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FunMed Random > Yuck ! > Flashcards

Yuck ! Flashcards

1
Q

what are sister and homologous chromosomes?

A

sister chromatids are identical copies of same chromatid (i.e both from mother / father)

homologous chromosome: a pair of chromosoemes, each derived from one parent

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2
Q

explain each phase of cell division

A

G0 phase: cells outside of cycle and have stopped dividing. can return to G1 phase.

G1 phase: normal growth phase. prep for DNA synthesis

S phase: DNA synthesised and duplicated

G2 phase: cell prepares for cell division.

M phase: proper cell division

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3
Q

what are the G phases?

A

gap / growth phases:

  • cell undergoes normal function.
  • NOT growing or replicating
  • allows cell time to monitor the env to check conditons correct for replication
  • act as regulatory phases / checkpoints: indicate of cell should continue dividing or undergo apoptosis
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4
Q

Explain the S phase

A

Synthesis Phase

DNA duplicated: 23 -> 46

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5
Q

explain the M phase

A

Mitotic phase:

Made of 4 stages:

Prophase, Metaphase, Anaphase, Telophase

then have cytokinesis (splitting of cytoplasm into 2)

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6
Q
  • explain process of crossing over / recombination. when does it occur?
  • explain what independent assortment. when does it occur?
A

Crossing over

MAIN SOURCE OF GENETIC VARIATION BETWEEN GENERATIONS = zygote

  • essentially a balanced translocation
  • occurs at chiasmata
  • can occur in prophase or metaphase

Independent assortment

  • sister chromatids during metaphase II, are randomly allocated from one side to the othe
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7
Q

what is difference between meiosis I and meiosis II? (general)

A

during anaphase in meisois II, get seperation of sister chromatids rather than homologous chromsomes

meisois II: more similar to mitosis

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8
Q

how is the cell cycle controlled? name and explain the checkpoints

A
  • very tightly regulated (if escape leads to cancer)

G1 checkpoint: end of G1. controls if cell enters S phase. is environment favourable? checks for growth factors, nutrients, cell size and DNA damage

G2 checkpoint: end of G2. environment favourable? is all DNA replicated? checks for cell size, DNA damage and DNA replication

Metaphase checkpoint: are all chromsomes attached to spindle?

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9
Q

what do transcription factors do?

how can transcription factors change cells?

A

- proteins that attach to promoter regions of gene and allow the gene to be transcribed. (if the DNA in promoter region is methylated, the transcription factor cant transcribe to the gene)

  • transcription factors can turn on at different times during cell differentation
  • as cells mature, different transcription factors can act on gene expression and change cells specification

-

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10
Q

what are the different commitment stages of cell differentiation?

A
  1. specification: capable of differentiating autonomously wihen placed in a neutral environment, not when placed in non-neutral env. reversible. (e.g. might be liver cell but dont know yet which cell)
  2. determination: capable of differentiating autonomously even when placed into another embryonic region. irreversible (committed to cell lineage bc have turned on more transcription factors).
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11
Q

describe basic differences between apoptosis and necrosis mechanisms

A

necrosis:. recovery possible.
occurs by: swelling of ER and mitochondria, membrane blebs, plasma membrane breaks bc can’t hold fluid inside. cells organelles released. inflammatory process undergone

(cells burst)

apoptosis: irreverisble. cells shrink and condense (including chromatin). cell fragments into apoptotic bodies. phagocytosis of apoptotic cells and fragments. avoids release of cell contents

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12
Q

why is apoptosis highly regulated?

what are two apoptopic pathways?

A

apoptosis cannot be stopped once is has started: regulation

2 pathways:

extrinsic apoptopic pathway

  • enviroment around the cell could cause cell death.
  • tumour necrosis factor (TNF) binds to death receptor. activates caspases

intrinsic apoptopic pathway:

  • targets the cell’s mitochondria -> activates caspases
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13
Q

explain how stem cell division occurs

A
  • stem cell division: asymmetrical or symmetrical
  • asymmetrical: one daughter cell becomes new stem cell, other daughter cell becomes differentiated
  • symmetrical: one stem cell divides into two stem cells OR stem cell will commit two daughter cells to differential lineages. both daughter cells have same fate
  • creates a constant pool or stem cells
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14
Q

explain what acetylcholine does in cardiac muscle

A

acetylcholine triggers membrane hyperpolarisation (moving away from potential to trigger activation)

  • acetylcholine binds to acetylcholine receptor on heart muscle (called muscarinic receptor)
  • muscarinic receptors are G protein coupled receptors that activate ionic channels via a second messenger cascade
  • this causes hyperpolarisation and a decrease in cardiac activity
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15
Q

explain effect of acetylcholine on skeletal muscle?

A

acetylcholine triigers membrane depolarisation in skeletal muscle

  • acetylcholine binds to skeletal muscle cell receptors called nicotinic acetylcholine receptors (nAChR)
  • depolarisation occurs (action potential more likely to happen)
  • contraction of skeletal muscle
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16
Q

explain how g-protein linked receptor initites enzyme action

A
  • signal molecule binds to extracellular side of receptor
  • causes G protein to intracellular part of receptor
  • G-protein activated
  • subunit in G-protein activates enzyme
  • Activated enzyme leads to biological respons
17
Q

what are the 8 hallmarks of cancer?

A

all contribute to sustaining proliferative signalling -> then to tumour developement and malignant progression

  1. self sufficiency in growth signals
  2. insensitivity to anti-growth signals
  3. evading apoptosis
  4. limitless reproductive potential
  5. sustained angiogenesis
  6. tissue invasion and metastasis
  7. deregulating cellular energetics
  8. avoiding immune detection
18
Q

give over view of cell signalling in normal cell when a growth factor binds to growth factor receptor xx

A
  • growth factor binds to receptor. two receptors interact (dimerization)
  • intracelllar side: phosphorylation of tyrosine
  • siganlling proteins bind to P-tyrosine
  • causes cascade of phosphorylation events
  • activates two pathways: MAPK pathway and PI3 Kinase Pathway
  • once pathways are activated, activate gene expression and transcription factors occur.
19
Q

explain the ras pathway and how mutation leads to kras cancer

A
  • when ras switched on: (normally ras is switched on by binding to GTP) can switch on ERK and AKT pathways. (ras regulates the pathways by turning on / off the ERK and AKT pathways)
  • mutated ras (kras): hydrolysis of bound GTP (first stage in pathway) occurs v slowly. GTP is bound to ras in unhydroloysed form - ras is permenantly switched on. continois proliferation and growth.
20
Q

where is type 4 collagen found?

A

basal membane

21
Q

where are reticular fibres found?

what role do they play / associated with?

A
  • supporting stroma for highly cellular organs (like liver).
  • found at boundary of connective tissue and epithelium.

- wound healing and scar tissue.

  • branching pattern -> loose to allow passage of cells and fluid
  • made of type III collagen. dont bundle
  • produced by fibroblasts
22
Q

which cells produce alpha smooth muscle actin? [1]

A

myofibroblasts

23
Q

what are the three main mechanism of gene alterations that activate oncogenes? [3]

A

- point mutations: single base change in DNA (e.g. Ras oncogene)

  • chromsomal rearrangements: translocation of chr activates oncogene by using regulatory elements from a highly transcribed gene to drive expression of oncogene

- gene amplification (e.g HER2)

24
Q

how does a point mutation in H-ras result in oncogene activation? what is the point mutation that occurs?

A
  • (ras is a GTPase (converts GTP into GDP)
  • normally regulates cell proliferation and survival)

- single nucleotide exchang_e GGC TO GTC_ in bladder cancers (glycine -> valine)

  • get different isoforms of ras gene resulting in different cancers (see photo)
25
Q

where is c-myc normally encoded?

where is IgH normally encoded?

explain cancer that occurs when the above translocate

A

- c-myc: found on chr 8

  • on chromsome 14, there is a gene that codes of IgH - has a very strong promoter
  • translocation of region of chr 8 and 14: myc gets translocated near to promoter of IgH
  • results in strong promoter driving the expression of myc: Burkitt lymphoma
26
Q

how does lymphoma occur?

A
  • strong promoter of IgH on chromosome translocates to chromsome 18
  • switches ON bcl-2 gene (anti-apoptotic protein) in active B-lymphocytes (is normally switched off)
  • cells that harbour mutations do not go into apoptosis
  • *- causes lymphomas:**
  • leukaemia
  • Non-Hodgkin lymphoma
  • solid tumours
27
Q

how does p53 mutation often occur?

A

point mutations - results in missense mutation - change in sequence in protein doesnt allow it conduct normal function

  • majority of mutations result in loss of function of p53’s ability to bind to DNA in a sequence specific manner and activate transcription of p53 target genes
28
Q

How is DNA damaged? [3]

A

1. replication errors (during S phase)

2. spontaneous damage - base sequence altered

3. mutagenic damage

a) endogenous (indirect acting carcinogens - need metabolic activation)
- alcohol
- polycyclic aromatic HCs
b) exogenous (direct acting carniogens)
- oxygen species
- chems
- X-rays
- UVs
- viruses and bacteria

29
Q

how does DNA damage occur by formation of DNA adducts in lung cancer?

A

in lung epithelial cells:

  • (benzopryene (BP) from smoke is oxidised (x2))- results in BPDE (ultimate carcinogen)
  • BPDE forms adduct with guanosine residues in lung epithelial cells
  • occurs often in tumour suppressor genes, such as p53

(mutations in p53 gene are more common in smkers than non smokers)

30
Q

explain other an example of DNA adducts causing cancers

A

oral and oespophageal cancers - caused by excess alchohol intake

  • reaction: ethanol –> acetaldeyde
  • acetaldeyde reacts with deoxyguanosine = weak mutagen. further reaction -> stronger mutagen (DNA adduct)
31
Q

how does DNA damage occur by UV radation ? and where

A
  • damage in basal cells of melansomes (particularly keratinocytes)
  • p53 implicated
  • formation of cylobutane pyrmindine dimers (CPD) covalent bonds form between 2 adjacent pyrimidines in same DNA strand. VERY STRONG BOND
32
Q

h-ras (and mutated k-ras) is an example of what type of protein? how work?

A

SIGNAL-TRANSDUCTION PROTEINS:

RAS if active, it SENDS GROWTH PROMOTING SIGNALS TO THE NUCLEUS

KRAS is continuously active (part of MAPK and PI3K pathways)

↓

Signals for cell division

↓

Continuous proliferation

33
Q

what does pRB do in normal cell? when causes cancer?

A

Phosphorylated Rb -> E2F is released -> Transcription and gene expression ->Progression from G1 to S phase

34
Q

give quick overview of how mestasis occurs

A
  1. vascularisation of tumour occurs
  2. cells detach from primary tumour
  3. BM is degraded :( and invasion into ECM occurs
  4. Intravasation of nearby blood vessels (need to breach membrane of enterocytes to do this)
  5. tumour cells circulate in vascualar system
  6. some cells adhere to walls of blood vessels
  7. Extravasation (leave blood vessels) to local tissues
  8. secondary tumour
35
Q

how do you grade and stage tumours?

A

Grading depends on:

  1. degree of anaplasia (degree of differentiation) -> more undifferentated = lower grade
  2. rate of growth

Stage depends on:

  1. size of tumour
  2. spread / extent of tumour
36
Q

what are paraneoplastic syndromes?

A
  • paraneoplastic syndromes: clinical syndromes not caused by direct invasion or metastasis of tumour which accompany malignant disease. non-metastatic manifestation of malignant disease
  • associated with malignancies in: lung, breast, gynaecologica and haemotoligcal tumours
  • arise from tumour secretion of hormones, peptides, cytokines -> interfere with normal metabolic pathways of hormones peptides

cause condition NOT directly associated with primary tumour. instead associated with excess of hormone / or cytokine etc

FunMed Random (19 decks)

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