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Pathology Flashcards

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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
Give an account on Hyperplasia (Define and Types) (P49)
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)
26
Define Atrophy (P50)
Decrease in size and weight of organ after the organ had reached its adult size
27
Give an account on Atrophy (Define and Types) (P50)
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.
28
Define Metaplasia (P51)
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.
29
Give an account on Metaplasia (Define,Types,Pathogenesis) (P51)
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.
30
Define Dysplasia (P52)
It is non -neoplastic disordered proliferation of cells, usually induced by prolonged cell irritation.
31
Give an account on Dysplasia (Define,Sites,Gross and microscopic pictures,Prognosis) (P52)
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
32
Define Carcinoma in Situ (CIS)
pre invasive stage of carcinoma involving full thickness of one epithelium and is characterized by sever dysplasia without invasion of basment membrane.
33
Give an account on Microscopic Features of Carcinoma in Situ and give 2 examples(sites) (P53)
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
34
Define Neoplasia (P54)
A new growth forming an abnormal mass caused by autonomous self controlling proliferation of cells. It is irreversible uncontrolled unlimited progressive and purposeless.
35
Compare Between Hyperplasia and Neoplasia (Table P54)
Hyperplasia: excited by stimulus, reversible, normal shaped cell, can be useful at times Neoplasia: no obvious stimulus, irreversible, abnormal cell shape and harmful
36
Discuss Morphology (Gross and Microscopic) of Benign Tumors (P55)
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
37
Discuss Morphology (Gross and Microscopic) of Malignant Tumors (P55,56)
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.
38
Enumerate Routes of spread of Malignant Tumors (P57,58,59)
Local spread: Tumor cells invade adjacent structures directly Distant spread (metastasis): -Lymphatic spread -Blood spread - transcoelomic spread - Transluminal spread
39
Discuss Lymphatic spread of Malignant Tumors (P57,58)
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
40
Discuss Hematogenous Spread of Malignant Tumors (P58)
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.
41
Discuss Transcoelomic Spread of Malignant Tumors (P59)
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.
42
Give an account on Mechanism of spread of Malignant Tumors (P60)
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
43
Define Locally Malignant Tumors and mention 2 examples (P61)
Are locally invasive and destructive but rarely give rise to metastases. Giant cell tumor of bone Some tumors of CNS
44
Enumerate Types of Papilloma and describe one (P63)
Squamous cell papilloma Villous papilloma: A benign tumor arise from urothelium and strongly pre-malignant Columnar cell papilloma
45
Define Adenoma (P63)
A benign tumor arising from glandular epithelium
46
Mention Microscopic Patterns of Adenoma in glands (P64)
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
47
Mention 3 sites of Squamous cell Carcinoma (P65)
Exocrine gland Endocrine gland Mucosal gland
48
Mention Predisposing Factors of Squamous cell Carcinoma (P65)
Prolonged exposure to skin to the sun Chemical carcinogenic Squamous metaplasia
49
Define Adenocarcinoma (P66)
malignant tumors arising from glandular epithelium of mucosal surfaces or glandular organs
50
Enumerate Types of Adenocarcinoma (P66,67)
Well differentiated adenocarcinoma Mucin secreting carcinoma Carcinoma simplex
51
Define Carcinoma (Table P69)
Malignant tumor of epithelium
52
Compare between Carcinoma and Sarcoma (Table P69)
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
Define Teratoma (P70)
Are germ cells tumors that arise from neoplastic transformation of germ cells.
54
Discuss Types of Teratoma (P70,71)
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
Define Embryonic Tumors and give 2 examples (P71,72)
Are malignant tumors derived from embryonic cell remnants in infants and young children Hepatoblastoma of liver Nephroblastoma of liver
56
Define Hamartoma and Give 2 examples (P72)
A tumor like developmental malformation formed of noncapsualted mature tissues of the affected organ but arranged haphazardly Lung hamartoma Kidney hamartoma
57
Enumerate 3 Chronic Inflammatory diseases that are precancerous (P73)
Bilharziasis Ulcerative colitis Atrophic gastritis
58
Mention Steps of Carcinogenesis (P74)
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
Discuss Steps of Carcinogenesis (tumorigenesis) (P74)
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
Mention 4 viruses that been implicated in causing neoplasms (P77,78)
EPV Hepatitis B virus Human papilloma virus Human T lymphotropic virus
61
Mention Dangerous Benign Tumors (P78)
They arise in vital organs like brain Aris in hollow organs cause obstruction They produce hormones Some begnin can become malignant
62
Mention 5 causes of death in Malignant Tumors (P78)
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
Discuss 4 causes of death in Malignant Tumors (P78)
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
Enumerate Causes of malnutrition in Malignant Tumors (P78)
loss of appetite Interference of food intake Chronic toxemia Cachexia Anemia
65
Define Cachexia (P79)
marked decrease of body fat and lean body mass, weakness, anorexia and anemia
66
Define paraneoplastic syndrome
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
Define Hyperemia (P82)
It increased blood flow to an organ
68
Define Congestion (P83)
it is a passive process caused by impaired blood outflow from the tissue resulting in increased blood contents
69
Give an account on Types and effects of congestion (P83)
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
Compare between Exudate and Transudate (Table P85)
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
Mention Causes of Edema (P86)
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
Enumerate 3 causes of Generalized Edema (P86)
Cardiac edema Nutritional edema Renal edema
73
Define Thrombosis (P87)
A pathological state resulting in formation of solid compact mass inside uninjured cardiovascular system
74
Discuss Etiology of Thrombosis (P87,88)
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
Discuss mechanism of Thrombosis (P88)
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
Discuss Sites and Types of Thrombi (P89)
Pale thrombi: made predominantly of platelets. Found in fast moving blood. Red thrombi: When thrombi form in slow moving blood.
77
Discuss Effect and fate of Thrombi (Any 4 effects)
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
Define Embolism (P90)
Is an insoluble mass circulating in the blood stream
79
Enumerate all types of emboli (P90)
Air emboli Fat emboli Tumor emboli Parasitic emboli Amniotic fluid emboli Thrombo emboli
80
Mention Types of Emboli (P90)
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
Mention Course of emboli of thrombotic origin (P91)
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
Mention Source and effects of Pulmonary Embolism
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
Define Ischemia (P93)
Decrease of arterial blood supply to organ or tissue due to occlusion of its artery
84
Mention Causes and effects of Acute Ischemia (P93)
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
Discuss Causes and effects of Chronic Ischemia (P93,94)
Atherosclerosis Arteritis Artery compression via tumor
86
Define Infarction (P94)
An infract is an area of ischemic necrosis caused by occlusion of vascular supply
87
Mention Types of infarctions and causes of each type (P94)
Red Infracts: Venous occlusion, loose tissue, congested tissue Pale infracts: Artery occlusion in solid organs like heart
88
Define Gangrene (P95)
Massive tissue necrosis followed by putrefaction
89
Mention Etiology and types of Gagrene (P95)
The necrosis is caused mainly by ischemia Dry gangrene Moist gangrene Infective gangrene Gas gangrene
90
Compare between Dry and Moist Gangrenes (Table P97)
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
Give an account on Diabetic Gangrene (Cause and Pathological Features) (P97)
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
Give an account on Gas gangrene (P97,98)
Characterized by elaboration of several gasses which is very serious
93
Define Toxemia and mention 2 examples (P100)
Organismal toxins in the circulation Tetanus Bacillary dysentery
94
Define Septicemia (P101)
Circulation of large numbers of bacteria which are multiplying in the blood stream
95
Define Pyaemia (P101)
Circulation of septic emboli
96
Mention types of Pyaemia and causes of each type (Table P102)
Pulmonary pyaemia: cellulitis, abscess Systemic pyaemia: Lt heart vegetations Portal pyaemia: Septic thrombophlenitits of GIT veins
97
Mention Sites of Primary TB (P106)
Lungs, tonsils, intestine
98
Discuss fate of Primary pulmonary TB complex (P107,108)
Most heal Spread: directly, blood spread, or bronchial spread Encapsulation: Lung and nodal lesion get encapsulated
99
Mention Complications of 2ry Pulmonary TB (P109)
Hemoptysis Spread of infection Rupture cavity Infected sputum can spread infection Lung fibrosis Swallowing of infected sputum causing intestinal TB
100
Define Gumma (P114)
Localized area of syphilitic granulation tissue which undergoes yellow causes necrosis
101
Enumerate Diseases Caused by HPV (P121)
Common warts Genital warts Cancer warts
102
Give an account on urothelial changes in bilharzial cystitis (P129)
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
Mention Effects of Portal Hypertension (P132)
Splenomegaly Ascites Piles
104
Define Regeneration (P36)
The replacement of the damaged cells by same cell type
105
Define Angiogenesis (P38)
process of new blood vessel development from existing vessels
106
Give an account on Angiogenesis (P38)
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
Discuss Factors that influence tissue repair (P41)
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
Discuss Healing by first intention (P41,42)
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
Compare between Healing by first intention(Primary union) and healing by second intention (secondary union) Table P44
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
Mention Complications of wound healing (P44)
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
Define Keloid (P44)
Keloid formation: over done repair formed from excessive fibroblast proliferation after dermal injury
112
Give four complications of Bilharzial cystitis
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
Mention types of actinomycosis (117, 118)
Cervicofacial actinomycosis Intestinal actinomycosis Pulmonary actinomycosis Skin actinomycosis
114
Mention complications of 2ry intestinal TB (111, 112)
Intestinal hemorrhage Stenosis of lumen Fistulae between two intestinal loops Septic peritonitis Spread
115
Give an account on fate of primary tubercle (107,108)
High immunity: Lesion completely fibrosed and large caseous lesions are encapsulated Low immunity: spread wither directly, lymphatically or through blood vessels.
116
Enumerate disease caused by EBV (121)
Infectious mononucleosis Burkitt's lymphoma Nasopharyngeal cancer

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