Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Semester 4 > MOD > Flashcards

MOD Flashcards

(73 cards)

Start Studying
1
Q

what is influenza

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how do NKcells and macrophages activate each other

A

macrophages—-IL-12—>nkc

NKC——IFN-gamma—-> macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

3 cell check points

A

late G1

before entering mitosis

during chromosomes aligned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what family CASPases lead to programmed cell death

A

BCL2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

drugs affecting M phase

A

colchicine
vinca alkaloids
palcitaxel (taxol)

stabilise free tubulin–> prevents chromosomes being pulled apart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what specific Cyclin-CDK complex works during G1

A

cyclin D - CDK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic Granulomatous Disease

A

Mutation in NADPH component

Defect in oxidative burst

= Phagocytosed microbes cant be killed leading to recurrent infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Chediak-Higashi Syndrome

A

Defective phagosome-lysosome fusion

= Phagocytosed microbes cant be killed leading to recurrent infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what bacteria causes whooping cough

A

bordetella pertussis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what acid components for gram +ve and -ve bacteria
+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
26
how are very large bacteria destroyed that cannot be taken up by macrophages
Ab bind to their antigens and Fc of Ab is recognised by eosinophils--->degranulation
27
herpes viridae common properties
icosahedral nucelocapsid dsDNA, linear enveloped ability to lay latent then reactivate
28
HIV structure
2 RNA (enveloped) reverse transcriptase protease integrase 2 viral proteins: gp120 gp41
29
human hepatitis virus
``` A B C D E ```
30
gastrointestinal infections
rotavirus | norovirus
31
consequences of parovirus
decreased erythropoiesis (reduced RBC lifespan <120days) erythema infectosum (slapped cheek) + red rash on trunk and limbs
32
what does HA bind to on host cells (influenza virus)
sialic acid
33
why so much influenza mutation
due to RNA polymerase not having proof reading/low selectivity leads them to make many different esp. type A
34
antigenic shift | antigenic drift
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
secondary infection
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
how CMV (cytomegalovirus) evades immune
decreases MHC I--> decrease in viral peptide presentation to CD8+
37
what examples of virus that make non-replicating cells---> divide--> cancer cells
papillomavirus | Hep B,C
38
high risk HPV
16,18,31,45
39
how papillomavirus--> cancer
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
4 type of toxins
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
action of alpha-lecithinase
a bacteria enzyme that splits lecithin on host membrane - allowing lysis to occur
42
endotoxins actions
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
super antigen of staphylococcus aureus and strep pyogenes
Staph A - toxic shock syndrome toxin(TSST) strep P - streptococcal pyrogenic exotoxin (SPE)
44
what happens during toxic shock syndrome
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
how can streptococcus A lead to rheumatic heat disease
molecular mimicry (immunopathology) Ab produced against it start attacking heart/bone due to similar structure
46
molecules that act as opsonins
IgG1 and 3 (phagocytes had a receptor to bind to Fc region of Ab) C3b CRP
47
replication cycle of rotavirus
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
what is protein A
binds to Fc regions of IgG --> preventing opsonisation function of IgG--> prevents phagocytes binding
49
what Ig does not fix complement
IgA | so pathogens can coat with IgA--> no complement
50
adaptive immune evasion
- 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
innate immune evasion
- 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
how many driver mutations for carcinogenesis
2-8
53
alkylating-like agents
direct chemical carcinogens form covalent bonds between guanines on DNA preventing strand seperation decreasing DNA replication used in chemotherapy
54
function of tumour promoters
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
physical carcinogens
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
viral carcinogens properties to cause cancer
- must have stable Association with cells - must not kill the cell - must evade immune surveillance HPV/HepB/HepC/Epstein barr
57
``` agenesis aplasia atresia dysplasia anaplasia ```
``` 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
heterotopia | hamartoma
``` Heterotopia = well developed tissue in wrong site hamartoma = disorganised tissue in appropriate site ```
59
classification of tumours
EPITHELIAL - benign = adenomas/papillomas - malignant = carcinomas MESENCHYMAL - benign = -omas (except melanoma/thyroma/semiroma) - malignant = sarcinomas
60
clues that a cancer is hereditatory
- young age onset - bilateral cancer/ multiple cancers in same individual - close relatives affected - patterns of cancer matching specific syndromes (eg. ovarian + breast)
61
KRAS
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
c-myc condition example where this is common
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
BCR-ABL1
robertsonian translocation of BCR 22 + ABL 9 philadelphia chromosme = changed chromosome 22 continuous tyrosine kinase activity
64
DNA repair enzymes for - single strand breaks/insertions/deletions - ds breaks
single strand - base excision repair = PARP - nucleotide excision repair = XP polymerase - mismatch = MSH2/MLH1 ds -recombination repair = BCR1/2/ATM/ATR/DNA PKA
65
tumour invasion mechanisms
- increased mechanical pressure - hypoxia--> angiogenesis - increased motility of malignant cells (EMT) - degradative enzymes
66
how hypoxia--> angiogenesis in cancer
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
EMT loss of/acquisiton of
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
what are normally on healthy cells that inhibit MMPs
TIMPs | tissue inhibitors of metalloproteinases
69
``` different grading systems of bladder kidney prostate breast ```
``` bladder = low/high kidney = fhurman 1 to 4 prostate = Gleason 1 to 5 breast = bloom-richardson 1 to 3 ```
70
different staging systems (just list)
Ann Arbor - Hodgkins Dukes - colorectal FIGO - gynaecological TNM = tumour nodes metastises
71
dukes staging
``` A = Within colon/bowel walls B = invaded past bowel walls but NOT in nodes C = spread to lymph nodes ```
72
ann arbor staging
``` 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
metaplasia examples of -columnar--> squamous -squamous--> columnar
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions