PRELIM Flashcards
This the study of the structural and function changes in cells tissues, organs and organs that underlie disease.
PATHOLOGY
changes in morphology
STRUCTURAL
reproduce without the process of telophase
PROKARYOTIC
reproduce through sexual reproduction
EUKARYOTIC
CORE OF PATHOLOGY:
- Etiology or Cause.
- Pathogenesis or mechanism of development.
- Morphology or the structural alterations induced in the cells and organs of the body.
the functional consequences of the morphologic changes
Clinical significance
the body reacts (repair)
INFECTION
Example of infection
TB
Example of infection is TB
Caused by
Mycobacterium tuberculae or acid fast bacilli
dye used after collecting the specimen
Acid fast stain
Mycobacterium leprae and tuberculae has the same mode of treatment
quadruple antibacteria
has the same mode of treatment (quadruple antibacterial)
Mycobacterium leprae and tuberculae
genesis of cancer
CARCINOMA
Our forefathers have always believed that infirmity was caused by
evil spirits
This involves the examination of the ill body parts, the most obvious tool for which is
autopsy
WHAT it was stopped by the church because according to them, human is a sacred body AND WHEN
Holy ghost
In 14th century
German physician who is considered the father of Pathology.
RUDOLF VIRCHOW
Based on the Eber’s papyrus discovered in the Nile Valley which speaks of the different types if bone injuries.
EGYPTIANS
They are also credited for their contribution the art for serving the dead called EMBALMING.
EGYPTIANS
EGYPTIANS, They are also credited for their contribution the art for serving the dead called.
EMBALMING.
Based on theWHATdiscovered in the Nile Valley which speaks of the different types if bone injuries.
Eber’s papyrus
Based on the Eber’s papyrus discovered in WHERE which speaks of the different types if bone injuries.
Nile Valley
Father of medicine
HIPPOCRATES
He wrote different theories of disease.
HIPPOCRATES
He also wrote on wounds, inflammation and tumors, hemorrhoids, malaria and tuberculosis.
HIPPOCRATES
He is one of the founders of Zoology
ARISTOTLE
ARISTOTLE
He is one of the founders of
Zoology
WHO Laid the ground work in human anatomic dissection.
ARISTOTLE
He is by considered as the greatest medical figure of medicine
GALEN OF PERGAMUM
Two Types of etiologic factors of disease:
INTRINSIC OR GENETIC
ACQUIRED
A problem in the organism e.g. congenital
INTRINSIC OR GENETIC
from within the organism/ born with it
INTRINSIC OR GENETIC
DIFFRENET TYPES OF ACQUIRED
Infections- caused by bacteria, virus, protozoa, and fungus
Nutritional- edge of an acceptable normal range
Chemical- form of vitamins
Physical-
caused by bacteria, virus, protozoa, and fungus
Infections-
edge of an acceptable normal range
Nutritional
form of vitamins
Chemical
form of accidents, inhalation, radiation, and any physical hazard
Physical
born with the disease; present during 1-2 years
CONGENITAL
causes abnormality to the baby
TERATOGENIC EFFECT
is a substance that interferes with normal fetal development and causes congenital disabilities
teratogen
explosion of radiologic power plant
CHERNOBYL
termination; NOT more than 20 weeks or age of viability; NOT more than 500 grams
ABORTION
PATHOGENESIS MEANING
PATHO= abnormality
GENESIS= creation of
This is the production and development of disease
PATHOGENESIS
refers to the sequence of events in the response of cells or tissues to injury
Pathogenesis
This is the development of a disease and the chain of events leading to that disease.
Pathogenesis
Refers to the structural changes in the cell or tissue
MORPHOLOGY
It is the process of progression and nature of disease
MORPHOLOGY
Development of morbid condition or disease more specifically the cellular events and reactions and other mechanisms occurring in the development of disease
MORPHOLOGY
A change in a patient’s/subject’s clinical status regarded as important, whether or not it is due to an intervention in the context of a clinical trial
CLINICAL SIGNIFICANCE
A property of cells, tissues, and organisms that allows the maintenance and regulation of the stability and constancy needed to function properly.
HOMEOSTASIS
More severe physiologic stresses and some pathologic stimuli may bring about a number of physiologic and morphologic cellular change
ADAPTATION
Local reactive change in tissues following injury or irritation
INFLAMMATION
It is a progressive reaction in living tissues, accompanied or followed by the process of repair or healing
INFLAMMATION
The injury causes altered metabolism which liberates compounds which initiates inflammatory process
INFLAMMATION
It is a protective reaction of the body to localize or dispose the injurious agent and set the stage for tissue repair
INFLAMMATION
Conditions show the signs of inflammatory reaction in other portions of the body like the lung and joints.
INFLAMMATION
SIGNS OF ACUTE INFLAMMATION
PAIN / DOLOR
HEAT / CALOR
REDNESS / VASCULAR CONGESTION / RUBOR
TUMOR
Produced by swelling and tension of tissues caused by the exudates with pressure on the nerves
PAIN / DOLOR
Accumulation of chemical substances like kinins and hydrogen ion, irritate the nerve endings
PAIN / DOLOR
There is disruption of cellular and tissue function
PAIN / DOLOR
the fluid produced by a wound as it heals
EXUDATE
Increase in the temperature of the particular area
HEAT / CALOR
Primarily due to dilatation of blood vessels and increase in the amount of circulation in the area
HEAT / CALOR
A response of body tissues to injury or irritation
REDNESS / VASCULAR CONGESTION / RUBOR
This characterized by pain and swelling and redness and heat
REDNESS / VASCULAR CONGESTION / RUBOR
Primarily due to vascular dilation and congestion
REDNESS / VASCULAR CONGESTION / RUBOR
A swollen part, swelling, protuberance.
TUMOR
This is an abnormal growth of body tissue
TUMOR
Swelling is due to the accumulation of exudates within the tissue
TUMOR
This is almost always secondary to tissue trauma or injury
TUMOR
is added to the organ name to indicate an inflammatory reaction.
itis
An injury or illness can involve acute, or short-term, inflammation.
ACUTE INFLAMMATION
can continue for months or years. It either has or may have links to various diseases.
CHRONIC INFLAMMATION
Agents Causing Cell Injury:
Physical
Chemical
Traumatic
Microbial
Immunologic
Radiation
FUNDAMENTAL RESULTS OF INJURY TO THE TISSUE
HYPERTROPHY
HYPERPLASIA
ATROPHY
METAPLASIA
DYSPLASIA
DEGENERATION
NECROSIS
COMMON TYPES OF NECROSIS
COAGULATION NECROSIS
CASEOUS NECROSIS
GUMMTOUS NECROSIS
LIQUIFACTIVE NECROSIS
FAT NECROSIS
GANGRENE
refers to an increase in the size of cells resulting in an increase in the size of the organ
HYPERTROPHY
Increase in the cell size depend on nutrition and extraneous stimulus
HYPERTROPHY
Enlargement or overgrowth of an organ or part of the body due to the increased size of the constituent cells
HYPERTROPHY
Most commonly seen in somatic body parts secondary to exercise
HYPERTROPHY
an increase in the number of cells in an organ or tissue
HYPERPLASIA
This results in the in increase volume of the organ or tissue
HYPERPLASIA
This is an increase in the rate of reproduction of cells probably influenced by hormones
HYPERPLASIA
This sets the stage in abnormal cellular proliferation which brings carcinomatous growth in the organ
HYPERPLASIA
Acquired decrease in the size of an organ that were once normal
ATROPHY
It may be caused by a reduction in size or number of component cells
ATROPHY
It could also be caused by inadequate nutrition or oxygenation
ATROPHY
There is disturbance in function
ATROPHY
results from a reduction in the structural components of the cell
ATROPHY
These cells have decreased function but are not dead
ATROPHY
Most Common Causes of Atrophy:
Decreased in work load
Inadequate nutrition
Loss of endocrine stimulation
Aging
Pressure
This is a reversible change in which one adult cell is replaced by another adult cell type
METAPLASIA
This may generally be a part of normal maturation process or caused by some sort of abnormal stimulus
METAPLASIA
is not synonymous with dysplasia and is not directly considered carcinogenic
METAPLASIA
An abnormal development of cell or tissue, often a precancerous stage of growth
DYSPLASIA
This alteration in size, shape, and organization of adult
DYSPLASIA
This has always been considered a pre-cancerous lesion reoffered to an in situ lesion
DYSPLASIA
There is disturbance of intracellular metabolism
DEGENERATION
There is swelling of the cell with organelle engorgement
DEGENERATION
Accumulation in the cytoplasm of substances that normally are invisible, absent or present only in small amounts
DEGENERATION
They vary in severity and are generally reversible
DEGENERATION
commonly produced by the cutting off of the blood supply thus causing infarction.
COAGULATION NECROSIS
tissue death
INFARCTION
cheesy macroscopic appearance, architectural outline is lost.
CASEOUS NECROSIS
Seen in tuberculosis infection
CASEOUS NECROSIS
seen as a consequence to syphilis infection
GUMMTOUS NECROSIS
the dead area softens and eventually liquefies
LIQUIFACTIVE NECROSIS
It is primarily seen in central nervous system injury
LIQUIFACTIVE NECROSIS
seen in pancreatic disease where there is a release of enzymes that exacerbate tissue injury
FAT NECROSIS
necrosis with the presence of putrefaction of bacteria
GANGRENE
This requires immediate amputation and antibiotic coverage with broad spectrum antibiotics
GANGRENE
Intrauterine Viral Infections:
Rubella
Cytomegalovirus (CMV)
Varicella-Zoster (VZV)
Enteroviruses
HIV
Hepatitis C
Hepatitis B
Japanese Encephalitis
Perinatal and Neonatal Infections:
Human Herpes Simplex
Enteroviruses
HIV
Hepatitis B
Previously Known as TORCH Infections:
Toxoplasmosis, Other( syphilis)
Rubella
Cytomegalo virus
Herpes
Hepatitis which is acquired post-natally
Hepatitis which is acquired post-natally
signs that hydrocephalus, diffuse intracranial chorioretinitis
toxoplasma gondi
cardiac defects, sensrineural hearing loss, cataracts
rubella virus
micrcephalus, periventricular calcification
cytomegalovirus
signs that vesicular lesions, keratoconjunctivitis
herpes simplex virus
signs that bullous macular and eczematous skin lesions involving the palms and the soles; rhinorrhea dactylitis and other signs of osteochronditis and periostitis
treponerma pallidum
signs that lim abnormalities, cicatricial lesions
varicella-zoster-virus
signs that severe thrush, failure to thrive, recurrent bacterial infections, calcifications of the basal ganglia
human immunodefiency virus
which is acquired post-natally
Hepatitis
this term is now obsolete due to HIV
TORCH
Most fetuses, if infected during the first trimester, will suffer from a
syndrome of congenital malformation.
Also known as GERMAN MEASLES
The fetus is most at risk in the first 16 weeks gestation
RUBELLA
RUBELLA
Also known as GERMAN MEASLES
The fetus is most at risk in the first 16 weeks gestation
Causative Organism:
Rubella virus ( togaviruses RNA)
RUBELLA
Route of Infection:
via respiration as the virus is concentrated in the nasopharyngeal secretions.
RUBELLA
Incubation Period:
14-21 days.
RUBELLA
Symptoms:
Mild pyrexia
Arthralgia
Rash which persists for a week and always affects the face
Lymphadenopathy in the postauricular, deep cervical, and suboccipital lymph node precedes the appearance of the rash and persists for 3 weeks
Risk of Fetal Transmission: RUBELLA
50-60% of fetuses are affected if maternal primary infection is in the first month of gestation.
22% in the second month, 6-10% in the third to fourth month.
RUBELLA
Routine Antenatal Screening:
Vaccination ( avoid pregnancy for 3 months)
RUBELLA
Maternal Screening:
Routine rubella IgG in the first trimester
If infection is suspected perform rubella IgM
RUBELLA
Prevention:
Vaccination before or after pregnancy (not during).
In acute infection: droplet precautions.
In neonatal infection: contact precautions.
In the United Kingdom this causes more congenital abnormalities than rubella.
Infects 50-60% of women of childbearing age.
CYTOMEGALOVIRUS (CMV)
Causative Agent: CYTOMEGALOVIRUS (CMV)
CMV (Herpes virus DNA)
Maternal Symptoms: CYTOMEGALOVIRUS (CMV)
Usually mild or asymptomatic, fever with/without lymphadenopathy, sore throat.
Transmission: CYTOMEGALOVIRUS (CMV)
DIRECT (person to person contact)
Saliva
Milk
Urine
Semen
Tears
Stools
Blood, Cervical secretions Vaginal Secretion
INDIRECT
Contaminated fomites
In Primary Cytomegalo Viral Infection:
30-40% of fetuses will be infected
2-4% of them will develop severe malformations at birth.
In Recurrent Cytomegalo Viral Infection:
1% of fetuses will be infected and the rest will appear normal at birth, but later in life, they may suffer from delayed speech and learning difficulties
due to cerebral calcification and Sensorineural hearing loss.
A small group will have chorioretinitis.
Complications of Fetal CMV Infection Include:
Micro-& hydrocephaly
Chorioretinitis
Cerebral calcification
Mental retardation
Heart block
Petechiae
Maternal Screening: CMV Infection
Not recommended
Prevention: CMV Infection
Hand washing( especially after changing diapers)
