Path Quiz 6 Material

Front 1

Describe 2 general classifications of asbestos

Back 1

1. Serpentine - curly configuration
2. Amphobile asbestos - straight fibers.

Front 2

What is one member of the serpentine classification of asbestos?

Back 2

Chrysotile "white asbestos". Has a fiber quality.

Front 3

What is one member of the amphobile asbestos family?

Back 3

Crocidolite "blue asbestos". May cause mesothelioma.

Front 4

What aspect of crocidolite makes it particularly hazardous?

Back 4

Fibers are very long and narrow. Can travel axially in the air stream and get deep into the lungs.

Front 5

Name 7 pathological manifestations of asbestos.

Back 5

1. Hyaline pleural plaques.
2. Asbestosis (parenchymal fibrosis of lung).
3. Mesothelioma (malig.neoplasm of pleural surface).
4. Carcinoma of lung parenchyma. (smoking=cofactor)
5. Carcinoma of other organs.
6. Rounded atelectasis.
7. Benign pleural effusions.
4.

Front 6

Describe 2 general classifications of asbestos

Back 6

1. Serpentine - curly configuration
2. Amphobile asbestos - straight fibers.

Front 7

What is one member of the serpentine classification of asbestos?

Back 7

Chrysotile "white asbestos". Has a fiber quality.

Front 8

What is one member of the amphobile asbestos family?

Back 8

Crocidolite "blue asbestos". May cause mesothelioma.

Front 9

What aspect of crocidolite makes it particularly hazardous?

Back 9

Fibers are very long and narrow. Can travel axially in the air stream and get deep into the lungs.

Front 10

Name 7 pathological manifestations of asbestos.

Back 10

1. Hyaline pleural plaques.
2. Asbestosis (parenchymal fibrosis of lung).
3. Mesothelioma (malig.neoplasm of pleural surface).
4. Carcinoma of lung parenchyma. (smoking=cofactor)
5. Carcinoma of other organs.
6. Rounded atelectasis.
7. Benign pleural effusions.
4.

Front 11

4 ways smoking may exacerbate asbestos.

Back 11

1. Impeding mucous ciliary clearance & macrophage activity.
2. Increasing asbestos infiltration.
3. Facilitating binding of asbestos.
4. Carcinogens from cig. adsorb onto surfaces of asbestos which acts as vehicle to deliver or retain them in lung.

Front 12

A low dose of asbestos is associated with what condition, regardless of smoking status?

Back 12

Mesothelioma.

Front 13

A higher dose of asbestos + smoking causes an increased risk in what condition?

Back 13

Carcinoma of the lung parenchyma.

Front 14

A modest level of asbestos is associated with what condition?

Back 14

Benign pleural changes.

Front 15

High asbestos exposure is associated with what condition, regardless of smoking?

Back 15

Asbestosis

Front 16

What is an Ames test?

Back 16

Screening test for possible carcinogens using strains of Salmonella Typhimurium that are unable to synthesize histadine.Carcinogen causes mutation that allows it to produce histadine.

Front 17

What advantage does Ames test offer over animal models?

Back 17

Allows for testing potential carcinogens outside of animals so that the animals' metabolism will not effect it.

Front 18

Describe how a chemical test of carcinogens is used?

Back 18

Test agent's chemical properties are evaluated. i.e. "bay region" of polycyclic molecules.

Front 19

What is Allergenic Alevolitis (aka Hypersensitivity penumonitis)?

Back 19

Combined Type 3 (Ab response) and Type 4 (T cell). Some causal agents are Thermophilic Actinomycetes.

Front 20

Name 3 toxic gases that can cause non-cardiac pulmonary edema.

Back 20

1. chlorine
2. phosgene
3. cadmium

Front 21

What is pneumoconosis?

Back 21

Inflammation commonly leading to fibrosis of the lungs caused by the inhalation of dust in various occupations, characterized by pain in chest, cough c little/no expectoration, dyspena, reduced thoracic excursion, cyanosis and fatigue after exertion.

Front 22

Describe 2 categories of inorganic dusts that can cause pneumoconosis.

Back 22

1. Fibrogenic (silica, asbestos, silicates.

2. Non-Fibrogenic (iron, tin, barium)

Front 23

What is Simple Coal Workers' Pneumoconioses?

Back 23

Pneumonoconiosis from accumulation of carbon and silica in the lungs from inhaled coal dust. Silica content produces fibrous nodules. Char by coal dust macules located adjuacent to respiratory broncioles.

Front 24

What are coal dust macules?

Back 24

1-2mm diameter aggregates of carbon laden macrophages located adjacent to respiratory bronchioles .

Front 25

What is silicosis?

Back 25

Simple (enlarged hilar lymph nodes surrounded by Ca.
Acute (alveoli filled c protein-rich fluid, causes fast death).

Front 26

List 6 noxious toxic gases.

Back 26

1. Ammonia NH3.
2. Sulfur Dioxide. SO2.
3. Chlorine. Cl.
4. Nitrogen Dioxide. NO2.
5. Ozone. O3.
6. Phosgene.COCl2.

Front 27

What disease is associated with oxides of nitrogen gases.

Back 27

Silo Filler's disease, which causes damage to epithelial lining of airway and bronchiolitis obliterans (scarring).

Front 28

Describe how carbon monoxide inhalation can cause death.

Back 28

CO binds more avidly c hemoglobin than does oxygen. Hem not avail to bind O2. CO causwes shift in dissociation curve, so taht remaining unbound hemoglobin is prevented from releasing O2 (Left shift).

Front 29

Describe 8 effects of lead poisoning.

Back 29

1.Anemia via -erthrypoieis, +hemolysis, -RBC life span. (Have +ALA excretion in urine due to build of intermediates in hemoglobin synethesis.
2. Reticulocytosis. Bone marrow releases more immature RBCs to +RBC production and compensate for anemia.
3. Colic.
4. Renal tubular acidosis (Fanconi's syndrome). Intranuclear inclusions.
5. CNA damage (encephalopathy, ADD-like symptoms)
6. Peripheral neuropathy.
7. Epiphysis lead lines.
8. Lead line at gingival margin dur to precipitates of lead sulfide.
2.

Front 30

Describe a classic microscopic sign of lead exposure.

Back 30

Basophilic stippling of RBCs (blue-staining stops on RBCs)

Front 31

What form of taking in metallic Hg is hazardous?

Back 31

Inhalation.

Front 32

What form of mercury is most toxic?

Back 32

Organic (methylated ) mercury. Is soluble and absorable by GI system.

Front 33

What is the leading cause of neonatal deaths?

Back 33

Congenital anomalies.

Front 34

What is the primary cause of chromosomal neonatal deaths?

Back 34

Trisomy. (15, 16 - the ones that lead to death. Not 21,18,13.

Front 35

Describe 4 char of Turners syndrome (XO)

Back 35

1. fluid in abdomen.
2. Webbing of neck skin.
3. Horsehoe kidney.
4. coarctation of aorta.
(may be mosaic)

Front 36

Describe 4 char of triploidy (69 chromosomes)

Back 36

(Note; more dangerous if extra set from father).
1. large head.
2. spina bifida/NTDs
3. hydrocephalus
4. syndactly

Front 37

Describe 4 char of Trisomy 21 (down's syndrome)

Back 37

1. palpebral fissure.
2. simian crease
3. wide space b/w 1st/2nd toe
4. little finger turned in.

Front 38

4 char of Trisomy 18 (Edward's syndrome)

Back 38

1. Cleft lip/palate
2. Radial aplasia
3. Missing thumb.
4. absent radial bone.

Front 39

Describe the 3 general categories of congenital anomalities in neonates.

Back 39

1. Malformation (poor formation, something wrong in embryolic process).
2. Deformation. (result of abnormal forces on normal tissues that change their appearance or position).
3. Disruption. Morphologic defect resultinf from extrinsic interference with a normal process (amniotic banding)

Front 40

Give an example of malformation + deformation.

Back 40

Renal agenesis. Malformation causes no kidney; deformation caused by lack of embryonic fluid.

Front 41

List 6 potential causes of disruption.

Back 41

1. Radiation.
2. Chemical/drug.
3. Metabolic. (PKU, diabetes)
4. Infectious (rubella, toxoplasmosis)
5. Immunologic.
6. Thermodisruptive.

Front 42

List 4 causes of congenital anomalies.

Back 42

1. Chromosomal defects.
2. Single gene defects.
3. Environmental defects.
4. Multifactoria defects.

Front 43

What distinguishes a dominant single gene defect from a recessive one?

Back 43

Dominant - mutation in gene that codes for structural protein (achondroplasia, sickle cell)
Recessive - mutations that code for enzymes (Meckel syndrome, osteogenesis imperfecta, storage disorders)

Front 44

Describe characteristics of Meckel syndrome.

Back 44

1. Polydactyly
2. cystic kidneys
3. cystic liver
4. encephaloceles

Front 45

2 examples of multifactorial disorders.

Back 45

1. Cleft palate.
2. Neural tube defects.

Front 46

6 Laws of Teratogenesis.

Back 46

1. Susceptibility depends on genotype.
2. Susceptibiity depends on developmental stage of exposure.
3. Cause malformations by specific pathologic mechanisms.
4. Maternal factors may influence teratogenicity.
5. Manifestations include death, malformations, growth retardation,functional impairment & transplacental tumorogenesis.
6. Manifestations range in frequency and severity.

Front 47

Describe features of FAS.

Back 47

1. Small size.
2. small brain.
3. short palpebral fissure.
4. Facial dysmorphism.

Front 48

What is a syndrome?

Back 48

A recognizable pattern of anomalies which is known or thought to be causally related.

Front 49

Describe features of DiGeorge Syndrome

Back 49

1. Thymic aplasia.
2. Deficient parathyroids.
3. Congenital defects in heart and great vessels (gene mutation prevents 3rd and 4th pharyngeal pouches from developing properly).

Front 50

What is a sequence?

Back 50

A pattern of cascade anomalies that can be explained on the basis of a single initiating event.

Front 51

What form of taking in metallic Hg is hazardous?

Back 51

Inhalation.

Front 52

What form of mercury is most toxic?

Back 52

Organic (methylated ) mercury. Is soluble and absorable by GI system.

Front 53

What is the leading cause of neonatal deaths?

Back 53

Congenital anomalies.

Front 54

What is the primary cause of chromosomal neonatal deaths?

Back 54

Trisomy. (15, 16 - the ones that lead to death. Not 21,18,13.

Front 55

Describe 4 char of Turners syndrome (XO)

Back 55

1. fluid in abdomen.
2. Webbing of neck skin.
3. Horsehoe kidney.
4. coarctation of aorta.
(may be mosaic)

Front 56

What is Prune Belly Syndrome?

Back 56

Pattern of cascade anomalities due to defect in posterior urethral valves obstruct the urethra, leading to backup of urine in bladder & kidney.

Front 57

What is the acronym for the most common association of defects.

Back 57

VATER
1. Vertebral Anomalies.
2. Anal Atresia.
3. T-E Fistula.
4. Radial Dysplasia.

Front 58

What is hydrops?

Back 58

Accumulation of edema in fluid of fetus during intrauterine growth.

Front 59

Describe causal mechanisms of hydrops?

Back 59

1. Congestive heart failure.
2. Portal hypertension.
3. Lymphatic or vascular obstruction.
4. Hypoalbuminemia.

Front 60

Describe 2 general classifications of Hydrops.

Back 60

1. Immune (Rh, hemolytic anemia.
2. Non-immune (cardiac malformations, chromosomal abnormality, monochorionic twins, infection, anemia, tumors)

Front 61

Describe 6 potential causes of intrauterine growth retardation.

Back 61

1. Placental problems.
2. Confined placental mosaicism.
3. Maternal vascular disease.
4. Multiple gestations.
5. congenital anomalies.
6. congenial infecions.

Front 62

What time defines perinatal mortality, postneonatal mortality?

Back 62

Perinatal - greater than 20 weeks of gestation to 1st month of life.

Postneonatal - 1 month to 1 year.

Infant death = death within first year of life.

Front 63

list 5 common causes of infant death.

Back 63

1. Birth defects.
2. Prematurity.
3. SIDS
4. Maternal complications.
5. Accidents.

Front 64

List causes of perinatal death.

Back 64

1. Fetal infection (ascending, maternal hematogenous infection (TORCH), Syphilis, Varicella
2. Tumors of infancy

Front 65

Examples of benigan neoplasia in early life.

Back 65

Benign tumors -
* Hemangioma
* Teratoma - cells from all three germlines (contain variety of different tissues)
* Hamartoma - overgrowth of tissues whieh are normally present in that organ.

Front 66

Examples of malignant neoplasms in early life.

Back 66

1. Wilm's Tumor
2. Neuroblastoma (small blue-stained tumors).

Front 67

What factors does the Gompertz approach to aging take into account?

Back 67

1. Life Span.
2. Probability of dying
3. Survivorship.
4. Life expectancy.

Front 68

What is the main reason for increasing life expecancy.

Back 68

Reduction in childhood mortality.

Front 69

Have maximum life span and the rate of aging changed?

Back 69

No. max = 120 and rate of aging hasn't changed.

Front 70

What is the Gompertz equation?

Back 70

probability of dying = infant death rate + (rate of dying)(time)

Front 71

What can be said of a disease that doesn't follow the Gompertz relationship?

Back 71

Then it is not age-related.

Front 72

What happens to the death curve as you remove attributable events?

Back 72

Move toward programmed death.

Front 73

Describe 6 theories of aging.

Back 73

1. DNA damage and repair.
2. Error catastrophe (prob c proteins lead to genetic abnormality).
3. Oxidation & free radicals.
4. Immunologic (prob secondary)
5. Neuroendocrine. (hypothal-pituitary axis)
6. Programmed aging (Hayflick #, telomerase)

Front 74

Describe how error catastrophe can cause aging?

Back 74

Problem with proteins associated with chromosomes lead to genetic abnormality and aberrant protein synthesis & death.
Protein & nuclei acid glycosylation . X-linking impairs passage of nutrients.

Front 75

What does trymadine incorporation into DNA measure?

Back 75

Measure of DNA repair (i.e. unscheduled DNA synthesis).

Front 76

What enzyme is important in aging?

Back 76

DNA helicase.

Front 77

What is the role of SIRT1 in aging?

Back 77

SIRT1 is a gene product that inhibits Bax, a protein that leads to apoptosis and preventing accumulation of fat.

Front 78

Effect of caloric restriction on SIRT1?

Back 78

As calories do down, SIRT1 levels down up. SIRT1 inhibits Bax and therefore limits apoptosis.

Front 79

Describe 2 ways immunity changes with age.

Back 79

1. Less protection against infection.
2. More antibodies directed against normal tissue.

Front 80

Describe results of inactivation of growth pathways.

Back 80

1. Decrease glucose or insulin-signaling.
2. Upregulate antixodant enzymes.
3. Accumulation of glycogen & fat.
4. Growth hormone and insulin-like growth factor act to promote stress.
5. Sexual maturity delayed and fertility decreased.
6. Intellectual development retarded.
7. Lessened osteoarthritis.

Front 81

Caloric intake, free radical damage & insulin-like peptide are related to?

Back 81

Oxidative Injury.

Front 82

Describe a histological change associated with aging.

Back 82

Lipofusein - derived from mitochondria. Is a marker of aging that has no bearing on cardiac function.

Front 83

What is distinction between aging vs age-related change?

Back 83

Aging is inevitable with age. (loss of position sense).
Age-related means that something is associated with aging and occurs at an older age. (AD disease)

Front 84

List 5 neurological consequences of aging.

Back 84

1. - central processing.
2. Maintained verbal skills.
3. Nigrostriatal pathway decline.
4. Receptor organ change.
5. Sleep shortened with arousals.

Front 85

Describe ways to increase SIRT1.

Back 85

1. Quercetin & piceatannol (tea & apples)
2. Reservatol (grapes & red wines)