Term
| These drugs work by preventing the formation of thromboxane and inhibiting the production of prostaglandins. |
|
Definition
|
|
Term
| These drugs work by preventing the formation of thromboxane and inhibiting the production of prostaglandins. |
|
Definition
|
|
Term
| This class of drugs is used to Tx acute ischemic chest pain and valvular disorders/replacement. |
|
Definition
|
|
Term
| This class of drugs works by preventing the binding of fibrinogen to GP receptors. |
|
Definition
| Platelet Glycoprotein Inhibitors |
|
|
Term
| This class of drugs is used as antithrombotic agents and in percutaneous coronary interventions. |
|
Definition
| Platelet Glycoprotein Inhibitors |
|
|
Term
| This class of drugs blocks the formation of prothrombin and other clotting factors, and deactivates Vitmain K. |
|
Definition
|
|
Term
| This class of drugs catalyzes the conversion of fibrin-bound plasminogen to plasmin (initiating fibrinolysis). |
|
Definition
|
|
Term
| This class of drugs can be used to Tx AMI when catheterization is delayed, Throbmosis CVA, and PVTs/PEs. |
|
Definition
|
|
Term
| This class of drugs replaces missing clotting factors. |
|
Definition
|
|
Term
| This class of drugs is used to Tx hemophilia. |
|
Definition
|
|
Term
| This type of hemostatic agent inhibits plasminogen and plasmin-mediated fibrinolysis. |
|
Definition
|
|
Term
| This type of hemostatic agent mostly works by absorbing plasma from the blood. |
|
Definition
| Topical Hemostatic Agents |
|
|
Term
| This class of drugs is used to stop hemorrhaging. |
|
Definition
| Hemostatic Agents (Tranexamic Acids and Topical Agents) |
|
|
Term
| If you see a drug that ends in "-statins", it most likely belongs to this class of drugs. |
|
Definition
|
|
Term
| Antihyperlipidermics work by... |
|
Definition
Lowering LDL
Lowering Triglycerides
Raising HDL |
|
|
Term
| Indications for use of Red Blood Cells (Packed Cells). |
|
Definition
-Pts w/ a symptomatic deficiency of O2 carrying capacity or tissue hypoxia
-Tissue hypoxia due to inadequate circulating red cell mass
-Hemoglobin level below 6 g/dl
-Complications of sickle cell disease |
|
|
Term
| Contraindications for Red Blood Cell admin. |
|
Definition
a. Chronic, asymptomatic anemia
b. Infection
c. Minor surgery
d. Uncomplicated pregnancy |
|
|
Term
| Precautions for admin of Packed Cells. |
|
Definition
a. Must administer supplemental O2 and O2 sat must be continuously monitored throughout the transfusion
b. Anaphylactoid rxn
c. Allergic rxn
d. Destruction of transfused cells
e. Circulatory overload |
|
|
Term
| Indications for frozen plasma use. |
|
Definition
a. Active bleeding due to deficiency of multiple coagulation factors
b. Severe bleeding due to warfarin therapy
c. Massive transfusion w/ coagulation bleeding |
|
|
Term
| Contraindications of frozen plasma use. |
|
Definition
a. Increasing blood volume or albumin concentration
b. Coagulotherapy that can be corrected with vitamin K admin |
|
|
Term
| Precautions of frozen plasma Tx. |
|
Definition
a. Bacterial contamination
b. Hypothermia |
|
|
Term
| What is the appropriate Tx for suspected AMI/ACS? |
|
Definition
| MONA (morphine, oxygen, nitrates, aspirin) |
|
|
Term
| What is the appropriate Tx for suspected STEMI? |
|
Definition
| MONA, but avoid nitrates with R. sided HF |
|
|
Term
| What is the appropriate Tx for suspected NSTEMI? |
|
Definition
|
|
Term
| What is the appropriate Tx for suspected Stable Angina? |
|
Definition
| Nitrates, CCB, and B-Blockers |
|
|
Term
| What is the appropriate Tx for suspected Prinzmetal's (Variant) Angina? |
|
Definition
|
|
Term
| What is the appropriate Tx for suspected Unstable Angina? |
|
Definition
Primary-aspirin
Secondary-nitrates and B-blockers
CCBs are used only in refractory cases, and morphine should be cautiously admin'd. |
|
|
Term
| ID the components of the acronym MONA. |
|
Definition
Morphine
Oxygen
Nitrates (Nitroglycerin)
Aspirin |
|
|
Term
| Discuss the role of O2 admin for AMI and angina. |
|
Definition
| Regarded as the single most important Tx for ischemic chest pain; goal of AMI/angina Tx is to correct O2 imbalance by reducing demand and increasing supply (O2 admin achieves the latter). |
|
|
Term
|
Definition
a. Facilitates cellular energy metabolism
b. Maintains aerobic metabolism |
|
|
Term
|
Definition
| Supplement O2 for Pts suffering ischemic chest pain to maintain O2 sat @ or >94%. |
|
|
Term
| Side effects of O2 admin. |
|
Definition
a. Free radicals
b. Reflex coronary vasospasm
c. Claustrophobia |
|
|
Term
|
Definition
Nitro breaks down into nitric oxide in smooth muscle cells resulting in vasodilation.
-Decreases preload/afterload
-Relieves coronary spasm
-Increases collateral blood flow |
|
|
Term
|
Definition
-Angina/cardiac-related chest pain
-Pulmonary edema |
|
|
Term
| Side-effects pf nitrate use. |
|
Definition
-HypoTN
-HA
-Decreased platelet aggregation
-Reflex tachycardia (due to hypoTN) |
|
|
Term
| Contraindications of nitrate admin. |
|
Definition
-Systolic BP<90 mm Hg
-Increased ICP
-Hypersensitivity
-Be cautious of inferior wall MI or R. ventricle involvement |
|
|
Term
| Actions of ASA (aspirin). |
|
Definition
a. Prevents the formation of thromboxane A2
b. Inhibits the production of prostaglandins |
|
|
Term
|
Definition
a. Ischemic chest pain
b. Valvular disorders |
|
|
Term
| Uses for morphine sulfate. |
|
Definition
1. Used for pain relief in ischemic chest pain
a. Stimulates opioid receptors (Mu)
b. Causes vasodilation (esp. of veins) and decreases preload/afterload
c. Stimulates histamine release
d. Reduces anxiety |
|
|
Term
|
Definition
| Decrease myocardial force (thus, decreasing O2 demand) |
|
|
Term
| What are the side-effects of CBBs? |
|
Definition
Toxicity results in direct extension of therapeutic effects:
-Serious cardiac depression
-Cardiac arrest
-Bradycardia
-AV Blocks
-HF
These effects may be exacerbated in Pts taking B-blockers. |
|
|
Term
|
Definition
| Decrease HR, BP, and contractility. |
|
|
Term
| The chest pain of stable angina is a result of... |
|
Definition
| An O2 supply and demand issue. |
|
|
Term
| How do you Tx stable angina? |
|
Definition
| Nitrates (#1), CCBs, and B-blockers. |
|
|
Term
| What is the appropriate Tx of Prinzmetal's angina (vasospastic or variant)? |
|
Definition
| Nitrates and CCBs will relieve approx. 70% of all Pt's angina pain. |
|
|
Term
| What is the primary Tx of unstable angina? |
|
Definition
| ASA (aspirin) primary, nitrates and B-blockers secondary, and CCBs only in refractory cases. |
|
|
Term
| This drug should be used very cautiously in unstable angina as there is evidence of increased mortality. |
|
Definition
|
|
Term
| What is the proper Tx of STEMI? |
|
Definition
| MONA (however, avoid nitrates w/ R. sided STEMI) |
|
|
Term
| What is the proper Tx of UA/NSTEMI? |
|
Definition
|
|
Term
| What is the Tx of choice for high output HF? |
|
Definition
|
|
Term
| What is the Tx of choice for low output HF? |
|
Definition
| Dopamine (get the BP back up) |
|
|
Term
| What's the difference between high output and low output CHF? |
|
Definition
| Blood pressure (HO is HTN, LO is hypoTN) |
|
|
Term
| What is the compensatory response of the body to hypotension (4 items)? |
|
Definition
1. Increased sympathetic activity (SVR increases)
2. RAA System activation (increase volume)
3. Ventricular hypertrophy
4. Decreased Hb-O2 affinity at tissue sites |
|
|
Term
| What is EMS Tx of HF? Compare HO vs LO HF |
|
Definition
1. O2/ventilation/CPAP
2. Approp. STEMI/NSTEMI response
3. Nitrates-0.4 mg norm, 1.6 mg for HO
4. Diuretics (being questioned)
5. Morphine (being questioned), 2-4 mg starting dose |
|
|
Term
| What are the basic mechanisms of actions of anti-dysrhythmias (4 items)? |
|
Definition
1. Prolongation of effective refractory period
2. Na+ channel blockers
3. Ca++ channel blockers
4. Sympathetic (Beta) blockers |
|
|
Term
| A lengthened action potential leads to a prolonged... |
|
Definition
|
|
Term
| These drugs are not used in the prehospital setting, but can often lead to cardiac dysrhythmias. |
|
Definition
| Inotropics like Cardiac-Glycosides (digitalis type drugs) and digoxin. |
|
|
Term
| What makes cardiac glycosides and digoxin so dangerous? |
|
Definition
| Highly protein bound with a narrow therapeutic range (so slight alteration can result in toxicity) |
|
|
Term
| Glycosides are positive inotropes, and ________ dromotropes and _________ chronotropes. |
|
Definition
|
|
Term
| In certain Pts with a higher gut bacteria, what can cause a sudden toxic increase in digitalis? |
|
Definition
|
|
Term
| Inotropic meds work by prolonging the refractory period by increasing Ca++ concentration in the vicinity of contractile proteins, which is facilitated by... |
|
Definition
| Inhibiting the Na+-K+ Pumps |
|
|
Term
| Inotropic meds are used for... |
|
Definition
-Chronic Afib Tx
-Paroxysmal Atrial Tachycardia
-Aflutter
-SVT
-Acute HF |
|
|
Term
| What are the actions of O2? |
|
Definition
-Facilitates cellular energy metabolism
-Maintains aerobic respiration |
|
|
Term
|
Definition
| Supplemental O2 for Pts suffering ischemic chest pain to maintain O2 sat @ or >94%. |
|
|
Term
| What are the side-effects of O2 admin? |
|
Definition
-Increase in free radicals
-Reflex coronary vasospasm
-Claustraphobia |
|
|
Term
| What are the actions of nitrates? |
|
Definition
Broken down into nitric oxide, resulting in smooth muscle vasodilation
-Decreases preload/afterload
-Relieves coronary spasm
-Increases collateral blood flow |
|
|
Term
| What are nitrates used for? |
|
Definition
-Angina/cardiac-related chest pain
-Pulmonary edema |
|
|
Term
| What are the side-effects of nitrate admin? |
|
Definition
-HypoTN
-HA
-Decreased platelet aggregation
-Reflex tachycardia (due to HypoTN) |
|
|
Term
| What are the contraindications of nitrate admin? |
|
Definition
-Systolic BP < 90 mm Hg
-Increased ICP
-Be cautious of inferior wall MI or R. ventricle involvement |
|
|
Term
| What are the actions of ASA? |
|
Definition
-Prevents the formation of thromboxane A2
-Inhibits the production of prostaglandins |
|
|
Term
| What are the uses of ASA? |
|
Definition
-Ischemic chest pain
-Valvular disorders |
|
|
Term
| What are the actions of morphine for ischemic chest pain? |
|
Definition
| -Stimulates opioid receptors (Mu) -Causes vasodilation (esp. of veins) and decreases preload/afterload -Stimulates histamine releases -Reduces anxiety |
|
|
Term
| What is the action of Ca++ channel blockers? |
|
Definition
| Decreases myocardial force (decreasing O2 demand) |
|
|
Term
| What are the side-effects of CBBs? |
|
Definition
Toxicity results in direct extensions of therapeutic action:
-Serious cardiac depression
-Cardiac arrest
-Bradycardia
-AV blocks
-HF |
|
|
Term
| These types of drugs cause dissolution of fibrin clots via conversion of plasminogen to plasmin. |
|
Definition
|
|
Term
| What are the actions of digitalis? |
|
Definition
-Prolongs the refractory period
-Inhibits the Na+/K+ pump
-Positive inotrope
-Negative dromotrope
-Mildly negative chronotrope |
|
|
Term
| What are the uses of digitalis? |
|
Definition
-Chronic Tx of Afib, Aflut, PAT, and AVT
-Acute HF |
|
|
Term
| What are the side-effects of digitalis? |
|
Definition
-High degree AV blocks, PVCs, and bigeminal rhythms
-Pts complain of flu-like symptoms and visual hallucinations (green/yellow halos)
-Hypokalemia can cause dig-toxicity |
|
|
Term
| What are the five classes of anti-dysrhythmics? |
|
Definition
-Inotropics
-Class I (Na+ Channel Blockers)
-Class II (B-Blockers)
-Class III (K+ Channel Blockers)
-Class IV (Ca++ Channel Blockers) |
|
|
Term
| This class of antidysrhythmics slows phase 0, and prolongs phase 4. |
|
Definition
|
|
Term
| This class of antidysrhythmics depresses the pacemaker rate, conduction and excitability. |
|
Definition
|
|
Term
| This class of antidysrhythmics decreases the AP and refractory period; is used for emergency Tx of VTach/VFib. |
|
Definition
|
|
Term
| Quinidine and procainamide belong to what class of antidysrhythmics? |
|
Definition
|
|
Term
| Lidocaine and phenytoin belong to what class of antidysrhythmics? |
|
Definition
|
|
Term
| Drugs ending with "-olol" typically belong to what class of antidysrhythmics? |
|
Definition
|
|
Term
| These antidysrhythmics block B1 receptors, decreasing HR, contracility and conduction; used to Tx PSVTs and SVTs. |
|
Definition
|
|
Term
| This class of antidysrhythmics works by prolonging the AP by blocking K+ channels in cardiac muscle. |
|
Definition
|
|
Term
| Amiodarone and bretylium are examples of what class of antidysrhythmics? |
|
Definition
|
|
Term
| These antidysrhythmics (sp. amiodarone) are used to Tx pulseless VFib/VTach, ventricular dysrhythmias, and atrial dysrhythmias (off-label)? |
|
Definition
|
|
Term
| This class of antidysrhythmics blocks activated Ca++ channels, and they're used to Tx AFib/AFlut, and as a second line drug for PSVT. |
|
Definition
|
|
Term
| Verapamil is a Class ____ antidysrhythmic. |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Na+ Channel Blocker (Class IB) |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Na+ Channel Blocker (Class IA) |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Inhibiting AV node conduction, and increasing the AV node refractory period |
|
|
Term
| MagSulfate affects the... |
|
Definition
| Na+/K+ Pump, and some Na+, K+, and Ca++ Channels |
|
|
Term
|
Definition
| Inotrope, and inhibits the enzyme that breaks down cAMP |
|
|
Term
| What is the role of nitric oxide (NO) in smooth muscle contraction? |
|
Definition
| It is a potent vasodilator released by the vascular endothelium. |
|
|
Term
| What are the four categories of anti-HTN meds? |
|
Definition
Diuretics
Sympathoplegic Agents
Vasodilators
Angiotensin Blockers |
|
|
Term
| What are the 3 side-effects of most all anti-HTN meds? |
|
Definition
| Orthostatic HypoTN, dizziness, and HA |
|
|
Term
| How do diuretics function as anti-HTNs? |
|
Definition
| Lower BP by depleting the body of Na+ and water. |
|
|
Term
| How do sympathoplegic agents function as anti-HTNs? |
|
Definition
1. Lower BP by reducing PVR, inhibiting cardiac function, and increasing venous pooling in capacitance vessels
2. All accomplished by blocking actions of NE |
|
|
Term
| How do vasodilators function as anti-HTNs? |
|
Definition
| Relax smooth muscle arterioles |
|
|
Term
| How do angiotensin blockers function as anti-HTNs? |
|
Definition
| By blocking the production or action of angiotensin. |
|
|
Term
| What are the five subclasses of diuretics? |
|
Definition
-Thiazide diuretics
-Loop diuretics
-Potassium-sparing diuretics
-Carbonic anhydrase inhibitors
-Osmotic diuretics |
|
|
Term
| These diuretics work by inhibiting carbonic anhydrase (RBC enzyme), inhibit NaCl reabsorption, and increase Ca++ reabsorption. |
|
Definition
|
|
Term
| These diuretics inhibit the Na+/K+/2Cl- transport system, inhibit NaCl reabsorption, and increases Mg++ and Ca++ excretion. |
|
Definition
|
|
Term
| This type of diuretic is indicated for pulmonary edema, mild hyperkalemia, and acute renal failure. |
|
Definition
|
|
Term
| These diuretics antagonize the effects of aldosterone, and are most useful in Pts taking Digitalis. |
|
Definition
| Potassium-sparing diuretics |
|
|
Term
| What is a side-effect of Potassium-Sparing diuretics? |
|
Definition
|
|
Term
| This type of diuretic inhibits the breakdown of H2CO3, thus blocking NaHCO2 reabsorption. |
|
Definition
| Carbonic Anhydrase inhibitors |
|
|
Term
| This type of diuretic can be used to Tx glaucoma. |
|
Definition
| Carbonic Anhydrase inhibitors |
|
|
Term
| This type of diuretic is typically used in acute settings (i.e. ICP Tx), and consists of hypertonic solutions that cause fluid to shift into lumens. |
|
Definition
|
|
Term
| These diuretics work in the brain to stimulate A2 receptors (which blocks NE release); also inhibit renin and stop vasoconstricting Alpha1 activity. |
|
Definition
| Central A2 Adrenergic Agonists |
|
|
Term
| What are the 4 types of sympathoplegic agents? |
|
Definition
-Central A2 Adrenergic Agonists
-Alpha1 Blockers
-Beta Blockers
-Calcium Channel Blockers |
|
|
Term
| This sympathoplegic agent is indicated for mild-moderate HTN, and as a second-line drug for mild-moderate HTN in an acute setting. |
|
Definition
| Central A2 Adrenergic Agonists |
|
|
Term
| This sympathoplegic agent competitively binds to Alpha1 receptor sites, preventing NE action. |
|
Definition
|
|
Term
| Alpha1 Blockers are indicated for Pts with... |
|
Definition
-Chronic HTN
-Pheochromocytoma caused HTN |
|
|
Term
| This class of sympathoplegic agents tend to end in "-olol". |
|
Definition
|
|
Term
| What are the actions of Beta Blockers? |
|
Definition
i. Blocks B-receptors w/ different selectivity
ii. Beta blockade opposes B2-mediated vasodilation that may initially cause HTN
iii. – Chronotrope, - Inotrope, - Dromotrope
iv. Antagonize the release of renin |
|
|
Term
| Beta blockers are indicated for... |
|
Definition
i. HTN
ii. Antianginal
iii. Antidysrhythmic
iv. Glaucoma
v. Neurologic Diseases |
|
|
Term
| What side-effect of Beta Blockers is cause for concern? |
|
Definition
| May precipitate bronchospasm due to blocking of B2 receptors. |
|
|
Term
| This class of sympathoplegic agents tend to end in "-dipine". |
|
Definition
|
|
Term
| What are the actions of Ca++ Channel blocking sympathoplegic anti-HTNs? |
|
Definition
-Dilate peripheral arterioles by inhibiting Ca++ influx thru slow channels
-Reduce heart contractility, conduction and automaticity |
|
|
Term
| Verapamil, diltiazem, and nifedipine function how as Ca++ blockers? (what end of the spectrum) |
|
Definition
-Verapamil = 100% cardiac
-Diltiazem halfway between verapamil and nifedipine
-Nifedipine = 100% vasculature |
|
|
Term
| Ca++ Channel Blockers are indicated for... |
|
Definition
-Antianginal
-Antidysrhythmic
-Anti-HTN |
|
|
Term
| What are the subclasses of vasodilator anti-HTNs? |
|
Definition
-Central-acting agents
-Oral vasodilators
-Parenteral vasodilators |
|
|
Term
| How do central-acting agents works as anti-HTNs? |
|
Definition
| Depress the CNS, which causes vasodilation, which decreases BP. BOOM! |
|
|
Term
| What are the side-effects of central-acting agents? |
|
Definition
| Drowsiness and depression |
|
|
Term
| This subclass of vasodilators dilates smooth muscle arterioles, and in some cases stabilize the RMP, reducing contraction. |
|
Definition
|
|
Term
| This class of vasodilators works by dilating arterial and venous vessels by increasing NO release/opening K+ channels. |
|
Definition
|
|
Term
| What are the 4 sub-classes of angiotensin blockers? |
|
Definition
-ACE Inhibitors
-Angiotensin I Receptor Agonist
-Angiotensin II Receptor Blockers
-Renin Inhibitors |
|
|
Term
| This sub-class of angiotensin blockers works by stopping the conversion of angiotensin I to angiotensin II. |
|
Definition
|
|
Term
| These angiotensin blockers are indicated for post AMI w/CHF Pts, and to stabilize renal fxs in Pts w/ diabetic nephropathy. |
|
Definition
|
|
Term
| These angiotensin blockers block stimulation of post-synaptic Alpha1 receptors (inhibiting NE reuptake and reducing PVR in both arteries/veins). |
|
Definition
| Angiotensin I Receptor Antagonists |
|
|
Term
| Angiotensin I Receptor Agonsists are indicated for... |
|
Definition
|
|
Term
| This sub-class of angiotensin blockers works by blocking the release of renin from the kidney, negating the effects of the RAS. |
|
Definition
|
|
Term
| Why is polypharmacy common in the Tx of HTN? |
|
Definition
| Different drugs act on one of a set of interacting mutually compensatory mechanisms for maintaining BP (= more effective). |
|
|
