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ISLAMIC MEDICAL EDUCATION RESOURCES 04

0007-PATHOLOGICAL PROCESSES: REPAIR & RESTORATION OF EQUILIBRIUM (RUJU ILA AL ITIDAL)

Lecture to 1st year medical students by Professor Omar Hasan Kasule sr.

OUTLINE

6.5.1 PATHOLOGICAL PROCESSES

A. Inflammation

B. Genetic Disorders

C. Infection

D. Immunity

E. Neoplasia:

 

6.5.2 PATHOLOGICAL MANIFESTATIONS

A. WOUND HEALING

B. THROMBOSIS

C. EMBOLISM

D. EDEMA

E. CARDIOVASCULAR

 

6.5.1 PATHOLOGICAL PROCESSES

A. INFLAMMATION

Definition: Inflammation is protective. It destroys, dilutes, or walls off the injurious agent. It is followed by the repair process. Both the inflammatory reaction and the repair process could be harmful if they get out of control.

 

Acute inflammation: Acute inflammation has three components: vascular dilation, permeability, and cell migration. Vaso dilation increases blood flow. Increased permeability allows plasma protein and leucocytes to leave the circulation. Leucocytes migrate to the site of injury to phagocytise the micro-organism of other particulate matter causing the inflammation. Tissue damage is caused by release of toxic material. The chemical mediators of inflammation are: histamine, serotonin, the complement fixation system, the kinin system and the clotting system. Inflammation has the following systemic effects: fever, decreased slow wave sleep, decreased appetite, increased protein degradation, lower blood pressure, increased liver synthesis of acute-phase proteins, and increase in leucocytes.

 

Chronic inflammation: Chronic inflammation is inflammation prolonged for weeks or months and in which the processes of destruction and repair co-exist. It may be due to persistent infection, prolonged exposure to toxic agents, or autoimmune. It has 4 characteristics. The site of inflammation is Infiltrated by mono-nuclear cells, macrophages, lymphocytes, and plasma cells. Tissue destruction continues. Repair attempts are made using connective tissue to replace destroyed tissue. Fibrosis occurs when fibrous tissue is the replacement and angiogenesis when vascular tissue is the replacement. Granulomas may eventually form at the inflammation site.

 

B. GENETIC DISORDERS

Many advances have been made recently in understanding the molecular basis of human disease. This has given hope to development of new technology in the fight against disease. Disease diagnosis using molecular probes provided by recombinant DNA technology can identify many genetic diseases. Gene therapy is around the corner.

 

Mutations are permanent changes in DNA that can arise in both germ and somatic cells. There are three types of mutations:  genome mutations, chromosomal mutations, and gene mutations. Genome mutations involve loss of a whole chromosome. Chromosomal mutations involve rearrangement of chromosomes.

 

Mendelian disorders: Mendelian disorders are due to mutations in single genes. There are over 4500 Mendelian disorders but most are recessive and do not present any clinical problems. A gene can be recessive or dominant. In co-dominance both alleles are expressed. Mendelian disorders can present in three ways: autosomal dominant, autosomal recessive, and X-linked.

 

Single-gene disorders: Single gene disorders cause disease in the following ways: enzyme defects, defects in membrane receptor and transport systems, alterations in non-enzyme protein, and unusual reaction to drugs.

 

Polygenic disorders: 2 or more genetic factors are involved

 

Disorders with multifactorial inheritance: These are disorders with both environmental and genetic factors. More than one gene may be involved.

 

C. INFECTION

The following are the main categories of infectious agents: viruses, bacteria, bacteriophages, plasmids, transposons, fungi, protozoa, helminths, and ecto-parasites. Microbial infectious agents cause tissue damage by destroying the host cell, releasing endo and exo-toxins, and eliciting host cellular responses that lead to further damage. The organisms use the following immune evasion methods to avoid being destroyed by the host immune system: being inaccessible to the immune system, resisting lysis of phagocytosis, changes in their antigens, and causing immune suppression. The inflammatory response to infection may take any of the following forms: suppurative inflammation, granuloma formation, viral cytopathic inflammation, viral cytoproliferative inflammation, necrotizing inflammation, chronic inflammation and scarring.

 

D. IMMUNITY

The cells of the immune system are: T lymphocytes, B lynphocytes, macrophages, langhans cells, and NK cells.

 

The disorders of the immune system are: hypersensitivity, auto-immune disorders (break-down of self-tolerance), immunological deficiency syndromes (primary and acquired), and amyloidosis.

The host has mechanical and immunological surface barriers to infection. It is only when they are overwhelmed that hematogenous spread of infection occurs.

 

E. NEOPLASIA:

Neoplasia means new growth. It is excessive unco-ordinated autonomous growth. It ma be benign or malignant. The malignant growths differ from the benign by being poorly differentiated, anaplastic, growing rapidly, local invasion, and distant metastasis. The following factors are involved in neoplasia: age, heredity, and environment, and genetic changes. Environmental carcinogenesis can be chemical, radiation, or viral carcinogenesis.

 

Oncogenes: The discovery of oncogenes enables understanding of the molecular basis of carcinogenesis. Oncogenes are necessary for normal functioning of cells. They are activated by retroviruses, chromosomal translocation, gene amplification, and mutation. Tumor suppressor genes bring about a balance by mitigating the effects of oncogenes.

Multi-step carcinogenesis:  

Tumor immunity: Tumor antigens and immunological surveillance 

6.5.2 PATHOLOGICAL MANIFESTATIONS

A. WOUND HEALING

Types: wound healing may be primary union (healing by first intention) or secondary union (healing by secondary intention).

 

B. THROMBOSIS

Thrombosis is a pathological process being an extension of normal hemostasis. It is caused by the following: injury to the endothelium, alterations in blood flow, alterations in blood leading to hyper-coagulability. Thrombosis could develop into disseminated intra-vascular coagulation that depletes clotting factors and leads to hemorrage. Once formed the thrombus can have one of the following fates: propagation, embolisation, dissolution, organisation, and recanalisation.

 

C. EMBOLISM

Arises as a complication of thrombosis. Emboli could also be systemic, amniotic fluid, air and fat emboli.

 

D. EDEMA

Edema is accumulation of fluid in the intecelullar space. Inflammatory edema is due to increased vascular permeability. Non-inflammatory edema is due to hemodynamic changes such as increased hydrostatic pressure in congestive cardiac failure, decreased oncotic pressure in protein malnutrition, sodium retention, and lymphatic obstruction.

 

E. CARDIOVASCULAR

 

HYPEREMIA and CONGESTION

Due to CCF and venous obstruction

 

HEMORRHAGE

Due to injury

 

INFARCTION

Infarction is ischemic necrosis of a tissue or organ due to occlusion or arterial supply or venous drainage.

 

SHOCK

Shock is circulatory collapse. Its causes are: cardiogenic shock in congestive cardiac failure, hemorrhagic shock, septic shock and neurogenic shock (simultaneous failure of all control mechanisms).

Professor Omar Hasan Kasule July 2000