Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Chapter 5 - Cardiovascular System > Flashcards

Chapter 5 - Cardiovascular System Flashcards

1
Q

Think of the heart as 2 pumps – The right side is the small pump and it …

A

Pumps blood to the lungs and back to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The left side of the heart is the larger and stronger pump and it …

A

Pumps blood throughout the remainder of the body and back to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Veins carry blood ________ the heart

A

Towards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Arteries carry blood ________ the heart

A

Away from

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The purpose of the valves in the heart …

A

To allow blood to flow in a SINGLE direction and to prevent blood from flowing backwards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

(True/False) Valves pump blood through the heart

A

FALSE. Valves open and close passively in response to changes in blood pressure on either side of the valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vena Cava

A

Vessels returning blood to the RIGHT side of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Right Atrium

A

Receives blood from the superior and inferior vena cava and delivers it to the right ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tricuspid Valve / Right Atrioventricular (AV) Valve

A

Valve between the right atrium and right ventricle of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Right Ventricle

A

Lower chamber (right), pumps blood through the pulmonary trunk and arteries to the capillaries of the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pulmonic Valve

A

Valve between the right ventricle and the pulmonary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pulmonary Arteries

A

Carry blood from the right ventricle to the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pulmonary Veins

A

Carry blood from the lungs back to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Left Atrium

A

Receives blood from the pulmonary veins and delivers it to the left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mitral Valve / Left Atrioventricular (AV) Valve

A

Valve in the heart that controls blood flow from the left atrium into the left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Left Ventricle

A

Lower chamber (left), pumps oxygenated blood out through the aorta into systemic arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aortic Valve

A

Valve in the heart between the left ventricle and the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Aorta

A

Main trunk from which the systemic arterial system proceeds - Arises from the left ventricle of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ascending Aorta

A

Arises from the left ventricle and passes upward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aortic Arch

A

Bends over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Descending Aorta

A

Proceeds downwards (divided into upper/thoracic part and a lower/abdominal part)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When the heart beats the “lubb-dupp” sound you hear is what action?

A

The sudden closing of the valves in response to the pressure change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cardiac diseases related to mechanical functions include the following 3 things …

A

1) Muscular chambers fail to contract with sufficient strength. 2) Valves fail to close or open completely. 3) Unnatural holes connect chambers or major vessels, allowing blood to blow in abnormal directions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sinoatrial (SA) Node

** The hearts pacemaker **

A

Group of specialized conduction cells in the right atrium that depolarize more rapidly than any other cells in the heart.
These cells set the pace of the depolarization of the heart (the subsequent contraction that is felt is the pulse rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Depolarization Wave

A

“Firing” of cells through the heart (electrical conduction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Contractile Muscle Cells

A

Actually pump the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Conduction Cells

A

Modified muscle cells that initiate and conduct the depolarization wave along a specific conduction pathway so that the muscle cells contract in the proper order

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Automaticity

A

The ability to depolarize (fire) spontaneously and independently without any external stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

SA Node Depolarization

A

Sends a wave of depolarization outward in all directions through the right atrium and left atrium (as the wave of depolarization passes from one cardiac muscle cell to another, each cell contracts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

P Wave

A

Atrial depolarization (and contraction of atrial muscle cells) – appears as the small bump or deflection on ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

PR Interval

A

Period of conduction delay in the AV Node – appears as a flat line after the P wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

QRS Complex

A

Represents ventricular depolarization (and contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

T Wave

A

Ventricular repolarization- Ventricle muscle cells relax and repolarize (reset) to prepare electrically for the next depolarization wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Arrhythmia

A

Any deviation from the normal pattern of cardiac depolarization or repolarization, can result in tachycardia/bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

(True/False) ECG is not used to diagnose mechanical abnormalities to the heart (poorly functioning valves/weak cardiac muscle)

A

TRUE. ECG is only useful in identifying electrical abnormalities in the conduction pathway or detecting an increase in the overall mass of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Bundle Branches

A

Specialized conduction cell pathway that splits into right and left parallel tracts, they rapidly conduct the electrical impulse to the Purkinje Fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Purkinje Fibers

A

Modified cardiac fibers composed of Purkinje cells - interlaced network at the apex of the heart. Receives and distributes electrical impulse rapidly from the ventricular muscle cells, from the apex to the heart valves, and pushes blood through the pulmonic and aortic valves and out to the lungs and body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Ventricular Diastole

A

Relaxation phase between contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

End Diastolic Volume

A

Amount of blood that fills the ventricular chambers after the ventricular diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Venous Return

A

Volume of blood returning to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Venous Return System

A

Large veins carrying blood back to the heart from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Diuresis

A

Decreased blood volume as the result of water loss through the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Ascites

A

Fluid in the abdominal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Systemic Hypertension

A

Increased blood pressure within the systemic arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Aortic Stenosis

A

Narrowing of the opening around the aortic valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Mitral Valve insufficiency

A

Damage to the valve between the left atrium and left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Depolarization

A

When a cardiac or specialized conduction cell “fires”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Repolarization

A

When a cell resets itself in preparation to fire again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Resting State (polarized cell)

A

The cell is polarized (having two distinct ‘poles’ or segregated areas of electrical charge on either side of the cell membrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the 3 most prominent ions found in the body?

A

Sodium (Na+)
Potassium (K+)
Chloride (Cl-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Sodium-Potassium -ATPase Pump

Sodium-Potassium Adenosine Triphosphatase

A

Pump (specialized protein) located in the cell membrane that maintains the separation of sodium and potassium by active transport, which gets its energy from the enzyme ATPase (the cells stored energy molecule)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Fast Sodium (Na+) Channels

A

Channel that when open allows Sodium to rapidly move into the cell driven by its concentration gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Potassium (K+) Channels

A

When the charge within the cell becomes positive (+) enough the Sodium fast channels close and the Potassium channels open, allowing Potassium to be driven out of the cell because of its influx of positively charged Sodium ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

When a rapid influx of Sodium moves INTO the cell (making it positively charged +) this is referred to as …

A

Depolarization - because the two ion populations are no longer kept separated or polarized across the cellular membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

When the charge within the cell becomes positive enough, the Na+ fast channels close and the K+ channels open to allow Potassium to leave the cell. This is referred to as …

A

Repolarization - because the positive charges from the potassium are leaving the cell due the to influx of sodium ions entering the cell, causing the charge inside of the cell to become more negative again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Preload

A

The pressure exerted on the myocytes within the walls of the ventricles by the “load” or volume of blood in the ventricles just before ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Afterload

A

The tension or pressure the ventricles must create to eject blood out of the ventricles and into the aorta and pulmonary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How many phases of charge are there inside the cardiac muscle cell with depolarization and repolarization?

A

5 total

Phase 0-IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Phase 0

Depolarization

A

Sodium fast channels open, allowing positive sodium ions to rush into the cell and make it more positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Phase I

Repolarization

A

After the Na+ influx, sodium channels close, potassium channels open, K+ leaves the cell causing the charge inside the cell to become less positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Phase II

depolarization/repolarization curve

A

Opening of other Na+ and Ca++ channels causes a cause a further influx of positively charged ions that offset the loss of K+ creating a Plateau Phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q 
Phase III
(Repolarization - Baseline charge)
A

When slow Na+ and Ca++ channels shut, continued outward movement of positive K+ ions now takes the charge inside the cell to a negatively charged baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Phase IV

Resting State

A

Potassium channels close and the Sodium-Potassium ATPase Pump redistributes the Na+ ions from Phase 0 back outside the cell, while moving the K+ from Phase I, II, and III back into the cell.
This causes NO net change in charge inside the cell, so the line remains flat (resting) until the next stimulus opens the fast Na+ channels again (Phase 0)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the 4 specialized cells of the hearts electrical cardiac conduction system

A

SA Node
AV Node
Bundle branches
Purkinje Fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Do cardiac conduction cells depolarize and repolarize exactly the same as cardiac muscle cells do?

A

NO. With cardiac conduction cells there is no plateau phase, and in Phase IV the conduction cell moves gradually upward immediately after completion of repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Threshold

A

Once the phase IV slope attains a certain level of positive charge, the conducting cell depolarizes (fires) allowing Na+ and Ca++ ions to flow into the cell via their channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Refractory Period

A

The time in the depolarization/repolarization cycle when the cardiac cell cannot depolarize again until it has completed the repolarization phase of the cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Absolute Refractory Period

A

A cardiac cell (or nerve) is absolutely refractory to depolarization stimulus during Phase 0, no matter how strongly the cell is stimulated to depolarize again they will not

69
Q

Relative Refractory Period

A

Only a stronger than normal stimulus may be able to cause the sodium channels to open again, evoking a depolarization response

70
Q

(Atria/Ventricle) Flutter or Fibrillation

A

A continuous series of rapid, uncoordinated contractions

71
Q

Arterioles

A

Small artery blood vessels

72
Q

List 3 Catecholamines

A

Epinephrine
Norepinephrine
Dopamine

73
Q

What response do Catecholamines produce when they bind to Adrenergic (Catecholamine) receptors?

A

The combination of Catecholamines and Adrenergic receptors found on tissues and organs produces the physiologic changes observed as the “Fight or Flight” response

74
Q

Adrenergic Agonists

Sympathomimetic Drugs

A

Any drugs that have intrinsic activity on these adrenergic receptors can mimic the effects of Epinephrine and Norepinephrine

75
Q

Adrenergic Antagonists

A

Drugs that are able to bind to these adrenergic receptors but have NO intrinsic activity. They block catecholamine molecules from combining with receptors, which blocks their sympathetic effect

76
Q

List the 4 Adrenergic Receptors (Fight or Flight/Sympathetic) having the greatest role in adrenergic drug actions

A

Alpha-1 (α1)
Alpha-2 (α2)
Beta-1 (β1)
Beta-2 (β2)

77
Q

Stimulation of the Alpha-1 (α1) adrenergic receptors causes …

A
  • Vasoconstriction of precapillary arterioles in the skin, abdominal organs including the GI tract and kidney (shunts blood away from these organs and towards the heart and skeletal muscles)
  • Mydriasis (dilation of pupil)
78
Q

Stimulation of the Alpha-2 (α2) adrenergic receptors (located on the ends of adrenergic neurons) causes …

A
  • Inhibition of release of further norepinephrine from nerve terminal (regulates the release or norepinephrine)
79
Q

Stimulation of the Beta-1 (β1) adrenergic receptors (located primarily in the heart) causes …

A
  • Increased heart rate and force of contraction (Beta for beat!)
80
Q

Stimulation of the Beta-2 (β2) adrenergic receptors (found on smooth muscle cells surrounding arterioles that supply the heart and skeletal muscles and surrounding bronchioles) causes …

A
  • Increased bronchiole (bronchodilation) diameter by relaxing smooth muscle
  • Dilation of blood vessels in skeletal muscles (for fleeing or fighting)
81
Q

List the 2 Cholinergic Receptors (Rest and Digest/Parasympathetic) having the greatest role in cholinergic drug actions

A

Muscarinic Cholinergic Receptors

Nicotinic Cholinergic Receptors

82
Q

Stimulation of the Muscarinic cholinergic receptors cause …

A
  • Increased secretion and motility of GI tract
  • Slows heart rate (but has no effect on force of contraction)
  • Urination
  • Bronchoconstriction
83
Q

Stimulation of the Nicotinic cholinergic receptors cause …

A
  • Voluntary skeletal muscle contraction
84
Q

Tachycardia

A

Faster than normal heart rate

85
Q

Bradycardia

A

Slower than normal heart rate

86
Q

Ectopic Focus

A

Abnormal site or initial depolarization, often caused by damaged myocardial or conducing cells with membranes that leak Na+ into the cell more rapidly than normal (which is what produces spontaneous depolarization)

87
Q

(True/False) Similar to diagnosing mechanical abnormalities, ECG cannot be used to detect arrhythmia’s cause by ectopic foci

A

FALSE.

ECG can be used to detect these arrhythmia’s

88
Q

Premature Ventricular Contraction (PVC)

A

Ectopic focus located in the ventricles, which generates a single, large, bizarre wave on the ECG in place of the normal QRS complex

89
Q

Paroxysm

A

Multiple PVCs occurring one after the other in a short series of waves

90
Q

Ventricular Flutter

A

A longer series of PVCs

91
Q

Ventricular Fibrillation

Rapidly Fatal

A

Conduction disturbance is severe and depolarization wave is so totally disrupted it is not identifiable on ECG (ventricles are quivering and unable to produce a coordinated contraction to eject blood)

92
Q

Ventricular Tachycardia

A

Abnormal cell in the ventricles rapidly depolarizing and causing a rapid heartbeat

93
Q

Atrial Flutter

A

Premature electrical impulse that arises in the atria, resulting in a faster than normal heart rate
(Rhythm may be regular or irregular in frequency)

94
Q

Atrial Fibrillation

A

Very rapid contractions or twitching of the heart muscle in the atria. Ventricles will then contract more rapidly than normal
(Rhythm may be regular or irregular in frequency)

95
Q

Sinus Rhythm

A

Normal rhythm controlled by the SA node

96
Q

Tachyarrhythmia

A

Fast abnormal heart rhythm

can produce a faster ventricular heart rate or tachycardia

97
Q

Bradyarrhythmia

A

Slow abnormal heart rhythm

can produce slower than normal heart rate or bradycardia

98
Q

Supraventricular Rhythm

A

Indicates that the source or the arrhythmia is “above” the ventricles, meaning it originates in the Atria, SA Node, or AV Node

99
Q

Ventricular Arrhythmia

A

Indicates that the problem originates somewhere in the ventricles or conduction pathways to the ventricles

100
Q

Tolerance

A

Becoming resistant to the effects of a drug, occurs from upregulation (is not caused by induction of drug metabolism in cases of B1 blockers)

101
Q

Upregulation

A

Occurs after a B1-adrenergic receptor has been blocked by B1-Blocker drugs for a long period of time. This causes the cell to begin to produce more B1-Receptors on the cell surface.

102
Q

Negative Inotropic Effect

A

Causes a decreased force of contraction

103
Q

Automaticity

A

Capacity of a cell to initiate an impulse, such as depolarization, without an external stimulus

104
Q

Downregulation

A

Cells remove some of the B1-Receptors from the cells surface, reducing the number of receptors available, reducing the cells ability to respond to adrenergic drug stimulation
(also decreases the positive inotropic effect)

105
Q

Positive Inotropic Effect

A

Increases the strength of contraction in a weakened heart

106
Q

Class I

Antiarrhythmic Drugs

A

Sodium Influx Inhibitors - Work primarily by decreasing the rate of Na+ movement into the cell through the sodium fast channels

107
Q

List 2-4

(Class I) Antiarrhythmic Drugs

A
  • Lidocaine
  • Mexiletine
  • Procainamide
108
Q

Class II

Antiarrhythmic Drugs

A

B-Blockers (antagonists) Work by blocking the B1-Sympathetic nervous system receptors on the heart

109
Q

List 2-5

(Class II) Antiarrhythmic Drugs

A
  • Propanolol (non selective antagonists (can combine with B1 and B2 receptors)) older drug
  • Atenolol (Newer, selective B1 Blocker)
  • Esmolol (Newer, Selective B1 Blocker) Very short acting
  • Metoprolol (Newer, selective B1 Blocker)
  • Carvedilol (Newer, Selective B1 Blocker)
110
Q

Class III

Antiarrhythmic Drugs

A

Other antiarrhythmic Drugs - Work by inhibiting the potassium channels, making them slower to open and prolonging the repolarization period and extending the refractory period

111
Q

List 1-2

(Class III) Antiarrhythmic Drugs

A
  • Sotalol

- Amiodarone

112
Q

Class IV

Antiarrhythmic Drugs

A

Calcium channel blockers - Block the slow calcium channels in conduction system cells, decreasing automaticity

113
Q

List 1-3

(Class IV) Antiarrhythmic Drugs

A
  • Diltiazem
  • Verapamil
  • Digoxin
114
Q

Positive Inotropic Drugs

A

Drugs that increase the strength of contraction of a weakened heart, most work by making Ca++ more available to contractile proteins

115
Q

Inodilator Drugs

A

Drugs that have both a positive inotropic effect and a vasodilation effect

116
Q

Catecholamines

A

Increase the force on contraction through the B1-Receptors by causing a greater release of Ca++ from intracellular storage sites within the cardiac muscle

117
Q

What are the body’s 3 natural positive inotropic agents (catecholamines) ?

A
  • Epinephrine
  • Norepinephrine
  • Dopamine
118
Q

Dobutamine

A

Adrenergic drug that produces a positive inotropic effect by stimulating B1-Receptors in the cardiac muscle and the conduction system cells - strong positive inotropes, but only improve cardiac contractility for a relatively short period of time

119
Q

Pimobendan (Vetmedin)

A

Inodilator - Does not increase release of Ca++ from storage cell sites. Instead increases the Ca++ binding with the contractile elements, resulting in a more effective contraction of the cardiac muscle cell. Approved for Veterinary use in 2007.

120
Q

Digoxin

A

Positive Inotrope - Causes more Ca++ to be released from the intracellular storage sites, making more Ca++ available for the contractile elements, enhancing strength of contraction

121
Q

Vasodilator Drugs

A

Increase the diameter of blood vessels and are very important in treating CHF

122
Q

Arterial Vasodilators

A

Directly reduces the resistance the heart must overcome to successfully eject the blood from the ventricles
Reducing the amount of blood left in the ventricles after contraction
Reducing backup of blood in the atria and vessels returning blood to the heart
Reducing backup and lowered pressure decreases pressure in the capillaries
Reducing forces pushing water into tissues and ultimately decreasing edema formation

123
Q

Amlodipine

A

Arterial Vasodilator - Calcium channel blocker, can be used in dogs but used primarily in cats with hypertension secondary to kidney, hyperthyroid, or diabetes and not typically used to treat cardiac disease

124
Q

Hydralazine

A

Arterial Vasodilator - Directly causes arteriolar smooth muscle to relax, the mechanism by which this occurs is not yet completely understood, but thought to inhibit some Ca++ movement into smooth muscle cells. Used to relieve some signs of CHF caused by severe mitral valve insufficiency

125
Q

Nitroglycerine

A

Venous Vasodilator - Primarily relaxes blood vessels on the venous side of circulation, resulting in blood ‘pooling’ in the expanding venous blood vessels, reducing the volume of blood in the arterial side of circulation and decreasing arterial blood pressure

126
Q

Mixed “Balanced” Vasodilators

A

Theoretically combines the benefits of arterial vasodilation (lowered arterial BP, ease of ventricular ejection of blood) and Venodilation (lowered pulmonary circulation BP, decreased edema formation)

127
Q

Nitroprusside

A

Potent Mixed Vasodilator - used short term to help stabilize dogs/cats with severe dyspnea cause by pulmonary edema secondary to heart failure. Cannot be administered to patients that are hypotensive

128
Q

ACE Inhibitors

A

Mixed or balanced vasodilators that relax smooth muscle of both arterioles and veins.
Produce vasodilation by blocking/inhibiting Angiotensin Converting Enzyme (ACE) preventing formation of Angiotensin II (potent vasoconstrictor) and Aldosterone (hormone that increases blood volume by causing Na+ retention)
** Must be used with caution in animals with pre-existing kidney disease

129
Q

List 2-4

ACE Inhibitor Drugs

A
  • Enalapril
  • Benazepril
  • Lisinopril
  • Captopril
130
Q

Hypertension

A

Increased blood pressure

131
Q

Hyoptension

A

Decreased blood pressure

132
Q

Congestive heart Failure (CHF)

A

The heart muscle is too weak to eject sufficient blood to maintain normal tissue functions. Decreased cardiac output results in decreased arterial blood pressure

133
Q

Baroreceptors

A

Special pressure receptors located in the walls of large arterial blood vessels (primarily in carotid artery and aortic arch) detect change in blood pressure.
When BP is normal: receptors send a constant low-level signal to inhibit activation of the SNS.
When Arterial BP decreases: Stop sending the inhibitory signal, the SNS becomes activated (releasing epinephrine and norepinephrine to stimulate B1 and A1 receptors) which increases arterial BP

134
Q

Renin

A

A compound that is released into the blood when the specialized cells in the renal tubules detect decreased blood flow

135
Q

Angiotensinogen

A

A compound produce by the liver, product of Renin conversion

136
Q

Angiotensin I

A

Product of Angiotensinogen which is quickly converted by the Angiotensin-Converting-Enzyme (ACE) to Angiotensin II

137
Q

Angiotensin II

A

Product of Angiotensin I, one of the body’s most potent vasoconstrictors. Its release is designed to increase arterial BP and theoretically restore renal blood flow and urine formation
(but increased arterial pressure also causes increase to the hearts workload by increasing the volume of circulating blood)

138
Q

Aldosterone

A

Hormone released from the adrenal cortex when stimulated by Angiotensin II.
It increases Na+ reabsorption from the urine and pulls it back into the blood, causing a greater retention of Na+. This osmotically attracts and holds water in the blood, increasing the blood volume. This restores/maintains arterial BP but also creates a larger volume of blood for the heart to pump and increasing the workload

139
Q

Compensated Heart Failure

A

A patient whose body has successfully initiated the autonomic compensatory response to the weakened heart and falling arterial blood pressure

140
Q

Diuretics

A

Increase urine formation and promote water loss (diuresis). Diuretics work by either:

1) preventing reabsorption of Na+ or K+ from the renal tubules
2) They enhance Na+ and K+’s secretion into the tubules

141
Q

List 2-4 reasons Diuretics may be used

A

1) Reducing inappropriate accumulation of tissue fluid (pulmonary or cerebral edema)
2) Reducing blood volume
3) Reducing arterial pressure
4) Decreasing the workload on a failing heart in CHF

142
Q

Loop Diuretics

A

Referring to the ‘Loop of Henle” located within the renal tubule, which is where these drugs produce diuresis by inhibiting reabsorption of Na+ from the urine at the thick ascending segment of the Loop. Retained Na+ in the urine osmotically retains water in the urine and results in water loss via urine

143
Q

Furosemide (Lasix)

A

Loop Diuretic that inhibits reabsorption of Na+, storing Na+ in the urine and osmotically retaining water, resulting in water loss via urine. Helpful in increasing diuresis in early stages or renal damage/disease

144
Q

Ototoxicity

A

Toxicity associated with hearing or the inner ear. Furosemide and other Loop diuretics have been implicated in causing ion imbalances, changing the electrolyte balance in the inner ear, resulting in loss of hearing

145
Q

Thiazide Diuretics

A

After administration, Thiazides are secreted into the forming urine by the proximal convoluted tubule, pass the loop of henle without causing any effect, and then flow downstream to the initial segment of the distal convoluted tubule where they act to decrease resorption of Na+ and Cl-

146
Q

(True/False)

Thiazide diuretics have more of a diuretic effect than Furosemide

A

FALSE.
They are less potent than loop diuretics because of their site of action (distal convoluted tubule). Also typically used in conjunction with Furosemide when kidneys become less responsive to Furosemide alone.

147
Q

List 1-2

Thiazide Diuretics

A
  • Chlorothiazide

- Hydrochlorothiazide

148
Q

Potassium-Sparing Diuretics

A

Diuretics that do not secrete K+ ions, and actually increase Na+ ion excretion and retains K+ in the body instead

149
Q

Spironolactone

A

Potassium sparing diuretic. Competitive antagonist of Aldosterone. Useful for animals with excessive fluid retention from CHF that is unresponsive to Furosemide or Thiazide alone

150
Q

Osmotic Diuretics

A

Retains water in the renal tubules by its physical presence within the lumen of the renal tubule.

151
Q

Mannitol

A

Carbohydrate (sugar) that retains water in the renal tubules by its physical presence. Primarily used to reduce cerebral edema associated with head trauma, reduce damage to the kidneys when they are first injured by a poison or drug, and increase excretion of renally eliminated toxins

152
Q

Carbonic Anhydrase Inhibitors

A

May be used to decrease production of aqueous humor in the eye and reduce intraocular pressure in animals with glaucoma

153
Q

Acetazolamide

A

Carbonic Anhydrase Inhibitor - relatively weak diuretic effect - Not used to treat cardiac problems in Veterinary patients

154
Q

Aspirin (Acetylsalicylic Acid)

A

Inhibits platelet formation of prostaglandins and thromboxanes. This reduces aggregation (clumping) of platelets and reduces the chances for spontaneous platelet plug formation and subsequent larger fibrin clot formation

155
Q

(True/False)

Use of Aspirin in cats can reduce the risk of spontaneous platelet adhesion and thrombus formation. But it must be given in a 48 hour dose interval.

A

TRUE
Aspirin can be used in cats to help prevent thrombus formation associated with hypertrophic or congestive cardiomyopathy. 48 hour dosing is required because cats do not metabolize and eliminate the drug as readily as other species do

156
Q

Sedatives/Tranquilizers

A

Sometimes use of these drugs by merely calming the animal which reduces the heart rate and reduces the risk of fatal arrhythmia’s. They can also reduce the heart muscles oxygen consumption and improve the heart muscles effectiveness. As always sedatives effects need to be weighed against any possible adverse effects in these situations

157
Q

Aerophagia

A

A condition in which the animal is gasping for breath

158
Q

Hyperkalemia

A

High concentrations of potassium (K+) in the blood

159
Q

Hyponatremia

A

Low sodium (Na+) levels in the blood and body

160
Q

Hypovolemia

A

Low blood volume

161
Q

Edema

A

Fluid retention in tissues

162
Q

Syncope

A

Fainting

163
Q

Ataxia

A

Weakness

164
Q

Ascites

A

Accumulation of fluid within the abdominal cavity

165
Q

Is ascites associated/seen with left or right sided heart failure?

A

Left

166
Q

Pulmonary Edema

A

Accumulation of fluid within the tissue of the lungs

167
Q

Is pulmonary edema associated/seen with left or right sided heart failure?

A

Right

168
Q

Thrombus

A

Large fibrin clot

169
Q

Thromboxanes

A

Released by traumatized tissue and make platelets sticky so that they will adhere to each other at small breaks in blood vessels to form a platelet plug that stops the bleeding

Pharmacology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions