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BMS 109 > Pathobiology > Flashcards

Pathobiology Flashcards

1
Q

What is a disease?

A

Any state in which the health of the human organism is impaired. Consequence of a failure of homeostasis.

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2
Q

What is Pathogenesis?

A

Biological mechanisms causing clinically evident diseases.

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3
Q

What is Atiology?

A

Specific cause of a disease

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4
Q

What is a risk factor?

A

A variable exposure or biological charactorisic that makes disease more likely e..g working in a building site with aspesdos.

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5
Q

Intrinisic factors for disease? (4 and examples)

A

-Genetic e.g. mutation- sickle cell anaemia
-Metabolic e.g. Diabetes, gall stones
-Cellular e.g. Autoimmune- Alzheimers, arthritis
-Structural
e.g. congenital- spina bifida, Ebsteins anomaly
or e.g. Aquired-atheroma

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6
Q

Extrinsic Factors for disease? (4 and examples)

A
  • Physical e.g. trauma, bone fracture, radiation, temp= frost bite/ burns
  • Chemical e.g. toxic substances- tobacco lung damage
  • Biological e.g. Bacterial/ viruses/ fungi
  • Nutritional- malnutrition.
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7
Q

What are the 4 stages of development of disease?

A
  1. Aetiological agent e.g. bacteria primary cause.
  2. Pathogenic mechanisms e.g. acute inflammation
  3. Pathological Process e.g. Morpholoical features- skin abscess,
  4. overt disease and secondary consequences-complications e.g. septicaemia
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8
Q

How were inherited diseases first indentified?

A

Garrod- noticed blackened urine and kidney stones was inherited in the disease Alkaptonuria 1901

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9
Q

Who started a catalogue of human diseases that exhibited Mendelian inheritance?

A

William Bateson 1909.

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10
Q

4 types of Mendelian patterns of inheritance?

A
  1. Autosomal recessive e.g. cystic fibrosis
  2. Autosomal dominant e.g. Huntingtons
  3. Autosomal co-dominant e.g. Sickle cell anaemia
  4. X linked e.g. Duchenne Muscular Dystrophy, Haemophilia (A and B)
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11
Q

Sickle cell anamia causes?

A

point mutation causing a change in AA 6 of B subunit from Glycine (charged) to Valine (uncharged) which when aggregates forms crystalline structures. HB^A to HB^s

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12
Q

Why is the proportion of carriers so high in Sub-sarharan Africa?

A

HB^s confers a resistance to milaria

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13
Q

What enables the chromosomes to be visuallised and abnormalities in banding to be seen? Decade found?

A

Karyotyping, 1970’s

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14
Q

What are the symptoms of Duchenne muscular dystrophy?

A

Muscle wasting away, progressive, lethal in childhood or early adult.

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15
Q

What are the causes of Duchenne Muscular Dystrophy?

A

Deletion of a DNA sequence on the gene Dystrophin- Dystrophin proteins link muscle fibres to the extracellular matrix maintaining tissue integrity.

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16
Q

What is Alkaptonuria?

A

Homogentisic acid accumulates in joints, causing cartilage damage & back pain; precipitates as kidney / prostate stones;
high levels are excreted, blackening urine
- allows diagnosis.
-Autosomal recessive

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17
Q

What is huntingtons disease? Year found?

A

1872, late onset disease caused by a repeat of CAG in the huntington gene increasing the size of the polyglutamate tract (QQQQ) 36+ glutamate have.
This makes the Huntinton protein toxic to neurones causing massive neuronal loss in the basal ganglia and dilation of lateral ventricles.

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18
Q

Example of cancer causing virus? Found when? (Retrovirus)

A

Rous Sarcoma Virus was found by Rous in 1911. DNA sequence was captured from the chicken and showed that the V-Src oncogene, which encodes an abnormal hyperactive version of a tyrosine kinase (now a C src Proto-oncogene)

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19
Q

Chromosomal rearrangements that disrupt the Proto- oncogenes cause cancer, Give an example?

A

Chronic Myelagenous Lukaemia caused by translocation “Philadelphia Chromosome” causing the ABL proto-oncogene to become a hyperactive version of tyrosine kinase BCR-ABL.

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20
Q

What is a V-oncogene?

A

A nucleic acid sequence in a virus responsible for the oncogenicity of the virus (proto to oncogene)
It is derived from the host cellular proto-oncogene and acquired from the host by recombination.

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21
Q

How does Retinoblastoma develop?

A

retinal tumour that can be unilateral (only one eye) which is typically non-heridatory or bilateral (both) which are always heridtory.

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22
Q

Why are bilateral retinalblastomas always hereditory?

A

Loss of function of a tumour supressor gene. Non hereditory needs to have two somatic mutations in the same cell to get bilateral hence very rare, else if inherited only needs one as there is already a germline mutation in every cell.

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23
Q

What are SNPS?

A

Single nucleotide polymorphisms. 3x10^7 across the human genome. They are a variation in the nucleotide in a specific location within the genome.

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24
Q

How are SNPs used?

A

They are markers used to tell people apart for profiling and seeing links to susceptibity for diseases.
Genome wide analysis Studies of SNPs:
-Genome wide SNPs collected.
-Case vs control comparison of specific SNPS.
-SNPS identified that increase susceptibilty to certain diseases.
If associated ‘locus is associated’

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25
Q

Can summarize results of a genome wide analysis study of SNPs on which graph?

A

Manhatten plot.

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26
Q

What is genome imprinting?

A

Structural modifications to specific regions of particular chromosomes that prevents the transcription of genes in these regions.

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27
Q

At what stages are genes imprinted?

A

DNA sequences can be methylated on the cytosine bases in the gametes and reappear in the somatic tissues of the progeny. (removed during germ line development in embryo) Happens during spermogenesis/oogenesis.Imprinting dependent on the sex of offspring.

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28
Q

If one gene is imprinted what will happen to expression?

A

If say the maternal gene is imprinted then this gene will not get expressed and therefore the Paternal gene will be.

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29
Q

What materal gene is always imprinted?

A

SNORD116 (small nuclear RNA)

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30
Q

What paternal gene is always imprinted?

A

UBE3A (ubiquitin protein ligase)

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31
Q

Disease linked to no function of SNORD 116 if paternal is mutated?

A

Prader Willi Syndrome

-low muscle tone, short stature, cognitive diability, obsese

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32
Q

Disease linked to no function of UBE3A if maternal is mutated?

A

Angelman Syndrome

-congititve disability,siezures, frequent smiling, sleep disturbance.

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33
Q

How are genes imprinted?

A
  1. Transcription activators are lost to make the gene off (but inducible)
  2. DNA Methylation
  3. Recruitment of Methyl- C binding proteins
  4. Recruitment of repressors to stabilise the switching off.
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34
Q

What is Epidemiology?

A

Science concerned with the pattern of disease frequency in humans. Time, distribution, place, person

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35
Q

What does Epidemiology presume..? (2)

A

Disease doesnt occur randomly there is a pattern.

Disease has an identifiable cause

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36
Q

Epidemiology triangle- three components that can constitute to disease?

A

Host e.g. genetic, age, sex, immunization, behaviour
Agent e.g. chemical, infectious,radiation
Environment e.g. socioeconomic conditions, temp

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37
Q

Who was the first to do a epidemiology study on Cholera in London and found the epicentre was a water source?

A

John Snow

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38
Q

How many a year die of diahrea?

A

6million

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39
Q

How many deaths in UK every day due to smoking? a year? Worldwide?

A

320+, 120,000 yr, 4 million worldwide a year, 1/5 of all deaths.

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40
Q

Why do smokers on average live 7.5 years less?

A

lung, mouth, throat, larynx, bladder, cervix, kidney and pancreas cancer. But also respiratory diseases suhc as COPD and vascular diseases such as stroke or cornory heart disease.

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41
Q

How does the tobacco lead to emphysema?

A
  1. Tobacco irritates the throat and lungs
  2. Interracts with resident macrophages n the lungs
  3. Neutrophils are recruited through chemotactic facors
  4. Protease is secreted.
  5. Proteins are digested-tissue damage =emphysema
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42
Q

How does the smoke’s oxidants and free radicals lead to emphysema?

A
  1. Smoke is ful of oxidants and free radicals
  2. Leads to lower levels of antitrypsin (tripsin inhibitor)
  3. Proteases such as trypsin become more active and digest protein =emphysema
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43
Q

How does the tar in cigarettes lead to emphysema?

A
  1. Cilia are destroyed by the sticky tar reducing cilia action.
  2. Excess mucus is not wafted away.
  3. Infections are cuaght.
  4. Leading to chronic bronchitus and emphysema due to tissue damage.
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44
Q

WHat did Robert Koch discover?

A

25 years after John Snow’s death the reactive agent fror Cholera, also TB and Anthrax.

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45
Q

How does smoking lead to birth complications? (5)

A
  1. Hypoxia- starved of Oxygen due to increase in carboxyhaeomoglobin.
  2. Disrupts signalling.
  3. Maternal endocrine/ parocrine changes (decreased progesterone, increased protoglandins)
  4. Restricted blood flow to placenta due to nicotine caused vasoconstriction.
  5. Increased risk of membrane rupture- decreased maternal immunity.
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46
Q

What are the two broad responses to extinsic factors?

A
  1. Allergic e.g. asthma, laryngitus

2. Pneumoconiosis e.g. from dust

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47
Q

Inhled antigen to response steps:

A
  1. Inhaled pathogen’s antigens are recognised as being foreign.
  2. Mast cells have specific IgE receptors which IgE binds to.
  3. The antigen then binds to these receptors,
  4. This causes the release of Hisamine by the mast cell by exocytosis.
  5. This causes bronchconstriction, mucus secretion and oedema (swelling)
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48
Q

The dust reactions may be: (4)

A
  • Inert e.g. coal
  • Allergic e.g. causing extrinsic allergic alveolitis
  • Fibrous e.g. aspesdos, silicon
  • Neoplastic e.g.Lung carcinoma (abnormal growth of tissue)
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49
Q

WHat diseases can aspestos cause? (4)

A
  • Aspesosis
  • Lung cancer,
  • Mesothelioma
  • cancer of stomach, colon or rectum
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50
Q

How is Aspesdos bad?

A

Aspesdos fibres often get coated by calcium and iron =ferruginous body. Microphages injest the fibre, which increases the fibrogenic response via release of growth factors that increase the deposition of collapgen by fibroblasts.

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51
Q

The average human contains … cells and ….microbial cells. e.g. gut microbiome not just pathogens.

A

10^13
10^14
1/5 deaths are caused by pathogens

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52
Q

What are the three types of pathogens?

A
  • Obligate: can only survive in host usually very specific to host species.
  • Faculative: Present in the environment(reservoir) waiting for host.
  • Opportunistic: Normally benign but cause disease in comprimised host e.g. AIDS
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53
Q

What are virulence genes?

A

A few genes which enables the virus to become pathogenic.

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54
Q

How does Vibro Cholerae become virulent?

A

It needs to be infected by certain bacteriophages, which transfers the genes that encode cholera toxins to the bacteria, which cause the spread through diarrhoea etc.

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55
Q

The word to describe that fungi can change shape.

A

Dimorphism

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56
Q

Dimorphism is shown by Candida albicans how?

A

Consumed by macrophage in the yeast like state, but rapidly grows germ tubes to break the cell membrane and break free.

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57
Q

Dimorphism is shown by Histoplasma capsulatum how?

A

Changes state according to the temperature. In the soil grows as a mould with hyphae yet in a warm body changes to yeast morphology which can move better

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58
Q

Steps from sucking on an infected persons blood cycle of milaria?

A
  1. Anophilies mosquito sucks on an infected persons blood picking up the gametocytes of the plasmodium
  2. Fertilisation of the gametes and formation of a zygote.
  3. Invasion of gut and growth.
  4. Release of Sporozoits and migration to the siliviary glands.
  5. Mosquito sucks a persons blood and injects sporozoits.
  6. These replicate in the human liver
  7. These infect RBC’s
  8. Replicate and produce plasmodium gametes.
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59
Q

Three components that pathogens need to overcome?

A

Epithelium, flora and mucous.

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60
Q

How can come bacteria anchor themselves to the membrane?

A

With adhesins and P pili. These bind to receptor proteins on the cell surface (that are used for other functions)

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61
Q

What two reasons may pathogens want to hill host cells?

A
  1. Killing WBC’s helps pathogen envade the nervous system.

2. Killing host cells provides nutrition.

62
Q

Bacteria may have syringe like structures that can probe for host cells or inject into them, called…?

A

Type III secretions.

63
Q

Enteropathogenic E.coli makes the host cell produce Actin pedistals for it how?

A

Tir protein is sufficient to cause e polymerisation of actin filiaments. This is injected into the host cell through type 3 secretions creating a phosphorylated tir receptor, in which the ecoli intimin binds to and anchors the pathogen to the raised host cell.

64
Q

What is unusual about the pathogen Legionella pneumophila?

A

It replicates inside the macrophages that ingulf it.

65
Q

By what two methods can bacteria invade nonphagocitic cells?

A
  • Zipper method= like velcro- adhesin receptors attatch to adhesins of the bacteria and ingulf it.
  • Trigger mechanism= Rho family GTPase is injected into the host cell through tyoe 3 secretions which causes the polimerisation of the actin in the cell ingulfing the pathogen.
66
Q

………. secretes…….., a protein which is breaks down the membrane of a Phagosome. Once in the effects are stopped by….. which targets the protein for destruction and they begin replication.

A

Listeria
Hemolysin
PEST AA sequence.

67
Q

Steps for listeria entering into a cell? (lecture 5 i drew nice diagram look at that tbh)

A
  1. Listeria attatches to E cadherin receptor on surface.
  2. uptake by zipper mechanism into a phagosome
  3. hemolysin secretion
  4. hemolysin mediated membrane breaking.
  5. bacteria released and replicate.
  6. hemolysin now destoyed by PESt AA sequence by host cell.
68
Q

How does listeria enter the next cell down? (also see diagram lecture 5)

A

Act A is localised at the bottom end of the litereria. This is a site of actin polymiserisation to make it motile and push into the next cell.

69
Q

How do antibiotics work?

A

By disrupting the pathogens cellular processes e.g. replication,protein synthsis etc.

70
Q

Behavioural ways to get invaded, tell me about the cat and the rat

A

Toxoplasma gondii can only complete its life cycle in cats - but it gets from cat to cat travelling by rat. Infected rats loose their fear of cats and are even attracted to cat smells, therefore spreading it.

71
Q

Steps of lytic cell replication?

A
  1. Virus enters the cell and the DNA is uncoated.
  2. The DNA is replicated
  3. The coat protein is synthesised
  4. assembly of progeny viruses exit from cells as host cell lyses.
72
Q

Whats the difference between cell lytic or lysogenic cycle?

A

In lysis the virses are released as cell lyses whereas in lysogenic the viruses are budded off and the bacteriophage genome is put into the host cells e.g. HIV.

73
Q

What is the classification of viruses by their mRNA/ DNA strands called?

A

Bolrimore classification.

74
Q

What are type 1 viruses?

A

Adenoviruses- dsDNA which is then transcribed to mRNA directly. e.g. chicken pox, herpes, papilloma virus.

75
Q

What are type II viruses?

A

Small parvovirus SSDNA- uses DNA polymerase to make it double.

76
Q

What are type III viruses?

A

Rotaviruses- DSRNA- synthesises mRNA from.

77
Q

What are type IV viruses?

A

SSRNA- RNA makes polyproteins which are cleaved. e.. Polio viruses, toga viruses, yellow fever.

78
Q

What are type V viruses?

A

SSRNA- synethises the negative strand from this postitive strand by its RNA transcriptase, and the makes mRNA. e.g. ebola, influenza

79
Q

What are type VI viruses?

A

Retroviruses- go back into our genome, SSRNA-RT e.g. AIDS.

80
Q

What are type VII viruses?

A

DSDNA and had reverse transcripase e.g. Hepatitus B

81
Q

What is reverse transcripase?

A

used to generate complimentary DNA strand from an RNA template. Especially retroviruses.

82
Q

What is RNA transcripase?

A

Use an RNA template to make more RNA

83
Q

How does HIV enter into the host cell?

A

Antigens bind to cell surface receptors, fuse with membrane and uncoated.

84
Q

How does Influena enter into the host cell?

A

It is endocytosed into an edosome. It then uncoats.

85
Q

How do RNA viruses enter into the host cell?

A

Polio virus binds to PM, into an endosome and transcribes mRNA out of the endosome.

86
Q

How do adenoviruses enter into the host cell?

A

Endocytosed,lysis of the endosome and uncoating, mRNA released goes into the nucleus.

87
Q

How does a papillomovirus cause cancer?

A

Virus infects epithelial cells causing bengin tumours, but accidental integration of viral DNA into the hosts chromosome upregulates DNA replication, therefore creates a malignant tumour.

88
Q

The papillomovirus contains which oncogenes?

A

E6 and E7 turns up hosts DNA replication mechinery to make more virus initially but after integrated into the genome makes the host cells proliferate uncontrollably.

89
Q

How do the papillomoviruses stop controlled cell proliferation?

A

E6 binds to p53
E7 binds to Rb protein
which both regulate and inactivate cell proliferation.

90
Q

What are retroviruses?

A

Viruses that incorporate their genes into the hosts genome e.g. HIV and Mouse leukimia virus.

91
Q

Difference between C-Src and V-Src?

A

C-Src can be phosphorlyated at one end to regulate proliferation and inactivate, but the V-Src does not have the C terminus, and therefore is an oncogene version of C-Src. This is a kinase so causes a cascade reaction.

92
Q

Two types of immunity?

A

Innate-Non specific immunity which has no memory e.g. Low PH in stomach
Adaptive- More specific e.g. antibodies which bind to antigens and aggregate and destroy. Has a memory.

93
Q

What is the first physical line of defence? (3)

A
  1. Skin- epithelia may ahve tight junctions
  2. Chemical defensins e.g. antimicrobial agents such as sweat, sebum, Stomach PH Acidic
  3. Defensins
94
Q

What are defensins?

A

Peptides that disrupt the pathogens membranes allowing water to enter on their PM and essential nutrients to leave.

95
Q

Brief role of the lymphatic system in innate immunity?

A

Has WBC’s and drains the bodys toxins and unwanted material.

96
Q

Role of the thymus gland in innate immunity? Bone marrow?

A

Site of maturation of T cells.

above but B cells.

97
Q

6 key comonents of the innate immune system?

A
  • Physical barriers
  • Phagocytes
  • Immunological surveillance e.g. natural killer cells
  • Interferons- released in response to pathogens
  • Complement system
  • Inflammation as a defence.
98
Q

How are pathogens recognised as foreign?

A
  • General recognition signals
  • F-met- prokaryote protein synthesis- we dont make proteins this way.
  • Gram negative have LPS (lipopolysaccharides)
  • Foreign nucleic acid
99
Q

When foreign components found what happens to them?

A

Pattern- recognition particles bind
- these can be soluble e.g. Complement system
or membrane bound e.g. toll receptors

100
Q

What do Collectins do?

A

They are soluble pattern recognition receptors which bind to the carbohydrate sugar coatings of pathogens to make them as foreign. Phagocytes have receptors for collectins so can find and then engulf the pathogen.

101
Q

What does the complement system do?

A

Souble Pattern recognition receptors that complement the ability for antibodies and phagocytes in clearing microbes. They promote lysis of cells.

102
Q

What two different effects does the complement system have?

A

C3 cleaves in the pathogen cells to release C3a and C3b.

C3a recruits other cells such as the Tcells, whereas C3b binds to the surface of the antigens and cause lysis also.

103
Q

What role do the Phagocytes play in the innate immune response?

A

Can have pattern recognition receptors, Fc receptors (which bind to the Fc regions of antibodies) and C3b receptors (which bind to C3b tagged pathogens from the complement system).
They then engulf the pathogen.

104
Q

What cells in the innate immune system have Toll-like receptors?

A

Macrophages, neutrophils and epithelial cells

105
Q

What role do toll like receptors have in the innate immune system?

A

Bind to a range of pathogens proteins such as LPS and promote inflammatory response.

106
Q

Interferons are examples of what?

A

cytokines!!

107
Q

What is the role of interferons in the innate immune response?

A

Secretion evoked by DsRNA which we dont have. Can inhibit viral replication.

108
Q

Types of inferferons and impact?

A

Alpha interferons- Attract and increase no, of natural Killer cells.
Beta interferons- Slow inflammation and increase no. of natural killer cells.
Gamma interferons- Stimulates T lympthocytes.

109
Q

What are natural killer cells?

A

Immunological surveillance e.g target cells that have a low MHC 1 and Detroy bacteria

110
Q

How do T cells form?

A
  • Red Bone Marrow forms haemocytoblasts.
  • These differentiate into lymphoid stem cells.
  • Some migrate to the thymus.
  • Immature T cells differentiate from lymphoid stem cells.
  • As the T cells are exposed to anitgens in the lympth nodes, they mature and take part in cell mediated immunity.
111
Q

How do B cells form?

A
  • Red Bone Marrow forms haemocytoblasts.
  • These differentiate into lymphoid stem cells.
  • The B cells then differentiate and then take part into antibody mediated immunity.
112
Q

How do NK cells form?

A
  • Red Bone Marrow forms haemocytoblasts.
  • These differentiate into lymphoid stem cells.
  • The NK cells then differeniate and take part in immunological surveilance.
113
Q

What is cell mediated immunity?

A

What T cells do. This is does not involve antibodies, rather activation of Phagocytes, T cells and cytokines.

114
Q

Which cells are found in the primary follicle zone of the lymph nodes? Interfollicular zone? Secondary?

A

Primary FZ- B cells, Follicular dendritic cells
Secondary FZ- Follicular dendritic cells
IFZ- T cells

115
Q

WHat is antigen presentation?

A

When a phagocyte engulfs a pathogen but then displays the pathogens antigen on it’s surface to alert other cells, especially T cells.

116
Q

What are MHC’s?

A

Major histocompatability complex. They are cell surface glycoproteins that bind antigens and present them. Part of the Adaptive immune system.

117
Q

What are MHC 1’s?

A 
In all nucleated cells. 
Activates cytotoxic (killer) T cells.
118
Q

What are MHC 2’s?

A

More speciallised APC’s, inducible in many cells.

Activate T-helper cells.

119
Q

What are cytokines?

A

A number of substances such as interferons, interleukins and growthfactors which enable cell communication in the immune system.

120
Q

What two cells can T helper cells differentiate into? Functions?

A
  • Cytotoxic (killer) T cells- release cytotoxins e.g. perforin, lymphotoxin which results in apoptosis- kill cancer cells and infected cells.
  • T memory cells- recognise previous foreign invaders, making the secondary response to release antibodies much faster. Reserve
121
Q

What are the major players in the Adaptive immune system?

A

B lymphocytes- release antibodies
T lymphocytes- T memory and T killer
Antigen Presenting Cells
Follicular Dendritic cells

122
Q

T cells, B cells and APC’s circulate through the …….. On antigen presentation they…. and attracted to the site of infection by …….

A

lympoid tissue
Divide
Chemokines.

123
Q

What are the 5 types of Ig immunogloblin antibodies? Produced by? Order?

A

B cells produce: IgG, IgM, IgE, IgA, IgD.

(GMEAD

124
Q

What’s the structure of IgG?

A

Two antigen binding sites both identical and a constant region (Fc tail) which signals to macrophages.
most abundant Ig and first to the site of a reaction.

125
Q

What’s the structure of IgM?

A

10 binding sites, clusters the pathogens together so that they cant move and spread. Can be co-expressed with IgD.

126
Q

What’s the structure of IgA?

A

4 binding sites to aggregate pathogens.

127
Q

Each….. produces one …..of antibody which recognises different antigen …..

A

B cell
Varient
epitope ( part of antigen that antibody binds to)

128
Q

What is the general strucure of an antibody?

A

Made of two light chains and two heavy chains joined by disulfide bonds. The heavy chains have a hinge region to allow for antigen binding.
Has a hypervariable region which is specific to an antigen.

129
Q

How are antibodies useful?

A

Fc receptors, which are on nearly every cell in the innate and adaptive immune system, bind to these antibodies which are bound to the pathogens antigens. These are then recognised or directly phagocytosed.

130
Q

3 features of the Adaptive immune system?

A

Specicifity
Memory
Tolerance (immunotolerance of self)

131
Q

3 examples of autoimmune diseases?

A

Myasthesis Gravis, Chrones disease, Rheumatoid arthritis

132
Q

Difference between Necrosis and Apoptosis?

A

Necrosis: Loss of cell components by lysis. Not all of the debris is broken down, often due to physical damage.
Apoptosis: Programmed cell death, by phagocytosis.

133
Q

Reasons for Necrosis?

A

Trauma, Infections, reapid loss of cell energy, acute hypoxia, acute toxicity.

134
Q

Why is necrosis not completely uncontrolled?

A

Can be in the case of trauma, but cells can swell before and be intetional.

135
Q

Events that lead to apoptosis?

A

Shrinkage before, then nuclear breakdown, then phagocytosis recyling of the cell components. Requires protein synthesis.

136
Q

Necrosis is charactorised by? (4)

A

Inflammation, autolysis, debris (pus) and calcification

137
Q

Why would apoptosis happen?

A

Due to developmental cell loss, toxicity, removal of growth factors, deatchment from substate, or senescence e.g. Hayflicks limit.

138
Q

How do cells die in the brain due to insufficient blood blow to the brain?

A

Brain ischaemia, around the outside they die apoptosis but necrosis in the centre.

139
Q

Apoptosis in development?

A

C elegans 1100 cells in adult, exactly 131 die in development
Digit formation
metamorphis e.g. tadpole to frog.
Neurons destroyed until age 25.

140
Q

Apoptosis gene flow chart in c elegans..

A

EGL-1 Blocks CED9 which blocks CED4 which acitvates CED3 causing cell death.

141
Q

If reduce CED3 or CED4…

A

Gives excess of adult cells (reduces apoptosis)

142
Q

If reduces CED9…

A

Huge amounts of cell death.

143
Q

What gene intitiates apoptosis?

A

EGL-1

144
Q

What is the CED3 mammal homologue?

A

Caspases.

145
Q

What are caspases?

A

Protein activated by cleavage of procaspase. This then causes the caspase cascade.

146
Q

What is caspase 3 important for in development?

A

Breaking down:
DNA repair enzyme PARD
Lamin A
Huntingtin

147
Q

What is hyperplasia?

A

Issue growth containing excessive numbers of cells.

148
Q

WHat is metaplasia?

A

issue growth containing displaced but otherwise normal cells

149
Q

What is dysplasia?

A

Tissue growth where cells are abnormal

150
Q

What is Neoplasia?

A

Invasive abnormal tissue growth e.g. after metastasis.

151
Q

Benign vs malignant?

A

Malignant breaks though basement membrane and spreads (metastasis)

152
Q

How do cancer cells avoid apoptosis? (2)

A

B cell leukemas express high levels of BCL2 which is an antiapoptosis.
Lung and colon cancer cells secrete decoy molecules that bind and inactivate MHC receptors for antigen presentation.

BMS 109 (6 decks)

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