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Cell Injury Flashcards

1
Q

CELL INJURY

-Cellular injury occurs when_______

A

a stress exceeds the cell’s ability to adapt.

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2
Q

Slowly developing ischemia (e.g renal artery ________) results in ______

A

atherosclerosis

atrophy

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3
Q

acute ischemia (e.g., renal artery ____) results in ____.

A

embolus

injury

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4
Q

Neurons are highly resistant to ischemic injury

T/F

A

F

susceptible

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5
Q

skeletal muscle is relatively more resistant to ischemic injury

T/F

A

T

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6
Q

CAUSES OF CELL INJURY

Mention 5

A

inflammation
-hypoxia
-trauma
-nutritional deficiency or excess
-genetic mutation

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7
Q

HYPOXIA
-is the ______

A

Inadequate oxygenation of tissue

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8
Q

Normally, O2 diffuses (up or down?? a gradient from the atmosphere to the ___, to _____, and into the _________, where it attaches to heme groups

A

Down

alveoli

Plasma

red blood cells (RBCs)

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9
Q

In hypoxia, there is decreased synthesis of ______

A

adenosine triphosphate (ATP).

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10
Q

Causes of Hypoxia

Mention 3

A

ischemia
-hemoglobin related abnormalities
-Hypoxemia

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11
Q

Ischemia
-is the _________ or ________

Consequences of ischemia
(1) _____

(2)______

(3)_____

A

decreased arterial blood flow to tissue or venous outflow of blood from tissue.

Atrophy

Infarction of tissue

Organ dysfunction

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12
Q

(1) Atrophy ( ________ )

(2) Infarction of tissue (_______)

A

reduction in cell/tissue mass

localized area of tissue necrosis

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13
Q

Hypoxemia
-is the __________

A

decrease in Pao2 measured in an arterial blood gas

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14
Q

Normal Pao2(oxygen in plasma) depends on

*percent O2 in _____
*_______
*______
*diffusion of O2 from the alveoli into the ______

A

inspired air

Ventilation

Perfusion

pulmonary capillaries

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15
Q

Ventilation refers to ______

*Perfusion refers to _____

A

how much air is in alveoli

how much blood gets to lungs

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16
Q

Causes of Hypoxemia
-issue with Percent O2 in inspired air e.g ______
-issue with Ventilation e.g ________

-Respiratory acidosis: defined as ________

-Diffusion defect: is the decreased diffusion of O2 through the alveolar capillary interface into the pulmonary capillaries. Examples— _______,______

A

high altitude breathing

Respiratory distress syndrome

retention of CO2 in the lungs

interstitial fibrosis, pulmonary edema

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17
Q

Hemoglobin (Hb) related abnormalities
1) ______

2)______

A

Anemia

Carbon monoxide (CO) poisoning

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18
Q

Anemia
-is the ________

A

decrease in Hb concentration

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19
Q

Causes of anemia include

Decreased production of Hb (e.g., _______)
-causes of anaemia include Increased destruction of RBCs (e.g., ________)
-causes of Anaemia include Decreased production of RBCs (e.g., _____)
-causes of Anaemia include Increased sequestration of RBCs (e.g., ______

A

iron deficiency

hereditary spherocytosis

aplastic anemia

splenomegaly)

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20
Q

In Carbon monoxide (CO) poisoning
-Sao2 is __creased

A

De

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21
Q

-CO binds hemoglobin more avidly than oxygen

T/F

A

T

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22
Q

Classic finding from carbon monoxide poisoning is ______ appearance of skin.

Early sign of exposure is ______

significant exposure leads to _____ and ___

A

cherry-red

headache

coma and death.

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23
Q

Clinical findings in HYPOXIA

Mention 4

A

Cyanosis
-Confusion
-Cognitive impairment
-Lethargy

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24
Q

TYPES OF CELL INJURY

_____ and ____

A

Reversible and non-reversible

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25
Q

Cyanosis

??

A

bluish discoloration of skin and mucous membranes

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26
Q

the characteristic feature of reversible cell injury is _______

the characteristic feature of irreversible cell injury is _____

A

cell swelling

cell membrane damage

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27
Q

In reversible cell injury

-ATP production is ??
-protein synthesis is ??

A

Reduced

Reduced

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28
Q

In reversible cell injury

Which channels or pumps are compromised??

A

Calcium channel and Na/K pump

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29
Q

Ribosomal detachment occurs in ____ stage of cell injury

A

Reversible

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30
Q

Mitochondrial swelling occurs in ____ stage of cell injury

A

Reversible

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31
Q

There are no plasma membrane changes in reversible cell injury stage

T/F

A

F

There is blebbing

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32
Q

What nuclear changes are associated with reversible cell injury

A

Chromatin clumping

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33
Q

Myelin figures are mainly associated with what stage of cell injury

A

Reversible

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34
Q

What are myelin figures

A

Aggregation of peroxidized lipids of the cell membrane

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35
Q

Breakdown of cell membrane is associated with what stage of cell injury

A

Irreversible

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36
Q

Influx of _____ activates the degradative enzymes in the cell

This is a characteristic of _____ stage of cell injury

A

Calcium ion

Irreversible

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37
Q

Abnormal increase in ATP levels and production in irreversible cell injury stage

T/F

A

F

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38
Q

Rupture of lysosomes occurs in _____ cell injury stage

A

Irreversible

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39
Q

Steps of nuclear destruction

List them

A

Pyknosis
Karyorrhexis
Karyolysis

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40
Q

Pyknosis - _______
Karyorrhexis- ______
Karyolysis - _______

A

Nuclear condensation

Nuclear fragmentation

Nuclear dissolution

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41
Q

Presence of amorphous inclusions in the mitochondria is associated with ______ cell injury stage

A

reversible

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42
Q

Cell injury occurs at the limit of _____.

A

adaptation

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43
Q

A cell’s ability to adapt depends on:

the ______________

as well as the ________

A

nature of the stress (duration and aetiology)

nature of
the cell/tissue (brain/colon cells in hypoxia)

44
Q

Intracellular accumulations: The _______ of _______ may persist in some cells

A

after effects

reversible injury

45
Q

Reversible injury:__________ (within or outside?) a cell’s tolerance limit

A

Mild to moderate stressors

Within

46
Q

Irreversible injury: ______ and _____ stressors

A

Persistent and severe

47
Q

In reversible injury

offending stimulus is _______
Key features:
• Reduced _______
• Changes in ion concentration
lead to _________ and ______

A

removed

oxidative phosphorylation

water influx and cell swelling

48
Q

In irreversible injury

Damage has reached point of _____

E.g. is heart muscle. With increased hemodynamic load , _______ results and it is (reversible or irreversible?).

Persistently increased load leads to ________

A

no return.

hypertrophy; reversible

point of no return (cell death).

49
Q

Causes of cell injury

1._______/______
2.______ agents e.g. _______,________ etc
3._______ agents/drugs: Eg ___,____,____
4.______ agents:____,____,_____

A

Hypoxia /Ischaemia

Physical; mechanical trauma, extreme heat/cold

Chemical; Acid, insecticides, narcotics

infectious; Bacteria, viruses, fungi

50
Q

Hypoxia (reduced _______)

Ischaemia (reduced ______)

A

O2 supply

blood flow

51
Q

Which is most common between hypoxia and ischemia

A

Ischemia

52
Q

Hypoxia (reduced O2 supply) / Ischaemia (reduced blood flow) -
•________ failure
• Reduced ______
• Reduced _____ capacity of blood (e.g. carbon monoxide, sickle cells)
•______ loss

A

Cardiorespiratory

blood flow

O2 carrying

Blood

53
Q

causes of cell injury

4._______ agents
5._____ derangement
6.________ imbalances

A

Immunologic

Genetic

Nutritional

54
Q

Genetic derangements :
•_________ abnormalities e.g ______
• Susceptibility to _____ agents
• Deficiency of ________ (e.g. inborn errors of metabolism)

A

Chromosomal; Down’s syndrome

injurious

functional proteins

55
Q

Which can survive hypoxia longer

Skeletal or cardiac muscle

A

Skeletal

56
Q

ATP depletion resulting from cell injury

Mechanisms
• Most commonly results from
———— , ______ damage or ______
• The cell may resort to ______

A

ischaemia/hypoxia, mitochondrial, toxins

anaerobic glycolysis

57
Q

Consequences of ATP depletion in a cell

• Defective ___________ pump; ___ gain, ______
• Anaerobic glycolysis, reduction in
________, _______ , reduced IC enzyme activity
• Failure of __ pump, ____ (influx or efflux?) , ________ stimulation
•_______ synthesis disruption
•________ proteins

A

NA/K ATP-dependent ; H20; swelling

glycogen stores

lactic acidosis

Ca; Ca influx

enzyme

Protein

Misfolded

58
Q

Mitochondrial damage resulting from cell injury

Mechanism
• Damaged by increased ________,______,_____
Also,
• Toxins
• Genetic mutations

A

cytosolic Ca, ROS, hypoxia

59
Q

Consequences of mitochondrial damage

• Formation of _____, failure of
__________, ____ depletion
• Increased ______ formation
• Leakage of _______, & ______ , stimulation of ________

A

MPTP; oxidative phosphorylation

ATP

ROS

cytochromec & caspases

apoptosis

60
Q

Calcium influx resulting from cell injury

Consequence
•______, failure of ____ generation
• Activate ________ (______ damage), _____ (_______ damage), _______ (fragment ___, chromatin), ATPases (ATP
depletion)

A

MPTP

ATP

phospholipases; membrane

protease; cytoskeletal

endonuclease; DNA; chromatin

61
Q

Reactive oxygen species

Mechanism
• Generation: _________ during normal metabolic process, absorption of ______,
_______, breakdown of ______

• Removal: _________,
__________, enzymes eg
________, SOD etc,

A

Oxidation/reduction
radiant energy
leukocytes; drugs

spontaneous decay; antioxidants (Vit E,A)
catalase

62
Q

Consequences of reactive oxygen species

• Lipid _______, _____
damage
•________ of proteins, ______ enzymes
•_____________ breaks.

A

peroxidation

membrane

Oxidative modification

damaged

Single & double strand DNA

63
Q

Mechanism of defect in membrane permeability
•______
• Decreased _______ synthesis (from ___ depletion)
• Increased _____ breakdown (from
__________ )
• _______ damage by ______

A

ROS
phospholipid ; ATP

phospholipid; phospholipases

Cytoskeletal; proteases

64
Q

Consequences of defect in membrane permeability

• Mitochondrial membrane:
reduced ____ generation
• Plasma membrane: _________
• Lysosomal membrane: ______ of the cell

A

ATP

Cell content leakage

Enzymatic digestion

65
Q

Ischemic-hypoxic injury

Decreased generation of cellular ____.
• Failure of __ pump, influx of _____
•___ influx/release, enzyme activation
• Reduced ______ synthesis
• Reduced cell _____
• Destruction of ______, membrane _____

A

ATP

Na; H20; Ca

protein

glycogen

cytoskeleton

blebs

66
Q

Ischemic-hypoxic injury

1) ________,_________,_______ cells are solely dependent on
aerobic respiration and are rapidly susceptible to damage.

A

CNS neurons, myocardial and kidney

67
Q

Ischemic-hypoxic injury

  1. Due to low oxygen supply and subsequent anaerobic respiration, there
    is increased _____ accumulation in the cell (______) which leads to a (rise or fall?) in intracellular pH and clumping of _______
A

lactic acid

lactic acidosis; fall

nuclear chromatin

68
Q

Ischemic-hypoxic injury

  1. Reduced ATP generation also affects the integrity of the _____ There is reduced synthesis of ____ which are useful for membrane repair, impaired function of ______ pump ( _______ ) and impaired ___ pump resulting in excess ___ influx
A

plasma membrane.

phospholipids

NA-K ATPase; hydropic swelling

Ca; Ca

69
Q

Irreversible injury is associated with:
• Severe ______
• Extensively damaged _____
•________ swelling/damage

A

mitochondrial swelling

plasma membranes

Lysosomal

70
Q

Hypothermic therapy
• Mechanism: Reduction of temperature leads to reduction in ______, production of ______ and _______.

• Current meta-analyses: (useful or Not useful?) , infact may cause _______

A

cellular metabolic demands

free radicals

host immune response

Not useful; more mortality.

71
Q

Ischemia-Reperfusion injury

•Occurs as a result of ______ of _____ to _____ tissue.
• It may result in additional __________.
• Commonly seen in tissue damage ff M.I. & ________

A

restoration; blood flow; ischaemic

death of reversibly damaged cells

cerebral infarction

72
Q

Ischemia-Reperfusion injury

Mechanisms:
• Oxidative stress: Increased ____ generation
• Intracellular ___ overload
• Increased _________
• Activation of ________ by binding Ab e.g. ____

A

ROS

Ca

inflammation

complement system

IgM

73
Q

Chemicals induce injury by:
•________
• Conversion of __________

A

Direct cytotoxicity

chemicals to reactive metabolites

74
Q

Direct cytotoxicity:
• Mostly affects cells which are ____________ of such
chemicals E.g. HgCl, Cyanide, Chemotherapy drugs

• HgCl poisoning: Hg binds -___ grp of cell membrane proteins, increased
__________. Mostly affects cells of the _____
• Cyanide: Targets _____________, reduction in _____ generation

A

directly involved in the metabolism

SH; membrane permeability

GIT, Kidney

mitochondrial cytochrome oxidase

ATP

75
Q

Conversion to reactive metabolites:
• The chemical agent is metabolized to yield the ____ which interacts
with the target cells. Usually by _____ in ___ of ____.

• Mechanism: Formation of _______
• E.g. is _______(CCl4), ________.

A

toxin

cytochrome P450

sER; liver

free radicals

Carbon tetrachloride

Acetaminophen

76
Q

Microscopic features of reversible injury

Microscopic
•——— secondary to failure of energy dependent ion pumps responsible for maintaining homeostasis
• Fatty change. Seen in _____ and ———— cells ff hypoxic/toxic injury

Ultrastructural
• Plasma membrane alterations
e.g. ________,________,______
• Mitochondrial changes e.g._______
•_____ dilation
• Nuclear alterations

A

Cellular swelling; hepatocytes and myocardial

blebbing. Blunting, loss of microvilli

amorphous densities

Endoplasmic reticulum

77
Q

The point of transition from reversible to irreversible injury is m clear
cut.

T/F

A

F

It’s not

78
Q

Pathogenesis of irreversible injury

1) Membrane damage: excess accumulation of ____ in __________ due to ____ influx disabling its function
2. Ca ion influx : leads to phospholipase activation that ________ and destroy _____
3. Intracellular proteases are also activated and leads to destruction of
________
4. Activated endonucleases damage the ________.
5. Lysosomal membranes are compromised leading to leakage of their _______ (e.g. hydrolase, DNAase etc) digest cellular components

A

Ca; mitochondria; Ca ion

degrades membrane phospholipids ; cell membrane

cytoskeletal proteins

DNA in the nucleus

hydrolytic enzymes

79
Q

Damage of the nucleus in irreversible damage occur in 3 forms: ____,____,_____

A

Pyknosis, karryohexis, karyolysis

80
Q

Enzymes released from the cell can be detected by laboratory assays.
Examples include:

•________,_____ (myocardial infarction)

•______,______ (Acute pancreatitis)

•_________/________ (hepatocyte damage)

A

Cardiac troponins, CK-MB

Amylase, Lipase

Aspartate/Alanine aminotransferase

81
Q

Histology of reversible injury

Two major changes:
•_____
•______
• Others include increased ______ (_____ change)

A

Cellular swelling

Fatty change

eosinophilia

hyaline

82
Q

• Cellular swelling : results from failure of ____ in the _______ leading to ion and fluid imbalance.

• Fatty change : seen most especially in cells dependent on _______ e.g.
________,_________ cells.______ are seen within the cytoplasm

A

pumps

plasma membrane

lipid metabolism

hepatocytes, myocardial

Vacuoles

83
Q

the first manifestation of cell injury is usually _____

A

Cellular swelling

84
Q

Classic physical find in a patient with CO poisoning?

A

Cherry red appearance of skin

85
Q

Early sign of exposure to CO poisoning is ______?

A

Headache

86
Q

MPTP

A

Mitochondrial permeability transition pore

87
Q

The response of a cell to stress or injurious stimuli includes

Intracellular accumulation

T/F

A

T

88
Q

The response of a cell to stress or injurious stimuli includes

Pathologic calcification

T/F

A

F

89
Q

The response of a cell to stress or injurious stimuli includes

Neoplasia
T/F

A

T

90
Q

Cellular nonlethal injury is sometimes
called ________ or _______ .

A

hydropic change or vacuolar degeneration

91
Q

The CYTOPLASM of injured cells appears ______ and ______ when stained
with hematoxylin and eosin (H&E) due to loss of cytoplasmic RNA, which binds the blue hematoxylin dye.

A

red (eosinophilc)

92
Q

The eosinophilia becomes (more or less?) pronounced with progression toward necrosis.

A

More

93
Q

A breakdown product of DNA that commonly leaks out of the cell into the ecf is _______

A

Uric acid

94
Q

In injured cells

Cardiac muscle cells, for example, express cardiac-specific variants of the contractile protein _____, while bile duct epithelium expresses a specific isoform of the enzyme ________ and hepatocytes express _________

A

troponin

alkaline phosphatase

transaminases

95
Q

Cardiac-specific troponins can be detected in the blood as early as _____ after myocardial cell necrosis

A

2 hours

96
Q

Necrotic cells show increased CYTOPLASMIC _____ in H&E stains, attributable in part to the loss of _______ and in part to accumulation of denatured cytoplasmic _____ (which bind the red dye eosin).

A

eosinophilia

cytoplasmic RNA

proteins

97
Q

In coagulative necrosis ,

Presumably, the injury denatures not only _____ but also ___ and so blocks the proteolysis of the dead cells; as a result, intensely ___philic cells with indistinct or ____ nuclei may persist for days or weeks

A

structural proteins

enzymes

eosino; reddish

98
Q

In liquefactive necrosis

The necrotic material is frequently ________ (color) because of the presence of leukocytes and is called pus.

A

creamy yellow

99
Q

Ischemia-reperfusion injury:

Refers to the exacerbation of existing injury upon restoration of blood flow
to a tissue
T/F

A

T

100
Q

Ischemia-reperfusion injury Contributes to tissue damage following reperfusion in ______ infarction and ______ infarction

A

myocardial

cerebral

101
Q

Ischemia-reperfusion injury

Inflammation is not a contributory mechanism

T/F

A

F

It is

102
Q

Ischemia-reperfusion injury

Involves decreased generation of free radicals
T/F

A

F
Increased

103
Q

Most common cause of budd chiari syndrome is ???

A

Polycythemia Vera

104
Q

Classic finding in methemoglobinemia is ________________ And the patient would be _________

A

Chocolate-colored blood

Cyanotic

105
Q

Treatment of methemoglobinemia

It (reduces Or oxidizes?) iron from —— to ____

A

IV methylene blue

Reduce

3+ to 2+

House AMP (64 decks)

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