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N216 > Perfusion > Flashcards

Perfusion Flashcards

1
Q

Perfusion

A

the blood flow through arteries and capillaries delivering nutrients and oxygen to cells

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2
Q

Clotting

A

physiological process in which blood is converted from a liquid to a semisolid gel

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3
Q

Central Perfusion

A

Force of blood movement generated by cardiac output

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4
Q

Central perfusion requires

A

adequate cardiac function, bp, and blood volume

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5
Q

Central perfusion equation

A

Cardiac output (CO) = stroke volume x heart rate

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6
Q

Tissue or local perfusion

A

Volume of blood that flows to target tissue

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7
Q

Tissue or local perfusion requires

A

patent vessels, adequate hydrostatic pressure, and capillary permeability

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8
Q

When does impairment of central perfusion occur

A

cardiac output is inadequate

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9
Q

Reduced cardiac output results in

A

reduced oxygenated blood reaching the body tissues

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10
Q

If impaired central perfusion is not treated

A

if it is severe it leads to shock

if completely untreated leads to ischemia, cell death and cell injury

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11
Q

Impairment of tissue perfusion is associated witH

A

Loss of vessel patency

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12
Q

Impaired blood flow to affected body tissues leads to

A

Ischemia, cell death if uncorrected

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13
Q

Populations at greatest risk for impaired perfusion are

A

Middle aged and older adults
men
African Americans

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14
Q

Signs of inadequate central perfusion in infants

A

Poor feeding
Poor weight gain
Failure to thrive
Dusky colour

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15
Q

Signs of inadequate Central perfusion in Toddlers and children

A

Squatting and fatigue

Development delay

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16
Q

Ischemia

A

Poor blood supply to an organ

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17
Q

Ischemic Heart Disease

A

Poor blood supply to the heart muscle
Athersclerosis
Coronary artery disease

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18
Q

Myocardial Infarction

A

Necrosis, or death of cardiac tissue

Disabling or fatal

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19
Q

Hemostasis

A

General term for any process that stops bleeding

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20
Q

What is coagulation

A

Hemostasis that occurs because of the physiological clotting of blood

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21
Q

Thrombus

A

Technical term for a blood clot

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22
Q

Embolus

A

Thrombus that moves through blood vessels

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23
Q

Coagulation system

A

Each activated factor serves as a catalyst that amplifies the next reaction

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24
Q

Coagulation system Result is

A

Fibrin, a clot forming substance

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25
Q

Fibrinolytic System

A

The breakdown of clots and serves to balance the clotting process

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26
Q

Fibrinolysis

A

Mechanism by which formed thrombi are lysed to prevent excessive clot formation and blood vessel blockage

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27
Q

Fibrin

A

In the clot binds to a circulating protein known as plasminogen. This binding converts plasminogen to plasmin

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28
Q

Plasmin

A

Is the enzymatic protein that eventually breaks down the fibrin degradation products. This keeps the thrombus localized to prevent it from becoming an embolus

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29
Q

Systemic clotting Problem

A

Problem extends to entire body; is usually the result of a significant haematological event

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30
Q

Localized clotting problem

A

Problem is localized; is usually a problem in a vein or artery, either injury to a vessel or a clot within a vessel

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31
Q

Factors affecting Blood Flow

A

Pressure, Resistance and Neural control of total peripheral resistance

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32
Q

Pressure

A

Force exerted in a liquid per unit area

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33
Q

Resistance

A

Opposition to force

Diameter and length of the blood vessels contribute to resistance

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34
Q

Neuralcontrol of total peripheral resistance

A

Change in diameter of the vessels
Baroreceptors
Arterial Chemoreceptors

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35
Q

Factors affecting blood flow

A

Velocity
Laminar versus turbulent flow
Vascular compliance

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36
Q

Atherosclerosis

A

Type of blood vessel disorder

Begins with soft fat deposits that harden with age

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37
Q

Terms to describe the disease process of Atherosclerosis

A

Arteriosclerotic heart disease
Cardiovascular heart disease
Ischemic heart disease
Coronary artery disease

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38
Q

Atherosclerosis is the major cause of

A

Coronary Artery Disease

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39
Q

Step 1 of Atherosclerosis

A

LDL enters intimate through intact endothelium

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40
Q

Step 2 of Atherosclerosis

A

Intimal LDL is oxidized into pro inflammatory lipids

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41
Q

Step 3 of Atherosclerosis

A

oxidized LDL causes adhesion and entry of monocytes and T Lymphocytes across endothelium

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42
Q

Step 4 of Atherosclerosis

A

Monocytes differentiate into macrophages and then consume large amounts of LDL, transforming into foam cells

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43
Q

Step 5 of Atherosclerosis

A

Foam cells release growth factors (cytokines) that encourage Atherosclerosis

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44
Q

C-reactive protein CRP

A

Nonspecific marker of inflammation

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45
Q

What is increased in many clients with CAD

A

CRP C-reactive protein

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46
Q

Chronic exposure to CRP is associated with?

A

Unstable Plaques and oxidation of LDL cholesterol

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47
Q

Developmental stage: Fatty streak of Coronary Artery Disease

A

Earliest lesions
Characterized by lipid-filled smooth muscle cells
Potentially reversible

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48
Q

Developmental stages: Fibrous plaque of Coronary Artery Disease

A

Beginning of progressive changes in the arterial wall

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49
Q

Developmental stages: Fibrous plaque of Coronary Artery Disease - Lipoproteins Transport Cholesterol and other lipids where?

A

Arterial intima

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50
Q

Developmental stages: Fibrous plaque of Coronary Artery Disease - Fatty streak is covered by ________ forming fibrous plaque that appears_____________

A
  1. collagen

2. Grayish or whitish

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51
Q

Developmental stages: Fibrous plaque of Coronary Artery Disease- Result

A

Narrowing of vessel lumen

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52
Q

Developmental Stages: Complicated lesion of coronary heart disease

A

Continued inflammation can result in plaque instability ulceration, and rupture

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53
Q

Developmental Stages: Complicated lesion of coronary heart disease- Platelets accumulate and ______ forms.

A

Thrombus

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54
Q

Developmental Stages: Complicated lesion of coronary heart disease- result

A

Increased Narrowing or total occlusion of lumen

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55
Q

Collateral circulation

A

Normally, some arterial anastomoses (or connections) exist within the coronary circulation

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56
Q

Growth and extent of collateral circulation are attributed to two factors

A
  1. Inherited predisposition to develop new vessels (angiogenesis)
  2. Presence of chronic ischemia
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57
Q

Nonmodifiable Risk factors of CAD

A 
Age
Gender
Ethnicity
Family History
Genetic Predisposition
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58
Q

Modifiable Risk Factors of CAD

A 
Elevated serum lipids
Hypertension
Tobacco Use
Physical Inactivity
Obesity
Diabetes
Metabolic Syndrome
Psychological States
Homocysteine level
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59
Q

Nontraditional Risk Factors for CAD

A 
Markers of inflammation and thrombosis
Troponin I
Hyperhomocysteinemia
Adipokines
Infection
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60
Q

If an Embolus lodges in a coronary artery it causes a..,.

A

Myocardial Infarction

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61
Q

If an embolus obstructs a brain vessel it causes

A

Stroke (cerebrovascular accident)

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62
Q

If an embolus travels to the lungs it is a …

A

Pulmonary Embolus

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63
Q

If an embolus travels to a vein in the leg it is called a…

A

DVT Deep vein thrombosis

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64
Q

Events including an embolus are referred to as

A

Thromboembolic events

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65
Q

Thrombus Formation in Veins

A

Obstruction of venous flow leading to increased venous pressure

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66
Q

Factors of Thrombus formation in veins

A

Triad of Virchow

  • Venous Stasis
  • Venous endothelial damage
  • Hypercoagulable states
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67
Q

Triad of Virchow

A
  • Venous Stasis
  • Venous endothelial damage
  • Hypercoagulable states
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68
Q

Varicose Veins

A

Vein in which blood has pooled

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69
Q

With Varicose veins the veins are…

A

Distended, tortuous, and palpable

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70
Q

Varicose Veins are caused by

A

Trauma or gradual venous distension

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71
Q

Risk Factors for Varicose Veins

A 
Age
Female Gender
Family History
Obesity
Pregnancy
DVT
Prior Leg Injury
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72
Q

Chronic Venous Insufficiency

A

Inadequate venous return over a long period due to varicose veins or valvular incompetence

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73
Q

Superior Vena Cava Syndrome

A

Progressive occlusion of the superior vena cava that leads to venous distension of upper extremities and head

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74
Q

Peripheral Artery Diseases

A

Thromboangitis Obliterans

Raynaud Phenomenon

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75
Q

Tromboangitis Obliterans (Buerger’s Disease)

A

Inflammatory Disease of peripheral arteries

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76
Q

Tromboangitis Obliterans (Buerger’s Disease) is strongly associated with

A

Smoking

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77
Q

Tromboangitis Obliterans (Buerger’s Disease) is an ________ disease

A

Autoimmune

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78
Q

Tromboangitis Obliterans (Buerger’s Disease) Characterized by….

A

The formation of thrombi filled with inflammatory and immune cells

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79
Q

Tromboangitis Obliterans (Buerger’s Disease) Symptoms

A

Causes pain and tenderness in the affected area, also caused by slow and sluggish blood flow

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80
Q

Tromboangitis Obliterans (Buerger’s Disease) can lead to

A

Gangrenous lesions and amputations

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81
Q

Raynaud Phenomenon

A

Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes

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82
Q

Primary Raynaud Phenomenon

A

Vasospastic disorder of unknown origin

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83
Q

Secondary Raynaud Phenomenon

A 
Secondary to other diseases like: 
Collagen Vascular Disease
Smoking
Pulmonary Hypertension
Myxedema
Cold Environment
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84
Q

Manifestations of Raynaud Phenomenon

A

Pallor
Cyanosis
Cold
Pain

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85
Q

Anticoagulants are also known as

A

Antithrombotic drugs

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86
Q

Anticoagulants have no effect on…..

A

Blood clots that are already formed

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87
Q

Anticoagulants prevent

A

Intravascular thrombosis by decreasing blood coagulability

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88
Q

Anticoagulants are used prophylactilly to prevent

A 
Clot formation (Thrombus)
An Embolus (Dislodged Clot)
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89
Q

General Actions of Anticoagulants

A

Work on different points of the clotting cascade
Prevent intravascular thrombosis by decreasing blood coagulability
Do not lyse existing clots

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90
Q

Anticoagulants Indications

A

Used to prevent clot formation in certain settings in which clot formation is likely

  • Myocardial infarction
  • Unstable Angina
  • Atrial Fibrillation
  • Mechanical Heart Valves
  • Conditions where blood flow may be slowed or blood may pool
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91
Q

Anticoagulants Contraindications

A

Drug Allergy

Acute bleeding process or high risk of occurrence

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92
Q

Warfarin is strongly contraindicated in

A

Pregnancy

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93
Q

Low- molecular-weight heparins are contraindicated in

A

Patients with an indwelling epidural catheter risk of epidural hematoma

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94
Q

Anticoagulants Adverse Effects

A 
Bleeding- Risk Increases with increased dosages
Heparin induced thrombocytopenia
Nausea
Vomiting
Abdominal Cramps
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95
Q

Adverse effects of warfarin

A 
Bleeding
Lethargy
Muscle pain
Skin Necrosis
Purple Toes syndrome
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96
Q

Anticoagulants Drug- Drug Interactions

A

Interactions are profound and complicated
Enzyme Inhibition of metabolism
Displacement of the drug from inactive protein-binding sites
Decrease in Vit K absorption or synthesis by the bacterial flora of the large intestine
Alteration of platelet count or activity

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97
Q

Heparin Action

A

Inhibit clotting factors IIa (thrombin), Xa, and IX. Factors XI and XII are also inhibited but do not play as important a role

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98
Q

Low-Molecular- weight heparins

A

Enoxaparin (Lovenox)
Dalteparin (Fragmin)
Nadroparin Calcium (Fraxiparine)
Tinzaparin Sodium (Innohep)

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99
Q

Heparin Sodium

A

Natural Anticoagulant obtained form the lungs or intestinal mucosa of pigs

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100
Q

Amount of heparin given for DVT prophylaxis

A

5,000 units subcutaneously 2-3 times a day

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101
Q

Heparin Induced Thrombocytopenia

A

Abnormally low levels of platelets

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102
Q

Heparin Induced Thrombocytopenia Symptoms

A

Excessive bruising
Prolonged bleeding from cuts, gums, nose, in still and urine
Enlrged spleen

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103
Q

Type I Heparin Induced Thrombocytopenia

A

Gradual Reduction in platelets

Heparin Therapy can generally be continued

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104
Q

Type II Heparin Induced Thrombocytopenia

A

Acute fall in the number of platelets (more than 50% reduction from baseline)
Discontinue Heparin Therapy

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105
Q

Toxic effects Of heparin Symptoms

A 
Hematuria
Melena (blood in the stool)
Petechiea
Ecchymoses
Gum or Mucous Membrane Bleeding
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106
Q

When toxic effects of heparin occur

A

Stop drug immediately

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107
Q

How to reverse toxic effects of heparin

A

IV Protamine sulphate 1mg can reverse the effects of 100 units of heparin

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108
Q

Do not give subcutaneous doses of heparin within 5 cm of…

A 
The umbilicus
Abdominal incisions
Open wounds
Scars
Drainage tubes
Stomas
Areas of bruising or oozing
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109
Q

Do not ______ or __________ the heparin injection site

A
  1. aspirate subcutaneous injections

2. Massage

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110
Q

Heparin may cause

A

Hematoma formation

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111
Q

Heparin doses are given…

A

Subcutaneously

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112
Q

Name of Heparin Flush

A

Heparin Leo

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113
Q

The Risk of development of heparin induced thrombocytopenia has caused most hospitals to use

A

0.9% normal saline as a flush for heparin-lock IV ports

114
Q

Heparin flushes (100 units/mL) are still used for…

A

Central catheters

115
Q

Warfarin

A

Inhibits Vit k synthesis by bacteria in the gastrointestinal tract

116
Q

Warfari action

A

Inhibits Vit K dependent clotting factors II, VII, IX, and X which are normally synthesized in the liver

117
Q

Warfarin needs careful monitoring of the

A

Prothrombin time (PT)/ international normalized ratio (INR)

118
Q

What is normal INR (without warfarin)

A

0.8-1.2

119
Q

A therapeutic INR ( with warfarin) ranges from

A

2-3.5

120
Q

Warfarin may be started while the patient is still on heparin until…

A

PT/INR levels indcicate adequate anticoagulation

121
Q

Full their[eutic effects of warfarin take

A

Several days

122
Q

Antidote to warfarin is

A

Vit K

123
Q

Herbal products that have potential interactions with Warfarin are…

A 
Capsicum Pepper
Garlic
Ginger
Ginkgo
St. Johns Wort
Feverfew
124
Q

Reversible effects of warfarin by Vit K may take

A

36-42 hours

125
Q

When Vit K is given, Warfarinresistance will occur for up to

A

7 days

126
Q

Toxic effects of warfarin include

A

Severe bleeding

127
Q

Antithrombins Action

A

Inhibit thrombin (Factor IIa)

128
Q

Natural antithrombins

A

Human antithrombin III (Thrombate)

129
Q

Synthetic Antithrombins

A

Lepirudin (Refludan)
Argatroban (Argatroban)
Bivalirudin (Angiomax)
Dabigatron (Pradaxa)

130
Q

Direct acting Xa inhibitors action

A

Inhibit factor

131
Q

Direct acting Xa inhibitors examples

A

Fondaparinux (Arixtra)
Rivaroxaban (Xarelto)
Apixaban (Eliquis)

132
Q

Direct Thrombin Inhibitor

A

Dabigatran

133
Q

Antiplatelet drugs Prevent

A

Platelet adhesion

134
Q

Examples of anti platelet drugs

A 
Aspirin 
Clopidogrel bisulfate (Plavix)
Dipyridamole (Aggrenox, Persantine)
Prasugrel (Efficient)
Treprostinil (Remodulin)
Abciximab (ReoPro)
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
Anagrelide hydrochloride (Agrylin)
135
Q

Three major types of Antiplatelet drugs

A
  1. Glycoprotein platelet inhibitors
  2. Platelet aggregation inhibitors
  3. Protease activated receptor 1 antagonists
136
Q

Adverse effects of anti platelet drugs

A

Risk for inducing bleeding
drug-drug interactions
Monitor for abnormal bleeding

137
Q

Lipids

A

Triglycerides
Phospholipids
Steroids

138
Q

Triglycerides

A

Most common form of lipids
Major storage of fat in the body
Important energy source

139
Q

Phospholipids

A

Used for building plasma membranes

Found in egg yolks and soybeans

140
Q

Steroids

A

Most common is cholesterol
Important part of plasma membranes
Building block for Vit D, Bile acids, Cortisol, estrogen, and testosterone
Body only needs small amount of cholesterol

141
Q

VLDL- Very Low Density Lipoproteins

A

Primary carrier of triglycerides

VLDL eventually changes to LDL

142
Q

LDL- Low density lipoproteins

A

LDL transports cholesterol from liver to tissues and organs

Known as the bad cholesterol as it contributes to plaque deposits

143
Q

HDL- High Density Lipoproteins

A

Transports cholesterol back to the liver from organs and tissues to be broken down and mixed with bile for excretion
The good cholesterol

144
Q

Normal HDL level for males

A

1.94mmol/L

145
Q

Normal LDL level for males

A

<2.59mmol/L

146
Q

Normal Triglycerides levels for males

A

0.45-1.81mmol/L

147
Q

Normal cholesterol level for males

A

<5mmol/L

148
Q

Normal HDL levels for females

A

> 1.94mmol/L

149
Q

Normal LDL levels for females

A

<2.59mmol/L

150
Q

Normal Triglyceride level for females

A

0.40-1.52mmol/L

151
Q

Normal Cholesterol levels for females

A

<5mmol/L

152
Q

Pharmacotherapy In Lipid Disorders

A

Statins (HMG-COA Reductase Inhibitors)
Bile Acid Resins
Nicotinic Acids
Fibric Acid Agents

153
Q

Statins action

A

Inhibits HMG-COA reductase (enzyme needed to synthesize cholesterol) resulting in less cholesterol biosynthesis

154
Q

Atorvastatin (Lipitor) Uses

A

Primary Hypercholesterolemia
Elevated triglyceride levels
Prevention of heart attacks in those with mild elevated cholesterol

155
Q

Atorvastatin (Lipitor) Contraindications

A

Pregnancy category X

Active liver disease

156
Q

Atorvastatin (Lipitor) precautions

A 
Past liver disease
Alcoholism
Infections
Severe metabolic disorders
Electrolyte Imbalance
157
Q

Atorvastatin (Lipitor) adverse effects

A 
Abdominal Cramps
Constipation
Diarrhea
heart burn
Flatus
Rhabdomyolysis
ALS
Liver dysfunction
Pancreatitis
158
Q

Atorvastatin (Lipitor) Interactions

A

Do not take with grapefruit juice, may increase digoxin

159
Q

Atorvastatin (Lipitor) nursing consideration

A 
Asses nutrition
Asses muscle pain and tenderness
monitor bowel patterns
LFTs
Renal tests
Asses eys annually
160
Q

If taking Statins while child bearing age pt must

A

take birth control

161
Q

While on statins do not drink

A

large quantities of alcohol

162
Q

Take statins with evening meal to prevent

A

Stomach upset

163
Q

Bile acid Renins Action

A

Binds with bile acids thusnincreasing the excretion of cholesterol
Prevent resorption of bile acids from small intestine
Bile acids are necessary for absorption of cholesterol

164
Q

Bile Acids Prototype Drug

A

Cholestyramine (Questran)

165
Q

There are lots of GI side effects with Bile Acid Renins but no…

A

Systemic effects

166
Q

Nicotinic Acid Action

A

Acts by decreasing VLDL levels, decreasing triglycerides and increasing HDL levels
Thought to increase activity of lipase which break down minds
Reduces the metabolism or Catabolism of cholesterol and triglycerides

167
Q

Nicotinic acid is a

A

B complex vitamin

168
Q

Nicotinic acid prototype drug

A

Niacin (Niacin)

169
Q

Fibric Acid agents Action

A

Suppress the release of free fatty acids from adipose tissue, inhibits synthesis of triglycerides in the liver and increase secretion of cholesterol in the bile

170
Q

Prototype Fibric Acid Agent

A

Gemfibrozil (Lopid)

171
Q

Side effects of Fibric Acid

A 
Abdominal discomfort
Blurred vision
Diarrhea
Nausea
Headache
172
Q

Precautions of Fibric Acid

A

Increased risk of gallstones
Prolonged thrombin time
Increased liver enzyme levels

173
Q

Fibric Acid Interactions

A 
Oral anticoagulants (may need lower doses)
Statins ( increased risk for myostistis, myalgias, rhabdomyolysis)
174
Q

Adverse effects of garlic

A 
Dermatitis
Vomiting
Diarrhea
Flatulence
Antiplatelet activity
175
Q

Garlic can be used as…

A

Antispasmodic
Antihypertensive
Antiplatelet
Lipid Reducer

176
Q

Garlic drug interactions

A

warfarin & Diazepam

May enhance bleeding when taken with NSAIDS

177
Q

Garlic should be ______ after surgery

A

Discontinued

178
Q

Hypertension

A

Sustained elevation of systemic arterial BP

179
Q

As BP increases, so does the risk for

A

Myocardial Infarction, Heart failure, stroke and renal disease

180
Q

Cardiac output

A

the total blood flow through the systemic or pulmonary circulation per minute

181
Q

Cardiac output can be described as

A

Stroke volume multiplied by the heart rate for 1 min

182
Q

Systemic vascular resistance

A

The force opposing the movement of blood within the vessels

183
Q

a1 and a2 adrenergic

A

Vasoconstriction

184
Q

B1 adrenergic

A

Increased heart rate and conduction

185
Q

B2 adrenergic

A

Vasodilation and increased renin secretion

186
Q

Dopaminergic

A

vasodilation

187
Q

Primary symptoms of Hypertension

A

Hypertension is asymptomatic until it becomes severe and target organ disease has occurred

188
Q

Secondary Symptoms of Hypertension

A 
Ftaigue
Reduced Activity Tolerance
Dizziness
Palpitations
Angina
Dyspnea
189
Q

Primary Hypertension

A

Focus in primary related to prevalence in clinical practice

190
Q

Secondary Hypertension

A

Many causes; treatment aimed at eliminating the underlying cause

191
Q

Isolated systolic hypertension

A

Sustained elevation of SBP>= 140mm Hg and a DBP < 90 mm Hg

192
Q

Malignant Hypertension

A

Rapidly progressive hypertension
Diastolic pressure is usually >140 mmHg
Life threatening organ damage

193
Q

Orthostatic (postural) hypotension

A

Decrease in both systolic and diastolic BP upon standing

Lack of normal BP compensation in response to gravitational changes on the circulation

194
Q

Contributing Factors to Primary Hypertension

A 
\+ SNS activity
\+ sodium retaining hormones and vasoconstrictors
\+ sodium intake
Diabetes mellitus
> ideal body weight
\+ sodium intake
Excessive Alcohol intake
195
Q

Primary Hypertension Risk Factors

A 
Heavy Alcohol Consumption
Advancing Stage
Cigarette Smoking
Diabetes Mellitus
Elevated Serum Lipids
High Dietary Sodium
Gender
Family History
Obesity
Ethnicity
Sedentary Lifestyle
Socioeconomic Status
Psychosocial Stress
196
Q

Primary Hypertension Complications

A 
Hypertensive Heart Disease
Coronary Artery Disease
Left Ventricular Hypertrophy
Heart Failure
Cerebro-vascular disease
Peripheral Vascular Disease
Nephrosclerosis
Retinal Damage
197
Q

Secondary Hypertension Contributing Factors

A

Unprovoked Hypokalemia
Abdominal Bruit
Variable pressures with history of tachycardia, sweating, and tremor
Family History of Renal Disease

198
Q

Secondary Hypertension Causes

A

Contraction or congenital narrowing of the aorta
Renal disease such as renal artery stenosis and parenchymal disease
Endocrine Disorders
Neurological disorders
Sleep Apnea
Medications
Pregnancy- induced hypertension

199
Q

Lifestyle modifications for Hypertension

A 
Nutritional Therapy
Weigh Reduction
Modification in alcohol consumption
Physical activity 
Avoidance of tobacco products
Stress management
200
Q

Pharmacological Therapies of Hypertension

A 
Diuretics
Calcium Channel Blockers
ACE Inhibitors
Angiotensinogon II Receptors Blockers
Adrenergic Agents
201
Q

Diuretics

A

First line of treatment for hypertension

Lowers BP by decreasing blood volume

202
Q

Different. Classes of Diuretics

A

Loop/ High Ceiling Diuretics
Thiazide and Thiazide like diuretics
Potassium Sparing Diuretics

203
Q

Loop Diuretics Action

A

Inhibits reabsorption of Na and Cl from loop of Henle and distal renal tubule

204
Q

Therapeutic Effects of Loop Diuretics

A

Diuresis and subsequent mobilization of excess fluid

Decrease BP

205
Q

Half Life of Loop Diuretics

A

30-60 minutes

206
Q

Onset of Loop Diuretics

A

30-60 min PO

5 min IV

207
Q

Peak of Loop Diuretics

A

1-2 hours PO

30 min IV

208
Q

Contraindications of Loop Diuretics

A

Cross sensitivity with thiazides

209
Q

Caution Loop Diuretics

A 
Liver Disease
Electrolyte Depletion 
Diabetes
Hypoproteinemia
Severe Renal Impairment
210
Q

Side Effects of Loop Diuretics

A 
Blurred vision
Dizziness
Headache
Vertigo 
Hearing loss
Tinnitus
Hypotension
Hypovolemia
211
Q

Loop Diuretics Drug-drug interactions

A 
Antihypersensitives
Nitrates
Alcohol
Corticosteroids
Stimulant laxatives
NSAIDS
Lithium
212
Q

Thiazide Diuretics Action

A

Increases excretion of Na and water by inhibiting Na reabsorption from the distal tubule

213
Q

Thiazide Diuretics Prototype

A

Hydrochlorothiazide

214
Q

Thiazide Diuretics Indication

A

Antihypertensive

Thiazide diuretic

215
Q

Thiazide Diuretics Therapeutic Effects

A

Decrease Bp

Diuresis for edema

216
Q

Thiazide Diuretics Pharmacokinetics

A

Rapid PO absorption

217
Q

Thiazide Diuretics Half Life

A

6-15 hours

218
Q

Thiazide Diuretics Onset

A

2 hours

219
Q

Thiazide Diuretics Peak

A

3-6 hours

220
Q

Thiazide Diuretics Duration

A

6-12 hours

221
Q

Thiazide Diuretics Contraindications

A

Sulfa allergy

Anuria

222
Q

Thiazide Diuretics Caution

A

Renal/ liver impairment

Pregnancy- jaundice or thrombocytopenia in newborn

223
Q

Thiazide Diuretics Side effects

A 
Dizziness
Drowsiness
lethargy
Weakness
Hypotension
Glaucoma
Myopia
Steven Johnson Syndrome
Hypokalemia
Dehydration 
Hypomagnesemia
Hyponatremia
Hypovolemia
224
Q

Potassium Sparing Diuretics Action

A

Acts by blocking the normal exchanges of Na+ for K+ in the distal tubules and the body retains K+

225
Q

Potassium Sparing Diuretics prototype

A

Spironolactone (Aldactone)

226
Q

Potassium Sparing Diuretics Indications

A

Counteract K loss caused by other diuretics
Used with thiazides to treat edema or hypertension
Primary hyperaldosterone

227
Q

Potassium Sparing Diuretics Therapeutic Effects

A

Weak diuretic and antihypertensive

Conservation of K

228
Q

Potassium Sparing Diuretics percentage of protein binding

A

90%

229
Q

Potassium Sparing Diuretics Half life

A

78-84 min

230
Q

Potassium Sparing Diuretics peak

A

2-3 days

231
Q

Potassium Sparing Diuretics Duration

A

2-3 days

232
Q

Potassium Sparing Diuretics Contraindications

A

Hyperkalemia
Anuria
Renal Failure

233
Q

Potassium Sparing Diuretics Cautions

A

Liver dysfunction
Age related renal dysfunction increases risk for hyperkalemia
Diabetes increases risk for hyperkalemia
Concurrent use of K supplements

234
Q

Potassium Sparing Diuretics Side Effects

A 
Dizziness
Clumsiness
Headache
Arrhythmias
Steven Johnson Syndrome
Toxic epidermal necrolysis
Breast tenderness
Gynecomastia
Ireggular menstrual cycles
Agranulocytosis
235
Q

Potassium Sparing Diuretics Interactions

A 
Antihypersenstitives 
Alcohol
Nitrates
ACE inhibitors
ARBs
NSAIDS
K supplements
Cyclosporine
Tacrolimus
Digoxin
Litium
236
Q

Potassium Sparing Diuretics Interaction with Antihypersensitives, Alcohol and nitrates

A

Increases risk for hypotension

237
Q

Potassium Sparing Diuretics interaction with ACE Inhibitors, ARBs, NSAIDS, K supplements, Cyclosporine and Tacrolimus

A

Increases risk for hyperkalemia

238
Q

Potassium Sparing Diuretics interactions with Digoxin

A

May increase effects of digoxin

239
Q

Potassium Sparing Diuretics interactions with Lithium

A

May increase risk for lithium toxicity

240
Q

Potassium Sparing Diuretics Nursing Considerations

A 
Monitor intake and output, weigh daily
Monitor BP
Access for hypokalemia
Access for hyperkalemia
Access for skin rash- Steven Johnson Syndrome
241
Q

Calcium channel Blockers action

A

Block calcium from entering the cells thus limiting muscular contraction. This decreases vascular resistance.

242
Q

Two groups of calcium channel blockers

A
  1. Selective for blood vessels

2. Non- selective for blood vessels and the heart

243
Q

Calcium channel Blockers Prototype

A

Nifedipine (Adalat)

244
Q

Calcium channel Blockers Nursing Considerations

A

CCB reduce myocardial contractility & thus increases the risk of heart failure

245
Q

Calcium channel Blockers Contraindications

A

heart block

246
Q

Calcium channel Blockers monitor

A

Vasodilation and heart failure

247
Q

ACE stands for

A

Angiotension converting enzyme

248
Q

ACE inhibitors action

A

Inhibit angiotensin converting enzyme which assists in converting angiotensin 1 into angiotensin 2
Decreases BP by lowering peripheral resistance & decreasing blood volume

249
Q

ACE inhibitors Prototype

A

enalapril (Vasotec)

250
Q

ACE inhibitors Nursing considerations

A

Persistent cough
Postural Hypotension
Angioedema

251
Q

Angiotensin 2 Receptor Blockers (ARBs) Action

A

Blocks the effects of angiotensin II by blocking the receptors in the arteriolar smooth muscle and in the adrenal gland
Decreases BP by lowering peripheral resistance & decreasing blood volume

252
Q

ARBs are the class of choice in

A

Diabetes

253
Q

ARBs prototype

A

Nil

254
Q

ARBs Nursing Considerations

A

Monitor electrolytes
May also cause cough but not as frequent as with ACE
May cause birth defects
Patients appear more prone to upper respiratory infections

255
Q

ARBs Contraindications

A

Do not use in pregnancy

Do not take with potassium sparing diuretics

256
Q

Adrenergic agents

A 
Beta blockers (antagonists)
Alpha 1 Blockers (antagonists)
Alpha 2 Blockers Agonists
Alpha1 & Beta Blockers
Adrenergic Neuron Blockers
257
Q

Beta Blockers (antagonists) Action

A

Blocks both Beta1 and beta 2 thus inhibiting the fight or flight response

258
Q

Beta Blockers (antagonists) Prototype

A

Metoprolol (Lopressor)

259
Q

Beta Blockers (antagonists) Indication

A

Hypertension
Angina
Prevent MI and decrease mortality in recent MI
Management of stable heart failure, hypertension or cardiomyopathies

260
Q

Beta Blockers (antagonists) Therapeutic effect

A

Decreases BP, Heart rate, frequency of angina attacks

261
Q

Beta Blockers (antagonists) Contraindications

A 
Uncompensated heart failure
Pulmonary edema
Cardiogenic shock
Bradycardia
Heart block or sick sinus rhythm
262
Q

Beta Blockers (antagonists) Caution

A 
Renal and hepatic impairment 
Increased sensitivity in older adults
pulmonary disease
Diabetes
Hyperthyroidism
263
Q

Beta Blockers (antagonists) Side effects

A 
Fatigue
Weakness
Bradycardia
HF
Pulmonary edema
Respiratory distress
Hypotension
264
Q

Beta Blockers (antagonists) Nursing Implications

A

Monitor BP, ECG, HR, Intake and output, daily weight

Access for heart failure

265
Q

Alpha1 Blockers (Antagonists) Action

A

Blocks alpha1, thus causes the relaxation of blood vessels
Decreases BP
Used for enlarged prostate & urinary obstruction

266
Q

Alpha1 Blockers (Antagonists) Prototype

A

Doxazosin (Cardura)

267
Q

Alpha2-Adrenergic Agonists Action

A

Acts on the presynaptic adrenergic nerve terminal by tricking the body by converting the drug into a false transmitter and blocking the real norepinephrine.

268
Q

Alpha2-Adrenergic Agonists is the drug of choice for….

A

Pregnancy

269
Q

Alpha2-Adrenergic Agonists side effect

A

hypotension

270
Q

Alpha2-Adrenergic Agonists Prototype

A

Methyldopa (Aldomet)

271
Q

Alpha 1 & beta blockers Action

A

Acts on all sympathetic organs including the heart also dilates blood vessels and dilates pupils

272
Q

Alpha 1 & beta blockers Drug

A

Labetalol (Trandate, Normodyne)

273
Q

Beta & Alpha Antagonists Nursing Considerations

A

Baseline BP and HR reassess regularly
Do not administer if HR <60 bpm
Diabetics needs to monitor Blood glucose regularly
Monitor for fatigue, dizziness, orthostatic hypotension
May cause impotence

274
Q

Hypertensive Crisis

A

Severe abrupt increase in DBP
Rate of increase in BP is more important than the absolute value
Often occurs in clients with a history of hypertension who have failed to comply with medications or who have been unmedicated

275
Q

Hypertensive emergency =

A

evidence of acute target organ damage

276
Q

Clinical Manifestations of a Hypertensive Crisis

A 
Hypertensive Encephalopathy
Cerebral hemorrhage
Acute renal failure
Myocardial infarction
Acute left ventricular failure with pulmonary edema
Dissecring aortic aneurysm
277
Q

Hypertensive Crisis treatments

A

IV drug therapy: titrated to mean arterial pressure
Monitor cardiac and renal function
Neurological checks
Determine cause

278
Q

Vasodilators Action

A

acts directly to dilate smooth muscles

279
Q

Vasodilators are used in a …

A

Hypertensive Crisis

280
Q

Vasodilators Prototype drug

A

Hydralazine (app-hydralazine)

N216 (5 decks)

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