NUR 345 Exam 1 Study Topics

3 stages of GAS

alarm, resistance/adaptation, exhaustion/allostatic overload

cortisol

-secreted during stress; reaches all tissues
-stimulates gluconeogenesis
-elevation in blood glucose; affects protein metabolism
-anti-inflammatory
-immunosuppressive

immune system role

-stress directly r/t proinflammatory cytokines= cytokines storm
-link between stress, immune function with various disease and cancer
-immune system affected by neuroendocrine factors
-stress response decreases t cell cytotoxicity and b cell function

synopsis of stress response

-alarm: fight or flight
-resistance- if exposure to stress continue, your body adapts and reacts to stressor (last for brief period)
-fatigue-exposure is prolonged, you begin to feel and lose ability to manage other stressors effectively

aging and stress

-stress age syndrome: your ability to adapt to stress changes as you age
-excitability changes in limbic system and hypothalamus
-increased catecholamines, ADH, ACTH, and cortisol
-alterations of opioid peptides
immunosuppression and pattern of chronic inflammation
alterations in lipoprotiens
hypercoag of blood
free radical damage to cells

locus

position of gene along a chromosome

allele

a different form of a particular gene at a given locus

polymorphism

loci on a pair of chromosomes that have identical genes

homozygous

loci on a pair of chromosomes that have identical genes

heterozygous

loci on a pair of chromosomes that have different genes

genotype

combination of alleles an organism inherits from its parents

phenotype

organism appearance

chromosomes

-somatic and gametes

somatic cells

-contains 46 chromosomes (23 pairs)
-diploid cells

gametes

-sperm and eggs
-haploid cells

autosomes

-23 pairs of chromosomes- in individuals
-22 pair are all homologous

sex chromosomes

remaining pair of chromosomes
-homo: XX
-hetero: XY

karyotype

set of chromosomes a person has

aneuploidy

somatic

trisomy

presence of third copies of a specific chromosome

monosomy

presence of one copy of a specific chromosome

autosomal dominant inheritance

an allele may be disease-causing or normal
-average: half offspring will be normal, half will be heterozygous and express disease

crossover

-occurs during meiosis I
-can cause recombination of alleles located on same chromosome
-frequency of recombination used to map distance between loci on same chromosome

marker locus

used to predict development of genetic disease

multifactorial inheritance

-polygenic: variation in trains caused by the effects of several loci
-multifactorial trait: variation in traits caused by genetic and environmental factors; have a threshold of liability

cellular adaptations

physiological change or petrophysical changes

5 types of cellular adaptation

-atrophy
-hypertrophy
-hyperplasia
-metaplasia
-dysplasia

atrophy

decrease in cellular size, decrease in function

hypertrophy

increase in cellular size, increase in work demand of cell

hyperplasia

excessive growth of cells

metaplasia

chronic injury, irritation
-change in cells

dysplasia

abnormal development or an abnormal structure resulting from such growth
-persistent severe injury or irritation, cancerous growth

hypoxic injury

single most common cause of cellular injury
-results from: decrease oxygen (decreased RBC, reduced O2, respiratory/cardiovascular disease, poisoning of oxidation enzymes within cell)

cellular injury response synopsis

-decrease ATP, failure of Na-K pump and Na-Ca exchange,
-cellular swelling (burst, die)
-vacuolation: vacuoles in cytoplasm of neutrophils in response to infection/inflammation

Na-K pump dysfunction

-unable to produce sufficient ATP
normally: 3 Na out, 2 K in
-contributes to membrane polarity in excitable tissues
-maintains normal osmotic relationship between ions
-lacks of ATP can cause intracellular Ca levels

ischemia-reperfusion injury

-additional injury that can be caused by restoration of blood flow and oxygen
-increased intracellular calcium
-inflammation
-complement activation
-oxidative stress

free radicals

unstable b/c its unpair oxygen
-cause: lipid peroxidation, protein use alteration, DNA alteration, mitochondrial damage

hydropic degeneration

-injury-hypoxia-ATP decrease-Na/K failure- osmotic pressure increase-more water into cell-burst of ER- form vacuoles-extensive vacuolation-hydropic generation

apoptosis

programmed cell death
-expected mechanism to eliminate aged/injured cells

aging

-cellular aging: atrophy, decreased function, loss of cells
-tissue and systemic aging: progressive stiffness and rigidity, sarcopenia
-frailty: mobility, balance, muscle strength, bone density all decrease (fractures/falls)

lines of defense

-innate (natural)
-inflammation
-adaptive (acquired)

ESR

-erythrocyte sedimentation rate
-measure rate at which RBCs precipitate out of plasma
-mainly for chronic inflammation monitoring
-influenced by fibrinogen levels in blood

CRP

-acute phase protein
-can initiate, amplify, or sustain inflammatory process
-indicates active inflammation

goals of immunity/inflammation

-limit and control inflammation process
-prevent further infection
-initiate adaptive immune
-initiate healing

stages of inflammation

-vascular
-cellular

vascular

-vasodilation, increased vascular permeability

cellular

-movement of WBC from blood vessels into soft tissue/site of inflammation
-phagocytosis begins with large influx of neutrophils and macrophages

phagocyctosis

-digest microbes through phagocytes (macrophages and neutrophils)

phagocytes

-neutrophils
-eosinophils
-basophils
monocytes/ macrophages

neutrophils

-early inflammatory response, short lives
-ingest bacteria, dead cells, cellular debris
-most abundant

eosinophils

-mildly phagocytic
-against parasites, asthma, allergies

basophils

prevent prevalent granulocytes

monocytes

-produced in bone marrow- enter circulation-migrate to inflammatory site where develop into macrophages

macrophages

arrive at inflammatory site 24 hours after neutrophils

cellular components

-erythrocytes
-platelets
-leukocytes

3 types of leukocytes

-granulocytes: neutrophils, eosinophil, basophil
-monocytes
-lymphocytes

cytokines

-responsible for reactivating other cells and regulating the inflammatory response
-regulate inflammatory response by amplifying it or deactivating it
-stimulate liver to release (c reactive protein)

chemokines

synthesized by many cells (macrophages, fibroblast, endothelial cells) in response to proinflammatory cytokines

interleukins (IL)

produced primarily by macrophages and lymphocytes in response to stimulation of WBC

tumor necrosis factor-alpha

secreted by macrophages and toll-like receptor recognition

basophil

-in blood,
function same as mast cells

mast cells

-cellular bags of granules located in loose CT close to blood vessels (faster response bc its so close to BV)
-skin, digestive lining, respiratory tract
-contains histamine, cytokines, chemotaxis factors
-chemical release in 2 ways: degranulation and synthesis

-play a role in allergies (food, hay fever) due to release of histamine

degranulation

-release of the contents of mast cell granules
-chemotactic: neutrophil and eosinophil
-histamine: vascular effects

synthesis

-produces prostaglandins: pain
-arachidonic acid
-platelet activating factors

arachidonic acid

-prostaglandin (pain)
-leukotrienes (vascular effects)

histamine

H1: proinflammatory
-smooth muscle of bronchi

H2: antiinflammatory
-parietal cells of stomach mucosa (gastric acid)

natural killer cells

-recognize and eliminate cells infected with virus
-inhibitory and activating receptors that differentiate between normal and abnormal cells
-produce cytokines and toxic molecules

educative fluids

-serous
-fibrous
-purulent
-hemorrhagic

adaptive immunity

allows the body to recognize antigens, develops memory process

2 components of active immunity

-humoral: immunoglobulins (B lymphocytes)
-cellular: T cells

humoral

-immunoglobulins (antibodies)
-b lymphocytes
-binds to antigens on bacteria and viruses

cellular

-t cells
-kill target directly
-stimulate other leukocytes
-t cells differentiate into CD4 T helper cells and CD8

CD4 helper t cells

helps all other cells in immune system
-HIV targets this directly (defeats cells mediated and antibody mediated immune response, 2 of human's strongest immune mechanism for fighting antigens)

CD8 cytotoxic cells

-chief cells
-directly attack antigens

location of b cells

bone marrow

location of t cells

thymus

2 types of adaptive immunity

-active and passive

active immunity

exposure to antigen, immunization

passive immunity

performed antibodies or t cells are administered
(mother to fetus)

immunoglobulins

GAMED

IgG

-most abundant
-most protected against infection
-transporter across placenta
-classes 1-4

igA

-predominantly in blood
IgA2: bodily secretions (blood, sweat, tears)

IgM

-synthesized early in neonatal life
-physically largest, first antibody produced during primary response to antigen

IgE

-least concentrated in circulation
-allergic responses, parasites
-initiate inflammatory reaction to attract eosinophils

IgD

function as one type of b cell antigen receptor
-function not fully understood

Antibodies function

-direct and indirect

direct function of antibodies

-neutralization
-agglutination
-precipitation

neutralization

binding to antigen to receptor

agglutination

clumping of particles, occur if antigen is mixed and its corresponding antibody is isoagglutinin

precipitation

making soluble antigen to an insoluble one

indirect antibodies

-inflammation
-phagocytosis
-complement

peds immune system

-sufficient IgM
-deficient IgG and IgA

geriatric immune system

-decreased t cells activity
-decrease antibody response to antigen

causes of cancer

-alcohol
-genetic factors
-UV A and B radiation
-infection (HPV, h pyloric, hep b, hep c)

benign tumors

-adenoma
-fibroma
-hemangiomas
-lipomas

malignant tumors

-carcinoma
-adenocarcinoma
-sarcoma
-lymphoma:

carcinoma

epithelial tissue

adenocarcinoma

from ductal or glandular tissue
ex: breast cancer

sarcoma

mesenchymal tissue

lymphoma

lymphatic