiency causes the defective formation of collagen and osteoid tissue.
c- metals:
i- zinc deficiency: zinc is necessary for collagen synthesis.
ii- Calcium deficiency: Calcium is required for the maintenance of connective tissue and bone as well as other processes.

3- Hormones: e.g. cortisol depresses the repair.

4- Systemic disease: e.g. diabetes mellitus increases susceptibility to infection, so delay the repair.

5- Physical agents: e.g. ionizing radiation delays repair.

6- Chemicals and drugs e.g. cytotoxic drugs delay repair.

226
Q

What is the etiology of Carcinogenesis?

A

 These are the possible causes of cancer and the mechanisms involved in the transformation of a normal cell into a neoplastic cell.

 No single factor is responsible for the development of tumors alone.

 The role of some carcinogenic factors in carcinogenesis is established
while others are still unknown.

227
Q

What does the etiology of Carcinogenesis include?

A

A.Carcinogenic agents (carcinogens).
B. Preneoplastic (precancerous, premalignant) lesions.

228
Q

What are the carcinogenic agents?

A

These are agents which can produce malignancy

229
Q

What are carcinogenic agents classified into?

A
  1. Internal
  2. External:
    a) Physical (radiation)
    b) Chemical
    c) Infectious agents (viral, bacterial, and parasitic)
230
Q

What are the internal carcinogens?

A

A. Smegma: in uncircumcised males may produce penile carcinoma.

B. Hormones: The tumor growth is affected by hormones (hormone dependant tumors), in these cases, hormones act as promotors (second step in carcinogenesis).
E.g: Estrogen dependant hormones as Breast, ovarian, endometrial carcinoma.

231
Q

What are physical carcinogens?

A

A. Non-ionizing radiation

  • (ultraviolet rays, UVR): Cause skin tumors especially in faired skin as squamous cell carcinoma, basal cell carcinoma, and melanoma

b. Ionizing radiation

  • cause Leukemia, thyroid carcinoma, lung carcinoma, and osteosarcoma.
232
Q

What are chemical carcinogens classified into?

A

a. Direct-acting agents
B. Indirect acting agents that need metabolic convergence

233
Q

What are the direct chemical carcinogens?

A

 As alkylating agents (chemotherapy for malignancy)
 As cyclophosphamide, chlorambucil, busulfan may cause leukemia.

234
Q

What are indirect chemical carcinogens?

A
  1. Tar (tobacco products)
  2. Azo dyes
  3. Aflatoxins
  4. Nitrosamine
  5. Asbestos
235
Q

Effect of tar

A

may cause carcinoma of the lung, urinary bladder, oral cavity, larynx, and esophagus.

236
Q

Effect of Azo dyes

A

Food coloring agents (scarlet red, butter yellow) may cause liver malignancy (hepatocellular carcinoma).

237
Q

Effect of aflatoxins

A

The product of Aspergillus flavus fungus that contaminates grains and peanuts, may cause hepatocellular carcinoma.

238
Q

Effect of nitrosamine

A

converted to nitrosamine by bacterial flora in the stomach with achlorhydria may cause stomach carcinoma.

239
Q

Effect of asbestos

A

used in industries may lead to mesothelioma (malignant mesothelial tumor)

240
Q

What are the biological (infectious) carcinogens?

A

I. Bacterial carcinogens: Helicobacter pylori may cause gastric carcinoma or gastric B-cell lymphoma.

II. Parasitic carcinogens: Bilharzial cystitis may cause urinary bladder carcinoma.

III. Viral carcinogens: Examples:
 Human papillomavirus (HPV): Types 16 & 18 cause cancer cervix.
 Epstein Barr virus (EBV) causes Burkitt’s lymphoma or Nasopharyngeal
carcinoma.
 Hepatitis B virus causes Hepatocellular carcinoma.

241
Q

What are pre-neoplasia lesions?

A

These are non-malignant lesions that are well-recognized predispositions for malignancy.

242
Q

What do preneoplastic lesions include?

A

A) Hereditary premalignant Lesions (disorders)
B) Acquired preneoplastic lesions (disorders)

243
Q

What are hereditary premalignant disorders? (inherited cancer syndromes)

A

1) Autosomal dominant as Familial adenomatous polyps of the colon
2) Autosomal recessive syndromes of defective DNA repair (Xeroderma pigmentosa).
3) Familial cancers as breast, ovarian, colonic carcinomas

244
Q

What are acquired preneoplastic disorders? (Give examples)

A
  1. Chronic irritation as chronic ulcers and scars
  2. Hyperplastic proliferation: atypical endometrial hyperplasia and atypical mammary hyperplasia.
  3. Metaplastic lesions: as squamous metaplasia.
  4. Some benign tumors as adenomatous polyps of the colon.
  5. Dysplastic proliferation (as dysplastic bronchial mucosa in smokers) and Carcinoma in situ.
245
Q

What accompanies dysplasia?

A

 It often accompanies metaplasia or hyperplasia.

246
Q

What does dysplasia involve?

A

If involves the whole thickness, this is usually associated with changes similar to that of malignancy but the basement membrane is intact and no invasion of underlying connective tissue.

247
Q

What are other names for dysplasia?

A

It is called carcinoma-in-situ or intra-epithelial carcinoma pre-invasive carcinoma.

248
Q

What are preneoplastic lesions classified according to?

A

They are classified according to their malignant potential

249
Q

What are premalignant lesions classified into?

A

High-risk lesions:
 In which the development of cancer is invariable (100%)
 e.g. Multiple familial polypses, Xeroderma pigmentosa

Low-risk lesions
 : In which the incidence of malignancy is so low (3-5 %)
 e.g. Leukoplakia, endometrial hyperplasia, dysplasia.

250
Q

What is the definition of Carcinogenesis?

A

Carcinogenesis is a complex multistep process leading to the transformation of a normal cell to a neoplastic one capable of producing a mass ( conversion of a normal cell to malignant cell) by the action of carcinogens

251
Q

What are the steps of Carcinogenesis?

A

Carcinogenesis is a multistep process, it passes through 3 steps:
1. Initiation
2. Promotion
3. Progression and heterogeneity.

252
Q

What is initiation in Carcinogenesis?

A

This is the first step in carcinogenesis, induced by irreversible, nonlethal genetic material change (gene mutation) of the affected cell. This mutation may be inherited in germ cells or acquired by carcinogens.

253
Q

Are multiple mutations needed in initiation?

A

Multiple mutations are required usually affecting genes that regulate cell proliferation.

254
Q

What are cell cycle regulatory genes?

A

I. Proto-oncogenes and oncogenes
II.Tumor suppressor genes
III. Genes controlling apoptosis
IV. DNA repair genes

255
Q

Proto-oncogenes and oncogenes

A

-Proto-oncogenes are genes found in normal cells and are responsible for controlling normal growth and proliferation

-When they are mutated, they are active called oncogenes.

  • Proto-oncogenes are dominant genes and changes that affect them are usually acquired.

Example: Epidermal Growth factor receptor: EGFR in breast carcinoma

256
Q

Tumor suppressor genes

A

-These genes code the production of proteins that inhibit cell proliferation.

-The gene damage inactivates it.

-Tumor suppressor genes act as recessive genes and the absence of both copies is required for transformation, Mutations of tumor suppressor genes may be inherited or acquired

-Examples: P53 in most tumors, BRCA-1 & BRCA-2 in breast & ovary carcinoma.

257
Q

p53.

A

 It is called the guardian of the genome.

 Mutated in more than 50% of malignant tumors.

 When there’s damage to the DNA, P53 causes cell cycle arrest at G1 providing time for DNA repair then the cell re-enters the cell cycle again.

 If DNA repair is not successful, P53 activates BAX the proapoptotic gene and the cell dies by apoptosis, thus preventing the mutated cell from growth.

 Loss or mutation in P53 is common in urinary bladder, lung, breast, and ovarian carcinoma

258
Q

Genes controlling apoptosis

A

-Cell survival is regulated by genes that initiate and inhibit apoptosis. Normally, the BAX gene (proapoptotic) stimulates apoptosis while the bcl2 gene (anti-apoptotic) prevents programmed cell death.

Examples: Activation of antiapoptotic genes as Bcl2 leads to prolongation of the life span of genetically mutated cells and development of malignant tumors as in
Follicular B cell lymphoma.

259
Q

DNA repair genes

A
  • Normal human DNA is subjected to daily minor damage by body heat & ultraviolet rays, repair of this damage takes place by a group of DNA repairing enzymes called DNA ligases.

-Mutation in genes that control the expression of DNA ligases lead to the development of tumors as in Xeroderma Pigmentosa → frequent skin malignancies.

260
Q

What does promotion (colonial expansion) in Carcinogenesis mean?

A

Promotion means the proliferation of the initiated cells resulting in monoclonal expansion from a single initiated progenitor cell ( formation of tumor mass by replication of the initiated cells).

261
Q

What does the promotion of the tumor depend on?

A

Depends on 2 factors:

  • Intrinsic factors (kinetics of tumor cell growth).
  • Host factors (angiogenesis).
262
Q

What are the intrinsic factors that affect the promotion of the tumor?

A

The time is taken by a single transformed cell to appear clinically as a mass depends on Increased Cell production/cell loss ratio due to:
a) Increase in proliferation,
b) increase in telomerase activity and decreased apoptosis

263
Q

What are the host factors that affect the promotion of tumors?

A

Formation of new blood vessels for the nourishment of the tumor cells as the tumor can’t grow beyond 2 mm without vascularity.

 Angiogenesis occurs due to angiogenic Growth Factors:
- produced by Tumor cells
 FGF (fibroblast growth factor)
 VEGF “vascular endothelial growth factor”.
- produced by macrophages invading the tumor
 TGFα “transforming growth factor-alpha”
 TNF “tumor necrosis factor”

264
Q

What are tumor progression and heterogeneity?

A
  • Tumor progression means that the aggressiveness of tumors increases with time & acquire more malignant characters (as more invasiveness)
  • Although the tumor is monoclonal, by the time it is clinically evident, its constituent cells are very heterogeneous due to multiple mutations of different tumor cells.
265
Q

T-cells

A

 T-cells regulate macrophage activation and recruitment by secreting specific mediators (lymphokines)

 T-cells modulate antibody production and cell-mediated cytotoxicity and maintain immunologic memory

266
Q

NK cells

A

NK cells, as well as other lymphocyte subtypes, help defend against viral and bacterial infections

267
Q

What are the functions of lymphocytes and plasma cells?

A

a. Complex, mainly immunological.
b. B lymphocytes differentiate to produce antibodies.
c. T lymphocytes involved in control & cytotoxic functions.

268
Q

What are dendritic cells?

A

professional antigen-presenting cells that trigger immune responses to antigens.

269
Q

What is the function of dendritic cells?

A
  • They phagocytose antigens and migrate to lymph nodes, where they present those antigens.
  • Recognition of antigen and other co-stimulatory molecules by T cells —->recruitment of specific cell subsets to the inflammatory process.
270
Q

What are fibroblasts?

A
  • Fibroblasts are cells whose chief function is to produce components of the ECM.
  • They are the construction workers of the tissue, rebuilding the scaffolding of ECM upon which tissue is re-established.
271
Q

What do activated fibroblasts produce?

A

Activated fibroblasts produce cytokines and chemokines creating a tissue
microenvironment that further regulates the behavior of inflammatory cells.

272
Q

What are the effects of chronic inflammation?

A
  1. Fibrosis e.g. gall bladder (chronic cholecystitis), chronic ulcers.
  2. Impaired function e.g. chronic inflammatory bowel disease
  3. Rarely, increased; e.g. mucus secretion, thyrotoxicosis
  4. Atrophy e.g. gastric mucosa, adrenal glands
  5. Stimulation of immune response (Macrophage - lymphocyte interactions)
  6. Chronic inflammation can be complicated by fibrosis
273
Q

What is the definition of granuloma?

A

A distinct pattern of chronic inflammation in which the chief reactive cell is activated macrophage —>aggregates together forming nodular collections — >fuse to form tumor-like mass grossly.

274
Q

What is the pathogenesis of granuloma?

A

This type of reaction is Type 4 hypersensitivity reaction with the end result in macrophage activation:

1- Antigen presentation to inflammatory cells.
2- Lymphocyte-macrophage interactions
3- Macrophage activation occurs
4- Macrophage accumulation.

275
Q

Lymphocyte-macrophage interactions

A
  • Activated lymphocytes and macrophages influence each other.
  • Release mediators that affect other cells Lymphocyte- macrophage interactions
276
Q

Macrophage activation occurs by?

A
  • Cytokines from immune-activated T-cells.
  • Non-immunologic stimuli: endotoxin, fibronectin, mediators.
277
Q

What is the microscopic picture of granuloma?

A
  • It is characteristic with each irritant.
  • The irritant may be seen inside or outside the phagocytic cells.
  • The granuloma is formed of :
     Macrophages,
     Epithelioid Cells,
     Giant Cells,
     Lymphocytes
     Fibroblasts
278
Q

What are giant cells?

A
  • Multinucleated giant cells originate by the fusion of macrophages.
  • They have stronger phagocytic power than macrophages.
279
Q

What are the types of giant cells?

A

Langhans giant cells

  • have nuclei arranged in a horseshoe-shaped pattern around the periphery of the cell.
  • This type is characteristic (but not specific) for tuberculosis

Foreign body giant cells

  • have the nuclei dispersed in the cytoplasm
280
Q

What are the types of granuloma?

A

1- Infective granuloma: Bacteria, Virus, Parasite, Fungi

2- Non infective granuloma:
 Allergic granuloma: as Rheumatic fever
 Foreign body granuloma: foreign bodies as beryllium
 Granulomas of unknown cause: as sarcoidosis

281
Q

What is the definition of necrosis?

A

Local death of a group of cells or tissue within a living body.

282
Q

What are the causes of necrosis?

A

Living:-

• Bacteria.
• Fungus.
• Virus.

Non-living:-

  1. Physical causes; Excess heat or cold and mechanical trauma.
  2. Chemical agents: Poisons and drugs, Pancreatic secretion, Toxins e.g. diphtheria toxins
  3. Ischemia: Cut of arterial blood supply, causing ischemic
    necrosis as an infraction.
  4. Hypersensitivity reactions: i.e. antigen-antibody reaction as necrosis of tuberculous lesion.
  5. Free radicals e.g. 02, H202 & OH
283
Q

What is the pathogenesis of necrosis?

A
  1. Severe mitochondrial damage leads to marked reduction of ATP production with the metabolic shift to anaerobic glycolysis resulting in
    decrease intracellular PH (acidosis).
  2. Reduction of ATP results in loss of integrity of cellular membranes as disruption of lysosomal membranes and lysosomal enzymes set free.
  3. Increase intracellular Ca: ATP reduction leads to failure of Ca pump, Ca is normally maintained at extremely low levels by energy-dependent transport. Increased Ca leads to activation of the following enzymes:

Proteases: leading to the breakdown of cytoskeleton protein.

Phospholipases: leading to the destruction of membrane phospholipids.

Endonucleases: leading to the breakdown of DNA and chromatin fragmentation (pyknosis, karyorrhexis, and karyolysis).

284
Q

What is the N/E of the necrotic area?

A

The necrotic area is: (SODYI):

a. Swollen.
b. Opaque.
c. Well defined.
d. Pale yellow.
e. Surrounded by a zone of redness (acute
inflammation).

285
Q

What is the M/E of the necrotic area?

A

Cell membrane

> disappear and become indistinct, but the cellular outline is recognized.

Cytoplasm

> Swollen and coagulated (denaturation of protein)
Deeply eosinophilic (increased eosinophilia is due to
loss of normal basophilia “imparted by RNA in the
cytoplasm”
Increased binding of eosin to denaturated intra-
cytoplasmic protein).

Nucleus

> Pyknosis: Nuclei become condensed and dense.
Karyorrhexis: Nuclei become fragmented.
Karyolysis: Nuclei are dissolved.

286
Q

What are the clinical effects of necrosis?

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Fibrinoid necrosis

287
Q

Coagulation necrosis

A

Characteristic of infarction (areas of ischemic necrosis) in all of the solid organs except the brain.

288
Q

Liquefactive necrosis

A

Characteristic of brain infarction.

289
Q

Caseous necrosis

A

seen in tuberculous infection

290
Q

Fat necrosis

A

> occurs in abdominal emergency known as acute
pancreatitis (enzymatic fat necrosis).

> Occurs after trauma to the breast (traumatic fat necrosis).

291
Q

Fibrinoid necrosis

A

A special form of necrosis, visible by light microscopy, usually in autoimmune diseases e.g. polyarteritis nodosa (PAN)

292
Q

What is the fate of necrosis?

A

Depends on the size of the necrotic area:

Small area of necrosis: Healing occurs by regeneration or by granulation tissue and fibrosis.

Large area of necrosis:
• Surrounded by a fibrous capsule.
• Unabsorbed contents dry and may show dystrophic calcification (Necrosis associated with a change in pH of the tissue favoring the deposition of calcium)

293
Q

What is apoptosis?

A

> Programmed cell death, usually involving a single cell.

> Based on sequential activation of suicide pathway enzymes (Cell suicide).

294
Q

What are the causes of apoptosis?

A

Physiological: as in endometrium during the menstrual cycle.

Pathological:
- Viral hepatitis: Councilman bodies
- Cell death by cytotoxic T-lymphocytes
- Radiation cell injury

295
Q

What is the pathogenesis of apoptosis?

A

Extrinsic (Death receptor-initiated) pathway

© Active binding of death receptor (e.g. TNF receptor) by its ligand

© Cause activation of proteolytic enzymes that initiate apoptosis.

Intrinsic (Mitochondrial) pathway

© Withdrawal of growth factors (survival signals) increases the mitochondrial permeability.

© This leads to the release of molecules that activate proteolytic enzymes and initiate apoptosis.

296
Q

Compare between necrosis and apoptosis?

A

Necrosis
• Group of cells or tissue.
• Cell swelling.
• Cell membranes rupture early.
• Elicit inflammatory reaction around

Apoptosis
• Single cell or few cells.
• Cell shrinkage.
• Cell membranes remain intact until late.
• No inflammation.

Y1B2 (PPMIP & PPP) 📗 (7 decks)

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