PRELIM Flashcards
(143 cards)
1
Q
This the study of the structural and function changes in cells tissues, organs and organs that underlie disease.
A
PATHOLOGY
2
Q
changes in morphology
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STRUCTURAL
2
Q
reproduce without the process of telophase
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PROKARYOTIC
3
Q
reproduce through sexual reproduction
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EUKARYOTIC
3
Q
CORE OF PATHOLOGY:
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- Etiology or Cause.
- Pathogenesis or mechanism of development.
- Morphology or the structural alterations induced in the cells and organs of the body.
4
Q
the functional consequences of the morphologic changes
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Clinical significance
4
Q
the body reacts (repair)
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INFECTION
4
Q
Example of infection
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TB
5
Q
Example of infection is TB
Caused by
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Mycobacterium tuberculae or acid fast bacilli
5
Q
dye used after collecting the specimen
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Acid fast stain
6
Q
Mycobacterium leprae and tuberculae has the same mode of treatment
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quadruple antibacteria
7
Q
has the same mode of treatment (quadruple antibacterial)
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Mycobacterium leprae and tuberculae
8
Q
genesis of cancer
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CARCINOMA
8
Q
Our forefathers have always believed that infirmity was caused by
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evil spirits
8
Q
This involves the examination of the ill body parts, the most obvious tool for which is
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autopsy
9
Q
WHAT it was stopped by the church because according to them, human is a sacred body AND WHEN
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Holy ghost
In 14th century
9
Q
German physician who is considered the father of Pathology.
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RUDOLF VIRCHOW
9
Q
Based on the Eber’s papyrus discovered in the Nile Valley which speaks of the different types if bone injuries.
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EGYPTIANS
9
Q
They are also credited for their contribution the art for serving the dead called EMBALMING.
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EGYPTIANS
10
Q
EGYPTIANS, They are also credited for their contribution the art for serving the dead called.
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EMBALMING.
10
Q
Based on theWHATdiscovered in the Nile Valley which speaks of the different types if bone injuries.
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Eber’s papyrus
10
Q
Based on the Eber’s papyrus discovered in WHERE which speaks of the different types if bone injuries.
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Nile Valley
10
Q
Father of medicine
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HIPPOCRATES
11
Q
He wrote different theories of disease.
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HIPPOCRATES
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He also wrote on wounds, inflammation and tumors, hemorrhoids, malaria and tuberculosis.
HIPPOCRATES
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He is one of the founders of Zoology
ARISTOTLE
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ARISTOTLE
He is one of the founders of
Zoology
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WHO Laid the ground work in human anatomic dissection.
ARISTOTLE
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He is by considered as the greatest medical figure of medicine
GALEN OF PERGAMUM
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Two Types of etiologic factors of disease:
INTRINSIC OR GENETIC
ACQUIRED
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A problem in the organism e.g. congenital
INTRINSIC OR GENETIC
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from within the organism/ born with it
INTRINSIC OR GENETIC
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DIFFRENET TYPES OF ACQUIRED
Infections- caused by bacteria, virus, protozoa, and fungus
Nutritional- edge of an acceptable normal range
Chemical- form of vitamins
Physical-
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caused by bacteria, virus, protozoa, and fungus
Infections-
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edge of an acceptable normal range
Nutritional
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form of vitamins
Chemical
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form of accidents, inhalation, radiation, and any physical hazard
Physical
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born with the disease; present during 1-2 years
CONGENITAL
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causes abnormality to the baby
TERATOGENIC EFFECT
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is a substance that interferes with normal fetal development and causes congenital disabilities
teratogen
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explosion of radiologic power plant
CHERNOBYL
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termination; NOT more than 20 weeks or age of viability; NOT more than 500 grams
ABORTION
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PATHOGENESIS MEANING
PATHO= abnormality
GENESIS= creation of
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This is the production and development of disease
PATHOGENESIS
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refers to the sequence of events in the response of cells or tissues to injury
Pathogenesis
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This is the development of a disease and the chain of events leading to that disease.
Pathogenesis
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Refers to the structural changes in the cell or tissue
MORPHOLOGY
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It is the process of progression and nature of disease
MORPHOLOGY
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Development of morbid condition or disease more specifically the cellular events and reactions and other mechanisms occurring in the development of disease
MORPHOLOGY
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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
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A property of cells, tissues, and organisms that allows the maintenance and regulation of the stability and constancy needed to function properly.
HOMEOSTASIS
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More severe physiologic stresses and some pathologic stimuli may bring about a number of physiologic and morphologic cellular change
ADAPTATION
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Local reactive change in tissues following injury or irritation
INFLAMMATION
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It is a progressive reaction in living tissues, accompanied or followed by the process of repair or healing
INFLAMMATION
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The injury causes altered metabolism which liberates compounds which initiates inflammatory process
INFLAMMATION
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It is a protective reaction of the body to localize or dispose the injurious agent and set the stage for tissue repair
INFLAMMATION
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Conditions show the signs of inflammatory reaction in other portions of the body like the lung and joints.
INFLAMMATION
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SIGNS OF ACUTE INFLAMMATION
PAIN / DOLOR
HEAT / CALOR
REDNESS / VASCULAR CONGESTION / RUBOR
TUMOR
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Produced by swelling and tension of tissues caused by the exudates with pressure on the nerves
PAIN / DOLOR
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Accumulation of chemical substances like kinins and hydrogen ion, irritate the nerve endings
PAIN / DOLOR
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There is disruption of cellular and tissue function
PAIN / DOLOR
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the fluid produced by a wound as it heals
EXUDATE
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Increase in the temperature of the particular area
HEAT / CALOR
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Primarily due to dilatation of blood vessels and increase in the amount of circulation in the area
HEAT / CALOR
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A response of body tissues to injury or irritation
REDNESS / VASCULAR CONGESTION / RUBOR
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This characterized by pain and swelling and redness and heat
REDNESS / VASCULAR CONGESTION / RUBOR
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Primarily due to vascular dilation and congestion
REDNESS / VASCULAR CONGESTION / RUBOR
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A swollen part, swelling, protuberance.
TUMOR
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This is an abnormal growth of body tissue
TUMOR
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Swelling is due to the accumulation of exudates within the tissue
TUMOR
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This is almost always secondary to tissue trauma or injury
TUMOR
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is added to the organ name to indicate an inflammatory reaction.
itis
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An injury or illness can involve acute, or short-term, inflammation.
ACUTE INFLAMMATION
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can continue for months or years. It either has or may have links to various diseases.
CHRONIC INFLAMMATION
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Agents Causing Cell Injury:
Physical
Chemical
Traumatic
Microbial
Immunologic
Radiation
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FUNDAMENTAL RESULTS OF INJURY TO THE TISSUE
HYPERTROPHY
HYPERPLASIA
ATROPHY
METAPLASIA
DYSPLASIA
DEGENERATION
NECROSIS
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COMMON TYPES OF NECROSIS
COAGULATION NECROSIS
CASEOUS NECROSIS
GUMMTOUS NECROSIS
LIQUIFACTIVE NECROSIS
FAT NECROSIS
GANGRENE
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refers to an increase in the size of cells resulting in an increase in the size of the organ
HYPERTROPHY
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Increase in the cell size depend on nutrition and extraneous stimulus
HYPERTROPHY
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Enlargement or overgrowth of an organ or part of the body due to the increased size of the constituent cells
HYPERTROPHY
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Most commonly seen in somatic body parts secondary to exercise
HYPERTROPHY
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an increase in the number of cells in an organ or tissue
HYPERPLASIA
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This results in the in increase volume of the organ or tissue
HYPERPLASIA
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This is an increase in the rate of reproduction of cells probably influenced by hormones
HYPERPLASIA
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This sets the stage in abnormal cellular proliferation which brings carcinomatous growth in the organ
HYPERPLASIA
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Acquired decrease in the size of an organ that were once normal
ATROPHY
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It may be caused by a reduction in size or number of component cells
ATROPHY
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It could also be caused by inadequate nutrition or oxygenation
ATROPHY
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There is disturbance in function
ATROPHY
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results from a reduction in the structural components of the cell
ATROPHY
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These cells have decreased function but are not dead
ATROPHY
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Most Common Causes of Atrophy:
Decreased in work load
Inadequate nutrition
Loss of endocrine stimulation
Aging
Pressure
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This is a reversible change in which one adult cell is replaced by another adult cell type
METAPLASIA
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This may generally be a part of normal maturation process or caused by some sort of abnormal stimulus
METAPLASIA
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is not synonymous with dysplasia and is not directly considered carcinogenic
METAPLASIA
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An abnormal development of cell or tissue, often a precancerous stage of growth
DYSPLASIA
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This alteration in size, shape, and organization of adult
DYSPLASIA
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This has always been considered a pre-cancerous lesion reoffered to an in situ lesion
DYSPLASIA
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There is disturbance of intracellular metabolism
DEGENERATION
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There is swelling of the cell with organelle engorgement
DEGENERATION
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Accumulation in the cytoplasm of substances that normally are invisible, absent or present only in small amounts
DEGENERATION
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They vary in severity and are generally reversible
DEGENERATION
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commonly produced by the cutting off of the blood supply thus causing infarction.
COAGULATION NECROSIS
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tissue death
INFARCTION
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cheesy macroscopic appearance, architectural outline is lost.
CASEOUS NECROSIS
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Seen in tuberculosis infection
CASEOUS NECROSIS
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seen as a consequence to syphilis infection
GUMMTOUS NECROSIS
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the dead area softens and eventually liquefies
LIQUIFACTIVE NECROSIS
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It is primarily seen in central nervous system injury
LIQUIFACTIVE NECROSIS
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seen in pancreatic disease where there is a release of enzymes that exacerbate tissue injury
FAT NECROSIS
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necrosis with the presence of putrefaction of bacteria
GANGRENE
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This requires immediate amputation and antibiotic coverage with broad spectrum antibiotics
GANGRENE
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Intrauterine Viral Infections:
Rubella
Cytomegalovirus (CMV)
Varicella-Zoster (VZV)
Enteroviruses
HIV
Hepatitis C
Hepatitis B
Japanese Encephalitis
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Perinatal and Neonatal Infections:
Human Herpes Simplex
Enteroviruses
HIV
Hepatitis B
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Previously Known as TORCH Infections:
Toxoplasmosis, Other( syphilis)
Rubella
Cytomegalo virus
Herpes
Hepatitis which is acquired post-natally
Hepatitis which is acquired post-natally
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signs that hydrocephalus, diffuse intracranial chorioretinitis
toxoplasma gondi
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cardiac defects, sensrineural hearing loss, cataracts
rubella virus
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micrcephalus, periventricular calcification
cytomegalovirus
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signs that vesicular lesions, keratoconjunctivitis
herpes simplex virus
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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
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signs that lim abnormalities, cicatricial lesions
varicella-zoster-virus
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signs that severe thrush, failure to thrive, recurrent bacterial infections, calcifications of the basal ganglia
human immunodefiency virus
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which is acquired post-natally
Hepatitis
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this term is now obsolete due to HIV
TORCH
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Most fetuses, if infected during the first trimester, will suffer from a
syndrome of congenital malformation.
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Also known as GERMAN MEASLES
The fetus is most at risk in the first 16 weeks gestation
RUBELLA
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RUBELLA
Also known as GERMAN MEASLES
The fetus is most at risk in the first 16 weeks gestation
Causative Organism:
Rubella virus ( togaviruses RNA)
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RUBELLA
Route of Infection:
via respiration as the virus is concentrated in the nasopharyngeal secretions.
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RUBELLA
Incubation Period:
14-21 days.
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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
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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.
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RUBELLA
Routine Antenatal Screening:
Vaccination ( avoid pregnancy for 3 months)
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RUBELLA
Maternal Screening:
Routine rubella IgG in the first trimester
If infection is suspected perform rubella IgM
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RUBELLA
Prevention:
Vaccination before or after pregnancy (not during).
In acute infection: droplet precautions.
In neonatal infection: contact precautions.
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In the United Kingdom this causes more congenital abnormalities than rubella.
Infects 50-60% of women of childbearing age.
CYTOMEGALOVIRUS (CMV)
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Causative Agent: CYTOMEGALOVIRUS (CMV)
CMV (Herpes virus DNA)
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Maternal Symptoms: CYTOMEGALOVIRUS (CMV)
Usually mild or asymptomatic, fever with/without lymphadenopathy, sore throat.
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Transmission: CYTOMEGALOVIRUS (CMV)
DIRECT (person to person contact)
Saliva
Milk
Urine
Semen
Tears
Stools
Blood, Cervical secretions Vaginal Secretion
INDIRECT
Contaminated fomites
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In Primary Cytomegalo Viral Infection:
30-40% of fetuses will be infected
2-4% of them will develop severe malformations at birth.
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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.
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Complications of Fetal CMV Infection Include:
Micro-& hydrocephaly
Chorioretinitis
Cerebral calcification
Mental retardation
Heart block
Petechiae
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Maternal Screening: CMV Infection
Not recommended
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Prevention: CMV Infection
Hand washing( especially after changing diapers)
