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805 > Lecture 2 (Quiz 2) > Flashcards

Lecture 2 (Quiz 2) Flashcards

1
Q

Plasma Membrane

A

Phopholipid bilayer with proteins, lipids, and carbohydrates integrated into it at varying levels. (Fluid Mosaic) Acts as a protective membrane that regulates what enters and leaves a cell (selectively permeable),

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2
Q

Mitochondria

A

POWER HOUSE OF THE CELL. Takes oxygen and broken down components of the diet to make ATP. Houses ETC = largest ATP producer. Also utilizes proton gradient that the ETC produces to create ATP by pumping in protons.

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3
Q

Transport Types

A

Simple Diffusion
Facilitated Diffusion
Active Transport
Group Translocation

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4
Q

Rough Endoplasmic Reticulum

A

Covered in ribosomes, located directly by the nucleus, site of protein synthesis

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5
Q

Smooth Endoplasmic Reticulum

A

No ribosomes, connected to RER but further from the nucleus, site of lipid & carbohydrate synthesis as well as some detoxifying functions.

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6
Q

Golgi Apparatus

A

Final check and packaging point to send things out of cell or accept things in from out of the cell.

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7
Q

Categories of Cellular Stress/Injury Response (3)

A
  1. Reversible
  2. Adaptive
  3. Death
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8
Q

Reversible Response

A

Withstands assault with quick, adaptive change, then returns to normal. Short-term stress/injury

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9
Q

Adaptive

A

Changes structure/function to adapt and is USUALLY reversible when assault is gone. Longer term stress/injury

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10
Q

Death

A

Apoptosis or necrosis of cell with stress/injury is too severe

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11
Q

Types of Reversible Responses (2)

A
  1. Hydropic swelling

2. Accumulation of Macromolecules

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12
Q

Hydropic Swelling

A

Accumulation of water in cells that cause swelling of the organ (ex: hepatomegaly)

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13
Q

How does Hydropic Swelling Happen?

A

Sodium-Potassium pumps fail which disrupts their corresponding gradients, causing water to follow sodium into the cell.

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14
Q

Why do the pumps fail?

A

Decreased availability of oxygen (hypoxia) and increased concentrations of chemicals that inhibit the ETC cause the ETC to stop, the hydrogen gradient to not be maintained, and, therefore, ATP not to be produced. In most cells, 30% of their ATP supply goes to keeping the pumps going, even higher in organs like the brain (90%).

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15
Q

Issues Associated with Accumulation (3)

A
  1. Toxicity
  2. Inflammation
  3. Crowding that disrupts cellular function
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16
Q

Categories of Accumulation (3)

A
  1. Accumulation of Normal Substances
  2. Accumulation of Abnormal Proteins
  3. Accumulation of Indigestional Particles
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17
Q

Normal Substances to Accumulate (3)

A
  1. Lipids
  2. Carbohydrates
  3. Proteins
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18
Q

Examples of Accumulating Lipids

A
  • Chronic Alcohol Ingestion - preferentially metabolizes alcohols over lipids leading to excess fatty vacuoles in the liver (fatty liver)
  • Tay-Sachs Disease
  • Gaucher Syndrome
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19
Q

Example of Accumulating Carbohydrates

A

Diabetes Mellitus - impaired uptake of glucose causes it to enter filtrate and leads to excess glycogen stores in renal tubule cells

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20
Q

Example of Accumulating Proteins

A

Renal tubules accumulating proteins due to leaky glomerular capillaries, endocytosis of escaped proteins, or excess accumulation

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21
Q

How Abnormal Proteins Accumulate

A

Stress causes protein denaturation. The denatured proteins can then be fixed and refolded by things like chaperone proteins or be “murdered” via ubiquitination. If either of these pathways are not working properly, abnormal proteins can build up and accumulate in the cell.

22
Q

Types of Indigestional Particles (2)

A
  1. Exogenous - tattoos, Black Lung, etc.

2. Endogenous - Bilirubin

23
Q

Bilirubin Accumulation

A

Example of Endogenous Indigestional Particle Accumulation. Pigmented byproduct of metabolized RBCs and heme. Lots of reasons can lead to its accumulation like bad livers, excessive breakdown of RBCs, overproduction of hemoglobin, etc. If it does accumulate it causes a yellowing of the white of the eyes (sclera) and even the skin, in high levels.

24
Q

What causes brain damage in neonates?

A

Unconjugated Bilirubin

25
Q

Reasons Bilirubin Accumulates in Neonates (3)

A
  1. Rh-factor mediated hemolysis
  2. Lack of intestinal bacteria (metabolize conjugated bilirubin into unconjugated bilirubin which is reabsorbed)
  3. B-glucuronidase found in breast milk
26
Q

What is done to treat neonates with bilirubin accumulation?

A

Phototherapy (450 nm). Breaks down Bilirubin into water soluble photoisomers that can be excreted.

27
Q

Five Classes of Adaption to Stress

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
  5. Dysplasia
28
Q

Atrophy

A

Decrease in size and function. Minimizes nutrient consumption, energy consumption and production, and a decrease of organelles and structures (NOT cytosol).

29
Q

Causes/Example of Atrophy

A

Causes: Bedridden, disuse, ischemia, age, chronic injury/disease, lack of trophic signals (growth factors)

Example: Alzheimer’s, brain atrophy

30
Q

Hypertrophy

A

Increase in size and function due to increased physiologic or mechanical demands

31
Q

Hypertrophy Examples

A
  1. Increase in skeletal muscle cells size. Increased demand, increases myosin and actin, adds thickness to the cell (enlargening present cells, not adding more)
  2. Increase in heart muscle size to try and counteract weak muscle contractions
32
Q

Hyperplasia

A

Increase in cell number (mitosis).

33
Q

Hyperplasia Examples

A
  1. Increase in endometrial cells in response to estrogen to prepare for pregnancy
  2. Chronic irritation leading to calluses and corns
  3. RBC production when changing from low to high altitude
  4. Neutrophils (WBCs) increase during bacterial infections
34
Q

Metaplasia

A

Conversion of one cell type to another. Adaptive response to chronic injury.

35
Q

Metaplasia Examples

A
  1. Chronic smokers have a change from columnar with villi to stratified squamous
  2. Chronic acid reflux leads to cells of esophagus changing to cells of intestinal tract that produce things like goblet cells
36
Q

Dysplasia

A

Abnormal variations in size, shape, and arrangement with no pattern. Significant change to become cancerous.

37
Q

Irreversible Cell Death Reason + Paths

A

Injury too severe or prolonged to be repaired.

Paths:

  1. Apoptosis - precise & controlled, clean, via phagocytosis
  2. Necrosis - decomposes & “explodes,” leads to inflammation
38
Q

Apoptosis

A

“Programmed Cell Death.” Regulated tissue recycling (remodeling) can use this to balance between cell death and mitosis of new cells. Occurs in myocardial infarcation, cancer cell death, and Alzheimer’s as well

39
Q

Extrinsic Signals for Apoptosis

A
  1. Lack of survival signals activating cell (growth, cell to cell interactions, or oxygen)
  2. Activation of death receptors by Fas ligand.
40
Q

Intrinsic Signals for Apoptosis

A
  1. DNA damage too great
  2. Mitochondrial failure
  3. Oxidative stress
  4. P53 protein - key signal (cancer cells don’t have)
41
Q

Examples of Apoptosis

A
  1. Cellular aging leading to DNA damage and activating apoptosis signals
  2. Predetermined cell death by telomeres becoming too short after multiple mitotic cycles (can be offset b germ/stem cells lengthening the telomeres)
42
Q

Hypoxia v.s. Ischemia

A
  1. Hypoxia - oxygen deficiency that impairs ATP production
  2. Ischemia - most common cause of hypoxia, faster than other methods (lung disease, RBS disorders), involves lack of waste removal and nutrient delivery
43
Q

Brian + Hypoxia/Ischemia

A

Ischemia - most acute brain injury. Primary - stroke, secondary - vasospasm, conpression, etc.
Hypoxia - Less severe, still damaging

44
Q

Neurons + Oxygen

A

HYPERSENSITIVE to oxygen levels. High demand of ATP (80-90% used for NA+/K+ pumps), lack of oxygen storage molecules, can’t function anaerobically

45
Q

Hypoxia Events in Neurons (7)

A
  1. Lose ATP Production
  2. Na+/K+ Pumps Fail
  3. Hydropic Swelling
  4. Mitochondrial Failure
  5. Lactic Acidosis
  6. Excessive Glutamate
  7. Reperfusion
46
Q

Mitochondrial Failure Events (5)

A
  1. Control of intracellular calcium lost
  2. Destructive proteases activated
  3. Oxidative stress builds leading to free radical formation
  4. Membrane integrity lost
  5. Strong signals for apoptosis
47
Q

Lactic Acidosis

A

Lack of oxygen causing anaerobic fermentation to occur and lactic acid to build up. Damages membrane proteins and instigates apoptosis signals

48
Q

Excessive Glutamate

A

Excitatory amino acid that is released excessively during ischemia events and induces cell injury and impacts ion channels

49
Q

Ion Channels Affected by Glutamate

A
  1. AMPA - sodium floods into cell and depolarizes membrane
  2. NMDA - depolarized membrane causes magnesium to release. More sodium enters cell along with calcium which causes more reactive species to form and oxidative stress
50
Q

Reperfusion

A

Presents danger in prolonged ischemic events. Increased calcium overloads cells –> oxygen radicals form –> increased damage to proteins and membranes –> triggers apoptosis

805 (18 decks)

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