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AAW - IHO 4 > Tuesday 3 - memorize these sheets ILT > Flashcards

Tuesday 3 - memorize these sheets ILT Flashcards

1
Q

what leaks large molecules

A

post capillary venules

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2
Q

what cause Redness - Vasodilation

A

Histamine
PGE2
PGI2
Kinins

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3
Q

what molecules cause Swelling - Increased vascular permeability

A

Histamine
Peptido leukotrienes (LTC4, LTD4, LTE4)
Kinins

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4
Q

what molecules cause Pain - Causes pain or reduces the pain threshold

A

PGE
PGI
LTB4
Kinins

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5
Q

What molecules are Chemotactic - Directed migration of white blood cells

A

LTB4 (neutrophils, etc)

Peptido leukotrienes (eosinophils)

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6
Q

what molecule induces fever

A

PGE

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7
Q

What molecules cause bronchoconstriction

A 
Histamine
Peptido leukotrienes***
Kinins
PGD2
Thromboxane
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8
Q

what cause Hypotension

A

Kinins!!!!

Histamine

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9
Q

Histamine

A

Redness, heat, swelling and airway constriction – but not chemotaxis.

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10
Q

PGE2 and PGI2

A

vasodilate, increase vascular permeability and cause pain

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11
Q

PGD2 and thromboxane

A

bronchoconstriction

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12
Q

TXA2

A

causes platelet aggregation (and vasoconstriction)

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13
Q

PGI2

A

opposes platelet aggregation (and causes vasodilation)

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14
Q

LTB4

A

is chemotactic (PMNs) and reduces pain threshold

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15
Q

Kinins (Bradykinin and kallidin)

A

Everything
Also very strong vasodilator with resulting hypotension!!!!
Not a major chemotactic agent.

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16
Q

WHAT TYPE OF AGONISTS ARE ANTIHISTAMINES

A

inverse agonists - they lower levels of activity when bound to histamine receptors (historically called competative agonists)

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17
Q

H1 histamine receptor stimulation

A

Bronchoconstriction
Contraction of GI smooth muscle
Increased capillary permeability (wheal)
Pruritis (itch) and pain
Release of catecholamines from the adrenal medulla

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18
Q

H2 receptor stimulation by histamine will cause

A

Gastric acid secretion****
Inhibition of IgE-mediated basophil histamine release
Histamine release by antigen feeds back to turn off its own release
Inhibition of T lymphocyte mediated cytotoxicity
Suppression of Th2 cells and cytokines

generally slower

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19
Q

H3 and H4 receptors

A

Present on histaminergic nerve terminals (H3) and many immune cells (H4; eosinophils, dendritic cells, T cells, neutrophils). Histamine can regulate activity of all of these cells through the H3 and H4 receptors.

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20
Q 
Mixed H1 and H2 receptor mediated responses.
Cardiac effects (H1 and H2)
A
  • increased heart rate
  • increased force of contraction
  • increased arrhythmias
  • Slows AV conduction (primarily H1)
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21
Q

“triple response of histamine”

A
  • Vasodilation (H1 & H2)
  • Flare - H1 (probably H2 also)
  • Wheal - increased capillary permeability (edema) is primarily H1 but may also involve H2
  • Pain and itching (primarily H1)

then why are there four bullet points and five different Sx…….?

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22
Q

Metabolism and excretion of first generation antihistamines

A

Transformed to inactive metabolites in the liver and excreted in the urine.

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23
Q

Side effects of first generation antihistamines

A

 Sedation
 Drying of secretions
 GI disturbances

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24
Q

first gen anti hista Acute poisoning

A

Resembles atropine poisoning
Fixed - dilated pupils, Flushed face and fever with dry mouth
Dominant effect - excitation, hallucinations, incoordination, convulsions
Terminally - coma and cardiorespiratory collapse

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25
Q

ftwo first gen antihistamines and SE

A 
	Diphenhydramine (OTC)
Low incidence of GI side effects
Sedation
If you want sedative actions as well, use diphenhydramine
	Chlorpheniramine (OTC)
Most suitable for day time use

ANTICHOLINERGIC
ANTIMUSCARINIC

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26
Q

Second generation antihistamines

A

Minimal anticholinergic properties
Do not cause sedation and drying of secretions

Cetirizine (OTC)
Fexofenadine
Loratadine (OTC) (claratin)

Only small amounts cross the blood-brain barrier and they cause less sedation than first generation H1 antagonists

DONT HAVE ANTICHOLINERGIC EFFECTS (DON’T STOP THE SYMPATHETIC NERVOUS SYSTEM)

27
Q

Prostanoids - what makes them

A

Synthesis By Phospholipase A2

28
Q

Cyclooxygenase (COX)

makes what

A

• key enzyme for the two step synthesis of PGH2 in the cell

29
Q

COX-1

A
  • Found in platelets

* Constitutively expressed in most cells and is thought to protect the gastric mucosa

30
Q

COX-2

A
  • Not found in platelets
  • Expressed constitutively in the brain and kidney, but can be induced by certain serum factors, cytokines and growth factors in other tissues and at sites of inflammation.
  • The more important isozyme in the production of prostaglandins and thromboxane in inflammation.
31
Q

What prostaglandin receptor causes platelet aggregation

what are it’s natural agonists

A

TP

TXA2, PGH2

32
Q

all the non selective NSAIDS

A

• Aspirin – irreversibly acetylates COX
• tNSAIDs or traditional NSAIDS or non-selective COX inhibitors
o Older inhibitors of both COX1 and COX2
Ibuprofen- fewer GI side effects than aspirin, OTC
Naproxen, OTC
Ketorolac – promoted primarily for analgesia but is also anti-inflammatory
Ketoprofen - related to ibuprofen
Indomethacin, most potent NSAID, severe frontal headache & blood disorders
Sulindac
Piroxicam - once a day administration, can cause dose related serious GI bleeding

33
Q

• Selective COX2 inhibitor

or ‘coxib’

differences between it and nonselectives

A

Celecoxib (Celebrex) – 200 mg/day, 10-20X more selective for COX2

COX 2 is not in platelets, so COX 2 inhibitors dont inhibit clotting

less likely to cause gastic ulceration and intolerane, as well as hypersensitivity reaction

34
Q

disease associated with aspirin in children

A

Reye syndrome - encephalopathy and fatty liver following viral infection

35
Q

The peptide leukotrienes

A

LTC4, LTD4, LTE4

36
Q

HETEs

A

Arachadonic acid product

enhance directed and random migration of white blood cells

37
Q

LTB4

A

Chemotaxis of white cells
leukocyte adhesion
hyperalgesia

38
Q

LTC4, LTD4, LTE4

what do they do

A

The peptide Leukotrienes

Cause increased vascular permeability and swelling, leading to bronchoconstriction - important in asthma and anaphylaxis

Also recruit eosinophils

39
Q

leukotriene inhibitors

A

used for chronic asthma

Zileuton - inhibits 5-lipoxygenase, preventing the synthesis (!) of LTB,C,D,E4 DOES NOT SHIFT THE DOSE RESPONSE CURVE OF LEUKOTRIENES

Zarfirlukast and Montelukast - leukotriene receptor antagonist (LTD4 receptor) - Zarfirlukast inhibits a cytochrome P450 and may have drug interactions - Montelukast is prescribed more because of once daily administration without restrictions with regard to meals.

40
Q

Kinins

how they act on their different receptors

A

Bradykinin and Kallidin

Via B1 receptor - Bradykinin and kallidin are more active WITHOUT the terminal arg
• Chronic inflammatory effects
• induced after trauma**
• maybe involved with cytokine production and more long term effects
• Hypotension and pain

Via B2 Receptor - Kallidin and Bradykinin are more active here if they have terminal arginine
• potent vasodilators - **Hypotension***
• increased capillary permeability and edema formation
• algesic agents - cause pain and stimulate nerve endings

41
Q

how is histamine made

how is it broken down

A

histidine > L-histidine decarboxylase in mast cells and basophils, etc > histamine

enzymes for metabolism are widely distributed, metabolites have little/no activity

42
Q

What happens if you give oral histamine

A

nothing, it is inactivated in intestinal wall or liver or by bacteria

43
Q

Sx of intravenous administration of histamine

A 
BP drops
tachycardia
bronchoconstriction
flushing
headache
wheal
mucus production
gastric acid secretion
44
Q

Do H1 antagonists help with congestion?

A

NO

Sudafed, an alpha agonist that constricts blood vessels, however, does.

45
Q

how long does it take to see the effects of nasal steroids?

A

days.

they need to regulate transcription factors in order to work

46
Q

what type of receptor does prednisone bind

What are some adverse effect that she talked about in class

A

glucocorticoid receptor

osteoporosis, immunosuppresion, hyperglycemia

47
Q

diphenhydramine -

works on what symptoms of an allergic reaction

doesn’t work on inhibiting the release of what

A

blocks H1, primarily works against the itching effect

doesn’t inhibit the production of prostanoids

48
Q

most potent bronchoconstricor of the peptide leukotrienes

A

LTC4

49
Q

What shifts the histamine curve but not the acetylcholine curve?

A

Loratadine! The non drowsy antihistamines

50
Q

enzyme incubated with LTA4 causes production of substance that causes very potent bronchoconstriction. what enzyme is it?

A

LTA4 -> glutathione transferase -> LTC4

51
Q

function of angiotensin converting enzyme

A

AKA ACE

ACE degrades bradykinin (Bradykinin lowers BP)

also converts angiotensin 1 into 2, which constricts blood vessels, driving up blood pressure

2 fold effect!

52
Q

Mech of aspirin hypersensitivity

A

shunting of AA enzyme metabolites to the Leukotriene pathway

53
Q

What enzyme receptors is critical for neutrophil migration into the lung

A

C5a Receptor

54
Q

Mycophenolate Mofetil

A

Used to prevent organ transplat rejection

• Mechanism: A metabolite is an inhibitor of inosine monophosphate dehydrogenase (IMPDH), an important enzyme in the de novo pathway of guanine nucleotide synthesis. B and T cells are highly dependent on this pathway for cell proliferation, while other cell types can use salvage pathways

55
Q

Fexofenadine’s effects on a dose response curve of Acetylcholine

A

No change

fexofenadine is a second generation anti histamine

56
Q

What drugs can you use to pretreat someone who is going to possibly have an anaphylactic shock

A

Any of the Leukotriene inhibitors, Zileuton, Montelukast, the other “kast”

also prednisone

57
Q

what is the major enzyme that forms leukotrienes from arachidonic acid

A

lipoxygenase

58
Q

What synthesizes bradykinin and kallidin and where is it found

A

Kallifrein

found outside of cells in tissues and plasma

59
Q

Carboxypeptidase N

A

– found in plasma, modifies bradykinin by removing the terminal arginine

important in breaking down kinins

60
Q

LTA4 hydrolase

A

found in myelomonocytic cells (basophils and mast cells)

o Converts leukotriene A4 (cannot interact with any receptors) to leukotriene B4 (biologically functional substrate)

61
Q

glutathione transferase

A

Makes the peptide leukotrienes (C,D,E4) from LTA4 by adding glutathione AA (a peptide)

62
Q

Why is thrombosis a risky side effect of celecoxib?

A

because it doesn’t stop the formation of thromboxane, which is made via COX1 inside platelets

63
Q

What is the biggest difference betwee prednisone and cortisol

A

prednisone only acts on glucocorticoid receptors

‘cortisol work on mineralcorticoid receptors as well

AAW - IHO 4 (14 decks)

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