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PathoPharm > 1.3 Immunity, Inflammation, Infection > Flashcards

1.3 Immunity, Inflammation, Infection Flashcards

1
Q

transfer of antibodies from a mother to her infant and breast feeding.

A

natural acquired passive immunity

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2
Q

when a person is naturally exposed to antigens, becomes ill, and recovers. The body creates it’s own antibodies.

A

naturally acquired active immunity

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3
Q

Vaccinations, your body makes the antibodies after vaccinations.

A

artificially acquired active immunity

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4
Q

first type of antibody to respond to acute infection “first you got to get it from your mother!”

A

IgM

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5
Q

As we get over the infection and our bodies remember; they are much smaller.

A

IgG

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6
Q

Found in secretions and on mucous membranes, also in breastmilk!

A

IgA

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7
Q

Describe the manifestations of acute inflammation, including diagnostic testing

A 
Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolar (pain)
Functio laesa (loss of function)
Malaise
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8
Q

____ is an autmatic response to cell injury that neutralizes harmful agents and removes dead tissue

A

inflammation

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9
Q

relatively short duration; non specific early response to injury. aimed primarily at removing the injurious agent and limiting tissue damage

A

acute inflammation

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10
Q

longer duration lasting for days to years.

A

chronic inflammation

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11
Q

2 types of inflammatory mediators

A 
plasma derived (liver)
Cell-derived (WBCs, Platelets, Endothelial cells)
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12
Q

3 concepts for plasma proteins

A

coagulation factors (clot formation)

Complement system (complement cascade)

Kinins (bradykinin, kallidin)

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13
Q

increases vascular permeability that causes contractions of smooth muscle and dilation of blood vessels

A

bradykinin

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14
Q

a part of the immune system that enhances or complements the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promotes inflammation, and attack the pathogenic cell membrane

A

complement system

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15
Q

regulated acid production in GI tract

A

Histamine

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16
Q

dilates arterioles by stimulating release of nitric oxide

A

histamine

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17
Q

increases permeability of capillaries to allow WBCs and proteins so they can enter tissues

A

Histamines

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18
Q

trigger smooth muscle contractions in the bronchioles

A

leukotrines

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19
Q

increase permeability of venules

A

leukotrines

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20
Q

formed by the oxygenation of arachidonic acid by cyclooxygenases 1 and 2 (COX-1 & COX-2)

A

prostaglandins

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21
Q

induce vasodilation

A

prostaglandins

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22
Q

inhibit platelet aggregation

A

prostaglandins

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23
Q

induce fever by activating thermoregulatory center in hypothalamus

A

prostaglandins

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24
Q

can cause bronchoconstriction

A

prostaglandins

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25
Q

what is the opposite of prostaglandins?

A

Thromboxane A2

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26
Q

induces vasoconstriction

A

thromboxane A2

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27
Q

facilitates platelet aggregation

A

Thromboxane A2

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28
Q

is a potent eosinophil chemoattractant that moves eosinophils to the site of injury

A

platelet activating factor (PAF)

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29
Q

a very important mediator that induces fever, hypotension, tachycardia, release of neutrophils

A

cytokines

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30
Q

_____ storm can be lethal

A

cytokines

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31
Q

3 local response vascular changes that may occur with inflammation:

A

immediate transient response

immediate sustained response

delayed hemodynamic response

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32
Q

this local response occurs with minor injury

A

immediate transient response

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33
Q

this local response occurs with more serious injury and continues for several days and damages the vessels in the area

A

immediate sustained repsonse

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34
Q

this local response increased in capillary permeability that occurs 4 - 24 hours after injury

A

delayed hemodynamic response

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35
Q

in what stage do prostaglandins and leukotrienes affect blood vessels?

A

vascular stage

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36
Q

in what stage are arterioles and venules dilated causing cells to adhere to and migrate through endothelium?

A

vascular stage

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37
Q

redness and warmth and dilation are a result of which stage?

A

vascular stage

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38
Q

in what stage are capillaries more permeable and allows work to damaged tissue? this allow allows exudate to escape from the tissues. swelling and pain is a result.

A

vascular state

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39
Q

watery fluid that is low in protein content and results of plasma entering inflammed site

A

serous exudate

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40
Q

occurs when there is severe tissue injury that causes damage to blood vessels or a significant leakage of RBCs from the capillaries

A

sanguineous exudate

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41
Q

we see liquidy exudate as well as blood in the clear fluid

A

serasanguineous exudate

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42
Q

fibrinous exudate

A

contains fibrinogen that makes a sticky meshwork in the fibers of a blood clot

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43
Q

necrotic cells get into the membrane of the tissues

A

membranous exudate

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44
Q

exudate that contains pus. pus is also known as degraded WBCs and tissue debris.

A

Prulent (suppurative)

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45
Q

White blood cells that are involved in inflammation

A

ganulocytes & monocytes

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46
Q

examples of granulocytes

A

neutrophils
eosinophils
basophils
mast cells

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47
Q

monocytes are converted to ____ so that they can devour pathogens or damaged cells

A

monocytes

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48
Q

____ enter the injured area, express adhesive proteins, and attach to the blood vessel lining

A

leukocytes

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49
Q

what inflammatory mediators do leukocytes release at the injury area?

A 
histamine
serotonin
PAF
Cytokines
Nitric oxide
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50
Q

which leukocytes participate in the acute inflammatory response?

A

eosinophils
monocytes
neutrophils

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51
Q

what plays a role in the acute phase of the immune response?

A

granulocytes and monocytes

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52
Q

in what stage do inflammatory mediators cause WBC production causing WBC count to rise?

A

cellular stage

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53
Q

two types of leukocytes participate in the acute inflammatory response:

A

granulocytes (neutrophils, eosinophils, and basophils)

Monocytes (the largest of the WBCs)

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54
Q

in what stage does fever, lethargy, and skeletal muscle breakdown occur?

A

systemic acute-phase response

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55
Q

in what stage does the liver make fibrinogen and C-reactive protein (CRP)? this facilitates in clotting, binding to pathogens, and moderate inflammatory responses

A

systemic acute-phase response

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56
Q

_____ is where macrophages accumlate in the damaged area and keep releasing inflammatory mediators?

A

chronic inflammation

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57
Q

this type of inflammation is where fibroblasts proliferate and scar tissue forms

A

nonspecific chronic inflammation

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58
Q

this type of inflammation is where macrophages mass together around foreign bodies and connective tissue surrounds and isolates the mass

A

granulomatous inflammation

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59
Q

What 3 drugs are anti-inflammatory agents?

A

Salicylates

NSAIDs

Acetaminophen (paracetamol)

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60
Q

this drug blocks the inflammatory response, has fever blocking properties, and analgesic properties

A

salicylates

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61
Q

this drug inhibits the synthesis of prostaglandins

A

salicylate

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62
Q

this drug is prohibited to children under 19 who have had a viral infection

A

salicylates

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63
Q

this drug can cause Reye syndrome: liver failure, brain damage

A

Salicylate

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64
Q

this drug to drug interaction needs to be noted because it interferes with absorption

A

salicylate

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65
Q

symptoms of salicylism

A 
dizziness
tinnitus
difficulty hearing
nausea
vomiting
diarrhea
confusion
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66
Q

what is tinnitus?

A

ringing in the ears

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67
Q

symptoms of acute salicylate toxicity

A

hyperpnea, tachypnea, hemorrhage, excitement, confusion, pulmonary edema, seizures, tetany, metabolic acidosis, fever, coma

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68
Q

what is the prototype of salicylate?

A

aspirin

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69
Q

non-selective NSAIDs inhibit what?

A

COX-1 and COX-2

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70
Q

this drug inhibits synthesis of prostaglandins

A

NSAID

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71
Q

GI bleeding is a contradiction of what drug?

A

NSAID

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72
Q

this drug-to-drug interaction of decreased diuretic effect, decreased beta-blockers, and lithium toxicity of which drug?

A

NSAID

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73
Q

what is the prototype of NSAIDs

A

Ibuprofen

74
Q

this drug selectively inhibits COX-2

A

COX-2 inhibitors

75
Q

what is the prototype for COX-2 inhibitors?

A

Celecoxib

76
Q

what drug-to-drug interaction must be noted with COX-2 inhibitors?

A

sulfonamides (SULFA ALLGERGY!)

77
Q

this drug causes severe renal or hepatic dysfunction, late pregnancy

A

Celecoxib

78
Q

this drug can lead to stevens-johnson syndrome which is a skin rash that can be lethal

A

Celecoxib

79
Q

as a pyretic, this drug acts directly on thermoregulatory cells of hypothalamus. it causes vasodilation and diaphoresis both which lower body temp

A

acetaminophen

80
Q

what is the prototype of acetaminophenl?

A

paracetamol aka tylenol

81
Q

this drug is associated with significant risk of liver damage especially in overdose

A

acetaminophen

82
Q

this drug is often used in combination with opioid analgesics

A

acetaminophen

83
Q

this steroid hormone is produced in the adrenal cortex

A

corticosteroids

84
Q

this drug is a contrast with non-steroidal anti-inflammatory drugs (NSAIDS)

A

corticosteroids

85
Q

this drug is a short term treatment of many inflammatory disorders

A

glucocorticoids

86
Q

this drug gives the body a chance to heal from the effects of inflammation

A

glucocoroticoids

87
Q

what is a serious adverse reaction of glucocorticoids?

A

Hyperglycemia. this effects the glucose levels so be careful with diabetic patients.

88
Q

this drug can cause adrenal insufficiency which is the suppression of the adrenals. prolong use can cause adrenal glands to atrophy.

A

glucocorticoids

89
Q

what is the prototype of glucocorticoids?

A

prednisone

90
Q

tissues that contain the functioning cells of an organ or body part

A

parenchymal

91
Q

what is the support tissue of parenchymal tissue?

A

stromal tissues

92
Q

what are 3 types of body cells

A

Labile
Stable
Permanent cells

93
Q

continue to divide and replicate throughout life, replacing cells that are continually being destroyex

A

labile

94
Q

this type of body cell stops dividing when growth ceases

A

stable

95
Q

this body cell cannot undergo mitotic division

A

permanent cells

96
Q

this body cell cannot undergo mitotic division

A

permanent cells

97
Q

how can wounds heal?

A

Primary healing and secondary healing

98
Q

this is when tissue create small, clean wounds and have no tissue loss

A

primary healing

99
Q

this is when tissue has great loss that needs to be replaced and tissue contamination. Example: burn

A

secondary healing

100
Q

what are the 3 stages of wound healing?

A

inflammatory phase

proliferative phase

maturational or remodeling phase

101
Q

in this phase of wound healing, blood clot and phagocytes occur to stop the bleeding and destroy pathogens

A

inflammatory phase

102
Q

what will promote wound healing?

A

increased blood flow and oxygen delivery

103
Q

what is the main objective of the inflammatory response?

A

increased blood flow and oxygen delivery

104
Q

this is the body’s physiologic response to injury

A

inflammation

105
Q

this is the body’s physiologic response that provides defense and protection against foreign substances that lead to disease?

A

immunity

106
Q

this is the invasion of multiplication of microorganisms in body tissues

A

infection

107
Q

Granulocytes are _____

A

phagocytes

108
Q

____ are by far the most prevalent of the granulocytes

A

neutrophils

109
Q

_____ are granulocytes that are involved in the allergic reactions and can attack parasites such as worms

A

eosinophils

110
Q

____ are granulocytes that are also involved in allergic reactions and are able to release histamine, which helps trigger inflammation, and heparin, which prevents blood from clotting

A

Basophils

111
Q

this monocyte is a the bridge from innate to adaptive systems

A

dendritic cells

112
Q

excessive or inappropriate activation of the immune response to harmless non-self antigens

A

hypersensitivity

113
Q

this occurs when the body is damaged by the immune system, rather than by the antigen (often called allergen)

A

hypersensitivity

114
Q

what are the 4 types of hypersensitivity reactions?

A

Type 1: IgE-mediated
Type 2: antibody-mediated
Type 3: complement-mediated
Type 4: cell-mediated

115
Q

this type of hypersensitivity is commonly called “allergic reactions”

A

Type 1 hypersensitivity

116
Q

this type of hypersensitivity causes systemic or anaphylactic reactions

A

Type 1 hypersensitivity

117
Q

These are examples of what type of hypersensitivity: rhinitis, food allergies, bronchial asthma, hives, and atopic dermatitis

A

Type 1 hypersensitivity

118
Q

systemic response to the inflammatory mediators released in type 1 hypersensitivity

A

anaphylaxus

119
Q

histamine, acetylcholine, kinin, leukotrienes, and prostaglandins all cause what?

A

vasodilation

120
Q

what will happen if arterioles vasodilate throughout the body?

A

BP drops. No blood flow in the body.

121
Q

acetylcholine, kinin, leukotrienes, and prostaglandins all cause what?

A

bronchoconstriction

122
Q

what will happen when bronchioles constrict?

A

Decrease the ability to inhale and exhale. No oxygen flow in the body.

123
Q

_____ has a very strong genetic predisposition. These people have frequent hypersensitivity to multiple allergens.

A

atopy or atopic reactions

124
Q

this type of hypersensitivity is cytotoxic. meaning the certain immune cell is doing the damage.

A

Type 2 hypersensitivity

125
Q

in this type of hypersensitivity, IgG or IgM attack antigens on cell surfaces.

A

Type 2 hypersensitivity

126
Q

this type of hypersensitivity reaction is evident in blood transfusion and Rh disease

A

Type 2 hypersensitivity

127
Q

in this type of hypersensitivity reaction, antibodies bind to receptors and cause dysfunction. i.e Graves disease; myasthenia

A

Type 2 hypersensitivity

128
Q

in this type of hypersensitivity, an inflammatory response leads to tissue damage.

A

type 2 hypersensitivity

129
Q

this type of hypersensitivity reaction occurs when free-floating antigen + antibody = circulating immune complex

A

type 3 hypersensitivity

130
Q 
this type of hypersensitivity causes:
autoimmune vascultiis 
glomerulonephritis 
serum sickness 
arthus reaction
A

type 3 hypersensitivity

131
Q

in this type of hypersensitivity reaction, immune complexes deposit on walls of blood vessels and activate complement. usually complement is a good thing but in this case, over reaction is causing damage to the blood vessels. example: Vasculitis

A

Type 3 hypersensitivity

132
Q

in this type of hypersensitivity reaction, it is cell-mediated and sensitized T cells are attacking antigen

A

Type 4 hypersensitivity

133
Q

in this type of hypersensitivity reaction, is cell mediated and DELAYED compared to the others.

A

Type 4 hypersensitivity

134
Q

in this type of hypersensitivity reaction, it destroys all cells with a virus even if it’s not damaging a cell.

A

type 4 hypersensitivity

135
Q

in this type of hypersensitivity reaction, we see a delayed-type hypersensitive in TB test, allergic dermatitis test, and hypersensitivity pneumonitis.

A

Type 4 hypersensitivity

136
Q

what type of hypersensitivity reaction would be involved in latex allergy?

A

Type 1 or Type 4.
Type 1 causes anaphylaxis
Type 4 causes allergic dermatitis, skin reaction.

137
Q

this is when the immune system attacks self-antigens

A

autoimmune disorder

138
Q

Normally, self-reactive immune cells are killed in the lymphoid organs or suppressed by regulatory T cells. In ____, this self tolerance breaks down. Instead the immune system will destroy its own body tissues.

A

Autoimmunity

139
Q

When testing for autoimmune diseases, _____ will appear in the blood.

A

antitissue antibodies. i.e antithyroid antibodies

140
Q

A chronic inflammatory diseases characterized by formation of autoantibodies and immune complexes (type 3 hypersensitivity)

A

Systemic Lupus Erythematosus

141
Q

In what autoimmune disorder do we see an increased production of autoantibodies, particularly antinuclear antibodies which attack the nucleic acid that make the DNA in the cells. Ultimately damages DNA.

A

Lupus

142
Q

T/F: patients who suffer from autoimmune disease have hypoactive immune systems

A

false, in autoimmune diseases, the immune system is HYPERactive. It is attacking self-antigens and destroys its own body tissues.

143
Q

This is when there is an inadequate immune response due to impaired function of insufficient production of immune factors.

A

Immunodeficiency

144
Q

in ______ genetic mutation that causes decreased production (poorly functioning) components of the immune response (B cells, T cells, immunoglobins, complements, etc)

A

Primary (heritable) Immunodeficiency

145
Q

in ______ this is caused by another disease.

Aids, cancers (bone marrow and blood cells), medications (immunosupression), and environmental toxins

A

Secondary (acquired) immunodeficiency

146
Q

A person who has an immunodeficiency of any kinds is said to be ______. They are vulnerable to opportunistic infections.

A

Immunocompromised

147
Q

This is referred to when bacteria are not causing harm and may be beneficial

A

Colonization

148
Q

This is referred to when bacteria are harmful and causing disease

A

infection

149
Q

Microorganisms that are normally living in or on the body. Some are useful, many have no effect. These are opportunistic pathogens that are capable of causing disease if health and immunity are weakened.

A

Microflora

150
Q

This is a type of infectious agent that is small modified infectious host proteins. They are abnormally shaped versions of our own proteins. The cause normal proteins to shape like them.

A

Prion

151
Q

This is a type of infectious agent has a protein coat surrounding a nucleic acid core. It has no metabolic enzymes of their own. They insert their genome into host cell’s DNA. They use cell’s metabolic machinery to make new versions of itself.

A

viruses

152
Q

This is a type of infectious agent are cells without membrane-bound organelles (prokaryotes). They can live independently and use infected organism for food and shelter.

A

Bacteria

153
Q

This is a type of infectious agent can produce toxins.

A

Bacteria

154
Q

This is a type of infectious agent most require a cooler temperature than human core body temperature. So most infections are on the surface of the body.

A

Fungi

155
Q

This is a type of infectious agent includes protozoa, malaria, dysentery, roundworms, tapeworms, ticks, mosquitoes, mites, lice, fleas.

A

Parasites

156
Q

____ means bacterial toxins in the blood

A

sepsis or septicemia

157
Q

What are the common adverse effects of antibiotics?

A

GI upset & Superinfection.

158
Q

What are the 2 most common superinfections?

A

Clostridium difficile & Candidiasis (yeast)

159
Q

These antibiotics are grouped together in the class called Beta Lactam antibiotics.

A

Penicillin (including carbapenems) and cephalosporins

160
Q

Inflammatory bowel diseases occurs where?

A

primarily in the colon, small intestine, and the rectum

161
Q

2 examples we discuss for IBD

A

Crohn disease

Ulcerative colitis

162
Q

IBD with granulomatous lesions

A

Crohn disease

163
Q

IBD that is primarily submucosal

A

Crohn disease

164
Q

IBD that skips lesions

A

Crohns disease

165
Q

IBD that occurs primarily in ileum, secondarily colon

A

Crohn disease

166
Q

IBD with rare rectal bleeding

A

Crohn disease

167
Q

IBD where fistulas, strictures, perianal accesses are common

A

Crohn disease

168
Q

IBD where development of cancer is uncommon

A

Crohn disease

169
Q

IBD where ulcerative, exudative lesions

A

Ulcerative colitis

170
Q

IBD that is primarily mucosal

A

Ulcerative colitis

171
Q

IBD with continuous lesions

A

Ulcerative colitis

172
Q

IBD primarily in rectum and left colon

A

Ulcerative colitis

173
Q

IBD where rectal bleeding is common

A

Ulcerative colitis

174
Q

IBD where fistulas, strictures, perianal abscesses are rare

A

Ulcerative colitis

175
Q

IBD where development of cancer is relatively common

A

Ulcerative colitis

176
Q

IBD with “cobblestone” appearance

A

Crohn disease

177
Q

Stage of Crohn disease: People with mild to moderate Crohn disease are able to eat food normally without dehydration, fevers, stomach pain, blockages in their intestine, or losing more than 10% of body weight

A

Mild to moderate stage

178
Q

Stage of Crohn disease: If patient does not respond to treatment if they have high fevers, significant weight loss, stomach pain, or tenderness, occasional nausea or vomiting, or significant anemia

A

Moderate to severe stage

179
Q

Stage of Crohn disease: have symptoms despite taking steroids, or have high fevers, persistent vomiting, blockages in their intestine, or an abcess

A

Severe stage

180
Q

treatment of crohn disease

A

corticosteroids

antibiotics

181
Q

cells in adaptive immunity

A

B & T cells

PathoPharm (18 decks)

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