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Year 3 Sem 1 > Week 6 > Flashcards

Week 6 Flashcards

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1
Q

function of PTEN and consequences of mutation?

A

normally inhibits PI3K

mutation = endometrial carcinoma

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2
Q

example of GOF mutation in cyclins and CDKs?

A

D cyclin and CDK4 promote progression from G1-S

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3
Q

example of LOF mutation in cyclins and CDKs?

A

TSG mutation (p.16, RB, TP53) that inhibit G1-S

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4
Q

what part of the cell cycle does Rb protein control?

A

transition from G1 to S

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5
Q

function of E2F?

A

required for synthesis of DNA replication enzymes

when Rb is bound to E2F - transcription and translation is stopped

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6
Q

how do GF affect Rb proteins?

A

GF phosphorylate Rb- detaching it from E2F = allowing gene transcription/ mRNA translation and transition to S phase

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7
Q

what is contact inhibition?

A

the cell to cell connection of E cadherin to the next epithelial cell
loss of contact inhibition contributes to metastasis and local invasion

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8
Q

function of APC?

A

encodes factors that negatively regulate WNT pathway in colonic epithelium by forming a complex that degrades B-catenin

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9
Q

what is associated with a NF2 mutation?

A

neurofibromatosis type 2

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10
Q

how does TGF-B carry out its inhibitory functions?

A

activates inhibitors of CDK and suppressors of MYC

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11
Q

what is CDKN2a?

A

negative regulator of cell entry and progression

encodes TSG and ARF (stabilizes p53)

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12
Q

what is another name for Fas

A

CD95

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13
Q

why re mutations in apoptosis more important in blood cancers?

A

because it regulates the number of lymphocytes

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14
Q

how do cells become senescent in terms of replication?

A

shortened telomeres are interpreted by DNA repair machinery as double stranded breaks leading to cell cycle arrest via p53 and Rb and senescence

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15
Q

how does hypoxia stimulate angiogenesis?

A

via H1F1-alpha

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16
Q

how do cancer cells degrade the basement membrane?

A

they express matrix mellaproteases in higher amounts than normal cells

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17
Q

what is the basis for PET imaging?

A

warburg effect

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18
Q

what is micro satellite instability?

A

regions of receptive DNA sequences prone to shortening or extension when mismatch repair enzymes are defective

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19
Q

what is imatinib ?

A

BCR-ABL kinase inhibitor

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20
Q

how do we know what drugs are being used?

A 
needle syringe program reporting 
hospitalization s
monitoring scehmes - IDRS, EDRS, household surveys 
forensic capture 
sewage monitoring
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21
Q

what are the 3 pillars of harm minimization?

A

demand reduction
supply reduction
harm reduction

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22
Q

what are the 3 approaches to harm minimization?

A

priority actions
priority populations
priority substances

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23
Q

psychological steps for dependance? (8)

A

exposure to substance with abuse potential
positive aspects of neurochemical activation outweight negative aspects in the ind
environmental context is conducive to repeated use
repeated use results in receptor adaptation
downstream neurological function alters to adjust for receptor adaptation
tolerance- need more drug for same effect
tolerance fuels desire for more drug use
dependence - normal function requires increased level of binding
withdrawal - removal of substance produces adverse effects

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24
Q

general features of withdrawal from CNS stimulant/ depressant.

A 
sweating
N&V, appetite disturbances
restless, irritable, angry 
depression, anxiety 
loss of self-control
muscle/ abdo cramps
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25
how does alcohol cause seizures?
alcohol chronically stimulates GABA-A receptors so once you withdraw you can get seizures
26
what is the specific gravity of alcohol?
0.789
27
what are some discriminating features of FAS?
``` short palpebral fissure flat midface short nose indistinct philtrum thin upper lip ```
28
what are some associating features of FAS?
epicentral folds low nasal bridge minor ear abnormalities micrognathia
29
what is FLAGS in brief intervention of alcohol?
``` feedback listen advice goals strategies ```
30
what is the pharmacotherapy used in alcohol?
naltrexone- opioid receptor antagonist - decreases the effects of endogenous opioids = decreases feelings of rewards from alcohol acamprosate- inhibits NMDA receptor and activates GABAA receptors - decreases the 'need' for alcohol disulfiram - inhibits acetaldehyde dehydrogenase
31
what component does wernickes encephalopathy affect?
physiological component - nystagmus and ophthalmopleia
32
what components does korsokoffs psychosis affect?
psychological component/ behavioural component | often later at the irreversible stage
33
what are some symptoms of mild withdrawal in alcohol?
anxiety, agitation, nausea, tremor, tachycardia, hypertension, disturbed sleep
34
what are some symptom fo severe withdrawal by alcohol?
vomiting, severe agitation, disorientation/ confusion, paranoia, hyperventilation and delirium
35
when to use diazepam and oxazepam in alcohol withdrawal?
use diazpam during withdrawal and then taper off for management if liver is impaired use oxazepam
36
what are the different strengths of beer?
full: 4.8% mid: 3.5% low: 2.7%
37
what are the different strengths of wine?
red: 13% white: 11.5% champagne: 12%
38
what components in cannibis extracts exhibit therapeutic effects? when are they used?
cannabinol and cannabidiol | - epilepsy, MS, chemo induced nausea
39
MOA of nicotine?
agonist of nACH-R in CNS
40
MOA of NRT?
agonist of nACH-R
41
MOA of veranacline? adverse effects?
partial agonist at a4b2 nACH-R | serious psychotic symptoms
42
MOA of bupropion?
nACH-R antagonist | inhibits DAT= decrease DA uptake = increased in synaptic cleft
43
which HLA-As must we match in transplantation?
HLA-A,B, DR
44
how many HLA alleles should you try and match?
at least 6 but aim for 12 HLA-A,B, DR essential HLA-C, DQ would be good
45
how to interpret results of lymphocyte cross matching?
so recipient serum mixed with donor lymphocytes and add complement if donor specific Ab not present - complement is not activated and cannot lyse cells if donor specific Ab are present then Ab will bind to lymphocytes and complement is activated to lyse cells and the cells take up dye
46
what are some cell based assays used to determine if recipient Ab are present against donor Ag?
complement mediated lysis of donor cells (classical complement pathway) flow cytomery based methods
47
what are some ways anti-HLA levels can change?
blood transfusions, previous transplants, pregnancies (make HLA Ab against paternal HLA)
48
what are the 3 main occasions for immunosuppression in transplantation?
induction maintenance tx of acute and chronic rejections
49
immunosuppressive agents: Ab therapies?
IL2-R antagonist (basiliximab) - often used for induction therapy - binds IL2-R on alpha chain of T lymphocytes and prevents IL2 mediated acitvation lymphocyte deleting AB - anti-CD3 mAB = deplete T cells from recipient Ab against CD3
50
calcineurin inhibitors?
tacrolimus and cyclosporine = decrease synthesis of pro-inflammatory cytokines
51
mTOR inhibitors?
sorilimus | block T cell activation
52
antiproliferative agentS?
mycophenolates and azathioprine | used to stop tumour cell and T cell proliferation
53
what kind of graft rejection occurs when AB react with endothelium?
hyperacute graft rejection
54
what mechanism is used to decrease the chance of sensitized HLA Ag after blood transfusion?
blood transfusions with leuco-depleted blood product which decreases the chances of recipient becoming sensitized to donor HLA
55
consequences of long term use of calcineurin inhibitors?
nephrotoxicity
56
how does the blockade of costimulatory signal in T cells help transplant survival?
block induces transplantation tolerance and prevents allograft rejection (eg, anti-CD40 mAB or CTLA4 block to CD80/86)
57
what is graft vs host disease?
mature T cells injected in allogeneic transplant see the recipients cells in BM are foreign and initiate an immune response = inflammation (rashes, diarrhea, pneumotitis)
58
drugs to stop sustaining proliferative signalling?
EGFR inhibitors
59
drugs to stop evading growth suppressors?
cyclin dependant kinase inhibitors
60
drugs to stop avoiding immune destruction?
activating anti-CTLA4 mab
61
how to stop enabling replicative immunity?
telomerase inhibitors
62
how to stop tumour promoting inflammation?
selective anti-inflammatory drugs
63
how to stop activating invasion metastases?
inhibitors HGF k-met
64
how to stop inducing angiogenesis?
VEGF inhibitors
65
how to stop genome instability and mutations?
PARP inhibitors
66
how to stop resisting cell death
pro-apoptotic BH3 mimetics
67
how to stop deregulating cellular energetics?
aerobic glycolysis inhibitors
68
significance of ABL-BCR translocation?
ABL normally codes for TK pathway, so once BCR binds to it the TK pathway is constitutively active
69
what are some elevated biomarkers for alcohol dependance?
MVC GGT LFTs
70
symptoms of nicotine withdrawal?
``` dysphoria/ depressed mood anxiety weight gain insomnia difficulty concentrating breathlessness decreased HR ```
71
what does renal transplant pathology look like?
lots of inflammatory cells little purple nuclei predominately T cells (hyper acute will have neutrophils) nuclei all around the BV
72
what was the original transplant drug and why are we moving away from it?
calcineurin inhibitors however long term use causes nephrotoxicity so new Abs target IL2-R signalling or production = stops T cell proliferation
73
define some features of the effector stage in transplants?
cell mediated, Ab, complement Macrophages and T cells initiate an inflammatory response Ag presentation to T cells increases as expression of adhesion molecules, MHCII, chemokine and cytokines is unregulated this promotes shedding of intact, soluble MHC molecules that may be involved in the activation of indirect allorecognition pathway T cell cytokines promote macrophages infiltration, EC activation and more T cells = amplification of response
74
another name for microlymphocytotoxicity assay?
lymphocyte cytotoxicity assay
75
what are some sign of kidney graft rejection?
short term: infection, abcesses, hematuria, abdominal hernia | later: pylonephritis, kidney stones and kidney dysfunction
76
what are the main differences between BMT and HSCT?
BM- take stem cells directly HSCT- take stem cells from peripheral circulation (give GCSF to give the BM a jump start to pump more SC in peripheral blood)
77
3 main groups of complications associated with BM/HSCT?
infections non-infectious GVHD (so use T cell depleted SC)

Year 3 Sem 1 (12 decks)

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