Stress CHAP AND (feedback loop)Immunopathology, Neoplasia, Chromosome Abnormalities Flashcards by natalie brown

Any factor that creates a significant change in the body/environment
extreme stimuli ; too much too little

Stressors

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3 stages of stress response

Alarm
Resistance
exhaustion

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stress response where the defense is mobilized.

Alarm

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this stress response activates the hypothalus, sympathetic nervous system, and adrenal glands

Alarm

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stress response that elevates hormones and essential body systems are working at peak performance

Resistance

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stress response where Pt is unable to respond further or is damaged by increased demands

Exhaustion

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ACTH is secreted

- an increase in cortisol

what happens when our bodies our stressed

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Increase level of function in critical areas of body

Why we react when stressed

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increase BP and HR
Bronchodialation
Increase Blood Glucose
Arouse the CNS
Decrease inflammatory and immune response

Effects of stress

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what Increase level of function in critical areas of body when stressed

Brain: enhance cognition and short term memory
Heart: Increase HR, and Blood pressure
skeletal muscle: increase function

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specific disorders that are associated with stress

Vasoconstriction
elevated BP dysrythmia
Chronic infections: herpes
Stressful situation may increase asthma,seizure
May exacerbate chronic disorders:MS,RA,SLE, asthma, acne,ulcers eczema

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Prolonged stress creates high amounts of glucocorticoids that disrupt what 2 things?

intellectual function and memory

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Severe stress may cause

Acute renal failure
stress ucler
infection: depressed immune
impede tissue healing: decrease protein synthesis and tissue regeneration
PTSD: relive event, lack emotional response, dissociative state

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How do you cope with stress?

Recognize the stress and respond emotionally and behaviorally
-solve problem or learn to cope

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factors that interfere with appropriate response

fatigue
age
inadequate nutrition
insufficient knowledge
lack of emotional support

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strategies to beat stress

rest and healthy diet
regular exercise
distractive activities
counseling
relaxation techniques, imagery biofeedback
anti-anxiety meds
assess options or goals

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Cause and development of disease

pathology

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tracking the pattern or occurrence of disease( how transmitted and distributed)

epidemiology

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causes and effects of disease

Etiology

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Etiology can include (10)

-congenital defects
-inherited or genetic disorders
-microorganisms
-immunological dysfunction
-metabolic derangements (diabetes)
-degenerative changes
-malignancy
-burns/trauma
-environmental factors
nutritional deficiencies

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the maintenance of stable internal body conditions,

homeostasis

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objective indicators of disease: can be observed by someone else

Signs

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subjective feelings

Symptoms

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mechanisms of disease (something that causes disease)

Diet
germs
genes
proteins

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a return as input, of some of the output, as a regulatory mechanism ex:regulation of thyroid output by the amount of thyroid hormone that is produced

feedback loop

organelles functions

- mitochondria:energy production - endoplasmic reticulum:transport system - ribosomes:protein synthesis - golgi apparatus: carbohydrate synthesis - lysosomes:phagocytosis

cell injury

``` hypoxia-low oxygen anoxia- no oxygen toxicity- pathogens-bugs injure cells ischemia-lack of blood ```

death of cells

necrosis

liquefactive necrosis

Brain becomes liquid. enzymes break down tissue.

coagulative necrosis

heart- thick coagulative appearance, nuclei disintegrates

infected coagulative necrotic tissue- can be wet or dry

Gangrene

Seen in pts with PVD, Diabetes, and residual limb of amputees

Gangrene

occurs in tuberculosis- Granuloma with cheese like center

Caseous necrosis

lipolytic enzymes:work only on fat ex:pancreas rupture

Fat necrosis

hardening of necrotic tissue in arteries, heart valves: too much calcium ( a type of necrosis)

dystrophic calcification

development of bone where it is not usually found: (a type of necrosis) muscle fascia usually post trauma hip,knee and shoulder most commonly affected

Heterotopic calcification (ossification)

Reduction in size of cells | found in immobilizaiton

atrophy

increase in size of cells left ventricle occurs when cells don't divide (striated heart)

hypertrophy

increase in number of cells within tissue | ex:kidney, callous,corn, polyps

hyperplasia

decrease number of cells: ex when uterus returns to normal after preagnancy

involution/hypoplasia

change in cell type

metaplasia

cells change from squamous epithelial to columnar epithelial (squamous cells don't protect esophagus in acid reflex)

Barrett's esophagus

cellular changes that are abnormal. precursor to cancer

dysplasia

bodies response to injury promotes healing allows for homeostasis cardnal signs

inflammation

swelling that has sudden onset, short in duration

acute inflammation

swelling that can last for months/years

chronic inflammation

initial damage---> mast cells, and platelets release chemical mediators initial vasoconstriction->histamine release->blood vessels become permeable--> causes redness and edema to occur

inflammatory response

2nd stage:blood vessels become congested -->clotting occurs

2nd stage of inflammatory response

- polymorphonucleuocytes: phagocytes, engulf debris release cytokines - eosinophils: phogcytes, bacteriocidal - monocytes: precursor to machrophages - macrophages:phagocytes - platelets:release seratonin (blood clotting) - basophils:release histamine - lymphocytes and plasma cells: chronic inflammation

cells involved in inflammatory response

classification of inflammation -Water fluid -occurs when pressure gradient changes causes edema

transudate

classification of inflammation - water, protein, cells of inflammation - will cause edema

exudate

- serous:clear fluid - fibrinous:lot of fibrin - purulent: pus that is yellow or green (smells) - ulcerative: usually clear - pseudomembranous: membrane forms - granulomatous: walled off

description of types of inflammation

injury never heals or acute exacerbation LBP Ankle sprain Multiple sclerosis

Acute on Chronic

PTs tx for subacute phase

- Electrical stim - non thermal ultrasound - gentle AROM

PTs tx for chronic phase

- Electrical stim - ultrasound break down scar tissue, mobilize tissue reduce pain - Exercise as appropriate

wound healing 1st intention

clear margins and can be closed with stitches

wound haling 2nd intention

nonsurgical wound. subcutaneous tissue exposed too long

occurs with irreversible cell injury tissue will be different usually loss of function scar is formed 70%-80% strenght

Fibrous repairp

``` proliferation granulation organization scar tissue remodeling of scar tissue ```

2nd intention phase of wound healing

- attempts to minimize size of wound - wound shrinks form edges - phogocytes remove necrotic tissue - blood coagulation forms scab

contraction of a wound

deposition of fibrin occurs through the wound

organization

- formed from type III collagen fibers produced by fibroblasts - turn into type I collagen - nutrition for formation of collagen comes from bed of granulation tissue

scar tissue

maturation phase red appearance decreases takes 18 months to become fully healed

remodeling of scar

foreign bodies, size of wound, infection, age, diabetes

delays wound healing

raised area of scar that spreads beyond of original wound

keloid

excessive collagen formulation | thick scar, remain with boundary of original wound

hypertrophic scarring

Complications of scarring - form contractures - tendon can't glide over joint - fibrosis of lung of liver

adhesions

complications of scarring | -wound opens before fully healed

dehiscence

- removal of necrotic therapy | - eschar: hard and leathery , black or brown, must be removed

wound debridement

- use of scalpel, scissors or tweezers | - chemical debridement agents

wound debridement

(autolytic): use of wet or dry dressing on wound( not to be used on dry wounds)

-Mechanical debridement (autolytic)

what tissue should be recognized in wounds?

Necrotic tendon connective tissue

-right time -moist wound:need absorbent material (alginate) -dry wound: hydrocolloid- occlusive or semiocclusive -wet to dry -wet to wet -

Appropriate wound intervention

treatment that helps stimulate proliferative stage and increase granulation tissue

Ultrasound

treatment:Neg polarity stim wound healing

electrical stimulation

treatment: water under pressure

pulsatile lavage

treatment: heat increases perfusion rate

short-wave diathermy

treatment: UVC: antibacterial

ultraviolet radiation

treatment: may damage healing tissue | :heat may stimulate perfusion

whirlpool

applies negative pressure: decrease edema, increase healing, blood flow, stimulate granulation tissue.

Vacuum assisted closure

- natural immunity that resists infection (born with) | - skin, mucous memebranes, bactericidal substance in tears, nose , intestinal tract

innate immunity

acquired immunity from exposure to antigens

secondary immunity

a stimulus that elicits an immune response

antigen

Antibodies are specific to one What? meaning one virus.

one antigen

Cells of immune response

Lymphocytes: WBC T lymphocytes B lymphocytes

- local effects on a cell - sent to area of body where infection is located - Effective against virus, fungal, protozoa, cancer cells and transplanted tissue T went to T cell (thymus) to get their final insections

T- lymphocytes

two types of t lymphocytes

cytotoxic | helper

- help stimulate b lymphocytes and macrophages | - assist B cells in making antibodies

Helper cells

- kill infected cells | - several types suppressor cells nk cells

cytotoxic

- produce antibodies - IgE, IgG, and IgM - IgG and IgM activates with immunization - recognizes disease and attacks it

B lymphocytes

Ig E (early) is present in

allergies

Type 1 immediate Type 2 produce antibodies Type 3 immune complex reaction Type 4 delayed response: cell mediated

hypersensitivity reaction

type I hypersensitivity reaction

``` Immediate Asthma allergic rhinitis eczema anaphylactic shock IgE links with receptors on mast cells(produce bid hives) ```

-Antibodies react with antigens within own tissue -autoimmune diseases -Blood transfusions -Hemolytic disease of the newborn (HDN) RH pos baby with RH neg mom anti D immunoglobin shot to mom

Type II hypersensitivity

- immune complex reaction * antigens and antibodies combine and instead of getting rid of it it forms a mass. * Causes tissue destruction * Glomerulonephritis, (kidney disease) lupus, RA

Type III hypersensitivity

Delayed response -cell mediated hypersensitivity EX PPD , plant toxins, chemicals in personal care items, latex TB get shot go back a few days later to have read

Type IV hypersensitivity

- introduces weak or dead antigens- the body creates antibodies - helps protect from disease

Immunizations

moderate exercise boosts immune system - intense exercise increases NK cells - increases endorphens: diminish effects of pain, decrease depression, improve sleep

Exercise and the immune response

-Air, open wounds, body fluids, ingestion, direct contact, vector

Spread of infection

bacteria, virus, fungi, parasites

Agents to infection

- insects(west nile, lymes,plague,yellow fever | - parasites- infected water, through skin, through mouth

Vectors

Microorganism- One cell, no mitochondria, single chromosome

Bacteria

Microorganisms are named according to shape and size:

Bacilli:rod Cocci:spherical Spirilla:curved

Clostridium tetani: lockjaw

Bacilli

Borrelia burgdorfei: lymes disease

Spirals

streptococci: respiratory infection

Cocci

Staphylococci: skin infections

Cocci

Methicillin Resistant staphylococcus aureus

MRSA

spreads through skin to skin cuts or scrapes contaminated objects sharing personal hygiene objects

ways to get MRSA

- 1 in 100 carry the bacteria but don't get sick - recent surgery or hospitalization, elderly or -immune compromised - now seen more in community

MRSA

- these to not respond to antibiotics - need a living host to survive - contain DNA or RNA - kills host and matures rapidly

Viruses

-one type can exist in many forms -many times it changes or slightly mutates -difficult to treat because of the constant morphing -can alter host cell chromosomes: lead to malignant cells EX : HPV

virus

-mold yeast -requires moisture and warmth -only a few are pathogenic -usually cause infection on skin or mucous membranes EX Tinea pedis

Fungi

Tinea pedis

athletes foot

- found in many places: animals, plants, food, humans household surfaces - Warmth and moisture speed growth - reproduce by budding

Fungi

Fungus that invades superficial layers of skin

Tinea pedis

candida

yeast infection

- can be normal - causes infection in oral cavity: infants and immune compromised patients - vaginal infections:especially with antibiotics - opportunistic: can cause chronic damage

Candida

coccidioides immitis

Valley fever

- Can be independent some are parasites - Unicellular - plasmodium causes malaria - Most pathogens are parasites - Parasites: live in or on another living host - Trichomonas, malaria, amebic dysentery

Protozoa

STD causes inflammation

Trichomonas vaginitis

- causes malaria - live in red blood cells - RBC will rupture, release new microbes - transmitted by insects

Plasmodium

- protein like agents | - transmitts from blood or tissue to recipients ***brain Mad cows disease

Prions

What Grade of tumors: - resemble normal cells - grow slow - less aggressive

Grade 1 tumors

What Grade of tumors: | -cells are moderately different than normal cells

Grade 2 tumors

What Grade of tumors: Grade 3 and 4 - tumors do not look like normal cells - tumors grow rapidly - spreads more quickly

Grade 3 and 4 tumors

Staging of tumors is based on what 3 things

size- how big extent- how many spread- how fast

``` unusual bleeding change in bowel/bladder change in wart or mole sore that does not heal weight loss unexplained anemia or low hemoglobin persistent cough or hoarseness solid lump, often painless ```

Warning signs of cancer

Pain Obstruction Tissue necrosis

Local effects of tumors

``` Weight loss and cachexia anemia chronic fatigue infections bleeding paraneoplastic syndrome ```

systemic effects of tumors

tumor cells release substances that affect neuro function or blood clotting

paraneoplastic syndrome

most common skin cancer

basal cell

poor prognosis silent tumor hormonal and genetic factors

ovarian cancer

parts of body are sterile under normal circumstances. They should have no bacteria

lung, bladder, stomach

production of malignant or cancerous tumors

neoplasia

study of neoplasia

oncology

self limiting, does not usually spread

benign

uncontrolled growth, potential to spread

malignant

Single gene defect

- X linked, - autosomal recessive, - autosomal dominant

early indications: seizures, headache,drowsiness, vomiting, visual disturbance, impaired motor function

Brain tumors

Mutations of DNA sequencing during meiosis

hereditary disease

an autosomal recessive disorders

Cystic fibrosis

recessive disease trait probability

25% child will be born with unaffected genotype 50% born as carrier 25% child will be born affected

a single gene defect in the exocrine glands which causes the production of abnormally thick mucus - mucus affects lungs and airflow - affects the pancreas

Cystic Fibrosis

an autosomal dominant

Huntington disease marfan syndrome osteogenesis imperfecta

autosomal dominant

one parent affected | 50% chance of child's chances to get

``` disorder that manifests in midlife 5 out of 100000 people causes progressive atrophy of the brain causes chorea autosomal dominant ```

Huntington's disease

X-linked recessive disorders

Duchenne's MD Beckers MD Fragile X syndrom hemophilia A and B

More frequent with intermarriage (auto recessive)

sickle cell | cystic fibrosis

``` Rubella microcephaly (small head and brain) alcohol medications viruses- syphillis cmv infectious disease ```

Teratogens

TORCH

``` toxoplasma- mental redtardation other viruses- neuronal defects rubella eye defects cmv- heart, lung, spleen herpes- hear lung spleen issues ```

abormal sequencing, translocation. deletion, inversion, ring chromosomes

chromosome abnormalities

- maternal serum alpha-fetal protein test - ultrasound - amniocentesis - genetic counseling

prenatal testing

Developing an infection

- Body has defense mechanisms - Immune system fails to resist the infection - Organism may be resilient or high concentration - Transmission: through port of entry * ****Wound, insect bite, contaminated needle, inhaled, contaminated food, sexual contact

avoiding Developing an infection

Prevention of initial contact Standard precautions Clean/sterile technique Frequent hand washing

time period between contact with the infection and when symptoms appear

Incubation period:

S/S of an infection

- fatigue, HA, diarrhea, constipation, rash, severe pain, abscess - Inflammation

Treatment of an infection

- Must diagnose | - Antimicrobials: medication must target the correct pathogen

Antibiotic resistant bacteria

- Rapidly increasing in numbers - MRSA - VRE - VISA - MDR TB

PT treatment: for antibiotic resistant bacteria

if an infection looks worse, immediately let the Therapist know