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Nurs 711 Pharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What are the causes of primary hypertension? What are the treatments?

A

No identifiable cause
Chronic progressive disorder
Treatment aimed to control, not cure

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2
Q

What are the causes of secondary hypertension? What are the treatments?

A

Secondary hypertension is caused by something else (pheochromocytoma, renal artery stenosis)
The treatment is to fix the underlying condition that is causing the hypertension

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3
Q

Blood Pressure:
What is a normal blood pressure?

A

120/80

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4
Q

Blood Pressure:
What is an elevated blood pressure?

A

120-129/<80

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5
Q

Blood Pressure:
What is considered high blood pressure? (Stage one)

A

130-130/90+

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6
Q

Blood Pressure:
What is considered high blood pressure (stage 2)?

A

140+/120+

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7
Q

What can be some of the results of hypertension?

A

Heart disease
kidney disease
Stroke

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8
Q

What are some of the lifestyle moderations that can aid in reducing hypertension?

A

Sodium Restriction
DASH Eating plan
Alcohol Restriction
Aerobic exercise
Smoking cessation
Weight loss

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9
Q

A DASH diet is composed of?

A

Rich in fruits and vegetables, low fat dairy, whole grains, lean meat

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10
Q

What are the categories of medication that are used to treat hypertension?

A

Diuretics
Adrenergic Antagonists
RAAS inhibitors
Calcium channel blockers
Vasodilators

David Always Remembers Cardiovascular Vessels

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11
Q

What is the formula for cardiac output?

A

Heart rate x Stroke Volume

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12
Q

What is the formula for arterial pressure?

A

cardiac output x peripheral resistance

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13
Q

What are the systems that regulate blood pressure?

A

Sympathetic baroreceptor reflex
Renin-Angiotensin-Aldosterone system
Renal Regulation

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14
Q

What are the different diagnostics to test for damages from untreated hypertension?

A

EKG
UA (for protein)
Renal Function
Electrolytes
Lipid profile

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15
Q

Where is most cholesterol produced?

A

The liver

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16
Q

What are the various lipid types?

A

LDL
HDL
VLDL
Triglycerides

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17
Q

If a patient has high cholesterol, what do providers do?

A

They follow a set of guidelines from the ACC/AHA

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18
Q

Most treatment plans for high cholesterol are?

A

Very personalized

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19
Q

What are the 7 Therapeutic lifestyle changes that are recommended to patients with high cholesterol?

A

Maintain BP
Perform over 150 min of exercise
Low-Dose Asprin (only for certain Pts)
Control type 2 diabetes
Diet Control
Smoking cessation
Acess ASVD risk

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20
Q

What are the 4 classes of Lipid Medications?

A

HMG-CoA reductase inhibitors (statins)
Bile acid sequestrants
Ezetimibe
Fibrates

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21
Q

HMG-CoA reductase inhibitors (statins):
What is the prototype?

A

lovastatin

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22
Q

HMG-CoA reductase inhibitors (statins):
What is the method of action?

A

Inhibits liver enzyme HMG-CoA reductase

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23
Q

HMG-CoA reductase inhibitors (statins):
What are its uses?

A

Used to treat hypercholesterolemia
Primary and Secondary prevention of CV events (heart attack/stroke)

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24
Q

HMG-CoA reductase inhibitors (statins):
What are the benefits?

A

Lowers TC
Lowers LDL
Raises HDL

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25
Q

HMG-CoA reductase inhibitors (statins):
What are the adverse effects?

A

Metabolized by the same CYP enzyme as grapefruit juice

Myopathy and Rhabdomyolysis

Hepatotoxic

Tertraogenic

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26
Q

What is rhabdomyolysis?

A

A condition where the muscles break down and then are filtered through the kidneys. The urine becomes very dark because of the kidney damage that filtering the proteins from the muscle breakdown

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27
Q

What drug designed to reduce cholesterol is NOT secreted by the kidneys?

A

Bile Acid Sequestrants

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28
Q

Bile Acid Sequestrants:
What is the prototype?

A

Colesevelam

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29
Q

Bile Acid Sequestrants:
What is the MOA?

A

binds to bile acids in the intestine, preventing their reabsorption into the blood and promoting excretion lowering LDL levels.

-Not water soluble so they only work in the intestines

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30
Q

Bile Acid Sequestrants:
What are its uses?

A

Used to treat hypercholeserolemia

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31
Q

Bile Acid Sequestrants are often paired with?

A

Statins

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32
Q

Bile Acid Sequestrants:
What are the benefits?

A

Lowers LDL 15-30%
When paired with a statin it lowers LDL 50%

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33
Q

Bile Acid Sequestrants:
What are the adverse effects?

A

GI (Bloating, constipation)
Many Medication interactions

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34
Q

What education should you provide a patient that is taking Bile Acid Sequestrants?

A

There are many medication interactions so this medication should be taken alone

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35
Q

What is a class of cholesterol drugs that is a unique drug to reduce plasma cholesterol, that experiences poteintiation with a statin but does not protect the pts cardiovascular system?

A

Ezetimibe

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36
Q

Ezetimibe:
What is the MOA?

A

Blocks absorption of cholesterol in the small intestine

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37
Q

Ezetimibe:
What are its uses?

A

Used alone or in combination with a statin for total cholesterol or LDL reduction

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38
Q

Ezetimibe:
What are it’s benefits alone?

A

Lowers LDL 19%
Raises HDL 1-4%
Lowers Trig 5-10%

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39
Q

Ezetimibe:
What are its benefits when given with a statin?

A

It goes from lowering LDL 19% alone to 25% with a statin

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40
Q

Which class of cholesterol drug was cleared by the FDA, but then was noted to have post market effects?

A

Ezetimibe

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41
Q

What is the class of cholesterol drug that interacts with receptors to reduce VDL and to lower Triglyceride levels while slighty raising HDL?

A

Fibrates

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42
Q

Fibrates:
What is the prototype?

A

Gemfibrozil

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43
Q

Fibrates:
What is the MOA?

A

Interactions with certain receptors in the liver, reducing VLDL levels to lower Trigyclerides

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44
Q

Fibrates:
What is its use?

A

Used to lower tryglycerides, and boost HDL

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45
Q

Fibrates:
What are it’s adverse effects?

A

GI Effects
Watch for gallstones
Myopathy
Hepatotoxcity
Displaces Warfarin from Albumin

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46
Q

Why do Fibrates increase the likelyhood of getting gallstones?

A

While it reduceds VLDL and Triglycerides-it does increase the cholesterol within the gallbladder, leading to a increased chance of getting gallstones

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47
Q

What is a drug that was removed from high cholesterol treatment guidelines, but is still sold over the counter?

A

Nicotinic Acid (Niacin)

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48
Q

What is the treatment for someone who has an adverse reaction to Niacin?

A

If a pt experiences the intense flushing reaction from Niacin, an aspirin will treat it

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49
Q

What is Angina?

A

a mid-sternal chest pressure that radiates to the left arm, shoulder or jaw

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50
Q

When does Angina occur?

A

When the oxygen demand on the heart is greater than the oxygen supply

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51
Q

What are the 3 types of Angina?

A

Stable
Variant (Prinzmetals/Vasospastic)
Unstable

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52
Q

What is a stable Angina?

A

An angina that is brought on by activity and stabilized by rest

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53
Q

What is a variant Angina?

A

An angina caused by coronary artery spasms

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54
Q

What is an unstable angina?

A

An angina that is considered a medical emergency because it is not relieved by rest and is an indicator of an impending heart attack

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55
Q

What are the treatment goals for treating an angina?

A

Prevent ischemia and pain
Prevent MI and Death

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56
Q

Organic Nitrates:
What is the prototype?

A

Nitroglycerin

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57
Q

Organic Nitrates:
What is the MOA?

A

Within VSM converted to nitric oxid which causes vasodilation.
This vasodilation works on preload

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58
Q

What is preload?

A

The pressure of the blood coming back into the heart

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59
Q

Organic Nitrates:
At a normal doses, what structure is normally affected?

A

Veins

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60
Q

Organic Nitrates:
What are its uses?

A

Stable and Unstable: vein dilation decreases venous return thereby decreasing preload and reducing O2 demand on the heart

Variant: NTG relaxes the coronary vasospasms, increasing O2 supply

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61
Q

What are the Parmacokinetics of Nitroglycerin?
Administration

A

It is highly lipid soluble so it can be given SL, PO, transdermal and IV but can be rapidly inactivated by the liver due to first pass effect

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62
Q

What are the adverse effects of Nitroglycerin?

A

Headache
Orthostatic hypotension
Reflex tachycardia

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63
Q

What are the interactions with Nitroglycerin?

A

Other HTN drugs
Erectile disfunction drugs
Beta Blockers

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64
Q

What are the unique properties of Nitroglycerin Sublingual tablets/spray?

A

-Bypasses the first pass effect seen in other administration methods
-Tablets need to be protected from light and moisture
-Gives rapid relief of chest pain in 1 to 3 min

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65
Q

What is the maximum dose of Nitroglycerin Sublingual tablets/spray, and what precautions should be taken?

A

Dose every 5 minutes x 3 doses max

BP must be checked to ensure that BP and HR do not drop to low

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66
Q

Which form of the organic nitrates can be used as a propholaxtic for angina?

A

Nitroglycerin Transdermal Patches

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67
Q

Nitroglycerin Transdermal Patches:
What is the onset?

A

30-60 minutes

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68
Q

Nitroglycerin Transdermal Patches:
What should be monitored while using?

A

Watch for tachycardia and hypotension

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69
Q

Which organic nitrate is unstable, but may be used for heart failure patients?

A

Nitroglycerin IV

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70
Q

What is special about NG IV that isn’t common in other IV medications?

A

Nitroglycerin may be absorbed by plastic, so it is dispensed in a glass bottle

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71
Q

Nitroglycerin IV:
What is the starting dose?

A

The starting dose 5mcg/min titrating up and down

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72
Q

Nitroglycerin IV:
What is the onset?

A

Seconds

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73
Q

Nitroglycerin IV:
Why must this med be tapered when discontinuing?

A

Because of the vasodilation, if discontinued too quickly a pt can experience reverse rebound vasoconstriction

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74
Q

What type of angina would a beta blocker be used for?

A

Stable and Unstable

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75
Q

What are the adverse effects of a beta blocker?

A

Bradycardia
Reduced cardiac output
Precipitation of heart failure
AV Heart Block
Rebond cardiac excitation
Fatigue/depression

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76
Q

What is a drug used to treat Angina that is fairly new and reduces the accumulation of sodium and calcium in myocardial cells?

A

Ranolazine

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77
Q

Ranolazine:
What angine does it treat?

A

Stable

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78
Q

Ranolazine:
What is its brand name?

A

Ranexa

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79
Q

Ranolazine:
What are its uses?

A

Used to treat stable angina but does not reduce heart rate, blood pressure or vascular resistance

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80
Q

Ranolazine:
What are its drug interactions?

A

It is metabolized in the liver, by the CYP34 enzyme-therefore grapefruit juice and CYP inhibitors must be avoided

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81
Q

Ranolazine:
What should you watch for?

A

Ventricular dysrhythmias and HTN

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82
Q

What are the names of the two Calcium Channel Blockers?

A

Verapamil and Diltiazam

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83
Q

Calcium Channel Blockers:
What is it used for?

A

Used to treat stable and variant angina

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84
Q

What are the 3 classes of drugs used to treat Stable Angina?

A

Organic Nitrates
Beta Blockers
Calcium Channel Blockers

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85
Q

What are the two classes of drugs used to treat variant angina?

A

Organic Nitrates
Calcium Channel Blockers

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86
Q

What are the 4 things used to treat unstable angina?

A

Organic Nitrates
Oxygen
Beta Blocker
Anti-platelets

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87
Q

What are the 3 classes of Anticoagulants?

A

Heparin
Enoxaparin
Warfarin

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88
Q

Where in the body do anticoagulants work?

A

In the veins

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89
Q

What are the two classes of anti-platelets?

A

Aspirin
Clopidogrel

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90
Q

Alteplace (tPA) is considered what type of drug?

A

A thrombolytic

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91
Q

Where in the body to antiplatelets work?

A

In the arteries

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92
Q

Heparin:
What is it’s method of action?

A

Disrupts the coagulation cascade

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93
Q

Heparin:
How does Heparin disrupt the coagulation cascade?

A

By messing up the cogulation cascade so that the platelet plug is not reinforced

Antithrombin inactivates thrombin and factor Xa, therefore reducing the amount of fibrin

Without fibrin, the platelet plug is not reinforced

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94
Q

Heparin:
What is it used for?

A

DVTs, PEs
Heart Surgery and hemodialysis
With Thrombolytic post MI

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95
Q

Is Heparin teratogenic?

A

No, it does not cross the placenta and therefore is safe for use in pregnancy

96
Q

Heparin:
What are the adminstration/absorption pharmacokinetics?

A

Not available PO
Must be given SQ or IV

Concentration is in units
Rapid Acting

97
Q

Heparin:
What are the distribution pharmacokinetics?

A

The molecules are too large therefore not able to cross membranes thus parenteral administration is necessary

98
Q

Heparin:
How is it excreted?

A

Hepatic/renal

99
Q

Heparin:
What are the adverse effects?

A

Bleeding (Can be fatal)
Contraindicated in pts with high risk of bleeding
Heparin induced thrombocytopenia

100
Q

What is Heparin induced thrombocytopenia?

A

a medical condition where the use of the anticoagulant drug heparin leads to a decrease in the number of platelets (thrombocytes) in the blood, potentially leading to blood clots and serious complications. HIT can cause serious problems, including deep vein thrombosis and pulmonary embolism.

101
Q

Heparin:
What is used to monitor heparin besides the peak and trough?

A

Activated Partial Thromboplastin Time (aPTT)

102
Q

Heparin:
What is a normal aPTT?

A

40 seconds

103
Q

Heparin:
What is a desired aPTT on heparin?

A

Usually 60-80 seconds

104
Q

Heparin:
If an overdose occurs. what is given?

A

Protamine Sulfate IV injection

105
Q

Heparin:
If an aPTT gets over 100, what should be done?

A

Lower dose immediately or give Protamine Sulfate for overdose

106
Q

Which Anticoagulant drug mainly inactivates factor Xa thereby slowing production of fibrin and clotting?

A

Enoxaparin (Lovenox)

107
Q

Enoxaparin (Lovenox):
What are its uses?

A

Prevention and treatment of DVTs
Prevention of ischemic complications after UA and STEMI

108
Q

Enoxaparin (Lovenox):
What are the admin/absorption pharmacokinetics?

A

SQ injection
Based on body weight
q12 or q24 hours

109
Q

Enoxaparin (Lovenox):
What are the metabolism pharmacokinetics?

A

Processed in the liver, but much slower than heparin due to it’s longer half life

110
Q

Enoxaparin (Lovenox):
What are the adverse effects?

A

Same as heparin but greatly reduced
Increased risk of bleeding if also taking a antiplatelet med

111
Q

Enoxaparin (Lovenox):
What are the benefits of Enoxaparin as opposed to heparin?

A

Doesn’t require aPTT monitoring
Can be used at home
Fixed time dosing

112
Q

What is the considered acidic/normal/alkalotic pH on an ABG?

A

7.35/7.40/7.45

113
Q

What is the considered acidic/normal/alkalotic PaCo2 on an ABG?

A

<45/45-35/<35

114
Q

What is the considered acidic/normal/alkalotic HCO3 on an ABG?

A

22/22-26/26

115
Q

Respiratory acidosis is produced by?

A

HYPOventilation

this decreases the pH because decreased breaths retain CO2

116
Q

What are some of the causes of respiratory acidosis?

A

Asthma attacks, airway obstruction (COPD) ARDS, respiratory depression, pnemonia, PE

117
Q

What is ARDS?

A

Acute respiratory distress syndrome

118
Q

What are the treatments for respiratory acidosis?

A

Correct respiratory impairment with a:

Bronchodilator
Oxygen
Bipap

Sodium bicarbonate if very severe

119
Q

What is respiratory alkalosis produced by?

A

produced by HYPERventilation
Deep rapid breathing that blows off CO2 and increases the pH

120
Q

What are some of the causes of Respiratory alkalosis?

A

Fear/anxiety, hypoxia, salicylate OD(aspirin), pain, shock, trauma, CNS injury

121
Q

What is the treatment of respiratory alkalosis?

A

Bag over nose and mouth to breath in exhaled CO2

-could give a sedative if very anxious

122
Q

what is metabolic acidosis produced by?

A

Low bicarb levels in the body and a decreased pH

123
Q

What are the causes of metabolic acidosis?

A

Chronic Renal Failure
Severe diarrhea
Overproduction of lactic or keto acids (liver diseases)

124
Q

What are the treatments for metabolic acidosis?

A

Treat the correct cause
Give sodium bicarb-
PO if mild
IV if severe

125
Q

What are going to be some appearances of metabolic acidosis in a patient?

A

Hypotension
Tachycardia
high HR
weak pulses
N/V/D
Deep labored breathing called Kussmaul breathing to higher pH

126
Q

What is metabolic Alkalosis produced by?

A

Increased bicarb in plasma (Metabolic)
increased pH

127
Q

What is metabolic alkalosis caused by?

A

Excessive loss of gastric acid
Antiacid OD

128
Q

What is the treatment of Metabolic Alkalosis?

A

IVF 0.9% NS + KCL

(it makes the kidneys excrete bicarb lowering the pH

129
Q

If a patient has a kidney or liver disease, what should be considered when administering IV fluids?

A

Lactated Ringers contain things other than saline and therefore kidney and liver diseases can be affected by the administration of LR

130
Q

The intracellular fluid is?

A

The Fluid contained inside all body cells

131
Q

The extracellular fluid is?

A

All the fluid outside of the body cells

132
Q

What are the 3 subcomponents of the extracellular fluid?

A

Intravascular Fluid (blood vessels)
Interstitial fluid (tissue spaces)
Transcellular fluid (CSF, joint spaces, pleural spaces)

133
Q

What is the definition of osmolality?

A

Osmolality describes fluids inside the body, the solute concentration in fluid by weight

134
Q

A volume contraction is an isotonic contraction were?

A

equal amounts of sodium and water are lost which contributes to a decrease in total volume of extracellular fluid

135
Q

What is the treatment for a isotonic contraction?

A

Isotonic fluids (0.9% sodium chloride aka normal saline)

136
Q

A hypertonic contraction is a?

A

Hypertonic contraction were the loss of water exceeds the loss of sodium

137
Q

What are the causes of a hypertonic contraction?

A

Excessive sweating, severe burns, osmotic duiresis

138
Q

What is the treatment for a hypertonic contraction?

A

Drink water
Infuse HYPOtonic fluids (0.45% sodium chloride aka 1/2 normal saline or D5W

139
Q

What is a hypotonic contraction?

A

A volume contraction where the loss of sodium exceeds the loss of water

140
Q

What are the causes of a hypotonic contraction?

A

Excessive duiretics
Chronic renal insufficency
Increased intracranial pressure
Lack of aldosterone (Addison’s)

141
Q

What is the treatment for a hypotonic contraction?

A

The treatment depends on sodium levels and renal function

For mild=infuse isotonic fluids
For severe=infuse HYPERtonic fluids (3% sodium chloride)

142
Q

An increase in total volume body fluid could be caused by?

A

too much Intravenous fluid
Heart failure
Kidney disorders
Liver disease

143
Q

The treatment for an increase in total volume fluid would be?

A

diuretics

144
Q

What role does Potassium play in the body?

A

Conducts nerve impulses
Maintains the electrical excitability of the muscles in the heart
Levels are regulated by kidneys

145
Q

How are potassium levels affected by extracellular fluid?

A

ECF alkalosis enhances K uptake by cells

ECF acidosis enhances K kick out by cells

146
Q

How is potassium effected by insulin?

A

Insulin stimulates K uptake by cells

147
Q

What is the treatment of Hypokalemia?

A

Oral KCL in pill or liquid that differ by the speed of release but have adverse GI effects

IV KCL that must be given very diluted and slow because it is irritating to veins

148
Q

Heart rate and potassium levels have what type of relationship?

A

inverse

149
Q

What is the treatment of Hyperkalemia?

A

Withhold K-rich foods or supplements
Infuse insulin and glucose
If acidotic, sodium bicarb will correct pH
Use meds like Keyexalate to directly remove K through stool
Dialysis

150
Q

Most diuretics share the same method of action. What is this?

A

Blockage of Na and CL rebsorption which also blocks H2O absorption

151
Q

The increase of urine flow is directly related to the amount of ____________ __________________ that a duiretic blocks.

A

Na/Cl reabsorption

152
Q

What are the general therapeutic uses for diuretics?

A

Treatment of hypertension
Treatment of edema related to heart, renal or liver failure
For any reason that the patient may be retaining fluid

153
Q

What are the general adverse effects of Diuretics?

A

Hypovolemia
Acid/Base imbalances
Drop in BP
Tachycardia
Other Electrolyte imbalances

154
Q

What are the 4 categories of diuretics?

A

Loops (potassium wasting)
Thiazides (potassium wasting)
Potassium Sparing
Osmotics

155
Q

Which site on the kidney does mannitol exhibit it’s action?

A

Proximal Convoluted tubule

156
Q

What site of the kidney does furosemide exhibit it’s action?

A

Thick segment on the ascending limb of Henle’s Loop

157
Q

What site on the kidneys do Thiazides exhibit their action?

A

Early distal convoluted tubule

158
Q

What site on the kidney do Spironolactone and Triamterene exert their action?

A

Late distal convoluted tubule and collecting duct

159
Q

How long do Loop diuretics normally last?

A

Around 6 hours

160
Q

What is the MOA of Loop diuretics such as Furosemide (Lasix)?

A

Blocks Na/Cl/K reabsorption in the thick segment of the ascending loop of henlle

161
Q

Which diuretic produces the MOST fluid and electrolyte loss?

A

Furosemide

162
Q

When would Furosemide be prescribed?

A

When a significant fluid excess exits
Pulmonary edema
Edema that is unresponsive to other diuretics
Hypertension that is not controlled by other diuretics

163
Q

Is Furosemide potassium wasting or potassium sparing?

A

Potassium wasting

164
Q

PHARMACOKINETICS: Furosemide
What is the route?

A

PO or IV

165
Q

PHARMACOKINETICS: Furosemide
What is the onset of PO Furosemide

A

Slower onset around 60 minutes but lasts 6 hours

166
Q

PHARMACOKINETICS: Furosemide
What is the onset of IV route

A

IV works in 5 minutes but only lasts 2 hours

167
Q

PHARMACOKINETICS: Furosemide
Why would it be given IV instead of PO?

A

It’s given IV in situations that require immediate diuresis due to 5 minute onset time

168
Q

Which diuretic can be effective even when renal blood flow/GFR is low?

A

Furosemide

169
Q

What are the adverse effects of Furosemide?

A

Hyponatremia, HypoChloremia, Hypokalemia
Dehydration/Hypovolemia/Hypotension
Ototoxcity
Teratogenic

170
Q

What are the negative drug-drug interactions of Furosemide?

A

Digixon
Lithium
other ototoxic and hypertensive drugs

171
Q

What are the beneficial drug drug interactions of Furosemide?

A

K-sparing diurectics

172
Q

Thiazide Diuretivs such as Hydroclorothiazide use what method of action?

A

Blocks Na/K/Cl reabsorption in the early distal convoluted tubule

173
Q

What is the difference between loop diuretics such as Furosemide and Thiazides?

A

Thiazides cause less diuresis than loop drugs and are only effective with adequate GFR

174
Q

What are the uses of Thiazides?

A

Hypertension
Moderate Edema

175
Q

PHARMACOKINETICS:Thiazides
What is the route and onset of Thiazides?

A

PO only
Diuresis within two hours

176
Q

What are the adverse effects of Thiazides?

A

Hyponatremia, Hypochloremia, Hypokalemia
Hypovolemia
Teratogenic

177
Q

What are the negative drug drug interactions of Thiazides?

A

The same as the loop drug Furosemide
Digixon
Lithium
other ototoxic and hypertensive drugs

178
Q

Which diuretic has sulfa components so it is important to not give to a patient with a sulfa allergy?

A

Thiazides

179
Q

What is the MOA of Potassium sparing Diuretics?

A

Blocks Na/Cl reabsorption in the late distal convoluted tubule without excretion of potassium

180
Q

What is the main difference between Loops, Thiazides and Potassium Sparing drugs?

A

The main difference is even less diuresis that thiazides but maintain the potassium levels unlike both loops and thiazides

181
Q

What are the two categories of Potassium Sparing Diuretics?

A

Aldosterone Antagonists
Non-aldosterone antagonists

182
Q

What is an example of an aldosterone antagonist?

A

Spironolactone

183
Q

What is the MOA of the aldosterone antagonist Spirolactone?

A

inhibits the action of aldosterone in the distal nephron

184
Q

PHARMACOKINETICS: Spirolactone
How long is the onset?

A

Effects take around 48 hours to develop

185
Q

In addition to being an aldosterone antagonist, Spirolactone also is in another category. What is it?

A

K+ sparing diuretics

186
Q

What are the uses of Spirolactone?

A

Hypertension
Edema
Heart Failure
Polycystis ovarian syndrome

187
Q

What are the adverse effects of Spirolactone?

A

Gynecomastia
Menstrual irregularities
Impotence
Hirsutism
Deepening of voice

188
Q

What does Hirsutism mean?

A

Hair growth

189
Q

How does Spirolactone work?

A

It blocks steroid hormones

190
Q

What is an example of a non-aldosterone antagonist?

A

Triamterene

191
Q

What is the MOA of the non-aldosterone antagonist Triamterene?

A

Inhibits the Na/K mechanism directly

192
Q

What are the uses of Triamterene?

A

Use to treat hypertension and Edema
Normally added to a loop or thiazide to maintain potassium levels

193
Q

What are the adverse effects of Triamterene?

A

It is not well tolerated
Frequently causes nausea and vomiting
Leg cramps
Dizziness

194
Q

What is an example of an osmotic diuretic?

A

Mannitol

195
Q

What is the MOA of Mannitol?

A

Increases the osmotic pressure within the nephron, preventing reabsorption of some water and the result is increased urine flow with no effect on electrolytes

196
Q

What are the uses of Mannitol?

A

Reduce intracranial pressure
Reduce intraocular pressure
Prevent renal failure

197
Q

PHARMACOKINETICS: Mannitol
What route is mannitol given?

A

Must be given parentally because it does not cross the GI membranes

198
Q

What are the adverse effects of Mannitol?

A

Peripheral Edema
Headache
Nausea/Vomiting
Potiental for hypovolemia

199
Q

What are the two forms of Drugs for heart failure?

A

HFrEF
HFpEF

200
Q

When would you treat heart failure with a HFrEF?

A

When it is heart failure with a reduced LV Ejection Fraction and systolic dysfunction

201
Q

When would you treat heart failure with a HFpEF?

A

When it is heart failure with preserved LV Ejection Fraction and dyastolic disfunction

202
Q

What are the causes of systolic disfunction that you would treat with a HFrEF?

A

Cardiac remodeling from MI
Viral Myocarditis
Valve disease
HTN

203
Q

What are the causes of Diastolic dysfunction that you would treat with a HFpEF?

A

Cardiac remodeling from HTN
Diabetes
Obesity
OSA
COPD

204
Q

If the heart failure is the result of the heart loosing it’s ability to contract, therefore not able to pump, which drug would you use to treat it?

A

HFrEF

205
Q

What is the first line treatment for volume overload heart failure?

A

Diuretics

206
Q

Why are diuretics the first line treatment for volume overload caused by heart failure?

A

Reduction in blood volume helps venous and arterial pressure, edema and cardiac dilation

207
Q

Which diuretic is most commonly used for volume overload from heart failure?
When would other drugs be used instead?

A

Loops would be the most common especially for those retaining large amounts of fluids.

Thiazides can be used for minimal edema

A potassium sparing drug may also be used to balance hypokalemia

208
Q

What are considered the “cornerstone” of HF therapy?

A

ACE Inhibitors

209
Q

What are the long term benefits of using an ACE Inhibitor for HF?

A

The long term benefits include:
Slowed HF progression
Extended life expectancy

210
Q

How do ACE Inhibitors work to help treat HF?

A

The systemic vasodilation reduces afterload and improves perfusion to kidneys and other organs.

It also SLOWS or REDUCES Cardiac remodeling *****

211
Q

If you are taking an ACE Inhibitor, what other drug can you NOT take?

A

an ARB

212
Q

ARBS have similar hemodynamic benefits to ACEIs, but why are ACEIs preferred?

A

The ARBs don’t have the same slowing of cardiac remodeling as the ACEIs do

213
Q

Which drug was first contraindicated for heart failure due to decrease in cardiac contractility, but now are considered a first-line therapy at low doses?

A

Beta Blockers

214
Q

What are the specific Betablockers most common to aid in HF?

A

Carvedilol
Metoprolol

215
Q

What are the benefits of a beta blocker for heart failure?

A

Improve EF
Increase exercise tolerance
Slows the progression of heart failure
Prolongs survival of pt

216
Q

If taking a Beta Blocker for heart failure, what should you watch out for?

A

Fluid retention
Fatigue
Hypotension
Bradycardia

217
Q

What is the only drug that is an Inotropic Agent Cardiac glycoside?

A

Digoxin

218
Q

What is the MOA of the Cardiac Glycoside Digoxin?

A

Competitor for the same sight on Na-K-ATPase

Postive inotropic action increasing myocardial contractile force
Inhibits Na-K-ATPase causeing more Ca accumulation in myocytes

219
Q

What are the benefits of Digoxin?

A

Reduced symptoms
increases exercise tolerance
Decreases hospitalization
Does NOT increase life expectancy

220
Q

Would Digoxin be the first choice drug to use for HF?

A

No, it is an NTI drug and has adverse effects such as dysrhythmas, toxicity

221
Q

PHARMACOKINETICS:Digoxin
What is the absorption?

A

The absorption of Digoxin varies depending on the manufacturer but is always delayed by food

222
Q

PHARMACOKINETICS:Digoxin
What is the Distribution?

A

Protein bound

223
Q

PHARMACOKINETICS:Digoxin
What is the elimination?

A

renal excretion

224
Q

PHARMACOKINETICS:Digoxin
What is the half life?

A

A very long half life

225
Q

PHARMACOKINETICS:Digoxin
What theraputic levels do you want to keep Digoxin at since it is an NTI drug?

A

0.5-0.8 ng/mL

226
Q

What are the adverse effects of Digoxin?

A

Dysrythmias
Toxicity

227
Q

The signs of a Digoxin toxicity include?

A

GI: N/V, anorexia
CNS: Fatigue
Visual issues: Blurred vision with yellow halos around light
Cardiac:Dysrthymias

228
Q

Who is a patient that should NOT be given Digoxin?

A

Anyone with a heart rate of under 60

229
Q

What are the drug-drug interactions of Digoxin?

A

Diuretics (potassium effects)
ACEIs/ARBs (potassium effects)
Dobutamine/Dopamine (dysrthymias)
Verapamil (suppresses effects and increase levels)

230
Q

POTASSIUM EFFECTS:
Furosemide

A

Potassium Wasting

231
Q

POTASSIUM EFFECTS:
Thiazide

A

Potassium wasting

232
Q

POTASSIUM EFFECTS:
Spironolactone

A

Potassium Saving

233
Q

POTASSIUM EFFECTS:
Triamterene

A

Potassium Saving

234
Q

POTASSIUM EFFECTS:
Mannitol

A

No effect on Potassium

235
Q

POTASSIUM EFFECTS:
Digoxin

A

Due to the competitive inhibition for the Na-K-ATPase pump, if Digoxin levels are up, K+ levels are down

If K+levels are up, Digoxin levels are down

Nurs 711 Pharmacology (6 decks)

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