Cell Injury, Cell Death and Cell Adaptation #1 (1/11/16) Flashcards Preview

Pathology #1 > Cell Injury, Cell Death and Cell Adaptation #1 (1/11/16) > Flashcards

Flashcards in Cell Injury, Cell Death and Cell Adaptation #1 (1/11/16) Deck (32):
1

What is Etiology?

Origin of disease including underlying causes and modifiers (Why a disease occurs)

2

What is Pathogenesis?

Development of disease, from molecular/cellular changes to functional and structural abnormalities (How a disease occurs)

3

_____ is common to all forms of pathology.

Cellular injury

4

What are 7 causes of cell injury?

Hypoxia (decreased oxygen levels)
Infectious agents (TB, Herpes, Candidiasis)
Physical injury
Chemicals/drugs (Gingival hyperplasia, Burns)
Immune response (Allergic responses)
Genetic abnormalities (Downs, Cancer)
Nutritional imbalance (Scurvy, Diabetes)

5

T or F, Clinical signs and symptoms are usually several steps removed from the biochemical changes associated with cell injury?

True

6

What are common targets for cellular injury? (4)

Cell membranes
Mitochondria
Cell Proteins
DNA

7

What are the 6 Mechanisms of cell injury?

ATP depletion
Generation of ROS
Loss of Ca++ homeostasis
Altered membrane permeability
Mitochondrial damage
DNA and Protein damage

8

Describe the Hypoxia-Ischemia model....

1. So you get a thrombosis which blocks oxygen transport.
2. Oxidative phosphorylation decreases which decreases ATP production. (Increase in anaerobic glycolysis = decreased pH, lactic acid production, decreased glycogen stores and chromatin clumping)
2. This increases Na+ and Ca++ influx as we'll as K+ Efflux.
3. Leads to increased H20 influx
4. Leads to cellular swelling, membrane blebs, loss of villi and ER swelling.

9

The generation of ROS are associated with.....

- Inflammation
- Oxygen toxicity
- Chemical/drug metabolism
- Radiation
- Aging

10

How do ROS cause damage?

Lipid Peroxidation
Protein Fragmentation
Single Strand Breaks in DNA

11

Where are the major sites of single strand breaks by ROS?

Thymidine and Guanine

12

How are ROS's controlled?

Enzymes = Catalase, SOD and Glutathione peroxidase
Antioxidants = Vitamens E, A and C, Glutathione, cystine
Serum proteins that reduce/bind iron and copper needed to catalyze the formation of ROS.

13

How does Ca++ induced Cell injury proceed?

Increased cytoplasmic Ionic Ca++ can lead to ATPase, phospholipases, protein disruption (Via protease) and DNA damage (via endonuclease)

14

What determines the degree of cell injury?

- The Physiological state of the cell
- Intensity of the insult
- Duration of insult
- # of exposures to insult

15

What are the 3 possibilities after cell injury?

1. May be reversible
2. May result in adaptation
3. Cell death (Necrosis or apoptosis)

16

What are good examples of reversible cell injury?

Ischemia
Toxins
Infectious agents
Thermal injury

17

T or F, there is no biochemical event that equates with cell death.

True, there is no line in the sand that indicates recovery vs death.

18

What are the 4 types of Necrosis?

Coagulative = "Egg dropped into frying pan" = cells are frozen. Hypoxia-Ischemia.
Liquefactive = Liquid pus center (abscess)
Caseous = Granuloma forms around tissue with necrotic fluid in middle. (TB)
Enzymatic (Fat Necrosis) = Trauma to fatty tissue can release lipase that destroy fat.

19

Which type of Necrosis is most common?

Coagulative

20

What is Apoptosis important for (3 things)?

Normal cell turnover
Embryogenesis
Immune function

21

What are conditions that involve excessive apoptosis?

AIDS
Ischemia
Neurodegenerative diseases
myelodysplasia
Toxin induced liver injury

22

What are diseases that inhibit apoptosis?

Cancer
Autoimmune diseases
Viral diseases

23

Describe the morphology of Apoptosis...

1. Chromatin condensation
2. Progressive cell shrinkage
3. Plasma membrane blebbing
4. Apoptotic bodies
5. Phagocytosis = no inflammation

24

What are the 2 mechanisms of Apoptosis?

1. Mitochondrial (intrinsic) pathway
2. Death receptor (extrinsic) pathway
*END RESULT IS THE SAME WITH BOTH

25

What is the stimuli for Necrosis vs Apoptosis?

Necrosis is always pathologic, where apoptosis can be physiological or pathological.

26

______ occurs on a single cell basis where as ______ occurs at multiple cells.

Apoptosis = single cell
Necrosis = multiple cells

27

Is there inflammation with apoptosis?

No!

28

What is atrophy?

Decrease in cell size and function
From decreased:
- Nutrition
- Innervation
- Workload
- Blood supply

or Increased:
Age or local pressure

29

What is Hypertrophy?

Increase in cell size and function with concurrent increase in organ size and/or function.
From increased:
- Functional demand
- imbalance of nutrition
- hormonal stimulation (steroids)

30

What is Hyperplasia?

Increase in Cell NUMBER with concurrent increase in organ size/function.

31

What is Metaplasia?

Alteration in cell differentiation with concurrent alteration of tissue/organ function. *Squamous metaplasia of the bronchus due to smoking.
*Intestinal metaplasia of the esophagus

32

What are some examples of intracellular accumulations?

Triglycerides (Steatosis) = Fatty liver
Cholesterol= Yellow skin papules (Xanthoma) or in vessels (atherosclerosis)
Protein = Mallory bodies and Alzheimer's bodies
Carbs = Glycogen storage disease
Exogenous Carbon pigment = Anthracosis, Pneimoconicosis, amalgam tattoos, lipofuscin (Melanotic tattoo), Hemosiderin, Bilirubin.