Etiological and Predisposing causes.pptx

7/28/2019 Etiological and Predisposing causes.pptx

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Cellular Alteration


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ATROPHY

Decrease in cell size resulting from decreasedworkload, loss of nerve supply, decreased blood

supply, inadequate nutrition, or loss of hormonal

stimulation

Physiologic atrophy occurs due to aging

Disuse atrophy dec workload on muscle ->

shrinkage

Loss of nerve supply gradual atrophy -> muscle

wasting

Chronic Ischemia

Starvation and malnutrition


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HYPERTROPHY

Increase in the size of individual cells =increasing mass without increasing the number of

cells


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HYPERPLASIA

Common condition seen in cells under increasedphysiologic workload or stimulation

Capable of dividing and increasing their number

Physiologic hyperplasia puberty and pregnancy

Compensatory hyperplasia regenerates lost

substance

Pathologic hyperplasia abn stimulation of a gland

or other hormones


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METAPLASIA

Reversible change in which one type of adult cellis replaced by another type


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Cellular Injury and Death


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May be caused by microorganisms, lack ofoxygen, physical agents and radiation

Anoxia lack of oxygen

Apoptosis program cell death/ suicide


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ISCHEMIA

Critical lack of blood supply to a localized area

Reversible when O2 supply is back

May precede infarction of the tissue pathologic

changeAssociated with atherosclerosis

Classical conditions: Angina pectoris and

Intermittent claudification


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THROMBOSIS

Formation of a clot onthe intimal lining of the

blood vessels

May increase or totally

occlude blood flow in

the vessel


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EMBOLISM

Broken thrombus

travelling mass in the blood

Obstruction caused by an

embolusembolic

occlusion

Occludes the arterial

tributary, compromises

blood flow to the areasupplied


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INFARCTION

Occlusion of blood supply from an artery causes,localized area of tissue death due to lack of blood

supply

Infarcted tissue has red appearance due to

hemorrhage

Bacterial growth is common and may be present

in the area


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NECROSIS

Cell or tissue death

Cell dies mitochondria swells >

disrupted organelle function >

membranes rupture > lysosomalenzymes released to the tissues

Nucleus undergoes specific changes

shrinking, fragmenting, gradual fading


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Coagulative Necrosis

Usually results from lack of bloodsupply to an area

most common pattern of necrosis

Cell structure may be preserved

but nucleus, organelles are lost


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Caseation Necrosis

Also known as caseous necrosis

Long been described related to

tuberculosis

Structureless necrosis

Center is soft and friable with a

cheesy and crumbly appearance


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Fat Necrosis

Specific form of cellular death thatoccurs when lipases escape into fat

storages

Causes patchy necrosis of the

pancreas and surrounding tissues


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Gangrenous Necrosis

Combination of coagulative andliquefactive necroses

gangrene black, foul-smelling area that

is adjacent to the liver tissue Cause of tissue death is ischemia but

bacteria and leukocytes causes

liquefaction Coagulant necrosis is dominant dry

gangrene

Liquefactive necrosis is dominant wet


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APOPTOSIS

Distinctive type of cell death inwhich single or small groups of cells

are deleted from their tissue of

origin

Can be normal or programmed cell

deathMay be initiated by an endogenous

endonuclease that causes

destruction of the DNA in the cell


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SOMATIC DEATH

Is death of the body

Irreversible changes occur in cells

and organs due to lack of oxygen

supply

Rigor mortis develops due to

deplation of ATP in the musclesLiver Mortis reddish blue

Algor Mortis


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Etiological and Predisposing

Factors of Cancer


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The etiology of cancer is multifactorial,with genetic, environmental, medical,and lifestyle factors interacting to

produce a given malignancy.

Most cancer is caused by genetic

mutationsoften, by a series ofmutations.


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Abnormalities in the genetic material due to:

Error in DNA replication (randomlyacquired).

Effects of carcinogens, such as tobaccosmoke, radiation, chemicals, or infectious

agents.

Inheritance, and thus present in all cells

from birth.


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tobacco

Polycyclic aromatic, hydrocarbons, nitrosamines,aromatic amines, aldehydes (carcinogenic

agents)

Duration of smoking and number of cigarettes

smoked are + correlated with cancer risk

Oral cavity, pharyngeal, laryngeal, lung and

esophageal cancers are increased among

cigarette smokers

Alcohol exhibits synergistic effects further inc. oral

cancers

Passive smoking, inhaling second-hand smoke

increases the risk of lung cancer


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alcohol

Plays a role in induction of cancer by increasingeffectiveness of carcinogens

Chronic alcohol consumption commonly lead to

cirrhosis

Moderate alcohol ingestion breast cancer,

pancreatic cancer


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diet

High in fat and low- fiber diet large bowel,breast, prostate, ovary, endometrium, pancreas,

colorectal

Single diet preference

High temperature cooking

Direct ingestion of Aflatoxin B (molds found in

corn, barley, peas, rice, soybeans)

Pickled, salt- cured, processed, canned foods(nitrates)

Vitamin deficiencies


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chemicals

Asbestos, Chromium, Nickel, Cadmium

Pollution


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pharmaceutical agents

Arsenic compounds Diethylstilbestrol adenocarcinoma in preg

women

Estrogens endometrial and breast cancers

Androgens, oral contraceptives hepatic tumors

Alkylating agents

Immunosuppresive agents


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radiation

X- ray Uranium radioactive substances

Ionizing radiation

Ultraviolet radiation


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infectious agents

Carcinogenic or oncogenic viruses (DNA & RNAvirus)

- Hepa B, Hepa C

- Herpes simplex type 2

- Epstein Barr

- Human T- cell leukemia

- Human papillomaviruses


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endegenous hormones

Estrogen Testosterone


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genetics

Autosomal recessive disordersAutosomal dominant disorders

X-linked recessive disorders

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Etiological and Predisposing causes.pptx