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Semester 4 > SBT > Flashcards

SBT Flashcards

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
Q

what is given for gout

A

allopurinol (inhibits xanthine oxidase) decreasing uric acid

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26
Q

how glucocorticoids have an anti-inflammatory effect

A

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

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27
Q

side effect of corticosteroids

A

osteoporosis because glucocorticoids inhibit OSTEOBLASTS

gastric ulceration (dec. of COX1–> PGE2 decreased)

Cushings

lipodystrophy

cataract

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28
Q

methods bacteria can be resistant

A
  • drug inactivation
  • alter drug targets
  • efflux pumps
  • overproduction of targets
  • intrinsic permeability
  • metabolic by-pass
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29
Q

3 ways of gene transfer of bacteria

A

transformation - taking up free DNA and inserting into own

transduction - via bacteriophages

conjugation - via sex pilli transferring plasmids

30
Q

what can be given if we know the bacteria is beta-lactam resistant

A

augmentin = clavulanic acid + amoxicillin

C.A binds to beta-lactamase and prevents it degrading amoxicillin(that contains beta-lactam ring)

31
Q

how do gram +ve and -ve become resistant to beta-lactams

A

both have beta-lactamase

+ve—> alter binding proteins of b-lactam (eg. PBP)
-ve–> alter porins so it can’t enter

32
Q

4 ways a bacteria can become penicillin resistant

A
  • mutation of porin
  • mutation of PBP
  • acquire efflux pumps
  • accquire penicillinases (eg.b-lactamase)
33
Q

how to overcome penicillin resistance

A
  • reduce antibiotic use
  • new/modified drugs
  • combination therapy (preventing resistant bacteria from surviving and passing it on)
  • infection control
34
Q

how can antibiotics be bad for us (microbial antagonism)

A

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
Q

antibiotic classification

A

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
Q

antibiotics that inhibit cell wall synthesis (peptidoglycan)

A

penicillin/cephalosporins/vancomycin

37
Q

antibiotics that inhibit cell membrane of phospholipids

A

polymyxins eg. colistin

38
Q

antibiotics that target bacterial ribosomes

A

50s- erythromycin/chloramphenicol/linezolid

30s - tetracycline/ aminoglycosides/deoxyclcine

therefore preventing proteinsynthesis

39
Q

antibiotics targeting bacterial DNA

A

quinolones–> inhibiting DNA gyrase

rifampin/fidaxomicin –> inhibits RNA polymerase
(tb)

metronidazole- free radicals (anaerobic bacteria)

nitrofurantoin - free radicals (UTI)

40
Q

antibiotics that affect THFA

A

(for folic acid)

anti-folates

  • trimethoprim: decrease DHFR
  • sulphonamides: PABA competitive inhibitor
41
Q

difference between gram + and - cell wall

A

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
Q

peptidoglycan synthesis

+ antibiotics to prevent them

A

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
Q

what cell produces histamine during an allergic response (secondary)

A

mast cells –> igE receptors (+c3a/c5a) –> histamine

44
Q

triple response of lewis and what is responsible for this response

A

acute inflamation

reddening - due to localised vasodilation
flare - due to surrounding vasodilation
wheal - due to exudate fluid raising the skin

histamine

45
Q

when are eicosanoids synthesised

A

NOT stored

made my almost any cell

synthesised only when required (eg. by a stimulus: presence of cytokines/other eicosanoids/mechanical trauma)

46
Q

inhibitors of lipoxygenases

A

GSK2190915 = inhibits FLAP

esculetins inhibits lipoxygenases (preventing formation of leukotrienes + lipoxins)

47
Q

effects post leukotriene receptor binding

A 
act as chemoattractants 
bronchoconstriction
oedema
increased mucus
increased vascular permeability

therefore worsening asthmatic symptoms - should BLOCK the receptors
(leukotrienes more potent Than histamine)

48
Q

how to activate NF-kappa beta

A

IKB kinase–> phosphorylase IKBa–> releases NF-kb–> nucleus to increase inflammatory gene expression

49
Q

glucocorticoid drugs

A

dexamethasone/prednisolone/betamethasone/hydrocortisone

50
Q

therapeutic uses for mineralocorticoids (Aldosterone)

A 
adrenal insufficiency (addisions)
electrolyte dosorders (eg. cerebral salt wasting)
orthostatic hypotensin (eg. due to baroreceptor reflex fail)
51
Q

name for fungal infections

A

mycoses

52
Q

treatment for influenza(anti-viral drugs)

A

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
Q

herpes virus drug treatment (anti-virals)

A

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
Q

hepres virus resistance 2 main methods

A

mutant thymidine kinase
-foscarnet and cidovir = still effective as they do not need phosphorylation

mutant dna polymerase
-all drugs rendered ineffective

55
Q

viral hepatitis anti-viral

A

pegylated interferon alfa

56
Q

which hep can be fully cured and which cant

A

hep b - can’t

hep c- can

57
Q

what viral surface protein found on HIV

A

gp120

and co-recptor CCR5

58
Q

zidovudine (similar action to aciclovir) action

A

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
Q

anti-fugals

A

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
Q

anti-folates

A

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
Q

folate pathway

A

parasites
(PABA/Ptendine)–> dihydropteroarate diphosphonate——DHPS–>dihydrofolic acid—DHFR—->tetrahydrofolic acid–>FA

Humans
(Diet)——–DHPS—–>dihydro—–DHFR—->tetra—>FA

62
Q

alkylating agents

A

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
Q

prostanoid production from AA—>?

A

AA–> PGH2(prostaglandin endoperoxides)—>

  • PGE2 via tissue-specific isomerase
  • TXA via TXA synthase
  • PGI via PGI synthase
64
Q

2 products that can form from leukotriene A4

A

—LTA4 hydrolase—> LTB4 (chemoattractant)

—gluthamine transpeptide + AA—> sulpidopeptide leukotriene

65
Q

PG receptors

A

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
Q

which leukotriene receptor do you block to decrease the asthmatic symptoms

A

cys-LT (sulphidopeptide leukotriene’s receptor)

67
Q

PUFA (EHA/DHA) derived anti-inflammatory mediators

A

DHA = Docosatrienes and neuroprotectins

EHA = Resolvins

increase in LIPOXINS (because only LOX - 5 is blocked by EHA not other LOXs)

68
Q

how does NSAIDs cause closure of ductus arteriosus

A

decrease of PGs–> less vasodilation–> constricts and closes

we use indomethacin / ibuprofen

therefore giving PG analogues will keep it open(Alprostadil)

69
Q

folic acid synthesis inhibitors (antibiotics)

A

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
Q

criteria for choosing drug combination

A
  • 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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