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SBT Flashcards

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1
Q

histamine production / degradation

A

histidine —-histidine decarboxylase—> histamine

degraded by INMT and diamine oxidase

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2
Q

role of histamine

A

acute inflammation + gastric acid production

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3
Q

4 histamine receptors

A

H1 - SM: CNS/endothelium/lungs/arterioles
H2 - stomach / heart
H3 - presynaptic terminals
H4 - gut / bone marrow/ basophils

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4
Q

what inhibits histamine release

A

stimulation of B2-adrenergic receptors on mast cells/basophils

EG. Salbutamol

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5
Q

what cells produce histamine

A

ECL

mast cells (activated by igE, C3a,4a,5a) - pre-made granules w/ heparin+ acidic proteins released

neurones

basophils (blood)

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6
Q

what effects does histamine have

A

dilation (H1 - vascular SM)

constriction (H1- non-vascular SM eg. lungs)

sensitises nerve endings (H1)

increases permeability of post-venues (H1)

increases HR (H2)

increased gastric production (H2)

increased exocrine secretions due to increased BF

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7
Q

what are H1 and H2 antagonists used for

A

H1 Antagonists - to treat inflammatory
(1st gen = promethazine 2/3rd gen= terfenadine /fexofenadine)

H2 antagonists - to treat gastric problems
(ranitidine/cimetidine)

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8
Q

bradykinin synthesis and degradation

A

hageman factor cleaves pre-kallikrein

kallikrein cleaves HMWkinogen –> bradykinin

broken down by kinases (ACE/carboxypeptidase etc.)

therefore ACEi = bradykinin accumulation–> drycough

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9
Q

effects of Bradykinin

A

similar to histamine

  • vasodilation (dec. BP)
  • constriction of non-vascular SM (bronchi/gut)
  • increased permeability (exudate)
  • sensitised pain endings
  • arachidonic acid formation
  • chemotactic to leucocytes
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10
Q

serotonin synthesis + degradation

A

l-tryptophan —” hydroxylase—-> 5-hydroxy-l-tryptophan —“decarboxylase—> 5-hydroxy-tryptophan

broken down by MAO/aldehyde dehydrogenase

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11
Q

arachidonic acid production

A

2 ways

1step pathway = phospholipids—–Phospholipase A2—>AA

2 step pathway
-phospholipids—- phospholipaseC–> DAG—DAG Ligase—>AA

-Phospholipids—phospholipase D—>phosphatidic acid—–PLA2—->AA

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12
Q

what known initiators stimulate AA formation

A

bradykinin and adrenaline

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13
Q

type of COX

A

COX 1

  • active continously
  • physiological roles (vascular, renal-BF, platelet aggregation, gastric protection)

COX 2

  • needs to be stimulated
  • inflammatory

COX 3 - variant of COX 1 (CNS pain perception)

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14
Q

what does COX produce from AA

A

TXA (platelet aggregation, vasoconstriction)

PG

  • PGE2: gastric protection (by endothelial cells)
  • PGD2: bronchoconstricion, decrease platelet aggregation (by mast cells)
  • PGF2a: bronchoconstriction/uterine contraction

PGI2 (vasodilator, decrease platelet aggregation) endothelial cells

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15
Q

how are lipoxins(anti-inflammatory) and leukotrienes (inflammatory) produced

A

in leukocytes

5-LOX—> 5-HPETE—> 4-Leukotriene–>LTB4 (chemotaxis leucocytes) / sulphidopeptide leukotrienes (LTC,D,E4)

other lipoxygenases –> lipoxins

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16
Q

what 2 mediators work together during resolution stage to phagocytose/clear apoptic cells after acute inflammation

A

lipoxins

  • recruit monocytes
  • regulate activation of neutrophils

cyPG

  • inhibit macrophage activation
  • inhibit NF-kappabeta—> decrease inflammatory gene expression
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17
Q

receptors of eicosanoids

A

TXA—> TP receptors

sulphidopeptide leukotrienes –> cys-LT
LTB4—> BLT

prostaglandins—> DP/FP/IP/EP

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18
Q

why does blocking COX route worsen asthma symptoms

A

leukotrienes—> bronchoconstriction/oedema/mucus/vascular permeability

therefore blocking cys-LT receptors decrease effects of asthma

leyukotrine receptor antagonists = ____lukast

side effects = GI upset

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19
Q

poly-unsaturated fat intake effect on inflammation

A

decreases AA derived eicosanoids

contains DHA and EPA

DHA inhibits COX2, EPA inhibits 5-LOX

formation of anti-inflammatory mediators

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20
Q

what does 5-LOX require to work

A

FLAP

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21
Q

3 main effects of NSAIDS

A

BLOCKING COX

anti-pyretic

  • IL-1B normally increases PGE2–> decreases temp sensitive neurones, lowering threshold
  • decreasing PGE2

analgesic
-decreasing prostanoids that sensitise pain endings

anti-inflammatory
-decreasing PGE2/PGI2 inflammatory mediators

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22
Q

NSAIDs effects on bodily systems

skeletal/renal/CNS/GI/GU/cvs

A

skeletal
-decreases inflammatory SYMPTOMS for arthritis etc

renal

  • decrease BF
  • decreases Na excretion–> high BP

GI tract

  • new ones are friendly (COX2 specific)
  • but NSAIDs are acidic–> dec. tissue healing + GI contractions/nausea/dyspepsia (indigestion)

CNS

  • overdose: paradoxical hyperpyrexia/stupor/coma
  • avoid in chicken pox/influenza children—> Reye’s syndrome

Gential

  • PGE2/PGF2a for uterine contraction for labour
  • NSAIDs can delay labour but increase post-partum blood loss due to low TXA

resp

  • despite prostanoids–> bronchoconstriction, NSAIDs have no effect on airway tone
  • NSAIDs should be avoided by asthmatics as leukotriene pathway is not blocked (worsen)
  • overdose aspirin–> hyperventilaiton etc.
CVS
-increase bleeding time if COX1
-aspirin is beneficial as COX2 specific
endothelials can regenerate new COX2 but platelets cannot COX1
(platelets not targetted)
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23
Q

NSAID other indications

A

closure of PDA

dec. alzheimers risk

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24
Q

ulcerative colitis

A

inflammation of bowel (colon + rectum) due to high PG

aminosalicylates –> 5-ASA—> decrease eicosanoids by blocking COX/LOX

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25
what is given for gout
allopurinol (inhibits xanthine oxidase) decreasing uric acid
26
how glucocorticoids have an anti-inflammatory effect
block PLA2 --> decrease AA --> decreasing eicosanoids (therefore can be used by asthmatics) they decrease inflammatory genes/ increase anti-inflammatory gene expression block TF: AP-1 and NF-kappa beta (which normally increase inflammatory proteins) induce Ikappabetaalpaha which blocks NF-kappabeta
27
side effect of corticosteroids
osteoporosis because glucocorticoids inhibit OSTEOBLASTS gastric ulceration (dec. of COX1--> PGE2 decreased) Cushings lipodystrophy cataract
28
methods bacteria can be resistant
- drug inactivation - alter drug targets - efflux pumps - overproduction of targets - intrinsic permeability - metabolic by-pass
29
3 ways of gene transfer of bacteria
transformation - taking up free DNA and inserting into own transduction - via bacteriophages conjugation - via sex pilli transferring plasmids
30
what can be given if we know the bacteria is beta-lactam resistant
augmentin = clavulanic acid + amoxicillin C.A binds to beta-lactamase and prevents it degrading amoxicillin(that contains beta-lactam ring)
31
how do gram +ve and -ve become resistant to beta-lactams
both have beta-lactamase +ve---> alter binding proteins of b-lactam (eg. PBP) -ve--> alter porins so it can't enter
32
4 ways a bacteria can become penicillin resistant
- mutation of porin - mutation of PBP - acquire efflux pumps - accquire penicillinases (eg.b-lactamase)
33
how to overcome penicillin resistance
- reduce antibiotic use - new/modified drugs - combination therapy (preventing resistant bacteria from surviving and passing it on) - infection control
34
how can antibiotics be bad for us (microbial antagonism)
can kill our normal flora (as they can't distinguish between pathogenic bacteria and normal) this leads to overgrowth of bacteria---> toxins/harm eg. pseudomembranous colitis (overgrowth of clostridium difficile) ---> ulceration/diarrhoea
35
antibiotic classification
type of activity - bactericidial - kills (can give to immunosuppressed) - bacteriostatic - inhibits (relies on immune system to clear) spectrum of activity - broad eg. cefotaximir - narrow eg. penicillinG molecular structure -b-lactams eg. penicillins / cephalosporins
36
antibiotics that inhibit cell wall synthesis (peptidoglycan)
penicillin/cephalosporins/vancomycin
37
antibiotics that inhibit cell membrane of phospholipids
polymyxins eg. colistin
38
antibiotics that target bacterial ribosomes
50s- erythromycin/chloramphenicol/linezolid 30s - tetracycline/ aminoglycosides/deoxyclcine therefore preventing proteinsynthesis
39
antibiotics targeting bacterial DNA
quinolones--> inhibiting DNA gyrase rifampin/fidaxomicin --> inhibits RNA polymerase (tb) metronidazole- free radicals (anaerobic bacteria) nitrofurantoin - free radicals (UTI)
40
antibiotics that affect THFA
(for folic acid) anti-folates - trimethoprim: decrease DHFR - sulphonamides: PABA competitive inhibitor
41
difference between gram + and - cell wall
gram +ve have large peptidoglycan walls (made by enzymes on cell membrane) -ve have thinner but have lipopolysaccharide layer around peptidoglycan = very impermeable (therefore have PORINS) antibiotics get through gram +ve easier
42
peptidoglycan synthesis | + antibiotics to prevent them
cytoplasm: NAG---UDP---NAM with d-ala-d-ala transported to outside of cell membrane: cross links via transpeptidases/carboxypeptidases = PBP vancomycin - binds to d-ala cyclosterine - stops d-ala being added on cephalosporins/penicillin - inhibits PBP - preventing cross links
43
what cell produces histamine during an allergic response (secondary)
mast cells --> igE receptors (+c3a/c5a) --> histamine
44
triple response of lewis and what is responsible for this response
acute inflamation reddening - due to localised vasodilation flare - due to surrounding vasodilation wheal - due to exudate fluid raising the skin histamine
45
when are eicosanoids synthesised
NOT stored made my almost any cell synthesised only when required (eg. by a stimulus: presence of cytokines/other eicosanoids/mechanical trauma)
46
inhibitors of lipoxygenases
GSK2190915 = inhibits FLAP esculetins inhibits lipoxygenases (preventing formation of leukotrienes + lipoxins)
47
effects post leukotriene receptor binding
``` act as chemoattractants bronchoconstriction oedema increased mucus increased vascular permeability ``` therefore worsening asthmatic symptoms - should BLOCK the receptors (leukotrienes more potent Than histamine)
48
how to activate NF-kappa beta
IKB kinase--> phosphorylase IKBa--> releases NF-kb--> nucleus to increase inflammatory gene expression
49
glucocorticoid drugs
dexamethasone/prednisolone/betamethasone/hydrocortisone
50
therapeutic uses for mineralocorticoids (Aldosterone)
``` adrenal insufficiency (addisions) electrolyte dosorders (eg. cerebral salt wasting) orthostatic hypotensin (eg. due to baroreceptor reflex fail) ```
51
name for fungal infections
mycoses
52
treatment for influenza(anti-viral drugs)
zanamivir/oselatmivir they decrease NA on surface--> prevent spread of infection but only good when commenced early good prophylaxis effects resistance is rare but common in immunosuppressed Amantadine (rarely used) decrease HA/viral uncoating by blocking M2 proteins
53
herpes virus drug treatment (anti-virals)
aciclovir - HSV/VZV - CMV/EBV prophylaxis ONLY - safe because of greater affinity to HSV thiamine kinase than humans ganciclovir -CMV valaciclovir/valganiclovir = valine ester added to allow the above (Only IV) --> orally taken (prodrugs) forscarnet/cidovir - cmv but not first choice - toxic to kidney
54
hepres virus resistance 2 main methods
mutant thymidine kinase -foscarnet and cidovir = still effective as they do not need phosphorylation mutant dna polymerase -all drugs rendered ineffective
55
viral hepatitis anti-viral
pegylated interferon alfa
56
which hep can be fully cured and which cant
hep b - can't | hep c- can
57
what viral surface protein found on HIV
gp120 and co-recptor CCR5
58
zidovudine (similar action to aciclovir) action
prodrug for HIV needs to be phosphorylated 3 times (affinity to thymidine kinase in parasite higher) polarised =stays within infected cell ZDV phosphorylated =thymidine analogue will compete with dGTP for reverse transcriptase and so ZDVtriphosphate incorporated into viral DNA however ZDVTP = lack appropriate OH group = acts as chain terminator preventing viral replication (for aciclovir, it competes with guanine for DNA polymerase)
59
anti-fugals
polyene macrolides they target ERGOSTEROL(from lanosterol) hydrophobically form pores--> cell contents leaks out--> dies ``` amphotericin B (broad spectrum) N yastatin = thrush (vaginal/oral) ```
60
anti-folates
methotrexate - binds to DHFR (higher affinity to parasite's Than humans) - plus more DHFRs in parasites sulphonamides - PABA is structurally similiar so binds to DHPS - production of pseudofolate/sulfa-ptendine complex = causes bacteria cell to die proguanil - antifolate for malaria - targets late stage of asexual reproduction - must be metabolised to work--> cycloquanil - slow acting - not given to critical situations
61
folate pathway
parasites (PABA/Ptendine)--> dihydropteroarate diphosphonate------DHPS-->dihydrofolic acid---DHFR---->tetrahydrofolic acid-->FA Humans (Diet)--------DHPS----->dihydro-----DHFR---->tetra--->FA
62
alkylating agents
form highly reactive carbonic ion transfer alkyl groups to nucleophilic sites on DNA bases cause DNA damage - cross linkage - abnormal base pairing - dna strand breakage(decreasing cell proliferation) alkylation also damages RNA/Protieins used for cancer as it is a cytotoxic agent
63
prostanoid production from AA--->?
AA--> PGH2(prostaglandin endoperoxides)---> - PGE2 via tissue-specific isomerase - TXA via TXA synthase - PGI via PGI synthase
64
2 products that can form from leukotriene A4
---LTA4 hydrolase---> LTB4 (chemoattractant) ---gluthamine transpeptide + AA---> sulpidopeptide leukotriene
65
PG receptors
DP - vasodilation / decreases platelet aggregation/ bronchoconstriction FP - myometrial contraction / bonchoconstriction IP - vasodilation / decrease platelet aggregation / increase renin EP1 - bronchoconstriction / GIT SM contraction EP2 - bronchodilation / GIT SM relaxation / vasodilation/ increases intestinal fluid secretions EP3 - intestinal SM contraction / increase gastric mucosa/ decrease acid secretion
66
which leukotriene receptor do you block to decrease the asthmatic symptoms
cys-LT (sulphidopeptide leukotriene's receptor)
67
PUFA (EHA/DHA) derived anti-inflammatory mediators
DHA = Docosatrienes and neuroprotectins EHA = Resolvins increase in LIPOXINS (because only LOX - 5 is blocked by EHA not other LOXs)
68
how does NSAIDs cause closure of ductus arteriosus
decrease of PGs--> less vasodilation--> constricts and closes we use indomethacin / ibuprofen therefore giving PG analogues will keep it open(Alprostadil)
69
folic acid synthesis inhibitors (antibiotics)
sulphonamide (PABA competitive inhibitor for dihydropteroate synthases) + they produce pseudofolate/sulfa-pteridine = causes bacteria cell to die trimethoprim (dehydrofolate reductase inhibitor) - loads more DHFR in bacteria cells - affinity to DHFR is much more towards parasite's Proguanil = also a DHFR inhibitor methotrexate = folic acid analogue - anti-tumour - decreases Folic acid production by COMPETING for DHFR
70
criteria for choosing drug combination
- drug should be active on their own - should have different mechanisms of action (prevent competition) - have different toxicity profiles (otherwise summation of toxicity at same point) - use the drugs at doses close to their maximum tolerated levels

Semester 4 (10 decks)

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