Pathology Flashcards
Enumerate stimuli of Acute Inflammation (P21)
Infections
Trauma
Tissue necrosis
Foreign bodies
Immune reactions
Enumerate 4 beneficial effects of fluid exudate (P22)
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
Mention beneficial effects of fluid exudate (P22)
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
Mention steps of Leucocyte recruitment in acute inflammation (P22)
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.
Define chemotaxis (P22)
Leukocytes move towards site of infection along chemical gradient
Enumerate chemotactic factors (P23)
Bacterial products
Cytokines
C5
Products of AA metabolism
Define Phagocytosis (P23)
Recognition, attachment of particle to ingested by leukocytes then engulfment and killing of material.
Discuss Outcomes (fate) of acute inflammation (P25)
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.
Define abscess (P26)
A collection of pus (or a cavity containing pus) that may be caused by seeding of organisms into tissue by secondary infections.
Discuss fate and complications of an abscess (P26,27)
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
Define Carbuncle (P27)
Multiple communicating deep subcutaneous abscesses opening on skin by multiple sinuses, common on deep of the back of the neck
Define Cellulitis (P28)
Diffuse suppurtive inflammation, occurs in loose tissues as subcutaneous tissue
Enumerate all types of non suppurative inflammation (P28,29)
Serous inflammation
Fibrinous inflammation
Catarrhal inflammation
Pseudomembranous (membranous) inflammation
Allergic inflammation
Hemorrhagic inflammation
Mention all types of non suppurative inflammation and describe one of them (28,29)
Serous inflammation: moderate increase of vascular permeability of watery fluid occurring pleural.
Fibrinous inflammation
Catarrhal inflammation
Pseudomembranous (membranous) inflammation
Allergic inflammation
Hemorrhagic inflammation
Mention role of mediators in different reactions of inflammation (Table 31)
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
Pathologic features of chronic inflammation(P32)
Minimal edema fluid
Infiltration by blood monocytes and lymphocytes
Ongoing tissue destruction by inflammatory response
Attempts at healing by fibrosis
Discuss role of macrophages in chronic inflammation (P32)
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.
Mention cells of chronic inflammation and role of
lymphocyte (P32,33)
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
Define Granuloma (P33)
A specific patter of chronic inflammation characterized by localized aggregation of activated macrophages (granuloma)
Discuss Mechanism of formation of granuloma (P34)
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.
Enumerate Types of granuloma and mention one example of each type (P34)
Infectious granuloma: TB
Foreign body granuloma: by splinter
Granulomas of unknown etiology: Crohn’s disease
Define Hypertrophy (P48)
Increased size and weight of organ due to increase in size of its cells
Give an account on Types of Hypertrophy (P48)
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)
Define Hyperplasia (P49)
Increased size and weight of organ due to increase number of cells
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)
Define Atrophy (P50)
Decrease in size and weight of organ after the organ had reached its adult size
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.
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.
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.
Define Dysplasia (P52)
It is non -neoplastic disordered proliferation of cells, usually induced by prolonged cell irritation.
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
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.
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
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.
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
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
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.
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
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
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.
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.
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
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
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
Define Adenoma (P63)
A benign tumor arising from glandular epithelium
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
Mention 3 sites of Squamous cell Carcinoma (P65)
Exocrine gland
Endocrine gland
Mucosal gland
Mention Predisposing Factors of Squamous cell
Carcinoma (P65)
Prolonged exposure to skin to the sun
Chemical carcinogenic
Squamous metaplasia
Define Adenocarcinoma (P66)
malignant tumors arising from glandular epithelium of mucosal surfaces or glandular organs
Enumerate Types of Adenocarcinoma (P66,67)
Well differentiated adenocarcinoma
Mucin secreting carcinoma
Carcinoma simplex
Define Carcinoma (Table P69)
Malignant tumor of epithelium
Compare between Carcinoma and Sarcoma (Table P69)
Carcinoma: malignant tumor of epithelium, most common, usually above 40 years, rapid growth rate, infiltrative and expansive.
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Sarcoma: malignant tumor of mesenchyme, much less common, usually below age of 20, faster than carcinoma, rapid growth rate
Define Teratoma (P70)
Are germ cells tumors that arise from neoplastic transformation of germ cells.
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
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
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
Enumerate 3 Chronic Inflammatory diseases that are
precancerous (P73)
Bilharziasis
Ulcerative colitis
Atrophic gastritis
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
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.
Mention 4 viruses that been implicated in causing
neoplasms (P77,78)
EPV
Hepatitis B virus
Human papilloma virus
Human T lymphotropic virus
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
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
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
Enumerate Causes of malnutrition in Malignant Tumors (P78)
loss of appetite
Interference of food intake
Chronic toxemia
Cachexia
Anemia
Define Cachexia (P79)
marked decrease of body fat and lean body mass, weakness, anorexia and anemia
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
Define Hyperemia (P82)
It increased blood flow to an organ
Define Congestion (P83)
it is a passive process caused by impaired blood outflow from the tissue resulting in increased blood contents
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
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
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.
Enumerate 3 causes of Generalized Edema (P86)
Cardiac edema
Nutritional edema
Renal edema
Define Thrombosis (P87)
A pathological state resulting in formation of solid compact mass inside uninjured cardiovascular system
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)
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.
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.
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.
Define Embolism (P90)
Is an insoluble mass circulating in the blood stream
Enumerate all types of emboli (P90)
Air emboli
Fat emboli
Tumor emboli
Parasitic emboli
Amniotic fluid emboli
Thrombo emboli
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
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.
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
Define Ischemia (P93)
Decrease of arterial blood supply to organ or tissue due to occlusion of its artery
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
Discuss Causes and effects of Chronic Ischemia (P93,94)
Atherosclerosis
Arteritis
Artery compression via tumor
Define Infarction (P94)
An infract is an area of ischemic necrosis caused by occlusion of vascular supply
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
Define Gangrene (P95)
Massive tissue necrosis followed by putrefaction
Mention Etiology and types of Gagrene (P95)
The necrosis is caused mainly by ischemia
Dry gangrene
Moist gangrene
Infective gangrene
Gas gangrene
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.
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.
Give an account on Gas gangrene (P97,98)
Characterized by elaboration of several gasses which is very serious
Define Toxemia and mention 2 examples (P100)
Organismal toxins in the circulation
Tetanus
Bacillary dysentery
Define Septicemia (P101)
Circulation of large numbers of bacteria which are multiplying in the blood stream
Define Pyaemia (P101)
Circulation of septic emboli
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
Mention Sites of Primary TB (P106)
Lungs, tonsils, intestine
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
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
Define Gumma (P114)
Localized area of syphilitic granulation tissue which undergoes yellow causes necrosis
Enumerate Diseases Caused by HPV (P121)
Common warts
Genital warts
Cancer warts
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
Mention Effects of Portal Hypertension (P132)
Splenomegaly
Ascites
Piles
Define Regeneration (P36)
The replacement of the damaged cells by same cell type
Define Angiogenesis (P38)
process of new blood vessel development from existing vessels
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
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.
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
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
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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.
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.
Define Keloid (P44)
Keloid formation: over done repair formed from excessive fibroblast proliferation after dermal injury
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
Mention types of actinomycosis (117, 118)
Cervicofacial actinomycosis
Intestinal actinomycosis
Pulmonary actinomycosis
Skin actinomycosis
Mention complications of 2ry intestinal TB (111, 112)
Intestinal hemorrhage
Stenosis of lumen
Fistulae between two intestinal loops
Septic peritonitis
Spread
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.
Enumerate disease caused by EBV (121)
Infectious mononucleosis
Burkitt’s lymphoma
Nasopharyngeal cancer
