Exam 3 Flashcards
(532 cards)
1
Q
Basic functional unit of the kidney
A
Nephron
2
Q
Four functionally distinct regions of the nephron
A
Glomerulus
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
3
Q
Where does filtration occur in the kidney?
A
Glomerulus
4
Q
What is reabsorbed in the kidney?
A
99% of water, electrolytes, and nutrients
5
Q
Where does reabsorption occur in the kidney?
A
Specific sites along the nephron:
- Proximal convoluted tubule
- Loop of Henle
- Distal convoluted tubule
- Collecting duct (distal nephron)
6
Q
Through filtration and reabsorption, what is also regulated in the kidneys?
A
Sodium-potassium exchange
Regulation of urine concentration
7
Q
Three basic functions of diuretics:
A
- Cleansing of extra cellular fluid and maintenance of ECF volume and composition
- Maintenance of acid-base balance
- Excretion of metabolic wastes and foreign substances
8
Q
Three main classifications of diuretics:
A
Loop diuretics
Thiazides
Potassium-sparing
9
Q
Two types of potassium-sparing diuretics:
A
Aldosterone antagonists
Nonaldosterone antagonists
10
Q
Definition of diuretics
A
Drugs that increase urinary output
11
Q
Two major applications of diuretics
A
Treatment of hypertension
Mobilization of edematous fluid to prevent renal failure
12
Q
Mechanism of action of diuretics
A
Blockade of sodium and chloride reabsorption
13
Q
Best site of action of diuretics
A
Proximal tubule produces greatest diuresis
14
Q
Adverse effects of diuretics
A
Hypovolemia
Acid-base imbalance
Electrolyte imbalances
15
Q
Prototype drug for loop diuretics
A
Furosemide (Lasix)
16
Q
Mechanism of action of Furosemide (Lasix)
A
Acts on ascending loop of Henle to block reabsorption
17
Q
Pharmacokinetics of Furosemide (Lasix)
A
Rapid onset (PO 60 min; IV 5 min)
18
Q
Therapeutic uses of Furosemide (Lasix)
A
Pulmonary edema
Edematous states
Hypertension
19
Q
Adverse effects of Furosemide (Lasix)
A
Hyponatremia, Hypochloremia, dehydration
Hypotension (volume loss, relaxation of venous smooth
muscle)
Hypokalemia
Ototoxicity
Hyperglycemia
Hyperuicemia
20
Q
Can Furosemide (Lasix) be used during pregnancy? Why or why not?
A
No, because too risky when balancing fluid/electrolytes of both mom and baby
21
Q
Normal range of potassium levels
A
3.5-5.0
22
Q
Drug interactions of Furosemide (Lasix)
A
Digoxin
Ototoxic drugs
Potassium-sparing diuretics
Lithium
Antihypertensive agents
Nonsteroidal anti-inflammatory drugs
23
Q
Administration routes for Furosemide (Lasix)
A
Oral
Parenteral
24
Q
Another name for Thiazides and related diuretics
A
Benzothiadiazides
25
Effects of Thiazides and related diuretics
Similar to those of loop diuretics:
- Increase renal excretion of sodium, chloride, potassium, and water
- Elevate levels of uric acid and glucose
26
How is diuresis of Thiazides and related diuretics compared to loop diuretics
Considerably lower than that produced by loop diuretics
Not effective when urine flow is scant (unlike loop diuretics)
27
Prototype for Thiazides and related diuretics
Hydrochlorothiazide (HydroDIURIL)
28
How long does it take for hydrochlorothiazide to peak?
4-6 hours
29
Therapeutic uses for hydrochlorothiazide
HTN
Edema
Diabetes insipidus
30
Adverse effects of hydrochlorothiazide
Hyponatremia, hypochloremia, and dehydration
Hypokalemia
Hyperglycemia
Hyperuricemia
Impact on lipids, calcium, and magnesium
31
Effects of hydrochlorothiazide on pregnancy
During lactation, enters breast milk
32
Drug interactions with hydrochlorothiazide
- Digoxin
- Augments effects of hypertensive medications
- Can reduce renal excretion of lithium (leading to accumulation)
- NSAIDs may blunt diuretic effect
- Can be combined with ototoxic agents without increased risk of hearing loss
33
Potassium-sparing diuretics compared to other diuretics
Most modest increase in urine production
Decrease in potassium excretion
Rarely used alone for therapy
34
Two groups of potassium-sparing diuretics
Aldosterone antagonist
Nonaldosterone antagonist
35
Prototype drug for aldosterone antagonist potassium-sparing diuretics
Spironolactone (Aldactone)
36
Mechanism of action for Spironolactone
Blocks aldosterone in the distal nephron
Retention of potassium
Increased secretion of sodium
37
Therapeutic uses of spironolactone
HTN
Edematous states
Heart failure (decreased mortality in severe failure)
Primary hyperaldosteronism
Can be used for hormonal issues:
Premenstrual syndrome
Polycystic ovary syndrome
Acne in young women
38
Adverse effects of spironolactone
Hyperkalemia
Benign and malignant tumors
Endocrine effects
39
Drug interactions of spironolactone
Thiazide and loop diuretics
Agents that raise potassium levels
40
Prototype of osmotic diuretics
Mannitol (Osmitrol)
41
Action of Mannitol
Promotes diuresis by creating osmotic force within lumen of the nephron
42
Pharmacokinetics of mannitol
Drug must be given parenterally
43
Therapeutic uses of mannitol
Prophylaxis of renal failure
Reduction of intracranial pressure
Reduction of intraocular pressure
44
Adverse effects of mannitol
Edema
Headache
Nausea and vomiting
Fluid and electrolyte imbalance
45
How much does one liter of fluid weigh?
2.2 lbs
46
How much of the total body water is in intracellular fluid?
2/3
47
Where is extracellular fluid located?
Outside the cells:
Divided into the vascular compartment (blood vessels) and the interstitial space (the gaps between the cells)
48
Explain the renin-angiotensin-aldosterone system
Decreased renal perfusion initiates release of aldosterone.
Aldosterone is a mineral corticoid that retains sodium and where sodium goes, water goes.
Aldosterone also retains potassium.
49
Lab value for potassium
3.5-5.0 mEq/L
50
Lab value for sodium
135-145 mEq/L
51
Lab value for chloride
95-105 mEq/L
52
Lab value for magnesium
1.5 to 2.5 mEq/L
53
Lab value for serum creatinine
0.6 to 1.2 mg/dl
54
Lab value for BUN
10 to 20 mg/dl
55
Lab value for glucose
70 to 100
56
Lab value for platelets
150,000 to 400,000
57
Lab value for hemoglobin (Hgb)
F 12-16 g/dl
M 14-18 g/dl
58
Lab value for hematocrit (Hct)
F 37-47%
M 42-52%
59
What can cause an abnormal loss of fluids? And what symptoms would they have?
Vomiting, diarrhea, hemorrhage
Dehydration
Weak, low BP
Dry skin
60
What can cause someone to have fluid volume excess? And what symptoms would they have?
CHF, kidney failure
Crackles, dyspnea, edema
61
How would a pt be treated who has fluid volume excess?
Diuretics
62
What nursing interventions would be done for pts who have abnormal fluid volume?
Assess the pt
Daily weights
I & O
IV fluids
63
Types of drugs that act on the Renin-Angiotensin-Aldosterone System
Angiotensin-converting enzyme inhibitors (ACE inhibitors)
Angiotensin II receptor blockers (ARBs)
Direct renin inhibitors
Aldosterone antagonists
64
Main functions of the RAA system
All involved with blood pressure
Many involved with fluid volume
Many involved with electrolytes
65
How is the RAAS involved with blood pressure?
Actions of angiotensin II
Vasoconstriction
Release of aldosterone
66
Actions of aldosterone
Regulation of blood volume and blood pressure
Pathologic cardiovascular effects
67
How does aldosterone regulate blood pressure and blood volume?
When aldosterone is released form adrenal cortex, it acts on the distal tubular of the kidneys, causing release of sodium and potassium
Because of this BP and blood volume go down
68
How does the RAAS elevate BP?
Angiotensin II formed by renin and angiotensin-converting enzyme
- renin speeds up formation of angiotensin I from angiotensinogen
- Regulation of renin release
- Angiotensin-converting enzyme (kinase II) converts angiotensin I (inactive) to angiotensin II (highly active)
69
Main part of RAAS to increase BP or blood volume
Renin (its main purpose is to elevate BP)
70
Where are ACE enzymes (AKA kinase II) located?
On the surface of many blood vessels
In the lining of the vasculature of the lungs
(Even though we typically only think of it being involved with the renals)
71
Situations the RAAS helps to regulate BP in
Hemorrhage
Dehydration
Sodium depletion
72
When someone is experiencing low BP, how does the RAAS act on the body to fix it?
Constricts renal blood vessels
Acts on the kidney to promote retention of sodium & water, and the excretion of potassium
73
How do ACE inhibitors work?
By preventing Angiotensin II, which lowers the levels of angiotensin II, which can dilate vessels
74
Therapeutic uses of ACE inhibitors
Hypertension
Heart failure
MI
Diabetic and non diabetic nephropathy
Prevention of MI, stroke, and death in pts at high cardiovascular risk
75
How do ACE inhibitors help MI and heart failure?
By remodeling the heart and preventing more damage from happening
76
Adverse effects of ACE inhibitors
First dose hypotension (fall risk!)
Fetal injury (can’t take during pregnancy)
*Cough (due to increased bradykinin)
Angioedema (swollen face, need to be taken off)
Hyperkalemia
Dysgeusia and rash
Renal failure or **bilateral renal artery stenosis (contraindicated)
Neutropenia
77
Drug interactions for ACE inhibitors
Diuretics
Antihypertensive agents
Drugs that raise potassium levels
Lithium (b/c some cause lithium to accumulate in the body)
Nonsteroidal anti-inflammatory drugs
78
How should ACE inhibitors be administered?
- All administered orally, except for Enalapril (Vasotec) which is given IV
- May be administered without regard to meals, except for Captopril (capoten) and Moexipril
79
List 3 ACE inhibitors
Captopril (Capoten)
Enalapril (Vasotec)
Lisinopril (Prinivil)
80
Pharmacologic effects of ARBs
- Block access of angiotensin II
- Cause dilation of arterioles and veins
- Prevent angiotensin II from inducing pathologic changes in cardiac structure
- Reduce excretion of potassium
- Decrease release of aldosterone
- Increase renal excretion of sodium and water
- Do not inhibit kinase II
- Do not increase levels of bradykinin
81
Difference between ACE inhibitors and ARBs
ARBs do not increase bradykinin release in vasculature of the lungs. Because of this, they do not cause cough
82
Therapeutic uses of ARBs
HTN, heart failure, MI
Diabetic nephropathy
If unable to tolerate ACE inhibitors, next best protection against MI, stroke, and death from cardiovascular causes in high-risk patients
83
Adverse effects of ARBs
Angioedema
Fetal harm in pregnancy
Renal failure (**bilateral renal artery stenosis)
84
Administration of ARBs
All are given PO
85
List 3 ARBs
Losartan (Cozaar)
Valsartan (Diovan)
Telmisartan (Micardis)
86
Function of direct renin inhibitors
Binds tightly with renin and prevents the division of angiotensinogen to angiotensin I
87
Side effects of direct renin inhibitors
Angioedema
Cough
GI effects
Hyperkalemia
Fetal injury
88
Only drug approved for HTN in direct renin inhibitor class
Aliskiren (Tekturna)
89
Mechanism of action of aldosterone antagonists
Selective blockade of aldosterone receptors
90
Therapeutic uses of Eplerenone (Inspra)
HTN
Heart failure
91
Administration considerations for Eplerenone (Inspra)
Absorption is not affected by food
92
Adverse effects of Eplerenone (Inspra)
Hyperkalemia (can be severe)
93
Drug interactions of Eplerenone (Inspra)
Inhibitors of CYP3A4
Drugs that raise potassium levels
Use with caution when combined with lithium
94
Prototype for aldosterone antagonists
Spironolactone (Aldactone)
95
Mechanism of action for spironolactone (Aldactone)
Blocks aldosterone receptors, binds with receptors for other steroid hormones
96
Therapeutic uses of Spironolactone (Aldactone)
HTN
Heart failure
97
Adverse effects of Spironolactone (Aldactone)
*Hyperkalemia (b/c it is also a potassium sparing diuretic)
Gynecomastia
Menstural irregulatrities
Impotence
Hirsute said
Deepening of the voice
98
How do calcium channel blockers work?
*Prevent calcium ions from entering cells
99
Which parts of the body to calcium channel blockers have the greatest impact on?
Heart
Arteries
Arterioles
100
What are calcium channel blockers used to treat?
*HTN
*Angina pectoris
*Cardiac dysrhythmias
101
Other names for calcium channel blockers
Calcium antagonists
Slow channel blockers
102
What do calcium channels do?
Regulate the entry of calcium ions into cells
103
What are the 2 groups of CCBs?
Verapamil and diltiazem
Dihydropyridines
104
What are verapamil and diltiazem?
Agents that act on the vascular smooth muscle and the heart
105
What are dihydropyridines?
Agents that act mainly on vascular smooth muscle
106
How do calcium channel blockers work on vascular smooth muscle when they are open vs. blocked?
Open = contractile process
Blocked = *vasodilation
107
What do therapeutic doses of calcium channel blockers do?
Work selectively on peripheral arterioles and arteries, and arterioles of the heart
Do not have significant effect on veins
108
Why does blocking calcium channels cause vasodilation?
Calcium causes forceful contractions of the heart. If we relax the muscle by blocking some of the calcium, it makes contractions less forceful and allows smooth muscle to relax
109
Which receptor are calcium channels highly intertwined with?
Beta1 adrenergic receptors in the heart
110
Classifications of calcium channel blockers
Dihydropyridines
Non-dihydropyridines
111
Example of dihydropyridines group of calcium channel blockers
Nifedipine (Procardia)
112
Examples of non-dihydropyridines group of calcium channel blockers
Verapamil, Diltiazem (Cardizem)
113
Site of action for Dihydropyridines
Act primarily on arterioles
114
Site of action for verapamil and diltiazem
Act on arterioles and on the heart
115
Function of Verapamil (Calan, Covera-HS)
Agent that blocks calcium channels in blood vessels and acts on vascular smooth muscle and the heart
116
Hemodynamic effects of Verapamil
Direct effects on the heart and blood vessels (relaxes)
Reflex effects
117
Five direct hemodynamic effects of verapamil
- Block at peripheral arterioles (reduces arterial pressure)
- Block at arteries and arterioles of heart (increases coronary perfusion)
- Block at SA node (reduces heart rate)
- Block at AV node (decreases AV nodal contraction)
- Block in the myocardium (decreases force of contraction)
118
Indirect (reflex) hemodynamic effects of Verapamil
Baroreceptor reflex (may cause BP to jump back up)
119
Net effects of verapamil
Little or no net effect on cardiac performance
*Vasodilation accompanied by reduced arterial pressure and increased coronary perfusion
120
Administration of Verapamil
Can be given PO or IV
121
Therapeutic uses of Verapamil
Angina pectoris (vasopastic angina and angina of effort)
Essential hypertension (first line agent)
Cardiac dysrhythmias
122
Types of cardiac dysrhythmias verapamil can be used for
Atrial flutter
Atrial fibrillation
Paroxysmal supraventricular tachycardia
123
How does verapamil help with dysrhythmias
If dysrhythmias are really fast, verapamil slows down contractions causing rhythm to be more regular
124
Adverse effects of Verapamil
*Constipation (most common complaint)
*Dizziness, facial flushing, headache (from lowered BP/HR)
Edema of ankles and feet
Gingival hyperplasia
Heart block
125
Drug interactions of Verapamil
Digoxin (doesn’t work well with other drugs)
Beta-adrenergic blocking agents (could lower BP too much or cause dysrhythmias)
126
When is Verapamil given IV?
Only for dysrhythmias and Pt must be on cardiac monitor with resuscitation equipment immediately available
127
Actions of Diltiazem
*blocks calcium channels in heart and blood vessels (similar to verapamil)
Lowers blood pressure
128
How does Diltiazem lower blood pressure?
Arteriolar dilation
Direct suppressant/reflex cardiac stimulation = little net effect on heart
129
Therapeutic uses for diltiazem
Angina pectoris
HTN
Cardiac dysrhythmias (atrial flutter, atrial fibrillation, paroxysmal tachycardia)
130
Adverse effects of diltiazem
(Similar to verapamil, but less constipation)
Dizziness
Flushing
Headache
Edema of ankles and feet
*Exacerbates bradycardia, sick sinus syndrome, heart failure, second- or third-degree heart block
131
Drug interactions of diltiazem
Digoxin
Beta-adrenergic blocking agents
132
What are Dihydropyridines?
Agents that act mainly on vascular smooth muscle
Create a significant blockade of calcium channels in blood vessels
And *Minimal blockade of calcium channels in the heart
133
Prototype of dihydropyridines
*Nifedipine (Procardia)
134
Actions of Nifedipine
Vasodilation by *blocking calcium channels
Blocks in vascular smooth muscle
Very little blockade of heart Ca channels
Cannot be used to treat dysrhythmias
Less likely than verapamil to exacerbate pre-existing cardiac disorders (used more for BP)
135
Direct effects of nifedipine
Limited blockade of Ca channels in vascular smooth muscle (no direct suppressant effects on: automaticity, AV conduction, or contractile force)
136
Indirect effects of nifedipine
Lowered BP activates baroreceptor reflex
(Primarily with fast-acting vs. sustained release)
137
Net effect of nifedipine blocking calcium channels and causing vasodilation
*Lowered BP
*Increased heart rate
*Increased contractile force
(HR and contractile force not affected as much as BP)
138
Therapeutic uses of nifedipine
Angina pectoris
HTN
139
Adverse effects of nifedipine
Flushing
Dizziness
Headache
Peripheral edema
Gingival hyperplasia
Chronic eczematous rash in older patients
Reflex tachycardia (= increased cardiac O2 demand)
- & can increase pain for anginal patients
140
What can nifedipine be combined with to prevent reflex tachycardia?
Beta blocker
(This is ok b/c nifedipine does not lower HR as much as beta blockers do)
141
Vasodilator that works selectively to dilate arterioles
Hydralazine
142
Vasodilator that works selectively to dilate veins
Nitroglycerin
143
Vasodilator that works to dilate both arterioles and veins
Prazosin
144
What occurs when a drug dilates resistance vessels (arterioles)?
Cause a decrease in cardiac Afterload
145
What occurs when a drug dilates capacitance vessels (veins)?
Decreased force with which blood is returned to the heart, so decreased preload
146
Therapeutic uses of vasodilators
*Essential HTN
*HTN crisis
*Angina pectoris
Heart failure
MI
Pheochromocytoma
Peripheral vascular disease
Pulmonary arterial hypertension
Production of controlled hypotension during surgery
147
Main adverse effects related to vasodilation
* Postural hypotension
* Reflex tachycardia
* Expansion of blood volume
148
What should you tell a patient who first starts taking vasodilators?
*They may faint, feel dizzy or fatigued
149
Action of Hydralazine (Apresoline)
Selective dilation of arterioles
(Postural hypotension is minimal)
150
Therapeutic uses of Hydralazine (Apresoline)
Essential hypertension (PO)
Hypertensive crisis (IV)
Heart failure
151
Adverse effects of Hydralazine (Apresoline)
Reflex tachycardia
Increased blood volume
Systemic lupus erythematous-like syndrome
Headache
Dizziness
Weakness
Fatigue
152
Drug interactions of Hydralazine (Apresoline)
Other antihypertensive agents
Avoid excessive hypotension
(Combined with beta blocker to protect against reflex tachycardia and diuretics to prevent sodium and water retention and expansion of blood volume)
153
Action of Minoxidil (Loniten)
Selective dilation of arterioles
(More intense dilation than Hydralazine, but causes more adverse reactions)
154
Uses of minoxidil (Loniten)
Severe HTN that is unresponsive to safer drugs
155
Adverse effects of minoxidil (Loniten)
Reflex tachycardia
Sodium and water retention
Hypertrichosis (hair growth b/c can also be used topically as rogane)
Pericardial effusion
156
Fastest acting antihypertensive agent
Sodium Nitroprusside (Nitropress)
157
Action of sodium nitroprusside (Nitropress)
Causes venous and arteriolar dilation
158
Administration of Nitropress
*IV infusion (CCU)
159
Onset of Nitropress
Immediate (but BP returns to pretreatment level in minutes when stopped)
160
When is Nitropress used?
For hypertensive emergencies
(Pt must be hooked up to monitor b/c vasodilation effects are so strong)
161
Adverse effects of Nitropress
Excessive hypotension (Must lower pt’s bp slowly)
Cyanide poisoning (b/c of how it breaks down in body, creates cyanide build up)
Thiocyanate toxicity
162
Other vasodilators
ACE inhibitors
Angiotensin II receptor antagonists
Direct renin inhibitors
Organic nitrates
Calcium channel blockers
Sympathy lyrics
Nesiritide
163
What are nesiritides?
Drugs for pulmonary arterial hypertension
164
Prehypertension BP
120-130 / 80-89
165
Two categories of HTN
Primary (essential) HTN
Secondary HTN
166
Difference between primary and secondary hypertension
Primary (essential) HTN:
- no identifiable cause
- chronic, progressive disorder
- can be treated but not cured
Secondary HTN:
- identifiable primary cause
- possible to treat the cause directly
- some individuals can actually be cured
167
Who is more likely to have primary (essential) HTN?
Older adults
African Americans
Mexican Americans
Post menopausal women
168
Consequences of hypertension
Heart disease
- MI
- heart failure
- angina pectoris
Kidney disease
Stroke
169
Free lifestyle modifications for pts with HTN
Sodium restriction
DASH diet (fruits, veggies) & alcohol restriction
Aerobic exercise, smoking cessation
Maintenance of K+ and Ca+ intake
170
Formula for arterial pressure
Arterial pressure = cardiac output X peripheral resistance
171
What causes changes in cardiac output?
Heart rate
Myocardial contractility
Blood volume
Venous return
172
Systems that help regulate blood pressure
Sympathetic baroreceptor reflex
Renin-angiotensin-aldosterone system
Renal regulation of blood pressure
173
Patient education for taking BP medications
They must take them faithfully to bring BP down
If they don’t get BP under control, may have stroke or MI
Encourage them to get a BP cuff to check at home
Can cause impotence in men and makes them not want to take it
174
Drugs for hypertensive emergencies
Fenoldopam
Labetalol
Diazoxide
Clevidipine
175
Which BP meds are contraindicated during pregnancy?
ACE inhibitors
ARBS
Direct renin inhibitors (DRIs)
176
Which medications should be used for preeclampsia and eclampsia?
Labetalol
Magnesium sulfate (anticonvulsant)
177
Patho of heart failure
Cardiac remodeling (gets out of shape & bigger)
Physiologic adaptations to reduced cardiac output
178
Physiologic adaptations to reduced CO
Cardiac dilation
Increased sympathetic tone
Water retention and increased blood volume
Natriuretic peptides
179
Drugs that are used to treat heart failure
Diuretics
Drugs that inhibit the renin-angiotensin-aldosterone system
Beta blockers
Inotropic agents (Digoxin- cardiac glycoside, dopamine)
Vasodilators
180
Drugs that inhibit the RAAS
ACE inhibitors
ARBs (if ACE inhibitors are not tolerated)
Aldosterone antagonists
Direct renin inhibitors
181
What are inotropic agents?
Sympathomimetics
182
Types of sympathomimetics
Dopamine (Intropin)
Dobutamine
Phosphodiesterase inhibitors
183
How does dopamine work for heart failure?
Catecholamine
Activates beta1 adrenergic receptors in heart, kidney, and blood vessels
Increases heart rate
Dilates renal blood vessels
Activates alpha1 receptors
184
How does dobutamine work for heart failure?
Synthetic catecholamine
Selective activation of beta1 adrenergic receptors
185
Intravenous vasodilators used for acute care
*Nitroglycerin
*Sodium nitroprusside (Nitropress)
Nesiritide (Natrecor)
186
Principle adverse effects of nitroglycerin
Hypotension
Resultant reflex tachycardia
187
Principal adverse effect of Nitropress
Profound hypotension
188
Principle adverse effect of Nesiritide (Natrecor)
Sympatomatic hypotension
189
Functions of digoxin and cardiac glycosides
Positive inotropic actions:
- increase myocardial contractile force
- alter electrical activity of the heart
- favorable affect neurohormonal systems
190
What is Digoxin
A cardia (Digitalis) Glycoside
Naturally occurring compound
191
*Effects of Digoxin
Profound effects on the mechanical and electrical properties of the heart
Increases myocardial contractility
Increased cardiac output
192
Adverse effect of Digoxin
Can cause severe dysrhythmias
193
Relationship of potassium to inotropic action
Potassium levels must be kept in normal physiologic range
194
Hemodynamic benefits of Digoxin
Increased cardiac output
- decreased sympathetic tone
- increased urine production
- decreased renin release
195
*Heart rate of a pt taking digoxin that would cause you to hold the drug and call the provider
* <60
196
Drug interactions of Digoxin
Diuretics
ACE inhibitors
ARBs
Sympathomimetics
Quinidine
Verapamil
197
Half life of digoxin
About 1.5 days
198
Stage A of heart failure
No symptoms of HF
Management directed at reducing risk
199
Stage B of heart failure
TX is same as for stage A with the addition of ACE inhibitors or ARBs
200
Stage C of heart failure
Relieve symptoms
Diuretics
BB
digoxin
201
Stage D of heart failure
Worse
Multiple drugs
Diuretics
Repeated hospitalizations
Fluid management is constant
202
What does ASCVD stand for?
Atherosclerotic Cardiovascular Disease
203
What is cholesterol?
A component of all cell membranes and membranes of intracellular organelles
204
What is cholesterol required for?
Synthesis of certain hormones and bile salts
205
Where does cholesterol come from and what is it manufactured by?
Comes from dietary sources
Manufactured by cells, primarily in the liver
206
What are apolipoproteins?
Recognition sites for cell-surface receptors
207
Function of apolipoproteins
Activate enzymes that metabolize lipoproteins
And increase the structural stability of lipoproteins
208
What are the 3 classes of plasma lipoproteins that are relevant to coronary atherosclerosis?
Very-low-density lipoproteins (VLDLs)
Low-density lipoproteins (LDLs)
High-density lipoproteins (HDLs)
209
Which class of lipoprotein are triglycerides in?
VLDLs
210
Which category of lipoproteins is the greatest contributor to CHD?
LDLs
211
Which class of lipoproteins is cholesterol in?
HDLs
212
What happens with the inflammatory process of atherogenesis?
Infiltration of macrophages, T lymphocytes, and other inflammatory mediators
213
How old/often should you have cholesterol screened?
Every 5 years for adults over 20
214
What do we want HDL cholesterol levels to be?
> or equal to 45 mg/dL
215
What do we want LDL cholesterol levels to be?
< 100 mg/dL
216
What do we want triglycerides levels to be?
< 90 mg/dL
217
Factors in risk assessment of cholesterol
Identifying CHD risk factors
Identifying CHD risk equivalents:
- diabetes, atherosclerotic disease other than CHD
Identifying an individual’s CHD risk category
218
Therapeutic lifestyle changes for High-LDL cholesterol
Smoking cessation
Diet
Exercise
219
Three medication categories for high cholesterol
HMG-CoA reductase inhibitors
Bile-acid sequestration
Fibrates
220
Secondary treatment targets of cholesterol medication
Metabolic syndrome (increases risk for CHD & T2DM)
High triglycerides (levels above 150 mg/dL)
221
Factors of metabolic syndrome
High blood glucose
High triglycerides
High apolipoprotein B
Low high-density lipoprotein (HDL)
Prothrombotic state
Proinflammatory state
Hypertension
222
Treatment goals for metabolic syndrome
Reduce the risk for atherosclerotic disease
Reduce the risk for T2DM
Increase physical activity
(Want to make sure pts know that they have to turn this disease around otherwise they will have diabetes and heart problems)
223
Most effective drugs for lowering LDL
HMG-CoA Reductase Inhibitors (Statins)
224
What do Statins do?
Lower LDL cholesterol
Raise HDL cholesterol
Lower triglyceride levels
225
Nonlipid beneficial cardiovascular actions of statins
Promote plaque stability
Reduce the risk for cardiovascular events
Increased bone formation
226
Prototype for statins
Lovastatin/Mevacor
227
When is the best time to take a drug that lowers cholesterol?
In the evening
Because a lot of cholesterol synthesis takes place at night while sleeping
228
What happens if you stop taking statins?
Cholesterol goes back up to where it was before starting the drug
229
Mechanism of action for statins
Cholesterol reduction
230
Therapeutic uses of statins
Hypercholesterolemia
Primary and secondary prevention of CV events
Post MI therapy (bc it helps prevent plaque from building up in vessel walls)
Diabetes
231
Another popular statin drug
Rouvastatin (Crestor)
232
Nursing consideration for patients taking Crestor
If pt is Asian, may get very high levels of this drug and have to decrease dose to lower levels
233
Adverse effects of statins
Common:
- headache
- rash
- GI disturbances
Rare:
- *Myopathy/rhabdomyolysis
- hepatotoxicity
234
What is myopathy and rhabdomyolysis?
A rare side effect of stating drugs
Myopathy - injured muscle tissue and can develop into:
Rhabdomyolysis - muscle tissue breaks down and increased levels of creatinine kinase floats around and could get into renals
235
Which severe side effects should you watch for in a pt taking statins?
Muscle tenderness and weakness (could indicate myopathy/rhabdomyolysis
Jaundice, pt saying they don’t feel good (could indicate hepatotoxicity)
Need to draw liver enzymes to see if they’re elevated
236
Drug interactions of statins
Most other lipid-lowering drugs (except bile acid sequestration)
Drugs that inhibits CYP3A
*Use in pregnancy (Category X = contraindicated)
237
Dosing of statins
*should be once daily, in the evening
238
What should the patient have done before they start taking a cholesterol lowering medication?
We need to get a lipid profile on them
239
Function of Bile-Acid sequestrants
Primarily used as adjuncts to statins
Lowers LDLs
240
Prototype bile-acid sequestrant
Colesevelam/Welcol
241
Difference between Colesevelam/Welchol and other bile-acid sequestrants
Does not increase uptake of fat-soluble vitamins as other bile sequestrants do
Does not significantly reduce the absorption of statins, warfarin, digoxin, and most other drugs studies
242
Two other drugs in the bile-acid sequestrants group
Cholestyramine
Colestipol
243
Function of Colesevelam (Welchol)
Decrease in LDL cholesterol
(Increased VLDL levels in some patients)
244
Mechanism of action of Colesevelam (Welchol)
Increases LDL receptors on hepatocytes
Prevents reabsorption of bile acids
245
Use of Colesevelam (Welchol)
Reduces LDL cholesterol (with modified diet and exercise)
246
Adverse effects of Colesevelam (Welchol)
Constipation
247
Function of Ezetimibe (Zetia)
Inhibits cholesterol absorption
248
Which type of cholesterol drug is Ezetimibe (Zetia)?
Bile-Acid Sequestrant
249
Uses of Ezetimibe (Zetia)
Lower total cholesterol
LDL cholesterol
Apolipoprotein B
250
Adverse effects of Ezetimibe (Zetia)
Myopathy
Rhabdomyolysis
Hepatitis
Pancreatitis
Thrombocytopenia
251
Drug interactions of Ezetimibe (Zetia)
Statins
Fibrates
Bile-acid sequestrants
Cyclosporine
252
Most effective type of drug available for lowering TG levels
Fabric Acid Derivatives (Fibrates)
253
Main functions of Fibrates
Most effective drug for lowering TG levels
Can raise HDL cholesterol
Little or no effect on LDL cholesterol
254
Drug interactions for Fibrates
Warfarin (can increase risk for bleeding)
Statins (can increase risk for rhabdomyolysis)
255
3 Fibrates used in the United States
*Gemfibrozil (Lopid)
Fenofibrate (Tricor)
Fenofibric acid (TriLipix)
256
Prototype for Fibrins
Gemfibrozil (Lopid)
257
Effects of Gemfibrozil (Lopid) on plasma lipoproteins
Decreased plasma TG content
Decreased VLDL levels
Can increase HDL cholesterol
258
How does Gemfibrozil (Lopid) interact with warfarin?
Displaces warfarin from plasma albumin
Must measure INR frequently
259
Uses of Gemfibrozil (Lopid)
Reduces high levels of plasma triglycerides (VLDLs)
(Treatment reserved for pts who have not responded to diet modification)
Less effective than statins in reducing LDL
Can raise HDL but not approved for this use
260
Adverse of Gemfibrozil (Lopid)
Rashes
GI disturbances
Gallstones
Myopathy
Liver injury (hepatotoxic)
261
Other products that are used to alter plasma lipid levels
Lovaza - omega 3 acid
Fish oil - diet
Plant stanol and sterol esters
Cholestin
262
What are GP2B3A receptors?
Receptors on platelets (50,000-80,000 on each platelet)
Where anticoagulation medications go in and attach to decrease platelet aggregation
263
Stage 1 of hemostasis
Formation of platelet plug
Platelet aggregation
264
Stage 2 of hemostasis
Coagulation
Intrinsic and extrinsic coagulation pathways
265
Three major groups of drugs for thromboembolic disorders
Anticoagulants
Antiplatelets
Thrombolytics
266
What do anticoagulants do?
Reduce the formation of fibrin
267
Two mechanisms of action of anticoagulants
Inhibit the synthesis of clotting factors
Inhibit the activity of clotting factors
268
Two drugs in anticoagulant group of drugs for thromboembolic disorders
Heparin
Coumadin
269
Function of heparin
Enhances antithrombin
Rapid-acting anticoagulant
270
How is heparin administered?
By injection only (Cannot be absorbed so can’t be PO)
IV (Continuous and intermittent)
Deep SubQ
271
Therapeutic uses of Heparin
Preferred anticoagulant during pregnancy when rapid anticoagulation is required
Pulmonary embolism
Stroke evolving
Massive DVT
Open heart surgery
Renal dialysis
Low-dose therapy postoperatively
Disseminated intravascular coagulation (DIC)
Adjunct to thrombolytic therapy
272
Adverse effects of heparin
Hemorrhage
Heparin-induced thrombocytopenia
Hypersensitivity reactions
273
What is heparin-induced thrombocytopenia?
HIT syndrome: wipes out pt’s platelets
274
How do we know HIT syndrome is occuring?
Get a base line lab value before starting pt on the drug and compare after starting. If platelets keep decreasing, will know they are being wiped out
275
When is heparin contraindicated?
Thrombocytopenia, uncontrolled bleeding
During and immediately after surgery of the eye, brain, or spinal cord (could cause hematomas and put too much pressure in these areas)
276
*Antidote for overdose of Heparin
*Protamine sulfate
277
What is aPTT? When is it drawn, and why?
Activated partial thromboplastin time
Gives an indication of how effective the heparin is working.
Need to draw pt’s levels every 6-8 hours while they’re taking heparin
278
Normal levels of aPTT and what happens to the levels when a pt is taking heparin?
Normal is around 40 seconds. Want it to increase when they are on heparin
279
Difference between unfractioned heparin and low-molecular-weight heparins
Unfractioned heparin has a different molecular structure and can be given IV
Low-Molecular-Weight heparins are composed of molecules that are shorter than those found in unfractioned heparin
280
Therapeutic uses of Low-Molecular-Weight heparins
Prevention of DVT after surgery (including replacement of hip, knee)
Treatment of established DVT
Prevention of ischemic complications
281
What types of ischemic complications does Low-Molecular-Weight heparin prevent?
Pts with unstable angina
Non-Q wave MI
STEMI
282
How is Low-Molecular-Weight heparin administered?
SubQ
Dosage is based on body weight
283
Antidote for toxicity of Low-Molecular-Weight heparin
Protamine sulfate
284
Benefits and down-sides of Low-Molecular-Weight heparin
Costs more than unfractionated heparin
Does not require monitoring, can be given at home
285
Adverse effects and interactions of Low-Molecular-Weight heparin
Bleeding (but less than with unfractionated heparin)
Immune-mediated thrombocytopenia
Severe neurologic injury for pts undergoing spinal puncture or spinal epidural anesthesia
286
Types of Low-Molecular-Weight heparins
*Enoxaparin (Lovenox)
Dalteparin (Fragmin)
287
What is *Warfarin (Coumadin)?
*An oral anticoagulant
288
Uses of Warfarin (Coumadin)
Oral anticoagulant with delayed onset
Vitamin K antagonist
Blocks biosynthesis of factors 7, 9, 10 and prothrombin in coagulation cascade
Not useful in emergencies (since it’s PO)
Long term prophylaxis of thrombosis
289
Which patients would use Warfarin as a long-term prophylaxis of thrombosis?
For prevention of:
- Venous thrombosis and associated pulmonary embolism
- prevention of thromboembolism (in pts with prosthetic heart valves)
- prevention of thrombosis during atrial fibrillation
290
How to monitor treatment with warfarin:
*Prothrombin time (PT) - normal is 12 seconds
* Internal normalized ratio (INR)
291
Adverse effects of warfarin
Hemorrhage (give Vitamin K for toxicity)
Fetal hemorrhage and teratogenesis during pregnancy
Pts will bruise easily
292
Drug interactions of warfarin
Drugs that increase anticoagulant effects
Drugs that promote bleeding
Drugs that decrease anticoagulant effects
Heparin
Aspirin
Acetaminophen
293
Antagonist for Coumadin
Vitamin K
294
What should you educate a pt on when they begin taking Warfarin?
Don’t want them to eat too much vitamin K in their diet to cancel it out
Should wear a bracelet that says they’re on Coumadin
Will bruise easily
295
Difference between how direct thrombin inhibitors and heparin work
Direct thrombin inhibitors directly inhibit thrombin and heparin enhances the activity of antithrombin
296
Drugs that are direct thrombin inhibitors
Dibigatran etexilate (Pradaxa) (not important)
Hiruden Analog: Bivalirudin (Angiomax)
Lepirudin (Refludan)
297
Function of Angiomax
Prevents clot formation (combined with aspirin) in pts with unstable angina who are undergoing coronary angioplasty
298
Mechanism of action of Angiomax
Facilitates the actions of antithrombin
Prevents conversion of fibrinogen to fibrin
Prevents activation of factor XII
299
Adverse effects of Angiomax
Bleeding
Back pain
Nausea, headache
300
Use of lepirudin (Refludan)
Prophylaxis and treatment of thrombosis in pts with HIT
(Direct inhibition of thrombin)
301
Drug that is a selective factor Xa inhibitor
Rivaroxaban (Xarelto)
302
Function of Xarelto
Binds directly with factor Xa to cause inactivation
303
Use of Xarelto
Retention of DVT and PE after ortho surgery
Prevention of stroke in pts with atrial fibrillation
304
Adverse effects of Xarelto
Bleeding
305
How does aspirin function as an anti platelet drug?
Inhibition of cyclooxygenase
306
Adverse effect of aspirin
Increases risk for GI bleeding
307
How does Clopidogrel (Plavix) work as an anti platelet drug?
P2Y12, adenosine diphosphate receptor antagonist
308
How does Vorapaxar (Zontivity) work as an antiplatlet drug?
Protease-activated receptor-1 (PAR-1) antagonist
309
Therapeutic uses of aspirin
Ischemic stroke
Transient ischemic attack
Chronic stable angina
Unstable angina
Coronary stunting
Acute MI
Previous MI
Primary prevention of MI
310
Adverse effects of aspirin
Bleeding
GI bleeding and hemorrhagic stroke
(Enteric coated tablets may not reduce risk for GI bleeding)
311
Therapeutic uses of plavix
Prevents blockage of coronary artery stents
Reduces thrombotic events in pts with acute coronary syndromes:
- MI
- Ischemic stroke
- Vascular death
312
Adverse effects of Plavix
Similar to those of aspirin
313
How does Vorapaxar (Zonitivity) work as an antiplatlet drug?
Protease-activated receptor-1 PO
314
Emergency drugs used in chest pain situations via IV
Aggrastat
Integrilin
315
How does Eptifibatide (Integrilin) work?
Small peptide that causes reversible and highly selective inhibition of GP IIb/IIIa receptors
Effects reverse within 4 hours of stopping the infusion
316
Which type of drug is Alteplase (tPa)?
Thrombolytic Fibrinolytic Drug
317
Therapeutic uses of Alteplase (tPa)
Strong emergency critical care drug
MI
Ischemic stroke
PE
318
Major adverse effects of Alteplase (tPa)
*Bleeding
(Minor oozing to life-threatening amount)
Risk for intracranial bleeding higher than with streptokinase
319
Likely sites of bleeding in pts taking Alteplase (tPa)
Recent wounds
Needle puncture sites
Invasive procedure sites
320
What increases the risk of bleeding for a pt taking Alteplase (tPa)?
Anticoagulants increase risk for hemorrhage
(Blood replacement may need to be considered)
321
How can nurses minimize the risk of bleeding in pts taking Alteplase (tPa)?
Minimizing physical manipulation of the pt
Avoiding subQ and IM injections
Minimizing invasive procedures
Minimizing concurrent use of anticoagulants
Minimizing concurrent use of anti platelet drugs
322
How is Alteplase (tPa) administered?
IV
Pt must be hooked up to 2 IVs. One for the tPa and one for a regular drip (like NS)
Weight based and requires careful assessment
323
Where does pain from angina occur?
Sudden pain beneath the sternum, often radiating to left shoulder and arm
324
What causes angina?
*Oxygen supply to the heart is insufficient to meet oxygen demand
325
Two goals of angina drug therapy
Prevention of MI and death
Prevention of myocardial ischemia and anginal pain
326
What controls cardiac oxygen demand
Heart rate
Myocardial contractility
Intramyocardial wall tension (preload/Afterload)
327
What controls oxygen supply?
Myocardial blood flow
Myocardial perfusion only in diastole
328
Three forms of angina pectoris
Chronic stable angina (exertional angina)
Variant angina (Prinzmetal’s or vasospastic angina)
Unstable angina
329
Three families of antianginal agents
*Organic nitrates
*Beta blockers
*Calcium channel blockers
330
What can cause chronic stable angina?
Emotional excitement
Large meals
Cold exposure
CAD
331
Treatment strategy for chronic stable angina
Increase cardiac oxygen supply
Decrease oxygen demand
332
Therapeutic agents for chronic stable angina
Organic nitrates
Beta blockers
Calcium channel blockers
Ranolazine (newer drug with limited indications, can be combined with other drugs)
333
Non drug therapy for chronic stable angina
Avoid factors that can precipitate angina
Decrease risk factors
334
What causes variant angina?
Coronary artery spasm
335
Treatment for variant angina
Increasing cardiac oxygen supply
336
Therapeutic agents for variant angina
Calcium channel blockers
Organic nitrates
337
How can you tell if someone is having unstable angina?
Symptoms of angina at rest
New onset of exertional angina
Intensification of existing angina
338
Treatment strategy of unstable angina
Maintain oxygen supply
Decrease oxygen demand
339
Therapeutic agents for acute management of unstable angina
Anti-ischemic therapy
Antiplatelet therapy
Anticoagulant therapy
340
Types of angina nitroglycerin is used for
Stable and variant angina
341
Action of nitroglycerin
Vasodilator
342
Adverse effects of nitroglycerin
Headache
Orthostatic hypotension
Reflex tachycardia
343
Drug interactions with nitroglycerin
Hypotensive drugs
Phophodiesterase type 5 inhibitors (Viagra)
Beta blockers, verapamil, and diltiazem
344
Which group of antianginal meds does nitroglycerin fall into?
Organic nitrates
345
What should you know about a pt’s tolerance to nitroglycerin?
Can develop rapidly, and will cause cross tolerance to all other nitrates
To minimize, use the lowest effective dose
For long acting formulas, do 8 drug-free hours per day
346
Preparations and routes of nitroglycerin
Sublingual tablets
Sustained release oral capsules
Transdermal delivery systems
Translingual spray (most common)
Topical ointment
IV infusion
347
What should a pt do if they are having chest pain and have nitro with them at home?
Take one sublingual nitro and wait 5 mins. If they are still having chest pain, call 911 and take another tablet
348
Nursing considerations for nitroglycerin
If using long acting preparations, they should be discontinued slowly
349
All uses for nitroglycerin
Acute anginal therapy
Sustained anginal therapy
IV for perioperative control of BP
Treatment of heart failure with MI
Unstable angina
Uncontrolled exacerbations of chronic angina
350
Critical care organic nitrates
Isosorbide mononitrate (Imdur) & isosorbide dinitrate (Isordil)
Amyl nitrate
351
Beta blockers that can be used for angina
*Propranolol (Inderal)
*Metoprolol(Lopressor)
352
Function of propranolol and metoprolol for anginal pain
Decrease cardiac oxygen demand
353
Adverse effects of propranolol and metoprolol
Bradycardia
Decreased AV conduction
Reduction of contractility
Asthmatic effects
Use with caution in pts with diabetes
Insomnia
Depression
Bizarre dreams
Sexual dysfunction
354
Calcium channel blockers that can be used for angina
*Verapamil
*Diltiazem
*Nifedipine
355
Function of calcium channel blockers for angina
Block calcium channels in vascular smooth muscle
356
Types of angina calcium channel blockers can be used for
Stable and variant angina
357
Adverse effects of calcium channel blockers
Dilation of peripheral arterioles
Reflex tachycardia
Hypotension
Beta blockers
Bradycardia
Heart failure
AV block
358
Drug in new class of antianginal agents
Ranolazine (Ranexa)
359
How does Ranexa work?
Benefits are modest, works better in men
Does not reduce heart rate, BP, or vascular resistance
360
Side effects of Ranexa
Can prolong QT interval, and can lead to Vtach
Multiple drug interactions
361
Drugs used to prevent MI and death
Antiplatelet drugs
Cholesterol-lowering drugs
Angiotensin-converting enzyme (ACE) inhibitors
Antianginal agents
(All of these can be used in combination to help with angina or to prevent MIs, etc.)
362
Risk factors for angina
Smoking
High cholesterol
Hypertension
Diabetes
Physical inactivity
363
Management of variant angina
Calcium channel blocker, or long acting nitrate
If either of these alone is inadequate, add a nitrate
If combination fails, CABG may be indicated
(Beta blockers not effective with vasospastic angina)
364
Antiplatelet therapy for angina:
Aspirin (indefinitely)
- Clopidogrel (Plavix)
- Abciximab (ReoPro)
- Eptifibatide (Integrilin)
365
Anticoagulant therapy for angina
Subcutaneous LMW heparin or IV
Unfractionated heparin
366
Anti-ischemic therapy for angina
Nitroglycerin
Beta blockers
Supplemental O2
IV morphine
ACE inhibitor
367
Revascularization therapy for angina
Coronary artery bypass graft (CABG) surgery
Percutaneous transluminal coronary angioplasty (PTCA)
Comparison of CABG surgery with percutaneous coronary intervention (PCI)
368
Two types of myocardial infarctions
MI
STEMI (ST-Elevation MI)
369
Difference between a MI and a STEMI
MI: necrosis of the myocardium resulting from ischemia
STEMI: acute IM, causes elevation of the ST segment on the ECG
370
Pathophysiology of a STEMI
- Blood flow to a region of myocardium is stopped (by platelet plugging and thrombus formation)
- Hydrogen ions accumulate
- Local metabolic changes occur
- Myocardial injury triggers ventricular remodeling
- Degree of residual cardiac impairment depends on amount/location of damage
371
Pain symptoms of STEMI
Severe sub sternal chest pain
Crushing/constricting pain
Radiates down arm and jaw
372
Things to look for to determine if someone has had a STEMI
Chest pain
Characteristic ECG changes
Sweating, weakness, sense of impending doom
(But 20% of pts experience no symptoms)
Biochemical markers for MI
373
Routine drug therapy for management of STEMI
Oxygen
Aspirin (not NSAIDs) (have pt chew it)
Morphine (IV to relieve pain & decrease anxiety)
Beta blockers (give right after)
Nitroglycerin (to vasodilate)
374
What is reperfusion therapy for when managing STEMI
Pt will go to cath lab for reperfusion therapy.
To dissolve clots, and convert plasminogen to plasmin
375
Types of reperfusion therapy to manage STEMI
Primary percutaneous coronary intervention
Fibrinolytic (thrombolytic) therapy
376
Adjuncts to reperfusion therapy when managing an MI
Heparin
Antiplatelet drugs
377
What type of Fibrinolytic drugs are used for management of STEMI?
Alteplase (a tissue plasminogen activator)
Reteplase
Tenecteplase
378
What is primary percutaneous coronary intervention?
Primary = use of angioplasty rather than fibrinolytic therapy
Stents may be placed
379
What is the goal of primary percutaneous coronary intervention?
Primary PCI within 90 minutes of patient contact
380
What should all patient undergoing PCI receive?
An anticoagulant (IV heparin, bivalirudin) combined with
Antiplatelet drugs: aspirin plus either Clopidogrel, ticagrelor, or prasugrel
381
Function of fibrinolytic (thrombolytic) therapy?
Dissolves clots
382
How does fibrinolytic therapy dissolve clots?
Converts plasminogen to plasmin (proteolytic enzyme)
1. Alteplase, a tissue plasminogen activator
2. Reteplase
3. Tenecteplase
383
When is fibrinolytic therapy most effective?
When patient presents early
(Best for patients younger than 75 years)
384
Goal of fibrinolytic therapy
To improve ventricular function and reduce mortality
385
Adjuncts to reperfusion therapy when managing a STEMI
- Unfractionated heparin (used for treatment lasting less than 48 hours)
- Low-molecular-weight heparin (used for treatment lasting longer than 48 hours)
- Antiplatelet drugs:
- Low dose aspirin
386
Types of Antiplatelet drugs used adjunct to reperfusion therapy when managing a STEMI
Clopidogrel (plavix)
Glycoprotein (GP) IIb/IIIa inhibitors
387
Considerations when giving a pt aspirin adjunct to reperfusion therapy when managing a STEMI
May use aspirin concurrently with clopidogrel
Should take indefinitely
Higher dose should be given for PCI patients
388
How should ACE inhibitors and ARBs be used while managing STEMI
They decrease short-term mortality in all patients
Start treatment within 24 hours
389
Why should calcium channel blockers be used when managing STEMI
Antianginal, vasodilation, and antihypertensive actions
390
Complications that can occur due to STEMI
Ventricular dysrhythmias
Cardiogenic shock
391
What occurs with ventricular dysrhythmias after STEMI
Develop frequently and are major cause of death after MI
Prophylactic antidysrhythmics not successful
392
What causes cardiogenic shock after a STEMI
Results from tissue perfusion reduction
7-15% of post MI patients develop shock in first few days
393
How can patients who have had a STEMI improve their chances of having another one
Cholesterol control
Smoking cessation
Exercise
Blood pressure control
Diabetes control
394
*Which medications should post MI patients take?
Beta blocker
ACE inhibitor
Antiplatelet drug or anticoagulant
395
Symptoms of Diabetes Melkite’s
Sustained hyperglycemia
Polyuria
Polydipsia
Ketonuria
Weight loss
396
Other names for T1DM
Insulin dependent
Juvenile onset
397
Primary defect of T1DM
Destruction of pancreatic beta cells
398
What percentage of diabetes cases is type 1?
5-10%
399
Another name for T2DM
*Non-insulin dependent diabetes
Adult onset
400
What causes type 2 diabetes?
Insulin resistance and impaired insulin secretion
401
Short term complications of diabetes
Hyperglycemia and hypoglycemia
402
Long term complications of diabetes
Macrovascular damage
- Heart disease
- HTN
- Stroke
Hyperglycemia
Altered lipid metabolism
403
What can Macrovascular damage from diabetes cause?
Retinopathy
Nephropathy
Neuropathy
Gastroparesis
Amputation secondary to infection
404
What causes gestational diabetes?
Placenta produces hormones that antagonize the actions of insulin
Glucose can pass freely from the maternal to the fetal circulation (fetal hyperinsulinemia)
405
What can happen if proper glucose levels are not maintained during pregnancy?
To prevent teratogenic effects
406
How is someone diagnosed with diabetes?
Excessive plasma glucose is diagnostic of diabetes.
Patient must be tested in two separate ways, and both tests must be positive
407
Tests that can be used to diagnose diabetes
Fasting plasma glucose (FPG)
Casual plasma glucose
Oral glucose tolerance test (OGTT)
*Hemoglobin A1C
408
What does glucose level have to be to diagnose diabetes from a fasting plasma glucose test?
126 mg/dL or higher
409
What does glucose level have to be to diagnose pt with diabetes for a casual plasma glucose test?
200 mg/dL or greater
410
What does a pt’s glucose level have to be to diagnose with diabetes during an oral glucose tolerance test?
200 mg/dL or higher
411
What does hemoglobin A1C measure?
Measures the glucose that’s bound to the hemoglobin molecules in the blood
Gives snapshot of what glucose levels have been over last 3 months
412
What level of A1C is indicative of diabetes?
6.5% and above
413
Criteria for pts to be diagnosed with pre diabetes
Impaired fasting glucose between 100 & 125 mg/dL
Impaired glucose tolerance test
414
What happens when someone is diagnosed with pre diabetes
They are at an increased risk for developing T2DM
(Many people who meet prediabetes criteria never develop diabetes)
May reduce risk with diet changes and exercise and possibly with certain oral anti diabetic drugs
415
Primary goal of diabetes treatment
To prevent long-term complications
416
What needs to be controlled during diabetes treatment?
Tight control of blood glucose level
Control blood pressure
Control blood lipids
417
Treatment plan for T1DM
Integrated program of diet, self-monitoring of blood glucose, exercise, and insulin replacement
418
Dietary measures for T1DM
Total number of carbohydrates is more important than the type
Glycemic index
419
Treatment plan for T2DM
Requires comprehensive plan:
- modified diet and exercise
- drug therapy
Should be screened and treated for:
- HTN
- Nephropathy
- Retinopathy
- Neuropathy
- Dyslipidemias
420
Common target values while self monitoring blood glucose:
*80-130 mg/dL before meals
*<180 mg/dL 1-2 hours after meals
421
Goal for A1C for diabetic patients
Below 7%
But below 8% may be appropriate for pts with a history of severe hypoglycemia
422
How is insulin synthesized?
In the pancreas by beta cells within the islets of langerhans
423
What stimulates insulin release
A rise in blood glucose, usually by eating food
424
*Types of rapid acting insulins
Insulin lispro (Humalog)
Insulin aspart (NovoLog)
Insulin glulisine (Apidra)
425
*Types of short acting insulin
Regular insulin: Humulin R
Regular insulin: Novolin R
426
*Type of intermediate duration insulin
Neutral Protamine Hagedorn (NPH) insulin
427
*Types of long duration insulin
Insulin glargine (Lantus)
Insulin detemir (Levemir)
428
*Types of ultra long duration insulin
Insulin glargine (toujeo)
Insulin degludec (Tresiba)
429
Prototype for short-duration, rapid-acting insulin
Insulin lispro (Humalog)
430
Time frames of Humalog
Rapid onset (15-30 mins)
Peak: .5-2.5 hrs
Short duration (3-6 hrs)
431
When should Humalog be administered
Before (or even after eating)
Should be injected 5-10 minutes before meals
432
Routes of Humalog
Usually subQ
Or insulin pump
433
Time frames of NovoLog
Rapid onset 10-20 minutes
Peak: 1-3 hours
Short duration 3-5 hours
434
When should NovoLog be administered?
5-15 minutes before meals
435
Time frames of Apidra
Rapid onset 10-15 minutes
Peak: 1-1.5 hours
Short duration 3-5 hours
436
When should Apidra be administered
Close to the time of eating
437
Routes for regular insulin
SubQ injection
SubQ infusion
IM injection (used rarely)
IV
438
Time frames for regular insulin
Onset: 30-60 mins
Peak: 1-5 hours
Duration: 10 hours
439
Color of regular insulin
Clear
440
Time frames of NPH insulin
Onset: 60-120 hours
Peak: 6-14 hours
Duration: 16-24 hours
441
What can NPH insulins be mixed with?
Short acting insulins (to give more coverage)
442
What color are NPH insulins?
Cloudy
And must be rotated before admin
443
Administration of NPH insulin
SubQ injection only
Must be rotated before admin
444
Time frames of lantus
Onset: 70 minutes
Duration 18-24 hours
445
Time frames of levemir
Onset 60-120
Duration: 12-24 hours
446
Color of long duration insulin
Clear solutions
447
How long does Toujeo last?
24 hours
(Very concentrated)
448
How are toujeo and tresiba typically administered?
Usually come in prefilled pens
449
*Rules for mixing insulin
NPH with short-acting insulins
Short-acting insulin is drawn first (clear to cloudy)
450
How can insulin be administered through subcutaneous infusion?
Portable insulin pumps
Implantable insulin pumps
451
How should insulin be stored?
*unopened vials should be refrigerated until needed
Not frozen!
Can be used until expiration date if refrigerated.
Keep out of direct sunlight and extreme heat
452
How should mixtures of insulin be stored?
Mixtures in vials: stable for 1 month at room temp and for 3 months under refrigeration
Mixtures in pre-filled syringes: stored in refrigerator for at least 1 week, stored vertically with needle pointing up
453
*Therapeutic uses of insulin?
Principle use: diabetes mellitus
(Required by all type 1 and some type 2 pts)
IV insulin for DKA
Hyperkalemia (can promote uptake of potassium)
AIDS in the diagnosis of GH deficiency
454
Complications of insulin treatment
Hypoglycemia
Lipohypertrophy (lumpy looking skin from injecting in same spot)
Allergic reactions
Hypokalemia
455
Drug interactions with insulin
Hypoglycemic agents
Hyperglycemic agents
Beta-adrenergic blocking agents
456
Glucose level of hypoglycemia
*below 70 mg/dL
457
Treatment for a pt who has a blood glucose below 70
Rapid treatment for hypoglycemia is mandatory
Conscious pts: fast-acting oral sugar (OJ, glucose tabs, soda)
If swallowing or gag reflexes are suppressed: IV glucose or parenteral glucagon
458
Medication group for T2DM
Oral hypoglycemics
459
Prototype of oral hypoglycemics
Metforman (Glucophage)
460
What type of oral hypoglycemic is metformin?
Biguanides
461
Most common side effects of metformin
GI disturbances
Lactic acidosis (potentially fatal but rare)
462
Uses of metformin
T2DM
Prevention of T2DM
Gestational diabetes
PCOS
463
What are Sulfonylureas used for?
Oral hypoglycemic for T2DM only
Promote insulin release
464
Major side effects of Sulfonylureas
Hypoglycemia
Weight gain
465
Why does rosiglitazone (Avenida) have restricted use?
Can cause cardiac side effects
466
How do alpha-glucosidase inhibitors work?
Oral hypoglycemics that act on the intestine to delay absorption of carbohydrates
467
Two alpha-glucosidase inhibitors
Acarbose (Precose)
Miglitol (Glyset)
468
Adverse effects of alpha-glucosidase inhibitors
Flatulence
Cramps
Abdominal distention
Diarrhea
Liver dysfunction
469
How do DPP-4 inhibitors (AKA gliptins) work?
Oral hypoglycemics that promote glycemic control by enhancing the actions of incretin hormones
470
Adverse effects of DPP-4 inhibitors
Upper respiratory infection
UTI
Headache
471
Types of drugs other than insulin that can treat T2DM
GLP-1 receptor agonists (incretin mimetics)
Amylin mimetics
472
2 GLP-1 receptor agonists
Exenatide (Byetta)
Liraglutide (Victoza)
473
1 drug that is a amylin mimetic
Pramlintide (Symlin)
474
Acute complications of poor glycemic control
Diabetic ketoacidosis (DKA)
Hyperglycemic hyperosmotic nonketotic syndrome (HHNS)
475
*Characteristics of DKA
Hyperglycemia
Water loss
Altered fat metabolism
Ketoacids
Hemoconcentration
Acidosis
Coma
476
Treatment for DKA
*Insulin replacement
Bicarbonate for acidosis
Water and sodium replacement
Potassium replacement
Normalization of glucose levels
477
Symptoms of HHNS
- Large amount of glucose excreted in urine
- Dehydration and loss of blood volume
- Increases blood concentration of electrolytes and non electrolytes (particularly glucose)
- Increases hematocrit (blood thickens and becomes sluggish)
478
How does HHNS occur?
With T2DM with acute infection, acute illness, or other stress
479
What happens if HHNS is left untreated?
Can lead to coma or death
480
Management of HHNS
Correct hyperglycemia and dehydration with IV insulin, fluids, and electrolytes
481
Difference between DKA and HHNS
HHNS has little or no change in ketoacid levels and has little or no change in blood pH
HHNS also has no sweet or acetone smell to urine/breath
482
Difference between treating DKA and HHNS
HHNS does not get treated with bicarbonate because there is no acidosis to treat
483
How is severe hypoglycemia treated?
IV glucose to immediately raise blood glucose level is preferred
*Glucagon can be used if IV glucose is not available
484
How does *glucagon work for treating hypoglycemia?
Delayed elevation of blood glucose (promotes glycogen breakdown)
Will not work in starvation (b/c malnourished have little glycogen left to break down)
485
Patient teaching for pts with diabetes
Self glucose checks
Medications
Care of insulin
All the supplies
Syringes - put used ones in a container
Nutrition
S & S of hypo- and hyper- glycemic
If they’re sick, have surgery, run marathons, etc, will all require adjusting doses
Age of pt and family support
486
What functions do thyroid hormones have a profound effect on?
Metabolism
Cardiac function
Growth (promotes maturation in infancy and childhood development)
487
Hormones produced by the thyroid
Triiodothyronine (T3)
Thyroxine (T4, tetraiodothyronine)
488
Synthetic T3
Liothyronine
489
*Synthetic t4
*Levothyroxine
490
What is a serum TSH test used for?
Screening and diagnosis of hyperthyroidism
(Elevated TSH is indication of hyperthyroidism)
491
What are serum T3 or T4 tests used for?
Can measure total T4 or free T4
(Or total T3 or free T3)
492
What is hypothyroidism called in adults?
And in infants?
Myxedema in adults
Congenital hypothyroidism in infants
493
How is hypothyroidism treated in adults?
Replacement therapy with thyroid hormones
In almost all cases, treatment must continue lifelong
494
How is hypothyroidism treated in infants?
Replacement therapy with thyroid hormones
495
Clinical presentation of hypothyroidism in adults
Pale, puffy, and expressionless face
Cold and dry skin
Brittle hair or loss of hair
Lowered heart rate and temperature
Lethargy and fatigue
Intolerance to cold
Impaired mentality
496
Causes of hypothyriodism
Malfunction of the thyroid (usual cause)
Hashimoto’s disease (Chronic autoimmune thyroiditis)
Insufficient iodine in diet
Surgical removal of thyroid and destruction of thyroid with radioactive iodine
Insufficient secretion of TSH and TRH
497
Lifelong medications that are used to treat hypothyroidism
Levothyroxine (T4) (standard treatment)
*Liothyronine (T3) option
498
What can occur if someone has hypothyroidism during pregnancy?
In first trimester can result in permanent neuropsychological defects in the child
499
What can occur in infants who have hypothyroidism
May be permanent or transient
Can cause mental retardation and derangement of growth if not diagnosed and treated
500
Two forms of hyperthyroidism
Graves’ disease (most common form)
Toxic nodular goiter (Plummer’s disease)
501
Who does Graves’ disease most typically affect?
Women 20-40 years old
502
Notable symptom of Graves’ disease
Exophthalmos
503
Cause of hyperthyroidism
thyroid-stimulating immunoglobulins (TSIs)
504
Treatment of hyperthyroidism
Surgical removal of thyroid tissue
Destruction of thyroid tissue
Suppression of thyroid hormone synthesis
Beta blockers (ex: propranolol)
Nonradioactive iodine
505
Causes of thyrotoxic crisis (thyroid storm)
Patients with thyrotoxicosis who undergo significant stress (surgery, illness, etc.)
High levels of thyroid hormone
(Cannot be identified by laboratory testing)
506
Signs of thyrotoxic crisis
Hyperthermia (105° or higher)
Severe tachycardia
Restlessness
Agitation
Tremor
Unconsciousness
Coma
Hypotension
Heart failure
507
*Treatment of thyrotoxic crisis
*Potassium iodide, *Methimazole, and *Beta blocker
Sedation, cooling, glucocorticoids, IV fluids
508
Prototype thyroid hormone preparation for hypothyroidism
*Levothyroxine (Synthroid)
509
What is Levothyroxine (Synthroid)?
Synthetic preparation of thyroxine (T4) and drug of choice for *all types of hypothyroidism
Conversion to T3
510
Half life of Levothyroxine (Synthroid)
7 days
511
When should Levothyroxine be taken?
In the morning at least 30-60 minutes before breakfast
512
Adverse effects of Levothyroxine
Tachycardia
Angina
Tremors
Can intensify effects of warfarin
513
Drug interactions of Levothyroxine
Drugs that reduce Levothyroxine absorption
Drugs that accelerate Levothyroxine metabolism
Warfarin
Catecholamines (too much stimulation)
514
First-line drug for hyperthyroidism
Methimazole (Tapazole)
515
What type of drug is Methimazole (Tapazole)?
Thionamides
516
How long does it take for Methimazole to work?
May take 3-12 weeks for euthyroid state (may need to add something to help sooner)
517
Pros and cons of Methimazole
Does not cause liver damage associated with PTU
Does not destroy existing stores of thyroid hormone
More dangerous than PTU during lactation and during the first trimester of pregnancy
Considered a hazardous agent, handle with caution
518
Applications of Methimazole in hyperthyroidism
- Can be used alone for Graves’ disease
- Adjunct to radiation therapy until the effects of radiation manifest
- Suppress thyroid hormone synthesis in preparation for thyroid gland surgery (subtotal thyroidectomy)
- Patients experiencing thyrotoxic crisis (although PTU is preferred)
519
Function of propylthiouracil (PTU)
Inhibits thyroid hormone synthesis
Second line drug for Graves’ disease
520
Half life of PTU
90 minutes
521
How long does it take PTU to work?
6-12 months for full benefits
522
Therapeutic uses of PTU
Graves’ disease
Adjunct to radiation therapy
Preparation for thyroid gland surgery
Thyrotoxic crisis
523
Adverse effects of PTU
Agranulocytosis (most serious)
Hypothyroidism
Pregnancy and lactation
Can cause *severe liver damage
524
PTU vs. Methimazole
PTU can cause severe liver injury, meth does not
PTU has shorter half life, hence it requires 2-3 daily doses
PTU crosses placenta less readily than meth and achieves lower concentrations in breast milk
PTU blocks conversion of T4 to T3 in the periphery, meth does not
525
What is Radioactive Iodine-131?
Radioactive isotope of stable iodine
Emits gamma and beta rays
526
Half life of radioactive iodine 131
8 days
527
How long does it take radioactive iodine to work?
2-3 months for full effect
528
When is radioactive iodine used?
In Graves’ disease
Cannot be used in children or during pregnancy
529
Type of nonradioactive iodine
Lugol’s solution
530
What is Lugol’s solution used for?
Strong iodine solution used to suppress thyroid function in preparation for thyroidectomy
531
Adverse effects of Lugol’s solution
Brassy taste
Burning sensation in mouth and throat
Soreness of teeth and gums
GI injury
(These could all also be symptoms of mild toxicity)
532
How can beta blockers be used for thyroid issues?
For hyperthyroidism
Can suppress tachycardia and other symptoms of Graves’ disease
(Benefits derive from beta-adrenergic blockade, not from reducing levels of T3 or T4)
Also beneficial in thyrotoxic crisis
