module 2 Altered Cellular Biology

Question 1

1. What is the plasma glucose level necessary for homeostasis? Ca2+?
2. What happens when cells suffer an irreversible injury?
3. When cells adapt to pathological changes, is this temporary or permanent?
4. Name the 5 cellular adaptations:

Answer 1

1. 80-120 mg/dl, 8-10mg/dl
2. Either Apoptosis or necrosis
3. permanent
4. atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia

Question 2

1. Name the cellular adaptation in which there is a decrease in cell size, aka wasting away?
2. Why is the size reduced?
3. Name the potential causes of atrophy
4. How does atrophy work (what are it’s mechanisms)?
5. Name the cellular adaptation in which there is an increase in cell size without increasing number of cells:
6. Which two organs can become hypertrophic in a non-damaging, physiological sense?
7. Name an organ that be hypertrophic in a pathological sense:

Answer 2

1. atrophy
2. loss of intercellular substance
3. Decreased workload, Decreased blood flow, Decreased nutrition, Decreased endocrine stimulation (menopause). Denervation, and Aging (involution)
4. Decreased protein synthesis, and Increased protein degradation.
5. Hypertrophy
6. uterus (in pregnancy) and heart (when in response to a non-disease reason)
7. Left ventricle w/ valvular disease

Question 3

1. What is hyperplasia?
2. Hyperplasia of the ……… and ……… come from physiologic ……….. stimulation. Hyperplasia of the …….. and ……….. come from compensation (but are still physiological). think if you removed a kidney what would happen to the other
3. What are the 2 pathological triggers for hyperplasia?

Answer 3

1. Increasing the size by increasing the number of cells
2. Breast (nursing), and uterus, hormonal. Liver, and kidney
3. excessive hormones and growth factor stimulation.

Question 4

1. What is the name for the Reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type? Why does this happen (in response to what)? Is this a protective mechanism?
2. Give 3 examples of metaplasia:
3. What is one disadvantage to metaplasia?
4. What are the mechanisms of metaplasia?
5. What is dysplasia? What is it in response to? Is it an adaptation?
6. How is dysplasia graded and is it cancerous?
7. Give 2 examples of dysplasia:

Answer 4

1. metaplasia, chronic irritation, yes protective mechanism.
2. tobacco smoking causing squamous metaplasia, acid reflux causing gastric metaplasia (Barret esophagus), osseous metaplasia
3. may predispose to malignant transformation.
4. Reprogramming of stem cells to differentiate
   - Induced by cytokines, growth factors and other environmental signals
   - Retinoic acid may play a role.
5. presence of abnormal cells within a tissue or organ. In response to severe, constant irritation. Not an adaptation.
6. Graded from low, which may be reversible to high often synonymous w/ cancer
7. cervical from HPV or colon polyps.

Question 5

1. what happens if a cell is unable to maintain homeostasis?
2. What is hypoxia, and what causes it?
3. What is ischemia?
4. What is the single most common cause of hypoxia?
5. What are some causes of hypoxic injury?

Answer 5

1. if reversible, it will recover, if irreversible, it will die.
2. A state of reduced oxygen within the tissues. Ischemia causes it.
3. Insufficient blood flow to tissues
4. ischemia
5. Reduced O2 in air
   • Loss or reduced efficacy of hemoglobin
   • Decreased production of red blood cells
   • Resp or cardio disease
   • Poisoning of the oxidative enzymes (cytochromes) within the cells.

Question 6

1. Can hypoxic injury be worsened by restoration of
   blood flow and oxygen? What is this called?
2. In which ways does ischemia reperfusion cause further injury?
3. What are free radicals and What causes them?
4. How do free radicals injure cells?
5. How is excess intercellular calcium dangerous?

Answer 6

1. yes. called ischemia-reperfusion injury
2. it causes Oxidative stress, Increased intracellular calcium, Inflammation, and Complement activation
3. Reactive Oxygen Species (ROS) end products of O2 use. Caused by reperfusion, radiation, and toxins.
4. They damage DNA, cause misfolded proteins, and damage cell membranes.
5. it acts as an enzyme that activates other enzymes that breaks down membranes, reduces ATP production,
   breaks down nucleus) etc.

Question 7

1. Intracellular accumulations (aka infiltrations)and systemic manifestations are a result of ………….. ………. .
2. What types of substances accumulate in cells when they are injured?
3. What is dystrophic calcification vs metastatic calcification?
4. How do substances accumulate in cells, and what happens?
5. Give a classic example of cellular accumulation:
6. What enzyme is involved in breaking down alcohol in the liver and what is it’s end product? Why is this dangerous?
7. What are 2 more examples of cellular accumulation?

Answer 7

1. cellular injury.
2. Lipids, glycogen, protein, melanin, bilirubin, and calcium.
3. Both are an accumulation of calcium in cells. However, dystrophic occurs in areas of necrosis and atherosclerosis whereas metastatic occurs in normal tissues when there is hypercalcemia
4. via Inhalation, ingestion, infection. Cells can’t remove substances because their packing and transport mechanisms are shut down. Proteins get misfolded, and vital enzymes not produced.
5. fatty liver (shiny, smooth look).
6. alcohol dehydrogenase - aldehydes. Excess of aldehydes hinders liver ability to break down lipids.
7. bruising and bilirubin

Question 8

1. How does necrosis differ from apoptosis?

2. - 6. Name the 5 patterns of necrosis and their “key word”:

Answer 8

1. Necrosis: loss of membrane integrity, leakage of cellular components and triggers INFLAMMATORY RESPONSE. Necrosis cell swells/ apoptosis shrinks
2. Coagulative Necrosis: most common. Caused by ISCHEMIA. Not in CNS.
3. Liquefactive Necrosis: specific to CNS caused by ischemia or infection. Hydrolytic enzymes released.
4. Caseous: Cheese looking.. granuloma, Tuberculosis. Combo of coagulative and liquefactive.
5. Fat Necrosis: pancreatitis. Produces lipase, breaks down fats and blood vessels, forms calcium salts, hemorrhage
6. Gangrenous Necrosis: coagulative necrosis and bacterial infection. Dry and wet versions. Happens to limbs, intestines. Not a distinct pattern

Question 9

1. What are the 2 pathways to apoptosis?
2. What gene do both pathways signal to?
3. Name the gene that signals cell survival, countering the apoptosis gene?
4. What is an autophagic vacuole?

Answer 9

1. intrinsic pathway - signal comes from inside the cell (ex: protein misfolding) Bcl-2.

extrinsic pathway: signalled from outside cell (ex: Tumor Necrosis Factor calls cell to die).

2. Bcl-2 apoptosis gene
3. Bci
4. a package surrounding a part of the cell undergoing apoptosis so it doesn’t leak dangerous enzymes everywhere.