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D&D Unit 2 > Cell and Tissue Injury (complete) > Flashcards

Cell and Tissue Injury (complete) Flashcards

1
Q

What type of tissue is involved in most cellular injuries?

A

Epithelia

THIS INCLUDES:

  • Skin
  • Linings of body cavities/organs
  • Endothelia in blood vessels
  • Mesothelium
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2
Q

What are the 7 major causes of cell injury?

A

1) Physical agents
2) Chemical/drug agents
3) Infection
4) Immune response
5) Genetic abnormalities
6) Nutritional imbalance
7) Hypoxia

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3
Q

What are common physical agents involved in cell injury?

A

1) Trauma
2) Heat, burns
3) Cold
4) Electric shock

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4
Q

Describe burns as it relates to cell injury

A

Always think: which tissue layers have been burned (dermis, basal lamina, CT, or just epidermis)

Lead to neurogenic shock, anemia, hypermetabolism, and infections (duh!)

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5
Q

Describe hypothermia as it relates to cell injury

A

Basically —> CELLS FREEZE!

Salts precipitates out —> damages cells

Poor perfusion of tissues (blood flow issues)

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6
Q

Describe electric shock as it relates to cell injury

A

Disrupts neural impulses —> cardiac arrest

Can cause tetany and asphyxia (b/c of chest wall spasms)

Outcome is a function of:

1) tissue conductance (dry skin = worse conductor)
2) amount of heat generated
3) intensity of current

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7
Q

Describe how cell injury contributes to the pathogenesis of disease

A

Disease = cell injury

No X cell? —> disease related to X cells

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8
Q

Which types of cells are present in acute cell injury?

A

PMNs (polymorphonuclear leukocytes)

a type of WBCs

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9
Q

Which types of cells are present in chronic cell injury?

A

Lymphocytes

Macrophages

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10
Q

What are the classic examples of cell injury? AKA: REVERSIBLE

A

1) Cell swelling (membrane damage)
2) Increase in extracellular metabolites
3) Fatty change in hepatocytes

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11
Q

To what does an increase in extracellular metabolites lead?

A

Massive overproduction of intracellular molecules

Eg: too much glucose (extra) —> too much glycogen (intro)

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12
Q

What do fatty changes in hepatocytes cause?

A

Fat vacuoles accumulate under conditions of high fat metabolism (b/c of glucose metabolism shut down)

Eg: Starvation or excessive, chronic alcohol consumption

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13
Q

What is ischemic cell injury?

A

No oxygen

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14
Q

How do neurons respond to ischemic cell injury?

A

Can only go 3-5 min w/o oxygen

After that —> irreversible damage

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15
Q

How do cardiac myocytes respond to ischemic cell injury?

A

Can go 20 min w/o oxygen

After that —> irreversible damage

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16
Q

How do liver/renal epithelium respond to ischemic cell injury?

A

Can go up to 2 hours w/o oxygen

After that —> irreversible damage

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17
Q

How do skin and skeletal muscle cells respond to ischemic cell injury?

A

Can go up to several hours w/o oxygen

After that —> irreversible damage

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18
Q

What are free radicals?

A

Molecules with free/unpaired electron

19
Q

From where do free radicals come?

A

A result of thermodynamic breakdown/alteration of O2

H2O2: easily breaks down to 2 OH free radicals

Fe++ w/ H2O2 = Fe+++ and free radical + OH-

O2-: generated from O2 interaction with ER (called superoxide)

20
Q

How do free radical produce cell injury?

A

They react with everything! Including DNA, RNA, important stuff

They constantly take an electron from normal rxns (think Fe2+ becomes Fe3+, affects a lot of stuff)

21
Q

What happens when mitos are deprived of O2 due to ischemia/hypoxia?

A
  • Acute drop in ATP
  • ATP mobilized from creatinine phosphate/glycolysis processes
  • Causes increase in lactic acid (decrease in cellular pH)
  • Ion pumps stop working
  • Cell swells!
  • Increase in Ca++ (affects signaling)

IMPORTANT: Still reversible at this point

22
Q

What happens when cell pH drops to 4.5 b/c of ischemic injury?

A
  • Lysosomes burst (proteases/nucleases released)
  • Destroys nuclear chromatin —» also eventually DNA/protein
  • uh oh… irreversible
23
Q

What happens when you give hypoxic pts lots of O2?

A
  • AKA: reperfusion

- Accumulate lots of free radicals

24
Q

Compare and contrast necrosis and apoptosis.

A

Both —> cell death

Necrosis: unplanned, occur in clumps of cells — cell swells — can happen anywhere, observable

Apoptosis: planned, occur in isolated cells that receive specific signals — cell shrinks — usually only in immune system (difficult to observe)

25
Q

Contrast DNA segments resulting from necrosis and apoptosis.

A

Necrosis: random, lots of released unspecific endonucleases

Apoptosis: chopped into discrete segments (very purposeful, specific by a particular enzyme)

26
Q

What are the 4 types of adaptive responses of chronic cell injury?

A

1) Atrophy
2) Hypertrophy
3) Metaplasia
4) Hyperplasia

27
Q

What is atrophy?

A

Cell decreases in size and function

28
Q

What is hypertrophy?

A

Cell increases in size (organelles, function)

Ex: left ventricle enlarges to compensate for overload in chronic hypertension

29
Q

What is metaplasia?

A

One type of cell replaced by another

Ex: when columnar epithelia in bronchus replaced by squamous epithelia — b/c of cell (thermal) damage from cigarette smoke

30
Q

What is hyperplasia?

A

One cell type proliferates in a particular location

Ex: with an endocrine tumor that produces ACTH, the adrenal cortex cells multiply like crazy

31
Q

What are the major alterations in the cell membrane during cell injury?

A
  • Problems b/c of physical break or inactivated ion pumps —> osmotic imbalance
  • Osmotic issues —> cell swelling (ion accumulation)
  • Physical break is due to oxidation of the lipids inside

REMEMBER: ATP required for ion pumps, so if no ATP = problem

32
Q

What are the major alterations in the mitochondria during cell injury?

A
  • Swells due to H20 accumulation in matrix
  • There’s a disruption in O2 supply (interrupts ion pumps at mito surface)
  • Also interferes w/ ATP dependent ion pumps elsewhere
33
Q

What are the major alterations in the nucleus during cell injury?

A
  • In reversible injury: problems in nucleolus appearance

- Changes not well characterized b/c of some effect in rRNA synthesis —> decrease in protein synthesis

34
Q

What are the 4 major types of necrosis seen in human disease?

A

1) Coagulative necrosis
2) Liquefactive necrosis
3) Caseous necrosis
4) Fat necrosis

35
Q

Describe coagulative necrosis

A
  • Dead cell = ghost-like remnant of former self
  • Nucleus shrinks —> fragments —> disappears

Classic in heart after myo infarc

36
Q

Describe liquefactive necrosis

A
  • Dead cell dissolves away
  • Lysosomal hydrolases digest cellular components
  • Commonly seen in brain and spleen
  • Acute infection
37
Q

Describe caseous necrosis

A
  • Only seen in TB
  • Chalky white appearance (like milk protein casein)
  • Central portion of infected lymph node is necrotic
38
Q

Describe fat necrosis

A
  • Typically follows acute pancreatitis or trauma

- Fats hydrolyzed into free fatty acids –> precipitate w/ Ca++ to produce a chalky gray material

39
Q

What does infarction mean?

A

Necrosis secondary to vascular insufficiency

40
Q

What is pyknosis?

A
  • Intensely dark staining
  • Shrunken nucleus
  • Seen in necrotic (dead) cells
41
Q

What is karyolysis?

A
  • Fragmentation of pyknotic nuclei
  • Extensive hydrolysis of the pyknotic nucleus w/ staining loss
  • Represents breakdown of denatured chromatin
42
Q

Hypoxia induces which transcription factor?

A

hypoxia-inducible factor 1

HIF1 alpha/beta

43
Q

Compare and contrast exertional and classic heat stroke

A

Common: Hot, dry skin

Exert: lactic acidosis, lead to: ATN, DIC, organ failure

Classic: respiratory acidosis, lead to: hypotension, coma

D&D Unit 2 (10 decks)

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