Term
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Definition
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Definition
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Definition
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Definition
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Definition
|
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Term
| CLINICAL MANIFESTATIONS. The clinical manifestations of ARDS are progressive as follows: |
|
Definition
Dyspnea and hypoxemia with poor response to oxygen supplementation
Hyperventilation and respiratory alkalosis
Decreased tissue perfusion, metabolic acidosis, and organ dysfunction
Increased work of breathing, decreased tidal volume, and hypoventilation
Hypercapnia, respiratory acidosis, and worsening hypoxemia
Decreased cardiac output, hypotension, and death |
|
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Term
|
Definition
(Systolic BP 160 mmHg or
diastolic BP 100 mmHg)
Two-drug combination for most (usually
thiazide-type diuretic and ACE inhibitor
or ARB or beta-blocker or CCB) |
|
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Term
|
Definition
| Lymphocytes with receptors against self antigens are eliminated |
|
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Term
|
Definition
| these cells are suppress by regulatory T-cells and other mechanism |
|
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Term
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Definition
| Antibody producing cell- T-regulatory cells that suppress the immune response to self-antigen |
|
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Term
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Definition
| small antigen that binds to large molecule and induces an immune response |
|
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Term
|
Definition
| portion of the antigen that is recognized and bound by an antibody or specific lymphocyte. Antigenic determinant |
|
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Term
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Definition
| molecule that activates many the cell receptors regardless of their antigen specificity by binding in an usual location |
|
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Term
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Definition
| Presents endogenous antigen |
|
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Term
|
Definition
| presents exogenous antigen |
|
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Term
|
Definition
| a substance included in a vaccine to stimulate immune response |
|
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Term
|
Definition
| Lymphocytes with receptors against self antigens are eliminated |
|
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Term
|
Definition
| these cells are suppress by regulatory T-cells and other mechanism |
|
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Term
|
Definition
| Antibody producing cell- T-regulatory cells that suppress the immune response to self-antigen |
|
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Term
|
Definition
| small antigen that binds to large molecule and induces an immune response |
|
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Term
|
Definition
| portion of the antigen that is recognized and bound by an antibody or specific lymphocyte. Antigenic determinant |
|
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Term
|
Definition
| molecule that activates many the cell receptors regardless of their antigen specificity by binding in an usual location |
|
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Term
|
Definition
| Presents endogenous antigen |
|
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Term
|
Definition
| presents exogenous antigen |
|
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Term
|
Definition
| a substance included in a vaccine to stimulate immune response |
|
|
Term
| CD1 antigen-presenting molecules present exogenous___________ antigen |
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Definition
|
|
Term
| Helper T cells are MHC Class ___________ restricted, but cytoxi c cells are ___________MHC Class Restricted |
|
Definition
|
|
Term
| The secondary immune response also is called the ___________ response |
|
Definition
|
|
Term
| Cytokines secreted by the cell promote ___________ immunity; cytokines secreted by the cells promote ___________ immunity; cytokines secreted by th17 promote ___________; cytokines secreted by trey cells ___________ the immune response |
|
Definition
| Cellular; humoral; inflammatory; suppress |
|
|
Term
| class switch indicates that a b lymphoctye changes from producing ___________ to producing another class of IG |
|
Definition
|
|
Term
| Cytotoxic T cell kill their target by secreting ___________that make a pore in the membrane and injecting ___________ through the pore, causing apoptosis |
|
Definition
|
|
Term
| th1 cells activate macrophages by secreting___________ |
|
Definition
|
|
Term
|
Definition
| Define against parasites; degrade vasoactive substance released by mast cells. |
|
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Term
|
Definition
| release chemicals that initiate the inflammatory response |
|
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Term
|
Definition
| Eliminate virus-infected cells |
|
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Term
|
Definition
| Phagocytize microorganism and cellular debris;secrete chemicals that promote tissue healing; activate adaptive immunity |
|
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Term
|
Definition
| the first line of deference against microorganism |
|
|
Term
| Surfactants and other chemical defenses produced by lung epithelium are called ___________ |
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Definition
|
|
Term
|
Definition
| microorganism that normally colonized the body surfaces |
|
|
Term
| pattern recognization receptors |
|
Definition
| one innate immune cell can recognize many different type of pathogenic bacteria via this process |
|
|
Term
MAC is formed by activated___________cascade causes
___________ |
|
Definition
|
|
Term
| List the cells that are phagocyte innate |
|
Definition
|
|
Term
| List the cells that are non phagocytic innate |
|
Definition
| Mast, Natural killer cells |
|
|
Term
| List the cells that are adaptive |
|
Definition
|
|
Term
|
Definition
| Brief vasoconstriction, Vasodilation, Increased vascular permeability, Leakage of palm into tissue, Local edema |
|
|
Term
| Sequence the events that occur when a neutrophil phagocytes a microorganism in the tissue |
|
Definition
| Increased adhesion molecules, margination, diapedesis, cemotaxix, recognition and attachment, engulfment and formation of phagosome, formation of phagolysosome, destruction of microorganism |
|
|
Term
|
Definition
| is a pattern molecule associated with a pathogenic organisms |
|
|
Term
|
Definition
| is a molecular pattern that is associated with injured or stressed host cells. |
|
|
Term
|
Definition
| is nonspecific, meaning that one cell or other element will defend against many different type of antigens |
|
|
Term
|
Definition
| is specific meaning that one cell will defend against only one particular antigen. |
|
|
Term
| Sequence the events that occur when a neutrophil phagocytes a microorganism in the tissue |
|
Definition
| Increased adhesion molecules, margination, diapedesis, cemotaxix, recognition and attachment, engulfment and formation of phagosome, formation of phagolysosome, destruction of microorganism |
|
|
Term
|
Definition
| is a pattern molecule associated with a pathogenic organisms |
|
|
Term
|
Definition
| is a molecular pattern that is associated with injured or stressed host cells. |
|
|
Term
|
Definition
| is nonspecific, meaning that one cell or other element will defend against many different type of antigens |
|
|
Term
|
Definition
| is specific meaning that one cell will defend against only one particular antigen. |
|
|
Term
|
Definition
| are molecules that mark antigens for destruction by innate immune cells |
|
|
Term
|
Definition
| are signaling molecules that influence behavior of immune and other type of cells. |
|
|
Term
|
Definition
The phagocyte leaves the bloodstream and enters the tissue through interactions between leukocyte and endothelial
adhesion molecules and the process of diapedesis. |
|
|
Term
| In a healing wound, fibroblast, migrate to the area, which phagocytic cell secretes chemicals to attract them |
|
Definition
|
|
Term
| What is the function of the fibroblast |
|
Definition
| To secrete collagen to help scar tissue |
|
|
Term
| Does wound contraction occur before or after fibroblast migration and proliferation |
|
Definition
|
|
Term
| Another word for natural immunity and native immunity |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| containing many red blood cells |
|
|
Term
|
Definition
| Another term for purulent exudate |
|
|
Term
|
Definition
| watery with few proteins or cells |
|
|
Term
|
Definition
meaning that
original tissue structure and function have been restored if
little tissue has been lost or injured tissue is capable of regeneration. |
|
|
Term
|
Definition
involve extensive damage or tissues
incapable of regeneration heal by the process of repair
that results in the formation of a scar. |
|
|
Term
| The two stages of Resolution healing |
|
Definition
the
reconstructive phase, in which the wound begins to heal,
and the maturation phase, in which the healed wound is
remodeled. |
|
|
Term
| Order or development of mature CD4 cell |
|
Definition
| Lymphoid stem cell migrate to thymus, cell divides and differentiates developing t-cell receptors and surface markers, immunocompetent naive tell migrate to secondary lymphoid organs, APC presents processed antigen with MHC class II molecule to Tcellm cell differentiate and matures to CD4 cells. |
|
|
Term
| The Fab fragment binds to what |
|
Definition
| antigen, it consists of two chains. |
|
|
Term
| another name for an antigenic determinant |
|
Definition
|
|
Term
|
Definition
| active against parasites are important mediator of allergies |
|
|
Term
|
Definition
| Produced during the primary response to antigen, are the largest Igs |
|
|
Term
|
Definition
| Are the most abundant class of Igs are transported across the placenta |
|
|
Term
|
Definition
| has subclasses; one subclass is most abundant in body secretions |
|
|
Term
|
Definition
| function unknown in blood are surface receptors on developing b lymphocytes |
|
|
Term
|
Definition
| Plasma cell is the cell that makes antibodies; Antibodes are a protective part of immune system and normally defends us against bacteria and viruses. |
|
|
Term
|
Definition
an altered immunologic response to an
antigen that results in disease or damage to the host |
|
|
Term
|
Definition
is a disturbance in the immunologic tolerance
of self-antigens. |
|
|
Term
|
Definition
occurs when the
immune system of one individual produces an immunologic
reaction against tissues of another individual. Alloimmunity
can be observed during immunologic reactions against transfusions,
transplanted tissue, or the fetus during pregnancy. |
|
|
Term
| Type I: IgE-Mediated Hypersensitivity Reactions |
|
Definition
Most common allergies
(e.g., pollen allergies) are type I reactions. In addition, most
type I reactions occur against environmental antigens and are
therefore allergic. |
|
|
Term
II Tissue-specific
reaction |
|
Definition
IgG
IgM
Macrophages in tissues Frequently Autoimmune thrombocytopenic
purpura, Graves disease,
autoimmune hemolytic anemia |
|
|
Term
III Immune complex–
mediated reaction |
|
Definition
IgG
IgM
Neutrophils Yes Systemic lupus erythematosus |
|
|
Term
|
Definition
None Lymphocytes,
macrophages
No Contact sensitivity to poison ivy
and metals (jewelry) |
|
|
Term
|
Definition
| Steady state of tolerance to self-antigens or lack of immune reactions against environmental antigen. |
|
|
Term
|
Definition
| immune system of one individual produces an immunologic reaction against tissues of another individual |
|
|
Term
| Type II hypersensitivity is induced by 5 different mechanisms name them |
|
Definition
1. complement mediated lysis
2. opsonization and phagocytosis
3. neutrophil mediated tissue damage
4. antibody cell mediated toxicity
5. modulation of cellular function. |
|
|
Term
| Complement mediated lysis occurs when |
|
Definition
| IgG or IgM antibodies damage the cell membrane with resulting lysis of the cell membrane of the erythrocyte. This is seen in autoimmune hemolytic anemia or as a result of an ABO compatibility |
|
|
Term
| Opsonization and phagocytosis |
|
Definition
| occurs when opsonin bind to a membrane and phagocyte are attracted resulting removal by phagocytosis. |
|
|
Term
| Neutrophil mediated tissue damage |
|
Definition
| occurs through the attraction of neutrophils which release granules |
|
|
Term
| Antibody cell-mediated toxicity |
|
Definition
| ocuurs when ctyoxic cells which are not antigen specific release toxic substance to destry target cells |
|
|
Term
| Modulation of cellular function |
|
Definition
| The cell is not destroy but caused to malfunction. A perfect example of this is in Graves disease where autoantibodies bind to and activates receptors for TSH, thus resulting in production too much thyroxine and the failure of the negative feed back system |
|
|
Term
|
Definition
produced by macrophages and
lymphocytes in response to the presence of an invading microorganism
or activation of the inflammatory process. |
|
|
Term
|
Definition
are cytokines that primarily protect the host against viral
infections and play a role in the modulation of the inflammatory
response. I |
|
|
Term
|
Definition
mediated by the B lymphocytes
(B cells) and is the principal defense against extracellular
microbes and their toxins. The B cells differentiate into
antibody-
secreting plasma cells. The circulating antibodies
then interact with and destroy the microbes that are present
in the blood or mucosal surfaces |
|
|
Term
| Cell-mediated, or cellular, immunity |
|
Definition
is mediated by
the cytotoxic T lymphocytes (T cells) and functions in
the elimination of intracellular pathogens (e.g., viruses).
T cells develop receptors that recognize the viral peptides
displayed on the surface of infected cells and then signal
destruction of the infected cells. |
|
|
Term
The cytokines
involved in innate immunity include |
|
Definition
TNF-α and lymphotoxin;
interferons (IFN-γ, IFN-α, IFN-β); the interleukins IL-1, IL-6,
and IL-12; and chemokines (see Table 13.2). These substances
modulate innate immunity by stimulating the development of
cells involved in both innate and adaptive immunity, producing
chemotaxis within leukocytes, stimulating acute-phase protein
production, and inhibiting viral replication |
|
|
Term
Two acute-phase proteins that are involved in the defense
against infections |
|
Definition
mannose-binding ligand (MBL) and
C-reactive protein (CRP). MBL and CRP are produced in the
liver in response to activation of proinflammatory cytokines.
MBL binds specifically to mannose residues, and CRP binds
to both phospholipids and sugars that are found on the surface
of microbes. These substances act as “costimulatory” opsonins
and enhance the binding of phagocytic cells to suboptimally
opsonized invading microorganisms.25 They |
|
|
Term
Regulatory T cells (TR) are a subset of T lymphocytes that
function to control immune system responses |
|
Definition
These cells represent a subset of CD4+ cells that act as “negative
regulators” of the immune process34. They suppress
immune responses by inhibiting the proliferation of other
potentially harmful self-reactive lymphocytes. |
|
|
Term
| The primary function of cytotoxic T (CD8+) cells |
|
Definition
to monitor
the activity of all cells in the body and destroy any that threaten
the integrity of the body. CD8+ T cells recognize antigens that
are presented on the cell surface by MHC class I–derived
molecules that sample peptides from protein degradation productions
from inside cells infected by viruses or transformed
by cancer33 |
|
|
Term
|
Definition
the loss of cellular differentiation,
irregularities of the size and shape of the nucleus, and the loss
of normal tissue structure. |
|
|
Term
|
Definition
Cancers arising from connective
tissu |
|
|
Term
|
Definition
to preinvasive
epithelial malignant tumors of glandular or squamous cell origin.
Cancers develop incrementally, as they accumulate specific
genetic lesions. Careful surveillance for cancer often detects
abnormal growths in epithelial tissues that have atypical cells
and an increased proliferation rate compared with normal surrounding
tissue |
|
|
Term
|
Definition
are of
endocrine, neurologic, and/or immunologic etiology. These
syndromes are a result of hormonal production of ectopic peptide
by the tumor or from autoantibodies released in response
to the tumor.9 |
|
|
Term
| 18F-Fluorodeoxyglucose (FDG) |
|
Definition
Because it is missing a key hydroxyl group it cannot
be broken down by glycolysis and, thus, FDG accumulates in
cells. Because it is tagged with 18F, it can be imaged by positron
emission tomography (a PET scan) |
|
|
Term
|
Definition
for example,
anchorage-independent growth, lack of contact inhibition, and
immortality. |
|
|
Term
clonal proliferation
or clonal expansion |
|
Definition
That mutant cell may then have a selective advantage
over its neighbors; its progeny can accumulate faster than
its nonmutant neighbors |
|
|
Term
|
Definition
| promote cancer proliferation |
|
|
Term
|
Definition
are mutant genes that
in their normal nonmutant state direct synthesis of proteins that
positively regulate (accelerate) proliferatio |
|
|
Term
|
Definition
encode proteins that in their normal state
negatively regulate (halt, or “put the brakes on”) proliferation.
Hence, they also have been referred to as anti-oncogenes. |
|
|
Term
|
Definition
An example of a proto-oncogene would be a
growth factor (e.g., epidermal growth factor) or a growth factor
receptor (e.g., epidermal growth factor receptor). |
|
|
Term
|
Definition
|
|
Term
|
Definition
Cancers that arise because of these mutations
often depend on these mutant genes and proteins for their
continued growth and survival. |
|
|
Term
TYPES OF GENETIC LESIONS
IN CANCER |
|
Definition
1. Point mutations
2. Subtle alterations (insertions, deletions)
3. Chromosome changes (aneuploidy and loss of heterozygosity)
4. Amplifications
5. Gene silencing (DNA methylation, histone modification, microRNAs)
6. Exogenous sequences (tumor viruses).
Mary are found in as |
|
|
Term
|
Definition
the myc gene is
aberrantly placed under the control of a B-cell immunoglobulin
gene (Ig) present on chromosome 14. The Ig gene is very
active in maturing B lymphocytes. The t(8;14) translocation
alters the control of myc; its normal low level is switched to
high levels, as directed by an Ig gene promoter. MYC protein,
when inappropriately high, drives proliferation and blocks differentiation. |
|
|
Term
| chronic myeloid leukemia (CML), |
|
Definition
This translocation, t(9;22),This translocation fuses two
chromosomes in the middle of two different genes, bcr on chromosome
9 and abl on chromosome 22. The result is production
of a BCR-ABL fusion protein containing the first half of BCR
and the second half of ABL. BCR-ABL is a misregulated protein
tyrosine kinase that promotes growth of myeloid cells Imatinib,
a drug that specifically targets this tyrosine kinase, represents
the first successful chemotherapy targeted against the product
of a specific oncogenic mutation. Imatinib and related tyrosine
kinase inhibitors (TKIs) are highly effective in the treatment of
CML and, because of their specificity |
|
|
Term
|
Definition
Amplifications are the result of duplication of a
small piece of a chromosome over and over again, so that instead
of the normal two copies of a gene, tens or even hundreds of
copies are presen |
|
|
Term
The N-myc oncogene is amplified in 25% of
childhood neuroblastoma cases and confers a poor prognosis.17 |
|
Definition
| Result in Gene Amplification |
|
|
Term
| Gene amplification example |
|
Definition
The epidermal growth factor receptor erbB2 is amplified in
20% of breast cancers |
|
|
Term
|
Definition
are genes whose major function is to
negatively regulate cell growth and prevent mutations. Tumor
suppressors may normally slow the cell cycle, inhibit proliferation
resulting from growth signals, or stop cell division when
cells are damaged |
|
|
Term
|
Definition
a tumor suppressor gene, normally
strongly inhibits the cell division cycle (see Chapter 1). When
it is inactivated, the cell division cycle can proceed unchecked.
Rb is mutated in childhood retinoblastoma, and in many lung,
breast, and bone cancers as well. |
|
|
Term
|
Definition
involve
changes in the patterns of gene expression without a change in
the DNA. Epigenetic mechanisms may “silence” genes, such
as tumor suppressor genes, so that even though the gene is
present, it is not expressed and a cancer-suppressing protein
is not made. Genes
silenced by hypermethylation can be inherited, |
|
|
Term
Self-sufficiency in
growth signa |
|
Definition
| cancer cells stimulate their own growth; |
|
|
Term
Insensitivity to
anti-growth signals |
|
Definition
They proliferate even though there are anti growth signals present. epidermal growth factor (EGF) receptor HER2/neu
is up-regulated, and likely sends growth signals into the cell even
when growth factors are at very low levels. Inhibitors of HER2
and other EGF receptors that block this pathway are effective in
treating selected breast and lung cancers.34 |
|
|
Term
|
Definition
ability to secrete
growth factors that stimulate their own growth. |
|
|
Term
Up to one third of all cancers have
an activating mutation in the gene for an intracellular signaling
protein called |
|
Definition
|
|
Term
|
Definition
More advanced cancers
can, however, secrete multiple factors that stimulate new
blood vessel growth (called neovascularization or angiogenesis).
The angiogenic factors, such as vascular endothelial
growth factor (VEGF), platelet-derived growth factor (PDGF),
and basic fibroblast growth factor (bFGF), |
|
|
Term
|
Definition
monoclonal
antibody that inhibits VEGF; erlotinib, sorafenib, and sunitinib,
inhibitors of the VEGF and PDGF receptor tyrosine
kinases; and thalidomide |
|
|
Term
| tumor-associated macrophage, or TAM. |
|
Definition
Uses cytokines and cheekiness to attract monocytes or macrophages to the tumor, which The classical pro-inflammatory
macrophage (M1) is the primary macrophage in the acute
inflammatory response and is responsible for removal and destruction of infectious agents. During healing, however, a
different phenotype (M2) produces anti-inflammatory mediators
to suppress ongoing inflammation and induce cellular proliferation,
angiogenesis, and wound healing.64 TAMs appear to
phenotypically mimic the M2 phenotype. The transition to the
M2 phenotype is under control of Th2 cytokines (for example,
tumor necrosis factor-alpha [TNF-α], colony-stimulating
factor-2 [CSF2; also known as granulocyte/macrophage colony
stimulating factor or GM-CSF], interleukin |
|
|
Term
| How does TAM uses our pathophysiology to keep the tumor alive |
|
Definition
TAMs have diminished cytotoxic response, and develop the
capacity to block cytotoxic T-cell and NK cell functions and
produce cytokines that are advantageous for tumor growth
and spread. TAMs secrete cellular growth factors (for example,
TGF-β and fibroblast growth factor [FGF-2]) that favor tumor
cell proliferation, angiogenesis, |
|
|
Term
matrix
metalloproteinases (MMPs) and plasminogen activators |
|
Definition
Active
proteases digest the extracellular matrix and basement membranes,
creating pathways through which cells can move can and travel to other areas. |
|
|
Term
(epithelial-mesenchymal transition
[EMT]) |
|
Definition
increased migratory capacity, elevated resistance
to apoptosis, and the potential to redifferentiate into other
cell types. These properties permit the tumor cells to dissociate
from the primary tumor and be transported to a distal site. |
|
|
Term
|
Definition
T0 = Breast free of tumor
T1 = Lesion <2 cm in size
T2 = Lesion 2-5 cm
T3 = Skin and/or chest wall involved
by invasion |
|
|
Term
|
Definition
N0 = No axillary nodes involved
N1 = Mobile nodes involved
N2 = Fixed nodes involved |
|
|
Term
|
Definition
M0 = No metastases
M1 = Demonstrable metastases
M2 = Suspected metastases |
|
|
Term
|
Definition
are symptom complexes that are
triggered by a cancer but are not caused by direct local effects: They are most commonly caused by biologic
substances released from the tumor (e.g., hormones) or
by an immune response triggered by the tumor
of the tumor mass |
|
|
Term
|
Definition
Parathyroid hormone–related protein (PTHRP),
TGF-α, TNF, IL-1 |
|
|
Term
|
Definition
|
|
Term
|
Definition
RANK ORDER* CAUSE OF DEATH RATE†
PERCENT OF TOTAL
DEATHS
1 Diseases of the heart 194 24.2
2 Malignant neoplasms 186 23.3
3 Chronic lower respiratory diseases 45 5.6
4 Cerebrovascular diseases 42 5.2
5 Accidents (unintentional injuries) 39 4.9
6 Alzheimer disease 27 3.4
7 Diabetes mellitus |
|
|
Term
| Three factors (triad of Virchow) |
|
Definition
promote venous thrombosis:
(1) venous stasis (e.g., immobility, obesity, prolonged leg
dependency [e.g., air travel], age, heart failure [HF]), (2) venous
endothelial damage (e.g., trauma, medications), and (3) hypercoagulable
states (e.g., inherited disorders, malignancy, pregnancy,
oral contraceptives, hormone replacement, hyperhomocysteinemia,
antiphospholipid syndrome). |
|
|
Term
| Superior Vena Cava Syndrome |
|
Definition
is a progressive occlusion
of the superior vena cava (SVC) that leads to venous distention
in the upper extremities and head. |
|
|
Term
| Isolated systolic hypertension (ISH) |
|
Definition
elevated systolic blood pressure accompanied by normal diastolic
blood pressure (less than 90 mmHg). ISH is becoming
more prevalent in all age groups and is strongly associated with
cardiovascular and cerebrovascular events. |
|
|
Term
| Blacks and Cardiovascular |
|
Definition
In blacks, variants of the apolipoprotein L1 (APOL1)
gene are associated with hypertension and renal disease.23 |
|
|
Term
| Cardiovascular risk factors |
|
Definition
(1) family history of hypertension; (2) advancing age; (3) gender
(men younger than 55 and women older than 70 years); (4) black
race; (5) high dietary sodium intake; (6) glucose intolerance
(diabetes mellitus); (7) cigarette smoking; (8) obesity; (9) heavy
alcohol consumption; and (10) low dietary intake of potassium,
calcium, and magnesium.19 |
|
|
Term
High
levels of angiotensin II |
|
Definition
contribute to endothelial dysfunction,
insulin resistance, dyslipidemia, and platelet aggregation and
play an important role in the complications associated with the
metabolic syndrome |
|
|
Term
|
Definition
Secreted by the adipose cells, to interact with
the hypothalamus to control body weight and fat deposition through appetite
inhibition and increased metabolic rate. However, chronically high
levels of leptin associated with obesity result in resistance to these weightreducing
functions and have been found to increase sympathetic nervous
system activity, decrease renal sodium excretion, promote inflammation,
and stimulate myocyte hypertrophy |
|
|
Term
|
Definition
protein that is produced
by adipose tissue but is reduced in obesity. Decreased adiponectin
is associated with insulin resistance, decreased endothelial-derived nitric
oxide (vasodilator) production, and activation of the sympathetic nervous
and renin-angiotensin-aldosterone systems. |
|
|
Term
|
Definition
is
caused by an underlying disease process that raises peripheral
vascular resistance or cardiac output. If the cause is identified
and removed before permanent structural changes occur,
blood pressure returns to normal. |
|
|
Term
|
Definition
(rapidly progressive hypertension
in which diastolic pressure is usually greater than 140 mmHg)
can cause encephalopathy. |
|
|
Term
|
Definition
|
|
Term
|
Definition
(Systolic BP 140-159 mmHg or
diastolic BP 90-99 mmHg)
Thiazide-type diuretics for most
May consider ACE inhibitor, ARB,
beta-blocker, CCB, or combination |
|
|
Term
|
Definition
is a localized dilation or outpouching of a vessel wall
or cardiac chamber |
|
|
Term
|
Definition
is an extravascular hematoma
that communicates with the intravascular space. A common
cause of this type of lesion is a leak between a vascular graft and a
natural artery.Arteriosclerosis and hypertension are found in more than
half of all individuals with aneurysms. |
|
|
Term
loss of medial elastic lamellae and thinning of the
tunica media.64
Aneurysms most |
|
Definition
Inflammation (with the production of toxic oxygen
radicals) and changes in cytokines, such as TGF-β, activate
matrix degrading proteins and smooth muscle cell apoptosis
resulting |
|
|
Term
| The prevalence of abdominal aortic aneurysms |
|
Definition
2.9 to 4.9 cm in diameter ranges from 1.3% in men 45
to 54 years of age to 12.5% in men 75 to 84 years of age. For
women, the prevalence ranges from zero in the youngest to
5.2% in the oldest age group.5 |
|
|
Term
| Aneurysms in the heart present with |
|
Definition
dysrhythmias,
heart failure, and embolism of clots to the brain or other vital
organs. |
|
|
Term
| Pulmonary emboli originate |
|
Definition
in the venous circulation (mostly from the deep veins of
the legs) or in the right heart |
|
|
Term
Arterial emboli most
commonly originate |
|
Definition
in the left heart and are associated with
thrombi after MI, valvular disease, left heart failure, endocarditis,
and dysrhythmias. |
|
|
Term
| Thromboangiitis Obliterans (Buerger Disease) |
|
Definition
is an inflammatory
disease of the peripheral arteries. It is associated with smoking
in approximately 95% of cases—the other 5% are related
to frostbite, trauma, or the use of sympathomimetic drugs.70 |
|
|
Term
There are five primary criteria for the diagnosis of Buerger
disease: ( |
|
Definition
1) onset before age 50; (2) history of tobacco use; (3)
ischemia of the digits; (4) typical arteriographic findings; and
(5) exclusion of autoimmune disease, thrombophilia, diabetes,
and proximal embolic source |
|
|
Term
| Raynaud phenomenon and Raynaud disease |
|
Definition
is secondary to systemic diseases,
such as collagen vascular disease (e.g., scleroderma), chemotherapy,
cocaine use, hypothyroidism, pulmonary hypertension,
thoracic outlet syndrome, serum sickness, vasculitis,
malignancy, or long-term exposure to environmental conditions,
such as cold or vibrating machinery in the workplace. |
|
|
Term
|
Definition
is a form of arteriosclerosis in which thickening
and hardening of the vessel are caused by the accumulation Once these lipid-laden foam cells accumulate in significant
amounts, they form a lesion called a fatty streak (see Figure
32-12). These lesions can be found in the walls of arteries of most
of lipid-laden macrophages within the arterial wall, which leads
to the formation of a lesion called a plaque. Both innate and adaptive immunity play
a role in the development and progression of atherosclerotic
lesions.78These macrophages then release enzymes and toxic oxygen
radicals that create oxidative stress, oxidize LDL, and
further injure the vessel wall.
5. Growth factors also are released, including angiotensin
II, fibroblast growth factor, TGF-β, and platelet-derived
growth factor, which stimulate smooth muscle cell proliferation
in the affected vessel. |
|
|
Term
| Peripheral Artery Disease |
|
Definition
refers to atherosclerotic disease
of arteries that perfuse the limbs, especially the lower
extremities. PAD affects approximately 8 to 12 million Americans,
12% to 20% of whom are 65 years of age or older, and is
associated with significant morbidity and mortality. Prevalence
increases with age, and PAD disproportionately affects blacks. |
|
|
Term
An increased serum concentration of LDL is a strong indicator
of coronary risk. |
|
Definition
LDL is responsible for the delivery of
cholesterol to the tissues. Serum levels of LDL are normally
controlled by hepatic receptors for LDL that bind LDL and limit
liver synthesis of this lipoprotein |
|
|
Term
Low levels of HDL cholesterol also are a strong indicator of
coronary risk. |
|
Definition
HDL is responsible for “reverse cholesterol transport,”
which returns excess cholesterol from the tissues to the
liver, where it binds to hepatic receptors. HDL can remove excess cholesterol from the arterial wall through
several pathways, including mediating the efflux of cholesterol
from lipid-laden macrophages (foam cells) through the activation
of adenosine triphosphate (ATP)–binding cassette transporter
proteins (ABC proteins).HDL also participates in endothelial
repair and decreases thrombosis. As HDL cholesterol is transported,
it progresses through three subtypes of HDL: pre-β HDL,
HDL3, and HDL2. Apolipoprotein (ApoA-I) on the pre-β HDL |
|
|
Term
Type I: exogenous hyperlipidemia;
fat-induced hypertriglyceridemia |
|
Definition
Cholesterol normal
Triglycerides increased three times
Chylomicrons increased
Abdominal pain
Hepatosplenomegaly
Skin and retinal lipid deposits
Usual onset: childhood
Low-fat diet |
|
|
Term
| Type IIa: hypercholesterolemia |
|
Definition
Triglycerides normal
LDL increased
Cholesterol increased
Premature vascular disease
Xanthomas of tendons and bony
prominences
Common
Onset: all ages
Low-saturated-fat and
low-cholesterol diet
Cholestyraminea
Colestipolb
Lovastatinc
Nicotinic acidd
Neomycine
Intestinal bypass |
|
|
Term
Type IIb: combined hyperlipidemia;
carbohydrate-induced
hypertriglyceridemia |
|
Definition
LDL, VLDL increased
Cholesterol increased
Triglycerides increased
Same as IIa Same as IIa; plus
carbohydrate restriction
Clofibratef
Gemfibrozilg |
|
|
Term
| Type III: dysbetalipoproteinemia |
|
Definition
IDL or chylomicron remnants
increased
Cholesterol increased
Triglycerides increased
Premature vascular disease
Xanthomas of tendons and bony
prominences
Uncommon
Onset: adulthood
Weight control
Low-carbohydrate, low-saturated-fat,
and low-cholesterol diet
Alcohol restriction
Clofibrate
Gemfibrozil
Lovastatin
Nicotinic acid
Estrogensh
Intestinal bypass |
|
|
Term
Type IV: endogenous hyperlipidemia;
carbohydrate-induced
hypertriglyceridemia |
|
Definition
Glucose intolerance
Hyperuricemia
Cholesterol normal or increased
VLDL increased
Triglycerides increased
Premature vascular disease
Skin lipid deposits
Obesity
Hepatomegaly
Common onset: adulthood
Weight control
Low-carbohydrate diet
Alcohol restriction
Clofibrate
Nicotinic acid
Intestinal bypas |
|
|
Term
Type V: mixed hyperlipidemia;
carbohydrate and fat-induced
hypertriglyceridemia |
|
Definition
Glucose intolerance
Hyperuricemia
Chylomicrons increased
VLDL increased
LDL increased
Cholesterol increased
Triglycerides increased three times
Abdominal pain
Hepatosplenomegaly
Skin lipid deposits
Retinal lipid deposits
Onset: childhood
Weight control
Low-carbohydrate and low-fat diet
Clofibrate
Lovastatin
Nicotinic acid
Progesteronei
Intestinal bypass |
|
|
Term
|
Definition
An
estimated 47 million residents have a combination of obesity,
dyslipidemia, and hypertension |
|
|
Term
Nontraditional Risk Factors. Nontraditional, or novel,
risk factors for CAD include: ( |
|
Definition
(1) increased serum markers
for inflammation and thrombosis, (2) troponin I, (3)
hyperhomocysteinemia, (4) adipokines, (5) infection, (6) air
pollution, and (7) coronary artery calcification and carotid
wall thickness. |
|
|
Term
| Markers of Inflammation and Thrombosis |
|
Definition
Of the numerous
markers of inflammation that have been linked to an
increase in CAD risk (hs-CRP, fibrinogen, protein C, plasminogen
activator inhibitor), the relationship between serum levels
of CRP and CAD has been explored in the greatest depth. |
|
|
Term
Other markers of inflammation
associated with CAD include erythrocyte sedimentation rate,
von Willebrand factor |
|
Definition
von Willebrand factor concentration, uric acid, IL-6, IL-18,
TNF-α, fibrinogen, and YKL-40 is a 40 kDa (mass) glycoprotein
produced by inflammatory cells, cancer cells, and stem cells |
|
|
Term
| Troponin I. Troponin I (TnI) is |
|
Definition
is a serum protein whose
measurement is used as a sensitive and specific diagnostic test
to help identify myocardial injury during acute coronary syndromes.
Highly sensitive TnI assays are used in individuals
without a history of CAD to assess risk for future CHD events,
mortality, and heart failure |
|
|
Term
|
Definition
Hyperhomocysteinemia occurs
because of a genetic lack of the enzyme that breaks down homocysteine
(an amino acid) or because of a nutritional deficiency
of folate, cobalamin (vitamin B12), or pyridoxine (vitamin B6).
Although it has not been identified by the AHA as a major risk factor
for CAD, hyperhomocysteinemia is associated with increased LDL
oxidation, decreased endogenous vasodilators, increased smooth
muscle proliferation, and an increased tendency for thrombosis. |
|
|
Term
|
Definition
Adipokines are a group of hormones released
from adipose cells. The two that are most studied are adiponectin
and leptin. Leptin is primarily implicated in obesity, hypertension,
and diabetes (see |
|
|
Term
|
Definition
Angina pectoris is chest pain caused by
myocardial ischemia.The pain is
caused by the buildup of lactic acid or abnormal stretching
of the ischemic myocardium that irritates myocardial nerve
fibers. |
|
|
Term
|
Definition
Prinzmetal angina (also called variant
angina) is chest pain attributable to transient ischemia of the
myocardium that occurs unpredictably and almost exclusively
at rest.Serum markers of inflammation,
such as CRP and IL-6, may be elevated in individuals with
this form of angina. |
|
|
Term
| Nitrates improve coronary blood flow and reduce myocardial |
|
Definition
demand by decreasing peripheral vascular resistance and
venous return to the heart (preload) and thereby reduce cardiac
workload. Nitrates can be used for short-term symptom relief,
and long acting nitrates are available in several forms |
|
|
Term
|
Definition
The process of atherosclerotic plaque progression can be
gradual. However, when there is sudden coronary obstruction
caused by thrombus formation over a ruptured or ulcerated
atherosclerotic plaque, acute coronary syndromes result |
|
|
Term
| Myocardial infarction (MI) |
|
Definition
results when prolonged ischemia
causes irreversible damage to the heart muscle. |
|
|
Term
|
Definition
Unstable angina is the result of reversible myocardial
ischemia and is a harbinger of impending infarction.Unstable angina is a form of acute coronary
syndrome that results in reversible myocardial ischemia |
|
|
Term
| Diagnosis of unstable angina |
|
Definition
The ECG most commonly
reveals ST-segment depression and T-wave inversion
during pain that resolves as the pain is relieved.The serum
cardiac biomarkers (troponins, creatine phosphokinase-myocardial
bound [CPK-MB] and lactate dehydrogenase [LDH1])
remain normal. |
|
|
Term
|
Definition
is acute inflammation of the pericardium. The
etiology of acute pericarditis is most often idiopathic or caused
by viral infection by coxsackievirus, influenza, hepatitis, measles,
mumps, or varicella viruses |
|
|
Term
|
Definition
the accumulation of fluid in the pericardial
cavity, can occur in all forms of pericarditis. The fluid may
be a transudate, such as the serous effusion that develops with
left heart failure, overhydration, or hypoproteinemia.If the fluid is
serosanguineous, the underlying cause is likely to be tuberculosis,
neoplasm, uremia, or radiatio |
|
|
Term
| Restrictive cardiomyopathy |
|
Definition
is characterized by restrictive filling
and reduced diastolic volume of either or both ventricles with
normal or near-normal systolic function and wall thickness |
|
|
Term
|
Definition
Disorders of the endocardium, the innermost lining of the heart
wall, all damage the heart valves, which are made up of endocardial
tissue. |
|
|
Term
|
Definition
is the most common valvular
abnormality affecting nearly 2% of adults older than 65
years.5 The three common causes are: (1) congenital bicuspid
valve, (2) calcific degeneration related to aging, and (3) inflammatory
damage caused by rheumatic heart disease |
|
|
Term
|
Definition
Aortic regurgitation results from
an inability of the aortic valve leaflets to close properly during
diastole resulting from abnormalities of the leaflets or the aortic
root, or both. I |
|
|
Term
|
Definition
Mitral stenosis impairs the flow of blood
from the left atrium to the left ventricle. Mitral stenosis is most
commonly caused by acute rheumatic fever |
|
|
Term
|
Definition
Mitral regurgitation has a variety of
causes. The most common are mitral valve prolapse and rheumatic
heart disease. Other causes include infective endocarditis,
CAD, connective tissue diseases (Marfan syndrome), and congestive
cardiomyopathy |
|
|
Term
|
Definition
usually is associated with
dilation and failure of the right ventricle secondary to pulmonary
hypertension. Rheumatic heart disease and infective endocarditis
are less common causes |
|
|
Term
| Mitral Valve Prolapse Syndrome. |
|
Definition
a condition in which the anterior and posterior
cusps of the mitral valve billow upward (prolapse) into the
atrium during systole Mitral valve prolapse is the most common valve disorder in
the United States, with a prevalence estimated at 2.4%.5 Mitral
valve prolapse tends to be most prevalent in young women. |
|
|
Term
|
Definition
is a systemic, inflammatory disease caused
by a delayed immune response to infection by group A betahemolytic
streptococci.165 In its acute form rheumatic fever is a
febrile illness characterized by inflammation of the joints, skin,
nervous system, and heart.166 If untreated, rheumatic fever can
cause scarring and deformity of cardiac structures, resulting in
rheumatic heart disease (RHD). |
|
|
Term
The classic manifestations
of aortic stenosis are angina |
|
Definition
| angina, syncope, and heart failure. |
|
|
Term
|
Definition
Aortic regurgitation results from
an inability of the aortic valve leaflets to close properly during
diastole resulting from abnormalities of the leaflets or the aortic
root, or both. It can be congenital (bicuspid valve) or acquired.
Acquired aortic regurgitation can be caused by rheumatic heart
disease, bacterial endocarditis, syphilis, hypertension, connective
tissue disorders (e.g., Marfan syndrome and ankylosing
spondylitis), appetite-suppressing medications, trauma, or
atherosclerosis |
|
|
Term
| Congestive Heart Failure (CHF) |
|
Definition
The heart fails when it is unable to eject blood delivered to it by the venous system.Most common hospital admission diagnosis for persons >65 years old
2. Types
a. Left-sided heart failure (LHF; most common type) |
|
|
Term
| Right-sided heart failure (RHF) |
|
Definition
Definition—RV cannot effectively pump venous blood into the lungs.
• Blood pools under pressure in the venous system (blood builds up behind the failed
heart).
2. Pathogenesis
a. Increase in RV afterload (increased resistance to blood flow out of the RV)
• Examples—LHF (most common cause RHF), PH, PV stenosis, saddle embolus |
|
|
Term
| Acute myocardial infarction (AMI) |
|
Definition
Most common cause of death in adults in the United States
b. Prominent in males between 40 and 65 years old
c. No predominant sex predilection after 65 years old
d. At least 25% of AMIs are clinically unrecognizeda. Sequence for developing an AMI
(1) An atheromatous plaque is suddenly disrupted (see Fig. 5-15).
(2) Subendothelial collagen and thrombogenic necrotic material are exposed.
(3) Platelets adhere to the exposed material and eventually form an occlusive platelet
thrombus.
b. Role of thromboxane A2 in an AMI (refer to Chapter 15)
(1) Platelet aggregating agent that contributes to the formation of the platelet
thrombus
(2) Acts as vasoconstrictor and causes vasospasm of the artery to reduce
blood flow |
|
|
Term
|
Definition
Rheumatic heart disease Increased left atrial pressure; left atrial dilatation, atrial
fi brillation
Increased pulmonary venous pressure, leading to
pulmonary hypertension and right ventricular
hypertrophy |
|
|
Term
|
Definition
| Rheumatic heart disease Left atrial dilatation |
|
|
Term
|
Definition
causes:Senile calcifi cation of normal tricuspid valve
Calcifi cation of congenitally bicuspid valve
Rheumatic heart disease: Results
Left ventricular hypertrophy, due to pressure overload
(increased gradient across stenotic valve); ischaemia
of hypertrophic ventricular myocardium (angina,
arrhythmias, cardiac failure, sudden death) |
|
|
Term
|
Definition
Aortic incompetence Rheumatic heart disease
Infective endocarditis
Leaking prosthetic valve
Aortic root dilatation (aortic dissection,
arthritis, Marfan’s syndrome, syphilis |
|
|
Term
| Right ventricular failure |
|
Definition
pulmonary embolism
• obstructive lung diseases
• interstitial lung diseases |
|
|
Term
|
Definition
is a localized dilation of a vessel wall to which
the aorta is particularly susceptible. |
|
|
Term
13. The most common sources of arterial thrombotic emboli
from the heart |
|
Definition
are mitral and aortic valvular disease and
atrial fibrillation. Tissues affected include the lower extremities,
the brain, and the heart. |
|
|
Term
|
Definition
is spasm or occlusion of the coronary arteries and is
most often the result of atherosclerotic lesions that limit the
flow of blood to the heart.results in an imbalance between coronary supply of
blood and myocardial demand for oxygen and nutrients
such that reversible myocardial ischemia or irreversible
infarction may result. |
|
|
Term
|
Definition
assessed by measuring
serum enzymes, such as creatinine kinase and troponins, as
well as looking for characteristic changes in the ECG. Those
individuals at highest risk for complications present with
ST-segment elevations on the ECG (STEMI) and require
immediate intervention. Smaller subendocardial infarctions
are not associated with ST-segment elevations (non-
STEMI) but suggest that additional myocardium is still at
risk for recurrent ischemia and infarction. Management
may include thrombolytic drugs, antithrombotic |
|
|
Term
|
Definition
| s a bolus of matter that is circulating in the blood |
|
|
Term
|
Definition
| is a blood clot that remains attached to the vessel wall. |
|
|
Term
|
Definition
| inflammation caused by a thrombus. |
|
|
Term
| Isolated systolic hypertension i |
|
Definition
| is an elevated systolic pressure with a normal diastolic pressure. |
|
|
Term
|
Definition
| is the result of extremely complicated interactions of genetics and the environment, mediated by a host of neurohumoral effects. |
|
|
Term
|
Definition
| s systolic pressure equal to or greater than 160 mm Hg and diastolic pressure equal to or greater than 100 mm Hg. |
|
|
Term
|
Definition
| is an abnormal vasospasm of the coronary vessels that causes transient ischemia, unpredictably and usually at rest, and is more common in women. |
|
|
Term
|
Definition
| with activity, is often limited, and resolves with rest. |
|
|
Term
|
Definition
| s poor myocardial perfusion that does not cause angina and may be associated only with nonspecific symptoms such as fatigue, dyspnea, or a feeling of unease. |
|
|
Term
|
Definition
| is typically experienced as transient substernal chest discomfort, ranging from a sensation of heaviness or pressure to moderately severe pain. |
|
|
Term
|
Definition
| Approximately two-thirds of Americans older than 60 years of age have hypertension, and approximately 48% of those have adequately controlled hypertension. Hypertension is defined as a diastolic pressure of 90 mm Hg or higher or a systolic pressure of 140 mm Hg or higher. Between 25% and 37% of adults in the United States are prehypertensive. |
|
|
Term
|
Definition
| is a yellow lipid ring around the cornea |
|
|
Term
|
Definition
| Antibodies are primarily responsible for protection against viruses and bacteria and are part of the humoral arm of the immune system |
|
|
Term
| The antigenic determinant or epitope |
|
Definition
| s the precise portion of the antigen that is configured for recognition and binding of an antibody. |
|
|
Term
|
Definition
| is the matching portion on the antibody or lymphocyte receptor. |
|
|
Term
|
Definition
| is one that is not foreign to the host. |
|
|
Term
|
Definition
| is an antigen that induces an immune response. |
|
|
Term
| The J chain anchors together the IgA molecule |
|
Definition
| to form dimers and helps them resist degradation from enzymes. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| IgA-2 is found in the secretions of the body. |
|
|
Term
| Paroxysmal nocturnal dyspnea (PND) |
|
Definition
| occurs when individuals with heart failure or lung disease wake up at night gasping for air and must sit up or stand to relieve the dyspnea. |
|
|
Term
| Kussmaul respirations are characterized by |
|
Definition
| slightly increased ventilatory rate, very large tidal volume, and no expiratory pause. |
|
|
Term
|
Definition
| is commonly caused by disorders such as pulmonary fibrosis that stiffen the lungs or chest wall and decrease compliance. Restricted breathing is characterized by small tidal volumes and rapid ventilatory rate (tachypnea). |
|
|
Term
| Labored breathing occurs whenever there is an i |
|
Definition
increased work of breathing, especially if the airways are obstructed, as in chronic obstructive pulmonary disease (COPD). If the large airways are obstructed, a slow ventilatory rate, increased
CHAPTER 35
Alterations of Pulmonary Function 1249
1250 UNIT X The Pulmonary System
effort, prolonged inspiration or expiration, and stridor (high- pitched sounds made during inspiration) or audible wheezing (whistling sounds on expiration) are typical. In |
|
|
Term
| Cheyne-Stokes respirations a |
|
Definition
| re characterized by alternat- ing periods of deep and shallow breathing. Apnea lasting 15 to 60 seconds is followed by ventilations that increase in volume until a peak is reached, after which ventilation (tidal volume) decreases again to apnea.Cheyne-Stokes respirations result from any condition that slows the blood flow to the brainstem, which in turn slows impulses sending information to the respi- ratory centers of the brainstem. |
|
|
Term
|
Definition
| control of breathing such that minute volume (tidal volume × respiratory rate) is reduced. When alveolar ventilation is normal, carbon dioxide (CO2) is removed from the lungs at the same rate at which it is produced by cellular metabolism. This maintains arterial CO2 pressure (Paco2) at normal levels (40 mmHg). With hypoventilation, CO2 removal does not keep up with CO2 production and Paco2 increases, causing hypercapnia (Paco2 greater than 44 mmHg). |
|
|
Term
|
Definition
| s alveolar ventilation that exceeds meta- bolic demands. The lungs remove CO2 at a faster rate than it is produced by cellular metabolism, resulting in decreased Paco2 or hypocapnia (Paco2 less than 36 mmHg). Hypocapnia results in a respiratory alkalosis that also can interfere with tissue func- tion |
|
|
Term
|
Definition
| or increased CO2 concentration in the arterial blood (increased Paco2), is caused by hypoventilation of the alveoli.12 |
|
|
Term
|
Definition
| (1) depression of the respiratory center by drugs; (2) diseases of the medulla, including infections of the central nervous system or trauma; (3) abnor- malities of the spinal conducting pathways, as in spinal cord disruption or poliomyelitis; (4) diseases of the neuromuscular junction or of the respiratory muscles themselves, as in myasthe- nia gravis or muscular dystrophy; (5) thoracic cage abnormali- ties, as in chest injury or congenital deformity; (6) large airway obstruction, as in tumors or sleep apnea; and (7) increased work of breathing or physiologic dead space, as in emphysema. |
|
|
Term
| Acute Respiratory Failure |
|
Definition
| Respiratory (lung) failure is defined as inadequate gas exchange, that is, hypoxemia, in which Pao2 is ≤50 mmHg, or hypercapnia, in which Paco2 is ≥50 mmHg with a pH of ≤7.25. |
|
|
Term
|
Definition
| Pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura (which surrounds the lungs) or the parietal pleura and chest wall |
|
|
Term
| Primary (spontaneous) pneumothorax, |
|
Definition
| usually men) between ages 20 and 40 years, is most often caused by the spontaneous rupture of blebs (blister-like formations) on the visceral pleura, although there may be underlying pleural disease with emphysema-like changes.16 Approximately 10% of affected individuals have a sig- nificant family history of primary pneumothorax that has been linked to mutations in the folliculin gene (Birt-Hogg-Dubé- syndrome), which influences cell–cell adhesion.17 Bleb rupture can occur during sleep, rest, or exercise. The ruptured bleb or blebs are usually located in the apexes of the lungs. |
|
|
Term
| Secondary (traumatic) pneumothorax c |
|
Definition
| an be caused by chest trauma, such as a rib fracture, stab or bullet wounds, or a surgical procedure that tears the pleura; rupture of a bleb or bulla (larger vesicle |
|
|
Term
|
Definition
| is most commonly caused by transthoracic needle aspiration |
|
|
Term
|
Definition
| is the presence of fluid in the pleural space. The source of the fluid is usually blood vessels or lymphatic vessels lying beneath either pleura, but occasionally an abscess or other lesion may drain into the pleural space. |
|
|
Term
| Empyema (infected pleural effusion) |
|
Definition
| is the presence of pus in the pleural space. It is thought to develop when the pulmonary lymphatics become blocked, leading to an outpouring of contam- inated lymphatic fluid into the pleural space. Empyema occurs most commonly in older adults and children and usually develops as a complication of pneumonia, surgery, trauma, or bronchial obstruction from a tumor.21 Commonly documented infectious microorganisms include Staphylococcus aureus, Escherichia coli, anaerobic bacteria, and Klebsiella pneumoniaeIndividuals with empyema present clinically with cyanosis, fever, tachycardia (rapid heart rate), cough, and pleural pain. Breath sounds are decreased directly over the empyema |
|
|
Term
| Restrictive Lung Disorders |
|
Definition
| Restrictive lung disorders are characterized by decreased com- pliance of lung tissue. Pulmonary function testing reveals a decrease in FVC. Restrictive lung diseases can cause ventilation and perfu- sion mismatch and affect the alveolocapillary membrane, which reduces the diffusion of oxygen from the alveoli into the blood and results in hypoxemia |
|
|
Term
|
Definition
| is the passage of fluid and solid particles into the lung. |
|
|
Term
| There are three types of atelectasis: c |
|
Definition
compression, absorption, and surfactant impairment: 1. Compression atelectasis is caused by the external pres- sure exerted on lung tissue, such as occurs with tumors, or by fluid or air in the pleural space. Atelectasis at the base of the lungs can be caused by abdominal distention pressing on a portion of the lung, causing the alveoli to
collapse.
2. Absorption atelectasis results from gradual absorption
of air from obstructed or hypoventilated alveoli or from
inhalation of concentrated oxygen or anesthetic agents. 3. Surfactant impairment results from decreased produc- tion or inactivation of surfactant, which is necessary to reduce surface tension in the alveoli and thus prevent lung collapse during expiration. Surfactant impairment can occur because of premature birth, acute respiratory
distress syndrome, anesthesia, or mechanic |
|
|
Term
|
Definition
| Bronchiectasis is persistent abnormal dilation of the bronchi. It usually occurs in conjunction with other respiratory conditions that are associated with chronic bronchial inflammation, such as obstruction of an airway with mucous plugs, atelectasis, aspi- ration of a foreign body, infection, cystic fibrosis, tuberculosis, congenital weakness of the bronchial wall, or impaired defense mechanisms. |
|
|
Term
|
Definition
| s diffuse inflammation of the small airways or bronchioles. It is most common in children (see Chapter 36). In adults it usually occurs with chronic bronchitis, but can occur in otherwise healthy individuals in association with an upper or lower airway viral infection (e.g., respiratory syncytial virus [RSV]), or with inhalation of toxic gases. |
|
|
Term
| Bronchiolitis obliterans i |
|
Definition
| s a late-stage fibrotic process that occludes the airways and causes permanent scarring of the lungs. This process can occur in all causes of bronchiolitis, but is most common after lung transplantation and is associated with acute rejection and infection. |
|
|
Term
|
Definition
| is an excessive amount of fibrous or con- nective tissue in the lung. |
|
|
Term
| Idiopathic Pulmonary Fibrosis. Idiopathic pulmonary fibrosis (IPF) i |
|
Definition
| is the most common idiopathic interstitial lung disorder. It is more common in men than in women and most cases occur after age 60. |
|
|
Term
|
Definition
| epresents any change in the lung caused by inhalation of inorganic dust particles, which usually occurs in the workplace. As in all cases of environmentally acquired lung disease, the individual’s history of exposure is important in determining the diagnosis. Pneumoconiosis often occurs after years of exposure to the offending dust with progressive fibrosis of lung tissue. |
|
|
Term
|
Definition
| epresents any change in the lung caused by inhalation of inorganic dust particles, which usually occurs in the workplace. As in all cases of environmentally acquired lung disease, the individual’s history of exposure is important in determining the diagnosis. Pneumoconiosis often occurs after years of exposure to the offending dust with progressive fibrosis of lung tissue. |
|
|
Term
| Hypersensitivity Pneumonitis. |
|
Definition
| Hypersensitivity pneumonitis (extrinsic allergic alveolitis) is an allergic, inflammatory disease of the lungs caused by inhalation of organic particles or fumes. Many allergens (antigens) can cause this disorder, including grains, silage, bird droppings or feathers, wood dust (particularly redwood and maple), cork dust, animal pelts, coffee beans, fish meal, mushroom compost, grain molds, mists from standing water, and fumes from paints and resins. |
|
|
Term
| Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) |
|
Definition
| represents a spectrum of acute lung inflammation and diffuse alveolocapillary injury. In the United States, ALI/ARDS is estimated at 64 to 78 cases per 100,000 people.44 |
|
|
Term
| Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) r |
|
Definition
| The most common predisposing factors for ARDSaregeneticfactors,sepsis,andmultipletrauma(espe- cially when multiple transfusions are received); however, there are many other causes, including pneumonia, burns, aspiration, cardiopulmonary bypass surgery, pancreatitis, drug overdose, smoke or noxious gas inhalation, oxygen toxicity, radiation therapy, and disseminated intravascular coagulation.47,48 |
|
|
Term
| Exudative (Inflammatory) Phase (Within 72 Hours). ARD |
|
Definition
| he initial lung injury damages the alveolocapillary membrane. Lung injury activates neutrophils, platelets, macrophages, lung epithelial and endothelial cells, and uncontrolled inflammation. Inflammatory mediators include complement, cytokines, arachidonic acid metabolites, platelet-activating factor, reactive oxygen species, and other mediators (specifically tumor necrosis factor [TNF], interleukin-1 [IL-1], and IL-6).49 Activated complement factors and platelet aggregation result in intravascular microthrombus formation and further damage to lung capillaries.50 I |
|
|
Term
| ARDProliferative Phase (4 to 21 Days). |
|
Definition
| Within 1 to 3 weeks after theinitiallunginjury,thereisresolutionofthepulmonary edema and proliferation of type II pneumocytes, fibroblasts, and myofibroblasts. The intra-alveolar hemorrhagic exudate becomes a cellular granulation tissue appearing as hyaline membranes and there is progressive hypoxemia. |
|
|
Term
| Fibrotic Phase (14 to 21 Days). |
|
Definition
| after the initial injury, remodeling and fibrosis occur. The fibrosis progressively obliterates the alveoli, respiratory bronchioles, and interstitium, leading to a decrease in functionalresidualcapacity(FRC)andcontinuingV ̇/Q ̇ mismatch with severe right-to-left shunt. The result of this overwhelming inflammatory response by the lungs is acute respiratory failure. |
|
|
Term
| The new Berlin definition of ARDS pr |
|
Definition
| provides categories of severity based on hypoxemia: mild (200 mmHg < PaO2/FIO2 ≤ 300 mmHg), moderate (100 mmHg < PaO2/FIO2 ≤ 200 mmHg), and severe (PaO2/FIO2 ≤ 100 mm Hg).51a |
|
|
Term
|
Definition
| Asthma is a chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constric- tion of the airways, and variable airflow obstruction that is reversible.59 |
|
|
Term
|
Definition
| athogenesis of asthma, including those that influ- ence the production of IL-4, IL-5, and IL-13; IgE; eosinophils; mast cells; adrenergic receptors; leukotrienes; nitric oxide; and transmembrane proteins in the endoplasmic reticulum. |
|
|
Term
|
Definition
is the presence of air or gas in the pleural space
caused by a rupture in the visceral pleura (which surrounds the
lungs) or the parietal pleura and chest wall |
|
|
Term
|
Definition
air pressure in the pleural space equals barometric
pressure because air that is drawn into the pleural space
during inspiration (through the damaged chest wall and parietal
pleura or through the lungs and damaged visceral pleura) is forced
back out during expiration |
|
|
Term
|
Definition
however,
the site of pleural rupture acts as a one-way valve, permitting air
to enter on inspiration, but preventing its escape by closing during
expiration. |
|
|
Term
| Chronic obstructive pulmonary disease (COPD) |
|
Definition
is defined
as a “preventable and treatable disease with some significant
extrapulmonary effects that may contribute to the severity in
individual patients. Its pulmonary component is characterized
by airflow limitation that is not fully reversible. The airflow
limitation is usually progressive and associated with an abnormal
inflammatory response of the lung to noxious particles or
gases.”80 COPD |
|
|
Term
|
Definition
is the third leading cause of death in the United
States and is the sixth leading cause of death worldwide.80
Overall mortality from COPD has increased in the United
States over the past 30 years; however, mortality in women has
increased more than twice that much |
|
|
Term
|
Definition
| Pneumonia is infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites. It is the sixth leading cause of death in the United States and is responsible for more disease and death than any other infection.1 |
|
|
Term
|
Definition
| characterized by destruction of alveoli through the breakdown of elastin within the septa by an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of lung structural Cel- lular apoptosis and early cellular senescence contribute to loss of alveolar cells and reduced surface area for gas exchange. Alveolar destruction also produces large air spaces within the lung paren- chyma (bullae) and air spaces adjacent to pleurae (blebs). |
|
|
Term
| Pulmonary embolism (PE) i |
|
Definition
| s occlusion or partial occlusion of the pulmonary artery or its branches by an embolus. PE most commonly results from embolization of a clot from deep venous thrombosis involving the lower leg |
|
|
Term
| Pulmonary artery hypertension (PAH) i |
|
Definition
| is defined as a mean pulmonary artery pressure greater than 25 mmHg at rest.159 Pulmonary artery pressure is lower than systemic arterial pressure and is normally 15 to 18 mmHg. |
|
|
Term
|
Definition
| Idiopathic PAH is characterized by endo- thelial dysfunction with overproduction of vasoconstrictors (e.g., thromboxane and endothelin) and decreased production of vasodilators (e.g., nitric oxide and prostacyclin).159,160 Release of growth factors causes proliferation of endothelial cells, smooth muscle cells, and fibroblasts, resulting in patchy changes in pre- capillary pulmonary arteries (resistance vessels). T |
|
|
Term
|
Definition
| Increased cytosolic calcium (vasocon- striction), phosphodiesterases (modulate cellular proliferation), (vasoconstrictor), and adrenomedullin (vasodila- tor) also play a role in the pathogenesis of this disorder. |
|
|
Term
|
Definition
| is secondary to pulmonary artery hypertension and consists of right ventricular enlargement (hypertrophy, dilation, or both).167 |
|
|
Term
|
Definition
| Cor pulmonale develops as pulmonary artery hypertension creates chronic pressure overload in the right ventricle similar to that created in the left ventricle by systemic hypertension. |
|
|
Term
|
Definition
| (NSCLC, about 85% of all lung cancers) and neuroen- docrine tumors (about 14% of all lung cancers). |
|
|
Term
|
Definition
| NSCLC can be subdivided into three common types of lung cancer: squamous cell carcinoma, adenocarcinoma, and large cell undifferentiated carcinoma, and they each have cellular subtypes.1 |
|
|
Term
| on–Small Cell Lung Cancer (NSCLC) |
|
Definition
| Squamous Cell Carcinoma. Squamous cell carcinoma (SCC) accounts for about 30% of bronchogenic carcino- mas, representing a sharp decline in incidence in the past two decades. |
|
|
Term
| Adenocarcinoma. Adenocarcinoma |
|
Definition
tumor arising from glands) of the lung constitutes 35% to 40% of all bronchogenic carcinomas (Figure 35-24, B). Adenocarcinoma occurs more
frequently in women, in non-smokers, and in Asians. Envi- ronmental tobacco smoke, occupational carcinogens, viruses, hormones, and positive family history are associated with this tumor type. |
|
|
Term
Neuroendocrine Lung Tumors
Small Cell (Oat Cell) Carcinoma. Small cell lung carcinomas (SCLCs) |
|
Definition
| are the most common type of neuroendocrine lung tumors and constitute about 14% of bronchogenic carcino- mas, but cause 25% of lung cancer deaths.1 |
|
|
Term
| How many genes do humans have |
|
Definition
| Humans have approxi- mately 20,000 to 25,000 genes. A |
|
|
Term
| Amniocentesis. This procedure, which is usually carried out at |
|
Definition
about 16
weeks' gestation, involves the withdrawal of a small amount of amniotic fluid from the uterus |
|
|
Term
| Chorionic villus sampling (CVS). Carried out at |
|
Definition
| 10 to 12 weeks’ gestation, CVS is performed by extracting a small amount of villous tissue directly from the chorion. |
|
|
Term
| Analysis of fetal DNA in maternal circulation. |
|
Definition
y approximately 6 to 8
weeks' gestation, fetal cells can be found in the mother’s bloodstream and these cells (or cell-free fetal DNA) can be tested for some disease- causing mutations. |
|
|
Term
| Each DNA subunit—consisting of one |
|
Definition
| ne deoxyribose molecule, one phosphate group, and one base (see Figure 4-1)—is called a nucleotide. |
|
|
Term
|
Definition
| is the base pair substitution, in which one base pair is replaced by another. |
|
|
Term
|
Definition
| This alteration involves the insertion or deletion of one or more base pairs to the DNA molecule. |
|
|
Term
| RNA differs from DNA in that |
|
Definition
| uracil rather than thymine is one of the four nitrogenous bases. |
|
|
Term
| Transcription is the process by which |
|
Definition
| RNA is synthesized from a DNA template. The result is the formation of messenger RNA (mRNA) from the base sequence specified by the DNA mol- ecule. Transcription of a gene begins when an enzyme called RNA polymerase binds to a promoter site on the DNA. |
|
|
Term
|
Definition
| any of the RNA sequences are removed and the remaining sequences are spliced together to form the func- tional mRNA that will migrate to the cytoplasm. The excised sequences are called introns, |
|
|
Term
|
Definition
| The excised sequences are called introns, and the sequences that are left to code for proteins are called |
|
|
Term
| Translation is the process by which |
|
Definition
| RNA directs the synthesis of a polypeptide |
|
|
Term
| The most well-known example of aneuploidy in an auto- some is trisomy of the twenty-first chromosome, which causes |
|
Definition
| Trisomy 21 or down's syndrome Down syndrome is seen in 1 in 800 live births |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Individuals with at least two X chromosomes and a Y chro- mosome in each cell.1 in 1000 male births. About two thirds of the cases are caused by nondisjunction of the X chromosomes in the mother, and the frequency of the disorder rises with maternal age. |
|
|
Term
|
Definition
| Other symptoms include low birth weight, severe mental retardation, microcephaly (smaller than normalhead size), heart defects, and the typical facial appearance shown in Figure 4-17. The disease is caused by a deletion of part of the short arm of chromosome 5. |
|
|
Term
|
Definition
| it is associated with substantial cognitive impairment. With a relatively high population prevalence (affecting approximately 1 in 4000 males and 1 in 8000 females), fragile X syndrome is the second most common genetic cause of mental retardation (after Down syndrome). |
|
|
Term
|
Definition
| another well-known autosomal domi- nant condition and its main features are progressive dementia and increasingly uncontrollable movements of the limbs |
|
|
Term
| The penetrance of a trait i |
|
Definition
| is the percentage of individuals with a specific genotype who also exhibit the expected phenotype. Incomplete penetrance means that indi- viduals who have a disease-causing allele may not exhibit the disease phenotype at all, even though the allele and the associ- ated disease may be transmitted to the next generation. |
|
|
Term
| variable expressiv- ity in an autosomal dominant disease |
|
Definition
| is type 1 neurofibroma- tosis, or von Recklinghausen disease. Like the retinoblastoma gene, the neurofibromatosis gene normally encodes a tumor suppressor.The expression of this gene can vary from a few harmless café-au-lait spots (“coffee with milk,” describing the light brown color) on the skin to malignant tumors, scolio- sis, seizures, gliomas, hypertension, learning disabilities, and neuromas |
|
|
Term
|
Definition
| cystic fibrosis, occurs in about 1 in 2500 births. Approximately 1 in 25 whites carries one copy of an allele that can cause cystic fibrosis |
|
|
Term
| Important criteria for discerning autosomal recessive inheri- tance include the following: |
|
Definition
1. Males and females are affected in equal proportions.
2. Consanguinity is sometimes present.
3. The disease is seen in siblings but usually not in their parents. 4. On the average, one fourth of the offspring of carrier parents
will be affected. |
|
|
Term
|
Definition
| (for “sex-determining region on the Y”), |
|
|
Term
| Pedigrees for X-linked recessive conditions show the following distinctive features: |
|
Definition
1. The trait is seen much more often in males than in females because females must inherit two copies of the recessive allele (one from each parent) to express the disease, while males need only inherit one copy (from their mother) to express the disease.
2. Because a father can give a son only a Y chromosome, the trait is never transmitted from father to son.
3. The gene can be transmitted through a series of carrier females, causing the appearance of a “skipped generation.”4. The gene is passed from an affected father to all his daugh- ters, who, as phenotypically normal carriers, transmit it to approximately half their sons, who are affected. |
|
|
Term
| The most common and severe of all X-linked recessive dis- orders is |
|
Definition
| Duchenne muscular dystrophy (DMD), which affects approximately 1 in 3500 males. As its name suggests, this dis- order is characterized by progressive muscle degenerationAffected individuals are usually unable to walk by 10 to 12 years of age. The disease affects the heart and respiratory muscles, and death caused by respiratory or cardiac failure usually occurs before 20 years. |
|
|
Term
| The DMD gene is the largest gene ever found in the human, spanning more than 2 million DNA bases. It encodes a |
|
Definition
| a previously undiscovered muscle protein, termed dystrophin. |
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|
