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Year 3 Sem 1 > Week 6 > Flashcards

Week 6 Flashcards

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
Q

how does alcohol cause seizures?

A

alcohol chronically stimulates GABA-A receptors so once you withdraw you can get seizures

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26
Q

what is the specific gravity of alcohol?

A

0.789

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27
Q

what are some discriminating features of FAS?

A 
short palpebral fissure
flat midface
short nose
indistinct philtrum
thin upper lip
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28
Q

what are some associating features of FAS?

A

epicentral folds
low nasal bridge
minor ear abnormalities
micrognathia

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29
Q

what is FLAGS in brief intervention of alcohol?

A 
feedback
listen
advice
goals
strategies
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30
Q

what is the pharmacotherapy used in alcohol?

A

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

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31
Q

what component does wernickes encephalopathy affect?

A

physiological component - nystagmus and ophthalmopleia

32
Q

what components does korsokoffs psychosis affect?

A

psychological component/ behavioural component

often later at the irreversible stage

33
Q

what are some symptoms of mild withdrawal in alcohol?

A

anxiety, agitation, nausea, tremor, tachycardia, hypertension, disturbed sleep

34
Q

what are some symptom fo severe withdrawal by alcohol?

A

vomiting, severe agitation, disorientation/ confusion, paranoia, hyperventilation and delirium

35
Q

when to use diazepam and oxazepam in alcohol withdrawal?

A

use diazpam during withdrawal and then taper off for management
if liver is impaired use oxazepam

36
Q

what are the different strengths of beer?

A

full: 4.8%
mid: 3.5%
low: 2.7%

37
Q

what are the different strengths of wine?

A

red: 13%
white: 11.5%
champagne: 12%

38
Q

what components in cannibis extracts exhibit therapeutic effects? when are they used?

A

cannabinol and cannabidiol

- epilepsy, MS, chemo induced nausea

39
Q

MOA of nicotine?

A

agonist of nACH-R in CNS

40
Q

MOA of NRT?

A

agonist of nACH-R

41
Q

MOA of veranacline? adverse effects?

A

partial agonist at a4b2 nACH-R

serious psychotic symptoms

42
Q

MOA of bupropion?

A

nACH-R antagonist

inhibits DAT= decrease DA uptake = increased in synaptic cleft

43
Q

which HLA-As must we match in transplantation?

A

HLA-A,B, DR

44
Q

how many HLA alleles should you try and match?

A

at least 6 but aim for 12
HLA-A,B, DR essential
HLA-C, DQ would be good

45
Q

how to interpret results of lymphocyte cross matching?

A

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
Q

what are some cell based assays used to determine if recipient Ab are present against donor Ag?

A

complement mediated lysis of donor cells (classical complement pathway)
flow cytomery based methods

47
Q

what are some ways anti-HLA levels can change?

A

blood transfusions, previous transplants, pregnancies (make HLA Ab against paternal HLA)

48
Q

what are the 3 main occasions for immunosuppression in transplantation?

A

induction
maintenance
tx of acute and chronic rejections

49
Q

immunosuppressive agents: Ab therapies?

A

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
Q

calcineurin inhibitors?

A

tacrolimus and cyclosporine = decrease synthesis of pro-inflammatory cytokines

51
Q

mTOR inhibitors?

A

sorilimus

block T cell activation

52
Q

antiproliferative agentS?

A

mycophenolates and azathioprine

used to stop tumour cell and T cell proliferation

53
Q

what kind of graft rejection occurs when AB react with endothelium?

A

hyperacute graft rejection

54
Q

what mechanism is used to decrease the chance of sensitized HLA Ag after blood transfusion?

A

blood transfusions with leuco-depleted blood product which decreases the chances of recipient becoming sensitized to donor HLA

55
Q

consequences of long term use of calcineurin inhibitors?

A

nephrotoxicity

56
Q

how does the blockade of costimulatory signal in T cells help transplant survival?

A

block induces transplantation tolerance and prevents allograft rejection (eg, anti-CD40 mAB or CTLA4 block to CD80/86)

57
Q

what is graft vs host disease?

A

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
Q

drugs to stop sustaining proliferative signalling?

A

EGFR inhibitors

59
Q

drugs to stop evading growth suppressors?

A

cyclin dependant kinase inhibitors

60
Q

drugs to stop avoiding immune destruction?

A

activating anti-CTLA4 mab

61
Q

how to stop enabling replicative immunity?

A

telomerase inhibitors

62
Q

how to stop tumour promoting inflammation?

A

selective anti-inflammatory drugs

63
Q

how to stop activating invasion metastases?

A

inhibitors HGF k-met

64
Q

how to stop inducing angiogenesis?

A

VEGF inhibitors

65
Q

how to stop genome instability and mutations?

A

PARP inhibitors

66
Q

how to stop resisting cell death

A

pro-apoptotic BH3 mimetics

67
Q

how to stop deregulating cellular energetics?

A

aerobic glycolysis inhibitors

68
Q

significance of ABL-BCR translocation?

A

ABL normally codes for TK pathway, so once BCR binds to it the TK pathway is constitutively active

69
Q

what are some elevated biomarkers for alcohol dependance?

A

MVC
GGT
LFTs

70
Q

symptoms of nicotine withdrawal?

A 
dysphoria/ depressed mood
anxiety
weight gain 
insomnia 
difficulty concentrating 
breathlessness
decreased HR
71
Q

what does renal transplant pathology look like?

A

lots of inflammatory cells
little purple nuclei
predominately T cells (hyper acute will have neutrophils)
nuclei all around the BV

72
Q

what was the original transplant drug and why are we moving away from it?

A

calcineurin inhibitors however long term use causes nephrotoxicity so new Abs target IL2-R signalling or production = stops T cell proliferation

73
Q

define some features of the effector stage in transplants?

A

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
Q

another name for microlymphocytotoxicity assay?

A

lymphocyte cytotoxicity assay

75
Q

what are some sign of kidney graft rejection?

A

short term: infection, abcesses, hematuria, abdominal hernia

later: pylonephritis, kidney stones and kidney dysfunction

76
Q

what are the main differences between BMT and HSCT?

A

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
Q

3 main groups of complications associated with BM/HSCT?

A

infections
non-infectious
GVHD (so use T cell depleted SC)

Year 3 Sem 1 (12 decks)

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