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Fundamentals of disease > Stress CHAP AND (feedback loop)Immunopathology, Neoplasia, Chromosome Abnormalities > Flashcards

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

1
Q
  • Any factor that creates a significant change in the body/environment
  • extreme stimuli ; too much too little
A

Stressors

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2
Q

3 stages of stress response

A
  • Alarm
  • Resistance
  • exhaustion
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3
Q

stress response where the defense is mobilized.

A

Alarm

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4
Q

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

A

Alarm

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5
Q

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

A

Resistance

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6
Q

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

A

Exhaustion

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7
Q
  • ACTH is secreted

- an increase in cortisol

A

what happens when our bodies our stressed

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8
Q

Increase level of function in critical areas of body

A

Why we react when stressed

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9
Q 
increase BP and HR
Bronchodialation
Increase Blood Glucose
Arouse the CNS
Decrease inflammatory and immune response
A

Effects of stress

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10
Q

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

A
  • Brain: enhance cognition and short term memory
  • Heart: Increase HR, and Blood pressure
  • skeletal muscle: increase function
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11
Q

specific disorders that are associated with stress

A
  • 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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12
Q

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

A

intellectual function and memory

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13
Q

Severe stress may cause

A
  • 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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14
Q

How do you cope with stress?

A

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

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15
Q

factors that interfere with appropriate response

A
  • fatigue
  • age
  • inadequate nutrition
  • insufficient knowledge
  • lack of emotional support
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16
Q

strategies to beat stress

A
  • rest and healthy diet
  • regular exercise
  • distractive activities
  • counseling
  • relaxation techniques, imagery biofeedback
  • anti-anxiety meds
  • assess options or goals
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17
Q

Cause and development of disease

A

pathology

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18
Q

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

A

epidemiology

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19
Q

causes and effects of disease

A

Etiology

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20
Q

Etiology can include (10)

A

-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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21
Q

the maintenance of stable internal body conditions,

A

homeostasis

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22
Q

objective indicators of disease: can be observed by someone else

A

Signs

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23
Q

subjective feelings

A

Symptoms

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24
Q

mechanisms of disease (something that causes disease)

A

Diet
germs
genes
proteins

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25
Q

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

A

feedback loop

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26
Q

organelles functions

A
  • mitochondria:energy production
  • endoplasmic reticulum:transport system
  • ribosomes:protein synthesis
  • golgi apparatus: carbohydrate synthesis
  • lysosomes:phagocytosis
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27
Q

cell injury

A 
hypoxia-low oxygen
anoxia- no oxygen
toxicity-
pathogens-bugs injure cells
ischemia-lack of blood
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28
Q

death of cells

A

necrosis

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29
Q

liquefactive necrosis

A

Brain becomes liquid. enzymes break down tissue.

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30
Q

coagulative necrosis

A

heart- thick coagulative appearance, nuclei disintegrates

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31
Q

infected coagulative necrotic tissue- can be wet or dry

A

Gangrene

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32
Q

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

A

Gangrene

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33
Q

occurs in tuberculosis- Granuloma with cheese like center

A

Caseous necrosis

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34
Q

lipolytic enzymes:work only on fat ex:pancreas rupture

A

Fat necrosis

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35
Q

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

A

dystrophic calcification

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36
Q

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

A

Heterotopic calcification (ossification)

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37
Q

Reduction in size of cells

found in immobilizaiton

A

atrophy

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38
Q

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

A

hypertrophy

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39
Q

increase in number of cells within tissue

ex:kidney, callous,corn, polyps

A

hyperplasia

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40
Q

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

A

involution/hypoplasia

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41
Q

change in cell type

A

metaplasia

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42
Q

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

A

Barrett’s esophagus

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43
Q

cellular changes that are abnormal. precursor to cancer

A

dysplasia

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44
Q

bodies response to injury
promotes healing
allows for homeostasis
cardnal signs

A

inflammation

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45
Q

swelling that has sudden onset, short in duration

A

acute inflammation

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46
Q

swelling that can last for months/years

A

chronic inflammation

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47
Q

initial damage—> mast cells, and platelets release chemical mediators

initial vasoconstriction->histamine release->blood vessels become permeable–> causes redness and edema to occur

A

inflammatory response

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48
Q

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

A

2nd stage of inflammatory response

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49
Q
  • 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
A

cells involved in inflammatory response

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50
Q

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

A

transudate

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51
Q

classification of inflammation

  • water, protein, cells of inflammation
  • will cause edema
A

exudate

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52
Q
  • serous:clear fluid
  • fibrinous:lot of fibrin
  • purulent: pus that is yellow or green (smells)
  • ulcerative: usually clear
  • pseudomembranous: membrane forms
  • granulomatous: walled off
A

description of types of inflammation

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53
Q

injury never heals or acute exacerbation
LBP
Ankle sprain
Multiple sclerosis

A

Acute on Chronic

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54
Q

PTs tx for subacute phase

A
  • Electrical stim
  • non thermal ultrasound
  • gentle AROM
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55
Q

PTs tx for chronic phase

A
  • Electrical stim
  • ultrasound break down scar tissue, mobilize tissue reduce pain
  • Exercise as appropriate
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56
Q

wound healing 1st intention

A

clear margins and can be closed with stitches

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57
Q

wound haling 2nd intention

A

nonsurgical wound. subcutaneous tissue exposed too long

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58
Q

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

A

Fibrous repairp

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59
Q 
proliferation
granulation
organization
scar tissue
remodeling of scar tissue
A

2nd intention phase of wound healing

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60
Q
  • attempts to minimize size of wound
  • wound shrinks form edges
  • phogocytes remove necrotic tissue
  • blood coagulation forms scab
A

contraction of a wound

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61
Q

deposition of fibrin occurs through the wound

A

organization

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62
Q
  • 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
A

scar tissue

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63
Q

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

A

remodeling of scar

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64
Q

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

A

delays wound healing

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65
Q

raised area of scar that spreads beyond of original wound

A

keloid

66
Q

excessive collagen formulation

thick scar, remain with boundary of original wound

A

hypertrophic scarring

67
Q

Complications of scarring

  • form contractures
  • tendon can’t glide over joint
  • fibrosis of lung of liver
A

adhesions

68
Q

complications of scarring

-wound opens before fully healed

A

dehiscence

69
Q
  • removal of necrotic therapy

- eschar: hard and leathery , black or brown, must be removed

A

wound debridement

70
Q
  • use of scalpel, scissors or tweezers

- chemical debridement agents

A

wound debridement

71
Q

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

A

-Mechanical debridement (autolytic)

72
Q

what tissue should be recognized in wounds?

A

Necrotic
tendon
connective tissue

73
Q

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

A

Appropriate wound intervention

74
Q

treatment that helps stimulate proliferative stage and increase granulation tissue

A

Ultrasound

75
Q

treatment:Neg polarity stim wound healing

A

electrical stimulation

76
Q

treatment: water under pressure

A

pulsatile lavage

77
Q

treatment: heat increases perfusion rate

A

short-wave diathermy

78
Q

treatment: UVC: antibacterial

A

ultraviolet radiation

79
Q

treatment: may damage healing tissue

:heat may stimulate perfusion

A

whirlpool

80
Q

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

A

Vacuum assisted closure

81
Q
  • natural immunity that resists infection (born with)

- skin, mucous memebranes, bactericidal substance in tears, nose , intestinal tract

A

innate immunity

82
Q

acquired immunity from exposure to antigens

A

secondary immunity

83
Q

a stimulus that elicits an immune response

A

antigen

84
Q

Antibodies are specific to one What? meaning one virus.

A

one antigen

85
Q

Cells of immune response

A

Lymphocytes:
WBC
T lymphocytes
B lymphocytes

86
Q
  • 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

A

T- lymphocytes

87
Q

two types of t lymphocytes

A

cytotoxic

helper

88
Q
  • help stimulate b lymphocytes and macrophages

- assist B cells in making antibodies

A

Helper cells

89
Q
  • kill infected cells

- several types suppressor cells nk cells

A

cytotoxic

90
Q
  • produce antibodies
  • IgE, IgG, and IgM
  • IgG and IgM activates with immunization
  • recognizes disease and attacks it
A

B lymphocytes

91
Q

Ig E (early) is present in

A

allergies

92
Q

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

A

hypersensitivity reaction

93
Q

type I hypersensitivity reaction

A 
Immediate
Asthma
allergic rhinitis
eczema 
anaphylactic shock
IgE links with receptors on mast cells(produce bid hives)
94
Q

-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

A

Type II hypersensitivity

95
Q
  • 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
A

Type III hypersensitivity

96
Q

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

A

Type IV hypersensitivity

97
Q
  • introduces weak or dead antigens- the body creates antibodies
  • helps protect from disease
A

Immunizations

98
Q

moderate exercise boosts immune system

  • intense exercise increases NK cells
  • increases endorphens: diminish effects of pain, decrease depression, improve sleep
A

Exercise and the immune response

99
Q

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

A

Spread of infection

100
Q

bacteria, virus, fungi, parasites

A

Agents to infection

101
Q
  • insects(west nile, lymes,plague,yellow fever

- parasites- infected water, through skin, through mouth

A

Vectors

102
Q

Microorganism- One cell, no mitochondria, single chromosome

A

Bacteria

103
Q

Microorganisms are named according to shape and size:

A

Bacilli:rod
Cocci:spherical
Spirilla:curved

104
Q

Clostridium tetani: lockjaw

A

Bacilli

105
Q

Borrelia burgdorfei: lymes disease

A

Spirals

106
Q

streptococci: respiratory infection

A

Cocci

107
Q

Staphylococci: skin infections

A

Cocci

108
Q

Methicillin Resistant staphylococcus aureus

A

MRSA

109
Q

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

A

ways to get MRSA

110
Q
  • 1 in 100 carry the bacteria but don’t get sick
  • recent surgery or hospitalization, elderly or -immune compromised
  • now seen more in community
A

MRSA

111
Q
  • these to not respond to antibiotics
  • need a living host to survive
  • contain DNA or RNA
  • kills host and matures rapidly
A

Viruses

112
Q

-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

A

virus

113
Q

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

A

Fungi

114
Q

Tinea pedis

A

athletes foot

115
Q
  • found in many places: animals, plants, food, humans household surfaces
  • Warmth and moisture speed growth
  • reproduce by budding
A

Fungi

116
Q

Fungus that invades superficial layers of skin

A

Tinea pedis

117
Q

candida

A

yeast infection

118
Q
  • can be normal
  • causes infection in oral cavity: infants and immune compromised patients
  • vaginal infections:especially with antibiotics
  • opportunistic: can cause chronic damage
A

Candida

119
Q

coccidioides immitis

A

Valley fever

120
Q
  • 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
A

Protozoa

121
Q

STD causes inflammation

A

Trichomonas vaginitis

122
Q
  • causes malaria
  • live in red blood cells
  • RBC will rupture, release new microbes
  • transmitted by insects
A

Plasmodium

123
Q
  • protein like agents

- transmitts from blood or tissue to recipients ***brain Mad cows disease

A

Prions

124
Q

What Grade of tumors:

  • resemble normal cells
  • grow slow
  • less aggressive
A

Grade 1 tumors

125
Q

What Grade of tumors:

-cells are moderately different than normal cells

A

Grade 2 tumors

126
Q

What Grade of tumors: Grade 3 and 4

  • tumors do not look like normal cells
  • tumors grow rapidly
  • spreads more quickly
A

Grade 3 and 4 tumors

127
Q

Staging of tumors is based on what 3 things

A

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

128
Q 
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
A

Warning signs of cancer

129
Q

Pain
Obstruction
Tissue necrosis

A

Local effects of tumors

130
Q 
Weight loss and cachexia 
anemia
chronic fatigue
infections
bleeding
paraneoplastic syndrome
A

systemic effects of tumors

131
Q

tumor cells release substances that affect neuro function or blood clotting

A

paraneoplastic syndrome

132
Q

most common skin cancer

A

basal cell

133
Q

poor prognosis
silent tumor
hormonal and genetic factors

A

ovarian cancer

134
Q

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

A

lung, bladder, stomach

135
Q

production of malignant or cancerous tumors

A

neoplasia

136
Q

study of neoplasia

A

oncology

137
Q

self limiting, does not usually spread

A

benign

138
Q

uncontrolled growth, potential to spread

A

malignant

139
Q

Single gene defect

A
  • X linked,
  • autosomal recessive,
  • autosomal dominant
140
Q

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

A

Brain tumors

141
Q

Mutations of DNA sequencing during meiosis

A

hereditary disease

142
Q

an autosomal recessive disorders

A

Cystic fibrosis

143
Q

recessive disease trait probability

A

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

144
Q

a single gene defect in the exocrine glands which causes the production of abnormally thick mucus

  • mucus affects lungs and airflow
  • affects the pancreas
A

Cystic Fibrosis

145
Q

an autosomal dominant

A

Huntington disease
marfan syndrome
osteogenesis imperfecta

146
Q

autosomal dominant

A

one parent affected

50% chance of child’s chances to get

147
Q 
disorder that manifests in midlife
5 out of 100000 people
causes progressive atrophy of the brain
causes chorea
autosomal dominant
A

Huntington’s disease

148
Q

X-linked recessive disorders

A

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

149
Q

More frequent with intermarriage (auto recessive)

A

sickle cell

cystic fibrosis

150
Q 
Rubella 
microcephaly (small head and brain)
alcohol
medications
viruses- syphillis cmv infectious disease
A

Teratogens

151
Q

TORCH

A 
toxoplasma- mental redtardation
other viruses- neuronal defects
rubella eye defects
cmv- heart, lung, spleen
herpes- hear lung spleen issues
152
Q

abormal sequencing, translocation. deletion, inversion, ring chromosomes

A

chromosome abnormalities

153
Q
  • maternal serum alpha-fetal protein test
  • ultrasound
  • amniocentesis
  • genetic counseling
A

prenatal testing

154
Q

Developing an infection

A
  • 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
155
Q

avoiding Developing an infection

A

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

156
Q

time period between contact with the infection and when symptoms appear

A

Incubation period:

157
Q

S/S of an infection

A
  • fatigue, HA, diarrhea, constipation, rash, severe pain, abscess
  • Inflammation
158
Q

Treatment of an infection

A
  • Must diagnose

- Antimicrobials: medication must target the correct pathogen

159
Q

Antibiotic resistant bacteria

A
  • Rapidly increasing in numbers
  • MRSA
  • VRE
  • VISA
  • MDR TB
160
Q

PT treatment: for antibiotic resistant bacteria

A

if an infection looks worse, immediately let the Therapist know

Fundamentals of disease (19 decks)

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