Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fall17-Pharmacology > Block 3 > Flashcards

Block 3 Flashcards

1
Q

What are the main causes of hypertension?

A

Sustained pressure of 140/90 or higher

Specific cause is established in 10% of patients - 90% don’t know why

No cause = primary hypertension

Caused by disease = secondary hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the targets for antihypertensive drugs?

A 
BP is maintained by CO and TPR at:
Arterioles
Postcapillary venules
Heart
Kidneys

In people with high BP, their baroreceptors appear to be set at a higher level of BP than normal patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main categories of antihypertensive drugs?

A

Thiazide diuretics
ACE Inhibitors
CCBs

Combo treatments are usually ACEIs + CCBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are comorbid conditions where antihypertensive drugs are commonly used?

A

Diabetes, asthma, angina, arrhythmias, CHF

Commonly use CCBs!

V and D for arrhythmias
Dipines for CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the baroreceptor reflex?

A

It control BP

Activated when arterial wall stretches from increased pressure = it tells vagus to increase parasympathetic and decrease sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is baroreceptor adaptation?

A

During exercise there is an increase in BP + increase in HR

There is no reflex Brady after the increase in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes a renin release?

A

Either decrease in arterial pressure or increase in sympathetics

Renin then starts the RAAS system which leads to ANGII which is a potent vasoconstrictor

Releases aldosterone
Increases BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A decrease in arterial pressure does what to ADH?

A

Release of ADH to act on renal collecting duct to enhance water retention - gets fluid volume back, increases pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the MOA of diuretics?

A

They reduce fluid volume by causing water and electrolyte excretion in the renal tubules

Leads to decrease in CO

After several days urinary excretion returns to normal, CO returns to normal but BP stays low

In the long term it reduces the vessels reaction to NE (NE increases BP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are side effects of diuretics? Contraindications?

A 
Potassium depletion (coupled with Na+ reabsorption)
Restrict Na+ intake b/c of this

Bad for people with chronic arrhythmias or acute MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the diuretic drugs?

A

“Thiazides”

Hydrochlorothiazide - most common
Chlorthlidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the MOA for CCBs?

A

Block the entry of Ca+ into L-type channels in the heart and smooth muscle

Cause relaxation and dilation of arterioles

Slow conduction of the AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are side effects of CCBs? Contraindications?

A

Constipation (due to slowing of smooth muscle - GI tract)
Gingival hyperplasia with dipines - red swollen gums, bleeding and growing over teeth

**if exam says treated for high BP then gums bleed, think dipines!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the CCB drugs?

A

Verapamil - heart (no reflex b/c right on heart)
Diltiazem
Amlodipine - vessels (reflex tachy, b/c its on vessel Ca+ channels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the MOA of ACE Inhibitors?

A

They directly block the enzyme ACE

With ACE blocked, no AngI to AngII (potent vasoconstrictor)

Also with ACE blocked, Bradykinin is activated (potent vasodilator)

Also without AngII, decrease aldosterone which means less Na+ and more water retention

NET: vasodilation with less aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Who are ACEI most effective for?

A

Young white patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the use for ACEI?

A

Hypertension
CHF
24 hrs after MI
**Diabetic nephropathy!! B/c it protects the kidneys by dilating efferent arteriole to lower GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are side effects to ACEIs? What is the most common vs the most serious?

A

Most common: Dry cough - due to Bradykinin

Most serious: Angioedema - swelling of nose, throat, mouth, lips, and tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are contraindications to ACEIs?

A

Teratogenic - harm fetus

Renal failure in patients with bilateral renal artery stenosis! - b/c AngII constricts efferent arterioles to keep GFR in check
-in this condition, when the efferent dilates, it will cause renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the ACEI drugs?

A

“Prils”

Captopril
Lisinopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the MOA for ARBs?

A

They inhibit AT-1 receptors which block AngII

***They do NOT affect bradykinin! B/c they are later in pathway SO there is no cough

They vasodilation and prevent aldosterone secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the use for ARBs?

A

Hypertension
CHF
Diabetic nephropathy - b/c of dilation of efferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the side effects?

A

No true bad ones… they are better than ACEIs, but they are VERY expensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are contraindications for ARBs?

A

Teratogenic

Renal failure in bilateral renal artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the ARB drugs?

A

“Sartans”

Losartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

In patients 18 and older, of any race with chronic kidney disease and hypertension, what should we give them?

A

ACEI or ARB

They improve kidney outcomes!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are renin inhibitor MOA?

A

It stops the enzyme renin from converting angiotensinogen to AngI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the Renin Inhibitor drug?

A

Akiskiren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the side effects of Renin Inhibitor?

A

Teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the MOA for beta blockers?

A

Stop the effects of NE and epi on B1 receptors
-decrease CO

Also block B1 receptors on JGA cells to stop renin pathway

NET: decrease BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the use for beta blockers?

A

Hypertension - but not first line unless comorbid MI or angina

Arrhythmias, angina, MI, all cardiac conditions!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which drugs treat black and elderly?

A

Diuretics or CCBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Who are beta blockers most effective for?

A

Young white patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are side effects of beta blockers?

A 
Bronchoconstriction
Disrupt glucose control 
Hypotension
Bradycardia
Lethargy

**do NOT use with asthma and diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are beta blocker drugs?

A

“Olols”

Atenolol
Metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the MOA for alpha1 blockers?

A

Block a1 receptors in arterioles and venules to cause relaxation of smooth muscle and decreased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Use for a1 blockers?

A

Hypertension

Benign prostatic hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Side effects of A1 blockers?

A

Orthostatic postural hypotension - dizziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the A1 blocker drugs?

A

“Zosins”

Prazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the MOA for central alpha2 agonists?

A

Main action in brain

Reduce sympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the a2 agonist side effects?

A

Sedation and dry mouth
Hemolytic anemia

**always taper! Rebound hypertension is severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are A2 agonist drugs?

A

Methyldopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the drug of choice for chronic hypertension in pregnancy?

A

Methyldopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the MOA for labetalol and carvedilol?

A

Non selective blocker - a1, B1, b2

Decreases vascular resistance without a reflex tachy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the MOA for nebivolol?

A

Blocks B1

Vasodilates via nitric oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the drug of choice for hypertensive emergencies?

A

Labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the drug of choice for CHF?

A

Carvedilol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is CHF?

A

Congestive heart failure

The CO is not enough to provide the oxygen that the body needs

Usually accompanied by increase in blood volume and fluid - vessels are very dilated with blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are symptoms of left heart failure?

A

Pulmonary congestion
Peripheral edema
Right heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the #1 reason for decrease in CO?

A

A decrease in contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How do you decrease preload?

A

Decrease volume

Use diuretics to get rid of volume

This is in the veins - venodilate to decrease preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do you decrease afterload?

A

Dilate arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What do we want to do in CHF?

A

Slow down HR

Use beta blockers to do it - LOW DOSE always!! B/c we don’t want to decrease contractility just slow HR down a bit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is cardiac remodeling?

A

It involves fibrosis/stiffening of the heart muscle - it decreases function

**remodeling=death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the causes of cardiac remodeling?

A

Aldosterone - use ACEI/ARBs

NE and epi - too much symp activity - use beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the top 3 drugs to use in CHF?

A

ACEI/ARBs

Beta blockers

Diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the first line therapy in CHF?

A

ACEIs or ARBs

They inhibit AngII vasoconstriction (vasodilation reduces afterload)

They inhibit aldosterone sodium retention and water (reduces preload)

They prevent remodeling via blocking aldosterone

No remodeling means less mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does Metoprolol (beta blocker) do in CHF?

A

Improves symptoms

Decreases remodeling due to B1 receptor on JGA

Always use in combo with ACEI or diuretics

Remember dose is critical! LOW dose only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What do diuretics do in CHF?

A

Reduce preload

Does NOT do anything to aldosterone, so does NOT decrease mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are CHF diuretic drugs?

A

Hydrochlorothiazide
Furosemide - loop
Spironolactone
Eplerenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the only diuretics that affect aldosterone (decrease remodeling/mortality)?

A

Spironolactone
Eplerenone

Aldosterone receptor antagonists

They are K+ sparing b/c aldosterone is K+ wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is a Neprilysin Inhibitor?

A

Neprilysin is an enzyme that degrades BP lowering peptides

It decreases preload by reducing blood volume
It also increases the levels of bradykinin

Alternative to ACEI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the neprilysin inhibitor drug?

A

Sacubitril

Side effects: cough and angioedema (b/c of bradykinin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is a funny sodium channel blocker?

A

It decreases the depolarization of SA node which decreases HR withOUT affecting contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Should you use CCBs in CHF?

A

No - they provide no mortality benefit

Basically stay away from them here

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are ionotropic drugs?

A

They increase the contractility of the heart

They bind reversible to Na+K+ pump in cardiac cell (binds in place of K+)
-Na+ is trying to get out, K+ is going in

This increases Na+ inside the cell b/c it can’t get out without a K+ bound. Now Na+ is forced to use the Na+Ca+ pump instead
-Na+ out, Ca+ in

In total, more Ca+ inside the cell means increased forced of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the inotropic drug?

A

Digoxin

VERY scary - TI = less than 2 - you must take it at the exact same time each day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the use for inotropic drugs(digoxin)?

A

Very last ditch effort.

If ACEl, diuretics, and beta blockers all don’t work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are side effects of iontropic drugs (digoxin)?

A 
Severe arrhythmias
Nausea
Vomiting
Confusion
Blurred vision - yellowish halos/blurred yellow vision**** exam!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are some factors that predispose you to digitalis toxicity?

A

Hypokalemia - it enhances the binding of digoxin to the Na+K+ pump

Diuretics are usually K+ wasting!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What types of drugs are for ACUTE heart failure only?

A

Beta agonists - positive inotropic effects - only short term use
-dobutamine - acts on B1 receptor

Phophodiesterase inhibitors
-inamrinone
ONLY short term!! Long term = death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Where in the heart do a lot of drugs target to control the signal?

A

The AV node

It’s like the gate keeper to the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Which node initiates the beat?

A

SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the PR interval?

A

Atrial conduction - the signal moves from the SA to AV nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the P wave?

A

Atria are excited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the QRS complex?

A

Ventricles depolarize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the QT interval?

A

Ventricular conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the T wave?

A

Ventricles are depolarizing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What does a FAST response action potential look like?

A

Very steep phase 0 (depolarization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Where are the fast response action potential found?

A

In the heart muscle and Perkinje fibers

Most of the muscle in the heart is in the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What drugs work great in the ventricles

A

Na+ channel blockers

  • Na+ starts the action potential
  • when Na+ rushes in, phase 0 starts
  • when given a Na+ blocker - slope goes DOWN… HR goes down…. INCREASES QRS complex

K+ channel blockers

  • K+ depolarizers membrane and K+ is always inside the cell so it rushes out to depolarize
  • K+ blockers slow down repolarization
  • slope goes DOWN… INCREASES QT

Both drugs treat ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What does a slow response action potential look like?

A

Flatter curvier graph - no sharp spikes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Where is the slow response action potential?

A

In the SA and AV nodes

This is because it is a different type of tissue than muscle

SA node is pacemaker b/c it depolarizes faster than any other node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are 2 types of drugs that work in slow response action potentials?

A

Ca+ channel blockers

  • depress phase 0 and 4
  • PR interval INCREASES

Beta blockers

  • if you block beta you get less Ca+ coming in
  • depress phase 4 and 0

Use these 2 to treat SVT!

85
Q

What is SVT?

A

Supraventricular tachycardia!

ABOVE the ventricles

86
Q

What are PVCs?

A

Premature ventricular complexes

Usually non life threatening

87
Q

What is ventricular tachycardia?

A

3 or more PVCs

Monomorphic - consistent QRS configuration

Polymorphic - varying QRS - Torsade

88
Q

What is ventricular fibrilllation?

A

Electrical chaos

Death ensues rapidly without treatment

89
Q

What are the classes of antiarrhythmic drugs?

A

Class 1 - Na+ channel blockers

Class 2 - beta blockers

Class 3 - K+ channel blockers

Class 4 - Ca+ channel blockers

“Saved By Pharm Class”

90
Q

What are class 1 - Na+ channel blocker drugs?

A

1a - quinidine

  • all lead to torsade
  • also block K+ channel*
  • increase HR and arrhythmias
  • increase mortality!

1b - lidocaine
-given via IV - so acute

1c - flecainaide
-increase in mortality!

These are all bad news - only as backup drugs

91
Q

What are class 2 - beta blocker drugs for anti arrhythmias?

A

Atenolol
Metoprolol

Very useful in SVTs

Prolong PR interval

92
Q

What are Class 3 - K+ channel blocker drugs for antiarrythmias?

A 
Best - amiodarone 
-contains IODINE so causes thyroid issues**
Corneal deposits***
Blue skin*** 
-long 1/2 life (several weeks)

Dronedarone

  • no Iodine
  • shorter 1/2 life

Sotalol
-also blocks beta receptors so use for SVTs in addition to ventricular
Torsades due to K+

93
Q

What are class 4 - CCBs for antiarrythmics?

A

Verapamil
Diltiazem

Slowed conduction of AV/SA node

94
Q

What are other antiarrhythmic drugs?

A

Digoxin - increase PR interval due to slowing AV node

  • use for SVTs
  • may increase Ca+ in SA/AV node to increase HR

Adenosine

  • at high doses it decreases conduction (slows heart)
  • drug of choice for Acute SVT!!**
  • IV only 8 seconds
  • patient temporarily flatlines, then restarts
95
Q

What is angina?

A

Chest pain

96
Q

What is angina caused by?

A

Accumulation of metabolites in striated muscle that occurs when blood flow is inadequate to supply the oxygen to the heart

97
Q

What is the most common cause of angina?

A

Atheromatous obstruction of the large coronary vessels

This is “classic/stable” angina

98
Q

What is another name for stable angina?

A

Angina of effort or exercise

99
Q

What is is called when the stable angina changes in character, frequency, duration, and precipitating factors?

A

Unstable angina

This is a medical emergency! B/c is usually means there is a clot

100
Q

What is the therapy for primary angina?

A

Dilate and relax the smooth muscles

Nitrates
Beta blockers - although avoid this one if patients have vasospasm b/c it will make it worse
Ca+ channel blockers

101
Q

What is the key difference between beta blockers and Ca+ channel blockers in angina?

A

B blockers - decrease oxygen remains on the HEART

Ca+ channel blockers - vasodilate smooth muscle in peripheral vessels to decrease oxygen demands on heart
-dilate coronary vessels to increase oxygen delivery

102
Q

What 2 classes of drugs are preferred for vasospastic/variant angina?

A

Nitrates

Ca+ channel blockers

103
Q

What are we worried about with unstable angina?

A

It’s probably a clot, so add some aspirin in addition to other therapies

104
Q

If a patient is suffering from angina and also has diabetes, what is a good drug?

A

ACEI

To protect kidneys

105
Q

What is the most common and drug of choice for organic nitrates for angina?

A

Nitroglycerin

Sublingual for prompt relief of an angina attack

It relaxes smooth muscle by converting nitrite ions to nitric oxide
***aka its a prodrug! - active form is nitric oxide

NO to cGMP to vascular smooth muscle relaxation

106
Q

What are 2 other drugs other than nitroglycerin that relax smooth muscle via Nitric oxide?

A

Bethanechol (M3 receptor)

Histamine (H1 receptor)

107
Q

Exam!! Which administration of nitroglycerin is used for RELIEF of an angina attack?

A

Sublingual!

108
Q

Exam: which administration of nitroglycerin should be used to PREVENT angina?

A

Transdermal patch

109
Q

What does nitroglycerin do to the cardiovascular system?

A

At moderate to high doses it dilates the large veins causing pooling of blood - decreases preload and reduces the work of the heart

110
Q

What are the side effects of nitroglycerin?

A

Headache
Reflex tachycardia
Orthostatic hypotension

111
Q

What is something you have to worry about with a nitroglycerin patch?

A

You may build a tolerance

Only wear the patch for 12 hours when you are most active - that is when the heart is working harder

112
Q

What are 2 other organic nitrate drugs other than nitroglycerin?

A

Isosorbide mononitrate
Isosrbide dinitrate

Given orally
Same as nitroglycerin

113
Q

When taking nitrites what are the other drugs you should avoid?

A

PDE5 inhibitors (“fils”)

Extreme hypotension and death

114
Q

What is the most common drug to PREVENT stable angina?

A

Beta blockers

115
Q

What are 2 other drugs for stable angina PREVENTION?

A

Verapamil

Diltiazem

116
Q

What is a drug for vasospasm PREVENTION?

A

Dipines

117
Q

What is ranolazine used for?

A

In addition to other standard therapies for angina

It is a good drug but may cause torsades - it increases QT interval

118
Q

What is associated with high LDL and low HDL?

A

Premature or accelerated development of atherosclerosis

119
Q

What are the 3 most popular and powerful HMG Co-A reductase inhibitors?

A

Atorvastatin
Simvastatin
Rosuvastatin

“Statins”

120
Q

What do HMG Co-A reductase inhibitors (statins) do?

A

They competitively block the rate limiting step in the synthesis of cholesterol

Unregulated LDL receptors to clear LDL from blood

High intensity statins also raise HDLs and lower TGs

121
Q

What are side effects of statins?

A

Mild muscle pain
Myalgia

Caution with grapefruit juice!! It’s a p450 inhibitor***

122
Q

What is the MOA for fibrates?

A

Activate the enzyme that break down triglycerides to clear TGs from blood

Good for hypertriglycerides in combo with statins

123
Q

What is the MOA for niacin?

A

Reduces VLDL synthesis to lower LDLs

Decreases free fatty acid and TGs

Decreases metabolism of HDL so that level stays high

124
Q

What are side effects of Niacin?

A

Cutaneous flushing

Itching caused by prostaglandins = treat with NSAID

125
Q

What is the MOA for BAS (cholestyramine)?

A

Binds directly to bile salts which are made mostly of cholesterol to decrease recycling

This forces the liver to make more new ones so it pulls LDL out of plasma

126
Q

What are side effects of cholestyramine?

A

Increase TG levels - don’t use if this is already high

GI upset

Constipation

127
Q

What is the MOA for Ezetemibe?

A

Decrease GI uptake of cholesterol

Lowers plasma LDL

128
Q

What are side effects of Ezetemibe?

A

No many!

Usually combine with a statin

129
Q

What is the MOA for PCSK9 inhibitors? (Alirocumab)

A

It is an enzyme that degrades LDL receptors

SO this antibody drug prevents the enzyme action which increases the receptor number to lower LDLs

No side effects

However it is EXTREMEMLY expensive!! $14000 per year

130
Q

What are the 2 categories of strokes?

A

Ischemic (87%)
Hemorrhagic (13%)

Weakness on one side of body, inability to speak, loss of vision, vertigo, falling

131
Q

What is VTE?

A

Venous thromboembolism

It comes from either deep vein thrombosis or pulmonary embolism

DVT=leg swelling, pain, or warmth

PE = cough, chest pain, shortness of breath, hemoptysis

132
Q

What is a common tactic for stroke PREVENTION?

A

Antiplatelet drugs

133
Q

What are the 2 most common antiplatelet drugs?

A

Aspirin

ADP receptor blockers (clopidogrel)

134
Q

What is the MOA for aspirin?

A

It irreversibly stops the COX pathway to prevent synthesis of TXA2 (which causes platelet aggregation)

It stops it for the life of the platelet! (~10 days)

135
Q

What is the use for aspirin?

A

Prevents transient ischemic attacks (mini strokes) and ischemic stroke

Side effects - bleeding

136
Q

What is the MOA for ADP receptor blockers? (Clopidogrel)

A

Irreversibly inhibits ADP receptors which prevent platelet activation

137
Q

What is the use for clopidogrel?

A

Prevent TIAs (mini strokes) and strokes in patients that can’t tolerate aspirin

Side effects - bleeding

138
Q

What are other not as common prevention drugs for strokes?

A

Glycoprotein IIb/IIa Inhibitors - Abciximab

Phosphodieterase (PDE) III inhibitors - dipyridamole

139
Q

What is the MOA for glycoprotein IIb/IIa inhibitors (abciximab)?

A

Blocks binding of fibrinogen with it’s receptor to prevent platelet cross-linking

Use: coronary angioplasty to prevent clots

Side effects: bleeding

140
Q

What is the MOA for PDE III inhibitors (dipyridamole)

A

Block breakdown of cAMP, more cAMP means platelets don’t aggregate

Use: usually combined with aspirin for antiplatelet benefits

Side effects: bleeding

141
Q

What is used for IMMEDIATE stroke treatment?

A

Thrombolytics

Aka fibrinolytics or clot busters

142
Q

What is the main thrombolytic drug?

A

Alteplase

Aka tissue plasminogen activator (tPA)

Must use within 3 hours of stroke to decrease mortality and preserve organ function

143
Q

What is the MOA of alteplase?

A

Binds to fibrin bound plasminogen to catalyze the conversion of plasminogen to plasmin

Plasmin is a proteas that breaks up a clot

Side effects: bleeding and possible intracerebral hemorrhage

144
Q

Which drugs work in the clotting cascade to prevent VTE?

A 
Heparin
Enoxaparin 
Warfarin
Dabigatran
Rivaroxaban
145
Q

What is the MOA for heparin?

A

Very good drug - works fast but never use long term

Catalyze the binding of antithrombin III to factors 2a, 9a, 11a, 12a resulting in rapid inactivation

Given IV for rapid anticoagulation

Side effects: bleeding

146
Q

What is the antidote for heparin?

A

Protamine sulfate

It binds directly to heparin

***this is chemical antagonism

147
Q

What factors are rapidly inactivated by heparin?

A

2a
9a
11a
12a

148
Q

What is the MOA for enoxaparin?

A

Binds with AT 3 with primary activity against factor 10a leading to rapid inactivation

Given IV, use acutely

It’s like a baby heparin - longer 1/2 life

Side effects: bleeding

149
Q

What is the MOA for warfarin?

A

Decreases hepatic synthesis of vitamin K dependent factors 2, 7, 9, 10

Specifically blocks vit K reductase which prevents regeneration of vit K

Orally for long term anticoagulation

Side effects - atrial fibrillation
Bleeding
Lots of drug interactions
Monitor with PT-INR

150
Q

What is the antidote for warfarin?

A

Vit K - but takes a long time for liver to make

Fastest reversal with fresh frozen plasma

151
Q

What are the vitamin K dependent factors that warfarin prevents?

A

2, 7, 9, 10

152
Q

What is the MOA of direct thrombin inhibitors? Dabigatran

A

Directly inhibits thrombin

Oral anticoag
Atrial fibrillation

Side effects: bleeding
No need to monitor

It’s an alternative to warfarin, much quicker with less monitoring

153
Q

What is the MOA of direct factor 10a inhibitors? Rivaroxaban

A

Think Xa = rivaroXaban

It directly inhibits factor 10a

Orally
Also rapid and no need to monitor

Atrial fibrillation

154
Q

Which diuretic works in the proximal convoluted tubule?

A

Acetazolamide (carbonic anhydrase inhibitor)

Inhibits HCO3

Weak diuretic

155
Q

Which diuretics work in the ascending loop of henle?

A

Furosemide

Inhibit Na+K+Cl- transport that results in retention of Na+, Cl-, and water in the tubule

Most efficacious of the diuretics

156
Q

Which diuretic drugs work in the distal convoluted tubule?

A

Thiazides

Inhibit reabsorption of Na+ and Cl- causing water retention

Most commonly used diuretics

157
Q

Which diuretics work in the collecting duct?

A

The K+ sparing diuretics

Spironolactone - aldosterone antagonist
Amiloride - block Na+ channels

Prevent loss of K+

158
Q

Where is the primary site of active reabsorption?

A

Proximal convoluted tubule

Sodium bicarb (85%)
Sodium chloride (40-50)
Water passively (60%)
159
Q

What do carbonic anhydrase inhibitors do? (CA inhibitors)

A

They decrease bicarb reabsorption
Leads to metabolic acidosis systemically but chan use for glaucoma topically

Without CA you can’t break down bicarb into CO2 and water so it stays in the urine

If it stays in the urine it can’t be remade inside the cell

160
Q

What happens in the loop of Henle?

A

Specifically in the thick ascending limb, NaCl is actively reabsorbed

“Loops lose Ca+”

K+ is high in cell and this pump brings more K+ in

Some of the K+ starts to leak out back into the urine which causes a separation in between the cells due to the + charge
The open space means Mg+ and Ca+ get reabsorbed

SO with loop diuretic, you block the pump so it can’t reabsorb Na+ so Na+ and water stay in urine
Cells stay together, Mg” and Ca+ can’t get in to you lose them both in urine

161
Q

What happens in the distal convoluted tubule?

A

Thiazides block Na+/Cl- pump

This causes increased Ca+ reabsorption via another pump

“Thiazides save Ca+”

PTH regulates this pathway

Elderly lady with osteoporosis - give her a thiazide b/c she needs the calcium

Someone who suffers from kidney stones - give them a thiazide b/c we need to get Ca+ out of urine and reabsorbed

162
Q

What happens in the collecting tubule?

A

Most diuretics waste K+ b/c the more Na+ that comes in the more K+ leaves

Increase in Na+ inside means an increase in K+ lost

K+ loss also means H+ loss

K+ and H+ wasting = hypokalemia and alkalosis

K+ and H+ sparing = hyperkalemia and acidosis

163
Q

Aldosterone does what in the collecting tubule?

A

It increases Na+ reabsorption

So K+ and H+ wasting

Drugs are spironolactone and eplerenone b/c they block aldosterone receptors - no Na+ reabsorption

164
Q

What does the drug amiloride do in the collecting tubule?

A

Blocks Na+ channels so K+ and H+ sparing

Side effects: hyperkalemia and acidosis

165
Q

What is the one exception to the K+ = H+ rule?

A

Carbonic anhydrase inhibitors

They cause K+ loss BUT acidosis
B/c they mess with bicarb

They do NOT get rid of H+

166
Q

Which receptor is the problem in diabetes insipidus in the collecting tubule? What does this cause?

A

It’s a problem with the ADH receptor

This is the ONLY time you will urinate less on a thiazide

167
Q

What are the uses for Carbonic anhydrase inhibitor? What are the drugs?

A

Glaucoma - closed angle

“Zolamides”
Inhibit carbonic anhydrase to reduce IOP

Side effects: metabolic acidosis if systemically used

168
Q

What drugs are the loop diuretics?

A

Furosemide
Torsemide

Get rid of a lot of fluid quickly

Use: acute pulmonary edema
CHF
Edema

Side effects: affects ears! “My ears are ringing”
Hypokalemia alkalosis

169
Q

Why can you use thiazides for hypercalciuria? Stones in urinary tract?

A

They pull the Ca+ OUT of the urine! To be reabsorbed = this is good

170
Q

Why are thiazides good for hyperglycemia and hyperlipidemia?

A

They inhibit insulin release from beta cells

171
Q

What are the uses for potassium sparing diuretics? Spironolactone, eplerenon

A

They are aldosterone receptor antagonists

Treat secondary hyperaldosteronism, decrease remodeling

172
Q

Which is the potassium sparing diuretic that does NOT act on aldosterone receptors?

A

Amiloride

Blocks the Na+ channels

Side effects: hyperkalemia = spare too much

173
Q

What are the diuretics for hypertension?

A

Chlorothiadone

Hydrochlorothiazide

174
Q

What are the CCBs for hypertension?

A

Verapamil
Diltiazem
Dipines

175
Q

What are the ACE Inhibitors for hypertension?

A

Lisinopril

Captopril

176
Q

What are the ARBs for hypertension?

A

Losartan

177
Q

What is the renin inhibitor for hypertension?

A

Aliskerin

178
Q

What are the beta blockers for hypertension?

A

Atenolol

Metaprolol

179
Q

What are the a1 blockers for hypertension?

A

Prazosin

180
Q

What is the a2 agonist for hypertension?

A

Methyldopa

181
Q

What are the 3 uncategorized drugs for hypertension?

A

Carvedilol - CHF
Labetalol - hypertensive emergency
Nebivolol - B1 plus NO vasodilation

182
Q

What are the ACEI and ARBs for CHF?

A

Captopril
Lisinopril
Losartan

183
Q

What are the beta blockers for CHF?

A

Atenolol
Metaprolol
Carvedilol

**always use these in combination with an ACEI/ARB or diuretic

184
Q

What are the diuretics for CHF?

A

Furosemide
Hydrochlorothiazide
Spironolactone
Eplerenone

185
Q

What is the neprolysin inhibitor in CHF?

A

Sacubatril

186
Q

What it’s he funny sodium channel blocker in CHF?

A

Ivanbradine

187
Q

What are the positive ionotropics in CHF?

A

Digoxin
Dobutamine (ACUTE)
Inamrinone (ACUTE)

188
Q

What are the class I - Na+ channel blockers for arrhythmias?

A

Quinidine Ia
Lidocaine Ib
Flecainamide Ic

189
Q

What are the class III - K+ channel blockers in arrythmias?

A

Sotalol
Amiodarone
Dronedarone

190
Q

What are the class II - beta blockers in arrythmias?

A

Atenolol

Metaprolol

191
Q

What are the class IV - CCBs for arrythmias?

A

Verapamil

Diltiazem

192
Q

What are the others drugs used to target the atria in arrythmias?

A

Digoxin

Adenosine (ACUTE)

193
Q

What are the drugs for stable angina?

A

Nitrates - nitroglycerin, isosorbide mononitrate, isosorbide dinitrate
B blockers - atenolol, metoprolol
CCBs - Verapamil, diltiazem

194
Q

What are drugs for vasospastic angina?

A

Nitrates - nitroglycerin, isosorbide mononitrate, isosorbide dinitrate
CCBs - dipines

195
Q

What are drugs for unstable angina?

A 
Nitrates - nitroglycerin, isosorbide mononitrate, isosrbide dinitrate 
Beta blockers - atenolol, metaprolol
CCBs - verapamil, diltiazem
Aspirin
Heparin
196
Q

What is another drug for angina that is not well known but works with all the other antiangina drugs and causes torsade?

A

Ranolazine

197
Q

What are the HMG Co-A reductase inhibitors for hyperlipidemia?

A

Atorvastatin
Simvastatin
Rosuvastatin

198
Q

What is the drug that activates PPAR-alpha to increase breakdown of TGs?

A

Fenofibrate

199
Q

This drug lowers fatty acids and TGs, and increases HDLs but causes flushing and itching so much be pretreated with aspirin?

A

Niacin

200
Q

This drug binds to bile salts and reduce LDL?

It may increase TGs in the process

A

Cholestyramine - BAS

201
Q

This drug decreases GI uptake of cholesterol to decrease LDL and is usually combined with a statin

A

Ezetemibe

202
Q

This is the PCSK9 inhibitor to prevent the degradation of LDL receptors to lower LDLs

A

Alirocumab

203
Q

Which drugs are used as an antiplatelet prevention for strokes?

A

Aspirin
Clopidogrel - ADP mediated
Abciximab - IIb/IIIa inhibitor
Dipyridamole - PDE III inhibitor

204
Q

Which drug is the thrombolytic for stoke treatment?

A

Alteplase

205
Q

What are the anticoagulants to prevent thromboembolism?

A 
Heparin - AT3 to inactivate 2a, 9a, 10a,11a,12a 
Enoxaparin - AT3 to inactivate Xa
Warfarin - liver Vit. K 2,7,9,10
Dabigatran - direct thrombin inhibitor
Rivaroxaban - direct Xa inhibitor
206
Q

What are the diuretics in the PCT?

A 
CA inhibitors
Acetazolamide
Brinzolamide
Dorzolamide
Methazolamide
207
Q

What are the diuretics in the loop of Henle?

A

“Loops lose Ca+”
Furosemide
Torsemide

208
Q

What are the diuretics in the DCT?

A

Thiazides save Ca+
Hydrochlorothiazide
Chlorothiadione

209
Q

What are the diuretics in the collecting duct?

A

Spironolactone
Eplerenone
Amiloride

Fall17-Pharmacology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions