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Pathophysiology > Infection and Immune System > Flashcards

Infection and Immune System Flashcards

1
Q

Virulence

A
  • capacity to cause severe disease
  • how hard it is to treat an organsim
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2
Q

susceptibility

A
  • how prone the host is to the infection
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3
Q

what are the two groups most susceptible to COVID-19

A
  • people over the age of 60
  • those with underlying medical conditions
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4
Q

opertunistic infection

A

Secondary infection
- occurs after the treatment of another infection
- EXAMPLE: yeast infection

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5
Q

Nosocomial Infection

A

Hospital Acquired Infection

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6
Q

Aerobic

A
  • survives in an oxygen enviorment
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7
Q

Anaerobic

A

does not require oxygen

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8
Q

endotoxins

A
  • also known as pyrogens
  • cell wall released during cell death
  • when treated; cant prevent the toxic effects; causes the inflammatory process to be activated gram negative
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9
Q

exotoxins

A
  • secreted toxins
  • elicit the production of antitoxins
  • can produce a vaccine against them
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10
Q

how can you determine if a bacteria is gram + or -

A

gram stain

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11
Q

example of an exotoxin

A

diptheria

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12
Q

septicaemia / sepsis

A
  • bacteria in the bloodstream causing generalized infection
  • caused by gram negative bacteria
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13
Q

what are the 3 life threatening pathogens - “super bugs”

A
  • Staphylococcus aureus
  • Methicillin- resistant Staphylococcus aureus (MRSA)
  • Vanomycin- resistant Enterococci (VRE)
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14
Q

S. Aureus

A
  • adapted over time to become life threatening
  • common in nasal passages and on skin
  • becomes opportunistic
  • has developed an enzyme that destroys penicillin
  • some strains have developed into broad spectrum antibiotics (Methicillinlike antibiotics)
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15
Q

MRSA is spread through

A
  • spread through contact (person to person)
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16
Q

VREis spread through

A
  • spread through contact
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17
Q

H. pylori is resistant to

A

clarithromycin

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18
Q

Salmonellae is resistant to

A

flouroquinolone

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19
Q

Neisseria gonorrhoeae is resistant to

A

cephalosporins and flouroquinolone

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20
Q

What are the 6 steps in viral infection invasion

A
  1. attatchment
  2. penetration
  3. uncoating
  4. biosynthesis
  5. assembly
  6. release
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21
Q

attachment

A

virus attaches to epithelial cell

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22
Q

penetration

A

cell engulfs the virus

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23
Q

uncoating

A
  • virus contents released into the cell
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24
Q

biosynthesis

A

RNA enter the nucleus of the cell

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25
Q

Assembly

A

new phage particles are assembled

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26
Q

Release

A

new viral particles are made and released

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27
Q

treatment of viral infections

A
  • antiviral medications
  • immune system
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28
Q

Fungal infection

A
  • large, thick walled organism
  • opportunistic
  • treated with antifungal medications
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29
Q

what is the most common fungal infection

A

Candida albicans
- resides in the skin, GI tract, and vagina

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30
Q

how are fungal infections treated

A

antifungal medications

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31
Q

Parasitic infection

A
  • transmitted through vectors
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32
Q

Tapeworm symptoms

A

nausea, waekness, loss of appetite, abdominal pain, diarrhea, dizziness, weight loss and inadequate absorption of nutrients, bloating

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33
Q

malaria symptoms

A

fever, chills, headaches, nausea and vomiting, muscle pain and fatigue

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34
Q

nonspecific resistance

A

innate immunity

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35
Q

specific resistance

A

aquired or adapted immunity

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36
Q

adaptive (aquired) immunity

A
  • not present at birth
  • created in response to a foreign substance
  • active and passive
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37
Q

active immunity

A

natural or vaccination

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38
Q

passive immunity

A

maternal or artificial

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39
Q

Innate immunity

A
  • physical and chemical (skin, mucous membranes, hair, cilia, urine, deification and vomiting, lysozyme, gastric juice, saliva, sebum, )
  • non specific resistance (phagocytes, inflammation, fever)
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40
Q

Skin

A

A thick layer of dead cells in the epidermis provides a physical barrier to viruses, bacteria, and microbes. As the epidermis sheds, microbes are removed

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41
Q

Mucous membrane

A

produce mucus to trap microbes so they cannot spread to the rest of the body

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42
Q

Hair

A

filters microbes, dust, and pollutants from the air to prevent them from invading the body
– present in the nose and ears

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43
Q

Cilia

A

lines the upper respiratory tract and traps and propels inhaled debris to the throat so it can exit the body more quickly

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44
Q

Urine

A

flushes microbes out of the body via the urethers

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45
Q

Phagocytes

A

ingest and destroy microbes that pass into body tissues

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46
Q

Inflammation

A

localized response in the tissue that occurs when a tissues are damaged or in response to other stimuli

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47
Q

Fever

A

inhibits bacterial growth and increases the rate of tissue repair when an infection is presented in the body
- will start by increasing enzyme activity; if too high will diminish activity

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48
Q

what antibodies are found in breast milk

A

IgA and IgG

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49
Q

Lymphocytes

A
  • specific wbc
  • t cells and b cells
  • responsible for aquired immunity
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50
Q

b cells

A
  • produce antibodies
  • immunoglobulins
  • works against bacteria and viruses
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51
Q

T cells

A
  • react directly with antigen on surface
  • works against viruses and cancer cells
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52
Q

ADD mRNA

A
  • messanger RNA that introduce a viral protein which corresponds to the coating of the virus
  • body reproduces the viral protein attack to the cell wall
53
Q

Attenuated vaccine

A
  • a weekend virus or bacterium
  • produces protective antibodies against a specific pathogen without causing the potentially life threatening disease
  • must be stored and handeled carefully (can be destroyed by heat and light)
54
Q

example of attenated vaccines

A
  • measles, mumps, rubella, varicella
55
Q

Inactivated Vaccines

A
  • killed or extracts of bacterial or viral antigens
  • vaccine is grown in a culture media and then exposed to heat or chemical to activate it
  • can contain strains from multiple strains
  • need several doses or use adjuvant
56
Q

Inactivated vaccine examples

A
  • polio, hepatitis, rabies
57
Q

bacterial toxins vaccines

A
  • bacteria diseases that damage the body by secreting chemicals
  • can deactivate the toxin and then the deactivated toxins are injected created immunity
58
Q

bacterial toxin vaccine examples

A
  • tetanus, diphtheria
59
Q

Passive immunity

A
  • protection produced by an animal or human and transferred
  • disappears within weeks or months
  • primary response is often short lived
  • mother in utero, milk, immunoglobulin injection
60
Q

Primary immunodeficiency

A
  • born with it; genetic defect
  • part of the immune system is either absent or not functioning properly
61
Q

secondary immunodeficiency

A
  • acquired; caused by another condition
  • immune system is compromised due to an environmental factor
62
Q

Example of secondary Immunodeficiency

A
  • HIV, severe burns, chemotherapy, radation, diabetes, malnutrition
63
Q

Low T cell counts may be due to

A

viral infections(influenza), aging, immunodeficiency disorders, HIV, AIDS, cancers that effect the blood or lymph nodes (leukemia and hodgkins disease)

64
Q

T cell deficiencies

A
  • cellular
  • viral, fungal, yeast, and atypical microorganism
  • less severe symptoms
  • react directly against the antigen
  • mycoplasma legionella
65
Q

B cell deficiencies

A
  • humoral
  • recurrent and life threatening bacterial infections
  • b cells create anitbodies
66
Q

Common variable immunodeficiencies (CVID)

A
  • most common
  • immune system is unable to defend against bacteria and virusues
  • reccurent infections
67
Q

Severe combined immune deficiency (SCID)

A
  • most severe primary
  • few lymphocytes; thymus is underdeveloped
  • boy in the bubble
68
Q

CVID symptoms

A
  • respitory, sinuses, ears
69
Q

SCID symptoms

A
  • respiratory and GI issues, breathing problems, chronic cough, diarrhea, weight loss, ear infections, sinus infections, chronic lung disease
70
Q

Primary T lymphocyte deficiency example

A

DiGeorge Syndrome

71
Q

DiGeorge Syndrome

A
  • small part of chromosome 22 is missing
  • cardiac defects, abnormal facial features, cleft palate, hypocalcemia/hypoparathyroidism
  • no parathyroid gland, no detectable thymus in children (no T cell maturation)
  • no cure
72
Q

Conditions associates with secondary immune deficiencies

A
  • normal conditions; pregnancy, infancy, aging
  • psychological stress
  • diet
  • malignancies
  • trauma
  • infections
73
Q

AIDS

A
  • suppresses the immune response against itself and creates generalized immune deficiency against other pathogens
74
Q

AIDS transmission

A
  • through blood to blood contact, IV medication abuse, heterosexual and homosexual activity, and maternal and child transmission
75
Q

HIV is a ______

A

retrovirus

76
Q

retrovirus

A
  • inserts a copy of its RNA into DNA of a host cell
  • changes to genome of that cell (organisms DNA)
77
Q

What are the stages of HIV infection

A
  • acute
  • asymptomatic HIV
  • Symptomatic HIV
  • advanced HIV
78
Q

stage 1 of HIV

A

Acute
- occurs about 1-2 weeks after the initial infection
- virus undergoes massive replication
- patients may be asymptomatic or have flu like symptoms

79
Q

Stage 2 of HIV

A

Asymptomatic HIV
- chronic signs and symptoms are not present
- stage can last for 10-12 years
- virus proliferating in the lymph nodes

80
Q

what is used to monitor the progression of HIV

A

T cell count

81
Q

stage 3 of HIV has what 2 phases

A
  • early
  • late
82
Q

late symptomatic HIV

A
  • T cell count falls below 200cells per cubic millimeter
  • emergency of opportunistic infection and cancers
83
Q

stage 4 of HIV infection

A

Advanced
- t cell count of 50 cells
- high risk for opportunistic infections and malignancies

84
Q

treatment of HIV

A

antiretroviral therapy

85
Q

antiretroviral therapy

A
  • combination of medications (3 or more)
86
Q

Pediatric HIV children life expectancy

A
  • usually dont survive past their 2nd birthday
87
Q

signs and symptoms of pediatric HIV

A
  • failure to thrive, not reaching milestones, nervous system issues (seizures, walking), frequently sick from childhood illnesses
88
Q

Allergy

A
  • hypersensativity to enviormental antigens
89
Q

Autoimmunity

A
  • misdirected immune response that occurs when the immune system goes awry and attacks the body itself
  • body recognizes self antigens as foreign
90
Q

autoimmunity is more common in

A

women than men

91
Q

Alloimmunity

A
  • immune system of one individual produces an immunological response against tissues of another individual
  • through transfusion, transplantation , or mother to fetus
92
Q

hypersensitivity response type I

A

immunoglobulin E(IgE)
–mediated release of histamine
– most well known is anaphylaxis
– quick onset

93
Q

hypersensitivity response type II

A

IgM or IgG targeting membrane-associated antigens
– it is an antibody
-dependent process in which specific antibodies bind to antigens, resulting in tissue destruction, inflammation, or dysfunction.

94
Q

hypersensitivity response type 3

A

Deposit of abnormal antigen-antibody complexes in vessels, joints, heart, & kidney tissues
– call these “immune complexes”
– precipitate in various tissues
– serum sickness or lupus

95
Q

hypersensitivity response type 4

A

Mediated by T cells, do not involve antibodies
– Stevens-Johnson Syndrome
– it is felt that is triggered by drugs or an infection
– about 3 weeks after exposure entire body, skin and mucus membranes, will develop blisters or rash
– over time the top layer of skin dies and is shed
– healing takes several days

96
Q

!st exposure: IgE mediated

A
  • sensitization
  • mast cells produce eosinophils which cause the first reaction
  • T helper cells trigger B cells to create IgE antibodes to a specific antigen
  • IgE antibodies bind to mast cells ready for the next reaction
97
Q

IgE mediated subsequent exposures

A
  • more serious
  • mst calls that are sensitized react to subsequwnt exposure and release histamine
98
Q

IgE mediated early reactions

A
  • trigger smooth muscle contraction (mostly in bronchi; difficulty breathing)
  • causes vasodilation, increased permeability, fluid leaks, edema, hives
99
Q

IgE mediated late reactions

A
  • recruitment of other cells to the site
100
Q

IgE mediated late reactions are treated with

A

antihistamines, corticosteroids, epinephrine

101
Q

angioedema

A

swelling of the lower layer of the skin

102
Q

how do IgE mediated symptoms occur

A

Histamine binds with H1 and H2 receptors

103
Q

type 1 manifiestations

A
  • astma, itching, urticaria, conjunctivitis
  • wheal swelling
104
Q

Ananphylactic signs and symptoms

A
  • difficulty breathing, wheezing, stridor, increased heart rate, decreased blood pressure
105
Q

Anaphylactic treatment

A
  • corticosteriods
  • epinephrine administration
106
Q

Idiopathic thrombocytopenia

A
  • phagocytes destroy sensitized platelets in peripheral blood
  • petechiae, bleeding from gums, noes, bowl, low platelet count
107
Q

transfusion reactions

A
  • host antibodies react with foreign antigens on the incompatible transfused RBCs and mediate the destruction of these cells
108
Q

hemolytic diseases is newborns

A
  • mothers blood is imcomptiable with mothers blood
  • mother is Rh- and father is Rh +
109
Q

Type 2 hypersensitivity reactions examples

A
  • thrombocytopenia
  • transfusion reaction
  • hemolytic disease in newborns
110
Q

what is the universal recipient

A

AB+

111
Q

what is the universal donor

A

O-

112
Q

Hemolytic disease in newborns symptoms

A
  • mild: jaundice
  • severe: miscarriages
113
Q

Common examples of type 3 hypersensativity

A
  • allergy: wheat
  • autoimmune: systemic lupus erythematosus
114
Q

Which reactions are meditated by antibodies

A

type I, II, and III

115
Q

which reactions are mediated by T cells

A

Type IV

116
Q

Type IV hypersensitivity reactions examples

A
  • allergy: contact dermatitis
  • alloimmune: transplant rejection
117
Q

why are immunosuppresents given to organ donor recipients

A
  • prevent your immune system from attacking the new organ
118
Q

how long do organ donors take immunosuppresents

A

lifetime

119
Q

stress

A
  • bodys reaction to any change that requires adjustment or response
120
Q

what is our central stress response system

A
  • hypothalamic pituitary adrenal axis (HPA)
120
Q

HPA regulates

A
  • arousal, cognition, mood, sleep, metabolism, cardiovascular tone, immune and inflammatory reactions, growth, and reproduction
121
Q

dysregulation of HPA

A

loss of resilience and depletion of metabolic reserve (change of cortisol output)
- inflammation due to a variety of stressors, including emotional stress, undiagnosed infections, exposure to environmental toxins and pollutants, and food sensitivities or poor diet

122
Q

manifestations of dysregulation of HPA

A
  • obesity, depression, and anxiety
123
Q

HPA axis increases ______ levels in time of stress

A

cortisol

124
Q

what hormones increase during stress

A

cortisol, norepinephrine, and epinephrine

125
Q

stress effect on the immune system

A

suppresses the effectiveness by lowering the number of lymphocytes

126
Q

cortisol

A
  • carbohydrate, lipid and protein metabolism
  • anti-inflammatory effects
  • proinflammatory effects
127
Q

recovery from dysregulation

A
  • within 5-7 days but can take 3-6 months

Pathophysiology (9 decks)

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