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Year 3 Sem 1 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

important general features of immune responses to microbes?

A

response is mediated by both innate and adaptive effector mechanisms

response is distinct and specialized to effectively combat specific infectious agents

the ability to evade and resist the effector mechanisms that enable the microbe to survive

tissue injury and disease may be caused by the host response to the microbe

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2
Q

what are some ways of direct host damage?

A

exotoxin secreted by bacteria
endotoxins wall of gram negative bacteria
direct killing of host cells (pathogen replication lyses host cell)
physical blockage
secrete toxins that directly damage host cell
interfere with synthesis of protein metabolism, change signalling pathways in the host cell, produce enzymes that damage host cell

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3
Q

some examples of exotoxins?

A

clostridium tetani = tetanus (interferes with inhibitory neutrons)
staphylococcus aureus = toxic shock syndrome (release of toxins that act as super antigens = non specific T cell cytokine release)
streptococcus pyogenes = tonsillitis

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4
Q

some examples of endotoxins?

A

escherichia coli = gram neg sepsis
haemophilus influenzae = meningitis pneumonia
salmonella type = typhoid fever

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5
Q

examples of pathogens that cause direct cytopathic effect:

A 
variola = smallpox
varicella-zoster= chickenpox/shingles
hepatitis B virus
polio virus = poliomyelitis 
measles virus 
influenza virus 
herpes simplex virus = cold sores
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6
Q

what are some ways of indirect host damage?

A

immune complexes (HepB, malaria)
molecular mimicry
aberrant immune responses (T cells)
immune response against pathogen can lead to tissue damage in the host = granulomatous inflammation

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7
Q

what is a chemoattract for Th17 cells?

A

CCL20

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8
Q

what is a chemoattractant for monocytes?

A

CCL2 (produced by Th1)

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9
Q

what are some bacterial strategies for avoiding and manipulating host immune responses:

A

escape epithelial defences - degrade mucous
escape from phagocytes and innate immunity - capsules, Ig binding, opsonization
evade adaptive immunity - resistance to Ab via capsules

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10
Q

what are some ways that bacteria resist innate immune responses?

A

prevention of lysosome-phagosome fusion
escape into the cytoplasm from phagosome
resistance to lysosomal enzymes

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11
Q

what are the different serogroups of neisseria meningitides?

A

A, B, C, X, Z, W135

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12
Q

which Neisseria meningitides serogroups have the capsular polysarccharides?

A

A, C, W135 and Y

capsule used as a conjugate in vaccine

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13
Q

why is Nm serogroup B poorly immunogenic?

A

B capsular polysaccharide is poorly immunogenic because identical to the polysialic acid present in many human glycoproteins

group B vaccine is protein antigen based

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14
Q

hydroxyurea?

A

antimetabolite- urea analogue

- inhibits ribonucleotide reductase, thus interfering with the conversion of ribonucleotides to deoxy ribonucleotides

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15
Q

what phase do antimetabolites work at?

A

S phase

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16
Q

pharmacokinetics of alkylating agents?

A

cyclophosphamide- needs P450 metabolism in liver for activity

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17
Q

what phase do alkylating agents work?

A

not cell specific but predominantly S phase

cell cycle block at G2

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18
Q

adverse effects of platinum compounds?

A

myelosuppression, CINV

cisplatin = nephrotoxic, ototoxic

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19
Q

indication for platinum compounds?

A

primary tx for ovarian and testicular cancer

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20
Q

what phase do vinca alkaloids work?

A

M phase

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21
Q

what phase do taxanes work at?

A

G2-M phase

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22
Q

difference between vinca alkaloids and taxanes?

A

vinca alkaloids binds b tubulin and block polymerization with a-tubulin into MT = prevents spindle formation in dividing cells and causes arrest at M phase

taxanes: stabilize MT in non-functional polymerized state and thus can’t pull part for cell division

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23
Q

indications for taxanes?

A

ovarian cancer

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24
Q

at which phase do topoisomerase 1 inhibitors work at?

A

S phase

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25
Q

adverse effect of anthracylcines?

A

long term therapy can lead to cardiomyopathy

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26
Q

which drug is used as a chemical carceration in sex offenders?

A

cyproterone (anti-androgen) - has prosgestogenic effects that decrease production of testosterone

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27
Q

actions of mTOR1?

A 
protein synthesis
ribosome biogenesis 
cell survival
proliferation
angiogenesis
invasion
migration/ metastases
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28
Q

actions of mTOR2?

A

cell survival
cell cycle progression
actin remodelling

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29
Q

indications for nivolumab?

A

NSCLC, melanoma

30
Q

indications for ipilimumab?

A

metastatic melanoma

31
Q

mechanism of cytotoxic drug resistance: transport?

A

decreased accumulation of cytotoxic drugs in the cells due to increased expression of drug transport efflux pumps (P-glycoprotein)
decreased amount of drug uptake in cell

32
Q

mechanism of cytotoxic drug resistance: metabolic?

A

decreased metabolic activation of drug (5-FU)
increased inactivation of the drug (anti-metabolites)
increased concentration of target enzymes (methotrexate - DHFR)
decreased requirement for substrates/ utilization of alternative metabolic pathways

33
Q

mechanism of cytotoxic drug resistance: targets?

A

mutations leads to altered/ resistant target molecules
increased repair of drug induced dNA damage
inhibition of apoptosis

34
Q

difference between cocaine and methamphetamines?

A

cocaine: shorter duration of action; blocks reuptake of DA
meth: longer duration of action; blocks reuptake of DA and stimulates the release of DA from VMAT2

35
Q

what are some physical harms with stimulants?

A 
OD
renal failure
cardiac failure
seizure 
MI
rhabdomyolosis 
malnutrition
36
Q

long term effects of amphetamine use

A

chronic insomnia
psychosis - lasting up to weeks
HTN, abnormal HB, MI risk
self medication with psycho depressants
malnutrition, less resistant to infections (BBV)
brain damage: memory impairment, cognitive/ motor impairment, impaired thinking
violent, aggressive behaviour

37
Q

what are the 3 phases of amphetamine withdrawal and what is the onset and durations?

A

crash phase: 12-24 hrs after use, subsides 2-4 days
withdrawal phase: 2-4 days after use; subsides over 2-4 weeks
extinction phase: weeks to months

38
Q

what are some characteristics of the crash phase of amphetamine withdrawal?

A

low cravings
fluctuations in mood
disturbed sleep, exhaustion, fatigue
generalized aches and pain

39
Q

what are some characteristics of withdrawal phase of amphetamine withdrawal?

A

strong cravings
increased appetite
fluctuating mood
disturbed sleep, vivid dreams, insomnia,
poor concentration/ attention
disturbed thoughts/ perceptions that can re-emerge but were masked in crash phase

40
Q

what are some characteristics of extinction phase of amphetamine withdrawal?

A

gradual resumption to normal mood with periodic episodes of mood changes
disturbed sleep
episodic cravings

41
Q

more prominent effects of cocaine when compared to amphetmaines?

A

hyperthermia
pulmonary edema
seizures
muscle rigidity

42
Q

the effects of GHB?

A

seizures, resp depression, coma, N&V, aggression

hypnotic with narrow therapeutic window so ID is common

43
Q

what is the safe level of caffeine for adults?

A

<400mg/day for adults

44
Q

specific opiate withdrawal symptoms?

A

goosebumps, yawning, runny nose, abdo cramps, diarrhea

45
Q

specific withdrawal symptoms for alcohol?

A

tremors, confusion (seizures, delirium, hallucination), fever

46
Q

onset and duration of alcohol withdrawal?

A

3-24 hours

4-10days

47
Q

mechanism of dependance and withdrawal for cocaine?

A

increase expression of DAT
increased presynaptic DA receptors
presynaptic DA is depleted

48
Q

what is the safe level of caffeine per day?

A

<400mg/day

49
Q

Th1 functions in IC bacteria:

IL3 and GM-CSF?

A

IL3 and GMCSF= stimulate production of monocytes in BM

50
Q

Th1 functions in IC bacteria:

TNFa and LTa

A

act on local BV, activates endothelium to induce macrophage binding and exit from BV at the site of infection

51
Q

what is the chemoattractant for monocytes and where does it come from?

A

CCL2 made from Th1 cells

52
Q

how does escaping epithelial defences help -bacteria avoid immune response?

A

interfere with physical barrier - degrade mucus
attachment and colonization
evasion of immune recognition (antigenic variation and LPS)

53
Q

how do bacteria escape from phagocytes and innate immunity?

A

capsules, Ig binding, opsonization, complement

interfere with phagocytosis and phagocyte recruitment (degrades chemokine)

54
Q

how do bacteria evade adaptive immunity?

A

resistance to bacteria

interfere with cytokine secretion, Ag presentation

55
Q

what is the characteristic pathological feature tb?

A

tb cavity formed when caseated and liquefied centre of tubercular pulmonary lesion is discharged into a bronchus

56
Q

how is dx of tb made?

A

chest x ray
sputum is stained with stain for acid and alcohol fast bacilli
immune based tests (mantoux test)

57
Q

prevalence of lynch syndrome?

A

1:660 - 1:2000

58
Q

prevalence of hereditary breast and ovarian cancer?

A

1:1600

59
Q

prevalence of familial adenomatous polyposis?

A

1:8000

60
Q

prevalence of cowed syndrome?

A

1: 20 000

very rare

61
Q

prevalence of li-fraumeni syndrome?

A

very rare

62
Q

prevalence of von-hippel lindau syndrome?

A

1: 36 000

63
Q

difference between septic shock and toxic shock syndrome?

A

septic shock = mediated by macrophages and endotoxin (LPS)

toxic shock syndrome = mediated by T cell cytokines and endotoxin (staph aureus)

64
Q

What is the consequence of the immune suppression seen in severe sepsis?

A

The cytokine storm seen in sepsis can cause activation-induced cell death (T cells, dendritic cells, etc.) and suppression of antigen presentation leading to the loss of adaptive immune responses. Immunosuppressed patients are then at increased risk of opportunistic infection. Anti-inflammatory cytokines (e.g. IL-10) released to allow return to homeostasis also impair APC/T cell function.

Immunosuppression in severe sepsis predisposes patients to secondary infection that can delay recovery of organ function following the initial pro-inflammatory response. It also has important implications in the care of the elderly septic patients, as elderly patients exhibit increased susceptibility to both infection and septic shock.

65
Q

septic shock?

A

Septic shock: sepsis is the presence of an infection in the bloodstream that results in the excessive release of TNF-alpha from macrophages throughout the body. The systemic release of TNF-alpha into the blood causes vasodilation and increased vascular permeability, this, in turn, leads to loss of plasma volume and eventual shock, also known as septic shock. This damage to capillary endothelium and vessel wall vasodilation which may also lead to multiple organ failure due to ischaemia.

66
Q

how does neisseria meningitides evade immune response?

A

polysaccharide capsule
changes surface proteins (evade adaptive immunity)
This pathogen also produces IgA1 proteases which serve as a virulence factor by overriding mucosal immunity

67
Q

how does meningococcal present? (Nm)

A

septecemia and meningitis

68
Q

what class of bacteria is TB?

A

classified as acid fast bacteria due to their impermeability by certain dyes and stains.

69
Q

how does Tb spread?

A

M. tuberculosis primarily infects alveolar macrophages but can infect other cell types. It then transits to lung parenchyma where it can infect resident macrophages or other phagocytes like neutrophils. Have the ability to replicate inside macrophages. Immune signals produced by infected macrophages provide additional target for infection. Bacteria can also be taken up by DCs to circulate to thoracic lymph node, where they activate T cells. These T cells return to the infectious site and organise around infected macrophages to form granulomas, which serves as a reservoir for bacteria.

70
Q

Anti-TB drug resistance is a major public health problem that threatens TB care and control worldwide. Why has TB drug resistance emerged?

A

Spontaneous gene mutations in TB render the bacteria resistant to anti-TB drugs thereby increasing their chance of survival and consequent transmission to other people when not adequately treated. Because the standard treatment for TB calls for a strict six-month drug regime, compliance with the treatment is very often very challenging and rates of non-compliance or premature treatment interruption can be high, allowing for the development of drug-resistant bacteria that can then be transmitted to other people.

Year 3 Sem 1 (12 decks)

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