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Patho > Patho- inflammation - acid base imbalance > Flashcards

Patho- inflammation - acid base imbalance Flashcards

1
Q

what are the steps of acute inflammation?

A

Vascular response

cellular response

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2
Q

What is vascular response?

A

stat brief vasoconstriction
leukocytes, mast cells, and platelets release mediators histamine and prostaglandin
histamine and prostaglandin brings capillary dilation, increase cap permeability,dilates blood vessels and mediates pain
vasodilation increase blood flow to area which causes hyperaemia
increased cap permeability allows exudate to form
fluid and protein shift causing swelling and pain
pain causes immobilization

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3
Q

Vasoconstriction- vs- Vasodilation

A

Vasoconstriction- clotting occurs during

Vasodilation- brings resources to site

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4
Q

What is hyperaemia?

A

redness, flushed warm skin

caused by vasodilation

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5
Q

what is a histamine?

A

a protein that is released by leukocytes, mast cells, and platelets which causes capillary dilation –> chemical response takes longer than euro response
increase cap permeability
dilates blood vessels

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6
Q

what is prostaglandin?

A

prostaglandin is considered a local hormone
(acts on point of release, does different things at different sites)
brings cap dilation. dilates blood vessels and mediates plain

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7
Q

Why do you need increased cap permeability?

A

allows exudate to form

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8
Q

what is exudate?

A

proteins, cells and plasma

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9
Q

what does the fluid and protein shift cause?

A

swelling and pain

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10
Q

signs of inflammation

A

redness, warmth, swelling, pain

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11
Q

what do leukocytes, mast cells and platelets release?

A

mediators- histamine, and prostaglandin

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12
Q

What is the cellular response?

A

Chemotaxis of neutrophils and other WBC to site
margination on endothelium assisted by adhesion molecules (integrins and selections)
Diapedesis/ emigration into tissue spaces
phagocytosis of cell debris and foreign particles

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13
Q

what is chemotaxis?

A

movement of an organism in response to a chemical stimulus

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14
Q

what is margination?

A

process in which free-flowing leukocytes exit the central blood stream, and initiate leukocyte and endothelial cell interactions by close mechanical contact.

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15
Q

what are adhesion molecules

A

selectin and integrins

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16
Q

Selectins

A

type of adhesion molecule

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17
Q

integrins

A

type of adhesion molecule

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18
Q

what is diapedesis ?

A

is the movement of leukocytes out of the circulatory system, towards the site of tissue damage or infection

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19
Q

what is emigration

A

same as diapedesis

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20
Q

what are PCAM

A

platelet cell adhesion molecules

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21
Q

types of exudate?

A 
serous
purulent/ suppurative
hemorrhagic
fibrinous
membranous
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22
Q

what is serous exudate ?

A

watery, decreased proteins of cells

mild, acute inflammation

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23
Q

what is purulent/ suppurative exudate?

A

pus, WBC, necrotic debris
cloudy, foul odour
severe, acute inflammation

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24
Q

what is hemorrhagic exudate?

A

RBCs

severe injury

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25
Q

what is fibrinous exudate?

A

increased number of fibrinogen

forms sticky mesh

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26
Q

what is membranous exudate?

A

developing mucus membrane

necrotic cells in fibropurulent exudate

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27
Q

systemic manifestations of inflammation ?

A

malaise, fatigue, headache

fever

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28
Q

what does fever do ?

A

enhances phagocytosis and triggers immune response

inhibits reproduction and growth of pathogens

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29
Q

why is fever considered good?

A

enhances phagocytosis and triggers immune response, inhibits reproduction and growth of pathogens

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30
Q

what is the pathogenesis of fever?

A

Exogenous pyrogens–> endogenous pyrogens–> PGE 2—> hypothalamic receptor–> adj temp to set point via CAMP

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31
Q

what does the hypothalamic receptor do?

A

adjusts temperature set point via CAMP

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32
Q

What is CRP

A

C- Reactive protein

Hepatic protein

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33
Q

What does CRP do?

A

Produced in response to inflammation;
acts as a serum marker, role in defence via complement, non specific marker

has increased levels in atherosclerosis

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34
Q

what are some treatments of inflammation ?

A

Cold, Elevation, pressure, heat, NSAIDS, steroidal anti inflam drugs

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35
Q

What does cold do to inflm ?

A

decreases swelling–> increases vasoconstriction, less volume of blood–> decreased pressure –> decreased volume of exudate–> decreased swelling

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36
Q

What does elevation and pressure do to inflam?

A

decreased blood flow, decreases exudate, decreases swelling

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37
Q

what does heat do to inflam ?

A

stimulates phagocytosis

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38
Q

what do NSAIDS do to inflam?

A

decrease prostaglandin synthesis–> decrease in pain

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39
Q

What do steroidal anti- inflame drugs do to inflam?

A

decrease permeability
decrease WBC and mast cells at site
decrease prostaglandin and histamine release

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40
Q

what are the three types of abnormal immune response?

A

autoimmunity
hypersensitivity
immunodeficiency

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41
Q

what is immunodeficiency ?

A

partial or complete loss of immune response

increases risk of disease

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42
Q

what are the types of immunodeficiency ?

A

primary and secondary immunodeficiency

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43
Q

what is primary immunodeficiency ?

A

immunodeficiency that is genetic or congenital

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44
Q

what is secondary immunodeficiency ?

A

acquired or post natal immunodeficiency

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45
Q

is genetic primary or secondary?

A

primary

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46
Q

types of secondary immunodeficiency

A 
T- cell disorders
B- cell disorders
T&B- cell disorders
Complement disorders
phagocytosis disorders
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47
Q

what type of infection could cause secondary immunodeficiency ?

A

AIDS

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48
Q

causes of secondary immunodeficiency ?

A

Cancer treatments
infection (aids)
immunosuppressive drugs

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49
Q

What are T cell disorders?

A

Impaired T cell function

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50
Q

What are B cell disorders?

A

impaired Antibody production

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51
Q

What are T&B cells disorders

A

impaired immune function

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52
Q

what are complement disorders?

A

problems with complement

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53
Q

What are disorders of phagocytosis?

A

problems with macrophage, and t cells

54
Q

What are the treatments for immunodeficiency ?

A 
replacement therapy (gamma globulins)
marrow/ thymus transplant
55
Q

What is hypersensitivity?

A

immune response that is exaggerated or inappropriate

Inflm and tissue damage occurs

56
Q

what are the types of hypersensitivity?

A

Type 1- IG E mediated or ALLERGY
Type 2- Cytotoxic Hypersensitivity or tissue specific Hypersensitivity
Type 3- Immune complex Hypersensitivity
Type 4- T-cell mediated Hypersensitivity or delayed Hypersensitivity

57
Q

What is type 1 or IG E mediated (allergy) hypersensitivity

A

due to Allergens (drugs, food)
Rapid response

Sensitization of Mast cells;
1st exposure to allergen–> TH2–> B cell stimulation —> IG E forms and attaches to mast cells–> mast cells sensitized

Re- exposure;
Allergen binds to IG E on mast cell —> Mediators are released—> Inflm occurs—> target area becomes red, swollen, and pruritic

58
Q

examples of IGE mediated hypersensitivity?

A

allergy, asthma, anaphylaxis

59
Q

what is the most common type or hypersensitivity?

A

Allergy or IGE mediated

60
Q

What is type 2 IGM or IGG mediated hypersensitivity?

A

Antibodies mis target surface antigens on cells

Antibodies + antigens—> antigen bearing cell destroyed by complement, phagocytosis, and inflam

61
Q

What is an example of IGM OR IGG mediated hypersensitivity ?

A

incompatible blood transfusion

62
Q

What is shock?

A

actue hypoperfusion due to cardiovascular failure—> tissue hypoxia

63
Q

What happens during anaphylactic shock?

A

type 1 hypersensitivity —> mediator release—> excessive vasodilation and increased cap permeability —> circulatory failure, deem, bronchospasm

64
Q

What happens during septic shock?

A

vasodilation causes hypotension causes systemic inflm—> multi organ dysfunction

65
Q

What are antigens bearing cells destroyed by ?

A

complement, phagocytosis

66
Q

What is type 3 Immune complex hypersensitivity ?

A

antigen and antibody form AGAB immune complex–> which is deposited in tissues
often on endothelium

Inflm and tissue damage follows

67
Q

examples of type 3 immune complex hypersensitivity?

A

Glomerulonephritis, rheumatoid arthritis

deposits in smaller joints– causing inflam and damage to joints

68
Q

What is type 4 T cell Hypersensitivity reaction?

A

macrophage presents antigen to T cell –> T cell sensitized–> cytotoxic T cell—-> destroy of antigen bearing cell —> inflame damage

69
Q

What are the types of T cell hypersensitivity reaction?

A

Direct (stat)

delayed ( days)- d/t production of lymphokines

70
Q

Examples of T cell hypersensitivity ?

A

TB test

contact dermatitis

71
Q

What is autoimmunity?

A

self antigens are normally tolerated–>
self is considered foreign
antibodies target self antigens

Ab+AG= inflm damage and necrosis

72
Q

how can self tolerance be lost?

A

abnormal T cell activity–> no T cell suppression
Molecular mimicry—> similar epitope (mistaken identity)
Exposure of previously masked self antigens (by disease)
SLE–> Lupus

73
Q

what is neoplasia?

A

abnormal cell growth and differentiation

74
Q

what is neoplasm?

A

tumor–> abnormal mass, irreversible growth

75
Q

what is a benign tumour?

A

uncontrolled slow growth
may stop or regress
differentiated cells
non invasive in relation to a malignant tumour

76
Q

What is a malignant tumour?

A

disorderly, rapid growth
poorly differentiated cells
invasive and damaging

77
Q

What is cancer?

A

at least on malignant tumour d/t mutated genes –> primary cause

78
Q

what is oncogenes?

A

general term for any gene that causes cancer

79
Q

for benign tumours what suffix do you use?

A

OMA

80
Q

for malignant tumours how do you name them?

A

Carcinoma—> if epithelium

Sarcome —-> if mesenchyme ( non epithelial tissue after birth)

81
Q

prefix “ aden”

A

from glandulary epithelium

82
Q

prefix “osteo”

A

bone

83
Q

methods of spread of tumours

A

extension and invasion
seeding in body cavities
metastasis via blood or lymph

84
Q

What is metastasis ?

A

spread of cancer cells from primary to secondary site

85
Q

What is the most common site of metastasis ?

A

lymphatic tissue

then liver, lungs, bone and brain

86
Q

explain stage 1 metastasis

A

invades local tissue, embolism enter blood or lymph vessel

87
Q

explain stage 2 metastasis

A

travel via blood or lymph
reach area of resistance (cap bed)
attach to suitable site—> cytokines, growth factors

88
Q

Explain stage 3 metastasis

A

angiogenesis & cell growth at second site

89
Q

what is grading of tumours ?

A

restrictive to extensive

1-4

90
Q

what is staging of tumours?

A

clinical criteria, physical assessment at hospital—> using global TNM system

91
Q

T 0-4 ?

A

size of tumour

92
Q

Tx

A

can’t assess size of tumour

93
Q

T is

A

in situ= is in original position

94
Q

N 0-3

A

regional lymph nodes

95
Q

M 0-1

A

metastasis

96
Q

TNMx

A

can’t be assessed

97
Q

Treatments of cancer?

A 
Radiation therapy
Chemotherapy
Surgery
immunotherapy
hormone therapy
combination therapy
98
Q

explain radiation therapy

A

Necrosis via: free radical production and disruption of DNA bonds

99
Q

explain chemotherapy

A

targets cell division, prevents/ slows growth of cells

100
Q

explain surgery

A

excise tumour—> take more than malignant cells

101
Q

explain immunotherapy

A

uses cytokines and antibodies that stimulates immune response to destroy cancer cells

102
Q

explain hormone therapy

A

used for hormone responsive tumours—> disrupts regulatory function

103
Q

explain combination therapy

A

mix of above therapies

104
Q

problems associated with therapy?

A

difficult to focus on malignant cells only
damage normal cells as well
incidence of recurrence

105
Q

what are congenital abnormalities ?

A

any defects present at birth due too developmental errors during gestation

106
Q

when are you most vulnerable for congenital abnormalities ?

A

most vulnerable during organogenesis ( 15- 60 days post conception)
critical period different for each organ

107
Q

what are teratogens?

A

environmental or maternal facts causing birth defects

108
Q

examples of teratogens?

A

Thalidomide– limb reduction defects- 15 - 20 days post conception

alcohol- Fetal alcohol syndrome

malnutrition, cigarette smoke, infections—> rubella virus–> german measles

109
Q

what are the types of genetic abnormalities?

A

monogenic

mitochondrial gene

complex trait

chromosomal

110
Q

What is monogenic genetic abnormality

A

single gene defect

111
Q

What are the types of manginess genetic abnormalities?

A

1a- autosomal dominant –> 50 percent chance of inheriting

1b. autosomal recessive—> 25 percent affected, 50 percent carrier, 25 percent unaffected
1c. X linked recessive

112
Q

what chance do you have of inheriting an autosomal dominant genetic abnormality?

A

5o percent chance

113
Q

What chance do you have of inheriting an autosomal recessive genetic abnormality?

A

25 % affected
50 % carrier
25 % unaffected

114
Q

what are complex trait genetic abnormalities?

A

polygenic, genes and environment component

115
Q

what are types of chromosomal genetic abnormalities ?

A

numerical abnormalities

structural defects

116
Q

explain numerical abnormalities

A

extra or missing chromosome ( aneuploidy )

or

extra chromosome in a pair ( monosomy)
—> named by chromosome ( down syndrome, trisomy 21)

117
Q

explain structural defects of genetic abnormalities

A

inversion
translocation
deletion

118
Q

Fluid is…?

A

water and electrolytes

119
Q

dehydration ( volume deficit ) is

A

decrease of interstitial and intravascular fluids

120
Q

dehydration caused by

A

inadeq intake of fluids
loss due to 3rd spacing
increase skin, renal or gi loss

121
Q

edema is

A

increase in fluid volume from vascular space

122
Q

edema causes

A

increase of capillary hydrostatic pressure
decrease in colloid op ( pull pressure)
increase cap permeability
obstructed lymph flow

123
Q

what is 3rd spacing?

A

when fluid accumulates in trans cellular space such as body cavities, pleural spaces –> not easily exchangeable

124
Q

why is acid base unbalance so critical?

A

because it can denature proteins, and some proteins are enzymes, hemoglobin, antibodies
proteins are dependent on narrow ph ranges

125
Q

arterial blood gases important because?

A 
alkalosis= increase base
acidosis= increase of acid
126
Q

4 types of acid base imbalances ?

A

Respiratory acidosis
metabolic acidosis

respiratory alkalosis
metabolic acidosis

127
Q

what is the carbonic acid- bicarbonate buffer

A

C02+ H20 H2CO3 H(+) + HCO3-

carbon dioxide + water carbonic acid hydrogen Ion + bicarbonate ion

128
Q

Respiratory imbalance, what is it?

A

CO2 elimination problems

impaired ventilation–> increase of carbon dioxide pressure—> decrease in ph ( resp acidosis)

excess elimination of carbon dioxide —> decrease of carbon dioxide pressure—> increase in ph ( resp alkalosis )

129
Q

Metabolic imbalance, what is it?

A

increase or decrease in acid or base

increase acid/decrease base= Metb acidosis

increase base/ decrease acid= metb alkalosis

130
Q

Compensation for acid base imbalances ?

A

Kidney and lung compensate for each other—> normalizes ph

131
Q

treatment for acid base imbalances

A

oral and IV sol to normalize PH

treatment of underlying cause

Patho (2 decks)

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