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Pharmacology 1 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What is blood pressure?

A

Arterial pressure.

(cardiac output) x (peripheral resistance)

Cardiac output is determined by: HR, contractility, blood volume, and venous return.

Peripheral resistance is determined by: Arteriolar constriction.

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2
Q

How is BP controlled?

A

Autonomic Nervous System (sympathetic ns?)

Renin-Angiotensin-Aldosterone-System (RAAS): pronounced “raz”.

Renal Regulation: Renin is released from the kidneys…

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3
Q

What BP measure is considered hypertensive?

A

> 140/90 mm Hg

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4
Q

Explain Primary vs Secondary hypertension:

A

Primary: No specific cause of HTN can be identified. AKA “idiopathic” or “essential”.

  • Accounts for 90% of all cases.
  • May not be curable, but the disease can be managed such that the long-term consequences can be reduced.

Secondary: A specific cause is identified.

  • Accounts for 10% of all patients with HTN.
  • Correcting the comorbid condition will cure the associated HTN.
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5
Q

What certain diseases are associated with elevated blood pressure?

A
  • Cushing’s Syndrome
  • Hyperthyroidism
  • Chronic renal impairment
  • Pheochromocytoma
  • Arteriosclerosis
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6
Q

The consistent elevation of systemic arterial blood pressure:

A

Hypertension (HTN)

They start getting concerned about HTN when BP systolic is at 135

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7
Q

What are some risk factors for HTN?

A
  • Obesity
  • Smoking
  • Caffeine
  • Family history
  • Diabetes
  • Excessive salt/fat intake
  • Lack of exercise
  • Stress
  • Age
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8
Q

CCBs:

A

Calcium-Channel Blockers.

One of the most widely prescribed classes…

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9
Q

What 2 chronic diseases do CCBs treat?

A
  1. Hypertension. Often asymptomatic.
  2. CAD: Coronary Artery Disease

Other therapeutic uses:
Angina and Dysrhythmias

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10
Q

1 in 3 people have this:

A

High BP

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11
Q

Which systems are effected by high BP?

A

All.

The heart is the primary organ damaged by chronic HTN. It’s subjected to chronic pressure overload = LT ventricular hypertrophy. Left untreated = HF heart failure.

HTN accelerates the deposition of atherosclerotic plaque, creating or worsening CAD.

HF and MI are the most common causes of death in patients with HTN.

Creates major stress on kidneys; small arteries become injured, inflamed, and atherosclerotic=renal decline.

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12
Q

What is the mechanism of action for CCBs?

A

CCBs inhibit calcium from moving into the cell membrane thereby decreasing muscle contraction.

In normal physiology, calcium is needed in the automatic and conducting cells of the heart to help create an action potential & muscle contraction.

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13
Q

What are the effects seen on arteries of the heart from the CCB inhibition drugs?

A
  • Decreased force of contraction- reduced HR
  • Decreased velocity and conduction through the SA/AV nodes
  • Dilation of the blood vessels
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14
Q

This drug name is sometimes called the proprietary name, product name, or brand name:

A

Trade name.

Intentionally selected to be short and easy to remember.

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15
Q

Stroke, heart disease, and kidney disease are all possible effects of what condition?

A

Hypertension

Also asymptomatic

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16
Q

How do we treat HTN?

A

Treat the cause!

If no cause known, lifestyle changes.

Last resort: drug therapy.

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17
Q

Where is the effect of the CCBs seen?

A

Seen on arteries of the heart and blood vessels…

  • Decreased force of contraction- reduced HR
  • Decreased velocity and conduction through the SA/AV nodes
  • Dilation of the blood vessels = decrease BP
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18
Q

Name a prototype CCB:

A

nifedipine (Adalat CC, Procardia)

Use: to treat hypertension and angina

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19
Q

How does nifedipine work?

A

Works by blocking calcium channels in the vascular smooth muscle, including the coronary arteries which then decreases the amount of calcium available for muscle contraction

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20
Q

What other names is nifedipine known by?

A

Adalat CC
and
Procardia

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21
Q

What patient would you not give nifedipine to?

A

Those on digoxin because a side effect is a possible increase in digoxin.

Or alcoholic since alcohol perpetuates adverse effects!

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22
Q

Adverse effects of Adalat CC?

A

AKA nifedipine AKA Procardia

  • Hypotension
  • Headache
  • Dizziness
  • Flushing
  • Increased digoxin levels

Alcohol perpetuates effects!

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23
Q

Name a CCB prototype other than nifedipine:

A

verapamil (Calan)

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24
Q

How does verapamil work?

A
  • Works by blocking calcium channels in the vascular smooth muscle and cardiac muscle (myocardium)
  • Causes vasodilation of peripheral blood vessels
  • Reduces contractility of heart

Use:
To treat hypertension, angina & dysrhythmias - particularly the fast HR dysrhthmias.

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25
Q

What are some adverse effects of Calan?

A

AKA verapamil

Same as nifedipine, plus edema…

  • Headache
  • Fushed skin
  • Dizziness
  • Lightheadedness
  • Peripheral edema.
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26
Q

What does ACE stand for?

A

Angiotensin-Converting Enzyme

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27
Q

What class does Lisinopril belong to?

A

ACE inhibitor.

AKA Prinivil

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28
Q

What is the mechanism of action for ACE inhibitors?

A

Prevent the formation of angiotensin II from angiotensin I = Inhibits the action of ACE

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29
Q

All the drugs that end in “pril” belong to which class?

A

Angiotensin-Converting Enzyme Inhibitor.

30
Q

What is another name for Lisinopril?

A

Prinivil

31
Q

What IS angiotensin II?

A

Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex.

32
Q

What is aldosterone?

A

If decreased blood pressure is detected, the adrenal gland is stimulated by stretch receptors to release aldosterone, which increases sodium reabsorption from the urine, sweat, and the gut. This causes increased osmolarity in the extracellular fluid, which will eventually return blood pressure toward normal.

33
Q

What are some specific effects on the body caused from angiotensin II?

A
  • Vasoconstriction on vascular smooth muscle
  • Sympathetic nervous system activation
  • Hypertrophy (scarring) of the myocardial cells
  • Secretes hormone aldosterone-increases sodium reabsorption
34
Q

What happens to the body if the effects of angiotensin II are blocked (as with ACE inhibitors)?

A
  • Vasodilation
  • Sympathetic nervous system activation-blocked
  • Hypertrophy (scarring) to myocardium prevented
  • Aldosterone hormone blocked & sodium excreted-water follows salt
35
Q

What are the adverse side effects from Lisinopril (Prinivil)?

A
  • Angioedema: swelling just beneath the surface of the skin or mucous membranes. This is due to bradykinin not being broken down (angio II normally does but it’s being blocked by drug). May lead to airway obstruction.
  • Cough
  • Headache (BP drop
  • Dizziness (BP drop
  • Orthostatic hypotension (BP drop
  • Rash
  • Fetal injury & death: Blk Bx warning for pregnancy.
36
Q

What are ARBs?

A

Angiotensin II Receptor Blockers

37
Q

Name a drug from the Angiotensin II Receptor Blockers class:

A

losartan (Cozaar)

Prescribed for those who can not tolerate adverse effects of ACE inhibitors.

38
Q

What is the mechanism of action of Iosartan (Cozaar)?

A

Mechanism of action: blocks the actions of angiotensin II - (at receptor site).

Same pharmacological effects as ACE inhibitors.

39
Q

What are the adverse effects of Cozaar?

A

AKA Iosartan.

  • Headache
  • Dizziness,
  • Fetal toxicity & death
  • Increase in lithium levels may lead to toxicity
40
Q

What are some conditions that cause fluid buildup in the body?

A
  • Hypertension
  • Heart failure
  • Renal failure/ impairment
  • Hypervolemia
  • Edema
41
Q

What is the mechanism of action with diuretic therapy?

A
  • Blocking reabsorption of sodium, chloride and water and excrete in urine.
  • The drugs that block the most sodium from being reabsorbed are the most effective diuretics!
42
Q

What are the 3 classes of diuretics?

A

1) Loop or High-ceiling: block the reabsorption of sodium in the loop of henle
2) Thiazides: block the reabsorption of sodium in the distal tubule
3) Potassium-sparing: inhibits the actions of aldosterone in the distal tubule and collecting ducts, potassium is retained in the circulation.

43
Q

Which class of diuretic block the reabsorption of sodium in the distal tubule?

A

Thiazides.

44
Q

Which class of diuretic inhibits the actions of aldosterone in the distal tubule and collecting ducts?

A

Potassium-sparing diuretic.

45
Q

Which class of diuretic blocks the reabsorption of sodium in the loop of henle?

A

Loop
or
High-ceiling diuretic.

46
Q

This drug is the most effective diuretic available:

A

furosemide (Lasix)

  • Produce greatest loss of fluid and electrolytes
  • Block solute reabsorption of sodium and chloride
  • Prevents passive reabsorption of water
47
Q

Name some adverse effects of Lasix:

A

AKA furosemide

  • Electrolyte imbalances
  • Excessive fluid loss
  • Ototoxicity: a metabolite buildup that leads to hearing loss
  • hyperglycemia
48
Q

This drug is from the Thiazide class of diuretics:

A

hydro-chloro-thiazides (Microzide)

  • In the early segment of the distal convoluted tubule
  • Normally, only 10% of sodium is reabsorbed at this site, diuresis is lower than with loop diuretics
  • Not a good choice for those with renal impairment (loop diuretic instead)
49
Q

What are the adverse effects of hydro-chloro-thiazide?

A

AKA Microzide

  • Similar to loop diuretics –frequency is less
  • Loss of sodium, potassium, chloride
  • No ototoxicity
50
Q

Name a drug from the Potassium-sparing diuretic:

A

spironolactone (Aldactone)

  • Aldosterone antagonist
  • Causes excretion of sodium (and water) and retention of potassium
  • Works in distal nephron
  • Effect not seen for 2 days following administration
51
Q

What are the adverse effects of Aldactone?

A

AKA spironolactone

  • Hyperkalemia
  • Endocrine Effects: gynecomastia, menstrual abnormalities, impotence, hirsutism
  • Teratogenic effects in lab animals (so no pregnancy)
52
Q

What are some things you should mention to the patients receiving a diuretic, things they should be aware of?

A
  • Weigh as directed, report weight gain
  • GI upset… Take with food/milk
  • Avoid exercise in hot weather and prolonged standing due to increased risk of dehydration
  • Orthostatic hypotension
53
Q

What are some nursing considerations you should think of regarding diuretics?

A
  1. Take in morning (nocturisis)
  2. Problems with fluid and sodium loss?
  3. Potassium imbalance-supplements…
  4. Restrict intake of K+ rich foods (bananas, nuts, citrus fruits, potatoes, green leafy veggies)
54
Q

What type of lipid is the main storage for fat and is used as an energy source?

A

Triglycerides

55
Q

Which steroid is a component of cell membranes, and produced by the liver?

A

Cholesterol

Found in the foods we eat.

56
Q

These help transport cholesterol, triglycerides and phospholipids:

A

Lipoproteins

Classified according to composition, size, weight and density.

HDL: High Density Lipoprotein - made up of mostly protein.

LDL: Low Density Lipoprotein - made up of mostly cholesterol

VLDL: Very Low Density Lipoprotein - mostly triglycerides

57
Q

These lipoproteins protect against atherosclerosis and coronary heart disease:

A

HDLs

Promotes removal of cholesterol by transporting to the liver for destruction

Increased levels reduces the risk of CHD (coronary heart disease)

58
Q

Theses lipoproteins are rich in cholesterol and accounts for 2/3 of cholesterol:

A

LDLs

Contribute to development of atherosclerosis and CHD by transporting cholesterol to tissues and organs.

Stored in the lining of blood vessels - causing plaque build up.

59
Q

These lipoproteins are rich in triglycerides and deliver them to storage in adipose tissue:

A

VLDLs

Evidence suggests they contribute to atherosclerosis as well (as LDLs).

60
Q

Desirable lab value for total cholesterol:

A

Less than 200 mg/dL

61
Q

Optimal lab value for total LDLs:

A

Less than 100 mg/dL

62
Q

Desirable lab value for HDLs:

A

60 mg/dL or more.

63
Q

Normal lab value for triglycerides:

A

Less than 150 mg/dL

64
Q

3 drugs used for dyslipidemia:

A
  1. Atorvostatin (Lipitor)
  2. Cholestyramine (Questran) - bile acid sequestrant
  3. gemfibrozil (Lopid) - fibric acid drug
65
Q

Mechanism of action for Atorvastatin (Lipitor):

A

Statins inhibit HMG-CoA reductase thereby reducing the amount of cholesterol being made in the liver.

Also increases the LDL receptors on liver which encourages more LDL’s being removed from the blood.

66
Q

Atorvastatin (Lipitor) adverse effects:

A
  1. Myopathy/Rhabdomyolysis: muscle pain, breakdown of muscle fibers… spill into blood circulation.
  2. Teratogenic
  3. GI discomfort: cramping, diarrhea
  4. Hepatotoxicity.
67
Q

Benefits of statins:

A
  1. Enhance the ability of blood vessels to dilate
  2. Protect against Alzheimer’s disease and dementia
  3. Lower incidence of colorectal cancer.
68
Q

Mechanism of Action for cholestyramine (Questran):

A
  • Binds to bile acids in the intestines, forming an insoluble complex that contains cholesterol
  • Prevents reabsorption of bile acids - eliminated in feces
  • Liver makes more LDL receptors - reducing LDL levels in blood (similar to statins).
69
Q

cholestyramine (Questran) Adverse Effects:

A
  • No absorption is occurring so no systemic effects
  • GI discomfort:
    Abdominal pain
    Bloating
    Diarrhea
    Steatorrhea (excretion of abnormal quantities of fat with the feces owing to reduced absorption of fat by the intestine)
    Constipation
    Interference w/absorption of vitamins and minerals.
70
Q

Mechanism of Action for gemfibrozil (Lopid):

A
  • Activates enzyme lipoprotein lipase which increases the breakdown and elimination of triglycerides from the plasma
  • Most effective for treating high triglycerides but little effect on LDLs.
  • Usually combined with statins to have greater effect.
71
Q

gemfibrozil (Lopid) Adverse Effects:

A
  • GI discomfort

- Contraindicated in hepatic impairment and gallbladder disease.

72
Q

What are the treatment goals for hyperlipidemia?

A
  • Dietary changes
  • Weight control
  • Exercise
  • Smoking cessation

Pharmacology 1 (16 decks)

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