1. Histopathology --deals with study of tissues removed from the living body

2. Forensic pathology and autopsy work includes the study of organs and tissues removed at post-mortem

3. Cytopathology includes study of cells shade off from lesions (exfoliative cytology and fine needle aspiration cytology of official and deep seated lesion for diagnosis

4. Pathogenesis --Refers to the  sequence of events in the response of cells or tissues to the aetiologic agent, from the initial stimulus to the ultimate expression of the disease

5. There are two types of cell death

a. Necrosis

b. Apoptosis



6. Causes of Cell Injury

a. Oxygen deprivation

b. Chemical agents

c. Infectious agents

d. Immunologic reactions

e. Genetic defects


7. Pathology is a scientific study of structure and function of the body in disease; it deals with causes, effects, mechanisms and nature of disease.


8. Human pathology is conventionally divided into;

General pathology

Systemic pathology



9. Neoplasia  means new growth OR is an abnormal mass of tissue of which the growth exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after the cessation of the stimuli which evoked the change.


10. Benign tumour is the new mass which is localized at the site of origin and has no ability to infiltrate other tissues and it is well differentiated


11. Malignant tumour is the new mass which is poorly or completely differentiated(anaplastic) and capable of invading or infiltrate the other tissues


12. Benign and malignant tumours can be distinguished on the basis of

Ø Degree of differentiation

Ø Rate of growth

Ø Local invasiveness

Ø Distant spread


13. Metastasis-Is the spreading/dissemination of malignant tumours to the distant tissues


14. Anaemia----A reduction in the number of circulating red blood cells or reduced haemoglobin level in relation to age and sex.


15. Causes of Anaemia

Ø Increased red cell destruction (haemolysis)

Ø Excessive bleeding (haemorrhage

Ø  Decreased red cell production (aplasia)


16. Cause of Haemolytic Anaemia

Ø The most common causes of these are the antibodies which have the capacity to agglutinate the red cells in vitro either directly or after the addition of ant-human globulin (the Coombs test).  

Ø Intrinsic red cell abnormality (haemoglobinopathies)

Ø Sickle cell anaemia (common in our environment)

Ø Thalasaemia

Ø Hereditary spherocytosis, there is defect of red cell membrane that render cell spheroid, less deformable and vulnerable to splenic sequestration

Ø Glucose- 6 Phosphate Dehydrogenase Deficiency (G-6-PD deficiency



17. Regardless of the cause, haemolysis leads to

Ø Haemoglobinaemia

Ø Haemoglobinuria

Ø Haemosiderinuria


18. Acute reticulocytosis.indicate which type of anaemia?

Ø Haemorrhagic anaemia


19. Aplastic Anaemia---- is the type of anaemia due to bone marrow failure resulting to decreased of all cell lines


20. Megaloblastic anaemia – anaemia resulting from either folic acid or vitaminB12 deficiency


21. Anaemia of any chronic illness is morphologically termed as

Ø Normocytic normochromic anaemia or microcytic normochromic anaemia

22. Physiologic adaptations- usually represent responses of cells to normal stimulation by hormones or endogenous chemical mediators (e.g. the hormone-induced enlargement of the breast and uterus during pregnancy).


23. Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury eg. Left ventricular enlargement


24. What is Atrophy---It is a decrease in the size (shrinkage) of the cell, tissue or organ which is brought by decrease in substances within cells.  Atrophic cells may have diminished function but are not dead.


25. List five causes of atrophy

a. A decreased workload (e.g. immobilization of a limb to permit healing of a fracture)

b. Loss of innervations

c. Diminished blood supply

d.  Inadequate nutrition

e. Loss of endocrine stimulation

f. Aging (senile atrophy)


26. Hypertrophy--- An increase of cell size which results in the increase of organ size and thus the hypertrophied organ has no new cells just larger cells.


27. Hyperplasia--It is an increase in the number of cells in an organ or tissue usually results in increased size of the organ or tissue.


28. Metaplasia-A reversible change in which one mature differentiated cell type (epithelial or mesenchymal) is replaced by another mature differentiated cell type.


29. Dysplasia is characterized by a constellation of changes that include loss in the uniformity of individual cells as well as a loss in their architectural orientation


30. Apoptosis--A form of cell death in which a programmed sequence of events leads to the elimination of cells without releasing harmful substances into the surrounding area


31. Causes of Apoptosis

Ø Programmed cell death is as needed for proper development as mitosis

Ø The formation of the fingers and toes of the foetus requires the removal, by apoptosis, of the tissue between them.

Ø The sloughing off of the inner lining of the uterus (the endometrium) at the start of menstruation occurs by apoptosis.

Ø Programmed cell death is needed to destroy cells that represent a threat to the integrity of the organism.

Ø Cells infected with viruses , one of the methods by which cytotoxic T lymphocytes (CTLs) kill virus-infected cells is by inducing apoptosis

32. What is necrosis -- refer to a series of changes that accompany cell death, largely resulting from the degradative action of enzymes on lethally injured cells.


33. List the five types(patterns) of necrosis

Ø Coagulative necrosis

Ø Liquefactive necrosis

Ø Gangrenous necrosis

Ø Caseous necrosis

Ø Fibrinoid necrosis


34. Coagulative necrosis --A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved for at least several days


35. Liquefactive necrosis--microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest (liquefy) the tissue.


36. Gangrenous necrosis--When bacterial infection is superimposed, coagulative necrosis is modified by the liquefactive action of the bacteria and the attracted leukocytes (so-called wet gangrene).


37. Caseous necrosis is often enclosed within a distinctive inflammatory border; this appearance is characteristic of a focus of inflammation known as a granuloma example in TB


38. Fibrinoid necrosis----This pattern of necrosis is prominent when complexes of antigens and antibodies are deposited in the walls of arteries.


39. Ischemia, is a diminished blood flow to a tissue



40. An infarction that is, an area of tissue death (necrosis) due to a local lack of oxygencaused by obstruction of the tissue's blood supply.


41. Chronic inflammation is inflammation of prolonged duration (weeks to months to years) in which active inflammation, tissue injury, and healing proceed simultaneously.


42. Causes  of chronic inflammation are:

Ø Chronic inflammation following acute inflammation

Ø Recurrent attacks of acute inflammation

Ø Chronic inflammation starting from agents known to cause chronic inflammatory response rather than acute



43. General Features of Chronic Inflammation

Ø Mononuclear cell infiltration

Ø Tissue destruction or necrosis

Ø Proliferative changes


44. reticulo-endothelial system comprises which organs, list any five

Ø The liver (where they are called kupffer cells)

Ø Spleen

Ø  lymph nodes

Ø Central nervous system (microglial cells)

Ø Lungs (alveolar macrophages)


45. chronic inflammatory cells include lymphocytes, plasma cells, eosinophils and mast cells.


46. Chronic non-specific inflammation ---It is characterised by non-specific inflammatory cell infiltration such as chronic osteomyelitis and lung abscess.A variety of this type of chronic inflammatory response is chronic suppurative inflammation in which infiltration by polymorphs and abscess formation is additional features e.g. actinomycosis.


47. Chronic granulomatous inflammation--Granulomatous inflammation is a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages that assume an epithelioid appearance.Granulomas are encountered in certain specific pathologic states.


48. Granulomatous inflammation---Is defined as a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages that assume an epithelioid appearance.


49. Granuloma---It is defined as a circumscribed, tiny lesion, about 1 mm in diameter, composed predominantly of collection of modified macrophages called epitheliod cells and rimmed at the periphery by lymphoid cells.


50. Examples of Diseases with Granulomatous Inflammation

Ø Tuberculosis  ( causative organisms - Mycobacterium tuberculae)

Ø Leprosy (causative organisms -  Mycobacterium leprae)

Ø Syphilis (causative organism - Treponema pallidum)

Ø Cat-scratch disease (Gram-negative bacillus)

Ø Sarcoidosis (Unknown aetiology)

Ø Crohn’s disease or inflammatory bowel disease (Immune reaction against intestinal bacterial, self-antigens)

Ø Schistosomiasis

Ø Histoplasmosis

Ø Cryptococcal


51. Systemic Effect of Inflammation, Acute and Chronic

Ø Fever

Ø Increased heart rate and blood pressure

Ø Decreased sweating,

Ø wasting syndrome

Ø Anaemia

Ø Elevated Erythrocytes Sedmentation Rate (ESR)

Ø Amyloidosis


52. Chronic bronchitisis the inflammation of the bronchial mucous membrane, characterized by cough, hypersecretion of mucus, and expectoration of sputum over a long period of time and associated with increased vulnerability to bronchial infection.


53. Bronchiectasis--It is a permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, resulting from or associated with chronic necrotizing infections.


54. Lung emphysema is characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis


55. Atelectasis, also known as collapse, is loss of lung volume caused by inadequate expansion of airspaces.


56. Resorption atelectasis occurs when an obstruction prevents air from reaching distal airways.


57. Compression atelectasis (sometimes called passive or relaxation atelectasis) is usually associated with accumulations of fluid, blood, or air within the pleural cavity, which mechanically collapse the adjacent lung.


58. Contraction (or cicatrization) atelectasis occurs when either local or generalized fibrotic changes in the lung or pleura Favour expansion and increase elastic recoil during expiration.


59. Atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque.

60. An aneurysm is a localized abnormal dilation of a blood vessel or the heart.

61. causes of  aneurysms include

Ø Trauma

Ø Congenital defects (e.g. berry aneurysms)

Ø Infections (mycotic aneurysms), or syphilis

Ø Arterial aneurysms can also be caused by systemic diseases, such as vasculitis


62. Varicose veins are abnormally dilated, tortuous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support   When legs are dependent for long periods, venous pressures in these sites can be markedly elevated (up to 10 times normal) and can lead to venous stasis and pedal edema, even in essentially normal veins (simple orthostatic edema).


63. Features of the Varicose veins

Ø Wall thinning at the points of maximal dilation with smooth muscle hypertrophy

Ø Intimal fibrosis in adjacent segments

Ø Elastic tissue degeneration

Ø Spotty medial calcifications (phlebosclerosis)

Ø Focal intraluminal thrombosis (due to stasis)

Ø Venous valve deformities (rolling and shortening)


64. Point mutations result from the substitution of a single nucleotide base by a different base, resulting in the replacement of one amino acid by another in the protein product.


65. Frameshift mutations occur when the insertion or deletion of one or two base pairs alters the reading frame of the DNA strand.


66. Genetic disorders are divided into three major categories

Ø Those related to mutant genes of large effect (single gene mutations)

Ø Diseases with multifactorial (polygenic) inheritance

Ø Those arising from chromosomal aberrations


67. Autosomal dominant-- type of inheritance the mutated gene that determines the abnormal phenotype is dominant to that coding for normal development. Thus the presence of the abnormal gene inevitably leads to disease.


68. Examples of autosomal recessive diseases are

Ø Sickle cell anemia

Ø Thalassemias

Ø Congenital adrenal hyperplasia

Ø Metabolic disorder such as cystic fibrosis and phenylketonuria


69. A multifactorial physiologic or pathologic trait may be defined as one governed by the additive effect of two or more genes of small effect, conditioned by environmental, non-genetic influences.


70. The following features of multifactorial inheritance

Ø These have been established for the multifactorial inheritance of congenital malformations and, in all likelihood, obtain for other multifactorial diseases.

Ø The risk of expressing a multifactorial disorder is conditioned by the number of mutant genes inherited.

Ø The risk is greater in siblings of patients having severe expressions of the disorder.

Ø The rate of recurrence of the disorder (2% to 7%) is the same for all first-degree relatives of the affected individual.

Ø If parents have had one affected child, the risk that the next child will be affected is between 2% and 7%.

71. What is shock----A clinical syndrome which follows critical reduction of blood flow within the microcirculation with inadequate tissue perfusion and oxygen delivery to meet nutritional requirements of cells and removal of waste products of metabolism


72. Types of shock

ü Cardogenic shock

ü Hypovolaemic/haemorrhagic  shock

ü Septic shock

ü Anaphylactic shock

ü Neurogenic shock


73. Causes of cardiogenic shock include

ü Heart attack, heart failure and cardiomyopathy

ü Valvular heart disease (VHD)

ü Cardiac arrhythmias


74. Septic shock is a serious condition that occurs when an overwhelming infection/septicaemia leads to low blood pressure and low blood flow.


75. Anaphylactic Shock--Widespread immunoglobulin E hypersensitivity reaction to a specific antigen resulting in vasodilation and increased vascular permeability leading to decreased perfusion and impaired cellular


76. Cause of anaphylactic shock include

Ø Insect bites/stings, horse serum (used in some vaccines), food allergies, and drug allergies.

Ø Pollens and other inhaled allergens rarely cause anaphylaxis.

Ø Some people have an anaphylactic reaction with no identifiable cause


77. Common causes of spinal injury are

Ø Spinal cord injury

Ø Central nervous system injuries

Ø Severe pain


78. Compensatory mechanisms of shock involves:

Ø Increased heart rate

Ø Constriction of peripheral blood vessels

Ø Dilatation of coronary and cerebral vessels


79.  List the five causes of insulin secretin

Ø glucose metabolism in the cells(The normal blood glucose is maintained within the narrow range of 4.4 – 6.6 mmol/L. (80 –120mg/dl)

Ø It maintains appropriate concentration of sugar in the plasma and the cells/tissues

Ø stimulate lipogenesis and increases fat storage (fat sparing effect)

Ø  stimulate protein synthesis directly

Ø  assist the maintenance of intracellular potassium ion concentration.


80. Acute complication of diabetes mellitus are

Ø Diabetic ketoacidosis (DKA) nonketotic hyperosmolar state (NKHS), Hypoglycemia are acute complications of diabetes.



81.  Chronic complication of diabetes mellitus

• The vascular complications of DM are further subdivided into

ü Microvascular

• Retinopathy

• Neuropathy

• Nephropathy

ü Macrovascular Complications

• Coronary Artery Disease

•  Peripheral Vascular disease leading to diabetic foot

•  Cerebrovascular disease

Ø Nonvascular complications include problems such as

• Gastroparesis

• Sexual dysfunction

• Skin changes


82. nnate immunity (also called natural, or native, immunity) is mediated by cells and proteins that are always present and poised to fight against microbes and are called into action immediately in response to infection.

83. Immediate (Type I) Hypersensitivity --- This results from the activation of the CD4+ helper T cells by environmental antigens, leading to the production of IgE antibodies, which become attached to mast cells


84. Antibody-Mediated (Type II) Hypersensitivity These disorders are caused by antibodies that bind to fixed tissue or cell surface antigens and promote phagocytosis and destruction of the coated cells or trigger pathologic inflammation in tissues


85. Immune Complex-Mediated (Type III) Hypersensitivity The disorders are caused by antibodies binding to antigens to form complexes that circulate and may deposit in vascular beds and stimulate inflammation, typically secondary to complement activation


86. T-Cell-Mediated (Type IV) HypersensitivityThe disorders are cell-mediated immune responses in which T lymphocytes cause tissue injury, either by producing cytokines that induce inflammation and activate macrophages, or by directly killing host cells.


87. Autoimmunity is a state in which the body’s immune system fails to distinguish between self and non self by formation of auto antibodies against one’s own tissues.


88. Haemostasis---A process that prevents excessive blood loss in the body.


89. Thrombosis---It is the formation of a clot in the blood that either blocks, or partially blocks a blood vessel.


90. Risk Factors for Thrombosis

Ø Age (as the age increases so the risk)

Ø Obesity

Ø Varicose veins

Ø Immobility

Ø Pregnancy

Ø High estrogen levels

Ø Previous history of DVT

Ø Surgery and trauma of the pelvis, lower limbs

Ø Heart failure

Ø Recent myocardial infarction

Ø Lower limb paralysis

Ø Cigarette smokin


91. Platelet adhesion ---When platelets detect damage to a blood vessel they begin to adhere to the exposed surfaces


92. Platelet release reaction --Once stuck to a site of damage, the platelets begin to change

93. Mural thrombi--Thrombi occurring in heart chambers or in the aortic lumen

94. Arterial thrombi---These occur in the arteries and are frequently occlusive and are produced by platelet and coagulation activation


95. Venous thrombosis (phlebothrombosis)--Occur along veins and are almost invariably occlusive, and the thrombus can create a long cast of the lumen


96. An embolism is an obstruction in a blood vessel due to a blood clot or other foreign matter that gets stuck while travelling through the bloodstream


97.  What are the functions of the extracellular matrix

Ø Mechanical support for cell anchorage, cell migration, and maintenance of cell polarity.

Ø Control of cell growth.

Ø ECM components can regulate cell proliferation by signaling through cellular receptors of the integrin family.

Ø Maintenance of cell differentiation.

Ø  Storage and presentation of regulatory molecules. For example, growth factors like FGF and HGF are excreted and stored in the ECM in some tissues.

Ø Scaffolding for tissue renewal.

Ø The maintenance of normal tissue structure requires a basement membrane or stromal scaffold.


98. Primary wound healing

ü This is also known as healing by first intention.

ü Occurs within hours of repairing a full-thickness surgical incision when edges of the wound are in aposition.

99. Delayed primary wound healing

ü Occurs if the wound edges are not reapproximated immediately

100. This is also known as healing by secondary intention. ----Secondary healing results in an inflammatory response that is more intense than with primary wound healing.

101. Pneumonia is inflammation of lung parenchyma due to infectious agent( eg. Bacteria) while pneumonitis is inflammation of lung paranchyma due to chemical substances (eg. Aspiration of food, water )


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