Stress CHAP AND (feedback loop)Immunopathology, Neoplasia, Chromosome Abnormalities Flashcards
- Any factor that creates a significant change in the body/environment
- extreme stimuli ; too much too little
Stressors
3 stages of stress response
- Alarm
- Resistance
- exhaustion
stress response where the defense is mobilized.
Alarm
this stress response activates the hypothalus, sympathetic nervous system, and adrenal glands
Alarm
stress response that elevates hormones and essential body systems are working at peak performance
Resistance
stress response where Pt is unable to respond further or is damaged by increased demands
Exhaustion
- ACTH is secreted
- an increase in cortisol
what happens when our bodies our stressed
Increase level of function in critical areas of body
Why we react when stressed
increase BP and HR Bronchodialation Increase Blood Glucose Arouse the CNS Decrease inflammatory and immune response
Effects of stress
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
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
Prolonged stress creates high amounts of glucocorticoids that disrupt what 2 things?
intellectual function and memory
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
How do you cope with stress?
Recognize the stress and respond emotionally and behaviorally
-solve problem or learn to cope
factors that interfere with appropriate response
- fatigue
- age
- inadequate nutrition
- insufficient knowledge
- lack of emotional support
strategies to beat stress
- rest and healthy diet
- regular exercise
- distractive activities
- counseling
- relaxation techniques, imagery biofeedback
- anti-anxiety meds
- assess options or goals
Cause and development of disease
pathology
tracking the pattern or occurrence of disease( how transmitted and distributed)
epidemiology
causes and effects of disease
Etiology
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
the maintenance of stable internal body conditions,
homeostasis
objective indicators of disease: can be observed by someone else
Signs
subjective feelings
Symptoms
mechanisms of disease (something that causes disease)
Diet
germs
genes
proteins
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
