Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
152 Cards in this Set
- Front
- Back
Name some conditions (not diseases) promoting the development of edema.
|
- Altered blood circulation (increased arterial and venous pressure)
- Altered blood composition (decreased osmotic gradient, salt and water retention) - Inadequate lymphatic drainage |
|
Name some diseases promoting the development of edema.
|
CHF
Hepatic cirrhosis Nephritis, Nephrosis, Renal damage due to HTN Diseases involving increased steroid hormone secretion Pre-eclampsia, toxemia Hypersensitivity reactions (anaphylactic shock, etc) |
|
What is the Distal Diluting Site?
|
a segment consisting of cortical diluting portion of ascending limb and the early section of the distal tubule
|
|
What might be an indication of neprhotoxicity of drugs?
|
Drug induced glucosuria and aminoaciduria
|
|
Which organic compounds can be secreted and reabsorbed by diffusion?
|
depends on lipid solubility, pKa, pH, etc. (glucose, amino acids, vitamins, etc)
|
|
What is an example of an organic compound that uses carrier mediated reabsorption?
|
uric acid
|
|
What are the most widely used diuretics?
|
thiazides
|
|
How do thiazides cause Hypokalemia?
|
potassium excretion is stimulated by an increasing sodium load presented to the distal exchange sites because of its non-reabsorption at an earlier site.
They also cause plasma volume contraction. The reduced plasma volume acts as a stimulus for aldosterone secretion which also encourages potassium loss. (a combination of these 2 mechanisms causes hypokalemia) |
|
How do thiazides cause hyperuricemia?
|
They decrease the excretion of uric acid in the tubule. Thiazides and uric acid compete for the same secretory mechanism of the renal tubule
|
|
How do thiazides decrease calcium excretion?
|
parathyroid hormone dependent Gs phosphorylates calcium channels, increases calcium reabsorption
|
|
How do thiazides cause hyperglycemia?
|
they may decrease the release of insulin and increase glucose intolerance. Important in Type 2 DM
|
|
What is excreted in excess in the urine of people taking Loop agents and thiazides?
|
NaCl
|
|
What is secreted in excess in the urine of people taking loop diuretics?
|
NaCl
|
|
What is secreted in excess in the urine of people taking carbonic anhydrase inhibitors?
|
NaHCO3
|
|
What do venodilator drugs do?
|
reduce preload by redistributing blood from the heart to the peripheral veins
|
|
What do arteriodilator drugs do?
|
reduce afterload by dilating arteries to decrease peripheral vascular resistance
|
|
What drugs affect contractility?
|
Inotropic drugs increase contractility
Beta adrenergic blockers decrease contracility |
|
How is digitalis toxicity treated?
|
with potassium and NEVER with calcium
|
|
How does digitalis cause bradycardia in normal hearts?
|
By decreasing vagal stimulattion due to:
- sensitization of arterial baroreceptors - stimulation of central vagal nuclei - increased SA node sensitivity to actylcholine |
|
How does digitalis cause bradycardia in failing hearts?
|
sympathetic tone is already high then as digitalis increases myocardial contractility sympathetic tone will be reduced
|
|
Is cardiac output increased in both normal and failing hearts by digitalis?
|
no just failing hearts due to increased peripheral vasoconstriction in individuals with normal heart function
|
|
What actions result in electrical effects of digitalis?
|
direct action on myocardial cells
Indirect action by parasympathetic stimulation |
|
In whom does digitalis cause diuresis?
|
in edematous patients with CHF as a result of hemodynamic improvement
|
|
What is the most common cause of death due to digitalis toxicity?
|
Ventricular fibrillation
|
|
How do you treat digitalis toxicity? (other than potassium)
|
discontinue digitalis administratin
Lidocaine, phenytoin, propranolol immunotherapy with Digitalis Immune Fab |
|
What do pharmicokinetic interactions of digitalis do?
|
they either enhance toxicity or reduce effectiveness
|
|
What do pharmacodynamic interactions of digitalis do?
|
they enhance toxicity
|
|
Why does hypothyroidism predispose one to digoxin intoxication?
|
by reducing renal clearance which elevates serum digoxin levels
|
|
Where are fast-response fibers found?
|
atria
ventricles bundle of His Purkinje fibers |
|
Where are slow-response fibers found?
|
SA node
AV node |
|
What is excitability?
|
the ability of a myocardial cell to respond to a stimulus by producing and action potential
|
|
What is automaticity?
|
spontaneous diastolic depolarization during phase 4.
i.e. the cell's inherent ability to initiate a cardiac impulse |
|
What is ERP (effective refractory period)?
|
the shortest interval at which a premature stimulus results in a propagated response.
|
|
What is the Action Potential Duration (APD)?
|
the time interval between the point of depolarization and repolarization
|
|
Which drugs slow phase 3 repolarization?
|
thioridazine
TCA-S Class I A Class III |
|
What do you really need to differentiate between in order to administer Verapamil?
|
know if the pt has ventricular or supraventricular tachycardia because if administered to pts with ventricular tachy it can cause ventricular fib, severe hemodynamic deterioration, or death
|
|
What are some common CV complications of HTN?
|
CAD leading to heart failure
Stroke Renal Failure |
|
What is normal BP?
|
<120
<80 |
|
What is prehypertension?
|
120-139
80-89 |
|
What is Stage 1 Hypertension?
|
140-159
90-99 |
|
What is Stage 2 Hypertension?
|
>=160
>=100 |
|
What is the most common cause of treatment failure in HTN?
|
non-compliance
|
|
How much do antihypertensives reduce BP?
|
almost all antihyptertensives will lower BP by at least 10% in mild to moderate HTN
|
|
What diastolic pressure would be dangerous in elderly hypertensives?
|
coronary perfusion may become inadequate at diastolic pressures <90mmHg --> morbidity and mortality may increase
|
|
What is the first line drug of choice for tx of HTN in most pts?
|
Thiazides
|
|
Which conditions are compelling indications for the initial use of other antihypertensive drugs (not thiazides)? What drugs would you use?
|
Certain high risk conditions:
- DM, Kidney disease, IHD, HF, Cerebrovascular disease Drugs: - ACE inhibitors, angiotensin-receptor blockers, beta-blockers, Ca2+ channel blockers |
|
What is the "polypill"?
|
One tablet that would include:
- a statin - an ACE inhibitor - a Thiazide diuretic - a beta blocker - aspirin - folic acid |
|
Which 2 doctors thought up the "polypill"?
|
Nicholas J Wald
Malcom R Law |
|
What type of pts would you prescribe loop diuretics for?
|
severe HTN cases, pts with renal insufficiency, CHF
|
|
Why should vasodilators not be used for monotherapy?
|
because the antihypertensive effects tend to diminish with time because of reflex tachycardia and increased renin secretion. Most effective when combined with other drugs to prevent the undesirable side-effects
|
|
Why are oral nitrates no longer used for chronic antihypertensives?
|
because they become ineffective as tolerance develops
|
|
Where are AT1 receptors located (angiotensin II receptors)?
|
predominate in vascular smooth muscle and cause most of the known actions of angiotensin II
|
|
Where are AT2 receptors located?
|
present in many tissues but they are not related to the regulation of CV homeostasis
|
|
What is the etiology of Variant/Prinzmetal's angina?
|
spasm or constriction in atherosclerotic coronary vessels
|
|
What is the treatment of variant/Prinzmetal's angina?
|
reversed by nitrates or calcium channel blockers
|
|
What is the etiology of classic/atherosclerotic "angina of effort"?
|
atheromatous obstruction of large coronary vessels especially with exercise
|
|
What is the treatment of classic/atherosclerotic "angina of effort" ?
|
if uncontrolled by drugs may require coronary bypass or angioplasty
|
|
How much O2 does the heart normally extract at rest?
|
75% of the O2 in arterial blood
|
|
What is coronary blood flow directly related/proportional to?
|
perfusion pressure
duration of diastole |
|
How can additional O2 be made available to the heart?
|
only by increasing O2 delivery through coronary blood flow
|
|
What is the major mechanism for all currently used antianginal drugs?
|
decreasing O2 demand through reduced cardiac work
|
|
What is another mechanism (not the major one) for altering O2 balance for angina?
|
increasing O2 supply through coronary vasodilation - ineffective becuase of "coronary steal phenomenon"
|
|
What drugs improve regional flow distribution (in the heart for angina)?
|
nitrates
calcium channel blockers beta blockers |
|
What drugs increase coronary blood flow?
|
nitrates
calcium channel blockers |
|
What drugs decrease heart rate and contractility?
|
beta blockers and some calcium channel blockers
|
|
What drugs decrease preload?
|
nitrates
|
|
What drugs decrease afterload?
|
calcium channel blockers
|
|
What is "Monday Disease"?
|
People who manufacture explosives are chronically exposed to high nitrate levels. This may cause tolerance leading to Monday disease. Headache and dizziness on Mondays b/c of the tolerance to the nitrates diminishes on weekends; symptoms gradually disappear during weekdays as tolerance develops again with continuous exposure
|
|
What are the 2 functions of intracellular calcium?
|
1. triggers muscular contraction in both the myocardium and vascular smooth muscles
2. required for pacemaker activity of the SA node and for conduction through the AV node |
|
In the heart and vascular smooth muscle, calcium channels have 2 actions...
|
opened by beta stimulation to enhance calcium entry and closed by CCAs to inhibit calcium entry
|
|
What drugs are more effective in variant angina?
|
nitrates and CCAs are more effective than beta blockers because beta blockers will not dilate spastic coronary blood vessels
|
|
What are the most common drug combinations used for angina?
|
beta blockers + CCAs
2 CCAs potentially harmful effects of CCAs or beta blockers can be prevented by combined tx with nitrate and vice versa Reflex tachycardia can be minimized by combining nitrates with CCAs or Beta blockers |
|
What is the target of Heparin Sodium and Low Molecular Weight Heparins?
|
Activated clotting factors
|
|
What is the target of Lepirudin, Bivalirudin, and Argatroban?
|
Inhibits thrombin
|
|
What is the target of Warfarin?
|
Clotting factor synthesis
|
|
What is the target of Protamine sulfate?
|
Binds heparins
|
|
What is the target of Vitamin K1?
|
Competes with Warfarin
|
|
What is the target of t-PA, Streptokinase, Urokinase, and Anistreplase?
|
Activates plasminogen to plasmin
|
|
What is the target of aminocaproic acid and tranexamic acid?
|
inhibits plasminogen activation
|
|
What is the target of aspirin?
|
irreversibly inhibits thromboxane synthase
|
|
What is the target of Plavix and Ticlid?
|
Inhibits ADP receptors
|
|
What is the taret of Abciximab, Eptifibatide and Tirofiban?
|
Inhibits GPIIb/IIIa receptors
|
|
What is the target of Cilostazol?
|
phosphodiesterase II inhibitor
|
|
What is hemostasis?
|
the arrest of bleeding when blood vessels are damaged
|
|
In what 3 ways is hemostasis achieved?
|
1. vascular contraction
2. platelet adhesion, activation, and aggregation 3. fibrin formation and reinforcement of the platelet plug (coagulation) |
|
What does Tissue Factor Pathway Inhibitor (TFPI) do?
|
blocks the activity of TF/VIIa
|
|
What does Protein C along with its cofactor Protein S do?
|
destroys factors Va and VIIIa
|
|
What does Thrombomdulin do?
|
on endothelial cells, allows activation of protein C by thrombin
|
|
What does ATIII do?
|
a plasma protease inhibitor that inactivates clotting factors
|
|
What does alpha1-antiprotease and alpha2-macroglobuin do?
|
like ATIII, inactivate clotting factors
|
|
What does alpha2-antiplasmin do?
|
inactivates plasmin
|
|
What does plasmin do?
|
Digests fibrin and many of the clotting factors
|
|
How is plasminogen cleaved to plasmin?
|
tissue plasminogen activator released from endothelial cells
|
|
What is a white thrombus?
|
the initial plug formed by platelets in high-pressure arteries
|
|
What is a red thrombus?
|
a mesh-like thrombus that includes RBCs
|
|
What does aPTT measure?
|
time to clotting following addition of calcium, negatively-charged phospholipids and kaolin (aluminum silicate)
aPTT is a measure of the intrinsic coagulation pathway |
|
What does PT measure?
|
time to clotting following addition thrombosplastin (a brain extract containing tissue factor and phospholipids) these values are usually normalized to an international standard and presented as the international normalized ratio (INR)
this is a measure of the extrinsic pathway |
|
Where is endogenous heparin found?
|
in mast cells, in the plasma, and in the endothelial layer of mast cells
|
|
What is heparin a mix of?
|
sulfated mucopolysaccharides
|
|
What is Heparin-Induced Thrombocytopenia?
|
a new thrombus while on heparin therapy is assumed to be heparin induced; discontinue heparin and use alternatives: lepirudin (in pts with hepatic insufficiency), argatroban (in pts with renal insufficiency), bivalirudin, or danaparoid
|
|
What is Arnica (leopardsbane, wolfsbane)?
|
an herbal produce puported to relieve bruising and help reduce pain and inflammation associated with skin wounds and infections - no scientific evidence to support these claims
|
|
What drug group do these drugs belong to?
Acetazolamide Brinzolamide Dorzolamide |
Carbonic Anhydrase Inhibitors
|
|
What drug group do these drugs belong to?
Furosemide Ethacrynic Acid |
Loop Diuretics
|
|
What drug group do these drugs belong to?
Bumetanide Torsemide |
Newer Loop Diuretics
|
|
What drug group do these drugs belong to?
Hydrocholorothiaizide |
thiazides
|
|
What drug group do these drugs belong to?
Metolazone Indapamide |
Compounds related to Thiazides
|
|
What drug group do these drugs belong to?
Amiloride Triamterene |
Potassium Sparing Drugs
|
|
What drug group do these drugs belong to?
Spironolactone Eplerenone |
Aldosterone Antagonists
|
|
What drug group do these drugs belong to? Mannitol
|
Osmotic diuretics
|
|
What drug group do these drugs belong to?
Vasopressin Desmopressin |
ADH Agonists
|
|
What drug group do these drugs belong to?
Demeclocycline Lithium Conivaptin Tolvaptan |
ADH antagonists
|
|
What drug group do these drugs belong to?
Inamrinone Milrinone "-none's" --> "nuns!!" |
Phosphodiesterase inhibitors
|
|
What drug group do these drugs belong to?
Dobutamine Dopamine |
Sympathomimetics
|
|
What drug group do these drugs belong to?
Levosimendan Pimobendan |
Calcium sensitizers
|
|
What drug group do these drugs belong to?
Nesiritide |
B type Natriuretic peptide (BNP)
|
|
What drug group do these drugs belong to?
Captopril Enalapril |
ACE inhibitors
|
|
What drug group do these drugs belong to?
Losartan Valsartan Candesartan? |
Angiotensin II receptor inhibitors
|
|
What drug group do these drugs belong to?
Bisoprolol Carvedilol Metoprolol |
Beta blockers
|
|
What drug group do these drugs belong to?
Sodium nitroprusside Hydralaxine Isosorbide dinitrate |
Vasodilators
|
|
What class of drugs do these drugs belong to?
Quinidine Procainamide Disopyramide |
Class IA antiarrhythmics
(Na+ channel blockers) |
|
What class of drugs do these drugs belong to?
Lidocaine Phenytoin Tocainide Mexiletine |
Class IB antiarrhythmics
(Na+ channel blockers) |
|
What class of drugs do these drugs belong to?
Flecainide Propafenone Moricizine |
Class IC antiarrhythmics
(blocks ALL sodium channels) |
|
What class of drugs do these drugs belong to?
Propranolol |
Class II antiarrhythmics - Beta blockers
|
|
What class of drugs do these
drugs belong to? Amiodarone Sotalol Bretylium Ibutlilide Dofetilide |
Class III antiarrhythmics - K+ channel blockers
|
|
What class of drugs do these drugs belong to?
Verapamil Diltiazem Bepridil |
Class IV antiarrhythmics
Ca2+ channel blockers |
|
What class of drugs do these drugs belong to?
Adenosine |
Nucleoside that occurs naturally throughout the body
|
|
What class of drugs do these drugs belong to?
Magnesium Potassium |
the "other" antiarrhythmics
|
|
What class of drugs do these drugs belong to?
Methyldopa Clonidine |
Centrally acting sympathoplegic drugs - alpha 2 agonists
|
|
What class of drugs do these drugs belong to?
Mecamylamine Trimetaphan |
Ganglion blocking agents
|
|
What class of drugs do these drugs belong to?
Guanethidine Reserpine |
Adrenergic neuron-blocking agents
|
|
What class of drugs do these drugs belong to?
Phenelzine |
MAOIs
|
|
What class of drugs do these drugs belong to?
Prazosin Doxazosin Terazosin |
alpha1 blockers
|
|
What class of drugs do these drugs belong to?
Labetalol Carvedilol |
Combined alpha and beta blockers
|
|
What class of drugs do these drugs belong to?
Hydralazine Sodium Nitroprusside |
Vasodilators working through NO
|
|
What class of drugs do these drugs belong to?
Minoxidil Diazoxide |
Vasodilators - Drugs acting to open potassium channels
|
|
What class of drugs do these drugs belong to?
Verapamil Diltiazem Nifedipine Minodipine Amlodipine |
Ca2+ channel blockers
|
|
What class of drugs do these drugs belong to?
Captopril Enalapril |
ACE inhibitors
|
|
What class of drugs do these drugs belong to?
Losartan |
Angtiotensin Receptor blockers
|
|
What class of drugs do these drugs belong to?
Aliskiren |
Renin inhibitor
|
|
What class of drugs do these drugs belong to?
Nitroglyerin Isosorbide dinitrate |
Nitrates/Nitrites
|
|
What class of drugs do these drugs belong to?
Sildenafil Vardenafil Taladafil |
Phosphodiesterase Type 5 Inhibitors
|
|
What class of drugs do these drugs belong to?
Ranolazine |
partial fatty acid oxidation inhibitor
|
|
What class of drugs do these drugs belong to?
Cholestyramine |
Bile acid binding resins
|
|
What class of drugs do these drugs belong to?
Nicotinic acid (Niacin, Nicobid) |
drugs that impair synthesis of lipoprotiens
|
|
What class of drugs do these drugs belong to?
Lovastatin Pravastatin Simvastatin Fluvastatin Atorvastatin Rosuvasatin |
HMG-CoA Reductase Inhibitors
|
|
What class of drugs do these drugs belong to?
Gemfibrozil Fenofibrate |
Fibric Acid derivatives
|
|
What class of drugs do these drugs belong to?
Ezetimibe |
Inhibitor of cholesterol absorption
|
|
What class of drugs do these drugs belong to?
Heparin sodium Enoxaprin Warfarin |
anticoagulants
|
|
What class of drugs do these drugs belong to?
Protamine sulfate Vitamin K |
Agents for reversing anticoagulant effects
|
|
What class of drugs do these drugs belong to?
t-PA Streptokinase Urokinase Anistreplase |
Fibrinolytic agents
|
|
What class of drugs do these drugs belong to?
Aminocarpoic acid Tranexamic acid |
Antirfibrinolytics
|
|
What class of drugs do these drugs belong to?
Aspirin Clopidogrel Abciximab Ticlopidin |
Antiplatelet agents
|