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Cardiovascular Drugs Flashcards

1
Q

What are the components that make up chylomicrons?

A

Triglycerides (free FAs + glycerol)

Cholesterol

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2
Q

VLDL formation and metabolism

A
  1. synthesis of VLDL by liver
    • conains triglycerides and cholesterol esters
    • assembled in ER
  2. Hydrolyzed by LPL
  3. HDL is cleaved off
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3
Q

Uses of LDL

A

Hormone production

BIle acid production

Cell membrane synthesis

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4
Q

What results from high circulating LDL?

A

Form foam cells

(accumulate intracellular cholesterol)

Formation of athermatous plaques

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5
Q

Where are HDLs synthesized? What are their components? Why are they beneficial?

A

Liver and Intestines

phospholipid and apolipoproteins

Benefit: removal of excess cholesterol from cells = anti-atherogenic!

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6
Q

Optimal levels of:

  • Cholesterol
  • LDL
  • HDL
  • Triglycerides
A
  • Cholesterol: <200
  • LDL: <100
    • Goal: <160 unless there are other risk factors
    • Risk factors: CHD, diabetes, Vascular disease
  • HDL: >60
  • Triglycerides: <150
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7
Q

What is metabolic syndrome?

A
  • Abdominal obesity (precipitating factor)
  • Atherogenic Dyslipidemia (lipids the wrong way)
    • Small LDL, low HDL, High Tg
  • HTN
  • Insulin Resistance
  • Prothrombotic/Proimflammatory state

**All can be fixed by weight loss

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8
Q

Some causes of Secondary Dyslipidemia

A
  • Diabetes
  • Hypothyroidism
  • Obstructive Liver Disease
  • Chronic Renal Failure
  • Drugs (progestins, anabolic steroids, corticosteroids)
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9
Q

What are the effects of taking fish oil?

A
  1. Increase cell membrane fluidity
    • may help prevent hardening of arteries
  2. Alter receptor responses
  3. Antiarrythmic
  4. Decrease Triglycerides
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10
Q

Dose recommendations for Fish Oil

  • For Primary Prevention
  • For Secondary Prevention (previous CV event)
  • For Hypertriglyceridemia
A
  • For Primary Prevention
    • 500mg/day
  • For Secondary Prevention (previous CV event)
    • 1g/d
  • For Hypertriglyceridemia
    • 4g/d
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11
Q

What is the mechanism of action of statins?

A
  • Competitive inhibitors of HG CoA reductase (rate-limiting step in Cholesterol synthesis
    • reduced cholesterol in the liver
    • Increased LDL receptor formation and cycling (bring LDL and cholesterol into cell)

Final result:

  • Decrease LDLs
  • Raise HDLs
  • Decrease Triglycerides
    • decrease in VLDL synthesis
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12
Q

Change in lipid profile with use of statins

A
  • Decrease:
    • Total cholesterol
    • LDL
    • Triglycerides (TGs)
    • Apo-B
  • Increase:
    • HDL
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13
Q

Side effects of Statins

A
  • Hepatic
    • increased aminotransferases
  • Myalgia
    • May have Increased serum creatine kinase
      • could also be related to trauma or hypothyroidism
  • Proteinuria
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14
Q

What is the Mechanism of Action of Fibrates?

A
  • decrease cholesterolgenesis, hepatic lipogenesis, secretion of VLDL
    • increase LPL activity
    • Decrease LDL
  • increased oxidation of TG-derived FA
    • decrease TGs
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15
Q

What is the mechanism of action of Niacin (Nicotinic Acid)?

A
  • Decreased FFA from adipose to liver
  • Decreased VLDL synthesis
  • Decreased LDL synthesis
  • Increased HDL
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16
Q

What is the mechanism of action of bile acid sequestrants? What side effect is present?

A

Mechanism of action:

  • Bind bile acid in the intestine and prevent reabsorption
  • Livers need to produce more (use cholesterol)
  • Decreased cholesterol in the body

Side effect: bloating

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17
Q

Neuromuscular blockers

  • Function
  • Act on what receptor?
A

Function:

  • Paralysis (sequence below)
    1. mm of fine movement
    2. limbs
    3. trunk
    4. intercostals
    5. Diaphragm
  • No analgesic properties

Receptor: Nicotinic ACh receptor

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18
Q

Excretion mechanisms of non-depolarizing neuromuscular blockers

A
  1. Renal (Primary)
  2. Liver
  3. Hofmann Elimination
    • spontaneous breakdown
  4. Plasma (plasma esterases)

Recovery can be accelerated by cholinesterase inhibitor

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19
Q

How to accelerate recovery from paralysis with any non-depolarzing neuromuscular blocker

A

Recovery can be accelerated by cholinesterase inhibitor

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20
Q

Drugs enhancing curare-type Neuromuscular blockade

A
  1. Aminoglycoside antibiotics
  2. Calcium channel blockers
  3. Inhalation anaesthetics
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21
Q

Succinylcholine

  • Type of drug and structure
  • What is the initial response to administration?
A
  • Depolarizing neuromuscular blocker (anesthetic muscle relaxant)
  • Structure: looks like 2 ACh
    • cholinesterases terminate function
  • What is the initial response to administration?
    • Wave of fasciculation (achy feeling later)
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22
Q

Side effects and contraindications of Succinylcholine (depolarizing neuromucular blockade)

A

Side effects:

  • Myalgia (due to fasciculation)
  • Potasium release from skeletal muscle
    • hyperkalemia => arrythmias
  • Prolonged paralysis (with atypical pseudocholinesterase)
  • Malignant hyperthermia

Contraindications

  • extensive burns/soft tissue damage
  • Paraplegics
  • Spinal chord injury
  • DMD in children
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23
Q

Treatment of malignant hyperthermia

A
  • ***Dantrolene
  • Hyperventilation
  • Cooling
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24
Q

What is the mechanism of action of local anesthetics?

A

Block “fast” voltage-gated sodium channels in nerves to reversibly block conduction

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25
Q

Which nerve types are blocked by local anesthetic?

A
  • Small fibers: A-delta and C fibers
    • unmyelinated
    • Function: pain, temp, touch
  • Bigger ( A-alpha, a-beta, motor) = less sensitive

Autonomic > Pain fibers > Sensory fibers > Motor fibers

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26
Q

Two types of linkage present in local anesthetic molecules

A
  1. Ester link
  2. Amide link
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27
Q

Metabolism of Amide and Ester-type local anesthetics

A

Amide

  • Broken down in liver
  • P450 (problem with hepatic disease)

Ester

  • hydrolysis
  • Not in liver
  • Plasma cholinesterases

Drugs within both groups vary in duration

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28
Q

What is the result of the use of epinephrine (a vasoconstrictor) with (after) a local anesthetic?

A

Vasoconstrictor will

  1. Decrease absorption/redistribution
  2. Prolong duration of anesthesia
  3. Reduce risk of systemic toxicity
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29
Q

What intrinsic qualities of local anesthetics affect their duration of action?

A
  1. Protein binding
  2. Hydrophobicity
    • more lipid soluble, more potent
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30
Q

Bupivacaine

  • Use
  • Primary site of action
  • Risk
A
  • Use
    • Anesthetic for long-duration surgeries
    • Low dose for obstetrics
  • Primary site of action
    • spinal nerve roots
  • Risk
    • Cardiotoxicity
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31
Q

Etidocaine

  • Use
  • Primary site of action
A
  • Use
    • muscle relaxant during surgery (motor block)
  • Primary site of action
    • spinal nerve roots
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32
Q

With spinal anesthesia, a sympathetic block may occur. What are common results of a sympathetic block?

A
  • Vasodilation: results in
    • blood pooling
    • Reduced CO
  • Treatment:
    • fluids
    • vasoconstrictors
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33
Q

What is the function of Benzocaine?

A

Topical anesthetic

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34
Q

What is the function of a eutectic mixture of lidocaine and prilocaine?

A

anesthetic action to 5mm after topical administration

Eutectic = low melting point

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35
Q

What are some side effects of local anestetics?

A
  1. CNS
    • Simulation
    • Depression
  2. Heart: Depression
    • Decreased conduction
    • Decreased force of contraction
    • Decreased excitability
  3. Vascular
    • Vasodilation => decreased BP
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36
Q

Contraindications of anesthetic amides? Of anesthetic esters?

A

Amides: hepatic disease

Esters: low esterase activity

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37
Q

What are the components of the anesthetic state?

A
  1. Amnesia
  2. Sedation (decreased arousal)
  3. Hypnosis (unconsciousnenss)
  4. Immobility
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38
Q

First anesthesia and date of discovery

A

Ether, 1842

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39
Q

What is Minimum Alveolar Concentration (MAC)? How is it measured? What are its limitations?

A
  • Concentration of gas in alveoli that results in a lack of pain response in 50% of subjects
  • Measure concentration of expired air (at equilibrium)
  • Limitations:
    • 50% still respond to pain
    • may not lose consciousness

***Want to give dose >MAC***

High MAC = less potent, quick time to action

Low MAC = more potent

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40
Q

What is the Mechanism of Action of General Anesthetics?

A
  1. increase GABA receptor activity
  2. increase activity of potassium channels
  3. Decrease activity of ACh receptors
  4. Decrease activity of glutamate receptors
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41
Q

What are the function and contraindications Barbiturates?

A

General anesthetic

Con: Porphyria

Clearance (rapid, but continued infusion helps)

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42
Q

Propofol

  • Function
  • characteristics:
    • analgesia
    • clearance
A
  • Function: General anesthetic
  • Poor analgesia, poor respiratory depression
  • High degree of clearance (rapid recovery)
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43
Q

Etomidate

  • Function
  • Used in which special population? Why?
  • Toxicity effect on adrenals
A
  • Function:
    • General anesthetic
  • Cardiostable => use in patients at risk of hypotension
  • Toxicity
    • causes suppression of adrenocortical stress response
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44
Q

Ketamine

  • Function
  • Side effects
  • Use in special populations
  • Toxicity effects
A
  • Function
    • General IV anesthetic
  • Side effects
    • increased BP (increased cerebral blood flow)
    • Bronchodilator
  • Use in special populations
    • At risk for Hypotension
    • Bronchospasm
  • Toxicity effects
    • emergence delirium
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45
Q

Cause and Treatment for malignant hyperthermia

A
  • Cause:
    • hypermetabolism
  • Treatment:
    • dantrolene
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46
Q

Clinical problems of IV anesthetics

A
  1. Respiratory depression
    • low response to CO2 or hypoxia
  2. CV depression
  3. Muscular rigidity (Opioids)
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47
Q

Which General anesthetics are used in patients at risk of hypotension?

A

Etomidate

Ketamine

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48
Q

Which general anesthetic is used in patients at risk for bronchospasm?

A

Ketamine

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49
Q

Which general anesthetic is associated with emergence delirium?

A

Ketamine

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50
Q

Which general anesthetic is used to increase cerebral blood flow?

A

Ketamine

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51
Q

Inhalation anesthetics are what molecule type?

A

Halogenated hydrocarbons

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52
Q

What is Henry’s Law? What are its implications?

A

Concentrations of drug in liquid = partial pressure of gas x solubility

The amount of gas which is soluble does not contribute to partial pressure and does not enter other tissues

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53
Q

What is the effect of the blood/gas partition coefficient on induction and duration of anesthetic?

A
  • Partition coefficient measures solubility
  • Higher = longer time to induction
  • Higher = longer duration of action
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54
Q

What is the blood/gas coefficient of NO? What is it’s potency?

A

Low coefficient

Not potent (short effect) but quick effect

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55
Q

What is the blood/gas coefficient of Halothane? What is it’s potency?

A

High coefficient

Potent, but takes time for effect

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56
Q

Halothane

  • Blood/gas co-efficient
  • Toxicity
A
  • High coefficient: potent but takes time for action
  • Toxicity:
    • Liver tox: hepatitis and hepatic necrosis
    • Malignant hyperthermia
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57
Q

Cause and Treatment of malignant hyperthermia

A

Cause: hypermetabolism

Treatment: dantrolene

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58
Q

Desflurane

  • Important side effect
  • MAC
A
  • inhaled anesthetic
  • Strong airway irritant
  • MAC = 6%
    • not soluble
    • Faster effect
    • Shorter duration (not potent)
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59
Q

Sevoflurane

  • MAC
A
  • Inhaled anesthetic
  • Not an airway irritant
  • MAC = 2%
    • more potent than desflurane
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60
Q

NO

  • Function
  • MAC
A
  • Inhalant anesthetic
  • MAC = 105%
    • quick induction
    • short action
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61
Q

Effect of blood-gas coefficient on induction time

A

Proportional

  • Low = short induction time
  • High = long “
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62
Q

Effect of MAC on Potency

A

Inversely proportional

  • Low MAC = Strong potency
  • High MAC = Weak potency
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63
Q

Effect of oil-gas coefficient on Potency

A

Measures lipid solubility

Proportional

  • High coefficient = strong potency (high lipid solubility)
  • Low coefficient = low potency
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64
Q

What is the mechanism of action of ACE inhibitors?

A
  1. inhibit Angiotensin I to AII
    • Reduce Na+ and water retention
    • Decrease afterload and wall tension
    • Inhibit cardiac remodeling
  2. Inhibit degradation of bradykinin
    • Prostaglandin synthesis
    • Vasodilation => Decreased BP
    • Increase renal blood flow

***Decreased TPR and effective circulating volume***

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65
Q

Where are ACE Inhibitors metabolized? What are the exceptions?

A
  • Kidneys
  • Exceptions: Kidneys and liver
    • Fosinopril
    • Spirapril
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66
Q

What is the effect of ACE inhibitors in patients with elevated plasma renin activity? How is their treatment modified?

A
  • Effect:
    • hyper-responsive to induced hypotension
  • Initial dose should be reduced
  • At-risk patients:
    • CHF, Na depletion
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67
Q

What are the therapeutic uses of ACE Inhibitors?

A
  1. Hypertension
    • especially in diabetic patients b/c are renal protective
  2. CHF
    • counteract ventricular remodeling
  3. L Ventricular Systolic Dysfunction
    • even w/o overt symptoms
  4. Acute MI
    • especially in diabetic and hypertensive patients
  5. Chronic Renal Failure
    • associated with T1DM
    • Captopril and Lisinopril
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68
Q

How do ACE Inhibitors counteract hypertension?

A
  1. Decreased TPR
  2. Increase Na+/water excretion at lower BP
  3. Increased arterial compliance
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69
Q

What drugs are used in Hypertension with Diabetes?

A

ACE Inhibitors

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70
Q

What drugs are used in MI with either hypertension or diabetics?

A

ACE Inhibitors

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71
Q

Which drugs are used to delay/prevent Chronic Renal Failure with Diabetes type I?

A

Captopril

Lisinopril

(ACE Inhibitors)

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72
Q

What is the MOA of renal protective effect in ACE Inhibitors?

A
  • Decrease BP and resistance => Decreased glomerular pressure
  • Decreased damage to GBM
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73
Q

What are the adverse effects associated with ACE Inhibitors?

A
  1. Teratogen (fetal hypotension)
  2. Acute renal failure
    • In diseases with decreased renal perfusion
    • CHF, bilateral renal stenosis, volume depletion (BP dependent on RAAS)
  3. Cough
  4. Angioedema
    • first-dose effect
  5. Hypotension
    • first-dose effect
  6. Hyperkalemia
    • In patients with renal insufficiency or who are taking drugs that promote K uptake
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74
Q

What is the MOA in ARBs?

A
  • Angiotensin II antagonists
    • selective competitive for AT1 receptors
    • Decrease TPR
    • Decrease effective circulating volume (increase Na+ and H20 excretion)
  • Inhibition is insurmountabile
    • blockade even with missed dose
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75
Q

What are the therapeutic uses of ARBs?

A
  1. High renin forms of hypertension
  2. Renoprotective in Type II Diabetes
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76
Q

What are the adverse effects of ARBs?

A
  1. Teratogen
  2. Hypotension/Acute Renal Failure
    • In patients whose BP is dependent on RAAS
  3. Hyperkalemia
    • In renal disease or taking drugs that promote K+ retention
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77
Q

What are the differences between ACE inhibitors and ARBs?

A

ARBs:

  • reduce activation of AT1 receptors more effectively
  • Do not affect Bradykinin levels
    • No cough
    • No angioedema

ACE Inhibitors:

  • Increased levels of Bradykinin
    • Cough
    • Angioedema
  • Increased Ac-SDKP
    • Promotes toxic anemia

Both:

  • Other side effects are the same
  • Affect RAAS
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78
Q

Aliskiren

  • MOA
  • Indications
  • Contraindications
A
  • MOA
    • Direct renin inhibitor
  • Indications
    • Hypertension
  • Contraindications
    • Diabetes
    • Renal Impairment
    • Use with ACE inhibitors or ARBs
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79
Q

What is diuretic braking?

A
  • Renal compensatory mechanisms that bring Na+ excretion in balance with intake
    • Activate SNS
    • Activate RAAS
    • Decreased arterial BP (decreased pressure natriuresis)
    • Hypertrophy of renal epithelial cells
  • **Important in the use of DIURETICS
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80
Q

What is the MOA of Carbonic Anhydrase Inhibitors (CAIs)?

A
  • Inhibit membrane and cytosolic Carbonic Anhydrase
    • excrete carbonic acid, Na+, and Cl-
    • Proximal tubule
  • Increased phosphate excretion
  • Decreased acid reabsorption in collecting duct
  • Renal effects
    • Increased afferent arteriolar resistance
    • Reduced Renal blood flow
    • Reduced GFR
  • Inhibition of CA in eye
    • decreased aqueous humor formation
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81
Q

Location of CAI action in the kidney

A

Proximal tubule

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82
Q

Indications of CAIs

A
  1. Glaucoma
    • Due to decreased aqueous humor and intraocular pressure
  2. Altitude sickness
  3. Correct metabolic alkalosis
    • Increased HCO3- secretion
    • Inhibit reuptake of weak organic bases
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83
Q

Adverse effects of CAIs

A

Sulfonamide derivatives:

  1. allergic rxn in patients hypersensitive to sulfonamides
  2. Bone marrow depression
  3. Renal lesions
  4. Skin toxicity
  5. Metabolic / Respiratory Acidosis
  6. Renal calculi
  7. Direct renal ammonia into circulation
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84
Q

Contraindications of CAIs

A
  1. Hepatic cirrhosis
    • directs ammonia into circulation
  2. Hyperchloremic acidosis
  3. COPD
    • worsens respiratory acidosis
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85
Q

What is the MOA of Osmotic Diuretics?

A
  • Reduce the vertical osmotic gradient in the Loop of Henle
    • Results in reduced water reabsorption in the collecting ducts
  • Increased excretion of nearly all electrolytes
  • Renal:
    • Increased RBF (dilate afferent arteriole)
    • Total GFR unchanged
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86
Q

What are the therapeutic uses of Osmotic Diuretics?

A
  1. Acute Renal Failure
    • attenuate decreased GFR
  2. Reduce cerebral Edema
  3. Reduce IOP
  4. Dialysis disequilibrium syndrome
    • Hypotension and CNS effects
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87
Q

Contraindications and Adverse effects of Osmotic Diuretics

A
  1. Pulmonary edema
    • In CHF or pulmonary congestion
  2. Hyponatremia
  3. Hypernatremia and dehydration
    • con: aneuric patients from severe renal disease

Contraindications;

  1. Patients with active cranial bleeding
  2. CHF/Pulmonary congestion
  3. Aneuric patients with severe renal disease
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88
Q

What is the MOA of Loop Diuretics?

A

***Inhibit the Na-K-2Cl symporter in the thick ascending limb of the loop of henle***

  • Large effect on Na excretion
    • 25% normally reabsorbed here
  • Reduce vertical medullary osmotic gradient
    • Decreased water reabsorption in collecting duct
  • Furosemide increases venous capacitance (distensibility)
    • reduces pulmonary edema before diuresis begins
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89
Q

What is the elimination half-life of Loop diuretics? How does this affect treatment?

A

Short elimination half-life

Cannot be used for long-term therapy

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90
Q

What are the therapeutic uses of Loop Diuretics?

A

Conditions with edema:

  1. Pulmonary edema (diuresis and increased venous capacitance)
  2. CHF congestion
  3. Nephrotic syndrome
  4. Liver cirrhosis (ascites)
  5. Hyponatremia (used with hypertonic saline)
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91
Q

What are the adverse effects of Loop diuretics?

A
  1. Ototoxicity
  2. Fats go wrong way (LDL, cholesterol and TG up; HDL down)
  3. Hyperglycemia
  4. Hyperuricemia (leads to gout)
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92
Q

What are the contraindications of Loop diuretics?

A
  1. Postmenopausal osteopenic women
    • Calcium loss
  2. Hypersensitivity to sulfonamides
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93
Q

What is the mechanism of action of Thiazinde Diuretics?

A

***Inhibit Na/Cl symport in distal convoluted tubule***

  • Increased excretion of K+, Acid, Uric acid (but not with chronic use)
  • Decreased excretion of Ca2+, increased reabs. of Ca2+
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94
Q

What are the therapeutic applications of Thiazide diuretics?

A
  1. Hypertension (First-line agent)
    • Dose for anti-hypertensive effect is lower than for diuretic effect
  2. Nephrogenic diabetes insipidus (decreased urine volume)
  3. Calcium nephrolithiasis (stones)
  4. Osteoporosis
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95
Q

What are the adverse effects of Thiazide Diuretics?

A
  • Hypokalemia
  • Hyperglycemia
  • Increased lipid profile
  • ED
  • sulfonamide hypersensitivity
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96
Q

What effect results from combined use of thiazide diuretics and Quinidine?

A
  • Quinidine: prolonged QT
  • Thiazide diuretics: hypokalemia
  • Result:
    • Early after-depolarizations
    • Torsades de Pointes
    • Ventricular fibrillation
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97
Q

What is the MOA of Amiloride?

A

***Blocks epithelial Na+ channels in distal tuble and collecting duct***

  • Because uptake of sodium usually causes excretion of K+, blockage of this channel is K-sparing
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98
Q

What are the therapeutic applications of Amiloride?

A

Used in conjuction with more effective diuretics to reduce K+ excretion and prevent hypokalemia

  • Edema
  • Hypertension
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99
Q

What are the contraindications for Amiloride?

A
  • Hyperkalemia
    • Renal failure
    • K+ supplements
    • NSAIDs
100
Q

What is the MOA of Aldosterone Antangonist-Diuretics?

A
  • Decrease Na+ reuptake
  • Increase K+ reuptake/retention

Spironolactone: competitive antagonist of androgen receptors

  • Testosterone converted to estradiol
101
Q

What are the therapeutic applications of Aldosterone - antagonist Diuretics?

A
  1. Diuretic of choice with hepatic cirrhosis
  2. Coadministration with other diuretics for K+ sparing
  3. Primary Hyperaldosteronism
  4. CHF
102
Q

Which diuretic is used in hepatic cirrhosis?

A

Aldosterone-antagonist diuretics:

Spironolactone

Eplerenone

103
Q

What are the adverse effects common to all aldosterone-receptor antagonists? Those to spirolactone alone?

A

All:

  • Hyperkalemia
  • Peptic Ulcers

Spirolactone: (converts testosterone to estradiol)

  • Gynecomastia
  • Impotence
  • Menstrual irregularities
  • Breast cancer
104
Q

Nesiritide

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • Structure: synthetic B-type natriuretic peptide
    • decreased TVR
    • Increased SV
    • decreased pulm. congestion
  • Indications
    • Short-term management of decompensated HF
  • Side effects
    • Hypotension
    • Increased risk renal dysfunction
105
Q

What are the effects of B1 receptors?

A
    • inotrope
    • chronotrope
  3. Increased CO
  4. Increased Systolic BP
  5. Increased O2 consumption of heart

**B = fight or flight; B1 = heart effects of fight or flight

106
Q

What are the effects of B2 receptors?

A
  1. Vasodilation
    • Decreased TPR
    • Decreased diastolic BP
    • Increased blood to mm
  2. Glucose mobilization
  3. Bronchodilation

***B2 = non-cardiac effects of fight or flight

107
Q

What are the effects of alpha-1 receptors?

A
  1. Vasoconstriction
    • Increased vascular resistance
    • Increased BP (Systolic and Diastolic)
108
Q

What are the indications for alpha-1-selective agonists?

A
  1. Orthostatic hypotension
  2. Hypotension in shock
  3. Locally as congestants

Function: vasoconstriction

  • increased TPR
  • increase/maintain BP
109
Q

Phenylephrine and Pseudoephrine

  • MOA
  • Indications
  • Side effects
A
  • MOA:
    • selective alpha-1 agonists
  • Indications
    • Rhinitis (acts as nasal decongestant)
  • Side effects
    • rebound nasal vasodilation and congestion
110
Q

Mephentermine

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • alpha-1 agonist
    • release of NE
    • Causes increased BP, (+) ino, (+) chronotrope
  • Indications
    • Hypotension from spinal anesthesia
  • Side effects
    • CNS stimulation
    • Very high BP
    • arrythmias
111
Q

Metaraminol

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • alpha-1 agonist
    • release of NE
    • Causes increased BP, (+) ino, (+) chronotrope
  • Indications
    • Hypotension from spinal anesthesia
  • Side effects
    • CNS stimulation
    • Very high BP
    • arrythmias
112
Q

What drugs are used to treat hypotension associated with spinal anesthesia? What is their MOA?

A

Mephentermine

Metaraminol

MOA: (+) ino, (+) chrono, increased BP

113
Q

Midodrine

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • alpha-1 agonist
  • Indications
    • Conditions with autonomic insufficiency and postural hypotension
  • Side effects
    • CNS stimulation
114
Q

What drug is used for conditions with autonomic insufficiency and postural hypotension?

A

Midodrine

alpha-1 agonist

115
Q

Norepinephrine

  • MOA
  • Indications
A
  • MOA
    • Alpha and beta-1 agonist
    • a = vasoconstriction => Increased TPR => increased BP
    • b = increased contractility (no effect on CO)
  • Indications
    • Severe hypotension and shock
116
Q

Epinephrine

  • MOA
  • Indications
A
  • MOA
    • low dose: beta agonist
      • increased HR and contractility
      • Increase CO, systolic BP
      • Bronchodilation
    • High dose: alpha agonist
      • vasoconstriction
  • Indications
    • Asthma
    • Anaphylaxis
    • Locally decrease blood flow to extend local anesthetic effect
117
Q

Dopamine

  • MOA
  • Indications
A
  • MOA
    • Low dose: D1 and beta1 agonists
    • increased HR, CO (beta effects)
    • increased renal perfusion (D1 effect)
      • renal and splanchnic flow
  • Indications
    • Hypotension and shock
      • treats decreased CO and renal function
    • Acute Heart Failure if BP is low
118
Q

What is the MOA of alpha-2 receptor agonists?

A

stimulate receptors in CV control centers in the CNS to reduce sympathetic nerve outflow and BP

119
Q

Metaproterenol

  • MOA
  • Indications
A
  • MOA
    • beta-2 agonist
  • Indications
    • Long-term treatment COPD and asthma
120
Q

Terbutaline

  • MOA
  • Indications
A
  • MOA
    • beta-2 agonist
  • Indications
    • asthma and COPD
121
Q

Albuterol

  • MOA
  • Indications
A
  • MOA
    • beta-2 agonist
  • Indications
    • asthma (symptomatic relief)
122
Q

Salmeterol

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • beta-2 agonist
  • Indications
    • long acting
    • treat COPD
  • Side effects
    • increased HR
    • Hyperglycemia
123
Q

Formoterol

  • MOA
  • Indications
A
  • MOA
    • beta-2 agonist
    • long-acting
  • Indications
    • Asthma
    • exercise-induced bronchospasm
    • COPD
124
Q

What is the suffix for beta-2 agonists?

A
  • terol
  • terenol

Isoproterenol is a non-selective beta agonist (1 and 2)

125
Q

Isoproterenol

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • non-selective beta agonist
  • Indications
    • Bronchodilator
    • Torsades de pointes
  • Side effects
    • Hypotension
    • Arrhythmia
126
Q

Which drug is indicated to reduce local blood flow in surgery to increase length of effectiveness of local anesthetics?

A

Epinephrine

127
Q

Which drugs are indicated for use as a nasal decongestant?

A

Phenylephrine

Pseudoephrine

(alpha-1 agonists)

128
Q

What drug group is indicated for treatment of asthma?

A

beta-2 agonists

  • terol
  • terenol
129
Q

What are the effects of alpha-2 receptors?

A

Decrease sympathetic outflow

Decreased: HR, BP

130
Q

Phenoxybenzamine

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • non-selective alpha receptor blocker
    • Irreversible
  • Indications
    • Treatment of Pheochromocytoma
  • Side effects
    • Orthostatic hypotension w/ reflex tachycardia/arrhythmia (alpha-2-blockade)
    • Inhibit ejaculation
131
Q

Phentolamine

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • non-selective alpha antagonist
      • competitive, reversible
    • Stimulates GI smooth mm and secretion
  • Indications
    • diagnose Pheochromocytoma
      • Relieve pseudo-obstruction on bowel
    • Treat hypertensive crisis associated with MAOIs and tyramine
    • ED
  • Side effects
    • Orthostatic hyptotension w/reflex tachycardia and arrythmia
    • Inhibition of ejaculation
    • exacerbates peptic ulcer
132
Q

What drug is used to treat pheochromocytoma?

A

Phenoxybenzamine

non-selective alpha receptor antagonist

133
Q

What drug is used to diagnose pheochromocytoma and relieve pseudo-obstruction of bowel in this disease?

A

Phentolamine

non-selective alpha receptor antagonist

134
Q

Prazosin

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • selective alpha-1-receptor antagonist
  • Indications
    • Hypertension (monotherapy)
    • CHF
  • Side effects
    • Postural hypotension and syncopy
      • first-dose effect
135
Q

Suffix of selective alpha-1-blockers

A

-osin

like the ocean

Prazosin

Tamsulosin

etc.

136
Q

Tamsulosin

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • selective alpha-1-blocker (alpha-1A)
  • Indications
    • Benign prostatic hypertrophy
      • without HTN
  • Side effects
    • impaired ejaculation

Very little effect on BP, so less likely to cause orthostatic hypotension

137
Q

Terazosin and Doxazosin\

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • selective alpha-1-blockers
    • induce prostatic apoptosis
  • Indications
    • benign prostatic hyperplasia
      • associated w/HTN
  • Side effects
    • First dose syncopy and orthostatic hypotension
138
Q

What drug is used to treat Benign Prostatic Hyperplasia (BPH) without associated HTN?

A

Tamsulosin

139
Q

What drug is used to treat Benign Prostatic Hyperplasia (BPH) with associated HTN?

A

Terazosin or Doxazosin

140
Q

What are the indications for beta blockers?

A
  1. hypertension
  2. ischemic heart disease (angina, prophylactic)
  3. Acute MI
  4. CHF
  5. Arrhythmia
141
Q

What is the suffix associated with beta-blockers?

A

-olol

beta fish giving lolipop to heart

142
Q

What are the effects of non-selective beta-blockers?

  • CV
  • Respiratory
  • Metabolic
A
  • CV:
    • decrease CO
    • Decrease HR
    • Decreased BP in patients w/HTN but not normal patients
    • Decrease conduction
      • increase AV node refractory period
      • can cause heart block
    • decreased work capacity during exercise
  • Respiratory
    • Bronchoconstriction
      • Con: COPD and asthma
  • Metabolic
    • Decrease insulin sensitivity
      • delay recovery from hypoglycemia
      • blunt effects of hypoglycemia
      • CON: diabetes (I)
    • Lipids in wrong direction
143
Q

What are the therapeutic applications of Propranolol?

A

HTN

Angina (prophylactic)

144
Q

What are the side effects associated with Propranolol?

A
  1. Bronchoconstriction
  2. Arrhythmias
    • decreased HR
    • CHF
    • (-) AV conduction
  3. Hypotension
  4. fasting gypoglycemia
145
Q

From which beta-blocker must patients be weened? Why?

A

Propranolol

  • Effects of Long-term use
    • Receptor upregulation
    • Hypersensitivity
  • Effects of abrupt discontinuation
    • exacerbate Angina
    • increased risk of death
146
Q

What are the contraindications associated with Propanolol?

A
  1. Heart Block
    • decreased conduction
  2. Asthma/COPD
    • bronchoconstriction
  3. Diabetes
    • insulin insensitivity
147
Q

Esmolol

  • MOA
  • Indications
A
  • MOA
    • selective beta-1-antagonist
    • decrease HR and contractility
    • Extremely short-acting
  • Indications
    • emergency beta-block (pre-op where expect large increase in SNS activity)
      • arrhythmia
      • HTN
      • MI
148
Q

Cavedilol

  • MOA
  • Indications
A
  • MOA
    • alpha-1 and beta-receptor blocker
      • decreased HR and contractility (B1)
      • Bronchoconstriction (B2)
      • Decrease BP (A1)
    • Increase NO
    • Ca2+ blocker
    • Antioxidant (protective, decreased apoptosis)
    • inhibit RAAS (decrease Na/H2O retention)
  • Indications
    • CHF
      • anti-remodeling effect (decreased stress => decreased ventricular size)
149
Q

What are the symptoms of beta-blocker overdose? What is the treatment?

A
  • cardiodepression
    • Hypotension
    • bradycardia
    • prolonged AV conduction
    • widened QRS
  • Treatment
    • atropine (bradycardia), isoproterenol (hypotension)
150
Q

What does a depressed/elevated S-T segment on an ECG signal?

151
Q

What is the difference between typical and variant angina?

A

Typical:

  • Induced by exercise, eating, or emotional stress (active)
  • Cause: atherosclerotic coronary artery disease

Variant:

  • Occurs any time (even at rest)
  • Cause: coronary artery vasospasm w/coronary thrombosis
152
Q

How much time can elapse in ischemic injury before irreversible damage occurs?

A

15 minutes

early irreversible: 1 hour

Late irreversible: 1 day

Note: irreversible has Ca2+ influx, stimulates lysosomal enzymes to destroy cell

153
Q

What is the MOA of Nitroglycerin?

A
  • Reacts with thiol => nitrosothiol (CV1, p4-5)
  • Release NO
  • Stimulate guanylate cyclase (Increased cGMP)
  • deactivation of myosin light chain
  • Smooth mm relaxation
    • ​preferentially in veins
    • decreased: Oxygen demand
      • preload
      • afterload
      • ventricular size
      • wall stress
    • Decreased ventricular pressure facilitates blood flow into endocardium
154
Q

What is the therapeutic application of Nitroglycerin?

A

Acute angina/Prophylaxis

(peak effect in 3 minutes)

155
Q

What are the side effects of nitroglycerin?

A
  1. Angina
    • reach point where flow proportional to pressure (vessels @ max dilation)
      • increased dose => decreased BP and flow to heart => ischemia => angina
  2. Headache
    • cerebral aa. dilation
  3. Orthostatic hypotension
    • from preferred venodilation
  4. Syncopy
    • decreased arterial pressure
  5. Rapid onset of tolerance
    • reflex activation of SNS and RAAS
    • Thiol depletion/ROS production (inactivates NO)
156
Q

What are the contraindications of Nitroglycerin?

A
  1. PDE5 inhibitors
    • treat ED
    • potentiate vasodilatory effect
  2. alpha-1-receptor blockers
157
Q

Ranolazine

  • MOA
  • Indications
A
  • MOA
    • limits Na+ and Ca2+ influx into cardiac cells
      • prevents overload
      • decreases diastolic wall tension
    • Myocardium less stiff
      • increased filling
      • increased diastolic function
    • Increased exercise capacitance
  • Indication:
    • Angina
158
Q

Nicorandil

  • MOA
  • Indications
A
  • MOA
    • Dilates arteries and veins
    • reduce O2 demand of heart
  • Indications
    • Angina

(nitroglycerin effect)

159
Q

Perhexiline

  • MOA
  • Indication
A
  • MOA
    • shift heart from FA to glucose metabolism
      • decreases O2 demand
  • Indications
    • Angina
160
Q

Trimetazine

  • MOA
  • Indications
A
  • MOA
    • shift heart from FA to glucose metabolism
    • decreases O2 demand
  • Indications
    • Angina
161
Q

What diseases are commonly associated with ED?

A
  1. HTN
  2. Diabetes
  3. Hypercholesterolemia
162
Q

What is the MOA of PDE5 inhibitors? What important drug interaction should be prevented?

A

MOA

  • Inhibit GMP-specific phosphodiesterases
  • Increase cGMP (which is normally stimulated by increased NO)
  • Amplify actions of NO on vascular tissue => increased vasodilation

Drug interaction:

  • Nitroglycerin: extreme reduction in BP
  • alpha-1-receptor antagonists: same
163
Q

Which channel subtypes are inhibited by Ca2+ channel blockers?

A

L-Type

Mostly in CV tissue

164
Q

What are the indications for Ca-channel blockers?

A

Major

  1. MI
  2. HTN
    • DHPs if hypertensive crisis
  3. Cardiac Arrythmia
    • Not DHPs
    • Verapamil best, or diltiazem

Minor

  1. Cardioprotection
  2. Migraine
  3. Esophageal spasm
165
Q

Nifedipine

  • MOA
  • Indications
  • Side effects
  • Contraindications
A
  • MOA
    • Calcium channel blocker (1,4 DHP)
      • inhibits recovery of channel
    • lipid-soluble
    • (-) cNMP phosphodiesterase, so vessels stay dilated
    • baroreceptor reflex occurs
  • Indications
    • Hypertensive crisis
  • Side effects
    • Hypotension
    • Peripheral Edema
    • Headache
  • Contraindications
    • heart failure or conduction abnormalities
166
Q

What is the MOA of Nifedipine?

A
  • class = 1,4-DHP
  • Ca-channel blocker
    • inhibits recovery of channel
  • lipid-soluble
  • (-) cNMP phosphodiesterase, so vessels stay dilated
  • baroreceptor reflex occurs
167
Q

What are the therapeutic applications for Nifedipine?

A

Hypertensive crisis

168
Q

What are the side effects of Nifedipine?

A

Headache

Hypotension

Peripheral edema

169
Q

Verapamil

  • MOA
  • Indications
  • Side effects
  • Contraindications
A
  • MOA
    • Ca-channel blocker
      • inhibits recovery
    • Hydrophilic, so action depends on frequency of receptor opening
  • Indications:
    • HTN
    • Arrhythmias
      • A-Fib
      • re-entry tachycardia thru AV node
      • supraventricular tachycardia
  • Side effects
    • Bradycardia
    • Heart Block
    • Hypotension
    • Peripheral edema
  • Contraindications
    • SA or AV conduction abnormalities
170
Q

Diltiazem

  • MOA
  • Indications
  • Side effects
  • Contraindications
A
  • MOA
    • Ca-channel blocker
    • inhibits recovery
    • Hydrophilic, so action depends on frequency of receptor opening
  • Indications:
    • HTN
    • Arrhythmias
      • A-Fib
      • re-entry tachycardia thru AV node
      • supraventricular tachycardia
  • Side effects
    • Bradycardia
    • Heart Block
  • Contraindications
    • SA or AV conduction abnormalities
171
Q

What is the MOA of Verapamil? What is its indication?

A
  • MOA
    • Ca-channel blocker
    • inhibits recovery
    • Hydrophilic, so action depends on frequency of receptor opening
  • Indications: Arrhythmias
    • supraventricular tachycardia
    • re-entry tachycardia thru AV node
    • A-Fib
172
Q

What are the side effects of Verapamil? What are its contraindications?

A
  • Side effects
    • Bradycardia
    • Heart Block
    • Hypotension
    • Peripheral edema
  • Contraindications
    • SA or AV conduction abnormalities
173
Q

What is the MOA of Diltiazem? What are its indications?

A
  • MOA
    • Ca-channel blocker
    • inhibits recovery
    • Hydrophilic, so action depends on frequency of receptor opening
  • Indications: Arrhythmias
    • supraventricular tachycardia
    • re-entry tachycardia thru AV node
    • A-Fib
174
Q

What are the side effects of Diltiazem? What are its contraindications?

A
  • Side effects: VERY MILD
    • Some Bradycardia
    • Some cardiodepression
  • Contraindications
    • SA or AV conduction abnormalities
175
Q

Bepridil

  • MOA
  • Indications
  • Side effects
  • Contraindications
A
  • MOA
    • Ca-channel blocker
  • Indications
    • Angina
  • Side effects
    • prolonged AP (prolonged QT)
    • May cause Torsade de pointes in susceptible individuals
  • Contraindications
    • Arrhythmia
    • Prolonged QT
176
Q

What are the physiological causes of increased vascular pressure in hypertension?

A
  1. Smooth muscle hypertrophy and hyperplasia
  2. enhanced sensitivity to constrictor stimuli
  3. reduced sensitivity to dilator stimuli
177
Q

What are the 5 first-line agents for treatment of HTN?

A
  1. Thiazide diuretics (used first)
  2. ACE inhibitors
  3. Calcium Channel Blockers
  4. beta-blockers
  5. alpha-1-blockers
178
Q

What drug reduces the risk of stroke in HTN patients?

A

Thiazide diuretics (chlorothiazide, chlorthalidone)

179
Q

What is believed to be the long-term effect of thiazide diuretics that results in decreased BP?

A

Decreased peripheral vascular resistance

180
Q

Which drugs are used for hyptertensive patients with MI, Myocardial ischemia, or Heart Failure?

A

beta-blockers

181
Q

What is the most likely mechanism of beta-blockers leading to decreased BP?

A

decreased plasma renin activity

182
Q

Which drugs are used for diabetic patients with HTN?

A

ACE inhibitors

Exert renal-protective effect

183
Q

Which drug has a side effect of hypertrichosis? What is its vascular indication?

A

Minoxidil

Hypertensive emergency

184
Q

Minoxidil

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • opens K channels, depolarizing cells
    • vasc. smooth muscle dilates
  • Indications
    • hypertensive emergency
  • Side effects
    • hypertrichosis
185
Q

Hydralazine

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • K channel activation
    • NO production
    • arteries > veins (little orthostatic hypotension)
  • Indications
    • Hypertension (short-term)
      • use with beta-blockers and diuretics (see SE’s)
    • CHF
      • with isosorbide dinitrite
  • Side effects
    • reflex SNS activation and fluid retention
    • Drug-induced Lupus
186
Q

What drug can cause Lupus?

A

Hydralazine

187
Q

Nitroprusside

  • MOA
  • Indications
A
  • MOA
    • directly produces NO
    • stimulates cGMP-mediated vasodilation
  • Indications
    • Hypertensive emergencies
188
Q

Fenoldopam

  • MOA
  • Indications
  • Side effects
  • Contraindications
A
  • MOA
    • D1 receptor agonist
    • dilates arteries
  • Indications
    • Hypertensive crisis
  • Side effects
    • Increased HR
    • Headache
    • increased intraocular pressure
  • Contraindications
    • Glaucoma
189
Q

Alpha-methyltyrosine

  • MOA
  • Indications
A
  • MOA
    • false substrate for tyrosine hydroxylase
    • inhibits NE synthesis and decreases BP
  • Indications
    • HTN in pheochromocytoma
190
Q

Methyldopa

  • MOA
  • Indications
A
  • MOA
    • alpha-2-agonist
    • converted to methyl-NE in the brain
      • causes vasomotor centers to decrease NE production
      • decreased vasoconstriction
  • Indications
    • HTN
191
Q

Drugs that treat Pheochromocytoma

A
  1. Phenoxybenzamine
    • chronic treatment
    • surgical resection
  2. Phentolamine
    • diagnosis
    • treat pseudo-obstruction of bowel
  3. Alpha-methyl-tyrosine
    • HTN
192
Q

What drug is used to treat HTN in patients with benign prostatic hyperplasia (BPH)?

A

Terazosin

Doxazosin

193
Q

Guanethidine and Guanadrel

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • Deplete NE stores from sympathetic nerve terminals
    • Results in a massive release at first
  • Indications
    • HTN, rarely used
  • Side effects
    • Hypertensive Crisis w/first dose
194
Q

Reserpine

  • MOA
  • Indications
  • Side effects
A
  • MOA
    • Blocks the VMAT transporter (no NE into vesicles)
    • Depletes terminal of NE stores
  • Indications
    • HTN
  • Side effects
    • May have hypertensive crisis
    • psychotic disorders
      • mimic paranoid schizophrenia
195
Q

Tamsulosin

  • MOA
  • Indications
A
  • MOA
    • alpha-1A-agonist
    • relaxes muscles in bladder neck and prostate
  • Indications
    • HTN with BPH
    • BPH (urinary tract symptoms)
196
Q

Why are guanethidine and guanadrel not currently used as anti-HTN?

A

They cause a large release of NE from nerve terminals, resulting in hypertensive crisis

197
Q

Which drug can cause side effects mimicking paranoid schizophrenia?

198
Q

What drug is used for HTN patients with angina?

A

beta-blocker

199
Q

What drug is used for HTN patients with MI?

A

beta-blocker

Thiazide diuretics

200
Q

What drug is used for HTN patients with CHF?

A

beta blocker

thiazide diuretics

201
Q

What drug is used for HTN patients with a high stroke risk?

A

Thiazide diuretics

202
Q

What drug is used for HTN patients with kidney disease?

A

thiazide diuretics

203
Q

What drug is used for HTN patients with diabetes?

A

thiazide diuretics

204
Q

What drug is used for HTN patients with asthma?

A

ACE inhibitors

ARBs

205
Q

What drug is used for HTN patients with Migraines?

A

beta-blocker (Propanolol)

206
Q

What drug is used for pregnant HTN patients?

A

Methyldopa

207
Q

What drug is used for HTN patients with Atrial fibrillation?

A

Verapamil

Diltiazem

beta-blocker

208
Q

What drug is used for HTN patients with supraventricular tachycardia?

A

Verapamil

Diltiazem

beta-blocker

209
Q

What drug is used for HTN patients with osteoporosis?

A

Thiazide diuretics

210
Q

What drug is used for HTN patients with renal calculi?

A

thiazide diuretics

211
Q

What drug is used for HTN patients with glaucoma?

A

beta-blockers

212
Q

What is the effect of using Diuretics with ACE inhibitors?

A

antihypertensive

controls K levels

Controls excessive reflex AII effects

213
Q

What is the effect of using Diuretics with hydralazine?

A

Prevent fluid retention from hydralazine

214
Q

What is the effect of using Diuretics with beta-blockers?

A

beta-blocker controls reflex activation of CV and RAAS from diuretic

215
Q

What is the effect of using Diuretics with beta-blockers and Ca-channel blockers?

A

refractory HTN

216
Q

What are the causes of cardiac remodeling in CHF? What drugs can be used to reduce this effect?

A
  • Causes:
    • SNS stimulation
    • RAAS
  • Drugs:
    • Beta-blockers
    • ACE inhibitors
217
Q

What are the effects of vasodilator therapy on the failing heart?

A
  • Venodilation: reduced preload
    • decreased pulmonary congestion
    • Little effect on SV
  • Arteriodilation: Decreased afterload
    • increase SV
  • Together:
    • increase perfusion
    • relieve pulm congestion
    • Reduce ventricular chamber size
218
Q

Which venodilators are used in the treatment of CHF?

A
  1. Hydralazine with isorbide dinitrite
  2. ACE inhibitors
219
Q

What are the effects of beta-blockers in CHF?

A
  • reduce arrhythmia
  • reduce water retention (RAAS inhibition)
  • Reduce myocyte apoptosis
    • reduced cardiac remodeling
220
Q

What is the MOA of digitalis?

A
  1. (+) INO
    • increases intracellular Ca2+
    • Increases contractile strength
  2. Increased ventricular performance
    • Increased CO
  3. Automaticity = increase rate of Vm rise in phase 4
    • create ectopic foci/DAD/arrhythmia
  4. Inactivate SA node at high dose
    • create ectopic foci
  5. Increase vagal and decrease SNS to heart
    • decreased nodal conduction
    • Block SA node => heart block!
221
Q

What are the side effects of Digitalis?

A

arrhythmia

Heart Block

222
Q

What drug is contraindicated for use with digitalis?

A

Quinidine

increases digitalis plasma concentration

223
Q

What is used to treat digitalis overdose?

A

Fab Fragments

224
Q

What is the therapeutic application of digitalis?

225
Q

What drugs are indicated when ventricular remodeling is present even if the patient is asymptomatic?

A

ACE inhibitors

Beta-blockers

226
Q

What drugs are indicated in acute heart failure when SBP is over 90?

A
  1. Furosemide (loop diuretic)
    • relieves congestion only
  2. Nitroprusside
    • increased perfusion and relieves congestion
227
Q

What drugs are indicated in acute heart failure if SBP <90?

A
  1. Levisomendan
    • Ca2+ sensitizers
  2. Amrinone
    • increase cAMP
    • (+) INO
  3. Dobutamine
    • Beta-1-agonist
    • stimulates the heart
  4. Dopamine
    • (+) INO
    • Peripheral constrictor
    • renal dilator for increased perfusion
228
Q

What are the actions of thrombin in the clotting cascade?

A
  • Forms and stabilizes the fibrin clot
  • Reactivates the coagulation cascade
  • Triggers platelet activation
229
Q

What cleaves fibrin?

230
Q

Expression of what receptor is the final common pathway to platelet aggregation?

A
  • GP IIb-IIIa
    • Binds fibrinogin and platelets stick together
    • Binds vWF
231
Q

What activates platelets to express GP IIb-IIIa and initiate aggregation?

A
  1. thrombin receptor
  2. ADP
  3. TXA2
232
Q

Aspirin

  • MOA
  • Time to peak action
A
  • MOA:
    • perminant inactivation of COX 1 and 2
    • inhibits TXA2 synthesis
    • Inhibits platelet aggregation
  • Time to peak action: 30-40 minutes
233
Q

Mechanisms of anti-platelet agents

A
  1. Inhibit TXA2
  2. GP IIb/IIIa antagonist
  3. ADP receptor inhibitor
  4. PAR-1 receptor inhibitor
234
Q

What is the effect of ADP receptor inhibitors?

A

anti-platelet aggregation

235
Q

What is the pathology of NSTE acute coronary syndrome?

A
  • Not completely occlusive
  • site of plaque rupture
  • Expose GPIIb-IIIa
  • Platelets cross-link

No ST elevation on ECG

236
Q

What is the pathology of STE MI?

A
  • Caused by complete occlusion
  • Stabilization of platelet aggregation by fibrin

ST elevation on ECG

237
Q

Unfractioned Heparin

  • MOA
  • Limitations
A
  • MOA:
    • Binds anti-thrombin III
      • inactivates Factors IIa, Xa, IXa, XIIa
  • Limitations:
    • Neutralized by platelet factor 4 (PF4)
    • Requires continuous anticoagulant monitoring
238
Q

What is the benefit of Low Molecular Weight Heparin over Unfractionated Heparin?

A

Easier administration

More predictable response, so no monitoring needed

239
Q

Warfarin (Coumadin)

  • MOA
  • How does Vit K affect warfarin activity?
  • Limitations
A
  • MOA: Anti-thrombin
    • inhibits Vitamin K Oxide Reductase
    • Inhibits factors II, VII, IX, and X as well as proteins C and S (can’t be carboxylated)
    • Affects extrinsic pathway
    • Measured by Prothrombin time!!!
  • Dependent by Vit K levels in the body
    • works best with low Vit K
    • High Vit K = need higher dose
  • Limitations
    • Narrow Therapeutic Range
240
Q

What does CHADS2 score measure? What are the factors considered? How does that score affect medication regimine?

A
  • measures stroke risk in A Fib patients
  • CHADS2
    • Congestive heart failure
    • Hypertension
    • Age >75
    • Diabetes
    • Stroke or TIA (worth 2 points)
  • Meds:
    • Score = 0 = aspirin
    • Score = 1 = aspirin or warfarin
    • Score >1 = warfarin
241
Q

Which coagulation pathway does warfarin affect? How is the effect measured?

A

Extrinsic pathway

Prothrombin Time (PT)

242
Q

What is the advantages of Direct Thrombin Inhibitors?

A
  • Affects only one factor
  • Independent of anti-thrombin III
243
Q

What is the effect of Factor Xa inhibitors on thrombin activity, thrombin generation, and platelet function?

A
  • No inhibition of thrombin activity
  • Inhibits thrombin generation
  • No effect on platelet function (unlike heparin)
244
Q

What is the effect of tPA?

A

fibrinolytic

activates plasmin

245
Q

Clotting cascade

Pharmacology (12 decks)

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