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PHARMACOLOGY > 4. CARDIOVASCULAR SYSTEM > Flashcards

4. CARDIOVASCULAR SYSTEM Flashcards

1
Q

…form physiological system that is responsible for supply of O2 and nutrients to organism and participation in elimination of metabolic waste

A

-heart, blood, blood vessels and lungs

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2
Q

effectiveness of cardiac muscle depends upon

A

O2 levels in blood

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3
Q

function of heart is regulated by

A

autonomous nervous system that controls its rhythm and contractility

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4
Q

heart is impacted by

A

-catecholamines (noradrenaline)
-dopamine
-prostaglandins
-acetylcholine
-renin-angiotensin-aldosterone system

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5
Q

cardiac muscle contraction mechanism: following stages (7)

A
  1. increase in myofibril membrane permeability for Na ions > flow of Na ions across membrane into cell and depolarization of membrane
  2. entry of Ca ions into cells and/or release from sarcoplasmic reticulum
  3. increase in concentration of Ca in cell will lead to reaction between ATP, myosin and actin > result ATP release > myosin-actin complex is formed and contraction occurs
  4. expulsion of K from cell with participation of Na, K-ATPase and depolarization of membrane terminated access of Ca into cell
  5. potential of cell membrane depends upon difference in concentrations of Na and K ions inside cell and external surface of cell
  6. cell membrane is selectively more permeable for K ions during diastole compared to Na
  7. this results in different charges occurring between internal and external surface and action of sodium-potassium pump becomes possible
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6
Q

positive inotropic effect

A

-systolic contraction of heart becomes faster and improves
-tone of myocardium improves
-dimension of dilated myocardium are reduced > minute and beat rate increase
-blood circulation becomes faster
-venous blood pressure drops=lisäävät sydänlihaksen supistumisvoimaa

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7
Q

negative chronotropic effect

A

slow-down in heart beat=hidastaa sydämen sykettä

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8
Q

negative dromotropic effect

A

inhibitor of impulse formation and impulse transmission system =Ne hidastavat impulssien johtumista sydämen johtoradassa.

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9
Q

positive bathmotropic effect

A

increase in myocardial irritability

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10
Q

substances impacting cardiac function: cardiotonics

A

-substances that restore energy resources of heart
-primarily for treatment of chronic heart failure

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11
Q

substances impacting cardiac function: cardiac stimulants

A

-substances that mobilize on short-term basis energy resources of heart
-used temporarily stimulate heart

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12
Q

ACE inhibitors

A

Angiotensin-converting-enzyme inhibitors

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13
Q

ACE inhibitors: mechanism of action

A

-inhibit conversion of inactive angiotensin 1 to active angiotensin 2 > reduces arteriolar resistance and glomerular filtration rate in glomerular capillaries

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14
Q

angiotensin is polypeptide that

A

-constricts blood vessels
-increases secretion of aldosterone
-facilitates central and peripheral effects of sympathetic nervous system

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15
Q

ACE inhibitors increase concentration of

A

bradykinin

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16
Q

activity of noradrenaline is reduced and activity is increased in

A

plasma

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17
Q

vasoconstrictor effect of angiotensin 2 is

A

reduced

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18
Q

excretion of sodium and water is

A

increased
(angiotensin 2-mediated release of aldosterone is decreased: aldosterone-mineralocorticoid, responsible for reabsorbtion of water and ions in kidney)

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19
Q

vasodilator effect of

A

bradykinin is maintained

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20
Q

REPRESENTATIVES of ACE inhibitors

A

-benazePRIL
-captoPRIL
-enalaPRIL
-fosinoPRIL
-quinaPRIL
-ramiPRIL

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21
Q

use of ACE inhibitors

A

hear failure

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22
Q

heart failure ACE inhibitors increase

A

-cardiac output and performance of heart

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23
Q

ACE inhibitors in heart failure: improve

A

-hemodynamics
-improve quality of life
-delay mortality
in dogs and cats

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24
Q

ACE inhibitors are classified also as

A

vasodilators

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25
Q

ACE inhibitors in renal failure: simultaneous administration of ACE inhibitors and diuretics (e.g furosemide) lead to same effect as in case of

A

simultaneous administration of diuretics and cardiac glycosides > risk of occurrence of hypokalemia or ventricular arrhythmia is higher when glycosides are administered

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26
Q

ACE inhibitors in renal failure: combination of for example

A

captopril-digoxin

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27
Q

drug interactions: ACE inhibitors potentiate effect of diuretics, but

A

-renal flow decreases > (angiotensin 2 maintains glomerular filtration rate, with ACE inhibitors GFR is decreased)
-it can lead to azotemia (plasma urea concentration increases)

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28
Q

NSAIDs may diminish effect of

A

ACE inhibitors

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29
Q

side effects of ACE inhibitors - relatively safe for

A

dogs

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30
Q

ACE inhibitors side effects: vomiting,

A

diarrhoea and anorexia may be experienced

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31
Q

side effects of ACE inhibitors sometimes an excessively sharp and powerful drop

A

in blood pressure

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32
Q

side effect ACE inhibitors hypo..

A

hypokalemia

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33
Q

captopril-bioavailability in dogs after administration through oral route

A

75%

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34
Q

captopril-full GIT tract bioavailability

A

30%

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35
Q

captopril - maximum effect is reached

A

1-2 hours after administration

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36
Q

captopril-primary effect in dogs

A

vasodilation

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37
Q

enalapril-bioavailability of

A

65%, maximum effect is reached after 2 hours

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38
Q

enalapril-duration of effect

A

12-14 hours

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39
Q

enalapril-effect: clinical improvement in dogs with heart failure due to

A

dilated cardiomyopathy or mitral regurgitation

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40
Q

lisinopril-bioavailability of

A

25-50%, fullness of GIT does not impact bioavailability

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41
Q

lisinopril-maximum effect is reached

A

6-8 hours after administration

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42
Q

benazepril-bioavailability

A

increases with repeated dosing, slight accumulation of drug

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43
Q

benazepril-for treatment of

A

congestive heart failure in dogs

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44
Q

cardiotonics i.e. cardiac glycosides i.e. digitalis glycosides- by acting on processes regulating cardiac function using cardiac glycosides it is possible to

A

-strengthen systolic contraction
-increase heart rate per minute
-reduce myocardial oxygen demand
-increase energy resources of heart = glycogen and creatine content of myocardium

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45
Q

using cardiac glycosides : such effect can also be achieved using

A

beta-adrenomimetics (temporarily)

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46
Q

cardiotonics-representatives: digitoxin, digoxin and gitoxin- glycosides obtained from

A

leaves of common foxglove (Digitalis purpurea)

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47
Q

cardiotonics- k-Strophanthidin-glycoside obtained from

A

seeds of Strophantus hispidus

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48
Q

cardiotonics-g-Strophanthidin-glycoside of

A

Strophanthus gratus

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49
Q

cardiotonics-Convallatoxin-glycoside extracted from

A

lily-of-valley (Convallaria majalis)

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50
Q

cardiotonics-Scillared-glycoside extracted from

A

squill

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51
Q

cardiotonics-pharmacokinetics depends on

A

lipid solubility and number of OH groups in structure - breakdown induced by gastric acid

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52
Q

digitoxin is absorbed best from

A

GIT - descending order as follows: digoxin, celanide, strofantin(not absorbed at all-injection)

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53
Q

water soluble Digitalis Glycosides (DG) are

A

injected into vein , onset action is within minutes

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54
Q

Digitalis Glycosides (DG) are partially bound to

A

blood proteins
-digitocin only has on OH group, absorbed well GIT
-strofantin has 5 OH groups , is not absorbed at all

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55
Q

DG primarily absorbed

A

in small intestine subsequent to p.o. administration

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56
Q

digoxin and digitoxin are absorbed in dogs and cats

A

p.o. 75-90% (strofantin 5-10%)

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57
Q

DG biotransformation

A

in liver, excreted through kidneys
-accumulated in addition to heart also in liver, kidneys, GIT

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58
Q

digitocin excreted

A

at slowest rate and strofantin is excreted at fastest rate

59
Q

DG effect is

A

similar between substances

60
Q

DG have direct impact on

A

-heart working capacity
-have effect on mechanism and contraction events of cardiac muscle, its excitation

61
Q

DG normalise

A

-oxygen demand of myocardium
-as result of that-performance of heart increases

62
Q

DG reduce activity of

A

K-Na-ATPase

63
Q

DG result of K-Na-ATPase activity reduction

A

-concentration of extracellular K and intracellular Na increase
-concentration of intracellular Ca increases
-strengthening and quickening systolic contraction of heart and POSITIVE INOTROPIC effect occurs

64
Q

DG reflexive mannes ….effect occurs

A

negative chronotropic effect occurs
-irritation of aortic arch and carotid sinus receptors due to strengthen pulse induces bradycardia throug vagus nerve

65
Q

DG extracardiac effect

A

-increase diuresis
-due to faster blood circulation
-blood supply of kidneys improves
-diuresis increases
-swellings resolve

66
Q

DG relocation of

A

-blood in organism
-part of blood relocated cardiac blood pool organs
-abdominal cavity blood vessels
-cardiac load decreases

67
Q

DG toxicity, side effects: humans experience

A

central nervous system effects:
hallucinations, psychosis, delirium, coma, yellow vision disturbances, lack of appetite, nausea, vomiting

68
Q

DG vomiting id both in animals and humans caused by

A

direct irritation of trigger zone of 4th ventricle of brain

69
Q

DG cardiac effect: side effect

A

-blocked impulse transmission
-extrasystoles
-ventricular fibrillation
-AV block

70
Q

DG toxicity : dogs primarily experience

A

irritation of GIT, loss of body weight, life-threatening arrhythmia, anorexia and vomiting

71
Q

DG (Digitalis Glycosides) if toxic reactions appear

A

-treatment should be terminated
-it may be necessary to administer K into vein

72
Q

DG primarily used in

A

small animals and horses

73
Q

DG indication

A

heart failure

74
Q

DG some treatment regimes, initially a loading dose is

A

administered i.e. so-called digitalization
- treatment is continued with maintenance dose = 1/5 to 1/8 of initial dose

75
Q

DG indication could be also

A

atrial fibrillation

76
Q

DG preventive digitalization-before lengthy

A

heart surgeries, cardiac glycosides may be administered in order to reduce toxicity of anaesthetics

77
Q

DG …. unless weak compared to beta-agonist and amrinone, milrinone

A

positive inotropic effect

78
Q

DG main effect

A

diuretic effect

79
Q

DG … vascular baroreceptor function

A

increased

80
Q

DG…. sympathetic activity

A

decreased

81
Q

DG …. increase parasympathetic nerve activity to sinus node, ratio and AV node

A

anti arrhythmic effects
-used for controlling supra ventricular tachyarrhytmias

82
Q

DG cats are more … than dogs and require .. doses

A

-sensitive
-lower

83
Q

DG doses are smaller in case of

A

liver impairment and kidney impairment

84
Q

DG contraindications are shock from loss off

A

shock from loss off blood , liver impairment and kidney impairment, ventricular arrhythmias

85
Q

non-glycoside inotropic agents : Bipyridine derivatives

A

lisää lihaksen supistumisvoimaa

86
Q

amrinone- non-glycoside inotropic agents: …effect

A

positive inotropic effect= lisää sydämen supistumisvoimaa

87
Q

amrinone gives

A

stronger heart rate

88
Q

amrinone heart rate does not

A

increase

89
Q

amrinone-O2 requirement of cardiac muscle is

A

reduced

90
Q

amrinone used for

A

short-term inotropic support in small animals with myocardial failure

91
Q

milrinone …. more potent than amrionen - effect ..

A

-20-30x
-similar

92
Q

milrinone contraindication - unsuitable for

A

chronic heart failure, side effects occur

93
Q

cardiac stimulants : (2)

A

-beta-adrenomimetics
-methylxanthines

94
Q

cardiac stimulants: heart contraction power

A

increases and positive inotropic effect occur (stronger heart muscle contraction)

95
Q

cardiac stimulants-cardiac energy resources

A

are used up more quickly-duration of action short-followed by complete exhaustion

96
Q

cardiac stimulants-used in case of

A

acute heart failure-for energizing animals on short term basis that have been sick for long period of time

97
Q

adrenaline-it stimulates

A

beta-adrenorreactive systems
-has positive chronotropic and inotropic effect (nostaa sydämen sykettä ja voimistaa sydänlihaksen supistumista)

98
Q

adrenaline- heart becomes

A

-quicker, performance increases, O2 req. of heart increase
-ventricular irritability increases, extrasystoles and fibrillation may occur

99
Q

dopamine (cardiac stimulants) precursor for …, decreases …., increases ….

A

-noradrenaline
-ventricular filling pressures
-cardiac output

100
Q

dobutamine (heart stimulant) synthetic …., … effect

A

-catecholamine
-inotropic

101
Q

caffeine, euphylli, aminophylline-methylxanthines : they have …. and …. effect

A

positive chronotropic and inotropic
=ventricular contraction strengthens, systole becomes more powerful
-rapid onset and duration of action is short

102
Q

methylxanthines-were used in

A

heart failure
> failures caused by infectious disease > as stimulant for CNS in case of general weakness
(not animals)

103
Q

analeptics:

A

heptaminol, diprophyllin, diprophyllin

104
Q

supportive treatment of acute cardiovascular and/or respiratory insufficiency (analeptic treatment)

A

heptaminol + diprophyllin

105
Q

cardiovascular analeptic

A

heptaminol

106
Q

heptaminol-action is related to

A

peripheral release of norepinephrine

107
Q

heptaminol … blood flow in aorta and has …. and …. effect > especially in case of weak heart work. … corona blood flow

A

-increases
-positive inotropic and chronotropic action
-increases

108
Q

diprophyllin (methylxantin) is

A

fosfodiesterase inhibitor , derivate of theophylline

109
Q

diprophyllin has …. and … action

A

analeptic and ccardiorespiratory

110
Q

diprophyllin relaxes…,dilates…, stimulater … and …, and increase

A

-bronchospasms
-coronary arteries
-respiration and cardiac work
-blood flow to heart

111
Q

antiarrhythmic agents reduce

A

impulse conduction system automaticity > activity of impulse origins outside sinus node is reduced and rhythm of heart normalizes

112
Q

antiarrythmic agents classified

A

1-4(5) classes

113
Q

lidocaine, quinidine, procainamide, aim aline, ethmozine, ethacizine

A

class 1 antiarrhythmic agents

114
Q

class 1 anti arrhythmic agents block …. . impulse conduction

A

-inflow of Na and Ca into cell
-speed and myofibril excitation decreases

115
Q

class 1 anti arrhythmic agents used for

A

treatment of acute ventricular arrhythmias but due ti several side effects use is limited

116
Q

propranolol, oxprenolol, atenolol, esmolol

A

class 2 anti arrhythmic agents

117
Q

class 2 antiarrhthmic agents basis of mechanism of action of

A

beta-adrenergic blocking agents is to block effect of catecholamines on impulse generation and impulse conduction of heart, reducing flow of Na ions into cell

118
Q

class 2 anti arrhythmic agents cardiovascular system effect is varied

A

-direct beta-adrenergic blockade
-stabilising effect of membranes
-selective effect on various tissues

119
Q

class 2 anti arrhythmic to treat

A

supraventricular and ventricular arrhythmias

120
Q

class 3 anti arrhythmic agents

A

-solatol
-amiodarone

121
Q

class 3 anti arrhythmic agents suppress

A

rhythm disorders caused by excess of catecholamines and having antiadrenergic effect

122
Q

class 3 anti arrhythmic agents do not impact

A

ion transport

123
Q

class 3 anti arrhythmic agents lower

A

blood pressure
>increase fibrillation threshold, are used to prevent sudden death due to ventricular arrhythmias

124
Q

class 4 anti arrhythmic agents

A

-verapamil
-nifedipine, amlodipine
-diltiazem=for slowing ventricular rate in case of atrial fibrillation

125
Q

class 4 anti arrhythmic agents are … blockers

A

calcium channel blockers

126
Q

class 4 anti arrhythmic agents suppress

A

permeation of Ca into cells > reducing cardiac muscle contractility and heart rate normalizing rhythm, blood vessels dilate

127
Q

class 4 anti arrhythmic agents do not impact

A

Na-K ion exchange

128
Q

class 4 anti arrhythmic agents treatment

A

paroxysmal supraventricular tachycardia

129
Q

pimobendan- derivative of

A

benzimidazole-pyridazinone is non-sympathomimetic, non-glycoside inotropic agent that has potent vasodilatory effect

130
Q

pimobendan used in dogs in treatment of

A

congestive heart failure caused by dilated cardiomyopathy or valvular disease (mitral regurgitation and/or tricuspid regurgitation)

131
Q

pimobendan has …. and positive… -inodilator

A

vasodilator and positive inotropic

132
Q

levosimendan increases

A

calcium sensitivity to myocytes by binding to troponin C in calcium dependent manner
-increases contractility without raising calcium levels

133
Q

levosimendan relaxes

A

vascular smooth muscle by opening adenosine triphosphate sensitive potassium channels

134
Q

levosimendan is used to manage

A

acutely decompensated congestive heart failure

135
Q

substances that cause dilation of blood vessels

A

-prazosin (alfa 1-blocker)
-nitroglycerin
-nitroprusside
-captopril
-enalapril

136
Q

dilation of blood vessels : propentofylline : peripheral …. increases

A

-vasodilator
-increases flow of blood into brain, as well as cardiac and skeletal muscle > this inhibits aggregation of blood platelets and improves flow properties of erythrocytes

137
Q

propentofylline used to improve

A

cerebral blood circulation and peripheral blood supply in dogs, administered in tablet form

138
Q

amlodipine: treatment of

A

systemic hypertension in cats

139
Q

amlodipine is a

A

voltage dependent calcium-channel blocker that is part of dihydropyridine group, selectively binding to L-type calcium channels in smooth muscle of blood vessels, cardiac muscle and cardiac nodal tissue

140
Q

amlodipine prefers L-type

A

calcium channels in smooth muscle of blood vessels, thereby lowering vascular resistance

141
Q

primary blood pressure-reducing effect of amlodipine is derived from

A

its direct relaxant effect on arteries and arterioles

142
Q

effect of amlodipine on venous blood circulation

A

is low

143
Q

amlodipine … effect endures and decreases depending upon dose

A

antihypertensive

144
Q
A

PHARMACOLOGY (14 decks)

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