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exam 2 Flashcards

1
Q

Increase the amount of urine produced
Increase sodium excretion
-prevent cells lining the renal tubule from reabsorbing sodium in the filtrate
-sodium, other ions, and water are lost in the urine
-those that block the most sodium work the best
Used for
heart failure, pulmonary edema, hypertension, renal disease, liver disease, hyperkalemia, glaucoma

A

Diuretics

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2
Q

Types of Diuretics

A 
Thiazide
Loop
Potassium sparing
Carbonic anhydrase inhibitors
osmotic
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3
Q

ii. Hydrochlorothiazide (Hydrodiuril) (HCTZ) - can be used in children
iii. Chlorothiazide (Diuril) - IV route for pts with pulmonary edema
iv. Indapamide (Lozol) - edema with HF, liver/renal failure, often combo with antihypertensives (Lisinopril/HCTZ) Produces 10-20 mmHg drop in BP

A

Thiazide Diuretics

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4
Q

Block the chloride pump in the early distal tubule
-sodium passively moves with chloride to maintain electrical neutrality
-keeps chloride and sodium in the filtrate
This segment of the tubule is impermeable to water and 90% of sodium is already reabsorbed
a. So there’s not a lot of sodium and water to get rid of at the end and that’s why it’s a mild diuretic
-little increase in the volume of urine produced
-mild diuretic when compared to others
Ability to produce diuresis diminishes with reduced blood flow through the kidney
-Diminished blood flow to the kidneys makes it not work as well
–Lasix or loop diuretic and every measures against it

A

MOA of thiazide diuretics

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5
Q

I. Hypotension – because they’re losing sodium and water

ii. Hypokalemia - weakness, muscle cramps, arrhythmias
iii. Hypercalcemia - fatigue, confusion, weakness, N&V
iv. Increased uric acid levels - interferes with secretory mechanism
- Worried for patients with gout
v. Hyperglycemia - hypokalemia reduces insulin secretion
- If hyperkalemic and could have slightly elevated BS and worried about that in patients with diabetes

A

Adverse effects of thiazide diuretics

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6
Q

i. Fluid and electrolyte imbalances
- Check potassium levels before administering a diuretic
ii. Severe renal disease
- Kick kidney and make them work a little better
- - Thiazidide less kick
iii. Systemic lupus erythematosus
- renal failure (degeneration), and adding something that adds a kick sends them to renal failure
iv. Diabetes mellitus
v. Gout
vi. Hyperparathyroidism
- Controls calcium levels in our body and hyperparathyroidism

A

cautions with thiazide diuretics

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7
Q

I. Digoxin toxicity may occur due to hypokalemia

  • -Digoxin helps with heart failure and helps heat beat harder/faster to help with heart failure
  • digoxin binds at the same place as potassium within the NA/K ATPase pump
  • requires close potassium monitoring
    ii. Decreased effectiveness of antidiabetic agents
  • dose adjustments may be needed due to increase in BS
    iii. Lithium toxicity
  • lithium chemically is similar to sodium
  • body saves lithium from the filtrate
A

interactions for thiazide diuretics

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8
Q

i. Work in the loop of Henle: which is where they get their name
ii. Also known as high-ceiling diuretics because they cause a greater degree of diuresis – so they pee a lot

A

loop diuretics

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9
Q

Furosemide (Lasix) - ped dosing
- IV of this onset is 5 mins
Bumetanide (Bumex) - 40X more potent than Lasix, shorter 1/2 life
Toresmide (demadex) - 2X as strong as Lasix, longer 1/2 life, once/day dose, less ototoxicity

A

types of loop diuretics

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10
Q

I. Block the chloride pump in the ascending loop of Henle where 30% of the filtered sodium is reabsorbed

  • results in copious amounts of sodium rich urine
  • -lots of urine coming out and all that fluid coming out makes blood slightly hypotonic. When blood travels to lungs, the hypotonic blood will help pull fluid out of the lungs and goes out of the kidneys and repeats
  • hypertonic intravascular fluid pulls fluid out of the interstitial space and delivers it back to the kidney
  • Only have an effect on blood that reaches the nephron
    ii. Inhibits symporter membrane protein, to block reabsorption of sodium and chloride
  • this action also blocks potassium reabsorption
A

MOA of loops diuretics

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11
Q

I. Dehydration - dry mouth, weight loss, headache

ii. Hypotension - dizziness, fainting
iii. Hypokalemia - weakness, muscle cramps, arrhythmias
iv. Hypocalcemia - weakness, muscle cramps, numbness and tingling of hands, feet, perioral, seizures
v. Hyperglycemia - hypokalemia reduces insulin secretion
vi. Increased uric acid levels -interferes with secretory mechanism
vii. Ototoxicity
- Effects nerves that come out of ear
- usually reversible
- occurs in high doses: infusion of 160 mg of Lasix and call you saying their ear is ringing

A

ADE of loop diuretics

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12
Q

I. Fluid and electrolyte imbalances

ii. Severe renal disease
- Does a big kick to the kidneys
iii. Systemic lupus erythematosus
- renal failure
iv. Diabetes mellitus
v. Gout

A

cautions of loop diuretic

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13
Q

I. Aminoglycosides (antibiotics) or cisplatin (anti-neoplastic)

  • Combined together and increased risk of ototoxicity
    ii. Anticoagulants
  • increased effects
    iii. NSAIDs
  • decreased loss of sodium & antihypertensive effects
    iv. Digoxin
    v. Lithium
A

interactions for loop diuretic

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14
Q

I. Not as powerful as loop diuretics

ii. Benefit is they retain potassium instead of wasting
- used for those clients at high risk of hypokalemia
- -maybe on lasiks and can’t get potassium down so give this drug

A

potassium sparing diuretics

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15
Q

iii. Spironolactone (Aldactone) prototype
- pediatric dosing with careful monitoring
iv. Amiloride (Midamor)
v. Triamterene (Dyrenium)
- Only available PO

A

types of potassium sparing diuretics

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16
Q

I. Spironolactone is a aldosterone antagonist

  • Aldosterone, found in adrenal gland, and helps to save sodium & water and excrete hydrogen and potassium
  • drug of choice for hyperaldosteronism
    ii. Others block sodium channels causing sodium to stay in the filtrate.
  • potassium is not excreted
    iii. Work in the late distal tubule & collecting ducts
    iv. Used as an adjunct with thiazide or loop diuretics
  • especially those at high risk of hypokalemia
  • digoxin, antiarrhythmics
A

MOA of potassium sparing

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17
Q

I. Hyperkalemia - lethargy, muscle cramps, arrhythmias

  • Check potassium levels before giving **
    ii. Binds to progesterone and androgen receptors
  • men - gynecomastia, impotence, diminished libido
  • women - menstrual irregularities, hirsutism, breast tenderness
A

AE of potassium sparing meds

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18
Q

I. Hyperkalemia

ii. Severe renal disease and anuria
iii. Pregnancy
- cause teratogenic effects in animals
- category D

A

cautions in potassium sparing

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19
Q

i. Diuretic effects is decreased if combined with salicylates (like asprin)
ii. Watch for hyperkalemia with ACE inhibitors

A

interactions with potassium sparing

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20
Q
  1. Block the effects of carbonic anhydrase enzyme in the proximal tubule
    - - Catalyst for sodium bicarb
    - - Sodium bicarb is a base in our body
    - carbonic anhydrase is the catalyst for sodium bicarbonate formation
    - prevents bicarbonate formation and reabsorption in the renal tubule
    - without bicarbonate sodium reabsorption does not occur
  2. Mild diuretic
    - adjunct to other diuretics when a more intense diuresis is needed
  3. Glaucoma, mountain sickness
    - Because it reduces the amount of fluid in the eye
    - Mountain sickness: reduce amount of sodium bicarb were making (base), body compensates by breathing harder to keep pH normal and helps us to breath better
  4. They work early in the process
A

carbonic anhydrase inhibitors

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21
Q

acetazolamide (Diamox)

Methazolamide (Zeptazane)

A

carbonic anhydrase inhibitors diuretics

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22
Q
  1. Metabolic acidosis
    - loss of bicarbonate
  2. Hypokalemia
    - potassium is lost in an attempt to retain sodium
  3. Monitor those on lithium
    - increased excretion
  4. Use with caution
    - fluid & electrolyte imbalance
    - renal or hepatic disease
    - adrenocortical insufficiency
    - respiratory acidosis
A

cautions with carbonic anhydrase inhibitors diuretics

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23
Q
  1. Pull water into the renal tubule without sodium loss
    - osmotic pull
    - large amounts of urine produced
    - work outside of the kidney, works in the brain
    - used to reduce intraocular pressure and increased ICP
A

osmotic diuretics

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24
Q

mannitol (osmitrol) - IV only: used in glaucoma to increase ICP, works early in process

A

osmotic diuretics

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25
Q
  1. Monitor client for sudden drop in fluid levels
    - N&V, hypotension, confusion, headache, cardiac decompensation, shock
    - continual monitoring
    - - CPV line, constant BP monitoring, telemetry

Contraindicated

  • rogressive renal disease, pulmonary congestion, intracranial bleeding, dehydration, HF
  • can exacerbate due to large fluid shifts
  • all this because it has a potential for a large fluid shift
A

cautions and contraindications

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26
Q

a. Monitor
- edema
- heart and lung sounds
- blood pressure and pulse before we give
- daily weight – same time, clothes and scale
- electrolytes
b. Administer early in the day
c. Ensure access to bathroom after administration
d. Provide potassium rich or low-potassium foods, potassium supplements may be needed
e. Provide fluids to prevent fluid rebound
f. Give with food if GI upset occurs
I. Also helps with compliance
g. Educate on importance of compliance

A

nursing considerations for diuretics

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27
Q
  1. Vessel spasm and constriction
    - – Collagen is exposed to air and makes the platelets become stick and adhere together and make plug. They make ADP and attracts other platelets and forms a weak plug that can be moved easily (not a blood clot)
    - – The same collagen makes a cascade
  2. Platelets become sticky and adhere together and to the damaged vessel
    - release adenosine diphosphate (ADP) which attracts other platelets
    - forms a weak plug
  3. When collagen is exposed the coagulation cascade is started
A

clotting process

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28
Q

I. Coagulation occurs when fibrin threads create a meshwork that traps blood constituents

ii. Two pathways
- intrinsic pathway is activated in response to the vessel injury inside the vessel
- extrinsic pathway is activated when blood enters tissue spaces
- - blood leaks on outside of the vessel
- inactive plasma proteins are converted to active forms
- formation of fibrin clot
iii. Intrinsic
- Hageman (XII) factor is activated by exposure to collagen
- - And starts extrinsic pathway
iv. Extrinsic
- release of tissue thromboplastin
- - intrinsic and extrinsic start the pathway of cascade
v. Start a number of reactions in the clotting cascade
vi. Last step - prothrombin activator converts clotting factor prothrombin to an enzyme thrombin
vii. Thrombin converts fibrinogen to long strands of fibrin
- clotting occurs in approximately 6 minutes
- - fibrin creates mesh work
viii. Several clotting factors including fibrinogen are proteins made by the liver
- vitamin K is required for production
- clients with serious hepatic impairment usually have abnormal coagulation

A

coagulation cascade

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29
Q

I. Clot removal

  • initiated 24 to 48 hours of clot formation, continues until clot is dissolved
    ii. Vessels near a fibrin clot secrete tissue plasminogen activator (TPA)
  • TPA converts inactive plasminogen, present in the clot, to active plasmin
  • plasmin digests fibrin strands
A

fibrinolysis

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30
Q

I. Thromboembolic - formation of thrombi

  • decreased blood flow through a vessel
  • results in tissue hypoxia, anoxia, and necrosis
  • damage to endothelial lining
  • CAD
    ii. Hemorrhagic - excess bleeding
  • less common
  • lack of clotting factors or platelets
  • hemophilia, liver disease, bone marrow failure
A

disorders affecting coagulation - not that significant

31
Q

I. Interfere with platelet aggregation

  • most work by blocking receptor sites on platelet membranes
  • Used to prevent clot formation in arteries
    • Anticoag: vessels or veins
    • Antiplatelet: arteries – like MI
  • MI, stroke, maintenance of AV grafts
A

antiplatelet agents

32
Q 
Aspirin 
Clopidogrel (Plavix)
ticlopidine (ticlid)
ticagrelor (brilinta)
Abcixmab (ReoPro)/Eptifibatide (integrilin) = IV
A

types of antiplatelet agents

33
Q

I. Bind irreversibly to the enzyme cyclooxygenase (COX) in platelets, this inhibits thromboxane A2 which is a powerful inducer of platelet aggregation
ii. Anticoagulant effect after a single dose can last up to a week
- discontinue 5-10 days before surgery
iii. Should only be used with other coagulation modifiers with physician approval
-Patient on coumadin: can’t take aspirin (NSAID) for headache
Side effects:
Gi upset, GI bleeding, tinnitus, dizziness

A

aspirin - blocks cox

34
Q

I. ADP receptor blocker
- irreversibly alters the plasma membrane of platelets, unable to receive chemical signals to aggregate
- discontinue 5 days before surgery
ii. Given orally for recent thromboembolic event such as stroke or MI
- can also be used to prevent clots following PCI (percutaneous coronary intervention)
iii. Similar efficiency as aspirin but more expensive
iv. Mainly used for those that cannot tolerate aspirin because of GI bleeding is lessened
Cautions
I. Bleeding disorder and recent surgery
ii. Closed head injuries
iii. Anagrelide (Agrylin) blocks platelet production at the bone marrow
- monitor for thrombocytopenia because it can cause them to not have enough platelets at all

A

Clopidogrel (Plavis)

35
Q

Adverse Effects
I. Bleeding: bruising, bleeding gums, black, tarry stools, change in LOC, abdominal pain
ii. Headache
iii. Dizziness
iv. Weakness
1-All 3 of those are also signs of bleeding
2.-All signs of hypertension

Nursing Considerations
I. Small, frequent meals to relieve GI upset*
ii. Bleeding precautions: soft toothbrush, electric razor, avoid contact sports, monitor for occult blood loss, avoid IM injections. care with fragile skin
iii. Monitor blood pressure and CBC for signs of bleeding
iv. Encourage a medical alert bracelet

A

Clopidogrel (Plavis) 2

36
Q

i. Interfere with the normal coagulation process by interfering with the clotting cascade and thrombin formation
ii. Heparin
iii. Warfarin (Coumadin)
iv. Enoxaparin (Lovenox)
v. Rivaroxaban (Xarelto)
vi. Dabigatran (Pradaxa)
vii. Apixaban (Eliquis)

A

anticoagulants

37
Q

I. Natural substance found in liver and lining of blood vessel

ii. Enhances the action of antithrombin III, protein that inactivates thrombin
- -Thrombin is the very last step – so if it is inactivated you can’t make fibrin
- prevents enlargement of existing clots and formation of new clots
- it does not dissolve existing clots
iii. Poorly absorbed by the GI tract so has to be IV or subq
- IV administration has immediate onset
- subq takes an hour
iv. IV is given by a weight-based nomogram
- weight, aPTT value, clinical indication every day
v. Normal activated partial thromboplastin time (aPTT) is 25-35 seconds
- therapeutic is 1.5-2 times greater than pretreatment (60-75ish is where we want to be)
- 90-100 is high and need to be worried about spontaneous bleeding
vi. During IV therapy an aPTT is drawn 1 time per day and every 6-8 hours after dose changes
vii. Stopping an infusion results in diminished action within hours
- Keep on bedrest because if they fall and hit their head they will bleed a lot into the brain
- discontinue 6-12 hours before surgery
- dosed 2 times a day, in the morning and night

A

Heparin

38
Q

I. Inhibits vitamin K and the hepatic synthesis of Factors II, VII, IX, X

    • Fairly hard to control and that’s why they come in so often to get an INR test because it’s not super stable
      ii. Used to maintain anticoagulation
  • afib, heart valves, venous thrombosis
    iii. Those on heparin are often switched to oral warfarin when stabilized
  • during transition the two drugs can be given concurrently for several days
  • warfarin onset is 3 days and last 4-5 days
    • because it takes 3 days to kick in, heparin can be given together. If you don’t, you will lose the therapeutic level
    • hep and lovenox can’t overlap
  • -hep and coumadin can overlap
    3. discontinue 4-5 days before surgery
  • Therapeutic INR levels are 2-3
A

Warfarin (Coumadin)

vitamin k is antidote

39
Q

I. Low molecular weight heparin

  • shortened, modified heparin molecules
  • inhibit Factor X
    ii. Advantages
  • duration is 2 to 4 times longer
  • -so usually once a day dosing for 7 days
  • produces a more stable response
  • can be given at home
  • -drug of choice for DVT prophylaxis
  • less likely to cause thrombocytopenia
    iii. Drug of choice for DVT prophylaxis following surgery
  • usually 1 time per day for 7-10 days
  • Other Anticoagulants
A

Enoxaparin (lovenox)

40
Q

I. Rivaroxaban (Xarelto), apixaban (Eliquis) super expensive

  • inhibit Factor Xa (a means it has been activated)
  • prophylaxis of DVT with knee or hip surgery, reduce risk of embolism due to afib
    ii. Dabigatran (Pradaxa)
  • inhibits thrombin (last step to create fibrin)
  • reduce risk of embolism due to afib

iii .As effective as warfarin

iv. No laboratory monitoring
v. Less drug interactions
vi. No food restrictions
vii. Expensive

A

other anticoagulants

41
Q

Cautions
I. Conditions with increased bleeding potential: trauma, spinal tap, GI bleed, surgery
ii. Warfarin is category X (will cause fetal demise)
iii. Warfarin has lots of drug-drug interactions: salicylates, erythromycin, cefazolin, amiodarone
2. close client monitoring when adding or removing a drug
iv. Combining with OTCs like NSAIDs
v. HIT - Heparin Induced Thrombocytopenia
-abnormal antibodies to heparin develop which activate platelets
- high risk for clots so monitor carefully
-usually appears 5-10 days after initiation of therapy
Nursing Considerations
I. Monitor for bleeding and bleeding precautions
ii. Monitor lab: INR (coumadin), aPTT (for heparin)
iii. know Antidote: heparin & lovenox are protamine sulfate; warfarin is vitamin K
iv. Self-administration techniques
- subq in abdomen because it is the most stable absorption
-don’t push out the air bubble from lovenox because it needs to be given deep in
-don’t rub the area because it will alter the way it is absorbed
v. Heparin comes from animal sources (beef lung or pig intestine), allergic reactions are possible OR religious preference

A

nursing considerations and precautions for anticoagulants

42
Q

iv. Urokinase (Abbokinase)
v. Alteplase (Activase, Cathflo) – will see this the most (Cathflo)
vi. Reteplase (Retavase)
work best when administered no more than 4 hours after clot formation
- monitor VS every 15 mins first hour, then ever 30 mins and for 1st 8 hours after
hold pressure on site for 30 mins

A

Thrombolytics

43
Q

Adverse Effects
I. Allergic reaction due to foreign proteins
- headache, flushing, fever, lethargy
ii. Human donors
- HIV, hepatitis
Nursing Considerations
I. Double check that the correct clotting factor is being used
ii. Administered through the IV route only
iii. Watch for signs of bleeding and thrombosis
iv. Type and crossmatch
v. Monitor for allergic reactions

A

Antihemophilic factor, VIII, (Bioclate)

44
Q 
Systemic
1. aminocaproic acid (Amicar)
Topical – give these more
1. absorpbale gelatin (Gelfoam)
2. human fibrin sealant (Atriss, Evicel)
3. microfibrillar collagen (Avitene)
4. thrombin (Thrombinar)
5. thrombin, recombinant (Recothrom
A

Hemostatic Agents
AKA antifibrinolytics
used to stop bleeding

45
Q

I. Used for surface injuries where clotting does not occur

ii. Available in sponge, spray, and powder
iii. Can be used in conjunction
- gelfoam and thrombin
iv. Thrombin is a bovine product
- allergic reactions are possible
v. Infection risk due to trapped bacteria

A

topical hemostatic agents

46
Q

I. Inhibits plasminogen activator
ii. Given oral or IV
iii. IV reduces bleeding in 1-2 hours
- aplastic anemia, hepatic cirrhosis, postoperative
iv. IV can cause hypotension or bradycardia
v. Excessive clotting
Contraindications/Cautions
1. DIC - tissue necrosis
2. urinary tract bleeding - promotes clots in renal pelvis or ureters
3. dizziness, drowsiness, headache - changes in cerebral blood flow, will it make clot in brain
4. N&V, cramps, diarrhea - clotting in GI tract
5. muscle pain, increased CPK - clots in muscle tissue
Nursing Considerations
I. Monitor for clinical response
ii. Monitor for signs of thrombosis
- chest pain, leg pain, difficulty breathing, confusion
- immediately discontinue the medication & notify provider
iii. Monitor the IV site for extravasation
iv. Monitor vitals and urine output

A

Aminocaproic Acid (Amicar) only systemic one of hemostatic agents

47
Q

Phase 0: depolarization, sodium channels open, sodium rushes into cell
Phase 1: sodium concentration equalizes
Phase 2:calcium slowly enters cell, potassium begins to leaves cell to counteract all the Na and Ca that entered in
- more calcium, harder/better heart will pump
Phase 3 – getting everything back - repolarization, sodium channels close, potassium rushes out of cell
Phase 4: cell rests, sodium-potassium pump resets cell

A

automaticity

48
Q

Goal: prevent or terminate dysrhythmias
Medications can cause serious side effects
Reserved for those who can’t control by other means: cardioversion, defibrillation, ICD, pacemaker
treating asymptomatic dysrhythmias with med is little-no benefit (med is short term treatment and bridges until you get long term treatment)

A

treatment of dysrhythmias

49
Q

Action potentials depend on the opening of sodium channels, blocking these channels will prevent depolarization
- slows impulse conduction across the heart, ectopic pacemakers will be suppressed, depress phase 0 (so it slows things down)
Use
most are reserved for treatment of life threatening ventricular arrhythmias
Quinidine/Procainamide - effective against a wider range of dysrhythmias
Lidocaine - drug of choice when monitoring isn’t available for exact arrhythmia

lidocaine prototype drug
procainamide, quinidine, propafenone (Rythmol) (see this most often in practice)

A

class 1 sodium channel blockers

50
Q

Adverse Effects
Potential to create new dysrhythmias or worsen existing ones
- Can lead to cardiac arrest
- Use this one if other things don’t work
Bradycardia and hypotension
-dizziness, syncope
Bone marrow depression
- Quinidine – older drug
N&V, diarrhea, dry mouth, urinary retention
- So give small meals, take with food
Cautions
Bradycardia or heart block without a pacemaker
- Slow conduction down in some form, so could make them bradycardic or cause heart block
- Assess BP and heart rate before administration
Heart failure, hypotension, shock
- If in heart failure be careful. Monitor closely when giving this
Electrolyte disturbances
Combined with other medications known to produce arrhythmias
- Digoxin (is used for heart failure, so be very careful when combining this), beta blockers
Quinidine
- when combined with digoxin monitor digoxin levels
– reserve for people who can’t use other things
- avoid grapefruit juice because it will enhance absorption
- avoid foods that alkalinize the urine
– milk can alkalinize urine

A

sodium channel blockers - class 1

51
Q 
Block beta1 receptors in heart
slow conduction through AV node - decreased HR
depression of phase 4
Uses:
Supraventricular tachycardia (Something above ventricle/atria based like afib, aflutter, SVT), PCVs, hypertension, Post MI pts
propranolol (Inderal) - prototype
acebutolol (Sectral): oral only
esmolol (Brevibloc): IV only
A

class 2 beta adrenergic blockers

52
Q

Adverse Effects
1. Hypotension, bradycardia, arrhythmias
2. Bronchospasm, dyspnea – important for patients with COPD/asthma
- blocking of beta2 receptors
3. Alterations in blood glucose
- mask effects of hypoglycemia
- B2 receptors in the liver control hepatic glucose production
- insulin resistance
4. Decreased libido, impotence – patients will stop taking
Cautions
1. Withdraw slowly to prevent rebound hypertension, dysrhythmias, and MI
2. Bradycardia, heart failure, shock
3. COPD, asthma
4. Diabetes( insulin dose adjustments, frequent blood sugar monitoring)

A

class 2 beta adrenergic blockers

53
Q

Block potassium channels and slow the outward movement of potassium (delays repolarization and lengthens the refractory period; phase 2-3)
Uses:
serious dysrhythmias r/t serious S/E (proarrhythmic, IV Amiodarone usually limited 2-4 days), used for variety atrial/ventricular dysrhythmias, Amiodarone isn’t drug of choice
amiodarone (Cordarone) - prototype
sotalol (Betapace) (beta-blocker with class III effects)
dronedarone (Multaq)

A

class 3 potassium channel blockers

54
Q

Adverse Effects
Bradycardia and hypotension in a significant number of patients
Worsen dysrhythmias or create new ones
Amiodarone can cause pulmonary and liver toxicity, is fairly common (has a significant half-life; mild liver injury is common; ALT is the best for liver specifically )
Dronedarone increases the risk of death in serious HF
-Black box warning: for Multaq - those with heart failure have increased risk of death; for Dronedarone - liver toxicity and pulmonary toxicity; pregnancy category X
N&V, weakness, dizziness

Cautions
Bradycardia, shock, AV block
- Coumadin with a fib and throw dronedarone with it, check the INR more frequently
Amiodarone can increase serum digoxin levels by 70%
Enhances the effects of anticoagulants

A

class 3 potassium channel blockers

55
Q

black movement of calcium across cell membrane (depresses generation of action potentials/delays repolarization in phase 1/2 - need Ca to have strong beat)
reduced automaticity in SA node and slowed impulse conduction through AV node
Uses:
Supraventricular dysrhythmias (afib, aflutter, SVT), hypertension, angina (helps relax vessels and get more oxygenated blood to heart)
diltiazem (Cardizem)
verapamil (Calan)

A

class 4 calcium channel blockers

56
Q

Treatment of choice for paroxysmal suprventricular tachycardia (Because acts fast)
Slows conduction through the AV node and decreases automaticity of the SA node
Given as a 1-2 second IV bolus and will reset everything in heart
**Dyspnea is common but self-limiting because of 10-15-second half life
- Let them know dyspnea will occur, but will go away fast

A

Adenosine (miscellaneous for cardiac dysrhythmias)

57
Q

Used primarily for heart failure
- positive inotropic effect – helps heart beat harder with each beat
- can eliminate dysrhythmias caused by cardiac hypoxia
Decreases automaticity of the SA node and slows conduction through the AV node
- slows calcium leaving cell
Can cause dysrhythmias, interacts with many meds
- careful monitoring is required, especially when you change drug regime
- serum levels (normal is 1.8) and electrolytes

A

Digoxin (miscellaneous for cardiac dysrhythmias)

58
Q

Assess VS
- monitor apical pulse for a full minute, blood pressure because if you give a hypotensive and they don’t have high BP it can cause BP to decrease
- educate on monitoring at home
Assess heart rhythm, may need continuous telemetry
Monitor daily weight – same time/scale/clothes
Assess for severe SOB, frothy sputum, profound fatigue, swelling extremities
Because this could be signs of HF or pulmonary toxicity
Monitor labs
- electrolytes, digoxin level, bone marrow suppression, coagulation studies, LFTs
- educate about routine lab work
Encourage medical alert bracelet
Titrate to smallest dose
Safety
- first dose at bedtime, get up slowly, good lighting, don’t double doses, don’t skip doses, 12 hours apart or 24 hours apart

A

Nursing consideration for cardiac dysrhythmias meds

59
Q

Progressive narrowing of coronary arteries, leads to decreased delivery of oxygen to cardiac muscle cells
- atheromatous plaques causes the narrowing
Plaques begin as fatty streaks, injure endothelial lining, causes an inflammatory response
- draw C reactive protein to tell basic informing on inflammation in body – tests CAD
Platelets, fibrin, other fats, collect on the injured lining narrowing the blood vessel
Scarring develops which causes the vessel to thicken
Atheromas can rupture and block a vessel
- Can travel down the vessel and get caught and that’s how an MI occurs

A

Coronary artery disease

60
Q 
Elevated cholesterol and lipids
- high fat diets
Unmodifiable
-genetic predisposition – CAD in children
-age
-gender: men are more prone until women hit post-menopausal and then we are even
Modifiable
-Smoking – damages endothelial lining
-sedentary lifestyle
-hypertension
-obesity
Often asymptomatic until something drastic happens
-At doctor and they test, or have heart attack and never go to doctor
Treatment
-Exercise
-Low-fat diet
-Smoking cessation
-Weight loss
-Stress management
-Control of blood pressure
-Control of blood sugar
-Medications
A

Risk factors for CAD

61
Q

Dietary fats are broken down to fatty acids (building block for triglycerides and phospholipids), lipids, and cholesterol by bile acids
- small units called micelles are absorbed in the small intestine
–triglycerides – float and get snagged on broken endothelial lining, stored in adipose tissue – use this for energy
Used for
1. energy
2. stored for future use
3. processed into lipoproteins

A

Fat metabolism

62
Q

Lipoproteins are produced mainly in the liver
Consist of cholesterol, triglycerides, and lipids
LDL – bad cholesterol and bad fats in body
-broken down for energy
-contain more cholesterol than HDLs
–cholesterol is bad for our body
-remnants are thought to initiate an inflammatory response
-ideally <129 mg/dL but really want <100
HDL – good, want more of
-used for energy
-pick up remnants of LDL for transport to liver
-like vacuum cleaner, suck up all the LDL bad stuff and recycles them
-increase during exercise
-ideally >60 mg/dL

A

LDL vs HDL

63
Q

Required for
-steroid hormone synthesis – like sex hormone (testosterone – need cholesterol in order to make that)
-cell membrane formation
–all cells have membranes, and to keep them intact we need cholesterol
Every cell in the body has the ability to produce cholesterol
-enzyme HMG-CoA – need this enzyme to make cholesterol
If dietary cholesterol is limited, cellular synthesis will increase
Total cholesterol <200

A

cholesterol

64
Q

Bind with bile acids in the intestines to form an insoluble complex that is excreted in the feces
-bile acids are high in cholesterol, so if we can bind up the bile acids we can get cholesterol down
cholestyramine (Questran)
colesevelam (WelChol)
colestipol (Colestid)

Use
Were a mainstay of treatment until discovery of statins
-produce 20% drop in LDL levels
Often combined with statins for those not able to achieve control with statins alone
Not used for monotherapy
Not absorbed systemically
-action is limited, only works when in intestines
-most are taken multiple times per day, up to 6 times a day
-compliance issue with this drug due to that

A

Bile acid sequestrants

not first line treatments

65
Q

Adverse Effects
Most are GI related: constipation, bloating, nausea, GI tract obstruction, malabsorption syndrome
Rash
Cautions
-Can bind many drugs and reduce their absorption
–warfarin, digoxin, penicillins, thiazide diuretics
can bind anything you take orally, so monitor when they start new medications so you know how they will affect them
Block absorption of iron and fat-soluble vitamins
-vitamin K – fat soluble vitamin used for clotting factors and antidote to coumadin
–so it patient takes coumadin and they don’t have vitamin K we need to watch for bleeding
-can lead to malnutrition
Caution with
-complete biliary obstruction
-abnormal intestinal function

A

Bile acid sequestrants

66
Q

Nursing Considerations
I. Monitor bowel sounds and function
ii. Administer before meals because it has to be in intestinal tract when food is there to bind the bile acids
iii. Powders should be mixed with at least 60 ml of any kind of liquid
- to prevent esophageal irritation
- the powder expands when it gets into GI tract if not mixed with enough water and can cause obstruction*
iv. Administer other medications 1 hour before or 4 hours after

A

Bile acid sequestrants nursing considerations

67
Q

HMG-CoA reductase is the primary regulatory enzyme for cholesterol biosynthesis
-All cells can produce own cholesterol to maintain cell membrane integrity with is important for cell integrity
As the liver makes less cholesterol, it responds by making more LDL receptors on the surface of liver cells
-further reduces serum levels of LDL and cholesterol
-more LDL on surface of liver cells and binds more serum to LDL and leaves lower levels of LDL and serum levels

atorvastatin (Lipitor) – prototype
pravastatin (Pravachol)
rosuvastatin (Crestor)
simvastatin (Zocor)

A

Statins

68
Q

Use
Reduce LDL 20 t0 40% - can be up to 60%
Lower triglycerides and VLDLs
-VLDLs are the primary carrier of triglycerides (fats that get stored in adipose tissue)
Increase HDLs to get lower levels of bad fats and higher level of good fats
Requires life-long treatment or until controlled through dietary/lifestyle changes – have to maintain the lifestyle change forever
Nursing Considerations
Best administered at night
-liver is processing most lipids
-best for those with a short half-life
Administer with food if GI upset occurs – Nausea, dyspepsia
Do not administer with grapefruit juice – increases absorption and can change levels
Monitor LFTs
Report increasing muscle pain*
-Legs or any part hurt unusually, contact us

A

Statins

69
Q

Adverse Effects
Usually mild and most often affect the GI tract
- dyspepsia, cramping, constipation, basic GI upsets
Muscle or joint pain, headache, dizziness
Rare rhabdomyolysis
-Breakdown of muscle tissue, which released things that are dangerous to our body: potassium, and 2 other things (TEGRITY)
–Can lead to cardiac issues, renal failure, muscle pain
–Must be treated right away
Cautions
Hepatic impairment
-all are metabolized/excreted through the liver except pravastatin (which is a renal excretion)
-Dose adjustments may be needed for renal impairment
-Pregnancy category X
-Rhabdomyolysis risk increased with
-erythromycin, cyclosporine (antibiotics), antifungals (systemic ones)
Can increase digoxin, warfarin, oral contraceptive levels
-So monitor patients closer: heart dysrhythmias, weakness

A

Statins

70
Q

Decreases the absorption of dietary cholesterol from the small intestine
Less cholesterol is delivered to the liver, the liver increases clearance of cholesterol from the serum to make up the difference
ezetimibe (Zetia)
Use
Blocks absorption of cholesterol by as much as 50%
-can cause the body to synthesize more cholesterol
-may combine with a statin
Not used as monotherapy – combined with Statin
Reduces LDL by about 20%
When combined with a statin LDL is reduced by an additional 15 to 20%

A

Cholesterol absorption inhibitors

71
Q

Adverse Effects
Usually well tolerated
-abdominal pain
-diarrhea – most common
-upper respiratory tract infection – equally common
–nasal stuffy, dripping nose, cough, sore throat
-joint & muscle pain – careful when combined with Statin because of that pain
Cautions
Don’t take with bile acid sequestrants
-Will inhibit absorption
Liver disease
metabolized by liver
-Cirrhosis, hepatitis – watch these patients very carefully
Warfarin levels may increase
Nursing Considerations
Assess bowel sounds and function
Access to bathroom
Monitor for signs of upper respiratory tract infection

A

cholesterol absorption inhibits

72
Q

Preferred drugs for severe hypertriglyceridemia
Exact mechanism of action is unknown
inhibit the breakdown of stored fat in adipose tissue
reduce hepatic production of triglycerides

fenofibrate (TriCor)
gemfibrozil (Lopid)
fenofibric acid (Trilipix) – most given

Cautions
Most common side effects are GI related
-cramping, diarrhea, dyspepsia
Headache, dizziness, cholelithiasis (get gallbladder stones, which can increase production of stones in stone – so watch in people with gallbladder disease)
Care with statins due to increased risk of rhabdomyolysis
Care with warfarin
-alters warfarin binding
-report bleeding or unusual bruising
May worsen gallbladder or liver disease
-report right upper quadrant pain
A

Fibrates

73
Q

Also called nicotinic acid or vitamin B3 and available OTC
Inhibits the release of free fatty acids from adipose tissue, increases rate of triglyceride removal from plasma
Reduces LDL by 20%
More side effects that statins and not nearly as effective
-most often used in lower doses as a supplement to statins or bile acid sequestrants

Cautions
Flushing and hot flashes occur in almost all patients
-premedicate with an aspirin
-take with cold water
GI effects are common
-nausea, gas, diarrhea
Increases levels of uric acid (forms crystals in all our joints)
-Watch for patients with gout
Available OTC but self-medication should not be attempted because they do not know the right amount

A

Niacin - Misc CAD and HCL

med surg pharm 1 (3 decks)

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