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Essential Medical Science - MoD > Lecture 3 MoD > Flashcards

Lecture 3 MoD Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

How to maintain a healthy living cell?

A

Preservation of genetic integrity
Normal enzyme content
Intact membranes and transmembrane proteins
Adequate supply of substrates and oxygen

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2
Q

What is cell injury?

A

Biochemical and/or morphological changes that occur when the steady state is perturbed by adverse influences.

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3
Q

Draw cell injury pathway

A

refer lecture

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4
Q

What is hyperplasia?

A

Increase in number of cells

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5
Q

What is hypertrophy?

A

Increase in the volume of an organ or tissue due to the enlargement of its component cells. (Increase cell size)

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6
Q

What is atrophy?

A

decrease in the size of cell

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7
Q

What is metaplasia?

A

Change in cell morphology

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8
Q

What are the different types of cellular adaptation?

A

Hyperplasia
Metaplasia
Hypertrophy
Atrophy

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9
Q

What are the aetiology of cell injury? (5)

A 
Low oxygen availability
Physical trauma
Chemical agents
Infectious organisms
Irradiation
Others:
-Immunological
-Lack of essential nutrients/vitamin
-Genetic disorders
-Ageing
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10
Q

What are the meaning of hypoxia, anoxia and ischaemia?

A 
Hypoxia = lack of oxygen
Anoxia = absence of oxygen
Ischaemia = lack of blood flow.
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11
Q

What causes hypoxia and anoxia?

A

reduction or loss respectively of oxygen delivered to cells, often caused by ischaemia

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12
Q

What will happen as the result of reoxygenation?

A

Reperfusion - generation of oxygen free radicals

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13
Q

What are the factors that cause physical trauma?

A 
Mechanical trauma
-Disruption of cell structure
-Thrombosis leading to ischaemia
Extremes of temperature
-Heat denaturation of proteins
-Ice crystals
-Fever
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14
Q

What are the examples of chemical agents that cause cell injury?

A 
Alcohol
Tobacco smoke
Drugs
Poisons
Environmental
Occupational
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15
Q

What are the examples of infectious organisms that cause cell injury?

A

Bacterial toxin

  • Exotoxins
  • Endotoxins
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16
Q

In what way does infectious organisms infect normal cells?

A

Hijacking of cell machinery by viral infection -> cell lysis

Collateral damage by inflammation

17
Q

Which organs have high sensitivity to radiation?

A

in bone marrow, gonads, intestines

18
Q

Which organs have low sensitivity to radiation?

A

Uterus, pancreas and adrenal

19
Q

What is the effect of radiation?

A

can induce inflammatory response several

hours after exposure

20
Q

What are the targets of cell injury?

A 
Mitochondrial function
Membrane integrity and function
Protein synthesis
Cytoskeleton
Genetic apparatus
21
Q

What are the events that have a central role in mediating effects on multiple intracellular systems?

A

Diminished oxidative phosphorylation and reduced ATP level

22
Q

What are the factors that lead to cellular swelling, loss of microvilli, blebs and ER swelling?

A

Activity of plasma membrane ATP-driven “sodium pump” is reduced, with consequent influx of sodium and calcium,

23
Q

What are the sequence of events that lead to lipid deposition?

A

Decreasing pH and ATP levels cause ribosomes to detach from rough endoplasmic reticulum and reduction in protein synthesis which lead to lipid deposition

24
Q

What can cause sublethal cell injury?

A

Cell (cloudy) swelling

Fatty change

25
Q

What is oxygen free radicals?

A
  • Highly reactive ions or molecules with single unpaired electron in outer orbital
26
Q

Explain oxygen free radicals toxicity?

A

Effector pathway of various types of cell injury
Chain reaction with molecules in membranes to produce additional free radicals
Also damages proteins and nucleic acids - apoptosis
Detoxification by superoxide dismutase and antioxidants e.g. vitamins A, C & E

27
Q

What are the things that can compromise cell membrane?

A

Can be compromised by bacterial toxins, viral proteins, complement, cytolytic lymphocytes, and various physical and chemical agents

28
Q

What are the effect of loss of membrane barriers?

A

Loss of membrane barriers leads to breakdown in metabolite gradients - point of no return?

29
Q

Due to loss of membrane barriers, Ca2+ will increased. What is the effect of that?

A

Increased Ca2+ in turn activates a number of enzymes, with potential deleterious cellular effects.

  • ATPases (thereby hastening ATP depletion),
  • phospholipases (which cause membrane damage),
  • proteases (break down membrane and cytoskeletal proteins)
  • endonucleases (responsible for DNA fragmentation)
30
Q

What is necrosis?

A

Cell death as result of lethal cell injury
Passive process
Incites an inflammatory reaction

31
Q

What are the different types of necrosis?

A 
Coagulative - most common
Caseous - tuberculosis
Colliquative - brain
Gangrene - wet and dry
Fat, fibrinoid
32
Q

What are the characteristics of coagulative necrosis?

A

Denaturation of intracytoplasmic protein
Dead tissue becomes firm and slightly swollen
Tissue shows retention of microscopic architecture
Typical of ischaemic injury (except in brain)
Cellular proteins may leak into blood

33
Q

What happened to the brain with colliquative necrosis?

A

Necrotic neural tissue is liable to total liquefaction and site is eventually marked by a cyst

34
Q

What are the characteristics of caseous necrosis?

A

Characteristic of tuberculosis
Cheese like
Cellular detail destroyed in this area, which is surrounded by granulomatous inflammation.
Dead tissue lacks any structure

35
Q

What is apoptosis?

A

‘Programmed cell death’ or ‘apoptosis’ (from Greek: falling off, as in leaves from trees)

36
Q

What is the mechanisms of apoptosis?

A

Apoptosis initiating factor (AIF) and cytochrome C are normally sequestered in mitochondria, but when released into the cytosol activate caspases, which are the effector molecules of apoptosis. Two important molecules you will hear about in cancer biology are involved. P53 (the ‘guardian of the genome’) is activated by DNA damage and causes the elimination of damaged cells by apoptosis. Mutations to p53 are very common in malignant tumours, thus allowing cells to accumulate genetic abnormalities and become malignant. Bcl-2 sequesters cytochrome C and thus inhibits apoptosis. Activating mutations leading to bcl-2 overexpression are another way that some tumours gain the ability to proliferate in an uncontrolled way.

Essential Medical Science - MoD (5 decks)

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