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108 Cards in this Set

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Diuretics are clinically used for the purpose of -------?
Diuresis - loss of water and reduction of extracellular volume
Name major side effects of diuretics?
Electrolyte imbalance
Name the three family groups of drugs that act on or closely associated with the Kidney?
1. Diuretics - thiazides, loop diuretics,K-sparing, aldosterone inhibitors, CA inhibitors, Osmotic agents, ADH agents

2. Non-diuretic inhibitors of Tubular transport: Uricosuric agents,

3.Renin angiotensin system: ACE inhibitors,AII receptor antagonist and Losartan potassium(imidazole - AT1receptors)
Name abnormalities in body fluid distribution where diuretics can be used?
Edema and Glaucoma
Why can thiazides be used for treatment of Calcium stones?
What is the mechanism of thiazide?

For both questions name the site of action
1. Stimulates the reabsorption of Ca2+ (distal tubule)
2. Inhibits the active reabsorption of NaCl (early distal convoluted tubule)
Thiazide increases the excretion of 4 electrolytes- name them and which of the 4 is excreted at high doses?
1. Na+, Cl-, K+ and HCO3-

2. HCO3- at high doses
Thiazides can be a weirdly enough -a derivative of?
Sulfonamides (many inhibit Carbonic anhydrase - leading to loss in HCO3-) in proximal tubule
Furosemide is specifically what type of drug?
Ethacrynic is specifically what type of drug?
1.Furosemide - Sulfonamide loop diuretic

2. Ethacrynic- Phenoxyacetic acid loop diuretic
What are the Toxic effects of Loop diuretics (such as Furosemide and ethacrynic acid)? (OH DANG)
1. Ototoxicity
2. Hypokalemia
3.Dehydration
4.Allergy (sulfa) - not seen in Ethacrynic
5. Nephritis (interstitial)
6.Gout
Name ADH antagonist? To treat what?
1. Demeclocycline and Lithium carbonate (make you not pee)

2. SIADH
1.Name an acidifing salt?
2.Why use it with Loop diuretics(high ceiling diuretics)
1.NH4Cl (lows PH and increase lumen of Cl- and Na+)
2.Counteract alkalosis of the loops
Name an Uricosuric drug (increase excretion of Uric acid)? May prolong the serum levels of Penicillin and used for Gout!

What other drugs can treat gout?
1.Probenecid
2. Sulfinpryrazone

3. Allopurinol (inhibits xanthine oxidase)
1. Mechanism of ACE inhibitors?
2. Effect on Bradykinin metabolism? 3.Action of Bradykinin?
Side effect?
1.Prevents the conversion of AGI to AGII
2. Increases Bradykinin levels (ACE acts to breakdown Bradykinin). Its is a vasodilator - drop in BP - COUGH.
Name some ACE inhibitors?
Side effects?
1. Captopril, enalapril and Lisinopril
2. CAPTOPRIL -
Cough and Angioedema
Proteinuria and Taste changes
hypOthension and Pregnancy
Rash and Increase Renin
Lower AGII
(also hyper-K)
Name an AGII receptor antagonist? metabolized in body by what?
Why use AGII instead of ACE inhibitor?
1.Losartan potassium
2.P450
3. No cough due to high Bradykinin levels
In heart failure what is dimishned - HR or Ventricular vol and pressure or Stroke volume?
Stoke volume
what drugs bind digitoxin and interfere with therapy?
Cholestyramine and Neomycin
What are some drug interactions with cardiac glycosides (Digoxin and digitoxin)?
1. Hypo-K (thiazides)- this increases toxicity of these drugs
2. Hypercalcemia- prolong as well the action as well as the toxicity
3. Quindine - displaces digoxin from tissue bind

bascially anything drug or condition that prevents Cardiac glycosides from binding to the Na K ATPase transporter
Name drugs used for the treatment of CHF?
1. Cardiac glycosides
2. ACE inhibitors -long term
3. other Inotropic - Amirione, Milrione
4. Dobutamine- short term
5. Diuretics
6. Vasodilators - Hydralazin, prazosin
What are the principal drug for the Tx of CHF and Certain Arrhythmias (atrial fibrillation and flutter and paroxysmal atrial tachycardias)?
How?
1. Cardiac Glycosides
2. CHF - (they increase contractility)
Atrial Fibrillation (They reduce conduction at AV node)
What is Digoxin's
1.Bioavailability (%)?
2.What % is bound to protein?
3. Half life
4. How is it excreted?
5. What condition can change the half-life?
1. 75% is bioavaible
2. 20-40% is protein bound
3. 40hours T1/2 (1.5days)
4. Secreted in the Urine
5. Renal insufficiency
When cardiac glycoside increase vagal activity on the heart what is the effect?
Inhibits SA node and delays conduction thru AV node
Mechanism of digoxin?
What happens to intracellular Na+(from ECM) and intracellular Ca+ (From SR)?
Function of Na+/Ca2+ Antiport?
1. Inhibits Na+/K+ ATPase (Na out:K in)
2. Na+ and Ca2+ increases
the increase in Ca2+- increases contractility
3.Na+/Ca2+ exchanger (Na+ in: Ca+ out)
Toxicity of digoxin?
(for 1 Tox. think Van Gogh)
Where is the most common site of action outside the heart?
1. Blurry yellow-green vision
2.Others - Arrhythmia, Nausea, Vomiting

Digoxin affects all excitable tissue
3. GI - this explains the GI Si/Sx
Digitalis has its action on which cell membrane transporter?
Na/K ATPase
Ryanodine has its action on which channel?
Activates Calcium release channel in the sarcoplasmic receptor
Calcium enters cardiac cells through which channel?
Voltage-gated calcium channel
Cytoplasmic calcium concentrations in cardiac cells can be decreased by sequestering calcium in the sarcoplasmic reticulum. Calcium enters the SR through which transporter?
Calcium pump in the wall of the SR
Calcium channel blockers have their effect on which calcium transporters?
Voltage-gated calcium channel
Name two ECG changes ellicited by digoxin administration
PR?
QT?
ST?
T-wave?
1. increase PR, decrease QT, scooping of ST segment, T-wave inversion
Which potentiates the effects of digoxin- hypo- or hyperkalemia?
hypokalemia-
K+ interferes with the binding of digioxin - the less resistance with to binding Hypo-K

K trys to prevent the bad effects of digoxin (with no K around - digoxin is free to be bad)
How does quinidine increase digoxin toxicity?
what are the two other things that increase digoxin toxicity?
1. Displaces Digoxin from tissue binding sites
2. Quinidine, Renal failure, Hypo-K
What is used to treat Digoxin toxicity?
1. Potassium (K+)
2. Lidocaine
3.Cardiac pacemaker
4. Anti-dig Fab Fragment
Many Antiarrhythmics are state dependent - most affect what tissue state?
Normally depolarized
What is the mechanism of class I anti-arrhythmic drugs?
What are the subsets?
1. Block Na+ channels
2. Class IA, IB, IC

Except IC blocks both K+ and Na+ channels
What type of antiarrhythmic are flecainide, encainide, propafenone?
Function?
Therapy for?
Limitation and Toxicity?
1.Class IC
2.Slow Conduction
3. V-Tachs --> Ventricular Fibrillations--> Supra VT
4. Last resort drugs too -toxic
Toxicity - Proarrhythmitic
What is the effect of Action potential by Class IC?
Class IB?
Class IA?
1. Class IC:None - effect
2. Class IB: Decreased (look at p321)
3. Class IA: Increased lead to - increased effective refractory period (ERP)
Name the 3 drugs of Class IB?
Tx for what?
1. Lidocaine, mexiletine, tocainide
2. Acute V-arrhythmia(esp. post MI) and digitalis induced arrhythmia
Do class 1A antiarrhythmics increase or decrease the effective refractory period, AP duration, and QT interval?
Increase ERP, increase AP duration, increase QT interval
This mneumonic is for class IA.
Queen Amy Proclaims Diso'sPyramid.
Quinidine, Amiodarone, Procainamide, Disopyramide, "Queen Amy Proclaims Diso's pyramid."
Toxicity of Quinidine?
1. Cinchonism - Dizziness and tinnitus (headaches)
2. Thrombocytopenia
3. Torsades de pointes
Why do we have Torsades de pointes with Quinidine use?
Increase QT
Side effect of Procainamide?
drug induced reversible SLE-like syndrome

others: not HIPP to have lupus

Hydralazine, INH, Procainamide and Phenytonin
What are the class II arrhythmic blockers?
Beta-blockers (both specific and non-specific)
In what classes can you find Amidarone?
Class 1A and Class III (K+ channel blocker)
What Antiarrhythmitic will cause Pulmonary fibrosis and hepatotoxity, hypothyroidism/hyperthyroidism (in addition to more)?
Amidarone
Does amiodarone increase or decrease AP duration?
Increase (K+ channel blocker)
Does sotalol increase or decrease the effective refractory period?
Increase (K+ channel blocker)
Does bretylium increase or decrease the QT interval?
Increase (K+ channel blocker)
Name a symptom of sotalol toxicity.
Torsades de pointes (K+ channel blocker)
Name three of the symptoms of amiodarone toxicity.
Pulmonary fibrosis, corneal deposits, hepatoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradychardia, heart block, CHF, hypothyroidism/hyperthyroidism. (Therefore, should check PFTs, LFTs, and TFTs)
What group make up the class IV antiarrhythmics?
Give two examples?
1.Calcium channel blocker
2. Verapamil and Diltiazem
What can be used to treat heart block?
Atropine
Propafenone is of what class? what other activity does it have?
1. Class IC
2. Some Beta antagonist activity
Describe Esmolol? and used when?
1.Short-acting Beta-blocker
2.To titrate block during surgery.
These drugs can prevent reflex tachycardia when a vasodilator is used?
Beta-blocker (the heart is being informed but it is not responding thanks to the blocker)
Cause of Gray man syndrome?
Amidarone
Class V antiarrhythmetic drugs include?
1. Adenosine - Purinergic receptors (for diagnosis and Tx of AV node block)
2. Digoxin (atrial flutter or A-fib)
Name a calcium blocker that can cause a serious arrhythmic condition - what is a major side effet?
1.Bepridil
2.This Ca2+ blocker Can cause ventricular arrhythmias
Tosades de pointes
This drug is a coronary vasodilator and it is used for prophylaxis of angina pectoris and it interferes with the reuptake vasodilator adenosine?
Dipyridamole
What is hydralizine's mechanims and clinical use?
increase cGMP --> smooth muscle relaxation. Vasodilates arteries > veins. Reduces afterload. Used for severe HTN or CHF
Mechanism: block type of calcium chanels of cardiac and smooth muscles to reduce contractility
voltage dependednt L type Ca
1.Rank the effects calcium block on vascular smooth muscle and on the heart?
2. How does Verapamil act in the heart?
3.Side effects?
smooth muscle nifedipine> diltiazem > verapamil
heart: verapamil> diltiazem> nifedepine

Verapamil slows down AV node conduction

3. Hypotension
Clinically, calcium channel blockers use to Tx what conditions?
HTN, angina, arrythmias (not nifedipine less effect on the heart)
A sudden Increase in baroreceptor activity means? What will be the reflex?
1. means a sudden increase in BP
2. Reflex: will be to lower BP: dilate vessel and reduce heart rate (less sympathetics)
Name a potential use of Mg+ to treat arrhythmias.
To treat torsades de pointes and digoxin toxicity
Name a potential use of K+ to treat arrhythmias.
Depress ectopic pacemakers, especially in digoxin toxicity
Name a use of adenosine in treating arrhythmias.
To diagnose and abolish AV nodal arrhythmias.
Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule
NaCl; early distal tubule
Does hydrochlorothiazide increase or decrease the excretion of calcium ion?
decrease
A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium
hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)
Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule
aldosterone; cortical collecting tubule
Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct
Triamterine and amiloride
Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect
Gynecomastia (antiandrogen effect)
Name three K+-sparing diuretics
Spironolactone, Triamterene, Amiloride (The K+ STAys.)
Diuretics are classified as carbonic anhydrase inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these causes in increase in urine NaCl?
All of them!
Which types of diuretucs increase urine K+?
All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop diuretics, thiazides.
Do carbonic anhydrase inhibitors increase or decrease blood pH?
Decrease, cause acidosis
Do K+-sparing diuretics cause acidosis or alkalosis?
Acidosis, decreases pH
Do loop diuretics cause acidosis or alkalosis?
Alkalosis, increases pH
Do thiazide diuretics cause an increase or decrease in blood pH?
Increase, cause alkalosis
Do loop diuretics increase or decrease levels of urine calcium ion?
Increase
Do thiazide diuretics increase or decrease levels of urine calcium ion?
Decrease
Antianginal therapy
p.319
Name four determinants of the level of myocardial oxygen consumption
There are five: end diastolic volume, blood pressure, heart rate, contractility, ejection time
Do nitrates affect preload or afterload?
preload
Do Beta-blockers affect preload or afterload?
afterload
What is the effect of nitrates on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
decrease EDV, decrease BP, increase contractility (reflex response), increase HR (reflex response), decrease ejection time
What is the effect of Beta-blockers on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
increase EDV, decrease BP, decrease contractility, decreased HR, increase ejection time
The effects of using nitrates and Beta-blockers together will: a) decrease myocardial oxygen demands by the same amount as using either alone, b) decrease myocardial oxygen demands by an amount greater than if each were used alone, or c) have no effect on myocardial oxygen demand
b) Decrease myocardial oxygen demands by an amount greater that if each were used alone
Nifedipine blocks -- channels
calcium (most effect in the blood vessels)
In its effects on myocardial oxygen consumption, is Nifedipine similar to Nitrates or B-blockers?
Nitrates (Nifedipine is similar to Nitrates)
In its effects on myocardial oxygen consumption, is Verapamil similar to Nitrates or B-blockers?
B-blockers
Dose nitroglycerin dilate arteries or veins more?
Veins>>arteries
Does nitroglycerin increase or decrease cGMP in smooth muscle?
Increase
In industrial exposure to nitroglycerine, weekend withdrawal is characterized by which three symptoms?
Tachycardia, dizziness , and headache ("Monday disease")
Toxic dosage of nitroglycerine causes which three symptoms?
Tachycardia, hypotension, headache
What is methyldopa?
Tx for what?
1. Potent False Neurotransmiter - inhibits sympathetic outflow - by inhibiting
a. presynaptic inhibitory alpha-receptors
b. Postsynaptic alpha2- receptors

2. HTN (reduces peripheral resistance)
What is the effect of cholestyramine on the serum triglyceride level?
Adverse effect of cholestyramine?
Is cholestyramine hydrophillic or hydrophobic?
1.Slight increase (cholestyramine is a bile acid resin)
The only one that even increases Triglyceride
2. Causes poor absorbtion of anionic drugs such as Warfarin and Digitalis
3.Hydrophillic:binds bile and exchanges it with Cl-
What is the effect of colestipol on HDL?
No effect! (colestipol is a bile acid resin)
What is the effect of lovastatin on HDL?
Increase (lovastatin is an HMG-CoA reductase inhibitor)
Name 2 side effects of pravastatin.
Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)
What is the effect of Niacin on HDL?LDL?Triglyceride?
1.HDL:Significant Increase
2.LDL: moderate decrease
3.Triglyceride: moderate decrease

Significant, moderate, Slight
What are the side effects of clofibrate?
Incease LFTs and cause myositis, mild to moderate dibetes insipidus(Clofibrate is a "Fibrate")
Which increases HDL most: simvastatin, niacin, or gemfibrozil?
Niacin
Which decreases triglyceride level most: colestipol, Atorvastatin, niacin, or bezafibrate?
Bezafibrate
What is the main effect of ezetimibe on
LDL, HDL and Triglyceride?

What type of drug is it?
1.LDL: decrease serum LDL (a cholesterol absorption inhibitor)
HDL:no effect
Triglyceride: no effect
Gemfibrozil increases the activity of which enzyme?
Lipoprotein lipase (which converts VLDL to IDL)