Patho Test 1

Front 1

Atrophy

Back 1

decrease of cell substance ... shrinks

Front 2

Metaplasia

Back 2

a reversible conversion from one adult cell type to another adult cell type. It allows for replacement with cells that are better able to tolerate environmental stressors

Front 3

Dysplasia

Back 3

deranged cell growth that results in cells that vary in size, shape, and appearance of mature cell

Front 4

Hyperplasia

Back 4

increase in number of cells of a tissue or organ

Front 5

Hypertrophy

Back 5

increase the amount of functioning mass by increasing cell size (can be good or bad – workout in the gym, but if gets too big then can’t come back and is bad: Sterlings law)

Front 6

biochemical lesions

Back 6

changes in chemical metabolic reactions

Front 7

suffix “–oma”

Back 7

Benign tumors

Front 8

sarcomas

Back 8

Malignant connective tissue

Front 9

carcinomas

Back 9

Malignant epithelial tumors

Front 10

lymphomas

Back 10

Cancers of lymphatic tissue

Front 11

leukemias

Back 11

Cancers of blood-forming cells

Front 12

Carcinoma in situ (CIS)

Back 12

-Pre-invasive epithelial malignant tumors
-of glandular or epithelial origin
-have not yet broken through the basement membrane or invaded the surrounding stroma

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Hyperplasia

Back 13

increase in the # of cells within tissue

Front 14

Hypoplasia

Back 14

organ is dwarfed

Front 15

Atrophy

Back 15

adult size organ - shrinks

Front 16

Hypertrophy

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enlargement of cells --> tissue-->organ

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Differentiation

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progeny of dividing stem cells become specialized to perform a particular task

Front 18

Metaplasia

Back 18

differentiating cell system under adverse conditions -->pattern of differentiation changes -->the dividing cells differentiate into types of cells not usually found in that area--may be regular or adaptive--reversible

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Dysplasia

Back 19

abnormalality in differentiation & proliferation of cell = variation in size, shape, appearance, arrangement

Front 20

Neoplasm

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1 -new growth
2 -abnormal mass of proliferating cells
3 -interferes with needs of host
4 -uncoordinated rate of growth
5 -functions independently of homeostatic control

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Characteristics of Neoplastic cells

Back 21

1 -Persistent proliferation
2 -Invasive growth
3 -Formation of metastases
4 -Immortality
5 -Etiology of cancer

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Immortality

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Unlike normal cells that die, cancer cells undergo endless divisions due to enzyme

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Persistent proliferation

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Unrestrained growth and division (most distinguishing property); malignant cells are unresponsive to feedback mechanisms

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Invasive growth

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malignant cells are free of constraints that inhibit invasive growth so penetrate adjacent tissues

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Formation of metastases

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Secondary tumors occurring at distant sites

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Etiology of cancer

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Alteration in DNA caused by chemical carcinogens, viruses, radiation; malignant transformation occurs in three stages (initiation, promotion, and progression)

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Effect of a Benign Neoplasm on Host

Back 27

-range of little to lethal
**occlude organ or structure --interfere with function of organ

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Effect of Malignant Neoplasm on Host

Back 28

-more aggressive & destructive
-causes severe malnutrition R//T effect of cytokines and response to tumor

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Benign Neoplasm

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-Non-cancerous (localized)
-Cells are cohesive
-Well defined borders(encapsulated)
-Cells move outward--DOES NOT SPREAD
-Growth is slow and can be stable

Front 30

Malignant Neoplasm

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-Growth is rapid & progressive
-Cells are not cohesive
-Iirregular expansion (unencapsulated)
-Invades and destroys tissue
-Proliferating cell --> break off & spreads-->secondary tumors

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Well differentiated

Back 31

--close resemblance to ancestors
-Benign neoplasm usually well differentiated

Front 32

Poorly differentiated

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--undifferentiated--only slight resemblance to ancestors--unspecialized proliferating elements
-Malignant neoplasm = poorly differentiated

Front 33

Metastases

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area of secondary growth

Front 34

ROUTES of metastases/metastasis

Back 34

-Vascular system --follows route
-Lymphatic system
-Across body cavity

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Metastasis

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process of discontinuous spread of malignant meoplasm

Front 36

Host Impact on Neoplasm

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1- ****Neoplasms needs O2 & Nutrients
2- Makes a vascular supply line from adjacent tissue
stroma-supporting framework **not a part of neoplastic cell
***body may modulate the growth of the stroma--antineoplastic defense
immunologic reaction from the body

Front 37

Anaplasia

Back 37

"dedifferentiation"
-A reversion of differentiation in cells
-Characteristic of malignant neoplasms

Front 38

antineoplastic defense

Back 38

***body may modulate the growth of the stroma
-Immunologic reaction from the body

Front 39

Cancer Cell Transformation

Back 39

1 -Independence from normal cellular controls
2 -Anchorage independent
3 -Immortal
4 -Anaplasia

Front 40

Cancer Stem Cells

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-Self-renew (Cell divisions create new stem cells)
-Multipotent (Ability to differentiate into multiple different cell types)

Front 41

Tumor cell markers

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(biological markers) are Substances produced by cancer cells or that are found on plasma cell membranes, in the blood, CSF, or urine

Front 42

Types of tumor cell markers

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Hormones
Enzymes
Genes
Antigens (ex. PSA)
Antibodies

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Tumor markers are used to:

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1- Screen and identify individuals at high risk for cancer
2- Diagnose specific types of tumors
3- Observe clinical course of cancer

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Cancer causing mutations

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Clonal proliferation or expansion:
-Due to a mutation, a cell acquires characteristics that allow it to have selective advantage over its neighbors
-Ex. Increased growth rate or decreased apoptosis (programmed cell death)
****Multiple mutations are required before cancer can develop

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Types of mutated genes

Back 45

1 -Secretion of growth factors (autocrine stimulation)
2 -Increased growth factor receptors
3- Signal from cell-surface receptor is mutated in the “on” position
4- Mutation in the ras intracellular signaling protein
5 -Inactivation of Rb tumor suppressor
6 -Activation of protein kinases that drive the cell cycle
7 -Mutation in the p53 gene

Front 46

ras

Back 46

intracellular signaling protein
(mutation can occur here)

Front 47

Angiogenesis

Back 47

-Growth of new vessels
-Advanced cancers can secrete angiogenic factors

Front 48

Telomeres and Immorality

Back 48

-Body cells are not immortal and can only divide a limited number of times
-Telomeres are protective caps on each chromosome and are held in place by telomerase
-Telomeres become smaller and smaller with each cell division
-With cancer telomeres don't become smaller/break off

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Proto-oncogene

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A normal, nonmutant gene that codes for cellular growth

Front 50

Oncogenes

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Mutant genes that in their nonmutant state direct protein synthesis and cellular growth

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Tumor-suppressor genes

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Encode proteins that in their normal state negatively regulate proliferation
Also referred to as anti-oncogenes
(fix mutated cells or sends signals to alert the rest of the body)

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Point mutations

Back 52

Changes in one or a few nucleotide base pairs

Front 53

Types of Mutation of Normal Genes

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1 -Point mutations
2 -Chromosome translocation
3 -Gene amplification
4 -Mutation of tumor-suppressor genes
5 -Loss of heterozygosity
6 -Gene silencing
7 -Mutation of Caretaker genes
8- Chromosome Instability

Front 54

Chromosome translocation

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A piece on one chromosome is transferred to another

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Gene amplification

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Duplication of a small piece of chromosome over and over
Results in an increased expression of an oncogene

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Mutation of tumor-suppressor genes

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Allows unregulated cellular growth

Front 57

Loss of heterozygosity

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Both chromosome copies of a gene are inactivated

Front 58

Gene silencing

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Whole regions of chromosomes are shut off while the same regions in other cells remain active

Front 59

Exposure to mutagens

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-If the mutation occurs in somatic cells, it is not passed to progeny
-If the mutation occurs in germline cells (sex cells - sperm and ova), it can be passed to future generations

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Implicated Viruses in Cancer

Back 60

1 -Hepatitis B and C viruses
2- Epstein-Barr virus (EBV)
3 -Kaposi sarcoma herpesvirus (KSHV)
3 -Human papillomavirus (HPV)
4 -Human T cell leukemia–lymphoma virus (HTLV)

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Bacterial Cause of Cancer

Back 61

Helicobacter pylori

Front 62

Chronic H-pylori infections are associated with:

Back 62

1 -Peptic ulcer disease
2 -Stomach carcinoma
3 -Mucosa-associated lymphoid issue lymphomas

Front 63

Environmental Risk Factors for Cancer

Back 63

1 -Tobacco
2 -Ionizing radiation
3 - Alcohol consumption
4 - Diet
5 -Obesity
6 -Occupational hazards
7 - Electromagnetic fields???
8 -Physical Activity
9 -Sexual Activity
10 -UV radiation

Front 64

Tobacco

Back 64

-Multipotent carcinogenic mixture (environmental risk factor)
-Linked to cancers of the lung, lower urinary tract, aerodigestive tract, liver, kidney, pancreas, cervix uteri, and myeloid leukemia

Front 65

Ionizing radiation

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-Emission from x-rays, radioisotopes, and other radioactive sources (environmental risk factor)

Front 66

-Ionizing radiation exposure causes:

Back 66

1- cell death
2- gene mutations
3- chromosome aberrations
-Bystander effects
-Poor gene repair
-Changes in gap junction intercellular communication

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Ultraviolet radiation

Back 67

(environmental risk factor)
Causes basal cell carcinoma, squamous cell carcinoma, and melanoma
Principal source is sunlight
Ultraviolet A (UVA) and ultraviolet B (UVB)
Promotes skin inflammation and release of free radicals

Front 68

Alcohol consumption

Back 68

(environmental risk factor)
Risk factor for oral cavity, pharynx, hypopharynx, larynx, esophagus, and liver cancers
Cigarette/alcohol combination increases a person’s risk

Front 69

Sexual reproductive behavior

Back 69

(environmental risk factor)
Carcinogenic types of human papillomavirus
High-risk HPV

Front 70

Physical activity

Back 70

(environmental risk factor)Reduces cancer risk
Decreases insulin and insulin-like growth factors
Decreases obesity
Decreases inflammatory mediators and free radicals
Increased gut motility

Reduces cancer risk
Decreases insulin and insulin-like growth factors
Decreases obesity
Decreases inflammatory mediators and free radicals
Increased gut motility

Front 71

Electromagnetic fields

Back 71

(possible environmental risk factor)
Carcinogenic?
Are they, or aren’t they?

Front 72

Occupational hazards

Back 72

(environmental risk factor)Substantial number of occupational carcinogenic agents:
Asbestos
Dyes, rubber, paint, explosives, rubber cement, heavy metals, air pollution,
Radon

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Diet

Back 73

(environmental risk factor)
Xenobiotics: toxic, mutagenic, and carcinogenic chemicals in food
-Activated by Phase I activation enzymes
-Defense mechanisms
Phase II detoxification enzymes
-Ex: Compounds produced in the cooking of fat, meat, or proteins
-Ex. Alkaloids or mold by-products

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Obesity

Back 74

(environmental risk factor)
-Correlates with the body mass index (BMI)
-Adipose tissue is active endocrine and metabolic tissue
-In response to endocrine and metabolic signaling, adipose tissue releases free fatty acids
-Increased free fatty acids gives rise to insulin resistance and ...
-causes chronic hyperinsulinemia
-Correlates with colon, breast, pancreatic, and endometrial cancers

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Most childhood cancers originate from the:

Back 75

Mesodermal germ layer
-mesodermal layer gives rise to connective tissue, bone, cartilage, muscle, blood, blood vessels, gonads, kidneys, and the lymphatic system

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Mesodermal germ layer gives rise to:

Back 76

Most childhood cancers originate from here.
1- connective tissue
2- bone
3- cartilage
4- muscle
5- blood
6- blood vessels
7- gonads
8- kidneys
9- lymphatic system

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Most common childhood cancers

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1- leukemias
2- sarcomas
3- embryonic tumors

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Embryonic tumors

Back 78

-Originate during uterine life
-Immature embryonic tissue unable to mature or differentiate into fully developed cells
-Commonly named with the term “blast”

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Etiology of Childhood cancers

Back 79

Genetic factors:
1- Oncogenes & tumor-suppressor genes
2- Chromosome abnormalities
Environmental factors:
1- Prenatal exosure to drugs or ionizing radiation
2- Increase parental age
3- Childhood exposure to drugs, ionizing radiation, or viruses

Front 80

Genetic Childhood factors

Back 80

1- Oncogenes & tumor-suppressor genes
2- Chromosome abnormalities
Aneuploidy (abnormal number of chromosomes), amplifications, deletions, translocations, and fragility

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Environmental factors

Back 81

1- Prenatal exposure to drugs (DES = >rate of uterine cancer) and ionizing radiation
2- Increased parental age (women & men, but especially women)
3- Childhood exposure to drugs, ionizing radiation, or viruses
Anabolic androgenic steroids, cytotoxic agents, immunosuppressive agents, Epstein-Barr virus, and HIV

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Childhood Cancer Prognosis

Back 82

-78% of children w/cancer are cured
-Children are more responsive and are better able to tolerate treatments
-More likely to be enrolled in clinical trials
-Long-term effects of treatment unknown
-Psychological ramifications
-High reoccurance rate

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Childhood Cancer Traits

Back 83

<1% of cancers
-Involves tissue
-Nonepithelial and mesenchymal
-Short latency
-Ecogenetic involvement
-Few prevention strategies
-Detection commonly accidental
-80% have metastasized at time of diagnosis
-Responsive to treatment
-Long-term consequences with treatment
>70% cure

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Adult Cancer Traits

Back 84

>99% of cancers
-Involves organs
-Carcinomas
-Long latency period
-Strong environmental and lifestyle influence
-80% preventable
-Screening linked to possible early detection
-Cancers are local or regional at time of diagnosis
-Less responsive to treatment
-Fewer long-term consequences
<60% cure

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Incidence rate

Back 85

Number of new cases of a disease reported during a specific period (typically 1 year) divided by the number of individuals in the population

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Prevalence rate

Back 86

Proportion of the population affected by a disease at a specific point in time

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Relative risk

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Incidence rate of a disease among individuals exposed to a risk factor divided by the incidence rate of a disease among individuals not exposed to a risk factor

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Polygenic

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Variation in traits caused by the effects of multiple genes

Front 89

Quantitative traits

Back 89

Traits that are measured on a continuous numeric scale

Front 90

Multifactorial trait

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Variation in traits caused by genetic and environmental or lifestyle factors (heart disease)

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Monozygotic

Back 91

identical twins

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Discordant trait

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A twin pair does not share a trait

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Concordant trait

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Both members of a twin pair share a trait

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Dizygotic

Back 94

fraternal twins

Front 95

Adoption studies

Back 95

Children born to parents who have a disease but are then subsequently adopted by parents lacking the disease are studied for the recurrence of the disease
(most prove genetic)

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Congenital malformations

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-Congenital diseases are present at birth or shortly after birth
-Most are multifactorial

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Adult Multifactorial Diseases

Back 97

1- Coronary Heart Disease
2- Alzheimer's
3- Familial Hypercholestremia
4- Hypertension
5- Breast Cancer
6- Colorectal Cancer
7- DM
8- Obesity
9- Alcoholism
10- Schizophrenia
11- Bipolar (??)

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Schizophrenia

Back 98

Severe emotional disorder characterized by delusions, hallucinations, and bizarre, withdrawn, or inappropriate behavior
-Recurrence risk among the offspring of one affected parent is 10 times higher than the general population
-Twin and adoption studies indicate that genetic factors are likely to be involved

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Bipolar affective disorder

Back 99

Genetics
Minimal environmental influence

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Alcoholism

Back 100

Alcoholism risk is 3 to 5 times higher in individuals with an alcoholic parent
Adoption studies
Offspring of nonalcoholic parents, when reared by alcoholic parents, did not have an increased risk
Twin studies
Concordance rates
MZ: >60%
DZ: <30%

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Alzheimer Disease

Back 101

Progressive dementia and loss of memory
Formation of amyloid plaques and neurofibrillary tangles in the brain
Risk of developing AD doubles in individuals who have an affected first-degree relative
Mutations in any of three genes that affect amyloid-beta deposition
Presenilin 1 (PS1)
Presenilin 2 (PS2)
Amyloid-beta precursor protein gene (APP)

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Obesity

Back 102

Body mass index >30
BMI = W/H2 (weight in Kg and height in meters)
Obesity is a substantial risk factor for heart disease, stroke, and type 2 diabetes
Adoptive studies
Body weights of adopted individuals correlated significantly with their natural parents’ body weights
Twin studies
Higher concordance in MZ twins than DZ twins

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DM II

Back 103

80% to 90% of all diabetes cases
Neither HLA nor autoantibodies are commonly seen in type 2
Patient has insulin resistance or diminished insulin production
Risk factors
High carbohydrate diet and obesity
Recurrence risk
0.90 MZ twin concordance rate
10% to 15% sibling recurrence

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DM I

Back 104

Autoimmune destruction of insulin-producing beta cells in the pancreas
T cell activation and autoantibody production
Onset before 40 years of age
Higher incidence with the offspring of diabetic fathers
Recurrence risk
0.55 MZ twin concordance rate
1% to 6% sibling recurrence

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DM (general)

Back 105

Leading cause of blindness, heart disease, and kidney failure
Two major types
Type 1 (insulin-dependent diabetes mellitus)
Type 2 (non–insulin-dependent diabetes mellitus)

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Colorectal cancer

Back 106

1 in 20 Americans will develop colorectal cancer
Second only to lung cancer
Risk factors
Genetics
High-fat and low-fiber diet are contributors

Front 107

Breast Cancer

Back 107

Affects 12% of American women who live to be 85
If a woman has a first-degree relative with breast cancer, her risk doubles
Recurrence risk increases if the age of onset in the affected relative is early and if the cancer is bilateral
An autosomal dominant form of breast cancer (5% of breast cancers) has been linked to chromosomes 13 and 17
Other genes are implicated

Front 108

Hypertension

Back 108

Risk factor for heart disease, stroke, and kidney disease
Studies show that 20% to 40% of blood pressure variations are genetic. This means that 60% to 80% are environmental.
Causes of hypertension
Sodium intake, lack of exercise, stress, obesity, smoking, and high-fat intake

Front 109

Familial Hypercholestrerolemia

Back 109

Autosomal dominant
1 in 500 is heterozygous for the FH gene; 1 in 1 million is homozygous for the trait
Serum cholesterol 300 to 400 mg/dL in heterozygote; 600 to 1200 mg/dL in homozygote
Cholesterol deposits in arteries and skin (xanthomas)

Front 110

Coronary heart disease

Back 110

Potential MI caused by atherosclerosis
Risk increases if:
There are more affected relatives
Affected relatives are female rather than male
Age of onset is younger than 55 years
Autosomal dominant familial hypercholesterolemia, high-fat diet, lack of exercise, smoking, and obesity

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What is health?

Back 111

Absence of disease?
Body’s ability to maintain homeostasis
Ability to meet demands on the body
Ability to adapt to external changes (vasoconstrict/vasodiolate)
Maintain constant internal environment (narrow limits)

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Causes of Variations in Normal Values

Back 112

-genetic makeup
-life experiences/interactions w/environment
-individuals’ control mechanism for body function
-the measurement process's error or capabilities
(If a value comes out wrong, do it again)

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Assessment of values

Back 113

-complex process
-know the variability of the measurement
(Ex. BP: know the high/low, time of day variations, what acceptable for that person)
-account for individual variation and baseline
-evaluate the measurement process/technique
****Evaluate the entire context of the individual
****Single measurement does not indicate abnormality

Front 114

Cultural influences

Back 114

what is a normal parameter? (weight, height)
what is assessed? (ex. attention deficit syndrome)
Doesn’t exist until you can test for it and have criteria.
what is accepted? (eccentric, Tourrette’s-Canadian small town)

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Disease

Back 115

1- Changes in an individual that causes health parameters to fall outside normal range.
2- Inability to maintain homeostasis
3- Inability to meet external demands (ADL)
3- It is an extension or distortion of normal processes. (Cancer - cell changes, MI-inflammation)
-Disease is the sum of physiologic processes that have been distorted.

Front 116

Disease Assessment

Back 116

1- Identify the process interfered with
2- Identify the character of the disturbance (how bad is it)
3- Identify secondary effects and disturbances

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Etiology

Back 117

Causes and/or reasons

Front 118

Disease Etiology = Causes and/or reasons

Back 118

causative agent or event
H1N1: Etiology: virus; resulting factor: pneumonia
Nausea/vomiting for three days ... OK for young adult; deadly for elderly and baby (age is a factor)
contributes of other factors:
-internal or external factors that provoke or contribute to the disease
-age
-nutritional status,
-physical status or problem

Front 119

Disease Etiology (other factors)

Back 119

Consider the contributes of other factors:
-internal or external factors that provoke or contribute to the disease
-age
-nutritional status,
-physical status or problem

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Pathogenesis

Back 120

development or evolution of a disease
Disease is dynamic with a rhythm and pattern (ex. 24 hr flu)

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Natural history of dx =

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evolution, impact, and duration
ex. rapid onset, prodrome, self-limited, chronic, remissions, exacerbations (asthma)

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Lesions

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structural changes - gross &/or microscopic caused by the disease

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Sub-clinical

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detected by lab results (kidney dx--CR level)

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Outcomes of Disease

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sequela/sequalae

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Complications

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new or separate process that results from some change caused by the primary dx

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Resolution

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host returns to a normal state