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250 Cards in this Set
- Front
- Back
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disease
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is defective biologic function
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etiology
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the cause of disease
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pathogenesis
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the natural history and development of disease
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lesion
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the anatomic abnormalities of a disease
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pathophysiology
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the abnormal functionality of a disease
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explain the difference between anatomic and clinical pathology
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anatomic pathology is the study of structural change
clinical pathology is the study of functional change |
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describe the relationship between structure and function
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structure and function are intimately related;
abnormal structure often produces abnormal function, and vice versa |
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symptom
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are complaints reported by the patient, or someone else and are a part of the medical history
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sign
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direct observations by the examiner (MD, PA, RN)
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explain the meaning of normal and abnormal
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normal and abnormal are terms applied to observations (ex: blood tests, physical findings, history, radiographs)
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explain the meaning between healthy and sick
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healthy and sick are terms applied to the underlying disease
(diseased structure or function) or lack of disease |
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describe differences among true positive, false positive, true negative, false negative tests
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these terms characterize test results according to whether or not the test correctly points to a healthy or diseased state.
most patients with a disease have abnormal results (tests that are true positives). most healthy patients have normal test results (tests that are true negatives). false-positive tests are ABNORMAL tests in healthy patients. false-negative tests are NORMAL tests in patients with disease. |
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meaning of normal range as it relates to medical tests
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a normal range is established for tests that have numerical results
normal range is defined by statistical methods to include 95% of test results in a population of healthy persons. it follows that 5% of healthy persons will have abnormal results |
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test sensitivity
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the ability of a test to be positive in the presence of disease
ex: a test is 99% sensitive if it is positive in 99 of 100 patients *known* to have the disease |
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test specificity
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the ability of a test to be negative in the absence of disease
ex: a test is said to be 99% specific if it is negative in 99 of 100 persons known NOT to have the disease |
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explain the concept of the predictive value of test results
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the purpose of testing is to determine who has the disease and who does not. a useful test has high predictive value; that is it accurately predicts who has/does not have disease.
If a test has many true-positives and few false-positives, the predictive value of a positive test is high. Likewise, if a test has many true-negative results and few false-negative results, the predictive value of a negative test is high. |
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why should sensitive tests be used first in the diagnostic process?
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positive results with a highly sensitive test include almost all people with disease, plus some that are healthy. it misses few who have the disease. this positive group can then be tested in follow up by a highly specific test.
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prevalence
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the prevalence of a disease is the number of individuals per 100,000 who have the disease at any given time.
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incidence
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is the number of new cases appearing each year
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why is it futile to test for disease in a population in which the prevalence of disease is very low?
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most positive results will be false-positive results
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acute disease
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arises rapidly, is accompanied by distinctive symptoms & lasts a short time
ex: acute otitis media |
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chronic disease
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usually begins slowly, with signs and symptoms that are difficult to interpret, persists for a long time, and generally cannot be prevented by vaccines or cured by medication
ex: arthritis |
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the purpose of inflammation
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the purpose of inflammation is to limit the extent and severity of injury, eliminate or neutralize the offending agent, and to initiate the repair process
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the main cell types in acute and chronic inflammation
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acute inflammation: neutrophils
chronic inflammation: lymphocytes, monocytes (macrophages) and plasma cells |
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acute inflammation
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acute inflammation occurs with short-term injury and lasts a few hours or a week or so.
features: a cell infiltrate of neutrophils |
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chronic inflammation
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occurs with persistent injury and lasts weeks or years.
features: an infiltrate of lymphocytes and monocytes (macrophages) an sometimes plasma cells |
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describe the sequence of events in acute inflammation
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vasodilation,
edema neutrophil infiltration monocyte & macrophage infiltration resolution |
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4 classic clinical signs of inflammation
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calor (heat)
rubor (redness) dolor (pain) tumor (swelling) |
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3 gross anatomic types of inflammatory exudate
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serous
fibrinous purulent |
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4 possible outcomes of acute inflammation
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-complete resolution
-scar -abscess -chronic inflammation |
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usual causes of chronic inflammation & examples
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-persistent infection: tuberculosis
-autoimmune disease: RA -persistent exposure to injurious agents: daily cigarette smoking |
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granulomatous inflammation
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-a special form of chronic inflammation characteristic of tuberculosis, but also seen in a few other conditions
-it features large nodules of macrophages, some of which merge to form giant cells with dozens of nuclei |
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outcomes of chronic inflammation
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scar and persistent chronic inflammation
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distant effects of inflammation
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involvement of lymphatics and lymph nodes, and systemic effects such as fever, malaise, leukoctosis, and poor appetite, the production of reactant proteins (like fibrinogen and CRP)
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2 important reactant proteins found in the blood in inflammation
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-C-reactive protein
-fibrinogen - accounts for elevated erythrocyte sedimentation rate (ESR) |
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the inflammatory response to various agents:
-bacteria -syphilis & other spirochetes -parasites -viruses |
-bacteria: produce a neutrophilic, acute, pyogenic (suppurative, purulent) inflammation
-syphilis/spirochetes: cause chronic inflammation (mostly lymphocytes) -parasites: invoke an infiltrate of eosinophils -viruses: evoke an infiltrate of lymphocytes |
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plasma derived mediators of inflammation
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the clotting system
the complement system the kinin system |
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plasma derived mediators of inflammation:
clotting system |
set of dozen proteins that interact w/ one another in a complex cascade to cause blood to clot
(activates the complement/kinin systems) |
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plasma derived mediators of inflammation:
complement system |
set of 2 dozen proteins that react w/ one another in chain reactions. products cause vasodilation, attract WBCs, and directly attack & destroy microbes
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plasma derived mediators of inflammation:
kinin system |
closely related to clotting system
consists of dozen or more proteins that cause vasodilation, increased endothelial cell permeability |
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brief explanation of a cell & of organization of tissues, organs, & organ systems
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a cell consists of a nucleus that is surrounded by cytoplasm, which is contained within a cell membrane.
-the nucleus is composed of DNA, which is organized into the genetic code, and which controls all cell activity. -the cytoplasm carries out the metabolic instructions of nuclear DNA. cells are organized into tissues, which are organized into organs, which are organized into organ systems |
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explain how genetic code is written into DNA
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the code is very long sequence of four specialized molecules, the DNA bases - adenine, thymine, guanine, cytosine ATGC respectively
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brief explanation of a cell & of organization of tissues, organs, & organ systems
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a cell consists of a nucleus that is surrounded by cytoplasm, which is contained within a cell membrane.
-the nucleus is composed of DNA, which is organized into the genetic code, and which controls all cell activity. -the cytoplasm carries out the metabolic instructions of nuclear DNA. cells are organized into tissues, which are organized into organs, which are organized into organ systems |
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explain how genetic code is written into DNA
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the code is very long sequence of four specialized molecules, the DNA bases - adenine, thymine, guanine, cytosine ATGC respectively
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explain the role of messenger RNA
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mRNA carries a copy of the genetic code from DNA in the nucleus to ribosomes in the cytoplasm, where the code is used to synthesize the protein coded by DNA
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the role of mitochondria
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mitochondria produce the energy required for metabolic processes
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apoptosis
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apoptosis is a natural, physiologic programmed cell death
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necrosis
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is pathologic death of cells because of injury
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explain the relationship of genes and environment in the pathogenesis of disease
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genese influence how we react to injury. some people are more disposed, other less disposed, to develop severe disease from a given injury
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what is the most common cause of cell injury
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hypoxia
-usually secondary to ischemia (low blood flow) |
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name one cell reaction resulting from mild acute cell injury
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acute mild injury- hydropic (vacuolar) change
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name one cell reaction resulting from mild chronic injury
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chronic mild injury - intracellular accumulations of fat, cholesterol, protein, glycogen, or pigments
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causes of cell atrophy
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reduced functional demand, inadequate blood supply,
lack of hormonal/neural support chronic injury cell aging |
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hypertrophy
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hypertrophy is tissue enlargement resulting from an increase in the size of individual cells
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hyperplasia
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is tissue enlargement resulting from increased number of cells
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dysplasia
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dysplasia is a premalignant change of cells typically seen in epithelium, in which the orderly arrangement of normal cells is replaced by a disorderly overgrowth of cells with enlarged, dark, irregular nuclei
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metaplasia
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metaplasia is the change of one cell type into another following stress or chronic injury; for example, the change of endocervical glandular epithelium into squamous epithelium as a result of chronic inflammation of the cervix (cervicitis)
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what is the consequence of severe, irreversible cell injury
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necrosis
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what is the most common CAUSE of necrosis and the most common TYPE of necrosis
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Coagulatie necrosis is the most common type of necrosis, it is most often caused by ischemia
(inadequate blood flow) |
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The Normal Range
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Used with numerical results
Defined by population sampling Standard Deviation (SD): natural variability of test results 95%: “normal” 5%: “abnormal” (2 SDs away) Therefore: Healthy people can have an abnormal test The reverse is also true: Sick people could have a normal test |
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DNA replication
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DNA is copied
The helix unwinds Bases are paired with their complimentary partners Held together by “centromere” Then DNA splits in half during Mitosis |
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Acute Injury
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#1: Hypoxia due to ischemia
Ex. Stroke Mild: hydropic (vacuolar) changes (reversible) |
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Chronic Injury
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Repeated injury
Ex. Hepatitis, Cirrhosis Intracellular accumulations of fat, cholesterol, protein, glycogen, or lipids (reversible) |
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atrophy
what it is, causes |
Decrease in size of an organ or tissue due to a decrease in mass of pre-existing cells
Causes: Reduced functional demand Loss of blood supply Lack of hormonal support Lack of neural support Chronic injury Cell Aging |
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Hypertrophy
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Increase in size of an organ or tissue due to an INCREASE in SIZE of cells
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metaplasia
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REPLACEMENT of one differentiated tissue by another
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Necrosis: elaborated
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-Pathologic death due to injury (#1: hypoxia from impaired arterial flow)
-Cellular swelling; entire sheets Tissue architecture disrupted. -Pyknosis, karyorrhesis, karyolysis = smudge of DNA Eosinophilia (RNA loss) -Disruption of organelles. Coagulative, caseous, or liquefactive destruction -Causes inflammatory rxn |
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Apoptosis: elaborated
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-Natural, programmed cell death
-Single cells: cell shrinkage. Cytoplasm and organelles condense. Minimum disruption of tissue. More intense stain. -Chromatin condensation along nuclear membrane. Laddering of DNA (200bp) -Apoptotic bodies; cytoplasm blebs; phagocytosis of apoptotic bodies (some contain nuclear fragments) -No inflammatory rxn |
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Disease is caused by...
Outcomes? |
Disease is caused by injury.
Outcomes: reparation, adaptation, or death (necrosis or apoptosis). |
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Types of Necrosis:
COAGULATIVE NECROSIS |
Hypoxic death (Infarct most common)
Heart, Kidney & Spleen Structure Preserved. Pale necrosis Inflammation Pyknosis, Karyolysis, Karyorrhexis |
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Types of Necrosis:
LIQUEFACTIVE NECROSIS |
Ischemic CNS.
Bacteria or fungus (staph, strep, E. coli) Enzymes: lysis Architecture not preserved. Cavity filled with liquid material/ empty |
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Types of Necrosis:
CASEOUS NECROSIS |
Bacterial or viral infections (most often TB, fungus)
Gross: Soft, grey-white and cheesy. Friable. Cell boundaries completely lost. Semi-solid. |
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Types of Necrosis:
FAT NECROSIS |
Injury to organs w/ high fat (Breast)
Enzymatic (acute pancreatitis) Enzymes digest triglycerides from fat FA form Ca salts: Dystrophic calcification: Chalky, gritty, white |
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chronic inflammatory cells
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lymphocytes
plasma cells monocytes macrophages |
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acute inflammatory cells
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neutrophils
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repair
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the body's collective attempt to restore normal structure and fucntion to the injured site
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regeneration
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one type of repair and is the complete or nearly complete restoration of normal anatomy and function by the regrowth of normal parenchymal cells and supportive tissue
-little or NO scarring is present |
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healing
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another type of repair that occurs when regeneration is partial or not possible
-some scarring is always present |
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what are the 2 main elements of the repair process?
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regeneration and fibrous repair (scarring)
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name the types of cells according to their ability to regenerate
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*Labile cells- divide continuously from a pool of stem cells
*Stable cells - have a reserve of stem cells & divide very slowly until stimulated by injury, after which they divide rapidly *Permanent cells - highly specialized, have no reserve of stem cells, and are incapable of division& regeneration |
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What is the importance of the basement membrane and extracellular matrix in the repair process?
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They provide structure upon which regenerating cells grow in an orderly manner
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Define: Wound
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A wound is the injury resulting from short-term injury at a discrete site
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List in sequence, the component steps in fibrous repair (scarring)
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1- fibrocyte migration
2- angioneogenesis 3- scar development |
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Causes of Inflammation
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Infection
Trauma Injury Physical (Thermal/Radiation) Chemical Immunologic Tissue death |
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Purpose of Inflammation
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Limit extent/severity of injury
Eliminate/neutralize offending agent Initiate repair process |
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Types of Inflammation:
SEROUS INFLAMMATION |
*Characterized by an effusion (thin watery fluid)
*Inc. vascular permeability Dec Protein *Skin blister Rheumatoid arthritis Viral infections |
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Types of Inflammation:
FIBRINOUS INFLAMMATION |
*Fibrin!
*More serious injury with increased vascular permeability Further inc. protein Inflammatory cells and serous fluid *Scab Mesothelial surfaces: Ex. Pericarditis after acute MI. |
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Types of Inflammation:
SUPPARATIVE (pyogenic) INFLAMMATION |
*Pus (neutrophils, necrotic cells, edema)
*Abscess- focal collection of inflammatory tissue from deep seeding of pyogenic bacteria Empyema: pus in body cavity *Pyogenic staphylococcal abscess (staph aureus). Acute appendicitis. |
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Acute Inflammation: more depth
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*Short term injury
*Lasts a few hrs/week *#1: Vasodilation w/ vascular gaps edema and neutrophil infiltrate Over time gives way to cells of chronic inflammation. *Outcome: complete resolution, scar, abscess, chronic inflammation |
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Chronic Inflammation: more depth
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*Chronic Inflammation
*Persistent injury *Lasts wks/yrs *Infection (TB), autoimmune (rheumatoid arthritis), chemicals (smoking) *Chronic inflammatory cells: characterized by lymphocytes, monocytes/macrophages, and plasma cells. *Outcome: scar or persistent chronic inflammation |
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Inflammatory response: exceptions to Bacteria
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*Chronic inflammation (lymphocytes)
*Syphillis/spirochetes |
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Distant Inflammatory Effects
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Involvement of lymphatics/lymph nodes
Systemic: fever, malaise, poor appetite, leukocytosis Production of Inflammatory proteins C-reactive protein Fibrinogen (elevated erythrocyte sedimentation rate) |
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Labile cells
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Divide continuously from pool of stem cells
*ex: Epithelium (skin & gut) |
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Stable cells
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*Reserve of stem cells, divide slowly until stimulated by injury- in which case divide more rapidly
*ex: Liver & kidney cells |
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Permanent cells
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*Highly specialized, no reserve of stem cells. Incapable of division and regeneration
*Heart & brain cells |
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Granulation Tissue: elaborated
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Mixture of new blood vessels, fibrous tissue, residual edema, & leukocytes.
Peak: few days into healing |
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Healing By Intention:
First Intention |
*Closely approximated edges
*Surgical incision *Inflammation-> Macrophage clean up -> neovascularization -> scarring |
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Healing By Intention:
Second Intention |
*Widely separated margins
*Skin or intestinal ulcers. *Same, but increased necrotic tissue. Re-epithelization is a longer process. |
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angiogenesis
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angiogenesis is the growth of new blood vessels into a wound
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Obstacles to normal repair
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-infection is the most common
-poor nutrition -steroid drug medication -diabetes -poor vascular supply -foreign body -mechanical forces that pull apart the wound |
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2 examples of pathological wound repair
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Keloid formation & Pyogenic granuloma.
-keloids are hyperplastic scars that are prominent, raised, or nodular, contain excess collagen -pyogenic granulomas are localized highly vascular collections of persistent granulation tissue |
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Blood pressure has 2 important functions:
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-to move blood through the blood vessels
-to aid in the diffusion of fluid across blood vessel walls from blood into tissues |
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Role of Endothelial Cells
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-separate blood from tissue, and act as a semipermeable membrane allowing passage of some substances from blood into tissues and blocking others
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For solutions with differing concentrations of dissolved substances on different sides of a semipermeable membrane:
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-solutions with a HIGH content of dissolved substances (salt) have HIGH osmotic pressure & attract H20 across the membrane from solutions with low content of dissolved substances
-solutions with a low content of dissolved substances have low osmotic pressure and favor loss of water across the membrane into solutions with a HIGH content of dissolved substances |
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What is the interstitial space?
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the space outside of blood vessels and between cells. it is the source of lymph fluid
everything that is exchanged between blood and tissue must pass through it. |
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Hemodynamic pressure
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is the pressure associated with moving blood through the vascular tree
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Hydrostatic pressure
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is the force exerted on blood vessel walls by the weight of a column of fluid (blood)
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Osmotic pressure
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osmotic pressure is a function of the amount of dissolved solids in water.
osmotic pressure is expressed as the amount of hydrostatic pressure that must be applied to fluid on one side of a membrane, the side with the lower water concentration (higher concentration of dissolved substances like salt), to prevent water from crossing the membrane from the side with the higher conc. of H20 (lower conc of dissolved substances) |
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describe the origin & flow of lymph fluid
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in capillaries the balance of blood pressure (hemodynamic pressure) and osmotic pressure forces a small amount of water out of blood vessels and into the interstitial space, where it replenishes interstitial fluid & enters the lymphatic system
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describe the origin and flow of lymph fluid
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in capillaries the balance of blood pressure (hemodynamic pressure) and osmotic pressure forces a small amount of water out of blood vessels and into the interstitial space, where it replenishes interstitial fluid and enters the lymphatic system
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briefly discuss body water compartments
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body water exists in several compartments, some of which are overlapping -- intravascular & extravascular, intracellular & extracellular.
-intravascular water is the main component of plasma, (an extracellular fluid) - most of the water in cells exists in extravascular tissues -clinically the most important compartment is intravascular fluid - blood cells and plasma. -more than 90% of plasma is water, 10% is protein, mainly albumin |
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briefly discuss body water balance
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almost all water is obtained from food and drink and is lost in stool, urine, perspiration, & respiratory air.
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Define Edema
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Edema is a shift of water from the vascular space into another compartment
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Types of Edema
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-inflammatory
-hydrostatic -osmotic -edema of lymphatic obstruction (lymphedema) **hydrostatic & osmotic edemas have LOW protein content **inflammatory & lymphatic edemas have HIGH protein content |
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Why does hydrostatic edema usually occur in the legs?
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Most edema occurs in the legs because hydrostatic pressure is highest there
(ie- the column of fluid - blood- above the lower leg is higher than at any other point in an erect patient) |
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How does proteinuria cause edema?
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Proteinuria (albuminuria) can cause protein to be wasted faster than it can be replaced by the liver; the result is low blood albumin (hypoalbuminemia). Since albumin accounts for most of the osmotic pressure in blood plasma, low albumin can therefore cause low intravascular osmotic pressure, which allows water to cross the vascular endothelium into the interstitial space.
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Hyperemia
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Active accumulation of blood (inflammation)
ex: sunburned skin, -the skin after exercise |
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Congestion
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Passive accumulation of blood (hydrostatic forces) associated with impaired venous outflow.
ex: the arm below and inflated blood pressure cuff. |
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Hemostasis
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The balancing act that keeps blood fluid.
Acts to stop blood loss: Vascular factors, Platelets, Coagulation factors |
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DIC
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Symptoms of CLOTTING and BLEEDING!
Consumes coagulation factors and platelets faster than the body can replace them Insufficient supply to stop blood loss. Spontaneous hemorrhage is the result |
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Petechia
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Smallest (1mm)
Pinpoint |
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Purpura
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A few mm
The middle man |
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Hematomas
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Cm
Pooled blood |
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Clotting
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-Designed to stop hemorrhages
-Structure: None clot= fibrin & platelets -Usually extravascular |
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Thrombosis
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-Pathologic process
-Architecture: Aggregation of platelets and white cells in layers -Intravascular |
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Embolism
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-Detached intravascular mass
-Thrombi are the MOST common. Can also be gas, or other solids/liquids. -Intravascular |
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Ischemia
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-Lack of O2 due to obstructed blood flow.
-Can cause infarct |
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Red Infarct
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-Hemorrhagic.
-Occurs in spongy tissue, or tissue with second blood supply. |
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White Infarct
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-Bloodless infarct.
-Dense solid tissue- heart or kidney. |
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Infarction:
slow or fast circumstances |
**If vascular occlusion occurs slowly- collateral circulation can develop
NO INFARCT! **If tissue is highly active metabolically, and there is low blood flow (not from occlusion) you can still have an infarct Even though the vessels are NORMAL |
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Shock
Cardiogenic |
Heart failure!
Ex. Infarct |
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Shock
Hypovolemic |
Dehydration
Hemorrhage Ex. Blood loss |
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Shock
Septic |
Bacterial endotoxins with severe systemic infection
Ex. Clostridium difficile |
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Stages of Shock
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Stages: Non-progressive, Progressive, Irreversible
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Benign
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*Grow slowly
*Do not metastasize *Rarely death *Round/smooth outline with fibrous capsule. *Adenoma |
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Malignant
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*Usually grow rapidly
*Can metastasize *Death… *Irregular outline, invading fingers Variegated surface: necrosis, hemorrhage, calcification, dark nuclei, mitotic figures *Sarcoma |
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Most common Cancers:
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MEN
Prostate (230,000) Lung (93,000) Colon & Rectum (72,000) WOMEN Breast (211,000) Lung (80,000) Colon & Rectum (73,000) |
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Most common Cancer Deaths:
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MEN
Lung (90,000) Prostate (30,000) Colon & Rectal (29,000) WOMEN Lung (73,000) Breast (40,000) Colon & Rectal (28,000) |
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congestion
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is a passive accumulation of excess blood in vessels resulting from hydrostatic forces
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hyperemia
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the active accumulation of excess blood in vessels owing to inflammation
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Define: hemostasis
& 3 elements of hemostasis that act to stop bleeding |
hemostasis refers to the combination of forces that maintain blood normally in a smooth, clot-free state & also stand ready to stop bleeding when it occurs.
-elements that act to stop bleeding: vascular factors, platelets, coagulation factors |
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Why is bleeding a problem with pts who have Disseminated Intravascular Coagulation (DIC)
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in DIC intravascular clotting consumes coagulation factors and platelets faster than the body can replace them, leaving blood without a sufficient supply of either;
*spontaneous hemorrhage is the result* |
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coagulation
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is a normal process that typically occurs outside of the vascular space
-intravascular coagulation is ALWAYS pathologic |
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Thrombosis
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is always a pathologic process and is always intravascular
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what is a clot made of?
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a clot is formed of FiBRIN, and entrapped blood cells and has NO internal architecture
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what is a thrombus made of?
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a thrombus is initially formed by pathologic aggregation of the formed elements of blood, in which platelets and white cells aggregate in layers, giving a thrombus its distinctive internal architecture
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define Embolus, and name the most common type of embolus
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an embolus is a detached intravascular mass (solid, liquid, gas) carried by blood to a distant site.
THROMBI are the most common emboli |
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define Ischemia
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ischemia is a lack of oxygen supply to tissue and is almost always caused by obstruction of blood flow.
-severe tissue ischemia can cause tissue death (infarct) |
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what is a white infarct
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is a bloodless infarct -- one that contains few RBC's.
-usually occur in ischemia in DENSE solid tissue like myocardium/ kidney |
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what is a red infarct?
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red infarct is a hemorrhagic infarct.
-these usually occur in loose, spongy tissue or in tissue with a second blood supply that continues to pump blood into the dead tissue |
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explain why arterial occlusion is not always followed by infarction, and why infarction may occur without arterial occlusion
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If vascular occlusion develops slowly and if collateral circulation is sufficient, complete occlusion of an artery may not produce an infarct because oxygenated blood can arrive by a secondary route.
-conversely, if blood flow is low, or blood is not carrying sufficient oxygen, infarction may occur in tissues supplied by patent vessels, esp. if the tissue is metabolically very active |
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name the types and stages of shock
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there are 3 types of shock:
-cardiogenic (pump failure) -hypovolemic (underfilled vascular space created by hemorrhage/marked vascular dilation -septic- assoc with bacterial endotoxins released during severe systemic infection. |
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the 3 stages of shock are...
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-nonprogressive,
-progressive -irreversible |
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Benign Neoplasms
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**Grow slowly, do not metastasize, and are usually not capable of causing death.
**Round/smooth outline with fibrous capsule. ex: Adenoma |
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Malignant Neoplasms
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**Grow rapidly, can metastasize, are capable of causing death.
**Irregular outline, invading fingers: Variegated surface: necrosis, hemorrhage, calcification, dark nuclei, mitotic figures. Growth is disorganized, normal structures are absent. ex: Sarcoma |
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name several types of carcinogenesis
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chemical (cigarette smoke)
radiation (x-ray or other ionizing radiation) viral (HPV) damage -all can alter the DNA to such an extent that the affected cell becomes malignant |
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define dysplasia,
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Dysplasia refers to a pre-malignant state of tissue (usually epithelium) that is atypical and clearly abnormal but not yet malignant.
(that is on its way but not completely autonomous) |
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define Carcinoma in situ
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Carcinoma in situ; is a malignant epithelium that has not penetrated the basement membrane, and therefore cannot metastasize.
-invasive carcinoma is a carcinoma that has invaded thru the basement membrane. -Some premalignant clinical conditions are HPV infx of cervix, Barrett metaplasia of esophagus, adenomatous polyps of colon, and chronic ulcerative colitis |
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explain the concept of doubling time and the growth of tumors
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a single malignant cell divides into One -> Two -> Four…. Etc.
*It takes 30 generations to reach detection size 1 gram/ size of a grape *Takes years (most of its life is before it becomes detectable) (it takes longer for tumor to go from one cell to grape, than from grape to football size) |
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tumor growth fraction
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tumor growth fraction is the percentage of tumor cells that are dividing
-tumors with high growth fraction grow more rapidly than do those with low growth fraction |
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why are the cells in a tumor that are most malignant the most likely to survive?
|
as the tumor grows, some tumor-cell variants develop mutations of one kind
-others develop mutations of a different kind -this variation of tumor cells is important for survival -some cells will be sturdier, more capable of defeating natural defenses |
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why do patients with immunodeficiency have increased risk for cancer?
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normal DNA and the proteins it encodes are recognized as self by the immune system and are therefore not subject to immune attack.
-injured DNA and its proteins become nonself and are subject to immune attack -most mutated cells are eliminated by immune system -pts w/ immune def. lack ability to eliminate mutated cells: and as result are more likely to develop neoplasms. -even in normal pts some cells can escape notice and develop into CA |
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explain paraneoplastic syndromes: give an example
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neoplasms may produce a general effect apart from the direct mass effect of the primary tumor/metastases.
-effect is usually the result of production of hormones by the tumor -ex: small cell carcinoma of the lung- produces variety of hormones, including ACTH which stimulates adrenal hyperplasia & Cushing syndrome |
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histologic grading
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histologic grading is microscopic (pathologic) assessment of the appearance of malignant cells
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histologic staging
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is a clinical exercise that assesses the size, location and degree of spread (if any) of the tumor, from its original state
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name 2 tumor factors found in blood & explain their use
|
1-PSA (prostate specific antigen)
2-carcinoembryonic antigen (CEA) -are tumor markers often found in blood in association with prostate (PSA) and colon (CEA) cancer. -they are NOT good sole screening tests for cancer because they are not very sensitive (too often the test result is negative in early disease=false negative) -levels of markers may be increased in non-neoplastic diseases, but they can be useful for monitoring tx/detecting recurrence of tumor |
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Metastases (places & facts)
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Locally/ Direct invasion
-Lymphatic invasion *Carcinomas -Vascular invasion *Sarcomas -Seeding body fluid and spreading through cavity Ovarian carcinoma through intraperitoneal spread |
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congenital deformation
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congenital deformations are caused by intrauterine mechanical factors.
ex- clubfoot is a deformation |
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congenital malformation
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congenital malformations are caused by intrinsic abnormalities of the embryologic developmental process.
ex- spina bifida |
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teratogen
-give example of chemical teratogen -give example of infectious teratogen |
a teratogen is an agent capable of inducing abnormal embryologic development to produce a fetal malformation
-most common are chemicals & viruses chemical- alcohol abuse -->FAS infectious - TORCH group, rubella |
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what is the TORCH group of teratogens?
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Toxoplasmosis
Rubella Cytomegalovirus Herpesvirus |
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cytogenetic disease
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cytogenetic disorders result from the absence or duplication of an entire chromosome
or to large scale structural dislocations of parts of a chromosome ex: Down Syndrome, three copies of 21 chromosome |
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single-gene (Mendelian) disease
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result from a defect of one gene and are inherited according to Mendelian principle
ex: sickle cell disease |
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polygenetic disease (resulting from multiple disease)
give examples |
its influence on the development of disease is associated with multiple genes, not usually identifiable.
ex: Type II DM - disease with clear polygenetic influences, these type of diseases are more common |
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autosomal dominant trait
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an autosomal dominant genetic characteristic requires only one copy of the gene (from mom or dad)
for the characteristic to be physically expressed |
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autosomal recessive trait
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requires two copies of the gene, one from each parent
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how is inheritance of genetic defects on the X chromosome different than gene defects on autosomes?
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principle difference is that a single defective recessive gene is expressed as disease when it occurs on an X chromosome.
-recessive genes are not expressed when they occur on autosomes unless BOTH copies of the autosome carry the same defective gene |
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name several examples of disease caused by single-gene defects
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-Gaucher disease
-familiar hypercholesterolemia -neurofibromatosis (von Recklinghausen disease) -Marfan syndrome -hemophilia A (classic) |
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how does cytogenetic disease differ from other genetic disease & give an example of a cytogenetic disease.
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a cytogenetic disorder is one in which there is:
-one or more extra chromosomes -a missing chromosome -large scale structural abnormalities such as missing parts (deletion), parts that are transported (translocation) to another chromosome, or parts that detach & reattach upside down (inversion). --in contrast other genetic diseases are caused by abnormalities in single genes (ex: Down syndrome) |
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explain the genetic abnormality in Turner Syndrome
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with abnormal meiosis in the testis, one sperm get both the X and Y, and the other gets no sex chromosome.
if the sperm with no sex chromosome fertilizes a normal X ovum the result is 45, X --> Turner Syndrome |
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Define: prematurity
& discuss associated risks |
an infant is premature if born before 37 weeks.
-premature infants are at higher risk for: -respiratory distress syndrome (due to immature lungs) -severe hyperbilirubinemia (can cause kernicterus, severe brain damage by deposits of bilirubin on floor of 3rd ventricle) |
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what's the differenc between prematurity and Small for Gestational Age (SGA)?
|
prematurity - born before end of 37th week of gestation
SGA - condition in which newborn infant weighs less than predicted for any given gestational age |
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Cystic Fibrosis
|
Defective chloride transport across epithelial cell membrane in ductal glands, and in respiratory/GI mucus glands
Low Cl-> Low Na-> dehydrated mucus Thick mucus -> obstruction Opportunistic infections |
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APGAR score
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An assessment of vigor: Maximum 10
More vigor: low perinatal morbidity and mortality and vice versa Rated 0,1,2 for the following: Heart rate Respiratory effort Muscle tone Color Response to catheter in nose |
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Perinatal Infection
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Perinatal period: From Week 28- Day 7
Most are bacterial Acquired during passage through the birth canal Or ascending infection from vagina into amniotic sac Whooping cough, diptheria, epiglottitis Most pediatric infections are viral: causing acute upper respiratory illnesses with fever, cough, rhinorrhea. Ex- measles, rubella, chickenpox, bronchiolitis, croup |
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SIDS
-risk factors |
RISKS
Under 6 months Prone sleeping position Prematurity Low birth weight Male sex Unmarried mothers <20 yrs Mothers who smoke Most with drug abuse Low socioeconomic condition African American ethnicity |
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Erythroblastosis Fetalis
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Rh-D negative mothers who develop Rh-D antibodies (due to prior pregnancy with Rh-D positive child)
Pregnant with subsequent Rh-D positive infant: Her antibody may attack infant’s red blood cells Causes hemolytic anemia |
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common perinatal infections of newborns
|
-most infections are bacterial and occur as infant passes thru vagina or from it traveling up thru vagina into embryonic sac
-most common: most are viral, many cause URI (w/ fever cough rhinorrhea) --> measles, rubella, chickenpox, bronchiolitis, croup bactieral -- whooping cough, diptheria, epiglottis |
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Define: Immunity
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a special function of lymphocytes & macrophages that defends the body against foreign (nonself) threats, mainly microbes
-by attacking and destroying the foreign substance |
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Define: autoimmune disease
|
diseases in which the immune system attacks the body's own tissues in addition to foreign ones
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what are the 2 principle nonimmune defense systems?
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1-surface barriers such as skin & mucosa
2- cellular and molecular nonimmune systems such as phagocytosis, natural killer cells, lysozymes, and the complement system |
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define: antigen
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an antigen is any substance capable of inciting an immune reaction
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define: antibody
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an antibody is an anti-antigen protein, an immunoglobulin, made by B cells to attack an antigen
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what are the 2 main types of immune cells?
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B-cells (B-lymphocytes) are programmed to produce and secrete circulating antibodies.
T-cells attack antigen directly by means of programmed receptors on their surface; no antibodies are involved |
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immunity
|
Lymphocytes and macrophages that defends body against foreign threats
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allergy
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Exaggerated but otherwise normal immune response against foreign antigen
**Against allergens- a sensitizing dose causes the hypersensitivity reaction **Mast cells! |
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autoimmune
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The immune system attacks self antigens.
Molecular mimicry: **Antigens on microbes or other foreign proteins share common antigenic features with self-antigens **Antibodies against microbe antigens cross-react with self-antigens |
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classify antibodies by type of protein...
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all antibodies are immunoglobulins & are found in the gamma globulin fraction of blood protein
there are 5 molecular types: -G,A,M,D, E. -the are formed quickly after antibody challenge and & constitute immediate response of the immune system for quick short-term protection. |
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The 5 molecular types & their prevalance & roles
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IgG: Most abundant, long term immunity
IgA: Secretory- protects mucosa IgM: Formed quickly after Ag challenge Provide quick short term protection IgD: IgE: involved in type 1 hypersensitivity Found in the gamma globulin fraction |
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Hypersensitivity:
Type I: Immediate hypersensitivity |
*Immediate Hypersensitivity
*Preformed antibodies. *Initial sensitizing exposure, causes reaction during subsequent exposure. *Anaphylaxis , Hay fever |
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Hypersensitivity:
Type II: Cytotoxic hypersensitivity |
*Antibody attaches directly to antigen.
*Causes cytolysis. *Immune hemolytic anemia Myasthenia Gravis |
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Hypersensitivity:
Type III: Immune complex hypersensitivity |
*Antigen and antibody form immune complex that incites inflammation or causes deposits
*Lupus, Farmer’s Lung |
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Hypersensitivity:
Type IV: Delayed Hypersensitivity |
T cell reaction independent of B cells (and Abs)
* T cell makes it different from other 3 types. ex: TB test |
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explain the immune reaction in type 1 hypersensitivity disease:
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*On first exposure IgE antibodies produced by B cells and attach to mast cells- coating mast cell with specific antibody against specific antigen
*On subsequent exposure antigen binds to IgE on mast cells *Triggers release of inflammatory and vasoactive substances (histamine and mast cell cytoplasmic granules) *Reaction attracts large numbers of eosinophils, causing local and peripheral blood eosinophilia. *Ex. Hay fever (allergic rhinitis), asthma |
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explain the principle difference between type 4 hypersensitivity reaction and the other 3 types
|
-Type 4 hypersensitivity is a T-cell immune reaction
-the other 3 types are B-cell system reactions |
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what is it meant by 'molecular mimicry'?
|
antigens on microbes or other foreign proteins share common antigenic features with self antigens.
-some antibodies made by the immune system against foreign antigens cross react with self-antigens; autoimmune disease is the result |
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Lupus
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Type III hypersensitivity (autoimmune disease)
Immune complexes deposit in tissue causing injury and inflammation Necrotizing vasculitis may affect any organ Heart Kidney Joints Skin Brain Serosal surface of lung, pericardia, peritoneal cavity |
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why can Type A blood not be transfused with Type B blood?
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Type A blood: have A Ag on RBCs **Also have anti-B anti-agglutinin- which agglutinates transfused type B red cells
**the minor crossmatch incompatibility betwen type A cells and AB plasma is not clinically significant |
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how are B & T cells affected during AIDS?
|
T-cells are attacked directly, and severely diminshed
-B cells also affected- react to HIV antigens and opportunistic infections but activity is ineffective w/out helper T cells (which are knocked out by HIV infx). result is increased but ineffective B-cell activity |
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most common AIDS risk groups in developed nations
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-homosexual males
-bisexual males -intravenous drug users -heterosexual contacts |
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Phases of HIV infection & appearance of AIDs
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Short “flu syndrome”: Sore throat, myalgia, fever and rash, high viral blood level, low T cell count.
Prolonged clinically quiet latent period: T cell count returns to normal (virus particles fall to low levels). Anti-HIV Abs. Crisis phase: T-cell count falls. AIDS-related neoplasms, opportunistic infections |
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explain the role of infections & AIDS defining neoplasms in HIV infection
|
Main types of malignancies: lymphoma, lymphocytic leukemia, plasma cell, Kaposi sarcoma, proliferations (multiple myeloma)
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3 types of malignancies of immune cells
|
-lymphoma
-lyhmphocytic leukemia -plasma cell proliferations (like multiple myeloma) |
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most common causes of death worldwide associated with Infection:
|
-respiratory infection
-HIV/AIDS -diarrheal diseases by infections -tuberculosis -malaria |
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infection
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the invasion of the body by a pathogen that results in tissue injury and inflammation
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contagion
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the spread of infections from one person to another
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nosocomial infection
|
an infection acquired at a hospital
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reservoir (of infection)
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a place where the pathogen exists and from which it spreads to new hosts
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carrier (of infection)
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a person or animal harboring the pathogen but suffering no obvious disease
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host (of infection)
|
infected person/animal
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vector (of infection)
|
an intermediate carrier, such as a mosquito, that carries pathogens from reservoir to patient
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crucial differences between bacteria and viruses
|
viruses are obligate intracellular parasites, are packets of protein without a cell wall
bacteria can live outside of cells, and are more complex structures |
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most common organ systems affected by the most common sources of infection:
|
GI tract
Respiratory tract Genital tract Skin |
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opportunistic pathogen
|
doesn’t cause disease in healthy people, but rather those with impaired immune systems
EX. Pneumocystic jiroveci pneumonia,cryptosporidial gastroenteritis, atypical tuberculosis, cytomegalic inclusion disease, cryptococcosis, toxoplasmosis, candidiasis, Pseudomonis aeruginosa infection |
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how to microorganisms spread in tissue
|
-they penetrate natural barriers (skin, GI mucosa, lungs, urogenital) epithelium to cause infections such as:
-abscess, diarrhea, pneumonia, or urinary infection --they may spread more after this by getting into blood or lymph |
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cellular inflammatory reaction to:
-bacteria -viruses -mycobacteria -fungi -parastici worms -protozoa |
bacteria - evoke NEUTROPHILS at the site and incr neutrophils in the blood
viruses - lymphocyte & monocyte reaction, few neutrophils mycobacteria & fungi - lymphocyte & monocyte reaction and formation of GIANT cell granulomas @ site of infxn parasitic worms- eosinophlic reax protozoa - lymphocyte & monocyte inflammation |
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dysentery
|
dysentery is severe, watery diarrhea with abd cramping & watery stools containing blood, pus & mucus
|
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|
what are several types of bacterial enteritis?
|
salmonellosis
shigellosis cholera |
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what are several STDs, the pathogen that causes them, and lesions associated with them (on the genitals)?
|
Syphilis - Treponema palladium
- an ulcer/canchre Gonorrhea - Neisseria gonorrhoeae -urethritis, prostatitis, epididymitis in men -salpingitis in women Chlamydia trachomatis - chlamydia infx, gonorrhea like manifestations in both sexes HPV- condyloma accuminata & dysplasia & cancer of cervix |
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what are several disease caused by Streptococcal organisms?
|
-acute streptococcal pharyngitis
-erysipelas -impetigo -UTI's -bacterial endocarditis -pneumonia -meningitis -dental caries, scarlet fever -acute rheumatic fever |
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what is a vector borne disease?
(including pathogen & vector) |
malaria- caused by Plasmodium protozoa & transmitted by mosquito bites
-rocky mountain spotted fever- caused by one of the Rickettsia and transmitted by ticks -Lyme disease -caused by spirochete Borellia burgdorfei - txm by ticks -Plague - is caused by Yersinia pestis & transmitted by rodent fleas |
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amebiasis
|
an infection by Entameoba histolytica, which infects hundreds of millions, most cases asympt.
but is 3rd most common fatal parasitic infx in world after malaria & schisomiasis. -infx acquired by eating food contaminated with shit that has amebic cysts in it. -ameba breaks out of cyst, invades colon, produces abd pain & diarrhea. invasion to portal blood produces amebic liver disease but could go to other organs too |
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|
what are the 2 parasitic diseases that cause the most morbidity and mortality
|
malaria & schistomiasis
|
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Clinical Phases of Infection
|
-after innoculation organism enters incubation period
-proliferates quietly or is destroyed by immune defense -prodrome - patient suffers from nonspecific symptoms -acute illness- during which typical symptoms are present -convalescent phase- symptoms fade & give way to ... -recovery - no symptoms present |
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|
Main causes of Death (in the western world)
|
#1: Cardiovascular disease
Stroke Malignancy Factors (in all 3): Diet Smoking Lack of exercise Alcohol is a factor in accidents Motor vehicle traffic accidents Firearms Acute toxic exposure (poisoning) Falls |
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|
Burns:
First degree burns |
without significant skin cell necrosis
-Erythema & edema |
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|
Burns:
Second degree burns |
Epidermal and superficial dermal necrosis
-Blisters |
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Burns:
Third degree burns |
Full thickness necrosis of epidermis and dermis
Deep skin appendages spared |
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|
what is a toxin?
some common examples of toxins? |
substance that threatens health/life
-lead -carbon monoxide -smoking |
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|
Carbon Monoxide
|
Leading cause of accidental poisoning death
Produced from incompletely burned fuel Gasoline, etc- 5% auto exhaust is CO Colorless and odorless Binds hemoglobin-> carboxyhemoglobin (bright red) Prevents O2 attachment-> anoxia |
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|
Lead
|
Older homes & factories
flaking lead based paint contaminated soil Earthen ware Impairs intellect, causes seizures, anemia of bone marrow, and renal failure |
|
|
Smoking
|
Cancer of lung, larynx, oral cavity, bladder, esophagus
Emphysema Generalized atherosclerosis Myocardial infarct Peptic ulcers |
|
|
Some examples of Chronic adverse reactions to medications:
|
-Steroids in treatment of rheumatoid arthritis
Can lead to Cushing syndrome: obesity, excess facial hair in females, diabetes, high blood pressure, fragile bones, immunocompromised -Estrogen replacement for postmenopausal osteoporosis/ hot flashes Increased breast cancer, thrombophlebitis, heart attack, stroke -Oral contraceptives Below normal risk: heart disease, decreased ovarian & uterine (endometrial) cancer If smoke: 3-10x normal risk of heart attack All: increased venous thrombosis & pulmonary thromboembolism |
|
|
Diseases other than lung cancer related to smoking
|
-emphysema
-generalized atherosclerosis -myocardial infarct -peptic ulcers -cancers of the larynx, mouth,bladder, esophagus |
|
|
What are several conditions associated with alcohol abuse?
|
-fatty liver
-cirrhosis -gastric ulcers -accidents -thiamine deficiency -cardiomyopathy, pancreatitis, HTN, spontaneous abortion, FAS -also associated with cancers of mouth, throat, larynx, esophagus,pancreas & bladder |
|
|
complications of intravenous drug abuse?
|
Coma and death
Pulmonary disease (foreign bodies) Kidney disease (immune complexes) Bacterial endocarditis (valves) |
|
|
malnutrition: marasmus
|
First stage,
Skeletal thinness Loss of muscle mass |
|
|
malnutrition: kwashiorkor
|
Second stage:
Loss of visceral protein Poor liver function: Generalized edema due to dec. albumin Infections from poor immune function |
|
|
obesity, BMI etc
|
18.5 underweight
Obesity Body mass index of >30 Body Mass Index Weight (kg)/Height(m)2 <18.5-24.9 normal 25.0-29.9 overweight 30.0-39.9 obese >/=40.0 morbidly obese |
|
|
metabolic syndrome
|
Lifesytle characterized
High carbs Lack of exercise Abnormalities: Abdominal obesity Abnormal glucose metabolism Abnormal plasma lipid levels Hypertension (high BP) At risk for diabetes and cardiovascular disease |
