1
Q
What is the drug class of furosemide (Lasix®)?
A
Loop diuretic (“water pill”).
2
Q
What is furosemide used for?
A
To treat hypertension, heart failure, and edema (fluid buildup).
3
Q
What key side effect should be monitored with furosemide?
A
Low potassium (hypokalemia) and dehydration.
4
Q
What is the drug class of hydrochlorothiazide (HCTZ)?
A
Thiazide diuretic.
5
Q
What is hydrochlorothiazide used for?
A
High blood pressure (hypertension) and mild fluid retention.
6
Q
What are important nursing considerations for HCTZ?
A
Monitor electrolytes, uric acid, and blood sugar; take in the morning.
7
Q
What is the drug class of spironolactone (Aldactone®)?
A
Potassium-sparing diuretic / Aldosterone antagonist.
8
Q
What does spironolactone do?
A
Removes sodium and water but keeps potassium.
9
Q
What is a major side effect of spironolactone?
A
High potassium (hyperkalemia) and possible gynecomastia in men.
10
Q
What is the drug class of digoxin (Lanoxin® or Toloxin®)?
A
Cardiac glycoside.
11
Q
What is digoxin used for?
A
Heart failure and atrial fibrillation.
12
Q
What must you check before giving digoxin?
A
Apical pulse for 1 full minute; hold if <60 bpm.
13
Q
What are signs of digoxin toxicity?
A
Nausea, vomiting, vision changes (yellow halos).
14
Q
What is the main goal of antihypertensive therapy?
A
To lower blood pressure and reduce the risk of heart and kidney disease.
15
Q
What is the goal of heart failure therapy?
A
To reduce the heart’s oxygen demand, improve pumping, and prevent further damage.
16
Q
What does “reduce afterload” mean in heart failure treatment?
A
It means lowering the pressure the heart must pump against, which decreases strain on the heart.
17
Q
Why is preserving left ventricular (LV) function important?
A
It keeps the heart strong and able to pump blood effectively.
18
Q
How do antihypertensive drugs improve quality of life in heart failure?
A
They help relieve symptoms like fatigue, swelling, and shortness of breath.
19
Q
Why does giving cardiac medications require critical thinking?
A
Because these drugs affect the heart and blood pressure — nurses must analyze vital signs, labs, and symptoms before and after giving them.
20
Q
What should be done before starting antihypertensive therapy?
A
Obtain a full health history and perform a head-to-toe physical assessment.
21
Q
Why is it important to check for contraindications?
A
To avoid dangerous drug interactions (e.g., herbal or OTC meds that raise BP or affect heart rhythm).
22
Q
Which conditions require caution when using antihypertensives?
A
Asthma (non-cardioselective beta blockers can worsen breathing) and diabetes (may mask low blood sugar).
23
Q
Why must liver and kidney function be considered?
A
Because these organs metabolize and eliminate drugs — if they’re impaired, the drug can build up and cause toxicity.
24
Q
What does “start low and go slow” mean?
A
Begin with a low dose and increase gradually to prevent side effects like dizziness or sudden BP drops.
25
Why do older adults need lower doses?
Their **renal and liver function decline with age**, so drugs stay in the body longer.
26
Why is ECG monitoring needed for IV antihypertensives?
To monitor for **arrhythmias**, **bradycardia**, or **sudden changes in blood pressure**.
27
What’s the difference between cardioselective and non-cardioselective beta blockers?
* **Cardioselective:** act mainly on the heart (safer for asthma).
* **Non-cardioselective:** affect both the heart and lungs (can cause bronchospasm).
28
What is the main goal of adrenergic drugs in treating hypertension?
To **reduce sympathetic nervous system (SNS)** activity, which lowers **heart rate, blood pressure, and renin release**.
29
What are the two main sites of adrenergic drug action?
1. **Central (brain)** → controls SNS outflow 2. **Peripheral (heart & blood vessels)** → blocks receptor response
30
What are examples of centrally acting alpha₂ agonists?
**Clonidine** and **Methyldopa**.
31
How do alpha₂ agonists lower blood pressure?
They **stimulate alpha₂ receptors in the brain**, reducing sympathetic outflow → less norepinephrine → ↓ HR, ↓ BP.
32
What kidney effect do alpha₂ agonists have?
They **decrease renin release**, reducing angiotensin II and vasoconstriction.
33
What are examples of alpha₁ blockers?
**Doxazosin**, **Prazosin**, and **Terazosin**.
34
What do alpha₁ blockers do?
They **block alpha₁ receptors** in arteries and veins → **vasodilation** → ↓ peripheral resistance and ↓ BP.
35
What other condition can alpha₁ blockers help with besides hypertension?
**Benign Prostatic Hyperplasia (BPH)** — they relax smooth muscle in the bladder neck and urethra.
36
What are examples of beta blockers?
**Propranolol**, **Metoprolol**, **Atenolol**.
37
How do beta blockers lower blood pressure?
They **block beta₁ receptors** in the heart → **slow heart rate**, **decrease contractility**, and **reduce renin secretion**.
38
What’s the difference between cardioselective and nonselective beta blockers?
* **Cardioselective:** target β₁ (heart only, safer for asthma). * **Nonselective:** block β₁ & β₂ (heart + lungs; can cause bronchoconstriction).
39
What are long-term effects of beta blockers?
↓ Peripheral vascular resistance and ↓ blood pressure.
40
What is an example of a dual alpha₁ and beta blocker?
**Labetalol (Trandate®)**.
41
How does labetalol work?
* **Beta₁ block:** slows heart rate & reduces contractility. * **Alpha₁ block:** causes vasodilation. → Combined effect: **lower BP + lower heart workload**.
42
What do alpha₂ agonists and beta blockers both reduce from the kidneys?
**Renin** — leading to less angiotensin II and lower BP.
43
What is the main therapeutic effect shared by all adrenergic antihypertensives?
**Lower blood pressure** and **decrease heart workload**.
44
What do adrenergic drugs do?
Lower blood pressure by blocking the “fight-or-flight” response.
45
Why aren’t beta blockers first-line for hypertension?
Other drugs lower heart risk better (like ACE inhibitors).
46
Why are beta blockers helpful in heart failure?
They **reduce heart strain** and **slow the heart rate**.
47
What heart problems do beta blockers treat?
**Angina, heart attack, arrhythmias, heart failure,** and **hypertension**.
48
What non-heart problems can beta blockers help with?
**Anxiety, migraines,** and **overactive thyroid (thyrotoxicosis)**.
49
What does clonidine do?
Lowers BP by **reducing nerve signals** from the brain.
50
What else can clonidine help with?
**Hot flashes, migraines,** and **withdrawal symptoms** (opioids, nicotine, alcohol).
51
What do alpha₁ blockers do?
**Relax blood vessels** to lower BP and help **urinary flow** in prostate problems (BPH).
52
How do alpha₁ blockers help heart failure?
Used with other heart meds to **improve blood flow** and **reduce pressure**.
53
What are some extra (off-label) uses of adrenergic drugs?
**Migraine prevention, anxiety relief, hot flashes,** and **withdrawal support**.
54
drug allergy
They can cause severe allergic reactions if the person is sensitive to the medication.
55
acute (uncontrolled) heart failure
They slow the heart rate, which can make pumping even weaker in an unstable heart.
56
bradycardia or heart block
They further slow the heart and can stop the heart from beating properly.
57
peptic ulcer disease
They can increase stomach acid and worsen ulcers.
58
liver or kidney disease
These organs clear the drug — if they don’t work well, the drug can build up and cause side effects.
59
asthma or COPD
Non-selective beta blockers block lung receptors (β₂) → cause bronchoconstriction and trouble breathing.
60
diabetic patients
They mask signs of low blood sugar (like fast heart rate) and reduce glucose release from the liver.
61
peripheral vascular disease (PVD)
They can reduce blood flow to hands, feet, and legs — making circulation worse.
62
bradycardia
A heart rate **below 60 bpm** caused by the heart slowing too much.
63
Why is bradycardia a concern with beta blockers?
It can cause **dizziness, fainting, or cardiac arrest** if the heart beats too slowly.
64
Why can beta blockers cause hypotension?
They **decrease heart rate and contractility**, which lowers blood pressure.
65
What symptoms can hypotension cause?
**Lightheadedness, fainting, and weakness.**
66
Why can beta blockers cause bronchoconstriction?
**Non-selective beta blockers** block β₂ receptors in the lungs → **airways tighten**.
67
Why is bronchoconstriction dangerous?
It can **worsen asthma or COPD**, causing **wheezing or shortness of breath**.
68
Why can beta blockers cause fatigue and dizziness?
Because they **slow the heart** and **reduce blood flow and oxygen** to tissues and the brain.
69
Why can beta blockers cause insomnia or vivid dreams?
Some (like **propranolol**) cross the **blood-brain barrier**, affecting the CNS.
70
Why can beta blockers cause hypoglycemia?
They **inhibit glucose release from the liver** and **mask warning signs** of low blood sugar.
71
Why can beta blockers also cause hyperglycemia?
They can **interfere with insulin release**, raising blood sugar levels.
72
What mental or general side effects can occur?
**Depression, drowsiness, weakness, constipation, or edema.**
73
Which patients are at higher risk for side effects?
**Diabetic, asthmatic, elderly, and heart failure patients.**
74
What should nurses always check before giving a beta blocker?
**Apical pulse and blood pressure** — hold if HR < 60 bpm or BP too low.
75
What must a nurse assess before giving a beta blocker?
The **indication**, **allergies**, and history of **asthma or COPD** (risk of bronchoconstriction).
76
Why is it important to assess for respiratory disease before giving beta blockers?
**Non-selective beta blockers** can cause **bronchoconstriction** and breathing problems.
77
How long should the apical pulse be taken before giving a beta blocker?
**1 full minute**.
78
What should the nurse do if the patient’s **HR is below 60 bpm**?
**Hold the medication** and **notify the prescriber.**
79
What should the nurse do if the **systolic BP is below 90 mmHg**?
**Hold the medication** and **report** to the provider.
80
Why check HR and BP before and after administration?
To monitor for **bradycardia** and **hypotension**, which can lead to fainting or cardiac arrest.
81
Why monitor electrolytes in patients on beta blockers?
To prevent **arrhythmias** and monitor **fluid balance**, especially if taking other heart meds.
82
Why is daily weight important for patients on beta blockers?
To detect **fluid retention** — sudden weight gain may mean **worsening heart failure**.
83
How much weight gain should be reported?
**2 kg (4.4 lbs) or more** in **1–2 days.**
84
Why monitor blood glucose in diabetic patients?
Beta blockers can **mask signs of hypoglycemia** and **alter blood sugar levels.**
85
What are signs of beta blocker overdose?
**Severe bradycardia, hypotension, fainting, or heart failure.**
86
What treatments are used for beta blocker overdose?
**Atropine** (raises HR), **vasopressors**, **gastric lavage**, **pacemaker**, or **dialysis.**
87
Why should patients never stop taking beta blockers suddenly?
It can cause **rebound hypertension, chest pain, or arrhythmias.**
88
What patient teaching helps prevent dizziness and falls?
**Rise slowly** from sitting or lying positions (orthostatic precautions).
89
What should the nurse assess before giving a beta blocker?
Health history, allergies, vital signs (BP & HR), and respiratory conditions like asthma or COPD.
90
How long should you count the apical pulse before giving a beta blocker?
1 full minute.
91
When should you hold a beta blocker?
If HR < 60 bpm or systolic BP < 90 mmHg.
92
What are the main goals of beta blocker therapy?
Improve cardiac output and lower blood pressure safely.
93
Why weigh the patient daily?
To detect fluid retention or worsening heart failure early.
94
When should weight gain be reported?
If the patient gains 2 kg (4.4 lbs) or more in 1–2 days.
95
What symptoms should patients report right away?
Weakness, dizziness, bradycardia, shortness of breath, or fainting.
96
Why shouldn’t beta blockers be stopped suddenly?
Can cause rebound hypertension, angina, or heart attack.
97
What should the patient do if they miss a dose?
Skip it and take the next dose as scheduled — don’t double up.
98
Why should patients change positions slowly?
To avoid fainting (syncope) from postural hypotension.
99
Why should heat exposure (saunas, hot tubs) be avoided?
Heat causes vasodilation, which can make BP drop too low.
100
What common side effect should patients be taught about?
Constipation — encourage fluids and fiber in the diet.
101
What should the nurse monitor in diabetic patients?
Blood glucose — beta blockers can mask symptoms of hypoglycemia or cause hyperglycemia.
102
What should nurses evaluate after giving beta blockers?
BP, HR, fluid balance, glucose levels, and therapeutic response.
103
What is the main action of ACE inhibitors?
They **block the enzyme ACE**, preventing **angiotensin I from converting to angiotensin II**, which lowers blood pressure.
104
Why do ACE inhibitors cause a dry cough?
They **increase bradykinin and substance P**, which can irritate the airways.
105
How do ACE inhibitors help in heart failure?
They **reduce preload and afterload**, easing the **heart’s workload** and improving pumping efficiency.
106
What electrolyte imbalance can ACE inhibitors cause?
**Hyperkalemia** (high potassium) due to **decreased aldosterone**.
107
What are the main therapeutic effects of ACE inhibitors?
**Vasodilation**, **lower blood pressure**, and **prevention of heart remodeling**.
108
Why are ACE inhibitors used for hypertension?
They **relax blood vessels** and **reduce fluid volume**, which lowers **blood pressure** and **heart workload**.
109
Why are ACE inhibitors drugs of choice for heart failure?
They **decrease preload and afterload**, helping the **heart pump more efficiently** and **reducing fluid buildup**.
110
What does “cardioprotective effect” mean with ACE inhibitors?
They **prevent ventricular remodeling** (thickening or enlargement) after a **heart attack**, preserving heart function.
111
Why are ACE inhibitors considered renal protective?
They **reduce pressure in kidney blood vessels** and **decrease protein in urine**, helping **slow diabetic kidney damage**.
112
Why might a patient be on an ACE inhibitor even without high BP?
For **heart or kidney protection**, especially in **diabetic** or **post-MI** patients.
113
Why do ACE inhibitors cause a dry, nonproductive cough?
Because they increase bradykinin and substance P, which irritate airway receptors. The cough stops when therapy is discontinued.
114
What is the most serious first-dose side effect of ACE inhibitors?
Hypotension — a sudden drop in blood pressure after the first dose, especially in patients on diuretics or with low sodium.
115
Why is it important to monitor potassium levels in patients on ACE inhibitors?
They reduce aldosterone, causing potassium retention (hyperkalemia) — which can lead to arrhythmias.
116
What renal effects should be monitored during ACE inhibitor therapy?
Elevated creatinine, BUN, or decreased urine output — can indicate reduced kidney function or acute kidney injury.
117
What rare but life-threatening reaction can occur with ACE inhibitors?
Angioedema — severe swelling of the face, lips, or throat; requires immediate emergency care.
118
Why should ACE inhibitors never be given to patients with a history of angioedema?
They can **trigger swelling of the face, lips, tongue, or airway**, which may lead to **life-threatening anaphylaxis**.
119
Why are ACE inhibitors contraindicated in patients with high potassium levels?
They **reduce aldosterone**, which causes the body to **retain potassium**, increasing the risk of **hyperkalemia and arrhythmias**.
120
Why should ACE inhibitors be avoided in pregnancy?
They are **teratogenic** — can cause **fetal kidney damage or death**, especially in the 2nd and 3rd trimesters.
121
Why are ACE inhibitors unsafe in patients with bilateral renal artery stenosis?
They **decrease blood flow to the kidneys**, which can cause **acute kidney failure**.
122
Why might ACE inhibitors be less effective for Black patients as first-line therapy?
They are **less effective in low-renin hypertension**, which is more common in Black populations, though still useful for **heart failure** or **combined therapy**.
123
What is the main mechanism of action of ARBs?
They **block angiotensin II from binding** to its **type 1 receptors**, preventing **vasoconstriction and aldosterone release**.
124
What is the main effect of ARBs on the body?
They cause **vasodilation** and **reduce sodium + water retention**, lowering **blood pressure** and **heart workload**.
125
How do ARBs differ from ACE inhibitors?
ARBs **do not increase bradykinin**, so they **don’t cause the dry cough** seen with ACE inhibitors.
126
What conditions are ARBs used to treat?
**Hypertension, heart failure, post-MI care,** and **diabetic kidney disease** (especially when ACE inhibitors aren’t tolerated).
127
What key nursing precautions apply to ARBs?
* **Monitor BP, potassium, and renal function** * **Avoid use in pregnancy or renal artery stenosis** * **Teach patients to rise slowly and report swelling or dizziness**
128
What are the main indications for ARBs?
Used to treat **hypertension** and **heart failure**, and for **patients who cannot tolerate ACE inhibitors** (e.g., due to cough or angioedema).
129
How do ARBs help lower blood pressure?
They cause **vasodilation** by blocking angiotensin II receptors → **relax blood vessels** and **reduce afterload/workload on the heart**.
130
Why are ARBs safer for some patients than ACE inhibitors?
They **don’t affect bradykinin**, so **no dry cough** and **lower risk of angioedema**.
131
What should nurses monitor or teach with ARBs?
* **Monitor:** BP, kidney function, potassium * **Teach:** rise slowly, avoid pregnancy, report swelling or breathing issues
132
What is the main difference in how ACE inhibitors and ARBs work?
ACE inhibitors block the **conversion of angiotensin I → II**, while ARBs block **angiotensin II receptors** directly.
133
What is a common side effect of ACE inhibitors that ARBs do not cause?
A **dry, nonproductive cough** caused by buildup of **bradykinin**. *(ARBs don’t affect bradykinin, so no cough.)*
134
Which drug class is better tolerated overall — ACE inhibitors or ARBs?
**ARBs** are generally **better tolerated**, with fewer side effects and no cough.
135
What side effect do both ACE inhibitors and ARBs share?
Both can cause **hyperkalemia** and require **monitoring of potassium and kidney function**.
136
What key safety consideration applies to both ACE inhibitors and ARBs?
Both are **contraindicated in pregnancy** (teratogenic) and should be avoided in **patients with renal impairment**.
137
What are the most common side effects of ARBs?
Upper respiratory infections and headache are the most common. Other mild effects include dizziness, fatigue, and insomnia.
138
Do ARBs cause cough like ACE inhibitors?
No — ARBs do not cause cough because they don’t increase bradykinin levels.
139
What serious adverse reaction can occur with ARBs?
Angioedema — swelling of the lips, tongue, or airway (rare but potentially fatal).
140
What electrolyte imbalance can ARBs cause?
Hyperkalemia (high potassium) — less likely than with ACE inhibitors, but still possible. Monitor serum potassium levels.
141
What are the signs of ARB overdose and how are they treated?
Overdose causes hypotension and tachycardia (sometimes bradycardia). Treatment: Supportive care with IV fluids to restore blood pressure and volume.
142
What should you always check before administering an ACE inhibitor or ARB?
Check **blood pressure** and **apical pulse rate**. Hold the medication if **BP < 90 mmHg** or **HR < 60 bpm** to prevent hypotension or bradycardia.
143
What lab values should be monitored with ACE inhibitors and ARBs?
* **Renal function:** Urea, creatinine, and GFR * **Electrolytes:** Potassium (K⁺) and sodium (Na⁺) High potassium (hyperkalemia) is more common with **ACE inhibitors**.
144
What adverse effects must nurses monitor for during ACE-I or ARB therapy?
* **Angioedema:** Swelling of face, lips, or airway (medical emergency) * **Cough:** Common with ACE inhibitors * **Hyperkalemia:** Causes muscle weakness and abnormal heart rhythms
145
What medications should be avoided with ACE inhibitors and ARBs?
Avoid **NSAIDs** and **potassium supplements** or **potassium-sparing diuretics** (e.g., spironolactone). They increase the risk of **renal impairment** and **hyperkalemia**.
146
What key teaching points should you give patients on ACE inhibitors or ARBs?
* Report **swelling of tongue, lips, or face** immediately. * **Do not use salt substitutes or potassium supplements.** * **Rise slowly** to avoid dizziness from low BP. * Report persistent **dry cough** (ACE only).
147
What are Angiotensin Receptor–Neprilysin Inhibitors (ARNIs)?
A **combination drug** made of an **ARB** (angiotensin II receptor blocker) and a **neprilysin inhibitor**. Example: **Sacubitril/Valsartan (Entresto®)** — used mainly to treat **heart failure**.
148
How do ARNIs work?
* **ARB:** Blocks angiotensin II receptors → causes **vasodilation** and prevents sodium/water retention. * **Neprilysin inhibitor:** Blocks the enzyme that breaks down **natriuretic peptides**, allowing them to stay active → promotes **sodium and water excretion** and **vasodilation**.
149
What are the main therapeutic effects of ARNIs?
* Lower blood pressure * Reduce fluid overload (acts like a mild diuretic) * Decrease cardiac workload * Improve heart function and survival in **heart failure**
150
What are the main side effects of ARNIs?
* **Hypotension** (from strong vasodilation) * **Hyperkalemia** (↑ potassium) * **Kidney dysfunction** * **Angioedema** (rare but serious) ⚠️ Do **not** use with ACE inhibitors — risk of severe swelling (must wait 36 hours between).
151
What should nurses monitor and teach patients taking ARNIs?
* Check **BP and HR** before giving. * Monitor **kidney function** and **potassium** levels. * Avoid **NSAIDs** and **salt substitutes**. * Teach to **rise slowly** and report **swelling or dizziness**.
152
What is the main use of ARNIs (e.g., Sacubitril/Valsartan)?
Used to treat **Heart Failure with Reduced Ejection Fraction (HFrEF)** — helps the heart pump more efficiently, lowers BP, reduces hospitalizations, and improves survival.
153
What are the main side effects of ARNIs?
* **Hypotension** (low BP)
* **Hyperkalemia** (high potassium)
* **Renal impairment**
* **Cough** (mild)
* **Angioedema** (rare but serious)
154
Why is angioedema a serious concern with ARNIs?
It causes **swelling of the tongue, lips, or airway**, which can block breathing.
It’s more likely in patients with a **previous reaction to ACE inhibitors or ARBs**.
155
Who should NOT take ARNIs?
* Anyone **allergic** to the drug
* **Pregnant or breastfeeding** patients
* **History of angioedema** from ACE-I or ARB
* **Patients who took an ACE inhibitor within 36 hours**
* Use caution in **older adults or those with kidney dysfunction**
156
What are key nursing considerations for ARNIs?
* Monitor **BP**, **K⁺**, and **kidney function**
* **Avoid ACE inhibitors and NSAIDs**
* Teach patients to **rise slowly**, report **swelling or dizziness**, and **avoid salt substitutes**
157
How do SGLT2 inhibitors work?
They **block glucose reabsorption in the kidneys** (proximal tubule), causing **glucose and sodium to be excreted in the urine**. This leads to **lower blood sugar, mild fluid loss, and decreased blood pressure**.
158
What are SGLT2 inhibitors used for?
* **Heart failure with reduced ejection fraction (HFrEF)** * May also be used in **Type 2 diabetes** They help by **reducing fluid overload**, **decreasing hospitalizations**, and **lowering cardiovascular mortality**.
159
When should SGLT2 inhibitors be avoided?
* **Severe renal impairment** (eGFR < 25) * **Hepatic dysfunction** * **Allergy or intolerance** If kidneys can’t filter well, the drug won’t work effectively and may cause harm.
160
What medications can interact with SGLT2 inhibitors?
**Diuretics** (like **Furosemide/Lasix** or **Hydrochlorothiazide**) — Both cause fluid loss, which can lead to **hypovolemia**, **low BP**, and **dehydration** when combined.
161
What should nurses monitor and teach patients taking SGLT2 inhibitors?
* Check **BP**, **eGFR**, and **electrolytes** regularly. * Watch for **dehydration** and **dizziness**. * Encourage **hydration** and teach to report low urine output or extreme fatigue. * Warn about **increased urination** and possible **yeast infections** (from sugar in urine).
162
What should you always check before giving an ARNI or SGLT2 inhibitor?
Check **blood pressure** and **apical pulse** — hold if BP is too low or pulse is irregular (risk of hypotension).
163
What signs should you assess for in a patient taking these meds?
Look for **heart failure symptoms** — chest pain, fatigue, crackles, ankle swelling, and shortness of breath.
164
How can you tell if the patient is retaining fluid?
Weigh daily — report if they gain **2 kg (4.4 lbs)** in 1–2 days. **Also:** Track intake & output — SGLT2 inhibitors cause increased urination.
165
What labs are important to monitor?
* **Kidneys:** Creatinine, BUN, GFR * **Electrolytes:** Potassium (K⁺) → ARNIs can raise potassium → risk for **arrhythmias**.
166
What are signs of high potassium (hyperkalemia)?
Use **MURDER**: Muscle weakness, Urine changes, Respiratory distress, Decreased heart strength, ECG changes, Reflex changes.
167
What are the main nursing priorities for ARNIs and SGLT2 inhibitors?
Monitor **BP, heart rhythm, fluid balance, kidney function, and potassium levels**. → Watch for **low BP, dehydration, and high K⁺**.
168
How do calcium channel blockers (CCBs) work?
They **block calcium channels** in the heart and blood vessel muscles, preventing calcium from entering → **muscle relaxation** and **artery dilation**.
169
How do CCBs help the heart?
They **relax coronary arteries**, increasing blood flow to the heart muscle and relieving **angina (chest pain)**.
170
What happens to blood pressure when a patient takes CCBs?
Arteries **dilate**, reducing **systemic vascular resistance** and **blood pressure**. (They **do not** dilate veins.)
171
Why are CCBs used for hypertension and angina?
Because they **reduce afterload** (resistance against which the heart pumps) and **increase oxygen to the heart**.
172
What’s one key thing CCBs *don’t* do?
They **do not dilate veins** — only arteries.
173
How do calcium channel blockers (CCBs) work?
They **block calcium channels** in heart and arterial smooth muscle → prevents contraction → causes **artery dilation** and **decreased blood pressure**.
174
What effect do CCBs have on the heart?
They **decrease heart rate**, **contractility**, and **workload** → making the heart use less oxygen.
175
How do CCBs lower blood pressure?
They **relax and widen arteries** (vasodilation), reducing **systemic vascular resistance (SVR)** → **lower BP**. *(They do not dilate veins.)*
176
What are CCBs used to treat?
* **Hypertension** * **Angina (chest pain)** * **Some arrhythmias (e.g., atrial fibrillation)**
177
When should CCBs be avoided?
Avoid in **acute or decompensated heart failure** because they reduce heart contractility.
178
Why are CCBs preferred in some patients?
* **More effective in Black patients and older adults.** * **Safer in respiratory diseases** (do not cause bronchoconstriction like beta blockers).
179
What should nurses monitor with CCBs?
* **BP** and **apical pulse** before giving (hold if HR < 60 bpm). * Watch for **dizziness, edema, bradycardia, and hypotension.** * Avoid **grapefruit juice** (increases toxicity risk).
180
What should you assess before giving a calcium channel blocker?
* Blood pressure and apical pulse (hold if HR < 60 bpm or SBP < 90 mmHg)
* Heart rhythm and rate
* Medication history (esp. beta blockers or digoxin)
* Indication for use (angina, hypertension, arrhythmia)
181
What signs of heart failure should you monitor for when giving a CCB?
* Daily weight and intake/output
* Crackles in lungs, shortness of breath, or hypoxia
* Peripheral edema and weak pulses
* Fatigue or poor tissue perfusion
💡 *CCBs can weaken heart contractions → may worsen HF.*
182
What are key nursing actions related to blood pressure and pulse?
* Monitor for hypotension and bradycardia
* Goal BP: < 140/90 mmHg (or < 130/80 mmHg with diabetes/renal disease)
* Never double up missed doses or stop abruptly (can cause rebound hypertension or angina)
183
Which labs should be monitored with CCBs?
* Electrolytes (especially calcium, potassium, magnesium)
* Renal function (BUN, creatinine, GFR)
💡 *Better perfusion at night may cause patients to urinate more.*
184
What patient teaching is important for calcium channel blockers?
* Change positions slowly (orthostatic hypotension)
* Avoid grapefruit juice (increases toxicity risk)
* Weigh daily for fluid retention
* Know target BP and when to call HCP
185
Why might CCBs be a preferred choice for some patients?
* Effective in Black patients and older adults
* Safer for patients with respiratory conditions (no bronchoconstriction)
* Used to prevent angina attacks by lowering heart workload
186
How do diuretics work?
They act in the **kidneys** to block the reabsorption of **sodium and water**, causing more urine to be produced. 💡 *Water follows sodium — less fluid in the bloodstream = lower BP and heart workload.*
187
What is the main goal of diuretics?
To **promote urine formation** and **remove excess fluid** from the body. This reduces **blood pressure**, **swelling (edema)**, and **heart workload**.
188
What conditions are diuretics used for?
* **Hypertension** (first-line for mild–moderate) * **Heart failure** (relieves fluid overload) * **Liver or kidney disease** (controls edema) * **High intracranial or intraocular pressure**
189
What are the advantages of diuretics?
* **Low cost** * **Safe and effective** * Can be used **alone or with other antihypertensives**
190
What are common side effects or risks of diuretics?
* **Dehydration** * **Electrolyte loss** (esp. potassium & sodium) * **Low blood pressure** 💡 *Monitor electrolytes, weight, and urine output closely.*
191
What should nurses teach patients taking diuretics?
* Take in the **morning** (avoid nighttime urination) * **Stand up slowly** to prevent dizziness * **Monitor daily weight** — sudden gain = fluid retention * **Eat potassium-rich foods** (bananas, oranges, spinach) unless on a potassium-sparing diuretic
192
Loop Diuretics (e.g., Furosemide / Lasix®)
They block sodium, chloride, and water reabsorption in the **Loop of Henle**, causing **strong, rapid fluid loss**.
193
Key nursing points for Loop Diuretics
* Monitor **K⁺** (risk of hypokalemia) * Track **I&O, daily weights, and BP** * Give in the **morning** * Causes **potent diuresis** used for heart failure and edema
194
Osmotic Diuretics (e.g., Mannitol)
They pull **water into renal tubules** from the bloodstream, increasing urine output and reducing pressure.
195
Uses of Osmotic Diuretics
* **High intracranial pressure (ICP)** * **High intraocular pressure (IOP)** * **Early renal failure protection**
196
Nursing points for Osmotic Diuretics
* **Monitor for dehydration** * **Not used for heart failure** (can worsen fluid overload before it helps)
197
Potassium-Sparing Diuretics (e.g., Spironolactone / Aldactone®)
They block **aldosterone** in the distal tubule, **holding potassium** but removing sodium and water.
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Key risks of Potassium-Sparing Diuretics
* **Hyperkalemia** (high potassium) * **Gynecomastia** in men
199
Nursing notes for Potassium-Sparing Diuretics
* **Avoid K⁺ supplements or salt substitutes** * Often used **with loop or thiazide diuretics** to balance potassium
200
Thiazide Diuretics (e.g., Hydrochlorothiazide / HCTZ / Microzide®)
They are **first-line drugs for hypertension** and used for mild heart failure-related edema.
201
How Thiazide Diuretics work
Block sodium and water reabsorption in the **distal tubule**, causing **moderate fluid loss**.
202
Key side effects of Thiazide Diuretics
* **Hypokalemia**, **hyponatremia**, dehydration * May increase **blood sugar** and **uric acid**
203
Carbonic Anhydrase Inhibitors (e.g., Acetazolamide)
Reduce reabsorption of sodium, water, and bicarbonate in the **proximal tubule**, causing mild diuresis and **metabolic acidosis**.
204
Uses of Carbonic Anhydrase Inhibitors
* **Glaucoma** * **Altitude sickness** * **Refractory edema**
205
Nursing considerations for Carbonic Anhydrase Inhibitors
* Monitor **electrolytes and pH** (risk for metabolic acidosis) * Rarely used for blood pressure
206
What is the most *prominent* group of adverse effects caused by furosemide?
**Fluid and electrolyte imbalances** — especially **hypokalemia, hyponatremia, hypochloremia, and hypomagnesemia** due to increased excretion through the kidneys.
207
What are signs and dangers of **hypokalemia** from furosemide?
**Muscle weakness, fatigue, and irregular heartbeat (arrhythmias)**. Low potassium can increase the risk of **cardiac complications**, so electrolytes must be monitored closely.
208
What causes **tinnitus or ototoxicity** with furosemide, and how can it be prevented?
Rapid or high-dose **IV administration** can damage the inner ear. To prevent it, **infuse the drug slowly** and monitor for **ringing in the ears (tinnitus)** — the **first warning sign**. Stop the infusion and notify the provider if it occurs.
209
What cardiovascular effects can result from excessive fluid loss with furosemide?
**Hypotension and dehydration**, which can cause **dizziness, fainting, and weakness**. Monitor **blood pressure, daily weights, and I&O** regularly.
210
How is **toxicity from furosemide** treated?
Treat with **fluid and electrolyte replacement therapy** — such as IV fluids, potassium, or magnesium supplements — as prescribed by the provider.
211
Why are these drugs called *potassium-sparing diuretics*?
Because they **remove sodium and water** from the body while **retaining potassium** — preventing **hypokalemia**.
212
What is the main *mechanism of action* of potassium-sparing diuretics?
They **block aldosterone** in the distal nephron, stopping sodium reabsorption and potassium excretion — leading to **increased urine output** without potassium loss.
213
What are the **main medications** in the potassium-sparing diuretic class?
**Spironolactone (Aldactone®)**, **Eplerenone (Inspra®)**, **Amiloride**, and **Triamterene** (often combined with HCTZ).
214
What is the **major adverse effect** of potassium-sparing diuretics?
**Hyperkalemia (high potassium)** — which can cause **muscle weakness, slow heart rate, and dangerous cardiac arrhythmias**.
215
What are key **nursing considerations** when giving potassium-sparing diuretics?
* Monitor **serum potassium** closely.
* Avoid **potassium supplements or salt substitutes**.
* Use caution with **ACE inhibitors or ARBs** (they also increase K⁺).
* Teach the patient to report **irregular heartbeat, weakness, or tingling** (signs of hyperkalemia).
216
Where in the nephron do potassium-sparing diuretics act?
They act in the **distal convoluted tubule** and **collecting duct** of the kidney — the last part of the nephron where fine-tuning of electrolytes occurs.
217
What is the **mechanism of action (MOA)** of potassium-sparing diuretics?
They **block aldosterone receptors**, preventing sodium and water reabsorption and **reducing potassium excretion**. This helps the body **excrete Na⁺ and water while conserving K⁺**.
218
Why are potassium-sparing diuretics considered **“weak” diuretics**?
Because most sodium reabsorption happens earlier in the nephron — by the time filtrate reaches their site of action, there’s **less sodium left to remove**, making their diuretic effect mild.
219
What are the **main therapeutic effects** of potassium-sparing diuretics?
They provide **mild diuretic and antihypertensive effects**, **increase survival in severe heart failure**, and **prevent potassium loss** (hypokalemia).
220
What is the **major risk** associated with potassium-sparing diuretics?
**Hyperkalemia (high potassium)** — can cause **muscle weakness, bradycardia, and cardiac arrhythmias**, especially if combined with ACE inhibitors or ARBs.
221
What are the main indications for potassium-sparing diuretics?
They’re used for heart failure, hypertension, hyperaldosteronism, and to reverse potassium loss caused by other diuretics (like loop or thiazide diuretics).
222
How do potassium-sparing diuretics help in heart failure?
They block aldosterone, reducing sodium and water retention, easing the heart’s workload, and increasing survival in severe heart failure.
223
What are the major contraindications for potassium-sparing diuretics?
* Hyperkalemia (already high potassium) * Severe kidney failure (can’t excrete potassium) * Anuria (no urine output) * Pregnancy or breastfeeding * Known drug allergy
224
Why is severe kidney failure an absolute contraindication for potassium-sparing diuretics?
Because poor kidney function prevents potassium excretion, leading to dangerous hyperkalemia and cardiac arrhythmias. Always check renal labs (BUN, creatinine, K⁺) before giving.
225
What are key nursing considerations for patients taking potassium-sparing diuretics?
* Monitor serum potassium and renal function. * Report if the patient isn’t urinating (anuria). * Avoid potassium supplements or salt substitutes. * Watch for signs of hyperkalemia: muscle weakness, bradycardia, irregular heartbeat.
226
Why does spironolactone (Aldactone®) cause hormonal side effects?
Because it not only blocks **aldosterone** but also **interferes with sex hormones** — it blocks testosterone and can slightly increase estrogen effects, leading to hormonal imbalances.
227
What is **gynecomastia**, and why can spironolactone cause it?
Gynecomastia is **enlargement of breast tissue in males**, caused by spironolactone’s **anti-androgenic (testosterone-blocking)** effect and mild **estrogen stimulation**.
228
How does spironolactone cause **amenorrhea** or **irregular menses** in women?
By **altering the balance of estrogen and testosterone**, it disrupts normal hormone cycles, leading to **missed or irregular periods**.
229
What is **postmenopausal bleeding**, and why might it occur with spironolactone?
It’s **unexpected vaginal bleeding after menopause**, caused by **hormonal stimulation of the uterine lining** from spironolactone’s endocrine effects.
230
What should the nurse teach patients about these hormonal side effects?
They are usually **reversible** when the drug is stopped. Teach patients to **report breast changes or menstrual irregularities**, and note that **eplerenone (Inspra®)** can be used instead if symptoms are distressing.
231
Hydrochlorothiazide (HCTZ)
one of the most frequently prescribed diuretics, mainly used to treat hypertension and mild fluid retention (edema).
232
Where do thiazide diuretics act in the nephron, and what do they block?
They act in the distal convoluted tubule, where they block sodium and chloride reabsorption, leading to increased excretion of sodium, chloride, and water.
233
What is the main effect of thiazide diuretics on blood pressure and electrolytes?
They lower blood pressure by reducing fluid volume but also cause potassium loss (hypokalemia) due to increased urinary potassium excretion.
234
What are examples of thiazide-like diuretics, and how do they differ from HCTZ?
Metolazone (Zaroxolyn®), Chlorthalidone, and Indapamide — they act similarly to thiazides but may have longer duration or be used in resistant cases (e.g., combined with loop diuretics).
235
What are key nursing considerations for patients taking thiazide diuretics?
* Monitor serum potassium and electrolytes.
* Watch for signs of dehydration (dry mouth, low urine output, dizziness).
* Encourage potassium-rich foods (bananas, oranges, potatoes).
* Assess blood pressure and daily weights to monitor fluid balance.
236
mechanism of action (MOA)
They act in the distal convoluted tubule to inhibit sodium and chloride reabsorption, causing increased excretion of sodium, chloride, water, and a small amount of potassium.
237
therapeutic effects
They reduce blood pressure in hypertensive patients and decrease edema by promoting mild, steady diuresis.
238
onset, peak, and duration
* Onset: 2 hours
* Peak: 3–6 hours
* Duration: 6–12 hours
💡 *This makes them ideal for long-term BP control, not emergencies.*
239
comparison to loop diuretics
They are similar but milder — both cause sodium and water loss, but thiazides act later in the nephron, have a slower onset, longer duration, and cause less potassium loss than loop diuretics.
240
nursing considerations
* Monitor potassium and sodium levels.
* Watch for signs of dehydration or hypokalemia.
* Encourage potassium-rich foods (bananas, oranges).
* Assess BP and daily weights to monitor fluid status.
241
What are the main indications for thiazide and thiazide-like diuretics?
* Hypertension (first-line treatment) * Mild to moderate edema due to heart failure, renal dysfunction, cirrhosis, steroid therapy, or estrogen therapy 💡 *These drugs are used for gentle, long-term fluid and blood pressure control.*
242
Why must a patient be urinating for thiazide diuretics to work?
Thiazides act in the distal convoluted tubule and are excreted through the kidneys. If there’s no urine output (anuria), the drug can’t reach its site of action and will be ineffective or unsafe. 💡 *If they’re not peeing, don’t give it!*
243
What are the main contraindications for thiazide and thiazide-like diuretics?
* Anuria (no urine output) * Severe kidney failure * Drug allergy (especially sulfa allergy) * Hepatic coma (esp. with metolazone) * Pregnancy or breastfeeding
244
How do thiazide diuretics help patients with hypertension and heart failure?
* Reduce blood pressure by lowering circulating fluid volume. * Reduce edema and cardiac workload in heart failure by promoting mild diuresis. 💡 *They “lighten the load” on the heart.*
245
What are key nursing considerations when giving thiazide diuretics?
* Monitor urine output, electrolytes (K⁺, Na⁺), and renal labs (BUN, creatinine). * Watch for dehydration or hypokalemia. * Encourage potassium-rich foods unless contraindicated. * Teach the patient to report muscle cramps, dizziness, or low urine output.
246
What pump does digoxin inhibit, and what is the result?
Digoxin inhibits the sodium-potassium ATPase pump, leading to increased intracellular sodium and decreased sodium-calcium exchange, causing calcium buildup inside cardiac cells.
247
How does increased intracellular calcium affect the heart?
It strengthens cardiac muscle contraction (positive inotropic effect), making each heartbeat more forceful and efficient.
248
How does digoxin affect heart rate and electrical conduction?
It slows conduction through the SA and AV nodes, producing a negative chronotropic effect (↓ heart rate), allowing more time for diastolic filling.
249
What are the main hemodynamic benefits of digoxin?
* ↑ Cardiac output (stronger pumping) * ↑ Diastolic filling time * ↓ Heart rate and workload * ↑ Overall cardiac efficiency 💡 *The heart beats slower but stronger.*
250
What are the main clinical uses of digoxin?
* Heart failure: improves contractility and output * Atrial fibrillation: controls ventricular rate by slowing conduction through the AV node 💡 *Used for hearts that need “stronger squeeze and slower rhythm.”*
251
How does digoxin affect stroke volume and heart size?
It **increases stroke volume** (more blood per beat) and **reduces heart size during diastole**, as the heart becomes stronger and more efficient at rest.
252
How does digoxin reduce venous pressure and congestion?
By improving cardiac output, it **decreases venous blood pressure** and **relieves vein engorgement**, reducing symptoms like **peripheral edema and jugular distention**.
253
What effect does digoxin have on coronary circulation?
It **increases coronary blood flow**, improving oxygen delivery to the myocardium and supporting stronger contractions.
254
What respiratory symptoms can improve with digoxin therapy?
It reduces **dyspnea, nocturnal cough, and cyanosis** by decreasing pulmonary congestion and improving oxygenation.
255
What are the overall benefits of digoxin therapy in heart failure?
* Promotes **tissue perfusion and diuresis** * Improves **exercise tolerance** and **quality of life** * Controls **symptoms** effectively ⚠️ *However, it does not reduce overall mortality.*
Pharm Lecture
flashcards
Decks in class (17)
# Cards
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Unit 1 (part 1)200
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Unit 2: Drugs Affecting The Autonomic NS278
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Unit 3: coagulation modifiers and anemia medications220
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Unit 3: coagulation modifiers and anemia medications163
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Unit 3: drugs for anemia75
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Lecture 4231
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Lecture 5: Drugs affecting the respiratory system245
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Lecture 6: Drugs Affecting GI131
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Lecture 7255
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Lecture 8184
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Lecture 9380
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Lecture 9 (Pt. 2)122
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Lecture 10225
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Lecture 10 pt. 2121
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Lecture 11168
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Lecture 11 (part 2)132
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Unit 12146
