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Pharmacology > module 12-13 > Flashcards

module 12-13 Flashcards

1
Q

What is coronary heart disease?

A
  • when coronary blood circulation fails to adequately supply the heart with blood
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2
Q

What is the primary cause of coronary heart disease?

A

athlerosclerosis

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3
Q

what is athlerosclerosis?

A

when plaques build up on the walls of the arteries, causing the artery to narrow, resulting in decreased blood flow to the heart

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4
Q

what is the relation between coronary heart disease and cholesterol levels?

A

people with high blood cholesterol are at risk of developing coronary heart disease

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5
Q

Cholesterol’s role in the body (3)

A
  • cell membranes
  • precursor of steriod hormones
  • precursor of bile salts
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6
Q

where does cholesterol come from? (2)

A
  • diet (exogenous)

- through synthesis (endogenous)

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7
Q

what percent of body’s cholesterol is endogenous vs exogenous

A
  • endogenous = 80%

- exogenous = 20%

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8
Q

Lipoproteins - structure

A
  • outer hydrophillic shell = phospholipids
  • core = lipophilic cholesterol and triglycerides
  • Apolipoproteins - embeded in phospholipid shell
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9
Q

Lipoproteins - function

A

transport cholesterol and triglycerides in the blood (since both are lipophilic, they cannot disolve in blood otherwise)

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10
Q

Apoplipoproteins function (3)

A

1) allow recognition by cells which may bind and ingest lipoproteins
2) activate enzymes that metabolize lipoproteins
3) increase the structural stability of lipoproteins

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11
Q

Lipoproteins with apoplipoprotein AI - function

A

transport cholesterol from non-hepatic tissue back to the liver

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12
Q

lipoproteins that contain apoplipoprotein B-100

A

transport cholesterol to non-hepatic tissue

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13
Q

how do we classify lipoproteins

A

based on density

very-low density lipoproteins, low density lipoproteins, high density lipoproteins

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14
Q

Very low density lipoproteins - function

A
  • deliver triglycerides from the liver to adipose tissue and muscle
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15
Q

Very low density lipoproteins - core composition

A

very rich in triglycerides

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16
Q

Very low density lipoproteins - athlerosclerosis

A
  • some studies show link to atherosclerosis
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17
Q

Very low density lipoproteins - apoplipoprotein

A

contain apoplipoprotein B-100, which allows them to bind to cells and transfer their lipid to cells

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18
Q

Low density lipoproteins - function

A

deliver cholesterol to non-hepatic tissue

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19
Q

Low density lipoproteins - core composition

A
  • cholesterol rich core = 60-70% of cholesterol in blood
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20
Q

Low density lipoproteins - apoplipoprotein

A
  • apoplipoprotein B-100 - which allows them to bin to cells and transfer their lipid to cells
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21
Q

Low density lipoproteins - athelosclerosis

A
  • clear link between LDL cholesterol adn development of atherosclerosis
  • higher the blood LDL level, the greater the risk of developing coronary heart disease
  • reducing blood LDL levels halts or even reverses atherosclerosis and has ben proven to decrease death from coronary heart disease
  • AKA “bad cholesterol”
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22
Q

High density lipoproteins - function

A

deliver cholesterol from non-hepatic tissue back to the liver. Promote cholesterol removal from the blood.
- aka the “good cholesterol”

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23
Q

High density lipoproteins - core composition

A

have cholesterol as their main core lipid and account for 20-30% of total blood cholesterol

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24
Q

High density lipoproteins - and coronary heart disease

A

elevated HDL decreases risk of coronary heart disease

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25
Q

High density lipoproteins - apoplioproteins

A
  • Apoplipoprotein - A-I (mediates benefical effect of HDL cholesterol)
  • also apoplipoprotein A-II, and A-IV
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26
Q

High density lipoproteins

A
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27
Q

Role of LDL cholesterol in atherosclerosis (6)

A
  • LDLs promote initiation of atherosclerosis
  • LDLs may move from blood into the sub-endothelial space of arterial epithelium where they may become oxidized
  • oxidation –> monocyte recruitment–> macrophage conversion
  • macrophages take up oxidized LDL becoming larger and vacuolated (aka foam cells)
  • Foam cells accumulate beneath epithelium, a fatty streak appears (followed by plateled adhesion, smooth muscle migration, collagen synthesis)
  • RESULT = atherosclerotic lesion with a lipid core and a tough fibrous plaque
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28
Q

what actually causes atherosclerosis?

A

not just LDL - atherosclerosis is primarily an inflammatory process (LDL causes a mild injury to arterial endothelium but it is the subsequent inflammatory response that mediates the development of atherosclerosis

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29
Q

Who should have cholesterol screening? (8)

A
  • males over 40, females over 50
  • females post-menopausal
  • patients with diabetes
  • patients who have heart disease or a family history of heart disease
  • patients with hypertension
  • patients who have central obesity (waist circumference M102cm, F88cm)
  • patients who smoke or have recently stopped smoking
  • patients with inflammatory (arthritis, lupus) or renal disease
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30
Q

Framingham Risk Score (FRS) (what, how calculate, risk levels, problems)

A
  • a cardiovascular risk assessment tool
  • encompases gender, age, total blood cholesterol, smoking status, HDL cholesterol and systolic blood pressure to calculate a risk
  • risk score = patients 10 year risk of developing coronary heart disease
  • High risk = score greater than 20%, between 10-19% is moderate risk, below 10% is low risk
  • NOTE - underestimates risk in youth, women, patients with metabolic syndrome
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31
Q

Patients with high risk of coronary heart disease- characteristics

A
  • Framingham Risk score of >20%
  • patients with diabetes
  • patients with heart disease
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32
Q

Patients with high risk of coronary heart disease - initiate cholesterol lowering treatment when….

A

trick question - all patients should be treated

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33
Q

Patients with high risk of coronary heart disease - LDL cholesterol target

A
  • <2mmol/L or >50% decrease in LDL cholesterol
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34
Q

Patients with moderate risk of coronary heart disease - characteristics

A
  • framingham risk score of 10%-19%
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35
Q

Patients with moderate risk of coronary heart disease - initiate cholesterol lowering treatment when…

A
  • LDL cholesterol >3.5 mmol/L
  • ratio of triglycerides/HDL cholesterol is >5.0
  • if significant inflammation is present
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36
Q

Patients with moderate risk of coronary heart disease - LDL cholesterol target

A
  • <2mmol/L or

- >50% decrease in LDL cholesterol

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37
Q

Patients with low risk of coronary heart disease

A
  • Framingham risk score <10%
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38
Q

Patients with low risk of coronary heart disease - initiate cholesterol lowering treatments when

A
  • LDL-cholesterol is >5.0 mmol/L
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39
Q

Patients with low risk of coronary heart disease - LDL cholesterol target

A
  • > 50% decrease in LDL cholesterol
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40
Q

Metabolic syndrome

A
  • combination of medical disorders that cause increased risk of coronary heart disease + type II diabetes
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41
Q

Characteristics of metabolic syndrome (5)

A

diagnosed when a patient has three or more of….

  • central obesity (waist circumference >102cm in men or 88cm in women)
  • elevated triglycerides (blood triglycerides >1.7 mmol/L
  • low HDL cholesterol (<1.03 mmol/L in men or 1.29 mmol/L in women)
  • Hyperglycemia (fasting blood glucose >5.6mmol/L
  • hypertension - BP > 135/85
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42
Q

Treatment of metabolic syndrom

A
  • decreasing risk for coronary heart disease and type II diabetes
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43
Q

metabolic syndrome prevelance

A

1/4 canadians

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44
Q

non-drug treatment of LDL cholesterol (4)

A
  • diet
  • weight control
  • exercise
  • cigarette smoking
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45
Q

non-drug treatment of LDL cholesterol - Diet (4)

A
  • intake less than 200mg/day of total cholesterol
  • intake of saturated fats as 7% or less of total calories
  • intake of soluble fiber 10-25 grams/day
  • plant stanols and sterols of 2 grams/day
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46
Q

non-drug treatment of LDL cholesterol - weight control

A
  • weight loss by dietary modification and exercise lowers LDL and decreases risk of coronary heart disease
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47
Q

non-drug treatment of LDL cholesterol - exercise (benefits x4, recommendation x1)

A
  • cardiovascular exercise benefits =
    • decrease LDL cholesterol,
    • elevate HDL cholesterol,
    • decrease insulin resistance,
    • decrease blood pressure
  • exercise for 30-60 minutes per day
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48
Q

non-drug treatment of LDL cholesterol - cigarette smoking

A
  • cigarette smoke decreases HDL and increasees LDL

- counsel patients to quit smoking

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49
Q

Drug treatment of elevated blood lipids (5)

A

1) statins
2) bile acid sequestrants
3) nicotinic acid
4) cholesterol absorption inhibitors
5) fibric acid derivatives

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50
Q

How is cholesterol synthesized?

A
  • in the liver via the mevalonic acid pathway
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51
Q

mevalonic acid pathway

A

1) acetyl CoA –>
2) HMG CoA –>
3) Mevalonic Acid –>
4) multiple other products –>
5) cholesterol

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52
Q

Statins (HMG-CoA Reductase Inhibitors) - mechanism of action

A
  • decrease hepatic synthesis of cholesterol by inhibiting the enzyme HMG CoA reductase, the rate limiting step of cholesterol synthesis
  • next, inhibition of HMG CoA reductase causes an upregulation of the hepatic LDL recelptors, allowing the liver to remove more cholesterol from blood
  • RESULT = decrease in LDL cholesterol blood levels
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53
Q

Benefits of Statins

A
  • decreased LDL cholesterol
  • increased HDL cholesterol
  • decreased triglycerides
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54
Q

Statins and Primary Prevention

A
  • Statins are effective at preventing coronary heart disease
  • statins decrease incidence of coronary events (ex heart attack) even in low risk patients with no history of coronary heart disease
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55
Q

Statins and secondary prevention

A
  • effective at preventing recurrent CV events in higher risk patients
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56
Q

primary prevention

A

prevent an incident form occuring

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57
Q

secondary prevention

A

prevent an event from occurring again

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58
Q

Statins prescription rate

A
  • atorvastatin (Lipitor) = highest prescribed drug in Canada

- Rosuvastatin is 4th highest prescribed drug in Canada

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59
Q

Pharmacokinetics of Atorvastatin (ADME) and bioavailibility

A

-

  • A - large fraction of absorbed dose extracted by the liver, low oral bioavailibility (<14%)
  • D - distribution is primarily to the liver but also to the spleen, adrenal glands, skeletal muscle
  • M - metabolized by CYP3A4
  • E - eliminated in the feces (minimal renal excretion)
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60
Q

pharmacokinetics of Rosuvastatin (ADME)

A
  • A - low oral bioavailibility (<20%), large fraction of absorbed dose is extracted by the liver (site of drug action)
  • D - distribution is primarily to the liver but also to skeletal muscle
  • M - not extensively metabolized
  • E - excreted in the feces, minimal renal excretion
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61
Q

Rosuvastatin considerations (2)

A
  • plasma rosuvastatin concentrations are approx 2x higher in asian patients (dose should start low at 5mg and caution should be used before increasing the dose.
  • should not be used in females who are pregnant or trying to become pregnant (cholesterol required for synthesis of cell membranes and hormones)
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62
Q

Adverse effects of statins (3)

A
  • generally well tolerated
  • most common = myopathy (muscle ache and weakness ) in about 1-5% of patients
  • Rhabdomyolysis (rare)
  • hepatotoxicity (rare)
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63
Q

Rhabdomyolysis (diagnosis, pathophysiology, associated symptoms, treatment)

A
  • muscle lysis with severe muscle pain
  • during significant muscle injury, muscle cell releases large a mounts of creatine kinase into blood stream…Rhabdomyolysis is diagnosed when blood creatine kinase is 10x above normal
  • also accompanied with hyperkalemia and may cause acute kidney failure
  • treatment = preserve kidney funciton via IV fluids
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64
Q

Nicotinic Acid - function

A
  • inhibits the hepatic secretion of VLDL. (since LDL is a by-product of VLDL degredation, nicotinic acid effectively reduces both VLDL and LDL)
  • also increases blood levels of HDL cholesterol
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65
Q

Nicotinic acid (Niacin) - adverse effects (5)

A
  • side effects limit its use
  • intense facial flushing,
  • hepatotoxicity,
  • hyperglycaemia,
  • skin rash,
  • increased uric acid levels
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66
Q

Bile-Acids - production

A
  • negatively charged molecules produced in liver from CYP7A1 mediated cholesterol metabolism
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67
Q

Bile-Acids - function

A

Are secreted into the intestine and function to aid in the absorption of dietary fats and fat soluble vitamins

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68
Q

Bile acids reabosption

A
  • undergo enterohepatic recycling and are therefore reabsorbed form the intestine
  • 95% of bile acids are normally reabsorbed form teh intestine
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69
Q

Bile Acid Sequestrants - mechanism of action

A
  • bile acid sequestrants are large positively charged molecules therefore they attract and bind bile acids (neg charge) in the intestine and prevent their absorption
  • this causes an increased demand for bile acid synthesis in the liver
  • to synthesize more bile acids, LDL cholesterol is required (therefore liver cells increase LDL receptors, resulting in an increased uptake of cholesterol from teh blood to the liver)
  • RESULT - decrease in plasma LDL cholesterol levels
70
Q

Bile acid sequestrants - adverse effects

A
  • are not absorbed = no systemic side effects
  • most side effects are limited to GI tract (constipation, bloating, etc.)
  • Drug-drug interaction - designed to bind to negatively charged moleules, they may decrease absorption of some drugs such as thiazide diuretics, digoxin, warfarin, certain antibiotics
71
Q

Cholesterol Absorption of dietary cholesterol

A
  • specific transport protein NPC1L1 = intestinal uptake of the majority of dietary cholesterol
72
Q

Cholesterol Inhibitor - mechanism of action

A
  • ezetimibe decreases intestinal cholesterol absorption by 54% and lowers blood LDL cholesterol by 15-20%
73
Q

Cholesterol inhibitor problems

A
  • decreased intestinal absorption of cholestorol can produce a compensatory increase in hepatic cholesterol synthesis
  • therefore, ezetimbe is often prescribed as an adjunct therapy along with a statin
  • approved combination pill called vytorin contains a statin iwth ezetimbe which can reduce LDL cholesterol by up to 60%
74
Q

Fibric Acid Derivative (Fibrates) - function

A
  • most effective class of drugs for lowering plasma triglyceride levels
  • increase HDL cholesterol
  • have almost no effect on LDL cholesterol levels
75
Q

Fibric Acid Derivatives - mechanism of action

A
  • fibrates bind to and activate a receptor in the liver called perozisome proliferator activated receptor-alpha (aka PPAR-alpha)

reduce hepatic triglyceride levels by inhibiting hepatic extraction of free fatty acids and thus hepatic triglyceride production

76
Q

perozisome proliferator activated receptor-alpha (PPAR-alpha) function (3)

A

1) increased synthesis of the enzyme lipoprotein lipase… which enhances clearance of triglyceride rich lipoproteins
2) decreased apoplipoprotein C-III production (ince apoplipoprotein C-III_ is an inhibitor of lipoprotein lipase) resulting in increased lipase activity
3) increased apoplipoprotein A-I and apopliporotein A-II levels resulting for increased HDL levels

77
Q

Adverse effects of fibrates (3)

A
  • increased risk of gallstones
  • myopathy (in a small fraction of patients… therefore careful in combination with statins)
  • hepatotoxicity
78
Q

Hypertension

A

elevated systemic arterial blood pressure

79
Q

What is blood pressure

A

measurement of the force against the walls of your arteries as the heart pumps blood through the body

80
Q

how is blood pressure measured

A

sphygamomanometer

81
Q

6 things to accurately measure blood pressure

A

1) patient must be seated for at least 5 minutes
2) no cafeine or nicotine within 30 minutes of measurement
3) feet should be touching the floor
4) arm should be elevated to heart level
5) two measurements in each arm should be taken 5 minutes apart
6) before a diagnosis of hypertension, the patient should have this repeated 3 times at least two weeks apart

82
Q

Systole

A

when the heart contracts

83
Q

Diastole

A

when the heart fills after a contraction

84
Q

Normal BP values

A

<120 systolic, <80 diastolic

85
Q

Prehypertension BP values

A

systolic 120-139 OR

Diastolic 80-89

86
Q

Stage one hypertension - BP values

A

Systolic of 140-159

Diastolic of 90-99

87
Q

Stage two hypertesnion - BP values

A

Systolic >160

Diastolic >100

88
Q

Types of hypertension

A
  • primary hypertension

- secondary hypertension

89
Q

Primary hypertension (what, prevelance, population)

A
  • hypertension of no known cause
  • 92% of all cases of hypertension
  • 90% of people over the age of 55 have hypertension
90
Q

Secondary hypertension

A
  • hypertension with an identifiable cause
  • EX - kidney disease, hyperthyroidism, pregnancy, erythopoietin, pheochromocytoma (tumour on adrenal gland releaseing epinephrine), sleep apnea, contraceptive use
91
Q

Consequences of hypertension (3)

A
  • chronic hypertension –> increased morbidity and mortality
  • untreated –> myocardial infarction, kidney failure, stroke, retinal damage
  • “silent killer”
92
Q

Why lower blood pressure

A
  • lower blood pressure = save lives (decrease morbidity and mortality)
  • decreases incidence of stroke, MI, heart failure (decrease 5mmHg = reduce stroke and heart attack by 20-35%)
93
Q

Determinants of blood pressure

A
  • Cardiac output

- peripheral resistance

94
Q

calculating blood pressure

A

BP = cardiac output x peripheral resistance

95
Q

Cardiac output - is determined by (4)

A

heart rate, heart contractility, blood volume, venous return

96
Q

Cardiac output and BP

A

increase in any of the cardiac output factors will result in an increase in blood pressure

97
Q

Peripheral resistance is determined by

A

arteriolar constriction

98
Q

peripheral resistance and BP

A
  • constriction of arteries and arterioles will cause BP to rise
99
Q

3 systems the body uses to regulate blood pressure

A

1) sympathetic nervous
2) the renin-angiotensin-aldosterone system (RAAS)
3) Renal Regulation of Blood Pressure

100
Q

Sympathetic nervous system (3)

A
  • helps us respond to stress (fight-or-flight response)
  • constantly active to keep body functions in homeostasis
  • reflex circuit = baroreceptor reflex that helps keep BP at a set level
101
Q

The baroreceptor reflex (5)

A
  • on the aortic arch and carotid sinus
  • they sense blood pressure and relay information back to the brainstem
  • BP too low –> sympathetic neurons stimulate the heart to cause increased cardiac output and smooth muscles on arteries causing vasoconstriction. Result = increase BP
  • BP too high –> sympathetic activity is decreased = decreased CO and vasodilation. Result = decrease BP
  • responds rapidly (seconds or minutes) to changes in BP
102
Q

The baroreceptor reflex and antihypertensive drugs

A
  • the baroreceptor reflex can oppose our attempts to decrease BP since the “set point” in patients with hypertension is high
103
Q

Renin-angiotensin-aldosterone system (RAAS)

A
  • a series of protein hormones
  • regulates blood pressure, blood volume, electrolyte balance
  • activate RAAS = kidney and vascular smooth muscle
  • takes hours to days
104
Q

Renin-angiotensin-aldosterone system and drugs

A

common target for blood pressure lowering drugs

105
Q

how the RAAS works

A 
Angiotensinogen -->
[Renin]
Angiotensin I (inactive) -->
[angiotensin converting enzyme]
Angiotensin II (active) -->
Aldosterone + antidiuretic hormone (ADH)
106
Q

Renin (function, where synthesized)

A
  • catalyzes formation of angiotensin I (from angiotensinogen)
  • rate limiting step
  • synthesized and secreted by juxtaglomerular cells of the kidney into the blood
107
Q

What increases renin release? (3)

A

1) decreased blood volume
2) low blood pressure
3) stimulation of beta 1 receptors on juxtaglomerular cells of kidney

108
Q

Angiotensin converting enzyme (ACE)

A
  • converts inactive angiotensin I into active angiotensin II
109
Q

Angiotensin II (3 functions)

A
  • potent vasoconstrictor (binds to its AT1 receptor to produce vasoconstriciton) –> increased BP
  • stimulates release of aldosterone from adrenal cortex
  • stimulates release of antidiuretic hormone (ADH) by posterior pitutiary
110
Q

Aldosterone

A
  • adrenal cortex

- acts on kidneys to increase sodium retention, which can increase water retention

111
Q

Antidiuretic hormone

A

causes water retention by the kidney

112
Q

Renin-Angiotensin-Aldosterone system - effect on blood pressure

A
  • when RAAS is activated, it causes vasoconstriction (which increases BP by increasing peripheral resistance)
  • it also causes increased retention of water and sodium (which increases blood volume, which increases CO, which increases BP)
113
Q

when should non-drug treatments be prescribed for hypertension?

A
  • diastolic BP of 90-95 mmHg

- can also be used in conjunction with drugs to augment the effectiveness

114
Q

What are non-pharmacologic interventions for hypertension (7)

A

1) decreasing body weight
2) restricting sodium intake
3) physical exercise
4) potassium supplementation
5) DASH diet
6) smoking cessation
7) alcohol restriction

115
Q

non-pharmacologic interventions for hypertension - decreasing body weight (2)

A

1) obese patients have increased insulin secretion, causing tubular reabsorption of Na+, causing increased water reabsorption resulting in a higher blood volume = increased BP
2) obese patients have increased activity of sympathetic nervous system

weight loss lowers BP in up to 80% of patients

116
Q

non-pharmacologic interventions for hypertension - restricting sodium intake

A
  • if salt levels are too high, it causes water to be reabsorbed from the kidney into the blood
  • causes increased extracellular blood volume = increased BP
  • recommendation = 5g per day (decreases systolic by 12 mmHg and diastolic by 6mmHg
117
Q

non-pharmacologic interventions for hypertension - physical exercise

A
  • regular exercise decreases BP by about 10 mmHg
  • regular exercise decreases extracellular fluid volume and circulating levels of plasma catecholamines
  • benefets seen even if patient doesnt restrict sodium or lose weight
118
Q

non-pharmacologic interventions for hypertension - potassium supplementation

A
  • high total body potassium =lower BP (increased potassium in diet will increase sodium excretion, decrease renin release, and cause vasodilation)
  • prefered source - fresh fruit and veg
  • DO NOT prescribe to patients taking ACE inhibitors
119
Q

non-pharmacologic interventions for hypertension - DASH diet

A
  • Dietary Approaches to Stop Hypertension
  • Diet rich in fruits, veg, low fat dairy, lean meats, whole grains, nuts, legumes
  • Diet excluding foods high in saturated fat, total fat, cholesterol
  • most patients achieve lower BP within 14 days
120
Q

non-pharmacologic interventions for hypertension - smoking cessasion

A
  • smoking acutely elevates BP (not linked to causal development of high BP)
  • encourage patient to quit since smoking and hypertension put patient at risk for development of cardiovascular disease
121
Q

non-pharmacologic interventions for hypertension - alcohol restriction

A
  • excessive alcohol consumption increases BP
  • alcohol can also decrease response to some antihypertensive medications
  • GOAL - less than 2 drinks per day (14 per week for men, 9 per week for women)
122
Q

sites of action for anti hypertensive medications (5)

A
  • vascular smooth muscle
  • RAAS
  • brainstem
  • heart
  • kidney
123
Q

anti hypertensive medications that act on vascular smooth muscle

A
  • calcium channel blockers

- thiazide diuretics

124
Q

anti hypertensive medications that act on the brainstem

A

centrally acting alpha 2 agonists

125
Q

anti hypertensive medications that act on the RAAS (5)

A
  • beta blockers
  • direct renin inhibitors
  • ACE inhibitors
  • ARBs
  • Aldosterone receptor antagonists
126
Q

anti hypertensive medications that act on the heart

A
  • beta blockres

- calcium channel blockers

127
Q

anti hypertensive medications that act on the kidney

A
  • thiazide diuretics
  • loop diuretics
  • potassium sparing diuretics
128
Q

3 types of diuretics (hypertension)

A

1) loop diuretics
2) thiazide diuretics
3) potassium sparing diuretics/aldosterone antagonists

129
Q

Diuretics function (hypertension)

A
  • block sodium and chloride ion reabsorption from nephron of kidney
  • create osmotic pressure –> prevents reabsorption of water
  • thus, excretion of water and sodium/choride ions
130
Q

Loop Dieuretics - sites of action

A
  • works at the ascending loop of Henle

- most effective (20% of Na+ absorption is absorbed at its site of action)

131
Q

Thiazide diuretics - sites of action

A
  • distal convoluted tubule

- where 10% of Na+ is absorbed (moderate intensity)

132
Q

Potassium sparing diuretics - sites of action

A
  • collecting duct

- least effective (1-5% of Na+ reabsorption is here)

133
Q

what determines a diuretics efficacy

A

percentage of sodium absorbed at the site of action

- increased absorption of sodium at one location = increased diuretic effect

134
Q

Loop diuretics (what, mechanism of action, when is it prescribed)

A
  • most effective diuretics availiable
  • work by blocking sodium and chloride ion reabsorption in thick ascending limb of loop of Henle
  • reserved for situations that requrie rapid loss of fluids (Edema, severe hypertension that does not respond to milder diuretics, severe renal failure)
135
Q

Adverse effects of loop diuretics (4)

A
  • hypokalemia (can cause fatal cardiac dysrhythmias)
  • hyponatremia
  • dehydration
  • hypotension
136
Q

Thiazide diuretics - mechanism of action

A

1) blocking sodium and chloride ion reabsorption in the distal tubule
2) decreasing vascular resistance

137
Q

Thiazide diuretics adverse effects (3)

A

1) hypokalemia (fatal cardiac dysrhythmias)
2) dehydration
3) hyponatremia

138
Q

Potassium sparing diuretics/aldosterone antagonists (function, mechanism of action, contraindications and indications, adverse effent)

A
  • minimal lowering of BP
  • act by inhibiting aldosterone receptors in collecting ducts (causing increased sodium excretion and potassium retention)
  • used in combination with thiazide and loop diuretics to counteract hypokalemia effects
  • don’t use with ACE inhibitors (they also conserve potassium)
  • adverse event = hyperkalemia
139
Q

Beta blockers mechanism of action

A

1) blocking cardiac beta 1 receptors (blocking these receptors decrease CO by preventing binding of catecholamines, resulting in decreased BP)
2) blocking beta 1 receptors on juxtaglomerular cells

140
Q

Beta blockres suffix

A

-olol (ex propanolol)

141
Q

Beta blockers (type of receptor interaction)

A

antagonists

142
Q

Classes of Beta Blockers

A
  • 1st generation - produce non-selective blockade of beta receptors as they inhibit both beta 1 (heart and juxtaglomerular cells) and beta 2 (lung) receptors
    2nd generation - selective blockage of beta 1 receptors
143
Q

Adverse effects of second generation beta blockers (4)

A

selective beta 1 receptor blockers

  • bradycardia
  • decreased cardiac output
  • heart failure (rare)
  • rebound hypertension/cardic excitation if withdrawn abruptly (therefore taper dose slowly over 10-14 days)
144
Q

Adverse effects of first generation beta blockers (6)

A
  • bradycardia
  • decreased cardiac output
  • heart failure (rare)
  • rebound hypertension/cardic excitation if withdrawn abruptly (therefore taper dose slowly over 10-14 days)
  • bronchoconstriction (blockade of beta 2 receptors in lung)
  • inhibition of hepatic and muscle glycogenolysis (dangerous in patients with diabetes who take too much insulin)
145
Q

How ACE inhibitors work

A

1) decreasing production of angiotensin II (decrease angiotensin II will cause vasodilation and decrease total blood volume)
2) inhibiting breakdown of bradykinin (elevated levels of bradykinin cause vasodilation)

146
Q

ACE inhibitors suffix

A
  • pril

ex catopril, ramipril

147
Q

adverse effects of ACE inhibitors *4

A

1) Side effects from decreased angiotensin II
- (cause 1st dose hypotension,…
- cause decreased aldosterone leading to potassium retention = hyperkalemia)
2) Side effects from increased bradykinin (
- (persistent cough
- angioedema)

148
Q

Drug interaction with ACE inhibitors

A

certain NSAIDs may decrease effect of ACE inhibitors

149
Q

Angiotensin receptor blockers - mechanism of action

A
  • block binding of angiotensin II to its receptor (AT1 receptor)
  • block the actions of angiotensin II but not its synthesis
  • causes vasodilation (block angiotensin II on arterioles)
  • causes increased sodium adn water excretion (decrease aldosterone release)
150
Q

angiotensin receptor blockers (ARBs) suffix

A
  • “sartan”

- EX losartan, valsartan

151
Q

angiotensin receptor blockers (ARBs) adverse effects

A
  • cause hyperkalemia
152
Q

Direct Renin Inhibitors - mechanism of action

A
  • bind to renin and block the conversion of angiotensinogen to angiotensin I
  • influence entire RAAS pathway
  • same effect as other classes of drugs
153
Q

Direct Renin Inhibitors - Adverse effects (4)

A
  • hyperkalemia - should not be used in combination with other drugs that may cause hyperkalemia
  • very low incidence of cough and angioedema
  • diarrhea
154
Q

Calcium Channel Blockers - mechanism of action

A
  • bring calcium from outside the cell to inside the cell (essential for muscle contraction in smooth muscle and heart)
  • bock entry of calcium into heart cells and smooth muscle cells, therefore decreasing contraction
155
Q

Calcium Channel Blockers - 2 types

A

1) dihydropyridine calcium channel blockers

2) non-dihydropyridine calcium channel blockers

156
Q

dihydropyridine calcium channel blockers - mechanism of action

A
  • significantly decrease calcium influz into smooth muscle of arteries resulting in relaxation of muscle around arteries (= vasodilation)
  • do not act on the heart (at therapeutic dose)
157
Q

dihydropyridine calcium channel blockers - suffix

A

“dipine”

ex - nifedipine, felodipine

158
Q

Dihydropyridine calcium channel blockers - adverse effects (6)

A
  • fluishing
  • dizziness
  • headache
  • peripheral edema
  • reflex tachycardia
  • rash
159
Q

non-dihydropyridine calcium channel blockers - mechanism of action

A
  • block calcium chanels in heart and smooth muscle of arteries
  • produce vasodilation of arteries and decrease cardiac output
160
Q

non-dihydropyridine calcium channel blockers - adverse effects (6)

A
  • constipation
  • dizziness
  • flushing
  • headache
  • edema
  • may compromise cardiac function
161
Q

Centrally acting alpha 2 agonists - mechanism of action

A
  • bind to and activate alpha 2 receptors in the brainstem
  • activate receptors decrease sympathetic outflow to heart and blood vessels
  • inhibit sympathetic outflow, centrally acting alpha 2 receptor agonists decrease cardiac output and peripheral resistance (sympathetic activity - increased CO and vasoconstriction)
162
Q

Centrally acting alpha 2 agonists - adverse effects (3)

A
  • drowsiness
  • dry mouth
  • rebound hypertension if withdrawn abruptly
163
Q

Target blood pressure (otherwise healthy individuals)

A

less than 140/90

164
Q

Target blood pressure (patients with diabetes or chronic kidney disease)

A
  • less than 130/80

- chronic kidney disease = lower BP slows progression of kidney damage

165
Q

Treatment of hypertension and kidney disease

A

use loop diuretics (not thiazide since these ones are ineffective)

166
Q

hypertension treatment algorithm - prehypertension (2)

A

1) lifestyle modifications

2) thiazide diuretic

167
Q

hypertension treatment algorithm - stage 1 hypertension

A

1) lifestyle modifications
2) thiazide diuretic
3) thiazide diuretic + ACEI, ARB, BB, or CCB

168
Q

hypertension treatment algorithm - stage 2 hypertension

A

1) lifestyle modification + thiazide diuretic + ACEI, ARB, BB, or CCB

169
Q

Complex hypertension treatment algorithm (moderate renal disease or diabetes)

A

1) lifestyle modification + thiazide diuretic + ACEI, ARB, BB, or CCB

170
Q

Complex hypertension treatment algorithm - severe renal disease

A

1) lifestyle modification + loop diuretic + ACEI, ARB, BB, or CCB

Pharmacology (6 decks)

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