Patho Exam 1 Red Text

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what is normal response to injury

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what is normal response to injury

Body NORMALLY reacts to injury through the inflammatory process

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neoplasm

Uncontrolled cell growth

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Idiopathic diseases

Without a known cause

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Iatrogenic diseases

physician produced

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Nosocomial infection

Infection acquired in the hospital

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Radiopaque

white on film (high density for X ray)

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Radiolucent

dark on film (low density on X ray)

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CT radiation load

Delivers higher dose of ionizing radiation than x-ray

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child (under 15) CT deaths

500 of these individuals might ultimately die

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MRI advantages over CT scan

MRI does not use ionizing radiation

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atrophy

Decrease in cell size or number

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12

hypertrophy

increase in size of cells

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13

hyperplasia

increase in number of cells

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Vascular supply is a limit on hypertrophy/hyperplasia

You can’t outgrow your blood supply!

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metaplasia

Conversion of a normal adult cell to another type of normal adult cell

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dysplasia

Always maladaptive (bad)

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dysplasia

Neoplasm (tumor or cancer) usually arises from dysplastic cells, which often arise from metaplastic cells

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Cell damage from low ATP

Na+ pumps fail, Water ALWAYS follows Na+

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19

necrosis is (reverisble or irreversible)

NECROSIS (Cell Death) IS IRREVERSIBLE

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Dr. David Pennington quote

“All of life is an effort to remain reduced”

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Ischemia

tissue effect from decreased oxygen supply

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Infarction

death of tissue due to sustained low/no oxygen supply

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What cell death causes inflammation

Dying (necrotic) cells produce acute inflammation as chemical mediators are released—inflammation does NOT occur with apoptosis

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what do the causes of inflammation v. necrosis look like

The causes of inflammation and necrosis are virtually identical

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apoptosis

Intentional, programmed death of a cell

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apoptosis v. necrosis

Apoptosis is normal and necessary - it is NOT necrosis

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Coagulation necrosis

Structure of tissue/organ maintained due to high protein content Lots of protein “scaffolding” supporting the tissue

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Liquefactive necrosis

Necrotic tissue becomes fluid Immune system (neutrophils) digests the “foreign” necrotic tissue Too little protein structure for coagulation necrosis Not enough protein scaffolding to maintain the tissue structure

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Caseous necrosis example

Tuberculosis

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Algor (sensation of cold) mortis (sign of death)

Room (environmental) temperature

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Rigor (rigid) mortis (sign of death)

Stiffened muscles

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Livor (purple/black/blue/bruised) mortis (sign of death)

Blood drains to dependent portions of body

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Antigen

large molecule (usualy protein)

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Specificity determined by protein shape segments or epitopes

Multiple different epitopes are present on a single antigen

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paratope

Glycoproteins (antibodies) have shape-specific indentation (paratope) that fits a specific epitope – lock for the key

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Humoral immunity

Antibodies for extracellular targets and free antigen

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Cell-mediated immunity (CMI)

Primarily cytotoxic T cells for intracellular targets

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CMI targets don't include

Does NOT respond to free antigen

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Clonal selection

When an epitope “fit” occurs between APC and a lymphocyte, lymphocyte is “selected” and activated

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Clonal expansion

Activated lymphocyte clones which can bind the epitope are stimulated to proliferate (divide) by helper T cells

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Natural Killer cells

Innate immune system (as opposed to adaptive immune system), Lack surface immunoglobulins; therefore, non-specific

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B cells

one epitope specificity, Become Plasma cells (part of B lymphocyte population), which produce massive amounts of epitope-specific antibody

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T cells

specific for one epitope

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classes of T cells

Helper T cells (CD4) Regulatory (Suppressor) T cells (CD4) Cytotoxic T cells (CD8) Memory T cells

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What do T cells respond to

respond to the combination of antigenic epitope and MHC molecule

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Dendritic cells

stellate macrophages specialized for antigen uptake, processing, and presentation

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Predominant antibody in anamnestic (secondary) response

IgG – most common, singleton

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48

Usually the first antibody produced during amnestic response

IgM – first produced, fiver (M for mega-size) Pentamer, macroglobulin

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Mast cells are studded all over with IgE – allergen binds one or two IgE sites, mast cell vomits histamine

IgE – ALLERGIES

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opsonization

binding and coating the invader (with complement or antibodies)

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MHC Class I

present on all nucleated host cells

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MHC Class II

present only on immune system cells (B lymphocytes, macrophages and related antigen-processing cells (APC) and some activated T lymphocytes (helpers and suppressors))

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Type I Hypersensitivity

allergy/atopic

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Type II Hypersensitivity

cytotoxic to cells (via antibodies)

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Type III Hypersensitivity

immune complex

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Type IV Hypersensitivity

delayed reaction (via cytotoxic T cells)

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Type I Hypersensitivity mech

IgE embedded in mast cells spew out histamine

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Type II Hypersensitivity mech

antibodies IgM or IgG bind to antigen on host cells

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Type III Hypersensitivity mech

response of antigens + antibody complex can get stuck to tissue/vasculature, and teh complement system and phagocytosis cause tissue damage

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Type IV Hypersensitivity mech

the secondary anamnestic response to an antigen causes the cytotoxic T cells to kill the cells and tissue and cuase inflammation

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Type I Hypersensitivity examples

seasonal allegies, atopic dermatitis, anaphylactic shock

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Type II Hypersensitivity examples

transfusion reactions, Rh rejection, some glomerulonephritis

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Type III Hypersensitivity examples

lupus, serum sickness, some glomerulonephritis

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Type IV Hypersensitivity examples

contact dermatitis, poison ivy

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Autoimmunity targets

Renal glomeruli and joints are frequent targets

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Autoimmunity sexual dimorphism

Females >> males

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Autoimmunity course

Exacerbation and remissions are the normal course

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Lupus

common in women, young adulthood (20s), kidney damage, wolf-like rash on face, spontaneous remission and exacerbation

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Schleroderma

worse outcomes, loss of facial flexibility, Raynaud's syndrome in fingers

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cell type distribution of tumors

a monoclonal tumor is inevitably composed of many subclones of the original cell

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carcinoma v sarcoma rates

Carcinoma is FAR more common than sarcoma

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Carcinoma

malignant tumor of epithelial-derived tissue

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Sarcoma

malignant non-epithelial (mesenchymal – connective tissue) tumor

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Mass Effect

expanding mass inside cranium compresses normal brain tissue

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Low grade neoplasia

low degree of histologic difference between neoplastic cells and origin cells

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High grade neoplasia

large histologic difference between neoplastic cells and origin cells

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Metastasis

non-contiguous spread (tumor cells break off and spread)

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Anaplasia

More primitive with loss of specialized structures ; The worse a neoplastic cell is, the more it regresses in maturity

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Benign tumors

DO NOT EVER metastasize!!!

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Most important (but not the only) determinant of malignant behavior

Non-contiguous spread to create a secondary tumor “distant” from the primary tumor

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Lymphatic metastasis

Invasive neoplastic cells enter/drain into lymphatic vessels -> LN -> beyond

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Hematogenous metastasis

Neoplastic cell invasion of blood vessels, typically veins -> usually to lungs or liver

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Implantation metastasis

Cells shed from tumor surface in a body cavity

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Carcinoma in Situ (CIS)

does not penetrate basement membrane

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Cancer cachexia

Weight loss, anorexia, anemia, malaise, weakness late in the course of tumors

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86

cancer mutations are (lethal or non-lethal)

nonlethal mutation

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87

cancer predisposition example

80% to 90%: no family history of breast cancer

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88

most common cause of cancer death in males/females

Lung cancer

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most common cancer affecting females

Breast cancer

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most common cancer affecting males

Prostate cancer

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cancer "survival"

Survival does not indicate cure; most cancer types recur, some prove fatal

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RBC IS ALL ABOUT THE SURFACE AREA!!

The biconcave structure of the normal RBC allows it to be more flexible and have more surface area

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RBC life span

~120 days • Old RBCs trapped and removed by macrophages in spleen/bone marrow • Abnormal fragility leads to early phagocytosis by M in spleen/BM

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Neutrophil life span

<12 hours

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95

High reticulocyte count in blood

indicates consumption of RBCs and increased production to replace them (bone marrow is functional)

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platelet life span

10 days in blood

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Heme

porphyrin ring that contains an iron atom

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98

Hgb A = α2β2

comprises 98% of normal hemoglobin

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All human hemoglobin has α chains

only the other chain pair varies

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100

hemoglobin tetramer

(4 globins and 4 hemes)

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