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Block 6 > PDA > Flashcards

PDA Flashcards

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
Q

What is the role of eicosanoids in GI secretion?

A

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

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26
Q

What limits therapeutic use of prostoglandins?

A

signficant adverse effects

short half-lives in circulation

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27
Q

How is aldosterone produced?

A

from zona glomerulosa cholesterol goes to prenenolone dexycortisoterone and then aldosterone

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28
Q

How is cortisol produced?

A

zona fasciculata and reticularis-cholesterol -> pregnenolone to deoxycortisol to cortisol

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29
Q

How is cortisol broken down?

A

reduction of A ring, sulfate conjugation and glucuronide conjugation

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30
Q

What are steroid therapy drugs usually used to tx?

A 
Adrenal insufficiency
rheumatoid arthiritis in progressive disease
osteoarthiritis for acute inflammation
allergic disases
inflammatory diseases
cerebral edema
shock--?
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31
Q

What are the three general properties of NSAIDs?

A

anti-inflammatory
anti-pyretic
analgesic

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32
Q

What is the mechanism of action of NSAIDs?

A

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

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33
Q

What is the major difference between aspirin and the other NSAIDs?

A

It is a irreversible inhibitor of the COX proteins.

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34
Q

What are the unique effects of aspirin that are unrelated to the inhibition of COX?

A 
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
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35
Q

What are the contrainidications indicated for all NSAIDS?

A

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

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36
Q

What are the toxicity problems linked directly to asprin?

A

Reye’s syndrome from aspirin and viral infections often in children. Liver failure
Salicylism

37
Q

How is histamine synthesized?

A

from esential amino acid L-histidine. By specific histidine decarboxylase using pyridoxal 5-phosphate as a cofactor.

38
Q

Where is histamine localized?

A

ubiquitous but highest in lung, skin and stomach. Mast cells, basophils as well as continual production

39
Q

What are the signs of histamine relase or injection?

A

burning itching sensation followed by intesnse warmth. Skin reddents BP falls and HR increases. Quickly bp recover and hives appear

40
Q

What is red-man syndrome?

A

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
Q

What is serotonin synthesized from?

A

the essential amino acid tryptophan

42
Q

What is the rate limiting step of serotonin synthesis?

A

tryptophan hydroxylase

43
Q

Where is the majority of serotonin stored and synthesized?

A

Enterochromaffin cells of GI mucosa–90% slow spontaneous release turnover 1 day
2nd most blood platelets–8%

44
Q

Where is the majority of CNS serotonin stored?

A

Rapid turnover 4 hours: midbrain Raphe nucleus

45
Q

What are the pharmacological actions of serotonin at GI?

A

GI smooth muscle contraction

emesis by 5-HT3

46
Q

What is carcinoid syndrome?

A

serotonin secreting tumors; and bradynkinin

Cause severe diarrhea and asthma

47
Q

What are the pharmacological actions of serotonin in the CV?

A

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
Q

What is Bezold-Jarisch reflex?

A

serotonin is a powerful activator of chemoreceptors in coronary vasculature which activates afferent vagal nerve endings”
bradycardia, hypotension and hypoventilation

49
Q

What is the pharm action of serotonin on platelets and CNS?

A 
platelet aggregation
Sensory perception
sleep
temp reg
neuroendocrine
learning and memory-short term
pain perception
drug abuse
emesis-5HT3
50
Q

What mental illnesses are associated with serotonin?

A 
affective disorders
schizophrenia
OCD
anxiety disorders- 5HT1A
Aggressive Behavior
51
Q

What is synthesized from serotonin in pineal gland?

A

Melatonin

52
Q

What are the mechanism of smooth muscle contraction?

A

Calcium-cell membrane
intracellular signalin-myosin light chain kinase
Rho kinase

53
Q

What are the mechanism of smooth muscle relaxation?

A

Signaling pathways inhibit contractile mechanism

paracrine factors-nitric oxide, dopamine, prostacyclin

54
Q

What is the juxtaglomerular cell?

A

modified smooth muscle found in media of afferent arteriole. Contain renin granules

55
Q

What is the macula densa?

A

Specialized epithelial cells found at point where distal tubule comes in contact with afferent arteriole; measure concentrationo f sodium in thick ascending limb

56
Q

What is renin?

A

acid protease that splits leucine-leucine bond of angiotensinogen giving angiotensin 1
produced in juxtaglomerular cells

57
Q

What is angiotensinogen or renin substrate?

A

alpha2 globulin, synthesized by liver, amino terminal sequence contain angiontensin 1

58
Q

What stimulates aldosterone production by zona glomerulosa cells of adrenal cortex?

A

potassium, ACTH and angiotensin 2

59
Q

What does aldosterone act on?

A

distal tubule and collecting ducts to enhance sodium reabsorption and potassium excretion

60
Q

What is the role of the intrarenal baroreceptor?

A

senses change in wall tension of afferent arteriole.

Wall tension inversely related to renin relase

61
Q

What is the role of the macula densa in renin relase?

A

senses change in sodium load, and this is inversely related to renin relase

62
Q

What is the role of renal sympathetic nervous system in renin release?

A

mediated by beta1 adrenergic receptors on JG cells

Renin release is increased by direct or indirect activation of renal sympathetic nerves

63
Q

What is the role of angiotensin 2 in renin release?

A

feedack inhibition

direct action by interaction with JG cells

64
Q

What is the role of angiotensin 2 on smooth muscle?

A 
AT1 receptor mediated
-vasoconstrictor
hypertrophy
At2 mediated
vasodilation-NO mediated
inhib proliferation of smooth muscle
promote apoptosis
65
Q

What is the role of angiotensin 2 on teh adrenal cortex?

A

stimulate aldosterone biosynthesis

66
Q

What is the role of angiotensin 2 on the CNS and sympathetic neruons?

A

promote thirst
ADH release
positive water balance

facilitates NE release
inhibit NE reuptake

67
Q

What is the role of angiotensin 2 on the heart?

A

hypertorphy of myocytes

increase in ECM production of fibroblasts

68
Q

How do the three classes of CCBs interact with each other?

A

allostericinteractions

1,4dihydropyridines act synergistically with each other and the others interfere incombinations

69
Q

What are the factors that account for preference of CCBs for CV cells?

A

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
Q

What type of cells do phenylalkylamines(verapamil and benzothiazepines(diltiazem) act on?

A

Cardiace cells

71
Q

What does 1,4dihydropyridines (nifedipine) act on preferentially?

A

arterial muscle cells

72
Q

What mechanism of action increases likelihood that phenylakylamines and benzothiazepines bind to cardiac cells?

A

Their binding site is deep within the channela nd therefore te rapid firing of cardiac cells increase opportunities for CCB binding.

73
Q

Why does the dihydropyridine CCB (nifedipine, almodipine) have a higher level of binding to vascular smooth muscle?

A

Binds with higher affinity to depolarized vascular smooth muscle, and vascular smooth muscle is more depolarized

74
Q

Why is diltiazem used to treat angina?

A

the beneficial effect is the reduced cardiac workload; SA node down adn reduces afterload

75
Q

Why is dilitiazem or verapamil used to treat supraventricular hypetension>

A

Reduce firing of SA node adn reduce conduction through AV node.

76
Q

Why is dihydropyridine used to treat hypertension?

A

Reduce blood pressure as a potent vasodilator. May trigger reflex tachycardia

77
Q

What are the adverse effects of calcium blockers?

A

vasodilator side effects, constipation, worse CHF, AV block

78
Q

In order what is the cost of diuretics?

A

Thiazides–>loop–>potassium sparing

79
Q

What is used to convert fibrinogen to fibrin?

A

Thrombin

80
Q

What primarily degrades the fibrin clot?

A

plasmin

81
Q

Warfarin is not used to treat clotting in emergencies?

A

Has no effect on active clotting factors

82
Q

Factor 5 Leiden causes what?

A

mutation that predisposes pateitns to clots

83
Q

What are the physical properties of heparin?

A

heterogenous mixture of polysaccharide negatively charged

84
Q

What occurs when heparin binds antithrombin?

A

allosteric hcange and encourages thrombin and active coagulation binds it

85
Q

What does heparin do?

A

prevent further clot formation prevent further extension of clot.

86
Q

What is heparin induced thrombocytopenia?

A

platelet coutn decreased by 50% major adverse reaction. Rare, autoimmune occurs in small amount.

87
Q

What is the difference between low molecular weight heparin and heparin?

A

Heparin inactivates 10a and thrombin whereas LMW heparin only inactivates 10a

88
Q

What is the mechanism of action of warfarin?

A

Prevents gamma-carboxylation of several glutamate residues in prothrombin. Blockade results in incomplete clotting factor production.

Block 6 (3 decks)

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