Pathoma: Growth Adaptations, Cell Injury and Cell Death Flashcards Preview

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Flashcards in Pathoma: Growth Adaptations, Cell Injury and Cell Death Deck (33)
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1

By what mechanism does cellular hypertrophy occur?

Gene activation, protein synthesis and increased production of organelles

2

By what mechanism does hyperplasia occur?

Stem cell activation

3

Tissues that cannot undergo hyperplasia

Cardiac, nervous and skeletal muscle

4

Pathologic hyperplasia that does not increase risk of cancer?

BPH

5

3 mechanisms by which organ atrophy occurs?

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

6

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

Stem cell reprogramming

7

Type of metaplasia that carries no increased risk for cancer?

Apocrine metaplasia of the breast

8

How does vitamin A deficiency cause keratomalacia?

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.

9

What is dysplasia?

Disordered cellular growth

10

When is dysplasia irreversible?

When cellular stress persists and it transitions to a carcinoma.

11

What is hypoxia?

Low oxygen delivery to tissue

12

Common causes of hypoxia

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

13

Common causes of hypoxemia

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

14

First sign of CO poisoning?

Headache

15

PaO2 and SaO2 in CO poisoning and methemoglobinemia?

PaO2 is normal. SaO2 is decreased.

16

Why treat patients with methemoglobinemia with methylene blue?

It helps reduce Fe3+ to Fe2+

17

How does hypoxia cause cellular injury?

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

Cellular features that indicate reversible injury

Loss of microvilli and membrane blebbing secondary to cellular swelling.

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

19

Signs of irreversible cellular injury

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

How does the nucleus change as the cell dies?

Pyknosis -> Karyorrhexis -> Karyolysis -> No nucleus

21

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

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

Characteristic histologic pattern of necrosis in the brain?

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

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

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

24

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

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

25

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

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

26

How does dystrophic calcification differ from metastatic calcification?

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

Characteristic histologic pattern of necrosis in vasculitis and malignant hypertension?

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

Examples of genetically-programmed apoptosis

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

29

Morphologic characteristics of apoptosis

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

Mechanics of apoptosis

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.