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Unit 8 > Path > Flashcards

Path Flashcards

0
Q

Infections that cause pseudo membranous inflammation

A

Diphtheria, clostridium difficile

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1
Q

Most common cause if a skin abscess

A

s aureus

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2
Q

What causes serous inflammation

A

Blister in second degree burns, viral pleuritis

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3
Q

What do lipoxins do

A

Inhibit transmigration/chemotaxis, enhance apoptosis, anti inflammatory mediators

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4
Q

What do resolvins do

A

Inhibit recruitment of inflammatory cells

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5
Q

Most common cause of chronic inflammation

A

Infection (tb, leprosy, hep c)

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7
Q

Most common cause of impaired wound healing

A

Infection

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8
Q

ST segment depression on ECG indicates:

A

subendocardial ischemia

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9
Q

(reversible/irreversible) change to cell: Na/K ATPase pump impaired

A

reversible

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10
Q

(reversible/irreversible) change to cell: CaATPase pump impaired

A

irreversible–cannot pump Ca2+ out of cytosol

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11
Q

increased cytosolic __ (ion): (a) Activation of phospholipase increases cell and organelle membrane permeability. (b) Activation of proteases damages the cytoskeleton.

(c) Activation of endonucleases causes fading of nuclear chromatin (karyolysis).
(d) Activation of ATPase leads to ↓ATP.
(e) activates caspases causing apoptosis of the cell.

A

Ca2+

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12
Q

NADPH oxidase is found in ____ cell membranes (type of cell)

A

phagocyte–neutrophils and monocytes

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13
Q

Consequences of free radical injury include cirrhosis and exocrine/endocrine dysfunction of the
_____ (organ).

A

pancreas

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14
Q

Salicylates, alcohol damage mitochondria; produce megamitochondria in ______ (cell type)

A

hepatocytes

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15
Q

(decreased/increased) drug detoxification causes lower than expected therapeutic drug levels.

A

increased detox > lower therapy

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16
Q

Induction of enzyme synthesis in the cytochrome P450 system produces _______ (organelle) hyperplasia

A

SER

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17
Q

name disease: defect in posttranslational modification lysosomal enzymes; deficient phosphotransferase

A

Inclusion (I)-cell disease

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18
Q

name disease: giant lysosomal granules (fusion defect); defect in formation of phagolysosomes

A

Chediak-Higashi

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19
Q

(dystrophic/metastatic) calcification: serum calcium and serum phosphate are normal

A

dystrophic

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20
Q

(dystrophic/metastatic) calcification: serum calcium is increased and/or phosphate

A

metastatic

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21
Q

(hypertrophy/hyperplasia) depends on the regenerative capacity of different cell types

A

hyperplasia

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22
Q

Barrett esophagus: ____ to ____ epithelium due to acid reflux in distal esophagus

A

squamous > glandular

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23
Q

bronchus in smoker, endocervix: _____ to _____ epithelium

A

glandular > squamous

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24
Q

(pale/hemorrhagic) infarctions: loose tissue, lung, bowel, testicle

A

hemorrhagic

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25
Q

(pale/hemorrhagic) infarctions: dense tissue, heart, kidney, spleen

A

pale

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26
Q

name disease: _______ of the toes in individuals with diabetes mellitus is a form of infarction that results from ischemia. Coagulation necrosis is the primary type of necrosis that is present in the dead tissue

A

dry gangrene

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27
Q

______necrosis: lysosomal enzyme destruction tissue by neutrophils

A

Liquefactive

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28
Q

cerebral infarction: (liquefactive/coagulative) necrosis

A

liquefactive

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29
Q

wet gangrene: (liquefactive/coagulative) necrosis

A

liquefactive

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30
Q

enzymatic fat necrosis leads to:

A

acute pancreatitis

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31
Q

______: calcium combined with fatty acids; dystrophic calcification

A

Saponification

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32
Q

(intrinsic/extrinsic) pathway of apoptosis requires TNF-a

A

extrinsic

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33
Q

main source of TNF-a

A

macrophages

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34
Q

_____: proinflammatory cell death using caspase-1

A

Pyroptosis

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35
Q

Microbial pathogens that may be killed by ______ include Salmonella typhimurium, Shigella flexneri, Legionella pneumophila

A

pyroptosis

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36
Q

(histamine/PGE2 and bradykinin) mediated: rubor, calor, tumor

A

histamine

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37
Q

(histamine/PGE2 and bradykinin) mediated: dolor

A

bradykinin and PGE2

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38
Q

the primary leukocytes in acute inflammation

A

neutrophils

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39
Q

(selectins/B-integrins): activated by IL-1 and TNF

A

selectins

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40
Q

(selectins/B-integrins): firm adhesion of neutrophils, activated by C5a and LTB4

A

B-integrins

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41
Q

Catecholamines and corticosteroids (stimulate/inhibit) activation of these neutrophil adhesion
molecules.

A

inhibit

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42
Q 
Inhibition of neutrophil β2-integrins, leads to an increase in the peripheral blood
neutrophil count (called \_\_\_\_\_\_)
A

neutrophilic leukocytosis

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43
Q

(neutrophilic leukocytosis/neutropenia): enhanced activation of neutrophil β2-integrins causes the total circulating neutrophil count to decrease

A

neutropenia

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44
Q

_____ (process) mediators: C5a, LTB4, bacterial products, IL-8

A

chemotaxis

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45
Q

opsonins __ and __: enhance neutrophil ability to ingest bacteria and recognize/attach

A

IgG and C3b

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46
Q

MPO=

A

myeloperoxidase system–oxygen dependent neutrophil killing of bacteria/fungi

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47
Q

(SOD/Fenton rxn) converts superoxide free radicals to H2O2

A

SOD

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48
Q

(SOD/Fenton rxn) converts peroxide to hydroxyl free radicals by iron

A

Fenton

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49
Q

end product of oxygen dependent MPO system:

A

bleach

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50
Q

____ (enzyme) deficiency: lack of NADPH interferes with normal function of the O2-dependent MPO system

A

G6PD–glucose 6 phosphate DHase

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51
Q

(chronic granulomatous dz/myeloperoxidase def): XLR

A

CGD

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52
Q

(chronic granulomatous dz/myeloperoxidase def): AR

A

MD

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53
Q

(chronic granulomatous dz/myeloperoxidase def): NADPH oxidase is absent

A

CGD

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54
Q

(chronic granulomatous dz/myeloperoxidase def): myeloperoxidase is absent

A

MD

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55
Q

(chronic granulomatous dz/myeloperoxidase def): respiratory burst is absent

A

CGD

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56
Q

(chronic granulomatous dz/myeloperoxidase def): peroxide is absent

A

CGD

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57
Q

(chronic granulomatous dz/myeloperoxidase def): bleach is absent

A

both

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58
Q

(IL-1 and TNF/IL-6): Initiate PGE2 synthesis in the anterior hypothalamus, leading to production of fever
Activate endothelial cell adhesion molecules

A

IL-1 and TNF

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59
Q

(IL-1 and TNF/IL-6): Primary cytokines responsible for increased liver synthesis of acute phase reactants (APRs), such as ferritin, coagulation factors (e.g., fibrinogen), and C-reactive protein

A

IL-6

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60
Q

(IL-8/IL-6): chemotaxis

A

IL-8

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61
Q

(histamine/NO): vasodilation, bactericidal

A

NO

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62
Q

(histamine/NO): vasodilation, increased vascular permeability

A

histamine

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63
Q

(complement/chemokines): synthesized in liver

A

complement

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64
Q

(complement/chemokines): produced by leukocytes, endothelial cells

A

chemokines

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65
Q

(chemokines/bradykinin): product of kinin system activation by activated factor XII

A

bradykinin

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66
Q

source of leukotrines (cell type)

A

leukocytes–converted from arachidonic acid by lipoxygenase-mediated hydroxylation

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67
Q

(prostaglandin/thromboxane A2): platelet aggregation

A

thromboxane A2

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68
Q

(prostaglandin/thromboxane A2): inhibits platelet aggregation

A

prostaglandin I2

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69
Q

histamine, NO, PGI2 participate in vaso (dilation/constriction)

A

vasodilation

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70
Q

thromboxane A2 participates in vaso (dilation/constriction)

A

constriction

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71
Q

histamine, bradykinin, LTC4, LTD4, LTE4, C3a, C5a participate in (producing pain/increasing venular permeability)

A

increasing venular permeability

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72
Q

PGE2, bradykinin participate in (producing pain/increasing venular permeability)

A

producing pain

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73
Q

PGE2, IL-1, TNF participate in (chemotaxis/producing fever)

A

producing fever

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74
Q

C5a, LTB4, IL-8 participate in (chemotaxis/producing fever)

A

chemotaxis

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75
Q

IL-_ stimulates acute phase reactant synthesis by liver

A

IL-6

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76
Q

two examples of noninfectious granulomatous inflammation

A

sarcoidosis, Crohn dz

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77
Q

two examples of granulomatous infections

A

TB, systemic fungi (histoplasmosis)

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78
Q

serum protein electrophoresis in acute inflammation: albumin (increases/decreases), no alteration in gamma-globulin peak

A

decreases

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79
Q

(increase/decrease) in gamma-globulin in chronic inflammation is due to the marked (increase/decrease) of synthesis of IgG in chronic inflam

A

increase, increase

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80
Q

stack of coins appearance

A

Rouleau RBCs stack

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81
Q

RBC rouleau: (increase/decrease) of fibrinogen/immunoglobulins, erythrocyte sed rate

A

increase all

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82
Q

C reactive protein is a marker of:

A

necrosis and disease activity

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83
Q

(IgM/IgG) predominant immunoglobulin in acute inflam

A

IgM

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84
Q

(IgM/IgG) predominant immunoglobulin in chronic inflam

A

IgG–increased serum IgG is key finding in chronic inflam

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85
Q

lung injury primary repair cell

A

type II pneumocyte

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86
Q

brain injury repair cells

A

astrocytes and microglial cells

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87
Q

primary cell in peripheral nerve transsection repair

A

Schwann

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88
Q

repair process in cardiac muscle damage

A

fibrosis (permanent tissue)

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89
Q

repair cell in muscle post exercise

A

satellite

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90
Q

glucocorticoids (simulate/inhibit) scar formation

A

inhibit

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91
Q

p53 protein product: inhibits Cdk4 (cell arrested in __ phase)

A

G1

92
Q

most critical phase in cell cycle

A

G1 to S phase

93
Q

proteins that control G1 to S phase in cell cycle (two)

A

cyclin D, Cdk4

94
Q

(IL-1/TNF): Activates macrophages; stimulates release of acute phase reactants

A

TNF

95
Q

(IL-1/TNF): Stimulates synthesis of metalloproteinases (i.e., enzymes containing trace metals)
Stimulates synthesis and release of acute phase reactants from the liver

A

IL-1

96
Q

(IL-1/TNF-a) is important in the formation and maintenance of TB and systemic fungal granulomas.

A

TNF-a. recruits cells for granuloma formation

97
Q

Multinucleated giant cell nuclei are usually located at the (center/periphery) of the granuloma.

A

periphery

98
Q

Cell types in TB granuloma: Epithelioid cells (activated macrophages) and mononuclear cells consisting of
CD(4/8) T cells, specifically, TH cells of the TH(1/2) type (memory T cells)

A

CD4 helper T cells

TH1

99
Q

(acute/chronic) inflam: serum protein electrophoresis=mild hypoalbuminemia

A

acute

100
Q

(acute/chronic) inflam: serum protein electrophoresis=polyclonal gammopathy, greater degree of hypoalbuminemia

A

chronic

101
Q

(acute/chronic) inflam: neutrophilic leukocytosis

A

acute

102
Q

(acute/chronic) inflam: monocytosis

A

chronic

103
Q

(acute/chronic) inflam: scar tissue formation, amyloidosis

A

chronic

104
Q

(acute/chronic) inflam: complete resolution or abscess formation

A

acute (or progresses to chronic inflam)

105
Q

(acute/chronic) inflam: scar tissue present

A

chronic

106
Q

(acute/chronic) inflam: necrosis is prominent

A

acute

107
Q

(acute/chronic) inflam: histamine is key mediator, along with prostaglandins and leukotriene

A

acute

108
Q

(acute/chronic) inflam: monocytes/macrophages are key mediators, also B and T lymphocytes, plasma cells, fibroblasts

A

chronic

109
Q

(mast cells/eosinophils): receptors for IgE

A

eosinophils

110
Q

(TLR/NK cells/NFκβ/PAMPs): “master switch” to nucleus for induction of inflammation

A

NFkB

111
Q

(TLR/NK cells/NFκβ/DAMPs/PAMPs): heat shock protein, chromatin-associated HMGB1, purine metabolites (ATP, adenosine, uric acid)

A

DAMPs

112
Q

Inflammosomes activate caspase-1 → (increase/decreases) secretion IL-1β and IL-18 → attract immune cells to sites of infection

A

increases

113
Q

(hemosiderin/ferritin/transferrin/hepcidin) keeps iron away from bacteria

A

hepcidin

114
Q

IFN-(α and β/γ): activation of macrophages

A

gamma

115
Q

IFN-(α and β/γ): inhibition of viral growth

A

alpha and beta

116
Q

CD40 ligands, cytokines, and (CD4/CD8) T cells are involved in isotype switching

A

CD4 helper T cells

117
Q

on which chromosome is the HLA system

A

(Major Histocompatiblity Complex=HLA): chromosome 6

118
Q

Type (I/II/III/IV) hypersensitivity: IgE antibody mediated activation of mast cells or basophils followed by acute inflammatory rxn

A

I

119
Q

IL-(4/5) causes plasma cells to switch from IgM to IgE synthesis.

A

4

120
Q

IL-(4/5) stimulates the production and activation of eosinophils.

A

5

121
Q

Type I hypersensitivity: APCs release IL-4 which induces CD4 T cells to become CD4 TH(1/2) cells that produce IL-4 and IL-5

A

TH2

122
Q

Type (I/II/III/IV) hypersensitivity: rhinitis and conjunctivitis, asthma, dermatitis, vomiting, diarrhea, anaphylaxis, edema, hives

A

I

123
Q

Type (I/II/III/IV) hypersensitivity: atopic (allergens), drug hypersensitivity (penicillin), transfusion rxn in IgA immunodef

A

I

124
Q

Type (I/II/III/IV) hypersensitivity: complement dependent antibody reactions

A

II

125
Q

Type (I/II/III/IV) hypersensitivity: cell lysis mediated by IgM or IgG, phagocytosis, IgE dependent cell-mediated cytotoxicity, Graves, myasthenia Gravis

A

II

126
Q

Type (I/II/III/IV) hypersensitivity: Goodpasture, pernicious anemia, ABO hemolytic dz of the newborn

A

II

127
Q

Type (I/II/III/IV) hypersensitivity: SLE, Arthus rxn (farmer’s lung), serum sickness

A

III

128
Q

Type (I/II/III/IV) hypersensitivity: Poststreptococcal glomerulonephritis,

A

III

129
Q

Type (I/II/III/IV) hypersensitivity: CD4 Helper T cell mediate granuloma formation

A

IV

130
Q

Type (I/II/III/IV) hypersensitivity: CD8 cytotoxic destruction of virus infected, neoplastic, or donor graft cells

A

IV

131
Q

Type (I/II/III/IV) hypersensitivity: initiated by the introduction of an allergen, which stimulates CD4 TH2 reactions and immunoglobulin E (IgE) production. IgE binds to Fc receptors on mast cells

A

I

132
Q

Type (I/II/III/IV) hypersensitivity: late phase mediators= prostaglandins, leukotrienes, platelet activating factor

A

I

133
Q

Type (I/II/III/IV) hypersensitivity: antibody directed against antigens on cell membrane or in ECM

A

II

134
Q

Type II hypersensitivity: (IgM/IgG) cell lysis–cold IHA, ABO mismatch

A

IgM

135
Q

Type II hypersensitivity: (IgM/IgG) cell lysis–Goodpasture, acute rheumatic fever

A

IgG

136
Q

Type (I/II/III/IV) hypersensitivity: circulating antigen-antibody complexes that damage tissue

A

III

137
Q

____ rxn in Type III hypersensitivity: formation of immunocomplexes at a localized site. Ex: farmer’s lung

A

Arthus rxn

138
Q

Type (I/II/III/IV) hypersensitivity: T cell-mediated immunity, often delayed

A

IV (DTH-delayed type hypersensitivity)

139
Q

Type (I/II/III/IV) hypersensitivity: controls TB infection, graft rejection, tumor surveillance

A

IV

140
Q

Type (I/II/III/IV) hypersensitivity: allergic contact dermatitis–poison ivy, topical drugs, rubber, chemicals

A

IV

141
Q

(cornea/kidney/bone marrow) transplant: best allograft survival rate

A

cornea

142
Q

(cornea/kidney/bone marrow) transplant: danger of transmitting Creutzfeldt-J-Dz

A

cornea

143
Q

(cornea/kidney/bone marrow) transplant: better survival if donor is living than cadaver

A

kidney

144
Q

(cornea/kidney/bone marrow) transplant: danger of graft-vs-host rxn and CMV infection

A

bone marrow

145
Q

most important requirement for successful transplantation

A

ABO blood grp compatibility

146
Q

hyperacute transplant rejection: Type II hypersensitivity, (reversible/irreversible)

A

irreversible

147
Q

acute transplant rejection: type II/IV, (reversible/irreversible)

A

reversible

148
Q

key cell in donor graft: (CD4/CD8/dendritic)

A

dendritic

149
Q

most common infection in transplant recipients

A

CMV

150
Q

solid organ transplantation: (Candida/Aspergillus) most common infection

A

candida

151
Q

bone marrow transplantation: (Candida/Aspergillus) most common infection

A

aspergillus

152
Q

in ____ rxn, donor T cells attack host MHC antigens located in the skin, bile duct epithelium, and mucosa of the GI tract.

A

Graft-vs-Host

153
Q

approx 90% of all autoimmune dz occurs in (men/women)

A

women (hormones thought to play a role)

154
Q

rheumatic fever: produced by (S pyogenes/Chlamydia trachomatis)

A

S pyogenes

155
Q

Reiter syndrome: produced by (S pyogenes/Chlamydia trachomatis)

A

chlamydia t

156
Q

Bacterial triggers of _______: S. pyogenes,

C. trachomatis, M. pneumoniae, C. jejuni

A

autoimmune dz

157
Q

Viruses as triggers of _______: coxsackievirus, measles virus, CMV, EBV, HHV-6, influenza virus

A

autoimmune dz

158
Q

SLE affects (older women/women of childbearing age/children)

A

mostly women of childbearing age

159
Q

most common visceral organ involved in SLE

A

kidney

160
Q

how do you differentiate between drug induced lupus and SLE

A

antihistone antibodies, ↓incidence renal/CNS disease, symptoms disappear when drug removed

161
Q

best screen for SLE

A

ANA (high sensitivity, not great specificity)

162
Q

(screen/confirm) for SLE: anti- dsDNA/anti-Sm antibodies; high specificity

A

confirm

163
Q

(SLE/Systemic sclerosis): ↑CD4 TH2 cells; ↑DNA-topoisomerase, centromere antibodies

A

systemic sclerosis

164
Q

most common initial sign of systemic sclerosis

A

raynaud

165
Q

what does CREST stand for

A

calcinosis, Raynaud, esophageal dysmotility, sclerodactyly, telangiectasia

166
Q

(infectious/noninfectious) inflammatory myopathies: polymyositis, dermatomyositis

A

noninfectious

167
Q

(polymyositis/ dermatomyositis): muscle atrophy is a prominent feature

A

dermatomyositis

168
Q

use corticosteroids to treat (polymyositis/ dermatomyositis)

A

both

169
Q

renal dz is (common/uncommon) in mixed connective tissue disease)

A

uncommon

170
Q

HIV is cytotoxic to CD (4/8) cells

A

4

171
Q

where is complement synthesized

A

in liver

172
Q

Complement: (C3a and C5a/C3b/C5b-C9): stimulate mast cell release of histamine

A

C3a and C5a

173
Q

Complement: (C3a and C5a/C3b/C5b-C9): opsonization

A

C3b

174
Q

Complement: (C3a and C5a/C3b/C5b-C9): cell lysis

A

C5b-C9

175
Q

Complement: (C3a/C5a): activation of neutrophil adhesion molecules, neutrophil chemotaxis

A

C5a

176
Q

(classical/alternative) complement pathway: C1, C4, C2; activated by ICs; requires antibody for activation

A

classical

177
Q

(classical/alternative) complement pathway: factor B, properdin, factor D; activated by endotoxins

A

alternative

178
Q

____ (complement) pathway: important in destruction of bacteria, fungi, viruses, does not require antibodies for activation

A

Lectin

179
Q

most common complement def (C2/C6-C9)

A

C2

180
Q

(C2/C6-C9) complement def: Increased susceptibility to disseminated Neisseria gonorrhoeae or Neisseria meningitidis infections

A

C6-C9 def

181
Q

most common overall organ involved in amyloidosis

A

kidney

182
Q

most common cause of death in shock

A

multiple organ dysfunction syndrome

183
Q

_____ produces fibrin thrombi in the microvasculature of most organs, leading to
tissue damage.

A

DIC

184
Q

(transudate/exudate): protein poor and cell poor fluid

A

transudate

185
Q

(transudate/exudate): protein rich, cell rich fluid

A

exudate

186
Q

(transudate/exudate): pitting edema, body cavity effusions, alteration in Starling Forces (HP, OP)

A

transudate

187
Q

(transudate/exudate): no pitting edema

A

exudate

188
Q

(oncotic/hydrostatic) pressure: favors movement of fluid (transudate) out of capillaries/venules.

A

hydrostatic

189
Q

(oncotic/hydrostatic) pressure: equates with the serum albumin level and opposes filtration of fluid out of
capillaries/venules.

A

oncotic

190
Q

in normal circumstances, (oncotic/hydrostatic) pressure is higher

A

OP is greater than HP

191
Q

(increased hydrostatic/decreased oncotic): pulmonary edema in LHF, peripheral pitting edema in RHF, portal HTN

A

increased hydrostatic

192
Q

(increased hydrostatic/decreased oncotic) pressure: nephrotic syndrome, malnutrition, cirrhosis, malabsorption

A

decreased oncotic pressure

193
Q

ascites in cirrhosis: increase in (hydrostatic/oncotic) pressure, decrease in (hydrostatic/oncotic) pressure

A

increase HP, decrease OP (hypoalbuminemia)

194
Q

in lymphatic obstruction, T cell cytokines stimulate _____ (cell type) to synthesize hyaluronic acid

A

fibroblasts

195
Q

example of activated coagulation system in thrombosis

A

DIC: disseminated intravascular coagulation

196
Q

(heparin and warfarin/plasmin) breaking down the thrombus to restore blood flow

A

plasmin (fibrinolytic system)

197
Q

(heparin and warfarin/plasmin) preventing formation of venous thrombi, not dissolving thrombi but preventing further formation

A

heparin and warfarin

198
Q

most common (venous/arterial) thrombus: coronary artery thrombus overlying an atherosclerotic plaque

A

arterial

199
Q

(gas/fat/paradoxical/systemic) embolism: Most frequently due to venous emboli passing through an atrial septal defect (ASD) or a ventricular septal defect (VSD) into the systemic circulation.

A

paradoxical

200
Q

(gas/fat/paradoxical/systemic) embolism: majority originate in left side of heart

A

systemic

201
Q

(gas/fat/paradoxical/systemic) embolism: most often due to traumatic fracture of long bones (femur) or pelvis

A

fat

202
Q

fat embolism patients are symptomatic in (most/few) cases

A

few (10%)

203
Q

(gas/fat/paradoxical/systemic) embolism: hypoxemia, increased A-a gradient, thrombocytopenia

A

fat

204
Q

____ embolism: occurs during labor or immediately postpartum

A

amniotic fluid–maternal mortality is 80%

205
Q

in amniotic fluid embolism: (dyspnea/bleeding) is due to DIC

A

bleeding

206
Q

in amniotic fluid embolism: (dyspnea/bleeding) is due to ARDS

A

dyspnea. also due to ARDS

207
Q

decompression sickness is a form of (fat/gas/paradoxical/systemic) embolism

A

gas–scuba and deep sea diving

208
Q

____ embolism: ↑pressure on lower extremity veins → stasis → thrombosis → embolism; dyspnea, pleuritic chest pain

A

pulmonary

209
Q

caisson disease caused by persistence of gas emboli in bone: (acute/chronic)

A

chronic

210
Q

loss of more than __% of blood produces shock

A

20%

211
Q

in hypovolemic shock, there (is/is not) an initial drop in Hb and Hct concentration

A

is not because there is an equal loss of RBCs and plasma

212
Q

best indicator of tissue hypoxia: mixed (arterial/venous) oxygen content

A

decreased mixed venous oxygen content

213
Q

_____ shock: increased anion gap type of metabolic acidosis due to lactic acidosis

A

hypovolemic

214
Q

(septic/hypovolemic) shock: warm skin, strong peripheral pulses, hypotension, DIC

A

septic

215
Q

(septic/hypovolemic) shock: cold/clammy skin, hypotension, tachycardia, ↓urine output

A

hypovolemic

216
Q

most common cause of cardiogenic shock

A

acute MI

217
Q

(cardiogenic/septic) shock: ↑CO, ↓LVEDP, ↓PVR, ↑MVO2

A

septic (initial phase)

218
Q

(cardiogenic/septic) shock: ↓CO, ↑LVEDP, ↑PVR, ↓MVO2

A

cardiogenic

219
Q

most common site for infection leading to sepsis

A

lungs

220
Q

endotoxins (LPS) are released by gram (+/-) bacteria

A

negative

221
Q

endotoxins (LPS) activate macrophages, releasing IL-1 and TNF. (IL-1/TNF) produces fever

A

IL-1

222
Q

endotoxins (LPS) activate macrophages, releasing IL-1 and TNF. (IL-1/TNF) damages endothelial cells, causing them to release vasodilators

A

TNF

223
Q

endotoxins activate the (classical/alternative) complement pathway. Anaphylatoxins C3a and C5a are produced which stimulate mast cells to release histamine

A

alternative

224
Q

MCC sepsis due to gram- (+/-) organisms (coagulase-negative Staphylococci)

A

positive

225
Q

E coli: most common cause of gram-(+/-) septic shock

A

negative

226
Q

Endotoxins damage tissue, causing the release of tissue thromboplastin, which activates the extrinsic coagulation system producing _____

A

DIC

227
Q

most common fungal cause of septic shock

A

Candida

Unit 8 (5 decks)

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