8 Cells And How They Replicate Flashcards

1
Q

Prokaryotes - Nucleus

A

No nucleus, DNA in nucleoid region

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2
Q

Eukaryotes - nucleus

A

True nucleus with a nuclear membrane

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3
Q

Prokaryotes - DNA structure

A

Generally circular, single chromosome

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4
Q

Eukaryotes - DNA structure

A

Multiple linear chromosomes within nucleus

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5
Q

Prokaryotes - membrane bound organelles

A

Absent

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6
Q

Eukaryotes - membrane bound organelles

A

Present (eg. Mitochondria and chloroplasts)

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7
Q

Prokaryotes - cell division

A

Binary fission

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8
Q

Eukaryotes - cell division

A

Mitosis and meiosis

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9
Q

Prokaryotes - size

A

1-10 um

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10
Q

Eukaryotes - size

A

10-100 um

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11
Q

Prokaryotes - metabolic diversity

A

High (including extremophiles)

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12
Q

Eukaryotes - metabolic diversity

A

Limited (autotrophic or heterotrophic)

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13
Q

Prokaryotes - cell wall composition

A

Common - peptidoglycan in bacteria

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14
Q

Eukaryotes - cell wall composition

A

Variable - cellulose in plants, chitin in fungi

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15
Q

Prokaryotes - ribosome

A

Smaller 70S

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16
Q

Eukaryotes - ribosome

A

Larger 80S in cytoplasm

Smaller 70S in mitochondria and chloroplasts

17
Q

Case study - treating bacterial vs fundal infections (A Cellular Approach)

A

Bacterial and fungal infections are common in healthcare / community

Require different distinct treatments - successful treatment relies on understanding cellular biology of the pathogen and that of the host

18
Q

Bacteria vs Fungi

A

Bacteria - prokaryote
Fungi - eukaryote

B - primary asexual reproduction
F - sexual and asexual through spores

Cell wall composition - bacteria composed of peptidoglycan and the fungi wall is composed of chitin

19
Q

How do AB treatments work (7)

A
  1. Cell wall synthesis inhibitors —> beta laxtams / glycopeptides / fosfomycin / bacitracin / alafosfalin
  2. DNA gyrase inhibitors - quinolones / coumermycin antibiotics
  3. Inhibition of DNA dependany RNA polymerase —> Rifampicin
  4. RNA synthesis inhibitors —> ansamycines
  5. Protein synthesis (30S and 50S) —> tetracyclines
  6. Folate synthesis inhibitors —> sulfonamides
  7. Cell membrane synthesis disruptors —> lipopeptides
20
Q

Case scenario - treating a patient with dual infections

A

Choose appropriate antibiotics and anti-fungals without causing harm or drug resistance

21
Q

Case scenario - treating a patient with dual infections (implications for medical practice)

A

Distinguishing between cell types matters in clinical settings

Accurate diagnosis and undertsanding of cellular biology it’s important in preventing treat,ent failures, drug resistance and unnecessary dysbiosis in the host

22
Q

Parasitic infections

A

Eukaryotic share some cellular structures with human cells / difficult to develop drugs that selectively target the parasite

23
Q

Cancer treatment

A

Cancer cells are eukaryotic But exhibit abnormal cell division and structural characteristics - some drugs target specific structures in cancer cells, such as rapidly dividing DNA, mutates protein receptors, or overexpressed enzymes

Understanding cancer cell structure and behaviour allows for the development of targeted therapies that aim to reduce harm to normal cells

24
Q

Autoimmune diseases

A

Immune system targets own body cells —> treatment focuses on modulating the immune system

Helps prevent damage to healthy cells

25
Q

Antibiotic selection in multi-drug resistant bacterial infections

A

Bacteria can develop resistances to break down the drugs (eg. Resistance to penicillin by producing enzyme beta-lactamase)

Requires the use of alternatives

Testing to determine what the bacteria is sensitive to

26
Q

Bacterial ribosome composition

A

70S (composed of 30S and 50S subunits)

27
Q

Eukaryote ribosome composition

A

80S (composed of 40S and 60S subunits)

28
Q

Why do some antibiotics target bacterial ribosomes

A

Antibiotics like tetracycline and erythromycin specifically bind to the bacterial subunits (either 30S or 50S), disrupting protein synthesis

These antibiotics prevent bacterial cells from making essential proteins, ultimately inhibiting growth or leading to cell death

29
Q

Why don’t antibiotics harm human cells?

A

Human cells have 80S ribsomones with different structural characteristics, so these antibiotics don’t recognise or bind to them effectively

Structural specificity means antibiotics can selectively inhibit bacterial cells without harming eukaryotic cells

30
Q

Examples of common ribosome targeting antibiotics - tetracycline

A

binds to the 30S subunit, blocking tRNA from attaching and halting protein synthesis

31
Q

Examples of common ribosome targeting antibiotics - erythromycin

A

binds to the 50S subunit preventing the ribosomes from moving along mRNA, stopping protein production

32
Q

Examples of common ribosome targeting antibiotics - Streptomycin

A

binds to the 30S subunit causing misreading of mRNA and resulting in faulty proteins

33
Q

Summary - Antibiotics targeting ribosomes

A

Selective targeting - antibiotics can selectively bind to bacterial ribosomes without affecting eukaryotic ribosomes

Structural differences in ribosome size and subunit composition is crucial for this selective effect

Implication for treatment - this selectivity allows antibiotics to combat bacterial infections without generally harming human cells