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WEEK 9 SEM 4 > Local Hormones- Inflammation and anti-inflammatory Agents > Flashcards

Local Hormones- Inflammation and anti-inflammatory Agents Flashcards

1
Q

What things can cause injury to body?

A

heat, UV light, and chemicals (physical and chemical agents), tissue necrosis, trauma

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2
Q

What is innate immune response?

A

fast
non-specific
minutes-hours

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3
Q

What is adaptive immune response?

A

specific to pathogen

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4
Q

What are the signs of inflammation?

A 
calor- warm bc more blood flow
rubour- red bc more blood flow
tumor- swell bc leaky venules
dolor- pain bc more sensitive pain neurones
functio laesa-loss of function
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5
Q

What happens during times of injury?

A 
mediators released
microvascular changes
leakage from venules and capillaries
accumulation of cells 12 hours after injury
repair 3-5 days after injury
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6
Q

What are the microvascular changes during injury?

A

more blood flow to area

vasodilation

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7
Q

What are the 2 ways liquid leaks out of venules and capillaries?

A

exudate

transudate

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8
Q

What is exudate?

A 
occurs during inflammation
bc of more space between endothelial cells of the blood vessels bc of inflammatory mediators
fluid is protein rich
SO more RBC in blood
so you get blood stasis and clotting
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9
Q

What is transudate?

A

not bc of inflammation
bc of less protein synthesis or increased protein loss in urine
occurs during liver and kidney diseases
decreased osmotic colloid pressure
SO fluidmoves into extracellular space-here the endothelial cell is permeable to only fluid

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10
Q

12 hours after injury, what cells accumulate?

A
  1. neutrophils and eosinophils accumulate
  2. they release factors
  3. cells leave capillaries bc endothelial layer of blood vessels contract bc cytoskeletal change due to toIL1 and TNF
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11
Q

Why is the inflammatory process beneficial?

A

antibody entry
fibrin formation
stimulates immune system
repair/healing

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12
Q

How does bleeding stop?

A

injured blood vessels get smaller- allow less blood through

platelets come to site and form a plug

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13
Q

How do the platelets form a plug?

A

adhesion- stick to wall of worn out blood vessel
activation
secretion- platelets release chemicals into bloodstream
aggregation

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14
Q

What does fibrin do?

A

weaves itself into a clot over the platelet plug

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15
Q

What are the harmful effects of inflammation?

A

destroy normal tissue
swelling
innapropriate inflammatory response

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16
Q

When is inflammatory swelling most serious?

A
  • If it occurs in enclosed spaces e.g. cranial cavity
  • can get acute meningitis or an intra-cerebral abscess
  • incracranial pressure rises to the point where blood cant easily come to the brain
  • depresses cardiac and respiratory centres = cause death
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17
Q

What are the 5 R’s of inflammation?

A

recognition of the injurious agent

recruitment of leukocytes

removal of the agent

regulation (control) of the inflammatory response

resolution, ie repair of the injury

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18
Q

Which hormones are important for increase in blood flow to injured area?

A

histamine and prostaglandins

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19
Q

Which hormones increase the permeability of the venule?

A

histamine and bradykinin

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20
Q

What are examples of local hormones?

A 
gastrin
CCK
glucagon
VIP
substance P
motilin
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21
Q

Local hormones communicate through basic cell signalling. What are the 3 mains parts of basic cell signalling?

A
  1. reception: binding of signal with a cellular protein
  2. transduction: binding triggers a series of cellular changes
  3. response: transduced signal elicits context-driven specific cellular
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22
Q

The responses can be nuclear or cellular. What is the difference?

A

cellular responses = rapid

nuclear responses = take time to occur bc need to synthesize diff proteins to see effects.

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23
Q

What kind of an amine is histamine?

A

dibasic vasoactive amine

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24
Q

What is histamine synthesized from?

A

synthesized from amino acid histadine by histidine decarboxylase

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25
Q

Where is histamine synthesized, stored and released from?

A

mast cells found in connective tissue
basophils found in blood
neurons in brain
histaminergic cells in gut

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26
Q

What receptors do mast cells express?

A

IgE, C3a and C5a

27
Q

What are c3a and C5a involved in?

A

chemotaxis

increase permeability of blood vessels

28
Q

Which neurones in the brain synthesize, store and release histamine?

A

tuberomammilary nucleus

involved in arousal, sleep, memory, energy and balance

29
Q

How is histamine released?

A

in secretory granules composed of negatively charged heparin and acidic proteins

30
Q

What is heparin important in?

A

distribution and control of catalytic activity of vasoactive amines like histamine and prostaglandins

helps keep these vasoactive amines inactive in the vesicles

proteoglycan is involved in regulating the enzymatic activity of mast cell proteases and to promote apoptosis

31
Q

When is histamine usually released?

A

during allergic reactions

32
Q

What is release of histamine inhibited by?

A

stimulation of B adrenoreceptors

33
Q

How many Histamine receptors are there?

A

4= all G proteins

H1,H2,H3,H4

34
Q

What does H1 receptor do?

A

H1 Gq coupled receptor
activates PLC
leading to PIP2 breakdown into DAG and IP3
it is in smooth muscles, endothelium, CNS, and sensory nerves

35
Q

What does H2 receptor do?

A

H2 Gs coupled receptor
activates adenylyl cyclase
converts ATP to cAMP leading to stimulation of PKA
found in parietal cells, heart, uterus, mast cells and neutrophils

36
Q

What does H3 receptor do?

A

H3 Gi receptor
leads to a decrease in cAMP
in presynaptic terminals and its stimulation decreases release of histamine (autoreceptor)

37
Q

What does H4 receptor do?

A

H4 Gi receptor
leads to decrease in cAMP levels
in basophils, bone marrow, and the gut

38
Q

What are cardiovascular effects of of histamine receptor activation?

A

dilate arterioles= less TPR (H1)
increase post-capillary venules permeability= less blood volume (H1)
increase heart rate (H2)

39
Q

What are nonvascular smooth muscle effects of histamine receptor activation?

A

bronchoconstriction (H1)

40
Q

What are algesic (pain) effects of histamine receptor activation?

A

pain, itch, sneeze= H1 RECEPTORS ON SENSORY NERVES

41
Q

What are the exocrine secretory effects of histamine receptor activation?

A

more blood flow so more secretions- runny eyes,nose, more mucus

42
Q

What are the effects on gastric acid of histamine receptor activation?

A

increased secretion of HCl (H2 receptors on parietal cells)

43
Q

What is promethazine used for?

A

H1 and H2 antagonist
if peanut allergy and someone having reaction give epinephrine, promethazine, and salbutamol (if the person also has asthma)

44
Q

What are the 2 main roles of histamine?

A 
acute inflammation (H1)
gastric acid secretion (H2)
45
Q

What is the triple response?

A

inject with histamine
acts on capillaries, veules- cause vasodilation
act on sensory nerves (c fibres)+ give pain
person gets REDNESS, FLARE AND WHEAL (RAISED SKIN)

46
Q

wHAT IS FLARE (SURROUNDING AREA TURNS RED) CAUSED BY?

A

Antidromic response= impulse conduction along nerve fibre in opposite direction to normal

conduction leads to neuropeptide release= cause arterial vasodilation

47
Q

What causes wheal (raised skin)?

A

exudation from capillaries and venules

48
Q

What dampens down gastric acid secretion?

A

PGE2

49
Q

What does PGE2 do?

A
  • dampen down gastric acid secretion
  • increase mucus secretion
  • cause vasodilation
50
Q

Give examples of H1 antagonists?

A

first generation:
•mepyramine, promethazine, diphenhydramine

second and third generation
terfenadine

51
Q

What is terfenadine?

A
  • H1 antagonist
  • prodrug
  • causes cardiac arrhythmia
  • p450 metabolises it into its active form
52
Q

Why is grapefruit bad with H1 antagonist?

A

inhibits P450

53
Q

Normally, what is the problem with H1 antagonists?

A
  • side effects
  • sedative, ie drowsiness
  • they have antimuscarinic actions - give atropine like effects like blurred vision, constipation
54
Q

What is promethazine?

A
  • H1 antagonist (1st generation)

- anti-emetic and can be used for motion sickness (anti-nausea and vomiting)

55
Q

What are H1 antagonists used for?

A

acute inflammation

56
Q

What are H2 antagonists used for?

A

gastric problems

57
Q

What are H2 antagonists?

A
  • cimetidine

- ranitidine

58
Q

What do H2 antagonists do?

A
  • they reduce gastric acid secretion in the treatment of duodenal and gastric ulcers and Zollinger-Ellison syndrome (duodenum & pancreas tumours which secrete gastrin)
  • increase INMT (enzyme involved in breakdown of histamine) activity so more rapid breakdown of histamine
  • mental confusion, dizziness, tiredness & diarrhoea sometimes as side effects
59
Q

Where is bradykinin found?

A
  • mast cell granules
  • endothelial cells
  • lungs
  • damaged tissue
60
Q

What are the effects of bradykinin?

A
  • pain
  • increased vascular permeability
  • vasodilation thus decrease in blood pressure
  • mobility of leukocytes (white blood cells are attracted to bradykinin)
  • contraction of visceral smooth muscle (in the gut and the bronchus)
  • stimulation of arachidonic acid metabolism
  • initiates phospholipase action which leads to release of numerous lipid mediators of inflammation
  • dry cough
61
Q

How is bradykinin broken down?

A
  • kininases I and II (ACE angiotensin converting enzyme, aminopeptidase P, carboxypeptidase
62
Q

What happens to a patient if they are given ACE inhibitor?

A
  • will usually have dry cough
    bc ACE if breaking down bradykining
    so ACE inhibitor means increase of bradykinin
63
Q

How does serotonin cause inflammation?

A
  • increase mast cells at injury site
  • enhance inflam reactions of skin, lungs, gut etc.
  • chronic inflammatory action of cancers of the skin, the lungs, and the pancreas is enhanced by serotonin
  • work with thromboxane A2 to stimulate platelet activity (by platelet aggregation) and vasoconstriction

WEEK 9 SEM 4 (9 decks)

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