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1
Q

What are the cardinal signals of acute inflammation?

A

vasodilation
increase vascular permeability
recruitment of neutrophils
ie often leads to edema

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2
Q

What are the signs of chronic inflammation?

A

can begin on its own, due to immune system, or as a continuation of an acute response

  • prolonged duration
  • participation by more monocytes, macrophages, etc
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3
Q

What are the potential harmful effects of inflammation?

A

Digestation of normal tissue through enzymatic attack such as by collagenases and proteases
swelling may lead to obstruction

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4
Q

What is the role of histamine in inflamation?

A 
biologic amine
vasodialates
increase vascular permeability
pain
activates by GPCR
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5
Q

What is the role of bradykinin in inflammation?

A 
peptide
vasodilation
increase microvessel permeability
pain
from endothelial cells
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6
Q

What is teh role of the complement system in inflammation?

A 
syntehsized by liver
chemotaxis-PMN
promote relase of neutrophil meadiators
increase vascular permeability
tissue injury
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7
Q

What is teh role of c reactive protein in inflmattion?

A 
plasma protein, produced in liver and adipocytes
marker of inflammation
-acute phase reactant
-activates complement
-mediates phagocytosis
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8
Q

What is the mechanism of action of C reactive protein?

A

binds to phospholipids in bacteria and damaged cells may be specific receptors in macrophages

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9
Q

What is the role of cytokines in inflammation?

A 
secreted proteins (IL-1 TNF-alpha)
-binds to specific receptors increase NFkappaB and AP-1 TF's leading to COX mediated fever, increased adhesion molecules and induce collagenase
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10
Q

Wha is teh role of Adenosine in inflammation?

A

from all cells, purine nuceloside from breakdown of ATP
increase extracellulary duing injury –anti-inflammatory–
inhibit cytokine activation
GPCR
ANTI-INFLAMMATORY

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11
Q

What are the roles of cell adhesion molecules?

A

family of proteins, source endothelial, platelets, leukcytes
-leukocyte adhesion to endothelium
-endothelium adhesion contribute to recruitement of platelets
calcium dependedn

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12
Q

What are the lipid mediators of inflammation?

A

prostoglandins, leukotrienes, glucocorticoids

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13
Q

What is the role of prostaglandins in inflmattion?

A 
from any cell
vasodialation
pain
fever
platelet aggregation
GPCR mediated
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14
Q

What is the role of leukotrienes?

A

from macrophages, neutrophils
increase vascular permeability
bronchoconstrictio
by activatio of GPCRs

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15
Q

What is the role of glucocorticoids in the inflammation response?

A 
produced by adrenal cortex
inhibits cytokines
inhibition of phospholipase A2
inhibition of COX2
inhibiton of cell adhesion
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16
Q

Leukotrienes: receptors identified for LTB4 and cysteinyl leukotrienes, LTC4 and LTD4 do what when activated?

A

coupled to specific G proteins and increase intracellular calcium

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17
Q

How do eicosanoids result in fever?

A

Result from production of PG, primarily PGE2, induce fever but don’t cotnribute to pyretic response.

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18
Q

What eicosanoids are involved in platelet aggregation?

A

TXA2: involved in platelet aggregation by stimulateing TP receptor
PGI2: inhibits platelet aggregation via stim of IP recpetor

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19
Q

What eicosanoids are involved in pain?

A

PGE2, sensitize afferent nerve endings to pain, COX2 in dorsal horn of spinal cord results in inflammation

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20
Q

What is the role of eicosanoids in reproduction?

A

PGI1=quiescent state of uterine activity durig early pregnancy
PGE2=initiation and progression of labor by inducing contractlity
PGF2–mediates uterine contractility during labor

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21
Q

What is the role of prostoglandins in cardio/vascular smooth muscle?

A

PGE2, PGI2: predominantly vasodilators
TXA2=vasoconstriction
PGF2=vasoconstriction

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22
Q

What is the role of PGs in fetal development?

A

maintain ductus arteriousus

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23
Q

Role of prostoglnadins in bronchial and tracheal smooth muscle?

A

PGE2, PGI2 relax
PGF2,, TXA2 constrict
LTC4, LTD4 constrict

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24
Q

Role of eicosanoids in the kidney?

A

PGE2, PGI2 increase renal blood flow and promote diuresis and natriuresis

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25
What is the role of eicosanoids in GI secretion?
PGE2 and PGI2 inhibit gastric secretion PGE2and PGI2 icnrease mucosal blood flow PGE2 stimulates viscous mucous and bicarb COX-1 important in syntehsis of cytoprotective PG
26
What limits therapeutic use of prostoglandins?
signficant adverse effects | short half-lives in circulation
27
How is aldosterone produced?
from zona glomerulosa cholesterol goes to prenenolone dexycortisoterone and then aldosterone
28
How is cortisol produced?
zona fasciculata and reticularis-cholesterol -> pregnenolone to deoxycortisol to cortisol
29
How is cortisol broken down?
reduction of A ring, sulfate conjugation and glucuronide conjugation
30
What are steroid therapy drugs usually used to tx?
``` Adrenal insufficiency rheumatoid arthiritis in progressive disease osteoarthiritis for acute inflammation allergic disases inflammatory diseases cerebral edema shock--? ```
31
What are the three general properties of NSAIDs?
anti-inflammatory anti-pyretic analgesic
32
What is the mechanism of action of NSAIDs?
Inhibition of cyclooxygenase, which leads to the conversion of arachidonic acid to prostoglandins The two forms that can be inhibited are COX-1 and COX-2
33
What is the major difference between aspirin and the other NSAIDs?
It is a irreversible inhibitor of the COX proteins.
34
What are the unique effects of aspirin that are unrelated to the inhibition of COX?
``` uric acid excretion -low levels decrease excretion -hight levels increase excretion CNS effects at high doses leads to delirium, nausea toxicity respiration--increase respiration rate ```
35
What are the contrainidications indicated for all NSAIDS?
GI irritation leading to ulcers Bleeding issues hypersensitivity Renal issues- complications arise from decreased blood flow Pregnancy--decrease uterine contractions, closure of ductus arteriosus prematurely
36
What are the toxicity problems linked directly to asprin?
Reye's syndrome from aspirin and viral infections often in children. Liver failure Salicylism
37
How is histamine synthesized?
from esential amino acid L-histidine. By specific histidine decarboxylase using pyridoxal 5-phosphate as a cofactor.
38
Where is histamine localized?
ubiquitous but highest in lung, skin and stomach. Mast cells, basophils as well as continual production
39
What are the signs of histamine relase or injection?
burning itching sensation followed by intesnse warmth. Skin reddents BP falls and HR increases. Quickly bp recover and hives appear
40
What is red-man syndrome?
Certian drugs, specifically vancomycin lead to a sudden release of histmine due to an increase in intracellular calcium via a number of different pathways.
41
What is serotonin synthesized from?
the essential amino acid tryptophan
42
What is the rate limiting step of serotonin synthesis?
tryptophan hydroxylase
43
Where is the majority of serotonin stored and synthesized?
Enterochromaffin cells of GI mucosa--90% slow spontaneous release turnover 1 day 2nd most blood platelets--8%
44
Where is the majority of CNS serotonin stored?
Rapid turnover 4 hours: midbrain Raphe nucleus
45
What are the pharmacological actions of serotonin at GI?
GI smooth muscle contraction | emesis by 5-HT3
46
What is carcinoid syndrome?
serotonin secreting tumors; and bradynkinin | Cause severe diarrhea and asthma
47
What are the pharmacological actions of serotonin in the CV?
potent vasoconstriction in large arteries and veins; also cranial blood vessels. Direct via 5HT2 on smooth muscle and 5HT1D or indirectly by amplification vasodilation in coronary arteries, arterioles, skeletal muscles and cutaneous blood vessels
48
What is Bezold-Jarisch reflex?
serotonin is a powerful activator of chemoreceptors in coronary vasculature which activates afferent vagal nerve endings" bradycardia, hypotension and hypoventilation
49
What is the pharm action of serotonin on platelets and CNS?
``` platelet aggregation Sensory perception sleep temp reg neuroendocrine learning and memory-short term pain perception drug abuse emesis-5HT3 ```
50
What mental illnesses are associated with serotonin?
``` affective disorders schizophrenia OCD anxiety disorders- 5HT1A Aggressive Behavior ```
51
What is synthesized from serotonin in pineal gland?
Melatonin
52
What are the mechanism of smooth muscle contraction?
Calcium-cell membrane intracellular signalin-myosin light chain kinase Rho kinase
53
What are the mechanism of smooth muscle relaxation?
Signaling pathways inhibit contractile mechanism | paracrine factors-nitric oxide, dopamine, prostacyclin
54
What is the juxtaglomerular cell?
modified smooth muscle found in media of afferent arteriole. Contain renin granules
55
What is the macula densa?
Specialized epithelial cells found at point where distal tubule comes in contact with afferent arteriole; measure concentrationo f sodium in thick ascending limb
56
What is renin?
acid protease that splits leucine-leucine bond of angiotensinogen giving angiotensin 1 produced in juxtaglomerular cells
57
What is angiotensinogen or renin substrate?
alpha2 globulin, synthesized by liver, amino terminal sequence contain angiontensin 1
58
What stimulates aldosterone production by zona glomerulosa cells of adrenal cortex?
potassium, ACTH and angiotensin 2
59
What does aldosterone act on?
distal tubule and collecting ducts to enhance sodium reabsorption and potassium excretion
60
What is the role of the intrarenal baroreceptor?
senses change in wall tension of afferent arteriole. | Wall tension inversely related to renin relase
61
What is the role of the macula densa in renin relase?
senses change in sodium load, and this is inversely related to renin relase
62
What is the role of renal sympathetic nervous system in renin release?
mediated by beta1 adrenergic receptors on JG cells | Renin release is increased by direct or indirect activation of renal sympathetic nerves
63
What is the role of angiotensin 2 in renin release?
feedack inhibition | direct action by interaction with JG cells
64
What is the role of angiotensin 2 on smooth muscle?
``` AT1 receptor mediated -vasoconstrictor hypertrophy At2 mediated vasodilation-NO mediated inhib proliferation of smooth muscle promote apoptosis ```
65
What is the role of angiotensin 2 on teh adrenal cortex?
stimulate aldosterone biosynthesis
66
What is the role of angiotensin 2 on the CNS and sympathetic neruons?
promote thirst ADH release positive water balance facilitates NE release inhibit NE reuptake
67
What is the role of angiotensin 2 on the heart?
hypertorphy of myocytes | increase in ECM production of fibroblasts
68
How do the three classes of CCBs interact with each other?
allostericinteractions | 1,4dihydropyridines act synergistically with each other and the others interfere incombinations
69
What are the factors that account for preference of CCBs for CV cells?
voltage-sensitive L-type Ca2+ channels are found on most tissues. However nervous and others have other types of Calcium channels and skeletal muscles have internal stores
70
What type of cells do phenylalkylamines(verapamil and benzothiazepines(diltiazem) act on?
Cardiace cells
71
What does 1,4dihydropyridines (nifedipine) act on preferentially?
arterial muscle cells
72
What mechanism of action increases likelihood that phenylakylamines and benzothiazepines bind to cardiac cells?
Their binding site is deep within the channela nd therefore te rapid firing of cardiac cells increase opportunities for CCB binding.
73
Why does the dihydropyridine CCB (nifedipine, almodipine) have a higher level of binding to vascular smooth muscle?
Binds with higher affinity to depolarized vascular smooth muscle, and vascular smooth muscle is more depolarized
74
Why is diltiazem used to treat angina?
the beneficial effect is the reduced cardiac workload; SA node down adn reduces afterload
75
Why is dilitiazem or verapamil used to treat supraventricular hypetension>
Reduce firing of SA node adn reduce conduction through AV node.
76
Why is dihydropyridine used to treat hypertension?
Reduce blood pressure as a potent vasodilator. May trigger reflex tachycardia
77
What are the adverse effects of calcium blockers?
vasodilator side effects, constipation, worse CHF, AV block
78
In order what is the cost of diuretics?
Thiazides-->loop-->potassium sparing
79
What is used to convert fibrinogen to fibrin?
Thrombin
80
What primarily degrades the fibrin clot?
plasmin
81
Warfarin is not used to treat clotting in emergencies?
Has no effect on active clotting factors
82
Factor 5 Leiden causes what?
mutation that predisposes pateitns to clots
83
What are the physical properties of heparin?
heterogenous mixture of polysaccharide negatively charged
84
What occurs when heparin binds antithrombin?
allosteric hcange and encourages thrombin and active coagulation binds it
85
What does heparin do?
prevent further clot formation prevent further extension of clot.
86
What is heparin induced thrombocytopenia?
platelet coutn decreased by 50% major adverse reaction. Rare, autoimmune occurs in small amount.
87
What is the difference between low molecular weight heparin and heparin?
Heparin inactivates 10a and thrombin whereas LMW heparin only inactivates 10a
88
What is the mechanism of action of warfarin?
Prevents gamma-carboxylation of several glutamate residues in prothrombin. Blockade results in incomplete clotting factor production.

Block 6 (3 decks)

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