Patho Exam 1 Red Text

what is normal response to injury

what is normal response to injury

Body NORMALLY reacts to injury through the inflammatory process

neoplasm

Uncontrolled cell growth

Idiopathic diseases

Without a known cause

Iatrogenic diseases

physician produced

Nosocomial infection

Infection acquired in the hospital

Radiopaque

white on film (high density for X ray)

Radiolucent

dark on film (low density on X ray)

CT radiation load

Delivers higher dose of ionizing radiation than x-ray

child (under 15) CT deaths

500 of these individuals might ultimately die

MRI advantages over CT scan

MRI does not use ionizing radiation

atrophy

Decrease in cell size or number

hypertrophy

increase in size of cells

hyperplasia

increase in number of cells

Vascular supply is a limit on hypertrophy/hyperplasia

You can’t outgrow your blood supply!

metaplasia

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

dysplasia

Always maladaptive (bad)

dysplasia

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

Cell damage from low ATP

Na+ pumps fail, Water ALWAYS follows Na+

necrosis is (reverisble or irreversible)

NECROSIS (Cell Death) IS IRREVERSIBLE

Dr. David Pennington quote

“All of life is an effort to remain reduced”

Ischemia

tissue effect from decreased oxygen supply

Infarction

death of tissue due to sustained low/no oxygen supply

What cell death causes inflammation

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

what do the causes of inflammation v. necrosis look like

The causes of inflammation and necrosis are virtually identical

apoptosis

Intentional, programmed death of a cell

apoptosis v. necrosis

Apoptosis is normal and necessary - it is NOT necrosis

Coagulation necrosis

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

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

Caseous necrosis example

Tuberculosis

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

Room (environmental) temperature

Rigor (rigid) mortis (sign of death)

Stiffened muscles

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

Blood drains to dependent portions of body

Antigen

large molecule (usualy protein)

Specificity determined by protein shape segments or epitopes

Multiple different epitopes are present on a single antigen

paratope

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

Humoral immunity

Antibodies for extracellular targets and free antigen

Cell-mediated immunity (CMI)

Primarily cytotoxic T cells for intracellular targets

CMI targets don't include

Does NOT respond to free antigen

Clonal selection

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

Clonal expansion

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

Natural Killer cells

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

B cells

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

T cells

specific for one epitope

classes of T cells

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

What do T cells respond to

respond to the combination of antigenic epitope and MHC molecule

Dendritic cells

stellate macrophages specialized for antigen uptake, processing, and presentation

Predominant antibody in anamnestic (secondary) response

IgG – most common, singleton

Usually the first antibody produced during amnestic response

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

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

IgE – ALLERGIES

opsonization

binding and coating the invader (with complement or antibodies)

MHC Class I

present on all nucleated host cells

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))

Type I Hypersensitivity

allergy/atopic

Type II Hypersensitivity

cytotoxic to cells (via antibodies)

Type III Hypersensitivity

immune complex

Type IV Hypersensitivity

delayed reaction (via cytotoxic T cells)

Type I Hypersensitivity mech

IgE embedded in mast cells spew out histamine

Type II Hypersensitivity mech

antibodies IgM or IgG bind to antigen on host cells

Type III Hypersensitivity mech

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

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

Type I Hypersensitivity examples

seasonal allegies, atopic dermatitis, anaphylactic shock

Type II Hypersensitivity examples

transfusion reactions, Rh rejection, some glomerulonephritis

Type III Hypersensitivity examples

lupus, serum sickness, some glomerulonephritis

Type IV Hypersensitivity examples

contact dermatitis, poison ivy

Autoimmunity targets

Renal glomeruli and joints are frequent targets

Autoimmunity sexual dimorphism

Females >> males

Autoimmunity course

Exacerbation and remissions are the normal course

Lupus

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

Schleroderma

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

cell type distribution of tumors

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

carcinoma v sarcoma rates

Carcinoma is FAR more common than sarcoma

Carcinoma

malignant tumor of epithelial-derived tissue

Sarcoma

malignant non-epithelial (mesenchymal – connective tissue) tumor

Mass Effect

expanding mass inside cranium compresses normal brain tissue

Low grade neoplasia

low degree of histologic difference between neoplastic cells and origin cells

High grade neoplasia

large histologic difference between neoplastic cells and origin cells

Metastasis

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

Anaplasia

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

Benign tumors

DO NOT EVER metastasize!!!

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

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

Lymphatic metastasis

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

Hematogenous metastasis

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

Implantation metastasis

Cells shed from tumor surface in a body cavity

Carcinoma in Situ (CIS)

does not penetrate basement membrane

Cancer cachexia

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

cancer mutations are (lethal or non-lethal)

nonlethal mutation

cancer predisposition example

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

most common cause of cancer death in males/females

Lung cancer

most common cancer affecting females

Breast cancer

most common cancer affecting males

Prostate cancer

cancer "survival"

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

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

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

Neutrophil life span

<12 hours

High reticulocyte count in blood

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

platelet life span

10 days in blood

Heme

porphyrin ring that contains an iron atom

Hgb A = α2β2

comprises 98% of normal hemoglobin

All human hemoglobin has α chains

only the other chain pair varies

hemoglobin tetramer

(4 globins and 4 hemes)