Immunity and infection Flashcards

1
Q

In the innate immune system what are the physical barriers

A

mucus skin saliva cilia coughing sneezing stomach acid

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2
Q

What is a white blood cell differential

A

check for leukocyte count

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3
Q

What does a left shift mean for a WBC differential

A

large amounts of neutrophils

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4
Q

Eosinophils are related to what two conditions

A

hay fever asthma

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5
Q

HIV attacks which cells

A

helper T

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6
Q

When your helper T’s are 250 microliters or less what happens

A

HIV turns to aids

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7
Q

What are the cardinal signs of inflammation

A

redness swelling heat pain function impariment

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8
Q

What complement protein are you born with

A

C3

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9
Q

What are the three ways the complement system gets activated called

A

Classical (slowest) Lectin Alternative (fastest)

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10
Q

Do all three complement pathways lead to the cleavage of C3 into C3b and a

A

yes

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11
Q

What does the classical pathway start with

A

the antibodies IgG or IgM

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12
Q

What does the alternative pathway start with

A

just C3

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13
Q

What does the lectin pathway start with

A

lectin binds with a sugar called mannose found on the surface of pathogens

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14
Q

Once the three complement pathways reach C3 what happens

A

C3 is cleaved into C3b and C3a

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15
Q

What is C3a’s purpose

A

to attract neutrophils According to the tutor, it also activates basophils and mast cells

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16
Q

What does C3b do

A

opsonizes the bacteria so phagocytes can recognize it or it acts as an enzyme for C5

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17
Q

What does C3 do to the C5

A

converts it into C5a & b C5a acts to stimulate the vascular phase of acute inflammation (where there brief vasoconstriction followed by rapid dialation and increased vascular permeability) C5b form together with C6,7,8,9 to form the membrane attack complex that pokes a hole in the microbe

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18
Q

What is the process of stimulating the adaptive immune response

A

after a phagocyte eats a microbe, it presents a piece of that microbe on its surface then presents that piece to a T cell the T cell then takes that antigen to a B cell who then differentiates into B plasma cells and memory cells the B plasma cells then mass produce antibodies

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19
Q

What is produced during the vascular phase of acute inflammation

A

histamine and nitric oxide

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20
Q

What are the effects of histamine and nitric oxide

A

vasodilation

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21
Q

Why is the decrease of blood flow caused by increased vascular permeability and vasodilation benefitial

A

enables clotting in the blood vessel helps localized infection

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22
Q

What type of protein increases during infection

A

C reactive proteins

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23
Q

What is a normal CRP level (C reactive proteins)

A

below 3 mg/L of blood

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24
Q

describe acute

A

rapid onset last between 2 weeks and 3 months

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25
Q

What cytokines inhibit viral replication

A

interferons

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26
Q

What is the most common Immunoglobin

A

IgG

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27
Q

What is the % of each Ig

A

75% IGG 15% IGA 10% IGM trace amounts for IGE and IGD

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28
Q

Which Ig is passed through the placenta

A

IgG

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29
Q

Which Ig is largest

A

IgM

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30
Q

Which Ig is the first to be produced

A

IgM

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31
Q

Where can IgE’s be found

A

basophils and mast cells

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32
Q

Cytotoxic T cells (CD8) have what MHC

A

I

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33
Q

Helper T cells (CD4) have what MHC

A

II

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34
Q

What are type I hypersensitivity disorders

A

mediated by IgE includes anaphylactic shock, bronchial asthma, and hay fever

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35
Q

What are type II hypersen disorders

A

anti-body mediated IgM or IgG includes A ntibody medieated cell destruction T ransfusion reactions H emolytic disease in newborns

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36
Q

What are type III hypersen disorders

A

involves the creation and deposition of insoluble antigen-antibody complexes that cause systemic and local immune complex disease Some causes are Antibodies, antivenom, foods

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37
Q

What are type IV hypersen disorders

A

cell mediated CD8’s kill antigen bearing target cells CD4’s release cytokines that damage and kill antigen containing cells examples: Hep A, TB test

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38
Q

If a B or T cell that is autoreactive escapes the first test in the lymphoid tissue how do they get suppressed (Two ways)

A

for these cells to proliferate after binding to a self-antigen , they need a secondary stimulating signals. With that secondary signal, they can cause more damage Suppression from suppressor T cells

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39
Q

A latex allergy might be a example of what type of hypersen

A

type IV

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40
Q

What is a immunodeficiency disorder

A

an abnormality in the immune system that leaves the person more susceptible to infections

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41
Q

What is a primary immunodeficiency

A

a genetic defect

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42
Q

What is a secondary immunodef

A

acquired

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43
Q

What type of virus is HIV

A

retro

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44
Q

What is it and what does a retro virus do

A

its an RNA virus that injects its DNA into the hosts DNA

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45
Q

What cell does HIV affect

A

CD4 T cells (cell mediated immunity)

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46
Q

How is HIV transmitted

A

through blood or body fluid (like semen, breast milk, and vaginal secretions)

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47
Q

What is the most frequent mode of transmission of HIV

A

sexual contacts

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48
Q

What is HIV’s pathogenesis

A

binds to CD4 molecule uses the hosts reverse transcriptase to turn RNA into DNA integrates its DNA into the hosts DNA the host cell then transcribes and translates proteins and in the process end up also transcribing and translating new HIV viruses protease cleaves some the polyprotein chains of the new viruses these new viruses then coat themselves with the cell membrane as they leave the host cell

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49
Q

What test is used for diagnosis of HIV

A

ELISA (enzyme-linked immunosorbent assay)

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50
Q

What are some common opportunistic pathogens that affect people with AIDS

A

Candida TB

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51
Q

What disease is a commonly associated with AIDS

A

dementia

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52
Q

What are the three phases of HIV infection

A

primary infection- symptoms similar to MONO like fever and fatigue, decrease in CD4 count latent period- no signs or symptoms, lasts average of 10 years, gradual drop of cd4 T cell count Stage 3 (overt AIDS)- occurs when CD4 T count drops below 200 cells/microliter, 2-3 years to death usually for people who don’t get treatment

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53
Q

HIV usually turns to AIDS after

A

7-10 years

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54
Q

What are some common conditions that AIDS patients get

A

opportunistic infections and cancers wasting syndrome dementia malignancies

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55
Q

What are some common examples of malignancies you can get from HIV

A

Kaposi sarcoma, non-hodgkins lymphoma, and non-invasive cervical carcinoma

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56
Q

What are pressure ulcers caused by

A

unrelieved pressure that impair blood flow and lymph

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57
Q

What does pressure ulcers cause

A

ischemia

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58
Q

What are the ways ischemia happens

A

unrelieved pressure shearing force moisture friction

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59
Q

Where do ulcer pressure usually occur

A

sacrum coccyx heels hips elbows knees ankles cranium

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60
Q

Who is at the most risk of ulcer pressures

A

injured elderly quadriplegia critical care setting

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61
Q

How do you prevent ulcer pressures

A

move patient every two hours

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62
Q

What are the stages of pressure ulcers and describe them

A

stage 1- reddened skin stage 2- skin loss of epidermis or dermis stage 3- skin loss involving damage or necrosis of subcutaneous that may extend to but not through the fascia stage 4- necrosis, damage to muscle, bone, supporting tissue

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63
Q

What type of disease is Psoriasis

A

immune mediated

64
Q

Is there a cure for psoriasis

A

no, lifelong

65
Q

Where is psoriasis usually found

A

knees elbows scalp

66
Q

What happens in psoriasis

A

skin cells are mistaken for pathogens, causing an immune reaction that cause a build up of cells giving a silvery look

67
Q

What are some bacterial skin infections

A

Cellulitis Impetigo

68
Q

What is Cellulitis

A

infection of the subcutaneous and dermis tissue, usually caused by staph aureus

69
Q

Where does cellulitis usually occur on the body

A

legs and face

70
Q

What is the pathology of cellulitis

A

inflammation of connective tissue and the dermis and subcutaneous

71
Q

What are the manifestations of Cellulitis

A

tingling feeling redness heat pain

72
Q

What is Impetigo

A

superficial skin infection caused by staph aureus or beta hemolytic streptococcus

73
Q

Is Impetigo contagious

A

highly

74
Q

What are some manifastations of impetigo

A

yellow honey crusted sores around the mouth

75
Q

Is impetigo itchy

A

it can be

76
Q

is impetigo painful

A

no

77
Q

How is impetigo spread

A

direct contact with the lesions

78
Q

How is impetigo treated

A

Bactroban or systemic antibodies in sever cases

79
Q

What is herpes simplex virus

A

infection of skin and mucous membranes

80
Q

Explain the two different types of HSV

A

HSV-1 : usually infects the mouth HSV-2 : usually infects genitals

81
Q

What are the primary symptoms of HSV-1

A

painful vesicles ulcers of the lips, tongue, and palate fever sore throat

82
Q

What are the recurrent symptoms of HSV-1

A

begin with burning or tingling in the area of the primary infection

83
Q

What are some factors that increase the chance of having an outbreak of HSV-1

A

stress ultraviolet B exposure

84
Q

Is there a cure for HSV

A

no, patients usually take antihistamines, antiinflams, and anesthetics sunscreen also helps block ultraviolet B

85
Q

What are shingles

A

vesicular eruption along dermatomal segment of the skin

86
Q

How are shingles and chicken pox related

A

they are both caused by the same virus, varicella-zoster chicken pox is more contagious but shingles can be transmitted through nonimmune contact

87
Q

How does age affect shingles

A

people older than 60 are the most effected

88
Q

What else increases the risk of getting shingles

A

HIV cancer treatments longterm corticosteroid treatments

89
Q

What are the symptoms of shingles

A

pain, tingling, and extreme sensitivity along the effected dermatome

90
Q

Where on the body does it usually effect

A

back to groin face thoracic region

91
Q

How long does HSV sores take to heal

A

2-6 weeks

92
Q

What is the prodromal phase of shingles preceded by

A

lesions (rash)

93
Q

How long might the prodromal phase of shingles last

A

1-3 days

94
Q

What do the lesions of shingles look like

A

erupted vesicles with erythematous bases that follow sensory nerves

95
Q

What is the lifespan of new crops of vesicles in shingles

A

erupt for 3-5 days dry up, form crusts, fall off last 2-3 weeks

96
Q

What are some complications that can arise from shingle vesicles on the face

A

they can damage the eye leading to blindness

97
Q

How is shingles treated

A

administration of antiviral agents preferably with 72 hours of the rash development vaccine

98
Q

What is scabies

A

a contagious disease caused by mites that burrow under the skins

99
Q

How is scabies transmitted

A

contact with person, bedding, or clothing

100
Q

What is the pathophysiology of scabies

A

eggs of the mites are laid in the stratum corneum, eggs hatch and become adults over the next 3 weeks

101
Q

What are the manifestations of scabies

A

appears after 3-5 weeks of infection the primary lesion are burrows, papules, and vesicles intense itching, worse at night secondary infections and crusting develop from scatching

102
Q

where on the body does scabies affect the most

A

hands and feet, webbed skin the most

103
Q

What is thrush (oral candidiasis)

A

fungal infection of candida albicans on the mucous membranes of the mouth

104
Q

What are the signs of thrush

A

thick white lesions on the tongue or inner cheek

105
Q

What are the symptoms

A

the lesion can be itchy and painful

106
Q

What are the risk factors of thrush

A

people coming off systemic antiboitics warm, moist environment pregnancy weakened immunity diabetes

107
Q

What is pediculosis

A

lice, parasites live on the surface of the skin and suck blood to survive

108
Q

How is lice transmitted

A

direct contact infected fomite

109
Q

What do lice secrete

A

toxic saliva

110
Q

What can the toxic saliva and mechanical trauma of lice cause

A

pruritis (severe itching)

111
Q

How often do female lice reproduce

A

every 2 weeks

112
Q

Who is most commonly affected by lice

A

children

113
Q

how is lice treated

A

medicated shampoo patient combing of the hair

114
Q

What is molluscum contagiosum

A

a highly contagious poxvirus, grows in the folicular epithelium

115
Q

How is molluscum contag transmitted

A

direct contact infected fomites

116
Q

What does molluscum contagiosum look like

A

the lesions are discrete, pitted, and dome shaped with little black dot in the middle

117
Q

Where does mollus contag affect on the body

A

anywhere

118
Q

What happens to the lesions of mollus contag

A

they erupt then scab over

119
Q

Is treatment of molluscum contag needed

A

usually not

120
Q

What is basal cell carcinoma

A

slow growing tumors in the deepest layer of the epidermis

121
Q

What causes basal cell car

A

damage from sun rays

122
Q

What does basal cell car usually look like

A

well defined lesions with rolled borders and depressed centers

123
Q

Does basal cell car metastisize out of the skin

A

no

124
Q

How does basal cell car grow

A

laterally

125
Q

What is chicken pox

A

contagious disease thats caused by the varicella-zoster virus

126
Q

What is the timeline of chicken pox

A

11-20 days of incubation contagious for 1-2 days before rash through 5 days after crusting

127
Q

What is the pathology of chicken pox

A

mascular rash papular vesicular crusted lesion

128
Q

Where does chicken pox affect the body

A

trunk face then later to the etremeties

129
Q

Is chicken pox itchy

A

yes

130
Q

What are some complications in adults with chick pox

A

H ematuria E pitaxis L aryngeal edema V aricella pneumonia

131
Q

What are the 5 things to monitor for skin cancers

A

A- asymmetry B- border C- color D- diameter E- evolving

132
Q

What is squamous cell carcinoma

A

Tumors that grow in the epidermis

133
Q

What are squam cell cars manifestations

A

red scaly patches with irregular borders open sores with raised borders and crusted surface

134
Q

Where is squam cell car commonly found

A

areas of the head shoulders back hands

135
Q

What areas are the most vulnerable

A

rim of ear and lower lip

136
Q

What is melanoma

A

cancer of melanocytes

137
Q

Is melanoma malignant

A

yes

138
Q

can melanoma metastisize

A

yes

139
Q

What are the risk factors of melanoma

A

sun exposure family history

140
Q

What does it look like

A

asymmetrical uneven borders more than one shade of color > 1/4 inches

141
Q

What are examples of granulocytes?

A

Basophils Eosinophils Neutrophils Mast cells

142
Q

What are examples of agranulocytes

A

Monocytes Macrophages Lymphocytes

143
Q

What is the bacterium that causes Lyme disease?

A

Borrelia Burgdorferi

144
Q

How is the disease transmitted to humans?

A

Bite of infected backlegged deer ticks

145
Q

What are typical symptoms of Lyme disease?

A

Fever, headache, fatigue, skin rash within 14 weeks

146
Q

Is Lyme disease curable?

A

Yes with antibiotics

147
Q

What is a distinguished feature of Lyme disease?

A

Target lesion/rash

148
Q

What is affected in first degree burn and what does it look like?

A

Epidermis; superficial, read

149
Q

What is affected in second degree burn and what does it look like?

A

partial/deep thickness- epidermis and some dermis; blisters, pain, edema, white & waxy

150
Q

What is affected in third degree burn and what does it look like?

A

full thickness- epidermis, dermis, subcutaneous tissue: critical, skin graft

151
Q

What is affected in fourth degree burn and what does it look like?

A

tissue beneath skin burned; muscle, tendons, ligaments, bones

152
Q

What is the pathophysiology of electrical injury?

A

Electrical current enters body –> follows tissue with low resistance –> exists at another site

153
Q

What are the manifestations of electrical injury?

A

Difficult to assess fuel extent of burn Tissue around exit wound most severely damaged

154
Q

What are the consequences of electrical injury?

A

Systemic: cardiac, acid-base, tissue necrosis Local: devascularazition –> amputation

155
Q

What is frost bite?

A

Injury due to exposure to extreme colder

156
Q

What is the pathophysiology of frost bite?

A

Ice crystal formation Blood vessels close to the skin constrict –> anoxia, release of inflammatory mediators Generation of oxygen free radicals Prostaglandins and release of proteolytic enzymes