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PED1003 pharmacology > Drug effects on other systems L19-25 > Flashcards

Drug effects on other systems L19-25 Flashcards

1
Q

local hormone

A

chemical messenger formed by tissue on which it acts

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2
Q

where is histamine formed

A

histaminocytes
histaminergic neurones
mast cells basophils

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3
Q

histamine formation

A

histidine break down by histidine decarboxylase to histamine

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4
Q

histamine breakdown

A

histamine oxidase breakdown if not stored

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5
Q

acute inflam response of mast cell

A

C3a/C5a receptors (complement component)
pathogen pattern receptors (pathogen)

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6
Q

hypersensitivity response of mast cell

A

immunoglobulin (Ig)E cell fixed antibody

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7
Q

arousal pathway

A

histamine neurones in TMN
spontaneously active
release histamine in wakefulness

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8
Q

emetic centre

A

histaminergic neurones in TMN receive vestibular input for sensory

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9
Q

mismatch of inputs to medulla

A

emetic (vomiting) centre activated in medulla

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10
Q

histamine receptor types

A

G-protein coupled
H1
H2
H3/4

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11
Q

H1

A

phospolipase C activated
triggers Ca2+

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12
Q

H2

A

adenlyl cyclase activated
triggers cAMP

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13
Q

H3/4

A

triggers cAMP

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14
Q

H1 functions

A

myosin phosphorylation
neuronal activation
nasal/bronchial secretions
vascular permeability
NFkB activation
sensory nerve endings
prociflam cytokine secretion

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15
Q

H2 functions

A

chronotropic heart rate increase

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16
Q

H1 and H2 functions

A

capillary permeability and dilation
inotropic increase of heart rate

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17
Q

rhinitis

A

inflammation within nose
sensory nerve ending stimulation
increases nasal secretions
capillary permeability and dilation

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18
Q

urticaria

A

sensory nerve ending stimulation
capillary dilation

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19
Q

anaphylaxis

A

rapid onset
HR rapid
consciousness loss
breathing difficulties

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20
Q

1st generation antihistamines

A

H1 receptor antagonists
prophylaxis

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21
Q

1st generation antihistamine pros

A

cheap/ effective
cross BBB ^ sedation and stops motion sickness
extra wanted effects due to broad selectivity

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22
Q

1st generation antihistamine cons

A

unwanted sedation/ adverse effects
can excacerbate other drugs anticholinergic adverse effects

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23
Q

muscarinic antagonist effects reversing parasympathetic activation

A

pupil dilation (blurred vision)
^ cardiac output
decreased exocrine gland secretion
decreased bladder contraction

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24
Q

a1-adrenoreceptor antagonist reversing sympathetic activation

A

vasodilation > hypertension/ dizziness

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25
Q

pros of 2nd generation antihistamines

A

add carbonyl groups (more polar)
less unwanted sedation
less anticholinergic effects

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26
Q

2nd generation antihistamines cons

A

don’t cross BBB as easily

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27
Q

gastric acid secretion pathway

A

stomach> gastric gland> parietal cell> proton pumps/ chloride co-transporter

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28
Q

peptic ulcer

A

perforation in lining of small intestine/ stomach
gram neg helicobacter pylori infection

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29
Q

peptic ulcer treatment

A

antimicrobials rid H.pylori
H2 antagonists competitively/ reversibly block histamine-binding

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30
Q

H2 antagonists cons

A

reoccurrence if H.pylori present and not erradicated
less effective for NSAID-induced ulcers
45 min action onset
affects other drug metabolism
decreases drug efficacy requiring acidic environment

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31
Q

H2 antagonists pros

A

all 4 effective for H.Pylori ulcers
heartburn effective
cheap
safe

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32
Q

Proton Pump Inhibitors

A

decrease H+ secretion
prodrug
acid resistant coating (removed in duodenum)
absorbed/ transported to parietal cell
metabolised to active and bind to PP
decrease gastric acid secretion

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33
Q

PPI pros

A

v effective
long duration

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34
Q

PPI cons

A

delayed action onset
increased risk of gut infection
gut pH above physio level

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35
Q

inflammation

A

local accumulation of fluid containing plasma proteins and white blood cells
non-specific/ dynamic/ 2nd line of defence against infection

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36
Q

inflammation functions

A

restricts damage/ infection
removes causative agent/ damaged tissue
allows immune cell access to site for repair

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37
Q

cardinal signs of acute inflammation

A

calor
dolor
oedema
erythema

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38
Q

innate responses inducing acute inflammation

A

bacteria-triggered cytokine/ chemokine release from macrophages
vasodilation/ ^vascular permeability
inflam cell migration > inflam mediators

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39
Q

cells recruited acute inflammation

A

macrophages
dendritic cells
eosinophils
neutrophils
basophils
mast cells

40
Q

4 inflammation stages

A
  1. tissue damage (sentinel cell activation)
  2. vasodilation and vascular permeability
  3. cell recruitment
  4. tissue repair (clotting/ annexin and fibrin release)
41
Q

eicosanoids

A

physio active lipid compounds
signalling molecules via enzymatic/non-enzymatic oxidation of arachidonic acid
prostanoids (prostaglandins, thromboxane)
leukotrienes

42
Q

prostaglandins

A

PGI2 > Prostacyclin (vasodilation/ stops platelet activation)
PGE2 > Prostaglandin (fever/pain and vascular permeability)
TXA2 > thromboxane (platelet activation and vasoconstriction)

43
Q

types of anti-inflammatory drugs

A

NSAID’s
glucocorticoids (steroidal anti-inflam)
immuno-suppressants
anti-histamines (antagonists of histamine receptors)

44
Q

non-opioid analgesics

A

paracetamol
aspirin (NSAID)
ibuprofen (NSAID)
celecoxib (NSAID)

45
Q

paracetamol pros / cons

A

:) analgesic/ antipyretic activity
:( no anti-inflam action/ liver damage on overdose

46
Q

aspirin pros/cons

A

:) acetylates COX
irreversible inhibitor
anti-platelet activity
:( ^risk of GI bleeding/ irritation

47
Q

ibuprofen pros/ cons

A

:) short-term analgesic
anti-inflam
:(gastric irritation/ ^ulceration risk

48
Q

celecoxib pros/cons

A

:) COX-2 inhibitor decreases side effects
:( ^risk of stroke/ heart attack following FDA cat.d use

49
Q

arachidonic acid on COX-1

A

housekeeper
many roles

50
Q

arachidonic acid on COX-2

A

Inflam cell activation
anti-inflam/ analgesic/ antipyretic

51
Q

side effects of non-opoid analgesics

A

immunosuppression
hyperglycaemia
growth impairment
natural corticosteroid synthesis suppression

52
Q

gene targets of non-opioid analgesics

A

^tyrosine aminotransferase (immunosuppressive)
^lipocortin (eicosanoid generation inhibition)
decrease NFkB regulated genes (COX)
decrease activator protein 1 regulated genes (wound-healing/ collagenase/ vit C/D metabolism)

53
Q

ACTH effects

A

adrenocorticotrophic hormone
^glucocorticoid hormones
^ cortisol proportion
^ w stress

54
Q

manufactured glucocorticoids

A

beclometasone (asthma inhaler)
hydrocortisone cream
prednisolone (allergies/ skin infection)

55
Q

glucocorticoid/ cortisol

A

prevents inflam mediator release
decreases TNF-a
twitches toward Th2 immune response via IgE

56
Q

Cushing’s syndrome

A

cortisol build up
latrogenic> long-term high dose cortisol use
endogenous> ACTH over-production in body
easy bruising/ purple striae/ muscle wastage/ atherosclerosis/ moon phase

57
Q

common bacterial targets for antibiotics

A

cell membrane
cell wall (e.g. penicillins)
protein synthesis (e.g. macrolides/ tetracycline)
RNA polymerase
DNA synthesis (e.g. fluroquinolones)
folate metabolism (e.g. sulphonamides)

58
Q

lactam

A

cyclic amide

59
Q

beta-lactam

A

lactam w heteroatomic ring structure (3C and 1N)

60
Q

types of penicillin

A

benzylpenicillin
broad spectrum
beta-lactamase resistant
extended spectrum
reversed spectrum (more g-)

61
Q

benzylpenicillin

A

original form
less active against gram negatives
acid labile
oral (Less absorbed)
parenteral (slow IV/ IM/ high availability)

62
Q

broad spectrum penicillin

A

amino group >penetration of outer membrane of g-
better absorption profile

63
Q

beta lactam antibiotic mechanism

A

inhibit enzyme (transpeptidases) > no links in peptidoglycan cell wall
swell and rupture of cell wall
multiplying organisms

64
Q

peptidoglycan monomer

A

N-acetylmuramic acid with N-acetylglucosamine and tetrapeptide connecting

65
Q

penicillin pharmacokinetics

A

A > varies
D> wide dist no CSF entrance
M> short half-lives (30-80mins)
E> kidney w 90% tubular secretion/ clearance reduction in neonates

66
Q

probenecid

A

inhibits tubular secretion

67
Q

penicillin adverse reactions

A

hypersensitivity
GIT disturbance
haemostatic effects

68
Q

folate biosynthesis

A

pABA>(dihydropteroate)>folate>(dihydrofolate reductase)>tetrahydrofolate>thymidylate synthesis> DNA

69
Q

Sulphonamide mechanism

A

blocks dihydropteroate synthetase
bacteriostatic

70
Q

sulphonamide pharmacokinetics

A

A> oral/ absorbed from stomach and intestines
D> wide inc. CNS
M>n-acetylation metabolism in liver
E>urine ~30mins

71
Q

sulphonamide adverse reactions

A

photosensitivity
stevens-johnson syndrome
hemopoietic disturbances

72
Q

fluoroquinolones

A

broad spectrum
gram+/g-
target DNA replication via TII topoisomerases
absorbed in upper GI tract/ excreted in tubular
CYP182 inhibition

73
Q

quinolone inhibition

A

DNA gyrase > supercoiling regulation and packaging (inhibited in gram negatives)
DNA topoisomerase IV > gyrase homologue (inhibited in g+)

74
Q

euk vs pro ribosomes

A

euk> 80S
pro> 70S
50S (23S/5S) and 30S sub-units

75
Q

macrolide mechanism of action

A

block peptide translocation
bind near RNA exit tunnel
peptidyl transferase RNA drop off

76
Q

macrolide ADME

A

A > capsules protect from gastric juices
D> crosses placenta not BBB
M>demethylation
E> excreted in bile

77
Q

macrolides adverse reactions

A

cholestatic hepatitis
GIT
transitory auditory impairments

78
Q

tetracycline mechanism of action

A

interrupts elongation phase of synthesis
sterically inhibits tRNA binding
unbinds/ rebinds/ futile loop

79
Q

tetracycline ADME

A

A> fasting state
M> long half-lives due to enterohepatic recirculation
E> bile / glomerular filtration

80
Q

hallmarks of cancer

A

resisting cell death
sustaining proliferative signalling
evading growth supressors
activating invasion/ metastasis
inducing angiogenesis
enabling replicative immortality

81
Q

cancer treatment options

A

surgery
biological
radiation
chemotherapy

82
Q

drugs affecting G1 phase

A

protein depleting

83
Q

asparagine + asparaginase

A

aspartic acid/ ammonia

84
Q

tamoxifen

A

S requires activation of hormone regulated genes and so replaces oestrogen in cancer cell to stop growth and proliferation

85
Q

Alkylating agents

A

ciplatin
nitrogen mustard
cyclophosphamide
daunorubicin

86
Q

antimetabolites

A

methotrexate
5-fluoruracil
6-mercaptopurine-A

87
Q

topoisomerase inhibitors

A

T1-irinotecan
T2-etoposide

88
Q

anthracyclines

A

inhibitx txn/replication
e.g. dauxorubicin

89
Q

BCR-ABL1 fusion protein function

A

tyrosine kinase ability

90
Q

PARP inhibitors

A

PARP (DNA damage repair) inhibition leads to double strand break
BRCA mutation in cancer cells die while normal cells survive

91
Q

distributional selectivity

A

useful for drugs equally toxic to host and parasite > selective parasite accumulation/ limited compartment/

92
Q

plasmodium life cycle

A

asexual reproduction
gametocyte development
RBC penetration

93
Q

4-aminoquinolones

A

accumulates in parasitic lysozomes, inhibiting digestion of host Hb
resistance in efflux of drugs from cells

94
Q

quinine methanols

A

binds to malarial pigment haemozoin >intercalates into DNA
erythrocytic
:)chloroquine resistance treatment

95
Q

8-aminoquinolones

A

radical cure
metabolised in liver
cytotoxic derivatives
haemolytic anaemia

96
Q

anti-folates

A

prophylactic
DNA synthesis inhibition
activated by CYP2C19/ cycloguanil

PED1003 pharmacology (6 decks)

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