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Semester 4 > MOD > Flashcards

MOD Flashcards

1
Q

what is influenza

A

a RNA virus creating a surface membrane around RNA containing glycoproteins: neuraminidase and haemaglutin

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2
Q

difference between streptococci and pneumocci

A

strep. pyogenes (group A strep) –> beta haemolytic on agar

strep. pneumoccus –> alpha haemolytic on agar
soluble to bile

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3
Q

difference between croup and acute epiglottis

A

croup = viral infection (parainfluenza virus)
acute epiglottis = bacteria so antibiotics will help (haemophiliac influenza)

croup = 3months to 3yrs
AE = 6yrs
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4
Q

how do natural killer cells work

A

activating receptors(ITAM) stimulated with unhealthy cells (virus infected cells)

inhibitory receptors(ITIM) stimulated with healthy cells

healthy cells express MHC I which inhibit NKC
virus containing cells do not express MHC I

they kill via

  • perforin –> pores
  • granzymes (A,B,C) to initiate apoptosis
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5
Q

how do NKcells and macrophages activate each other

A

macrophages—-IL-12—>nkc

NKC——IFN-gamma—-> macrophages

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6
Q

innate lymphoid cells

A

they produce cytokines

ILC1–> Th1-like/IFN-gamma (virus)
ILC2 —> Th2-like/IL5/IL13 (inflammatory)
ILC3 –> Th17-like/IL-17 (intestinal barrier function/lymphoid organogenesis)

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7
Q

3 cell check points

A

late G1

before entering mitosis

during chromosomes aligned

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8
Q

drugs acting on s phase

A

5-fluorouracil
-thymidine analogue - blocking thymidylate synthase (thymidine synthesis)

bromodeoxyuridine

  • thymidine analogue
  • can be detected by Ab
  • used to identify cells that have passed S phase (are replicating)
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9
Q

how are cells controlled during the checkpoints

A

cyclin-CDK complex controls cell progression

retinoblastoma protein is bound to E2F
cyclin-cdk phosphorylates retinoblastoma
E2F let go
can continue to express S-phase proteins so can progress on S phase

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10
Q

tumor protein 53

A

if DNA is damaged

TP53 is phosphorylated and acts as a TF

  • stimulates expression of CDKi to arrest cell
  • stimulate DNA repair protein expression

if repaired it enters back into cell cycle, if not –> apoptosis

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11
Q

what family CASPases lead to programmed cell death

A

BCL2

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12
Q

necrosis

A

accident death eg. due to low BF

lack of O2 --> lack of ATP
ion pumps stop working
water enters, cell swells
if BF is returned, it can be reversed
if not it will burst and proteolytic enzymes released from lysosomes

stimulates an inflammatory response

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13
Q

apoptosis

A

initial CASPases activated via ligand-induced dimerisation or cytochrome C

cleaves cystolic proteins eg. cytoskeleton/nuclear lamin

production of blebs (kept in vesicles)

phagocytose by macrophages

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14
Q

apoptosis

A

initial CASPases activated via ligand-induced dimerisation or cytochrome C

cleavage of pro-CASPases–> CASPases cascade

cleaves cystolic proteins eg. cytoskeleton/nuclear lamin

production of blebs (kept in vesicles)

phagocytose by macrophages

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15
Q

2 ways of activating the initial CASPases during apoptosis

A

extrinsic pathway = ligand-induced dimerisation

TNF = ligand that binds
cystolic part recruits death adaptor protein(FADD) to death domain
recruitment of 2 inactive CASPases
autoproteolysis of each other

intrinsic = cytochrome C
normally in mitochondria
release depends on BCL2 proteins (block the pores from Bad, Bax, Bid)

cytochrome in cytosol binds to APAF protein
recruitment of inactive CASPases

2xcytochrome C –> 2 inactive CASPases–> autoproteolysis of each other

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16
Q

what other 2 things play an important role related to cytochrome c (intrinsic pathway to activate CASPases)

A

survival signals –> phosphorylate Bad–> prevents it from binding to BCL2–> pores remained blocked–> no apoptosis

TP53—> stimulated pro-apoptotic –> apoptosis of unhealthy cells

(cancer = mutation of TP53–> No induced apoptosis/DNA repair)

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17
Q

release of enzymes during necrosis allows us to identify extent of necrosis

A

muscular dystrophy

  • CK
  • lactate dehydrogenase

heart attack
-lactate dehydrogenase

bone/liver disease

  • alkaline phosphotase
  • lactate D

haemolytic anaemia
-damaged erythrocytes—> LDH1/2

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18
Q

drugs affecting M phase

A

colchicine
vinca alkaloids
palcitaxel (taxol)

stabilise free tubulin–> prevents chromosomes being pulled apart

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19
Q

2 cyclin-cdk inhibtiors

A

CDKN1

  • stimulated by DNA damage (TP53)
  • gradually sequestered by G1 complexes–> others

CDKN2

  • stimulated by TGF-beta
  • inhibited by G1 complex
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20
Q

what specific Cyclin-CDK complex works during G1

A

cyclin D - CDK

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21
Q

Chronic Granulomatous Disease

A

Mutation in NADPH component

Defect in oxidative burst

= Phagocytosed microbes cant be killed leading to recurrent infections

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22
Q

Chediak-Higashi Syndrome

A

Defective phagosome-lysosome fusion

= Phagocytosed microbes cant be killed leading to recurrent infections

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23
Q

what bacteria causes whooping cough

A

bordetella pertussis

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24
Q

3 things that CD4+ cells do after activation from MHC II presented antigen

A

release cytokines—> B-cell Ab activation
TNF—> inflammation
IFN-gamma—> macrophages–> phagocytosis

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25
Q

what acid components for gram +ve and -ve bacteria

A

+ve = lipoteichoic acid

-ve = hylauronic and salcacid (LPS) - resistant properties that decrease opsonisation as these are present on host cells so no Ab against them

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26
Q

how are very large bacteria destroyed that cannot be taken up by macrophages

A

Ab bind to their antigens and Fc of Ab is recognised by eosinophils—>degranulation

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27
Q

herpes viridae common properties

A

icosahedral nucelocapsid
dsDNA, linear
enveloped
ability to lay latent then reactivate

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28
Q

HIV structure

A

2 RNA (enveloped)
reverse transcriptase
protease
integrase

2 viral proteins: gp120 gp41

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29
Q

human hepatitis virus

A 
A
B
C
D
E
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30
Q

gastrointestinal infections

A

rotavirus

norovirus

31
Q

consequences of parovirus

A

decreased erythropoiesis (reduced RBC lifespan <120days)

erythema infectosum (slapped cheek) + red rash on trunk and limbs

32
Q

what does HA bind to on host cells (influenza virus)

A

sialic acid

33
Q

why so much influenza mutation

A

due to RNA polymerase not having proof reading/low selectivity leads them to make many different

esp. type A

34
Q

antigenic shift

antigenic drift

A

shift

  • every 2-8yrs
  • minor
  • due to continual viral mutation –> eventually accumulating over time–> “drifted strains”—> disease

drift

  • only with type A influenza
  • genetic reassortment (mixing of genes between 2 strains whey they infect same host)
  • new strain = everyone lacks immunity
  • leads to pandemic
35
Q

secondary infection

A

infection with a different organism whilst being infected/after being infected by a previous organism

or due to being immunocompromised (eg. by HIV)–> other bacterial infections following

36
Q

how CMV (cytomegalovirus) evades immune

A

decreases MHC I–> decrease in viral peptide presentation to CD8+

37
Q

what examples of virus that make non-replicating cells—> divide–> cancer cells

A

papillomavirus

Hep B,C

38
Q

high risk HPV

A

16,18,31,45

39
Q

how papillomavirus–> cancer

A

circular DNA

  • E2 in contact–> down regulates E6/7 (in early region)
  • E6 surpresses TP53/stimulates telomerase gene
  • E7 surpasses retinoblastoma

when linear (to integrate into host DNA)

  • E2 cut
  • URR can recruit TF to express E6/7
  • uncontrolled cell division
  • cancer
40
Q

4 type of toxins

A

1 - on cell surface but not transported in (disrupting/comprising cell metabolism)

2- on cell surface causing membrane damage

3- transported into host cell –> intracellular damage

extracellular - damage cellular matrix and connective tissue

41
Q

action of alpha-lecithinase

A

a bacteria enzyme that splits lecithin on host membrane - allowing lysis to occur

42
Q

endotoxins actions

A

increase macrophages —> cytokines etc–> inc permeability–> leaky into extravascular space–> dec. BV–> shock and dec organ perfusion/failure

inc complement –> inc clotting cascade–> uncontrolled clotting–>DIC

+ due to clotting factors used up–>more bleeding

43
Q

super antigen of staphylococcus aureus and strep pyogenes

A

Staph A - toxic shock syndrome toxin(TSST)

strep P - streptococcal pyrogenic exotoxin (SPE)

44
Q

what happens during toxic shock syndrome

A

gram +ve bacteria—> superantigens–> over activation of T-cells–> massive cytokine release/response—> huge inflammation–> hypovolemic shock/gangrene/liver damage/rash etc. (endotoxin like symptoms)

45
Q

how can streptococcus A lead to rheumatic heat disease

A

molecular mimicry (immunopathology)

Ab produced against it start attacking heart/bone due to similar structure

46
Q

molecules that act as opsonins

A

IgG1 and 3 (phagocytes had a receptor to bind to Fc region of Ab)
C3b
CRP

47
Q

replication cycle of rotavirus

A

VP7 and 4 help attachment and entry into cell

VP6 for replication of their dsDNA

transcription with VP1,2,3

assembly of single and double shelled particles with the viral proteins etc.

enter ER and acquire outer shell

48
Q

what is protein A

A

binds to Fc regions of IgG –> preventing opsonisation function of IgG–> prevents phagocytes binding

49
Q

what Ig does not fix complement

A

IgA

so pathogens can coat with IgA–> no complement

50
Q

adaptive immune evasion

A
  • Fc binding sites–> reversed Ig binding–> no opsonisation
  • hiding inside cells /privileged sites
  • block MHC presentation (decreasing TAP protein)
  • express “decoy” MHCs
  • different strains of antigens(influenza)
  • latency
  • sIgA proteases
51
Q

innate immune evasion

A
  • teichoic acids–> inflammation–> increase damage of endothelial cells
  • protein A
  • igA on surface (cant fix complement)
  • leucodins (kill leucocytes)
  • capsule/LPS - blocks opsonisations
  • carbohydrates on surface/C5a proteases to block MAC formation
  • increase macrophage consumption of certain bacteria (shigella/TB/E.coli) –> macrophage invasion/prevent phagolysosome fusion/oxidation
52
Q

how many driver mutations for carcinogenesis

A

2-8

53
Q

alkylating-like agents

A

direct chemical carcinogens

form covalent bonds between guanines on DNA
preventing strand seperation
decreasing DNA replication

used in chemotherapy

54
Q

function of tumour promoters

A

they enhance cell growth - not cancer

need to give it AFTER a carcinogen to promote cancer
(by increase cell division–> increases likelihood of one of the cells getting 2 hits–> cancer)

55
Q

physical carcinogens

A

high frequency radiations eg. gamma rays/x-rays = IONISING

they directly damage DNA & form free radicals when react with water—> generate compounds that can indirectly damage DNA

UV =NON-IONISING not as high frequency but can form cyclobutane pyrimidine dimers (covalent bonds between 2 adjacent Cs/Ts

found in TP53 tumour suppressor genes–> cant function

56
Q

viral carcinogens properties to cause cancer

A
  • must have stable Association with cells
  • must not kill the cell
  • must evade immune surveillance

HPV/HepB/HepC/Epstein barr

57
Q 
agenesis 
aplasia
atresia
dysplasia
anaplasia
A 
agenesis = complete absence of organ + its primordium
aplasia = absence of organ due to incomplete development of its primordium
atresia = absence of opening (usually of hollow organs)
dysplasia = abnormal organisation of cells (usually at sites of metaplasia - "pre-malignant")
anaplasia = lack of differentiation
58
Q

heterotopia

hamartoma

A 
Heterotopia = well developed tissue in wrong site
hamartoma = disorganised tissue in appropriate site
59
Q

classification of tumours

A

EPITHELIAL

  • benign = adenomas/papillomas
  • malignant = carcinomas

MESENCHYMAL
- benign = -omas
(except melanoma/thyroma/semiroma)
- malignant = sarcinomas

60
Q

clues that a cancer is hereditatory

A
  • young age onset
  • bilateral cancer/ multiple cancers in same individual
  • close relatives affected
  • patterns of cancer matching specific syndromes (eg. ovarian + breast)
61
Q

KRAS

A

point mutation activated oncogene

tyrosine kinase receptors –> SH2 domain—> activated Ras

Ras + GDP = OFF
Ras + GTP = ON

point mutation(chromosome 12/13/18) causes constant activated Ras due to lack of GTPase activity

62
Q

c-myc

condition example where this is common

A

gene amplification activation of protooncogene–> oncogene

myc genes normally encode for TF

insertion of viral genome between 1st and 2nd exon of chromosome 8 –> unregulated expression of c-myc

dysregulated by its own promoter/enhancer

Burkitt’s lymphoma = chromsome 8 + chromosme 14 translocation

63
Q

BCR-ABL1

A

robertsonian translocation of BCR 22 + ABL 9

philadelphia chromosme = changed chromosome 22

continuous tyrosine kinase activity

64
Q

DNA repair enzymes for

  • single strand breaks/insertions/deletions
  • ds breaks
A

single strand

  • base excision repair = PARP
  • nucleotide excision repair = XP polymerase
  • mismatch = MSH2/MLH1

ds
-recombination repair = BCR1/2/ATM/ATR/DNA PKA

65
Q

tumour invasion mechanisms

A
  • increased mechanical pressure
  • hypoxia–> angiogenesis
  • increased motility of malignant cells (EMT)
  • degradative enzymes
66
Q

how hypoxia–> angiogenesis in cancer

A
  1. HIF1 induced
  2. promotion of angiogenic factors (VEGF/FGF2/TGF-B/HGF/SF)
    these are bound to ECM inactively but matrix metalloproteinases from cancerous cells allows them to be released
  3. tip cells grow down angiogenic factor gradient to tumour
67
Q

EMT loss of/acquisiton of

A

loss of

  • E-cadherin
  • epithelial shape
  • cell polarity
  • cytokeratin intermediated filament expression

acquisition of

  • N-cadherin
  • fibroblast-like shape/motility
  • invasiveness
  • vimentin intermediate filament expression
  • mesenchymal gene expression
  • protease secretion (MMP2/MMP9)
68
Q

what are normally on healthy cells that inhibit MMPs

A

TIMPs

tissue inhibitors of metalloproteinases

69
Q 
different grading systems of 
bladder
kidney 
prostate
breast
A 
bladder = low/high
kidney = fhurman 1 to 4
prostate = Gleason 1 to 5
breast = bloom-richardson 1 to 3
70
Q

different staging systems (just list)

A

Ann Arbor - Hodgkins
Dukes - colorectal
FIGO - gynaecological
TNM = tumour nodes metastises

71
Q

dukes staging

A 
A = Within colon/bowel walls
B = invaded past bowel walls but NOT in nodes
C = spread to lymph nodes
72
Q

ann arbor staging

A 
I = 1 lymph node
II = >1 but on same side of diaphragm
III = either side of diaphragm
IV = non-lymphorecticular organs affected

adding B is presents with symptoms = fever/night sweats/weight loss

73
Q

metaplasia examples of
-columnar–> squamous

-squamous–> columnar

A

columnar–> squamous

  • resp tract due to chronic irritation (eg. smoking)
  • stones in excretory ducts
  • endocervix as it everts @puberty

squamous–> columnar

  • barret’s oesophagus
  • helicobacter infected stomach

Semester 4 (10 decks)

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