Pathoma: Growth Adaptations, Cell Injury and Cell Death Flashcards

1
Q

By what mechanism does cellular hypertrophy occur?

A

Gene activation, protein synthesis and increased production of organelles

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2
Q

By what mechanism does hyperplasia occur?

A

Stem cell activation

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3
Q

Tissues that cannot undergo hyperplasia

A

Cardiac, nervous and skeletal muscle

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4
Q

Pathologic hyperplasia that does not increase risk of cancer?

A

BPH

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5
Q

3 mechanisms by which organ atrophy occurs?

A

Apoptosis, ubiquitin-proteosome degradation of cytoskeletal intermediate filaments and autophagy via vaculole-lysosomal degredation.

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6
Q

Mechanism by which the columnar cells in Barrett’s esophagus underwent metaplasia?

A

Stem cell reprogramming

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7
Q

Type of metaplasia that carries no increased risk for cancer?

A

Apocrine metaplasia of the breast

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8
Q

How does vitamin A deficiency cause keratomalacia?

A

Vitamin A is necessary for production of the thin squamous lining of conjunctiva. When it is absent, those cells undergo metaplasia to stratified keratinized squamous epithelium.

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9
Q

What is dysplasia?

A

Disordered cellular growth

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10
Q

When is dysplasia irreversible?

A

When cellular stress persists and it transitions to a carcinoma.

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11
Q

What is hypoxia?

A

Low oxygen delivery to tissue

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12
Q

Common causes of hypoxia

A

Ischemia (decreased arterial perfusion, decreased venous drainage or shock), hypoxemia (PaO2

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13
Q

Common causes of hypoxemia

A

High altitude, hypoventilation, diffusion defect and V/Q mismatch

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14
Q

First sign of CO poisoning?

A

Headache

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15
Q

PaO2 and SaO2 in CO poisoning and methemoglobinemia?

A

PaO2 is normal. SaO2 is decreased.

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16
Q

Why treat patients with methemoglobinemia with methylene blue?

A

It helps reduce Fe3+ to Fe2+

17
Q

How does hypoxia cause cellular injury?

A

Low O2 = low ATP production. Low ATP results in multiple problems:

  1. Na/K ATP pump dysfunction causes Na and H2O to build up in the cell and it swells
  2. Ca2+ ATP pump dysfunction causes Ca2+ build-up in cytosol
  3. Lactic acid build-up denatures proteins and precipitates DNA
18
Q

Cellular features that indicate reversible injury

A

Loss of microvilli and membrane blebbing secondary to cellular swelling.

Decreased protein synthesis from ribosomal dissociation from rER secondary to swelling.

19
Q

Signs of irreversible cellular injury

A

Plasma membrane damage results in enzyme leakage (troponins) and increased Ca entry.

Mitochondrial membrane damage results in loss of function of the ETC and cytochrome C leakage into cytosol.

Lysosomal membrane damage results in release of hydrolytic enzymes that are activated by already high intracellular Ca levels.

20
Q

How does the nucleus change as the cell dies?

A

Pyknosis -> Karyorrhexis -> Karyolysis -> No nucleus

21
Q

Characteristic histologic pattern of cell death in every organ except the brain?

A

Coagulative necrosis. Nucleus is absent, but cellular architecture is preserved by protein coagulation. Note that the area of infarcted tissue is typically wedge-shaped and pale. The area of infarction is red if blood re-enters after infarction.

22
Q

Characteristic histologic pattern of necrosis in the brain?

A

Liquefactive necrosis. This is a result of enzymatic lysis of cells and proteins. This also occurs in abscess (neutrophilic enzymes) and the pancreas (pancreatic enzymes)

23
Q

Characteristic histologic pattern of ischemia in a patient with lower limb or GI tract ischemia?

A

Gangrenous necrosis is coagulative necrosis that looks mummified, there may be superimposed liquefactive necrosis if the dead tissue becomes infected

24
Q

Characteristic histologic pattern of necrosis in a Tb or fungal infection?

A

Caseous necrosis. This occurs due to accumulation of fungal wall or mycobacterium in the infected necrotic tissue.

25
Q

Characteristic histologic pattern of necrosis in a woman hit in the breast by a baseball or a patient with acute pancreatitis?

A

Fat necrosis. This occurs because fatty acids release by trauma or lipases saponify with calcium to form a chalky-white necrotic tissue.

26
Q

How does dystrophic calcification differ from metastatic calcification?

A

Metastatic calcification deposits anywhere because there are high serum calcium or phosphate levels. In dystrophic calcification, dead tissue serves as a nidus for calcification and serum Ca is normal.

27
Q

Characteristic histologic pattern of necrosis in vasculitis and malignant hypertension?

A

Fibrinoid necrosis is a result of protein leakage into the vessel wall after it has been damaged, causing a bright pink/red stain on microscopy.

28
Q

Examples of genetically-programmed apoptosis

A

Endometrial shedding during the menstrual cycle, removal of tissue between toes in embryogenesis, CD8+ T-cell killing of virally infected cells, etc.

29
Q

Morphologic characteristics of apoptosis

A

Dying cells shrink, the nucleus fragments and apoptotic bodies fall from the cell. Macrophages eat these apoptotic bodies and eventually consume the cell WITHOUT ANY INFLAMMATORY RESPONSE!

30
Q

Mechanics of apoptosis

A

Cellular injury, DNA damage or decreased hormonal stimulation results in inactivation of Bcl2 in the mitochondia. This allows cytochrome c to leak into the cytosol from the inner mitochondrial membrane to activate caspases, proteases and endonucleases that breakdown the cytoskeleton and DNA.

31
Q

How does extrinsic receptor-ligand apoptosis occur?

A

FAS ligand binds FAS death receptor (CD95) on the target cell and activates intracellular caspases. This occurs in cellular selection in the thymus. Another mechanism is TNF binding to TNF-receptor on the target cell and caspase activation.

32
Q

How to CD8+ T-cells mediate apoptosis?

A

They secrete perforins to create pores in the target cell and granzyme enters the pores and activates caspases

33
Q
A