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Pharm Stuff > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Cardinal signs (5)

A
  • pain
  • heat
  • redness
  • swelling
  • loss of function
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2
Q

PAMP

A
  • pathogen-associated molecular patterns

- chemical recognised by PPR

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3
Q

PPR

A
  • pathogen recognition receptors

- receptors that recognise PAMP

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4
Q

PMN

A
  • polymorphnuclear cells

- e.g. neurophils

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5
Q

Cellular phase of inflammation

A
  • PMN - neurophils

- monocytes -> macrophages

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6
Q

Neurophils

A

is PMN

  • first to enter site of inflammation
  • phagocyte microbrial material
  • respiration burst (toxic oxygen products)
  • release proteases (anti-microbial activity)
  • mediators (recruit more leukocytes)
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7
Q

Monocytes/Macrophages

A
  • second to enter site of inflammation
  • phagocytosis
  • release host inflammatory mediators
  • present antigen to lymphocytes
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8
Q

Inflammatory mediators

A
  • synergistic and inhibitory interactions
  • positive and negative feedback pathways/cascades
  • temporal changes in cellular and mediator composition
  • emergent properties (simple -> complex interactions)
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9
Q

Diphernhydramine, chlopheniramine

A
  • H1 antagonists
  • cross BBB
  • sedation, treatment of motion sickness, allergies
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10
Q

Cetirizine, terfenadine

A
  • H1 antagonists
  • don’t cross BBB
  • allergies (only partially effective)
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11
Q

Ranitidine

A
  • H2 antagonist

- suppression of gastric secretion -> healing of duodenal ulcers

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12
Q

Anti-inflammatory mediators

A
  • histamine
  • kinins
  • lipid mediators (prostaglandins)
  • NSAID (non-steroidal anti-inflammatory drugs)
  • Anti-inflammatory steroids
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13
Q

Kinins

  • principal kinins
  • precursor
  • destruction
  • plasma half-life
  • effects
  • actions via (direct and indirect)
A
  • principal: bradykinin and kallidin
  • formed from kininogens (plasma protein precursors)
  • destroyed by carboxypeptidase N and angiotensin converting enzyme
  • plasma half-life: 20 min
  • effects: vasodilators, increase venular permeability, pain, contract smooth muscle
  • via beta2 (and beta1); some actions indirectly mediated by histamine or prostaglandin release
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14
Q

Icatibant

A
  • beta2 antagonist (blocks binding of bradykinin to beta2)
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15
Q

Prostaglandin

  • subclass
  • structure
  • metabolism
  • synthesis
  • receptors
  • effects in inflammation
A
  • subclass of eicosanoids and prostanoids
  • structure: 20C with a HO group at C15
  • rapidly metabolised
  • synthesis: from arachidonic acid to prostanoid via enzymes cyclooxygenase and relevant synthase
  • prostanoid receptors - GPCRs
  • effects: vasodilation, inhibit monocyte activation and suppress T cell activation, regulation of TH2 lymphocytes, fever, pain
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16
Q

NSAID

  • mechanism
  • anty-pyretic effect
  • analgesic action
  • anti-inflammaroty effect
  • toxicity
  • example
A
  • inhibition of COX (older unselective, newer selective for COX2)
  • inhibition of PGE2 -> thermostat back to normal
  • reduces PGE2 formation -> lower pain (also an effect on CNS)
  • inhibits formation of PGE2, PGD2 and PGI2 to reduce heat, redness and oedema of inflammation
  • damage to upper GI tract (inhibition of COX1 increases secretion and reduces mucus and bicarbonate),
  • aspirin
17
Q

COX

- types

A

cyclo-oxygenase

- COX1 (constitutive enzyme) and COX2 (induced at site of inflammation)

18
Q

Glucocorticoids

  • examples
  • mechanism of action
  • effects
A
  • anti-inflammatory steroid
  • e.g. prednisolone and betamethasone
  • suppress early event of inflammation (vasodilation, oedema, leucocyte infiltration and leucocyte activation)
  • effects: anti-inflammatoy and immunosuppressive (by supression of autacoids) and inhibition of histamine
19
Q

Effects of steroids

A
  • synthesis of new protein and suppression of protein synthesis
  • anti-inflammatory actions after several hours
  • reduced COX products -> oedema, reduced blood flow and reduced pain
  • reduced lipoxygenase products -> reduced leucocyte infiltration and activation, reduced bronchoconstriction
  • reduced expression of COX2, NOS, adhesion molecules and some cytokines
20
Q

TNFalpha effects

A
  • fever
  • acute phase protein release
  • cytotoxic for cells
  • activates granulocytes and macrophages
  • promotes bone resorbtion by osteoclasts
  • inhibit collagen synthesis and promotes breakdown
  • induces cytokine synthesis
  • promotes fibroblast proliferation
  • activates endothelial cells
  • promotes angiogenesis

Pharm Stuff (7 decks)

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