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Pathology Flashcards

1
Q

Enumerate stimuli of Acute Inflammation (P21)

A

Infections
Trauma
Tissue necrosis
Foreign bodies
Immune reactions

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2
Q

Enumerate 4 beneficial effects of fluid exudate (P22)

A

Dilution of toxins produce by bacteria

Transport of antibiotics

Delivery of oxygen and nutrients for active cells

Entry of antibodies, where they can help in phagocytosis

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3
Q

Mention beneficial effects of fluid exudate (P22)

A

Dilution of toxins produce by bacteria

Transport of antibiotics

Delivery of oxygen and nutrients for active cells

Entry of antibodies, where they can help in phagocytosis

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4
Q

Mention steps of Leucocyte recruitment in acute inflammation (P22)

A

Margination and rolling of leukocytes: neutrophils that were usually confined allowed to flow into plasma zone. Leukocytes then bind, detach and tumble on the endothelial cell (after it released adhesive material); a process called rolling.

Pavementing of Leukocytes: Adhesion of neutrophils to vascular endothelium is called pavementing

Emigration of leukocytes: After adhering to endothelial surface, Leukocytes migrate through vessel while by squeezing in between intra cellular junctions. This migration a long gradient is stimulated by Chemokines

Chemotaxis: After leaving blood, leukocytes move towards injury a long gradient by process called chemotaxis.

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5
Q

Define chemotaxis (P22)

A

Leukocytes move towards site of infection along chemical gradient

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6
Q

Enumerate chemotactic factors (P23)

A

Bacterial products

Cytokines

C5

Products of AA metabolism

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7
Q

Define Phagocytosis (P23)

A

Recognition, attachment of particle to ingested by leukocytes then engulfment and killing of material.

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8
Q

Discuss Outcomes (fate) of acute inflammation (P25)

A

Resolution: tissue is resorted to normal; necrosis debris cleared by phagocytes

Progression and spread: With weak immunity, bacteria may spread directly, causing inflamed region to widen or through lymphatics.

Chronic inflammation: flows acute if offending agent not removed

Fibrosis and scarring: repair after substantial tissue destruction.

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9
Q

Define abscess (P26)

A

A collection of pus (or a cavity containing pus) that may be caused by seeding of organisms into tissue by secondary infections.

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10
Q

Discuss fate and complications of an abscess (P26,27)

A

Fate:
Small abscess absorbed followed by healing
Large abscess ruptures and heal

Complications of abscess: Spread of infection directly or through lymphatics. Blood spread can cause septicemia

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11
Q

Define Carbuncle (P27)

A

Multiple communicating deep subcutaneous abscesses opening on skin by multiple sinuses, common on deep of the back of the neck

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12
Q

Define Cellulitis (P28)

A

Diffuse suppurtive inflammation, occurs in loose tissues as subcutaneous tissue

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13
Q

Enumerate all types of non suppurative inflammation (P28,29)

A

Serous inflammation
Fibrinous inflammation
Catarrhal inflammation
Pseudomembranous (membranous) inflammation
Allergic inflammation
Hemorrhagic inflammation

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14
Q

Mention all types of non suppurative inflammation and describe one of them (28,29)

A

Serous inflammation: moderate increase of vascular permeability of watery fluid occurring pleural.

Fibrinous inflammation

Catarrhal inflammation

Pseudomembranous (membranous) inflammation

Allergic inflammation

Hemorrhagic inflammation

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15
Q

Mention role of mediators in different reactions of inflammation (Table 31)

A

Vasodilation——–> Histamine and prostaglandins

Increased vascular permeability—-> histamine, C3a, C5a and Leukotrienes

Chemotaxis, Leukocyte, recruitment and activation—–>TNF, IL-1, Chemokines, C3a, C5a, Leukotrienes

Fever—> IL-1, TNF and prostaglandins

Pain–> prostaglandins and Bradykinin

Tissue damage—> Lysosomal enzymes of leukocytes and reactive oxygen species

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16
Q

Pathologic features of chronic inflammation(P32)

A

Minimal edema fluid

Infiltration by blood monocytes and lymphocytes

Ongoing tissue destruction by inflammatory response

Attempts at healing by fibrosis

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17
Q

Discuss role of macrophages in chronic inflammation (P32)

A

Activated by microbial products. Activation causes macrophages to stay longer at site of inflammation and increase their intracellular killing and degradation

Macrophages produce enzymes which degrades extracellular matrix

Macrophage produce many growth factors which influence the process of repair

After stimulus is illuminated the macrophages die or wander off into lymphatics.

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18
Q

Mention cells of chronic inflammation and role of
lymphocyte (P32,33)

A

Eosinophils are found sites around parasitic infections

Mast cells in atopic persons, mast cells are armed with IgE antibody specific for certain environment antigens

Neutrophils: chronic inflammation may continue to show extensive neutrophilic infiltrates as result of persistent microbes or necrotic ells.

Role of lymphocytes: Secrete antibodies and cytokines

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19
Q

Define Granuloma (P33)

A

A specific patter of chronic inflammation characterized by localized aggregation of activated macrophages (granuloma)

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20
Q

Discuss Mechanism of formation of granuloma (P34)

A

Immune-mediated granuloma: are formed by immune T cell mediated response to persistent, poorly degradable antigens.

Granulomas from after macrophages have initially digested the pathogenic organism. They pass through lymphatics to lymph nodes where they simulate antigens (T-lymphocytes)

T lymphocytes proliferate and migrate to inflammatory focus and secrete cytokines which active macrophage

Foreign body granuloma: elicited by inert foreign particles that are difficult to clear.

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21
Q

Enumerate Types of granuloma and mention one example of each type (P34)

A

Infectious granuloma: TB

Foreign body granuloma: by splinter

Granulomas of unknown etiology: Crohn’s disease

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22
Q

Define Hypertrophy (P48)

A

Increased size and weight of organ due to increase in size of its cells

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23
Q

Give an account on Types of Hypertrophy (P48)

A

Physiological as in pregnant uterus due to hormone stimulation and muscle hypertrophy in athletes

Pathological:
Adaptive types due to increased intra-luminal pressure as in Lt ventricular hypertrophy

Compensatory type: if one of a paired organ is out of function or surgically removed, the other organ undergoes hypertrophy (if one kidney is enlargement when other kidney is surgically removed)

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24
Q

Define Hyperplasia (P49)

A

Increased size and weight of organ due to increase number of cells

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25
Q

Give an account on Hyperplasia (Define and Types) (P49)

A

Increased size and weight of organ due to increase number of cells

Physiological: hormone hyperplasia (breast due to estrogen stimulation) and compensatory hyperplasia (bone marrow hyperplasia after hemorrhage)

Pathological: hormonal hyperplasia (endometrial hyperplasia in repeated anovulatory cycles) and Lymphoid hyperplasia (in response to antigenic stimulation)

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26
Q

Define Atrophy (P50)

A

Decrease in size and weight of organ after the organ had reached its adult size

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27
Q

Give an account on Atrophy (Define and Types) (P50)

A

Decrease in size and weight of organ after the organ had reached its adult size

Physiological: localized atrophy as thymus after puberty and breasts after menopause. Generalized atrophy in case of senility.

Pathological:

Localized atrophy: hormonal atrophy due to loss of hormonal stimulation, vascular atrophy, pressure atrophy, neuropathic atrophy (due to loss of innervation due to loss of muscle)

Generalized atrophy: affects all organs, heart is small, bones are week due to chronic malnutrition and starvation.

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28
Q

Define Metaplasia (P51)

A

Replacement of one mature differentiated cell type to another type it is usually an adaptive response to injury, where the new type of cell is more resistant to chronic injury.

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29
Q

Give an account on Metaplasia (Define,Types,Pathogenesis) (P51)

A

Replacement of one mature differentiated cell type to another type it is usually an adaptive response to injury, where the new type of cell is more resistant to chronic injury.

Epithelial metaplasia
Mesenchymal metaplasia

It is the result of reprogramming of stem cells that are know to exist in normal tissue, or of undifferentiated mesenchymal cells present in connective tissue.

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30
Q

Define Dysplasia (P52)

A

It is non -neoplastic disordered proliferation of cells, usually induced by prolonged cell irritation.

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31
Q

Give an account on Dysplasia (Define,Sites,Gross and
microscopic pictures,Prognosis) (P52)

A

It is non -neoplastic disordered proliferation of cells, usually induced by prolonged cell irritation.

Mucous membrane of cervix, bronchi, oral cavity, urinary bladder

Non specific gross appearance

Loss of normal orderly arrangement
Different shapes and sized and increased nuclear color
Increased mitosis
May be low or high grade

Low grade dysplasia is commonly reversible
High grade dysplasia passes to carcinoma in situe

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32
Q

Define Carcinoma in Situ (CIS)

A

pre invasive stage of carcinoma involving full thickness of one epithelium and is characterized by sever dysplasia without invasion of basment membrane.

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33
Q

Give an account on Microscopic Features of Carcinoma in Situ and give 2 examples(sites) (P53)

A

Diffuse cellular atypia involving the whole thicknes of the epithelium. Cells are pleomorphic with dark nuclei and numerous mitoses
No invasion of basement membrane

Bladder, cervix

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34
Q

Define Neoplasia (P54)

A

A new growth forming an abnormal mass caused by autonomous self controlling proliferation of cells. It is irreversible uncontrolled unlimited progressive and purposeless.

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35
Q

Compare Between Hyperplasia and Neoplasia (Table P54)

A

Hyperplasia: excited by stimulus, reversible, normal shaped cell, can be useful at times

Neoplasia: no obvious stimulus, irreversible, abnormal cell shape and harmful

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36
Q

Discuss Morphology (Gross and Microscopic) of Benign
Tumors (P55)

A

Well circumscribed globular. Most are capsulated, cut section of tumor is commonly uniform with no hemorrhage or necrosis.

Are perfectly differentiated (closely mimic cells nearby)
Rarely any hemorrhage or necrosis
Structural pattern is same as near by cells

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37
Q

Discuss Morphology (Gross and Microscopic) of Malignant Tumors (P55,56)

A

Appear as irregular non-capsulated mass, with ill defined infiltrating margin, cut section shows hemorrhage and necrosis.

Lack of differentiation, Cellular pleomorphism, nuclear bizarre in shape. Nuclear enlargement, abundant mitosis
Grow in sheets, loss of common structure. Carcinoma maybe graded according to degree of differentiation and highly undifferentiated are more agressive.

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38
Q

Enumerate Routes of spread of Malignant Tumors (P57,58,59)

A

Local spread: Tumor cells invade adjacent structures directly

Distant spread (metastasis):

-Lymphatic spread
-Blood spread
- transcoelomic spread
- Transluminal spread

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39
Q

Discuss Lymphatic spread of Malignant Tumors (P57,58)

A

Occurs more commonly with carcinoma than sarcoma. Can spread lymphatics embolism and lymphatic permeation

Lymphatic embolism: Malignant cells invade the wall of the lymphatic vessels forming tumor emboli and reach the lymph node

Lymphatic permeation: Tumors cells grow as solid columns inside lymphatics leading to lymphatic obstruction and lymphatic edema

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40
Q

Discuss Hematogenous Spread of Malignant Tumors (P58)

A

Emboli derived from primary tumors of organs drained by systemic veins

Emboli derived from tumors of lungs are carried through pulmonary veins to left side of the heart and systemic arterial circulation causing metastases in different organs

Emboli derived from tumors of organ drained by portal vein give rises to emboli to reach hepatic vein.

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41
Q

Discuss Transcoelomic Spread of Malignant Tumors (P59)

A

Transperitoneal spread from stomach, colon causes metastatic peritoneal nodules accompanied by hemorrhagic ascites

Transpleural and transpericardial spread: from lung or breast cancer resulting in metastases on diaphragm accompanied by hemorrhagic pleural

CSF: Malignant tumors of brain may give rise to tumor cells within CSF leading to metastases within lining of ventricles and base of skull.

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42
Q

Give an account on Mechanism of spread of Malignant
Tumors (P60)

A

Invasion of ECM: by loss of cellular cohesion then attachment of tumor cells to matrix components.

Then degradation of the ECM by proteolytic enzymes secreted by the tumor cells.

Tumors migration by pseudopodia which is mediated by tumor like cytokines.

Tumor cell mobility allows cells to come in contact with blood vessels.

Tumor cells cross vascular basement membranes reach circulation as tumor emboli

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43
Q

Define Locally Malignant Tumors and mention 2
examples (P61)

A

Are locally invasive and destructive but rarely give rise to metastases.

Giant cell tumor of bone
Some tumors of CNS

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44
Q

Enumerate Types of Papilloma and describe one (P63)

A

Squamous cell papilloma

Villous papilloma: A benign tumor arise from urothelium and strongly pre-malignant

Columnar cell papilloma

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45
Q

Define Adenoma (P63)

A

A benign tumor arising from glandular epithelium

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46
Q

Mention Microscopic Patterns of Adenoma in glands (P64)

A

Simple adenoma: consist of proliferated glands lined by cuboidal, separated by fibrovascular stroma

Fibroadenoma: consist of glandular and wide stromal proliferation

Cystadenoma: secretions are retained leading to cystic dilation

Papillary cystadenoma: cystadenoma in which epithelial lining in cyst proliferates forming papillae

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47
Q

Mention 3 sites of Squamous cell Carcinoma (P65)

A

Exocrine gland
Endocrine gland
Mucosal gland

48
Q

Mention Predisposing Factors of Squamous cell
Carcinoma (P65)

A

Prolonged exposure to skin to the sun

Chemical carcinogenic

Squamous metaplasia

49
Q

Define Adenocarcinoma (P66)

A

malignant tumors arising from glandular epithelium of mucosal surfaces or glandular organs

50
Q

Enumerate Types of Adenocarcinoma (P66,67)

A

Well differentiated adenocarcinoma

Mucin secreting carcinoma

Carcinoma simplex

51
Q

Define Carcinoma (Table P69)

A

Malignant tumor of epithelium

52
Q

Compare between Carcinoma and Sarcoma (Table P69)

A

Carcinoma: malignant tumor of epithelium, most common, usually above 40 years, rapid growth rate, infiltrative and expansive.
______________________________________
Sarcoma: malignant tumor of mesenchyme, much less common, usually below age of 20, faster than carcinoma, rapid growth rate

53
Q

Define Teratoma (P70)

A

Are germ cells tumors that arise from neoplastic transformation of germ cells.

54
Q

Discuss Types of Teratoma (P70,71)

A

Mature teratoma: are commonly cystic in ovary. Contains tuffs of hair, skin, teeth and bones.

Specialized teratomas: specialized teratomas differentiate along the line of a single abnormal tissue

Malignant teratoma: are rare tumors composed of embryonic elements resembling immature fetal tissue

55
Q

Define Embryonic Tumors and give 2 examples (P71,72)

A

Are malignant tumors derived from embryonic cell remnants in infants and young children

Hepatoblastoma of liver
Nephroblastoma of liver

56
Q

Define Hamartoma and Give 2 examples (P72)

A

A tumor like developmental malformation formed of noncapsualted mature tissues of the affected organ but arranged haphazardly

Lung hamartoma
Kidney hamartoma

57
Q

Enumerate 3 Chronic Inflammatory diseases that are
precancerous (P73)

A

Bilharziasis

Ulcerative colitis

Atrophic gastritis

58
Q

Mention Steps of Carcinogenesis (P74)

A

Initiation: Induction of certain irreversible changes in the genome of the cells.

Promotion: Promoters enhance the proliferation of initiated cells, an effect may contribute to the acquisition of additional mutation.

Neoplastic transformation: abnormal differentiation occurs and the cells undergo continuous purposeless uncontrolled irreversible proliferation

59
Q

Discuss Steps of Carcinogenesis (tumorigenesis) (P74)

A

Initiation: Induction of certain irreversible changes in the genome of the cells are not transformed and do not have growth autonomy

Promotion: promoters enhance the proliferation of initiated cells

Neoplastic transformation: Abnormal differentiation occurs and the cells undergo continuous purposeless uncontrolled irreversible proliferation.

60
Q

Mention 4 viruses that been implicated in causing
neoplasms (P77,78)

A

EPV
Hepatitis B virus
Human papilloma virus
Human T lymphotropic virus

61
Q

Mention Dangerous Benign Tumors (P78)

A

They arise in vital organs like brain
Aris in hollow organs cause obstruction
They produce hormones
Some begnin can become malignant

62
Q

Mention 5 causes of death in Malignant Tumors (P78)

A

Local organ destruction
Distant organ destruction by direct spread
Destruction of vital centers
Organ failure
Obstruction of lumen of hollow organs
Some tumors secrete hormones

63
Q

Discuss 4 causes of death in Malignant Tumors (P78)

A

Local organ destruction
Distant organ destruction by direct spread
Destruction of vital centers
Organ failure
Obstruction of lumen of hollow organs
Some tumors secrete hormones

64
Q

Enumerate Causes of malnutrition in Malignant Tumors (P78)

A

loss of appetite
Interference of food intake
Chronic toxemia
Cachexia
Anemia

65
Q

Define Cachexia (P79)

A

marked decrease of body fat and lean body mass, weakness, anorexia and anemia

66
Q

Define paraneoplastic syndrome

A

a set of signs and symptoms that can occur when you have cancer. The symptoms develop when a malignant tumor causes changes in your body that aren’t directly caused by the cancer itself. The tumor may secrete a hormone or protein that affects a particular body system

67
Q

Define Hyperemia (P82)

A

It increased blood flow to an organ

68
Q

Define Congestion (P83)

A

it is a passive process caused by impaired blood outflow from the tissue resulting in increased blood contents

69
Q

Give an account on Types and effects of congestion (P83)

A

Systemic congestion as occurs in heart failure
Localized congestion as in occlusion or external pressure on vein

Acute congestion: the vessels are distended and organs are grossly red in color and usually associated with interstitial edema

Chronic congestion: Gradual congestion is associated with edema, focal hemorrhages with RBC breakdown leading to accumulation of macrophages. May result in ischemia

70
Q

Compare between Exudate and Transudate (Table P85)

A

Exudate: high protein, high specific gravity, high fibrinogen content, rich in inflammatory cells, cloudy, due to inflammation

Transudate: Low protein content, low specific gravity, no fibrinogen, straw colored, increased hydrostatic pressure

71
Q

Mention Causes of Edema (P86)

A

Increase hydrostatic pressure: due to impaired VR

Reduced plasma osmotic pressure: hypoproteinemia

Lymphatic obstruction: as in lymphadenitis, edema of upper limb or inflammatory

Sodium retention: Excessive salt intake with renal insufficiency

Inflammation: in acute inflammation.

72
Q

Enumerate 3 causes of Generalized Edema (P86)

A

Cardiac edema
Nutritional edema
Renal edema

73
Q

Define Thrombosis (P87)

A

A pathological state resulting in formation of solid compact mass inside uninjured cardiovascular system

74
Q

Discuss Etiology of Thrombosis (P87,88)

A

Three primary factors (Virchow’s triad)

-Endothelial injury is the dominant cause of thrombosis

-Alterations in normal blood flow that is usually laminar

-Hypercoagulability any alteration of the coagulation pathways predisposes to thrombosis (heritable hypercoagulable states)

75
Q

Discuss mechanism of Thrombosis (P88)

A

Exposure of subendothelial collagen

Adhesion of the platelets to the exposed collagen which is mediated by factor VII. They then adhere to exposed thrombus

Platelets’ derive thromboxane A2 causes platelet contraction and platelet factor 3 forms thrombin to prothrombin

Thrombin leads to transformation of fibrinogen into fibrin. These fibrin deposit on platelet clot to encourage more deposits of platelets.

76
Q

Discuss Sites and Types of Thrombi (P89)

A

Pale thrombi: made predominantly of platelets. Found in fast moving blood.

Red thrombi: When thrombi form in slow moving blood.

77
Q

Discuss Effect and fate of Thrombi (Any 4 effects)

A

Fragmentation: thrombi may fragment, producing thrombo-emboli

Occlusion of an artery will result in ischemia and of vein will lead to congestion and edema

Organization: are invaded by granulation tissue which converts into scar

Canalization and Organization: as thrombus turns over a few weeks, into vascular granulation tissue, it recanalizes

Propagation: when thrombus occludes a vein completely the proximal column of blood clots till the next tributary. In the other tributary another thrombus is formed and when it occludes the lumen completely it results in formation of another clot proximal to it.

78
Q

Define Embolism (P90)

A

Is an insoluble mass circulating in the blood stream

79
Q

Enumerate all types of emboli (P90)

A

Air emboli
Fat emboli
Tumor emboli
Parasitic emboli
Amniotic fluid emboli
Thrombo emboli

80
Q

Mention Types of Emboli (P90)

A

Thromboembolism: dislodged or fragmented emboli. Effect depends on size of embolus.

Pulmonary emboli: from DVT. Only medium and big embolus are detected and can cause harm.

Amniotic fluid emboli: cause amniotic fluid which is full of baby debris enter maternal circulation.

Air emboli: due to injury of large neck or ruptured chest vein. Gas lodges in the vessels and it interferes with blood flow

Fat embolism: arise from severe trauma like fracture to long bones

81
Q

Mention Course of emboli of thrombotic origin (P91)

A

Emboli from systemic vein or right side of heart impact lung

Emboli from aorta or left side of heart impact in any organ

Emboli from portal vein impact in liver

Emboli form systemic vein may by-pass the lung through septal defect in the heart and impact in any organ.

82
Q

Mention Source and effects of Pulmonary Embolism

A

Source: large majority of pulmonary emboli come from the deep vein legs

Small sized: has no effect

Medium sized in healthy lung: no effect (lung has double blood supply)

Medium sized in patient with chronic venous congestion of lung: hemorrhagic infraction

Big embolus: Occluding the pulmonary trunk resulting in release of high amount of seritonin

83
Q

Define Ischemia (P93)

A

Decrease of arterial blood supply to organ or tissue due to occlusion of its artery

84
Q

Mention Causes and effects of Acute Ischemia (P93)

A

Thromboses
Embolus
Strangulation
Surgical ligature

Sudden occlusion of arteries with poor collaterals causes gangrene
Sudden occlusion of arteries with goo collaterals has no effect

85
Q

Discuss Causes and effects of Chronic Ischemia (P93,94)

A

Atherosclerosis
Arteritis
Artery compression via tumor

86
Q

Define Infarction (P94)

A

An infract is an area of ischemic necrosis caused by occlusion of vascular supply

87
Q

Mention Types of infarctions and causes of each type (P94)

A

Red Infracts: Venous occlusion, loose tissue, congested tissue

Pale infracts: Artery occlusion in solid organs like heart

88
Q

Define Gangrene (P95)

A

Massive tissue necrosis followed by putrefaction

89
Q

Mention Etiology and types of Gagrene (P95)

A

The necrosis is caused mainly by ischemia

Dry gangrene
Moist gangrene
Infective gangrene
Gas gangrene

90
Q

Compare between Dry and Moist Gangrenes (Table P97)

A

Dry: caused by occlusion of arterial supply, usually affect exposed limb, slow spread, strong line of separation and demarcation, natural amputation can occur

Moist: Occlusion of both artery and vein, affects internal organs, rapid spread, line of separation is absent and line of demarcation is poorly absent, natural amputation cannot occur.

91
Q

Give an account on Diabetic Gangrene (Cause and
Pathological Features) (P97)

A

Uncontrolled diabetes results in hyperlipemia, which leads to atherosclerosis at an earlier age. Usually at big toe. It is moist because low resistance and excess sugar in tissue.

92
Q

Give an account on Gas gangrene (P97,98)

A

Characterized by elaboration of several gasses which is very serious

93
Q

Define Toxemia and mention 2 examples (P100)

A

Organismal toxins in the circulation

Tetanus
Bacillary dysentery

94
Q

Define Septicemia (P101)

A

Circulation of large numbers of bacteria which are multiplying in the blood stream

95
Q

Define Pyaemia (P101)

A

Circulation of septic emboli

96
Q

Mention types of Pyaemia and causes of each type (Table P102)

A

Pulmonary pyaemia: cellulitis, abscess

Systemic pyaemia: Lt heart vegetations

Portal pyaemia: Septic thrombophlenitits of GIT veins

97
Q

Mention Sites of Primary TB (P106)

A

Lungs, tonsils, intestine

98
Q

Discuss fate of Primary pulmonary TB complex (P107,108)

A

Most heal
Spread: directly, blood spread, or bronchial spread
Encapsulation: Lung and nodal lesion get encapsulated

99
Q

Mention Complications of 2ry Pulmonary TB (P109)

A

Hemoptysis
Spread of infection
Rupture cavity
Infected sputum can spread infection
Lung fibrosis
Swallowing of infected sputum causing intestinal TB

100
Q

Define Gumma (P114)

A

Localized area of syphilitic granulation tissue which undergoes yellow causes necrosis

101
Q

Enumerate Diseases Caused by HPV (P121)

A

Common warts
Genital warts
Cancer warts

102
Q

Give an account on urothelial changes in bilharzial
cystitis (P129)

A

Transitional cell hyperplasia: mucosa becomes thickened

Transitional cell atrophy: reduction of cell layers due to ischemia

Squamous metaplasia: chronic irritation by the ova will produce change from a weaker transitional epithelium

103
Q

Mention Effects of Portal Hypertension (P132)

A

Splenomegaly
Ascites
Piles

104
Q

Define Regeneration (P36)

A

The replacement of the damaged cells by same cell type

105
Q

Define Angiogenesis (P38)

A

process of new blood vessel development from existing vessels

106
Q

Give an account on Angiogenesis (P38)

A

Proteolytic degradation of the parent vessel membrane by metalloproteinases

Migration and proliferation of endothelial cells towards the area of tissue injury and produce solid buds

Remodeling into capillary tubes

Recruitment of periendothelial cells to form the mature vessel

107
Q

Discuss Factors that influence tissue repair (P41)

A

General factors: nutrition (no vitamin C retards healing), metabolic status (diabetes delays healing), hormones (no steroids) and circulatory status

Local factors: infection, mechanical damage or foreign body.

108
Q

Discuss Healing by first intention (P41,42)

A

occurs in incised wounds, where little damage to the tissue on sides.

Blood clots on wound surfaces fibrin acts as glue which holds the cut surfaces together. After 24 hours there is mild inflammatory reaction, with fluid exudate which stat to digest the clot

Within 48 hours basal cells start to regenerate and migrate to bridge gap and afterwards continue to restore thickness of epidermis

Day 3 macrophages appear in inflammatory exudate and digest fibrin and cellular debris

Fibroblast lay down collagen which unite edges of wound

109
Q

Compare between Healing by first intention(Primary union) and healing by second intention (secondary union) Table P44

A

First intention: clean non gaping wound, minimal tissue damage, epithelial gap is closed firs by epithelial regeneration followed by epithelial regeneration followed by formation of granulation tissue in dermis, Line of incision are permanently, Complications are less common
_________________________________________________________
Second intention: gaping wound, extensive tissue damage, gap is wide so granulation tissue fills the wound from below upwards until reaches the epidermis, forming a base upon which epithelial cells can grow. Formation of large scar line of incision are permanently lost, complications are more common.

110
Q

Mention Complications of wound healing (P44)

A

Cosmetic deformities: due to extensive scarring

Excessive scar contraction: lead to contracture which is limiting of movement across joints

Keloid formation: over done repair formed from excessive fibroblast proliferation after dermal injury

Implantation epidermal cyst: during regeneration of the epidermis some epidermal cells may grown down the cut edges of dermis. They later are resorbed and can grown into cyst

Chronic ulcer, sinus or fistula: defective of repair in case of persistent infection or foreign body.

Carcinoma may develop from the edges of chronic ulcers and scar tissue.

111
Q

Define Keloid (P44)

A

Keloid formation: over done repair formed from excessive fibroblast proliferation after dermal injury

112
Q

Give four complications of Bilharzial cystitis

A

Terminal hematuria: Hemorrhage at the end of micturition due to squeezing out of ova during bladder constriction.

Secondary infections of the ulcers leading to fistulae

Malignant transformation of epithelium

Obstructive uropathy due to fibrosis causing hydro nephrosis

113
Q

Mention types of actinomycosis (117, 118)

A

Cervicofacial actinomycosis
Intestinal actinomycosis
Pulmonary actinomycosis
Skin actinomycosis

114
Q

Mention complications of 2ry intestinal TB (111, 112)

A

Intestinal hemorrhage
Stenosis of lumen
Fistulae between two intestinal loops
Septic peritonitis
Spread

115
Q

Give an account on fate of primary tubercle (107,108)

A

High immunity: Lesion completely fibrosed and large caseous lesions are encapsulated

Low immunity: spread wither directly, lymphatically or through blood vessels.

116
Q

Enumerate disease caused by EBV (121)

A

Infectious mononucleosis
Burkitt’s lymphoma
Nasopharyngeal cancer

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