Cell and Tissue Injury (complete) Flashcards by Eooooo m

What type of tissue is involved in most cellular injuries?

Epithelia

THIS INCLUDES:

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

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What are the 7 major causes of cell injury?

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

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What are common physical agents involved in cell injury?

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

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Describe burns as it relates to cell injury

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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Describe hypothermia as it relates to cell injury

Basically —> CELLS FREEZE!

Salts precipitates out —> damages cells

Poor perfusion of tissues (blood flow issues)

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Describe electric shock as it relates to cell injury

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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Describe how cell injury contributes to the pathogenesis of disease

Disease = cell injury

No X cell? —> disease related to X cells

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Which types of cells are present in acute cell injury?

PMNs (polymorphonuclear leukocytes)

a type of WBCs

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Which types of cells are present in chronic cell injury?

Lymphocytes

Macrophages

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

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

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To what does an increase in extracellular metabolites lead?

Massive overproduction of intracellular molecules

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

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What do fatty changes in hepatocytes cause?

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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What is ischemic cell injury?

No oxygen

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How do neurons respond to ischemic cell injury?

Can only go 3-5 min w/o oxygen

After that —> irreversible damage

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How do cardiac myocytes respond to ischemic cell injury?

Can go 20 min w/o oxygen

After that —> irreversible damage

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

Can go up to 2 hours w/o oxygen

After that —> irreversible damage

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

Can go up to several hours w/o oxygen

After that —> irreversible damage

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What are free radicals?

Molecules with free/unpaired electron

From where do free radicals come?

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)

How do free radical produce cell injury?

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)

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

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

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

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

What happens when you give hypoxic pts lots of O2?

AKA: reperfusion

- Accumulate lots of free radicals

Compare and contrast necrosis and apoptosis.

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)

Contrast DNA segments resulting from necrosis and apoptosis.

Necrosis: random, lots of released unspecific endonucleases Apoptosis: chopped into discrete segments (very purposeful, specific by a particular enzyme)

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

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

What is atrophy?

Cell decreases in size and function

What is hypertrophy?

Cell increases in size (organelles, function) Ex: left ventricle enlarges to compensate for overload in chronic hypertension

What is metaplasia?

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

What is hyperplasia?

One cell type proliferates in a particular location Ex: with an endocrine tumor that produces ACTH, the adrenal cortex cells multiply like crazy

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

- 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

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

- 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

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

- In reversible injury: problems in nucleolus appearance | - Changes not well characterized b/c of some effect in rRNA synthesis ---> decrease in protein synthesis

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

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

Describe coagulative necrosis

- Dead cell = ghost-like remnant of former self - Nucleus shrinks ---> fragments ---> disappears Classic in heart after myo infarc

Describe liquefactive necrosis

- Dead cell dissolves away - Lysosomal hydrolases digest cellular components - Commonly seen in brain and spleen - Acute infection

Describe caseous necrosis

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

Describe fat necrosis

- Typically follows acute pancreatitis or trauma | - Fats hydrolyzed into free fatty acids --> precipitate w/ Ca++ to produce a chalky gray material

What does infarction mean?

Necrosis secondary to vascular insufficiency

What is pyknosis?

- Intensely dark staining - Shrunken nucleus - Seen in necrotic (dead) cells

What is karyolysis?

- Fragmentation of pyknotic nuclei - Extensive hydrolysis of the pyknotic nucleus w/ staining loss - Represents breakdown of denatured chromatin

Hypoxia induces which transcription factor?

hypoxia-inducible factor 1 HIF1 alpha/beta

Compare and contrast exertional and classic heat stroke

Common: Hot, dry skin Exert: lactic acidosis, lead to: ATN, DIC, organ failure Classic: respiratory acidosis, lead to: hypotension, coma