TEST 1: Cellular Biology Flashcards

1
Q

Hyperplasia

A

-Increase in NUMBER of cells
-pathologic: menstruation
-pathophysiologic: BPH, anemia
-only in dividing cells (not in heart or brain)

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2
Q

Metaplasia

A

-one cell replaces another cell that’s better able to tolerate the environment
(Reversible) usually change isn’t beneficial
-pathological: not normal, no example
-pathophysiologic: lung Ca, GERD
-epithelial cells

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3
Q

Dysplasia

A

-not a true adaptation
-disorganized cell growth
-can lead to cancer/ pre-cancerous
-from chronic irritation/ inflammation (remove irritant cause)
-no “good” dysplasia

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4
Q

2 ways hypoxic- ischemic injury to cells can occur

A
  1. Mitochondrial injury
  2. Calcium influx injury
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5
Q

Mitochondrial injury that causes ischemic cell damage occurs by

A

-damage to cytochromes (proteins that are involved in electron transport)
-ATP synthesis fails, which causes failure of ion pumps to function (mitochondria can’t make ATP and thus have no energy)
-endoplasmic reticulum begins to fail (cells are swollen but doesn’t work well in that environment; still reversible)
-if hypoxia continues, structure starts to fail—> swollen, inflamed, cytoskeletal structure breaks down and ATP is lost—> cell death

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6
Q

Mitochondrial damage that is caused by calcium influx injury occurs by

A

-happens as a result of calcium influx into the cell by loss of function from NA/K and NA/Ca pumps
-more NA and Ca that goes into the cell results in increased cellular edema (potassium increases extracellularly)
-damage to the membrane makes it hard to produce ATP, nucleic acids, and ribonucleic acids
-increase Ca into the cell causes enzyme activation that leads to cell death

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7
Q

How do you know hypoxic injury is occurring

A

Lysosomes are digesting cytoplasmic and nuclear components, so lysosomes leak acid into the blood, causing:
-increases in lactic acid
-increases in troponin
-increases in transaminases

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8
Q

Reperfusion injury

A

-when oxygen is reintroduced to cells after hypoxia or ischemia
-huge amount of ATP production to attempt to repair, BUT this huge increase causes excessive oxygen reactive species, which leads to oxidative stress (body can handle only a small amount of ROS at a time)
-ROS damages the cell membrane

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9
Q

Oxidative stress

A

-associated with: aging, DM, CA, autoimmune disease (chronic inflammation)
-ROS that cause this: hydroxyl radicals, superoxide, hydrogen peroxide, nitric oxide
-you need SOME level of these in normal function in order to signal to cells to regulate enzymes and transcription factors

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10
Q

What are Reactive oxygen species & how to handle them

A
  • AKA “free radicals)
    -are electrically charged molecules (that have an unpaired electron) that scavenge for electrons to make to neutral which damages carbs, lipids, proteins, and DNA
    -antioxidants neutralize the effect of ROS (Vitamins, C,E, flavonoids, beta carotene)
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11
Q

Cell injury by chemical agents

A

-damages cell membrane integrity
-membrane either directly affected by the chemical agent or the free radicals that it generates
-can be due to one large injury or multiple small insults over time

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12
Q

Cell injury by chemical agents

A

-damages cell membrane integrity
-membrane wither directly affected by the chemical agent or the free radicals that it generates
-can be due to one large injury or multiple small insults over time

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13
Q

Cell injury from therapeutic drugs

A

-Tyelonal OD
-Antibiotics (vanco=renal) (quinolones= tendon rupture & nerve injury)

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14
Q

Cell injury from non- therapeutic drugs

A

-Arsenic: replaces phosphate in ATP (damaged mitochondrial function + cell death)
-cyanide: deadly after one exposure, blocks intracellular use of oxygen (results in hypoxic injury + cell death)
-Lead: disrupts calcium homeostasis (cells uptake leads instead of key elements)
-Mercury: binds with proteins and lipid soluble aka allows crossing into the BBB and accumulation in the brain

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15
Q

Arsenic

A

-is naturally found in soils/ water/ products
-used in leukemia treatment
-slow accumulation over time is deadly
-replaces phosphate in ATP and thus damaging mitochondria

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16
Q

Cyanide

A

-deadly after one exposire
-blocks the intracellular use of oxygen
-naturally occurring substance

17
Q

Lead

A

-found in soil, dust, water, old paint
-disrupts calcium homeostasis and is more readily up-taken than iron, vitamin d, calcium, magnesium, zinc
-builds up over time
-causes neuro developmental, musculoskeletal, endocrine, reproductive, and dental issues
-NO safe level for children

18
Q

Mercury

A

-found in soil, water, fish, seafood
-most problematic source is found in water, liquid at room temp
-binds with proteins, is lipid soluble so crosses the BBB and accumulates in the brain
-also generates nitrous oxide and free radicals that causes cell necrosis and apoptosis
-causes neurological toxicity

19
Q

Ethanol

A

-we ingest via alcohol—> absorbed by stomach/small intestines—> transported to liver—> distributed to all tissues and fluids in body—> liver enzymes metabolize ethanol to acetaldehyde
-when too much is consumed, liver converts to acetaldehyde that produces ROS (which in turns damages DNA, proteins, lipids)
- Body sees ETOH as a nutrient (specifically a carb that replaces nutrient rich foods) and leads to nutritional deficiencies (mag, b6, thiamine, folic)
-causes: wernicke encephalopathy, peripheral neuropathy, cirrhosis, portal HTN, hepatotoxicity

20
Q

Carbon Monoxide (CO)

A

-from combustion sources (wood, engine exhaust, propane)
-binds to hemoglobin, forming carboxyhemoglobin, which prevents oxygen transport
-CO levels > 10% indicate poisoning, need treatment levels > 30%
- causes: dizziness, confusion, tired, SOB
-treatment: 100% oxygen or hyperbaric oxygen chamber

21
Q

Physical agents that cause cell injury

A
  1. Temperature:
    -hypothermia
    slows metabolism, stops ATP production
    -hyperthermia
    increases metabolism + generates ROS
    -cell death from temp extremes
  2. Radiation
    -increases cellular reactivity
    -“safe” threshold of radiation (except nuclear weapons)
    -can cause cancer and genetic alterations
  3. Mechanical
    -trauma, rearrange cells, interferes with communication and protein synthesis
    -cause injuries from: compression, tension, shear, or torsion
22
Q

Apoptosis

A

-programmed cell death
-normal process of cells to maintain tissue homeostasis and eliminate damaged/ potential harmful cells
-during: cell shrinks, chromatin condenses, and cell fragments into membrane bound apoptotic bodies, which are then phagocytosed by macrophages (without triggering inflammatory response)
-this process relies on ATP and is characterized by activation of caspases
-cellular components are kept intact and does not have negative consequences

23
Q

Caspases

A

-are a family of aspartic acid specific enzymes that trigger proteolytic activity in response to signals received that induce apoptosis
-activated caspases cleave to other proteins in the system that initiate a series of reactions known as the “suicide cascade”
-Caspar activation triggers the mitochondrial (intrinsic pathway) and the death receptor (extrinsic pathway)

24
Q

Necrosis

A

-uncontrolled cell death that can result from trauma, infection, toxin, or ischemia
-not contained because injured cells swell and lose membrane integrity, then cell contents spill out into extracellular spaces which triggers an inflammatory response
-does not require energy and is considered a passive process

25
Q

Apoptosis issues

A

-Insufficient: allows for uncontrolled cell proliferation, can lead to cancer
-excessive: as seen in neuro degenerative disorders that result in a vital loss of neurons or autoimmune diseases

26
Q

Autophagy purpose

A

-Greek meaning “self- eating”
-process by which cells maintain their homeostasis and survival by degrading and recycling their own components
-self destructive process that delievers cytoplasmic contents to the lysosome for degradation
-process involves formation of autophages, which engulf damaged or superfluous cell complete and fuse with lysosomes where the components are degraded and recycled

27
Q

Mechanism of autophagy

A

-when cells are exposed to stress the autophagic process is triggered to maintain cell homeostasis
-catabolic process
-lysosomes (specialized organelles containing hydrolytic enzymes) are crucial to the process by breaking down cell components into their basic building blocks (amino acids, fatty acids, sugar). The salvaged nutrients are then re-used by the cell to to support essential functions: primarily ATP generation, repairing damaged structures, and sustaining cells through period la of metabolic stress

28
Q

Benefits of autophagy

A
  1. Nutrient recycling: provides essential nutrients/ energy but degrading non essential/ damaged cell components (especially during starvation/ nutrient scarcity)
  2. Damage control: removes damaged organelles such as mitochondria or misfolded proteins to prevent cellular dysfunction
  3. Cell homeostasis: helps maintain cell integrity/ function by constantly turning over cell components
29
Q

Autophagy energy requirement

A

-Autophagy is an energy dependent process requiring ATP
-by degrading and recycling cell components more ATP is generated (resulting a net gain of energy and nutrients for the cell)

30
Q

Autophagy pathological context

A

-Excessive/ diysregated activation: can lead to excessive degradation of cell components impairing essential functions + accelerating cell death (Alzheimer’s disease + cancer)
-in cancer can have a dual role, either promoting survival of cancer cells or contributing to cell death when over activated

31
Q

Hypoxia vs Ischemia

A

Hypoxia = lack of Oxygen

Ischemia = lack of blood flow