Growth Adaptations, Cellular Injury and Cell Death Flashcards Preview

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Flashcards in Growth Adaptations, Cellular Injury and Cell Death Deck (64)
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Mechanism of cellular hypertrophy

Increased cellular stress -> increased gene activation -> increased protein synthesis and production of organelles


Permanent tissues that can only undergo hypertrophy

Cardiac myocytes, skeletal muscle and nerve


Pathologic hyperplasia that does NOT have an increased risk for progression to dysplasia and cancer

Benign prostatic hyperplasia


Mechanisms of cellular atrophy

Apoptosis decreases cell number and decreased cell size occurs via ubiquitin-proteosome degradation of cytoskeletal proteins and vacuole autophagy of organelles.


Mechanism of metaplasia

Change in type of stress -> reprogramming of stem cells -> change in cell type to better hand stress. This most commonly occurs in surface epithelium.


3 types of epithelium

Squamous (keratinizing vs. non-keratinizing), columnar and transitional (urothelium).


Barrett esophagus metaplasia. What happens if the patient is treated and acid exposure decreases?

Esophageal non-keratinized squamous epithelium changes to columnar, non-ciliated, mucinous epithelium in response to increased gastric acid exposure in the esophagus. Remember that metaplasia is reversible and the epithelium can return to normal if the exposure is eliminated.


Type of metaplasia that does not increase the risk for cancer?

Apocrine metaplasia associated with fibrocystic changes in the breast.


Vitamin A deficiency metaplasia

Vitamin A is necessary for maintenance of the specialized squamous epithelium of the eye (conjunctiva). When vitamin A is deficient, the epithelium undergoes metaplasia


Myositis ossificans metaplasia

Inflammation of the skeletal muscle from trauma that results in metaplasia to bone within the muscle.


Consequence of longstanding pathologic hyperplasia or metaplasia?

Dysplasia, which is a disordered cellular growth pattern.


What is the distinction between dysplasia and cancer?

Cancer is irreversible and dysplasia is reversible.


Classic example of aplasia

Unilateral renal genesis from failure of cell production during embryogenesis.


Classic example of hypoplasia?

Streak ovary in Turner syndrome from decreased cell production during embryogenesis.


When does cellular injury occur vs. adaptation?

Injury occurs when the insult exceeds the cell's ability to adapt. This is determined by the type of stress, its severity and the type of cell affected.


Hypoxemia vs. hypoxia

Hypoxemia = low PaO2. Hypoxemia = low O2 delivery to tissue, leads to decreased ATP and cellular injury.


3 major causes of hypoxia

Ischemia (ACS, shock and Budd-Chiari syndrome), hypoxemia (PaO2


PaO2 and SaO2 in anemia

Both are normal in anemia


PaO2 and SaO2 in CO poisoning

PaO2 in normal, SaO2 will be decreased.


A patient is found dead in his house with a cherry red appearance to the skin. What symptom would have been the earliest sign of illness?

Headache -> confusion -> coma -> death in CO poisoning.


PaO2 and SaO2 in methemoglobinemia

PaO2 normal, SaO2 decreased to due oxidation of Fe2+ to Fe3+ and inability to bind O2.


A patient presents with cyanosis and chocolate-colored blood. What are risk factors for the condition he had.

Oxidant stressors such as sulfa drugs and nitrates can cause methemoglobinemia. Newborns can also develop methemoglobinemia due to immature machinery that reduces Fe3+ back to Fe2+.


Treating methemoglobinemia?

IV methylene blue reduces Fe3+ back to Fe2+ (Fe2 binds O2)


How does low ATP from hypoxia result in cellular injury?

ATP is necessary for Na-K pump. Lack of ATP results in Na accumulation in the cell, cellular swelling and cellular injury. ATP is necessary for the Ca pump. Lack of ATP results in Ca accumulation in the cell and enzyme activation. Finally, lack of ATP results in increased production of lactic acid via aerobic glycolysis. This reduces intracellular pH and causes precipitation of DNA and proteins.


Hallmark findings in reversible cellular injury.

#1 = cellular swelling. This manifests as loss of microvilli, membrane blebbing and swelling of the rough endoplasmic reticulum leading to the ribosomes falling off and reducing protein synthesis.


Hallmark findings in irreversible cellular injury.

Membrane damage. Plasma membrane (cardiac enzymes in MI, LFTs in hepatitis, increased intracellular Ca), mitochondrial membrane (ETC damage, cytochrome C-induced apoptosis) and lysosomal membrane (release of lytic enzymes into cytosol).


Hallmark findings in cellular death.

Hallmark = loss of the nucleus. The nucleus is lost by pyknosis (shrinks), karyorrhexis (breaks up) and karyolysis (broken down).


Mechanisms of cell death

Necrosis (involves a large group of cells, is followed by ACUTE INFLAMMATION and is never physiologic) and apoptosis.


Subtypes of necrosis

Coagulative, liquefactive, gangrenous, caseous, fat and fibrinoid necrosis.


Coagulative necrosis

Necrotic tissue that remains firm due to protein coagulation. Cellular architecture is preserved and nucleus is gone. This is the classic type of necrosis seen in ischemic infarction. Note the loss of nuclei and preserved architecture in the image on the left.