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1 STEP UWorld pathology > Patho infl. and recovery > Flashcards

Patho infl. and recovery Flashcards

1
Q

What 3 factors induce ROS production and lead to mitochondria damage?

A

Radiation, toxins, reperfusion

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2
Q

Where originates oxygen used to form ROS in reperfusion?

A

Restoration of arterial blood flow to an affected limb floods ischemic tissue with oxygen. This molecular oxygen reacts with enzymes (…) to form ROS.

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3
Q

Molecular oxygen reacts with …………. (3) to form ROS.

A

xantine oxidase, NADPH oxidaze, NO synthase

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4
Q

What 3 types of ROS are formed after molecular oxygen reacts with some enzymes?

A

superoxide, hydroxyl radicals, singlet oxygen

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5
Q

How ROS disrupt cellular functions? (3)

A

DNA mutations, protein synthesis disruption/protein damage, membrane lipis peroxidation

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6
Q

What are antioxidant enzymes that convert ROS to oxygen and water?

A

superoxide dismutase, glutathione peroxidase, calatase

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7
Q

What reaction is catalyzed by catalase/glutathione peroxidase?

A

hydrogen peroxide (H2O2) –> H2O (it is called detoxification)

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8
Q

When are neutralized ROS generated during cellular respiration?

A

Before it causes damage

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9
Q

What are the result molecules in detoxification?

A

Oxygen and water

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10
Q

Why there is ROS damage to cell after reperfusion if normally cells are capable to neutralize it?

A

Because in postischemic damage, the production of ROS exceeds the neutralizing capabilities of antioxidant enzymes (high oxidative stress) –> cell injury and death

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11
Q

What is high oxidative stress?

A

ROS exceeds the neutralizing capabilites of antioxidant enzymes

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12
Q

Eg there is prostata cancer with radiation treatment. What condition may develop?

A

acute radiation enteritis

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13
Q

What are 2 mechanisms that cause cell damage when used ionizing radiation?

A

DNA double-stranded breakage and generation of ROS

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14
Q

DNA double-strand breakage in ionizing radiation?

A

Breakage of both strands is required. Single-strand breaks can be repaired by polymerase

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15
Q

What is used to form ROS (tipo unstable molecules) by ionization?

A

WATER. Unstable molecules formed by the ionization of water.

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16
Q

Radiation-induced DNA damage impairs ………. and initiates ………….. of susceptible cells.

A

Mitosis; apoptosis

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17
Q

What are susceptible cells for radiation?

A

Intestinal crypt stem cells and other highly proliferative cells (eg, cancer cells, hematogenous precursors)

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18
Q

What immune response is innitiated by cellular damage due to radiation?

A

induced immune response –> increased proinflammatory cytokines + migration of leukocytes (eg neutrophils) –> Inflammation –> production of additional ROS that leads to contribution of radiation-induced tissue damage

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19
Q

What proinflammatory cytokines participate in radiation-induced cell damage?

A

IL-1, IL-6, TNF-alpha

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20
Q

What is the result of GI mucosal denudation due to radiation therapy?

A

decreased absorptive area –> diarrhea

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21
Q

What causes diarrhea in radiation therapy?

A

GI mucosal denudation –> decreased absorptive area –> diarrhea

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22
Q

What are late GI complications due to radiation therapy?

A

Intestinal fibrosis = strictures, adhesions, bowel obstruction

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23
Q

As an antioxidant, ………………….. neutralizes ROS, preventing …………..

A

superoxide dismutase; preventing cell injury.

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24
Q

Cytochrome P450 enzymes metabolize ……………. and ………..

A

endogenous toxins as well as drugs.

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25
Q

How can cytochrome P450 enzymes can lead to hepatotoxicity?

A

Cytochrome P450 enzymes metabolize endogenous toxins as well as drugs. They are capable of producing ROS, which can contribute to the hepatotoxicity seen with certain drugs.

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26
Q

What enzyme is bactericidal, but also causes oxidative damage to host cells?

A

myeloperoxidase

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27
Q

NADPH oxidase catalyzes the reduction of …………… to ………….., aiding in bacterial destruction by phagocytic cells.

A

molecular oxygen to superoxide free radicals

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28
Q

What reaction catalyzes NADPH oxidase?

A

reduction; molecular oxygen to superoxide free radicals

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29
Q

What is the effect on bacterias y superoxide free radicals that are produces by NADPH oxidase?

A

It aids bacterial destruction by phagocytic cells

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30
Q

Proteasome activity normally increases in …………………………..

A

response to oxidative stress

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31
Q

the ubiquitin-proteosome system is inhibited by ……………..

A

ionizing radiation

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32
Q

radiation-induced tissue damage occurs primarily through the ……………..

A

Generation of free radicals

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33
Q

Ionizing radiation causes …………… and ……………damage

A

cellular and DNA

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34
Q

What triggers progressive inflammation and tissue damage in radiation therapy?

A

Ionizing radiation causes cellular and DNA damage primarily through generation of reactive oxygen species, which can trigger progressive inflammation and tissue damage.

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35
Q

What breakdowns proteins?

A

Ubiquitin protease pathway

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36
Q

Viral infection. Need to activated cellular immune. What is needed for activation and what system participates?

A

Need viral protein presentation to effector immune cells (eg CD8 lymph). These proteins are broken down by ubiquitin protease pathway and hydrolyzed peptides are presented to effector cells.

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37
Q

What proteins are broken down by ubiquitin-proteasome pathway?

A

native and foreign intracellular (eg viral) proteins

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38
Q

What initiates UPP?

A

Ubiquitin ligase

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39
Q

What does ubiquitin ligase?

A

It recognizes proteins and catalyzes the attachement of ubiquitin

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40
Q

What specific feature have proteins that participate in UPP and eventually are broken down?

A

Those proteins are tagged with ubiquitin. Then they are broken down by proteosome to peptide fragments –> recycled to amino acids

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41
Q

What catalyzes breakdown of proteins in UPP?

A

proteasome; proteins to peptide fragments

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42
Q

What is presented to MHC class I in viral infection?

A

PEPTIDE FRAGMENTS!!!!!

The are got after proteins are broken down by proteasome

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43
Q

What cell process if initiated by cytotoxic CD8 when eg viral peptides are presented?

A

apoptosis

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44
Q

What process happens when apoptosis is initiated by cytotoxic CD8?

A

activation of caspase cascade through the release perforin and granzyme

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45
Q

What is activated by perforins and granzymes?

A

caspase cascade

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46
Q

What state is cachexia?

A

hypermetabolic

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47
Q

What drives cachexia?

A

elevated proinfalmmatory cytokines (eg TNF-alpha, IL-6)

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48
Q

What is stimulated by TNF-alpha and IL-6 in cachexia?

A

UPP, therefore there is the degradation of muscle proteins (actin, myosin)

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49
Q

In cancer-related cachexia, high levels of pro-inflammatory cytokines lead to increased ……………………….. of ……………….. proteins, which in turn leads to extensive skeletal muscle loss

A

ubiquitination of sarcomeric muscle proteins -_> extensive skeletal muscle loss

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50
Q

How is called the destruction of targeted proteins?

A

selective proteolysis

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51
Q

Oligopeptides formed within within proteasomes further degraded by …………………………. into ………..

A

cytosolic peptidase into individual amino acids

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52
Q

Necrosis is characterized by ……………………… and …………………………due to external factors such as infection, toxin, or trauma.

A

cellular injury and premature death

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53
Q

What are the reasons of necrosis?

A

external factors such as infections, toxins, trauma

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54
Q

Main change in necrotic cell?

A

irreparable damage to the cellular membrane with subsequent leakage of cellular contents

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55
Q

Duchenne and Becker muscular dystrophies are caused by X-linked mutations to the ……………….

A

dystrophin gene

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56
Q

Function of dystrophin?

A

Dystrophin provides mechanical stability to muscle cells during contraction.

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57
Q

Pathophysiology when dystrophin gene mutations?

A

Mutations are associated with membrane tears that allow calcium to enter the cell and cause myofiber damage

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58
Q

What happens to the cell when telomers shorten beyond a certain point?

A

the cell undergoes apoptosis or senescence

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59
Q

Reprogramming of undifferentiated mesenchymal cells (eg, connective tissue) is a form of ……………………

A

Metaplasia

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60
Q

………………………………….(eg, connective tissue) is a form of metaplasia

A

Reprogramming of undifferentiated mesenchymal cells

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61
Q

Acid phosphatase is found in the …………………………

A

lysosomes

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62
Q

What does acid phosphatase?

A

hydrolyzes organic phosphates

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63
Q

guanylate cyclase plays important role in …………………….. and ……………………… of ………………. (eg ……….. and ………………..)

A

activation and regulation of diverse physiologic processes (eg smooth muscle relaxation, retinal phototransduction)

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64
Q

What secondary signal is in smooth muscle relaxation and retinal phototransduction?

A

guanylate cyclase

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65
Q

Apoptosis is a means of carefully regulated cell death in which the cell activates …………………..

A

enzymes to degrade its own nuclear DNA and proteins

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66
Q

What is the membrane condition in apoptosis?

A

it is intact

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67
Q

Why there are no inflammation in apoptosis?

A

because no cell contents are leaked into the surrounding tissue

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68
Q

What are the apoptosis phases? (2)

A

initiation and execution

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69
Q

What happens in initiation phase in apoptosis?

A

protein-hydrolyzing caspases are activated

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70
Q

What happens in execution phase in apoptosis?

A

caspases bring about the cell death by cleaving cellular proteins and activating DNAses

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71
Q

protein-hydrolyzing caspases are activated in ………… phase

A

initiation

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72
Q

caspases bring about the cell death by cleaving cellular proteins and activating DNAses in ………….. phase

A

execution

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73
Q

The initiation of apoptosis occurs via signals from …………………………….

A

two separate pathways

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74
Q

What are 2 pathways that initiate apoptosis?

A

intrinsic (mitochondrial) and extrinsic (dead receptor)

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75
Q

In the intrinsic pathway, the mitochondria become more ………………….. and it leads to release of ………………………. into………………..

A

permeable; pro-apoptotic substances; into cytoplasm

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76
Q

Release of pro-apoptotic substances in intrinsic pathway in apoptosis happens in response to ………………………………… (2)

A

in response to stress or the cessation of survival signal

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77
Q

Where reside anti-apoptotic proteins?

A

in mitochondrial membranes and cytoplasm

78
Q

What are anti-apoptotic proteins?

A

Bcl-2 and Bcl-x

79
Q

When anti-apoptotic proteins are replaced by pro-apoptotic proteins?

A

When cell is exposed to stress or the cessation of survival signals

80
Q

What are pro-apoptotic proteins?

A

Bak, Bax, Bim

81
Q

What cause pro-apoptotic proteins?

A

The pro-apoptotic proteins allow for the increased permeability of the mitochondria, which results in the release of caspase-activating substances like cytochrome c.

82
Q

What is released when pro-apoptotic proteins replace anti-apoptotic proteins?

A

due to incr. mitochondria permeability - release of caspase-activating substances

83
Q

What is the key enzyme in apoptosis?

A

caspases

84
Q

What can activate caspases?

A

cytochrome c

85
Q

Where occur death receptors in apoptosis?

A

in the cell surface

86
Q

To what family belongs death receptors?

A

tumor necrosis factor receptor family

87
Q

What are 2 best known death receptors?

A

type 1 TNF receptor (TNFR1) and Fas (CD95)

88
Q

What is FADD?

A

death-domain containing adapter protein

89
Q

What happens when Fas cross-links with its ligands?

A

multiple molecules of Fas come together to form a binding site for FADD

90
Q

What happens when FADD binds Fas formed binding site?

A

FADD then binds an inactive form of a caspase, again bringing multiple caspase proteins together that through a cascade effect eventually induce caspase activation.

91
Q

Hemosiderin accumulation is common in patients who have ………………… or …………………….

A

hemolytic anemia or who undergo frequent blood transfusions

92
Q

Chronic inflammatory conditions are characterized by the persistent stimulation of …………………………………. (2)

A

Neutrophils and macrophages

93
Q

Persistent stimulation of neutrophils and macrophages in chronic inflammation leads to increase of ………….. (4)

A

Inflammatory cytokines such IL-1, IL-6, TNF and INF-gamma

94
Q

What are 2 important acute phase reactants?

A

fibrinogen and globulins (CRP)

95
Q

What influence has acute phase reactants on RBCs?

A

they cause RBCs to overcome their zeta potential (negative potential that separates them) –> rouleaux formation –> it is heavier than separate RBCs –> settle to the bottom of tube more quickly

96
Q

Etiology of fibrinoid necrosis?

A

Malignant hypertension, vasculitis

97
Q

Etiology of fat necrosis?

A

Acute pancreatitis, trauma (subcutaneous adipose tissue)

98
Q

Etiology of liquefactive necrosis?

A

CNS infarcts, severe bacterial infection (eg gangrene)

99
Q

Etiology of caseous necrosis?

A 
Mycobacterial infection
Fungal infections (histoplasma, cryptococcus, coccidioides)
100
Q

Etiology of coagulative necrosis?

A

irreversible ischemic damage outside CNS

101
Q

Difference between apoptosis and necrosis?

A

apoptosis - no membrane damage.

necrosis - loss of membrane integrity –> proinflammatory intracellular material leaks –> injury of surrounding tissue

102
Q

Necrosis is an uncontrolled process of cell death that results in …………………… of cellular proteins and ……………………. of cellular components

A

denaturation;

enzymatic digestion

103
Q

In most organs, irreversible ischemic injury typically results in ………………………… (what necrosis?)

A

coagulative necrosis

104
Q

Why in coagulative necrosis is maintained cellular architecture?

A

digestive enzymes denaturate before they destroyed cellular architecture, but nuclei are absent.

105
Q

How differs liquefactive necrosis and coagulative?

A

in coagulative - maintaines cellular architecture;

in CNS liquefactive - digestion of cellular constitutienst and liquefaction of necrotic tissue

106
Q

In what areas occurs fat necrosis?

A

in tissues with high numbers of adipocytes (pancreas, breast, subcutaneous fat)

107
Q

in fat necrosis: TG –> free fatty acids. What 2 factors cause this reactions?

A

active enzymes (eg lipases) or mechanical damage

108
Q

From where occurs enzymes in fat necrosis?

A

enzymes are released from damaged cells

109
Q

What combines with free fatty acids in fat necrosis?

A

it combines with calcium = saponification (calky-white deposits)

110
Q

What is seen under microscopy in fat necrosis?

A

anucleated adipocytes with calcium deposits

111
Q

what cells surround in caseous necrosis?

A

epithelioid macrophages and giant cells

112
Q

How is described material in the centre of granuloma? it is made of ……….

A

white, friable, cheese-like material. it is made up of CELL FRAGMENTS AND AMORPHOUS PROTEINACEOUS DEBRIS

113
Q

Why tissue architecture is preserved in coagulative necrosis?

A

Due to early denaturation of lytic enzymes

114
Q

2 microscopic changes in coagulative necrosis?

A

Cells are nucleated with eosinophilic cytoplasm.

Leukocytes eventually infitlrate and digest necrotic tissue

115
Q

What immune cells digest necrotic tissue in coagulative necrosis?

A

Leukocytes

116
Q

Fibrinoid necrosis results from ………………… (2)

A

Immune complex and/or plasma proteins (eg fibrin) that leak through the damaged intima and depositing within the vessel wall.

117
Q

How appear deposits in fibrinoid necrosis in histology?

A

circumferential ring of pink, amorphous material surrounding the vascular lumen. (proteinaceous material - nes leakina baltymai eg fibrin)

118
Q

How looks liquefactive necrosis?

A

infected abscess fluid is creamy yeallow due to dead leukocytes (pus)

119
Q

why abscess is yellow in liquefactive necrosis?

A

due to dead leukocytes (pus)

120
Q

How resolves brain infarcts?

A

it resolves into CSF-filled space

121
Q

Why occurs dystrophic calcification?

A

Dystrophic calcification occurs in areas of tissue injury or necrosis that escape removal by phagocytes

122
Q

What binds calcium in dystrophic calcification?

A

Phosphate ions bins calcium –> salts, which appear as white granules.

123
Q

How microscopically occurs dystrophic calcification?

A

amorphous, basophilic material on H&E stain

124
Q

How long it takes for dystrophic calcification to develop?

A

slowly - months and years following injury

125
Q

What type of necrosis in in kidney and heart?

A

coagulative

126
Q

Why there is not maintained cell architecture in brains in ischemia?

A

because there is lack of supporting architecture.

127
Q

How long it takes to manifest for liquefactive necrosis in brains?

A

it occurs within 10 days oof infarction

128
Q

What cells digest infarcted CNS tissue?

A

microglia (CNS macrophages)

129
Q

What replaces digested CNS tissue?

A

cystic space surrounded by astroglial scar (gliosis)

130
Q

How long it takes to form a cystic space + gliosis in CNS infarction?

A

months to years

131
Q

Fibrinoid necrosis. What material accumulates?

A

Accumulation of fibrin-like material in the walls of blood vessels

132
Q

fibrinoid necrosis in cerebral arteries can predispose a …………………….

A

hemorrhagic stroke

133
Q

What immune cells can be seen in fibrinoid necrosis?

A

neutrophilic infiltrates

134
Q

tuberculosis infection in CNS. Acute or chronic?

A

Chronic

135
Q

fat necrosis. What cells engulf what?

A

foamy macrophages contains engulfed lipids debris + release free fatty acids that combine with calcium.

136
Q

free fatty acids combine with calcium and form deposits. They are eosinophilic or basophilic?

A

basophilic

137
Q

Coagulative necrosis occurs following ………………

A

hypoxic cell death

138
Q

Wound healing process needed to …. (2)

A

restore continuity and tensile strength.

139
Q

4 stages of wound healing.

A

4 sequential (but overlapping) phases: hemostasis, inflammation, proliferation, and maturation.

140
Q

What phase occurs immediately after tissue injury?

A

hemostasis

141
Q

What is involved in hemostasis? (3)

A

small vessel constriction;
platelet aggregation;
clotting cascade activation;

142
Q

Result of hemostasis? (3)

A

platelet plugging, fibrin clot formation, and cessation of bleeding

143
Q

For relatively minor injuries, hemostasis is often accomplished within …………….

A

minutes

144
Q

The fibrin clot that is formed during hemostasis provides a ………………

A

scaffold for subsequent wound healing

145
Q

inflammation after wound injury usually starts within ……………………

A

hours of injury

146
Q

What cells primary participate in inflammation phase?

A

mast cells –> degranulate –> vascular permeability + CELLULAR INFILTRATION (neutrophil, monocytes)

147
Q

Function of neutrophils in inflammation phase?

A

digest bacteria, necrotic tissue and foreign debris

148
Q

Function of monocytes in inflammation phase?

A

secrete growth factors (TGF-beta, VEGF, IL-1, TNF-alpha) –> promote next phase of healing

149
Q

what 2 factors released from platelets in hemostasis phase?

A

PDGF, TGF-beta

150
Q

PDGF from hemostasis phase induces …….. in inflammation phase.

A

macrophages

151
Q

What factor from hemostasis activates macrophages in inflammation phase?

A

PDGF

152
Q

TGF-beta from inflammation phase induces …….. in proliferation phase.

A

fibroblasts

153
Q

What factor from inflammation activates macrophages in proliferation phase?

A

TGF-beta

154
Q

Proliferation, which begins during the ……….phase and continues for ………..afterward

A

inflammatory phase and continues for weeks afterwar

155
Q

3 processes that happens in proliferation phase?

A

epithelization, fibroplasia, angiogenesis

156
Q

What happens in epithelization?

A

Basal keratinocyte proliferation and migration of new epithelial cells form a new superficial epithelial layer that acts as a barrier to bacteria.

157
Q

what happens in fibroplasia?

A

Fibroblasts proliferate and synthesize ground substance and collagen, forming a matrix into which capillaries can grow

158
Q

What process during fibroplasia help to decrease wound size?

A

Simultaneous contraction of myofibroblasts (ie, differentiated fibroblasts that produce contractile proteins) helps decrease the wound size.

159
Q

What important proteins produce fibroblasts during fibroplasia?

A

differentiated fibroblasts that produce contractile proteins

160
Q

What happens in angiogenesis?

A

Proliferation and migration of endothelial cells from nearby blood vessels lead to ingrowth of new capillaries into the collagen matrix.

161
Q

Proliferate and migration of what cells happens in angiogenesis in proliferation phase? From where those cells migrate?

A

Endothelial cells;

nearby blood vessels

162
Q

Matrix in fibroplasia is formed from ………….

A

collagen (collagen matrix - here can grow new capillaries)

163
Q

The last phase of wound healing?

A

maturation

164
Q

What happens in maturation phase?

A

collagen remodeling and cross-linking

165
Q

the primary mechanisms by which the tensile strength of the wound increases?

A

collagen remodeling and cross-linking

166
Q

duration of hemostasis?

A

0 hours-1 day

167
Q

duration of inflammation?

A

3 hours- 5 days

168
Q

duration of proliferation?

A

3 days - 5 weeks

169
Q

duration of remodeling?

A

3 weeks - 2 years

170
Q

What factors are produced by fibroblasts in proliferation phase?

A

FGF, VEGF, extracellular matrix

171
Q

What enzymes plays a role in remodeling?

A

matrix metalloproteinases

172
Q

What types of collagen in remodeling?

A

type III –> type I

173
Q

hemostasis. 2 results?

A

vasoconstriction;

fibrin clot formation

174
Q

Inflammation. 3 results?

A

vasodilation;
incr. permeability;
inflmmatory cells chemotaxis

175
Q

Recurrent respiratory infections + dextrocardia –?

A

Kartagner syndrome

176
Q

Kartagner syndrome is a form of ………………

A

primary ciliaryy dyskinesia (PCD)

177
Q

Inheritance of Kartagner syndrome?

A

autosomal recessive

178
Q

Eukaryotic flagella and cilia are composed of …………

A

central core known as the axoneme

179
Q

the axoneme is anchored to the cell by a ………………..

A

basal body

180
Q

The axoneme of flagella and motile cilia consists of a …………

A

a circular array of microtubule doublets surrounding 2 central microtubules (9+2 arrangement

181
Q

Each doublet in cilia has an ………….. and ………..subunits which are connected to ………………..

A

Each doublet has an A and B subunit and is connected to the adjacent doublet via dynein arms.

182
Q

These dynein arms contain an …………. that generates energy to slide the microtubules past each other, producing ciliary movement

A

ATPase

183
Q

how happens ciliary movement?

A

These dynein arms contain an ATPase that generates energy to slide the microtubules past each other, producing ciliary movement.

184
Q

Primary ciliary dyskinesia can result from failure of the …………….. to develop normally.

A

dynein arms

185
Q

Why patients with PCD experience recurrent respiratory infections?

A

due to impaired mucociliary clearance

186
Q

What cardio pathology seen on xray in kartagner syndrome (PCD)?

A

dextrocardia

187
Q

impaired ciliary movement during embryogenesis can cause …………….

A

situs inversus (reversed right/left positioning of internal organs).

188
Q

genital manifestation in PCD in women and men?

A

Infertility in men (impaired sperm motility) and women (immobility of fallopian tube cilia)

189
Q

Deficiency of the C1 complement component causes increased susceptibility to ………………. bacteria and also predisposes to developing ………………………

A 
encapsulated bacteria (eg, Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis);
SLE
190
Q

Same manifestation in PCD and cystic fibrosis?

A

recurrent respiratory infections, infertility;

in PCD - sinus inversus (in cystic is not seen)

191
Q

Epithelial cell chloride channels are defective in ……………….

A

cystic fibrosis

1 STEP UWorld pathology (10 decks)

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