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PATHO > PRELIM > Flashcards

PRELIM Flashcards

1
Q

This the study of the structural and function changes in cells tissues, organs and organs that underlie disease.

A

PATHOLOGY

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2
Q

changes in morphology

A

STRUCTURAL

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2
Q

reproduce without the process of telophase

A

PROKARYOTIC

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3
Q

reproduce through sexual reproduction

A

EUKARYOTIC

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3
Q

CORE OF PATHOLOGY:

A
  • Etiology or Cause.
  • Pathogenesis or mechanism of development.
  • Morphology or the structural alterations induced in the cells and organs of the body.
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4
Q

the functional consequences of the morphologic changes

A

Clinical significance

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4
Q

the body reacts (repair)

A

INFECTION

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4
Q

Example of infection

A

TB

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5
Q

Example of infection is TB
Caused by

A

Mycobacterium tuberculae or acid fast bacilli

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5
Q

dye used after collecting the specimen

A

Acid fast stain

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6
Q

Mycobacterium leprae and tuberculae has the same mode of treatment

A

quadruple antibacteria

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7
Q

has the same mode of treatment (quadruple antibacterial)

A

Mycobacterium leprae and tuberculae

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8
Q

genesis of cancer

A

CARCINOMA

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8
Q

Our forefathers have always believed that infirmity was caused by

A

evil spirits

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8
Q

This involves the examination of the ill body parts, the most obvious tool for which is

A

autopsy

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9
Q

WHAT it was stopped by the church because according to them, human is a sacred body AND WHEN

A

Holy ghost
In 14th century

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9
Q

German physician who is considered the father of Pathology.

A

RUDOLF VIRCHOW

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9
Q

Based on the Eber’s papyrus discovered in the Nile Valley which speaks of the different types if bone injuries.

A

EGYPTIANS

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9
Q

They are also credited for their contribution the art for serving the dead called EMBALMING.

A

EGYPTIANS

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10
Q

EGYPTIANS, They are also credited for their contribution the art for serving the dead called.

A

EMBALMING.

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10
Q

Based on theWHATdiscovered in the Nile Valley which speaks of the different types if bone injuries.

A

Eber’s papyrus

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10
Q

Based on the Eber’s papyrus discovered in WHERE which speaks of the different types if bone injuries.

A

Nile Valley

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10
Q

Father of medicine

A

HIPPOCRATES

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11
Q

He wrote different theories of disease.

A

HIPPOCRATES

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12
Q

He also wrote on wounds, inflammation and tumors, hemorrhoids, malaria and tuberculosis.

A

HIPPOCRATES

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13
Q

He is one of the founders of Zoology

A

ARISTOTLE

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14
Q

ARISTOTLE
He is one of the founders of

A

Zoology

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14
Q

WHO Laid the ground work in human anatomic dissection.

A

ARISTOTLE

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14
Q

He is by considered as the greatest medical figure of medicine

A

GALEN OF PERGAMUM

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15
Q

Two Types of etiologic factors of disease:

A

INTRINSIC OR GENETIC

ACQUIRED

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15
Q

A problem in the organism e.g. congenital

A

INTRINSIC OR GENETIC

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15
Q

from within the organism/ born with it

A

INTRINSIC OR GENETIC

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15
Q

DIFFRENET TYPES OF ACQUIRED

A

Infections- caused by bacteria, virus, protozoa, and fungus
Nutritional- edge of an acceptable normal range
Chemical- form of vitamins
Physical-

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15
Q

caused by bacteria, virus, protozoa, and fungus

A

Infections-

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15
Q

edge of an acceptable normal range

A

Nutritional

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16
Q

form of vitamins

A

Chemical

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16
Q

form of accidents, inhalation, radiation, and any physical hazard

A

Physical

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17
Q

born with the disease; present during 1-2 years

A

CONGENITAL

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17
Q

causes abnormality to the baby

A

TERATOGENIC EFFECT

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17
Q

is a substance that interferes with normal fetal development and causes congenital disabilities

A

teratogen

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18
Q

explosion of radiologic power plant

A

CHERNOBYL

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18
Q

termination; NOT more than 20 weeks or age of viability; NOT more than 500 grams

A

ABORTION

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18
Q

PATHOGENESIS MEANING

A

PATHO= abnormality
GENESIS= creation of

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18
Q

This is the production and development of disease

A

PATHOGENESIS

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18
Q

refers to the sequence of events in the response of cells or tissues to injury

A

Pathogenesis

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19
Q

This is the development of a disease and the chain of events leading to that disease.

A

Pathogenesis

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20
Q

Refers to the structural changes in the cell or tissue

A

MORPHOLOGY

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20
Q

It is the process of progression and nature of disease

A

MORPHOLOGY

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21
Q

Development of morbid condition or disease more specifically the cellular events and reactions and other mechanisms occurring in the development of disease

A

MORPHOLOGY

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21
Q

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

A

CLINICAL SIGNIFICANCE

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22
Q

A property of cells, tissues, and organisms that allows the maintenance and regulation of the stability and constancy needed to function properly.

A

HOMEOSTASIS

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22
Q

More severe physiologic stresses and some pathologic stimuli may bring about a number of physiologic and morphologic cellular change

A

ADAPTATION

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22
Q

Local reactive change in tissues following injury or irritation

A

INFLAMMATION

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22
Q

It is a progressive reaction in living tissues, accompanied or followed by the process of repair or healing

A

INFLAMMATION

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23
Q

The injury causes altered metabolism which liberates compounds which initiates inflammatory process

A

INFLAMMATION

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23
Q

It is a protective reaction of the body to localize or dispose the injurious agent and set the stage for tissue repair

A

INFLAMMATION

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23
Q

Conditions show the signs of inflammatory reaction in other portions of the body like the lung and joints.

A

INFLAMMATION

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24
Q

SIGNS OF ACUTE INFLAMMATION

A

PAIN / DOLOR
HEAT / CALOR
REDNESS / VASCULAR CONGESTION / RUBOR
TUMOR

24
Q

Produced by swelling and tension of tissues caused by the exudates with pressure on the nerves

A

PAIN / DOLOR

25
Q

Accumulation of chemical substances like kinins and hydrogen ion, irritate the nerve endings

A

PAIN / DOLOR

25
Q

There is disruption of cellular and tissue function

A

PAIN / DOLOR

25
Q

the fluid produced by a wound as it heals

A

EXUDATE

25
Q

Increase in the temperature of the particular area

A

HEAT / CALOR

25
Q

Primarily due to dilatation of blood vessels and increase in the amount of circulation in the area

A

HEAT / CALOR

26
Q

A response of body tissues to injury or irritation

A

REDNESS / VASCULAR CONGESTION / RUBOR

27
Q

This characterized by pain and swelling and redness and heat

A

REDNESS / VASCULAR CONGESTION / RUBOR

27
Q

Primarily due to vascular dilation and congestion

A

REDNESS / VASCULAR CONGESTION / RUBOR

27
Q

A swollen part, swelling, protuberance.

A

TUMOR

27
Q

This is an abnormal growth of body tissue

A

TUMOR

27
Q

Swelling is due to the accumulation of exudates within the tissue

A

TUMOR

27
Q

This is almost always secondary to tissue trauma or injury

A

TUMOR

27
Q

is added to the organ name to indicate an inflammatory reaction.

A

itis

28
Q

An injury or illness can involve acute, or short-term, inflammation.

A

ACUTE INFLAMMATION

28
Q

can continue for months or years. It either has or may have links to various diseases.

A

CHRONIC INFLAMMATION

29
Q

Agents Causing Cell Injury:

A

Physical
Chemical
Traumatic
Microbial
Immunologic
Radiation

29
Q

FUNDAMENTAL RESULTS OF INJURY TO THE TISSUE

A

HYPERTROPHY
HYPERPLASIA
ATROPHY
METAPLASIA
DYSPLASIA
DEGENERATION
NECROSIS

29
Q

COMMON TYPES OF NECROSIS

A

COAGULATION NECROSIS
CASEOUS NECROSIS
GUMMTOUS NECROSIS
LIQUIFACTIVE NECROSIS
FAT NECROSIS
GANGRENE

29
Q

refers to an increase in the size of cells resulting in an increase in the size of the organ

A

HYPERTROPHY

29
Q

Increase in the cell size depend on nutrition and extraneous stimulus

A

HYPERTROPHY

30
Q

Enlargement or overgrowth of an organ or part of the body due to the increased size of the constituent cells

A

HYPERTROPHY

30
Q

Most commonly seen in somatic body parts secondary to exercise

A

HYPERTROPHY

30
Q

an increase in the number of cells in an organ or tissue

A

HYPERPLASIA

31
Q

This results in the in increase volume of the organ or tissue

A

HYPERPLASIA

31
Q

This is an increase in the rate of reproduction of cells probably influenced by hormones

A

HYPERPLASIA

31
Q

This sets the stage in abnormal cellular proliferation which brings carcinomatous growth in the organ

A

HYPERPLASIA

32
Q

Acquired decrease in the size of an organ that were once normal

A

ATROPHY

32
Q

It may be caused by a reduction in size or number of component cells

A

ATROPHY

33
Q

It could also be caused by inadequate nutrition or oxygenation

A

ATROPHY

33
Q

There is disturbance in function

A

ATROPHY

33
Q

results from a reduction in the structural components of the cell

A

ATROPHY

33
Q

These cells have decreased function but are not dead

A

ATROPHY

33
Q

Most Common Causes of Atrophy:

A

Decreased in work load
Inadequate nutrition
Loss of endocrine stimulation
Aging
Pressure

34
Q

This is a reversible change in which one adult cell is replaced by another adult cell type

A

METAPLASIA

34
Q

This may generally be a part of normal maturation process or caused by some sort of abnormal stimulus

A

METAPLASIA

35
Q

is not synonymous with dysplasia and is not directly considered carcinogenic

A

METAPLASIA

36
Q

An abnormal development of cell or tissue, often a precancerous stage of growth

A

DYSPLASIA

36
Q

This alteration in size, shape, and organization of adult

A

DYSPLASIA

37
Q

This has always been considered a pre-cancerous lesion reoffered to an in situ lesion

A

DYSPLASIA

37
Q

There is disturbance of intracellular metabolism

A

DEGENERATION

38
Q

There is swelling of the cell with organelle engorgement

A

DEGENERATION

39
Q

Accumulation in the cytoplasm of substances that normally are invisible, absent or present only in small amounts

A

DEGENERATION

40
Q

They vary in severity and are generally reversible

A

DEGENERATION

40
Q

commonly produced by the cutting off of the blood supply thus causing infarction.

A

COAGULATION NECROSIS

40
Q

tissue death

A

INFARCTION

40
Q

cheesy macroscopic appearance, architectural outline is lost.

A

CASEOUS NECROSIS

40
Q

Seen in tuberculosis infection

A

CASEOUS NECROSIS

40
Q

seen as a consequence to syphilis infection

A

GUMMTOUS NECROSIS

40
Q

the dead area softens and eventually liquefies

A

LIQUIFACTIVE NECROSIS

41
Q

It is primarily seen in central nervous system injury

A

LIQUIFACTIVE NECROSIS

41
Q

seen in pancreatic disease where there is a release of enzymes that exacerbate tissue injury

A

FAT NECROSIS

41
Q

necrosis with the presence of putrefaction of bacteria

A

GANGRENE

41
Q

This requires immediate amputation and antibiotic coverage with broad spectrum antibiotics

A

GANGRENE

41
Q

Intrauterine Viral Infections:

A

Rubella
Cytomegalovirus (CMV)
Varicella-Zoster (VZV)
Enteroviruses
HIV
Hepatitis C
Hepatitis B
Japanese Encephalitis

41
Q

Perinatal and Neonatal Infections:

A

Human Herpes Simplex
Enteroviruses
HIV
Hepatitis B

41
Q

Previously Known as TORCH Infections:

A

Toxoplasmosis, Other( syphilis)
Rubella
Cytomegalo virus
Herpes
Hepatitis which is acquired post-natally
Hepatitis which is acquired post-natally

41
Q

signs that hydrocephalus, diffuse intracranial chorioretinitis

A

toxoplasma gondi

41
Q

cardiac defects, sensrineural hearing loss, cataracts

A

rubella virus

41
Q

micrcephalus, periventricular calcification

A

cytomegalovirus

42
Q

signs that vesicular lesions, keratoconjunctivitis

A

herpes simplex virus

42
Q

signs that bullous macular and eczematous skin lesions involving the palms and the soles; rhinorrhea dactylitis and other signs of osteochronditis and periostitis

A

treponerma pallidum

42
Q

signs that lim abnormalities, cicatricial lesions

A

varicella-zoster-virus

42
Q

signs that severe thrush, failure to thrive, recurrent bacterial infections, calcifications of the basal ganglia

A

human immunodefiency virus

42
Q

which is acquired post-natally

A

Hepatitis

42
Q

this term is now obsolete due to HIV

A

TORCH

42
Q

Most fetuses, if infected during the first trimester, will suffer from a

A

syndrome of congenital malformation.

42
Q

Also known as GERMAN MEASLES
The fetus is most at risk in the first 16 weeks gestation

A

RUBELLA

42
Q

RUBELLA
Also known as GERMAN MEASLES
The fetus is most at risk in the first 16 weeks gestation

Causative Organism:

A

Rubella virus ( togaviruses RNA)

42
Q

RUBELLA

Route of Infection:

A

via respiration as the virus is concentrated in the nasopharyngeal secretions.

42
Q

RUBELLA

Incubation Period:

A

14-21 days.

42
Q

RUBELLA

Symptoms:

A

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

42
Q

Risk of Fetal Transmission: RUBELLA

A

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.

42
Q

RUBELLA
Routine Antenatal Screening:

A

Vaccination ( avoid pregnancy for 3 months)

42
Q

RUBELLA
Maternal Screening:

A

Routine rubella IgG in the first trimester
If infection is suspected perform rubella IgM

42
Q

RUBELLA
Prevention:

A

Vaccination before or after pregnancy (not during).
In acute infection: droplet precautions.
In neonatal infection: contact precautions.

42
Q

In the United Kingdom this causes more congenital abnormalities than rubella.
Infects 50-60% of women of childbearing age.

A

CYTOMEGALOVIRUS (CMV)

42
Q

Causative Agent: CYTOMEGALOVIRUS (CMV)

A

CMV (Herpes virus DNA)

42
Q

Maternal Symptoms: CYTOMEGALOVIRUS (CMV)

A

Usually mild or asymptomatic, fever with/without lymphadenopathy, sore throat.

42
Q

Transmission: CYTOMEGALOVIRUS (CMV)

A

DIRECT (person to person contact)
Saliva
Milk
Urine
Semen
Tears
Stools
Blood, Cervical secretions Vaginal Secretion
INDIRECT
Contaminated fomites

42
Q

In Primary Cytomegalo Viral Infection:

A

30-40% of fetuses will be infected
2-4% of them will develop severe malformations at birth.

42
Q

In Recurrent Cytomegalo Viral Infection:

A

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.

42
Q

Complications of Fetal CMV Infection Include:

A

Micro-& hydrocephaly
Chorioretinitis
Cerebral calcification
Mental retardation
Heart block
Petechiae

43
Q

Maternal Screening: CMV Infection

A

Not recommended

43
Q

Prevention: CMV Infection

A

Hand washing( especially after changing diapers)

PATHO (4 decks)

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