Diuretics
Name an example of a drug from the loop diuretics class as well as its mechanism
Furosemide, torsemide, bumenatide. Inhibit Na/K/2Cl in the loop of Henle.
B1 vs. B2 (in simple terms)
B1 - heart
B2 - lungs
Mechanism of action of dobutamine
B1-agonist
What is telmisartan?
ARB
T or F: Nitroglycerin causes vasodilation of veins > vasodilation of arteries.
True! By reducing preload on the heart (by decreasing venous return), it helps with the demand on the heart and chest pain!
These cause metabolic acidosis
Acetazolamide, K+-sparing diuretics
These drugs, when withdrawn quickly, can cause rebound HTN
A2-agonists
Mechanism of action of milrinone
Inhibits PDE3, leading to increased cAMP and calcium
Explain the RAAS.
Renin is produced by the JGA of the kidneys in response to lower perfusion. Renin cleaves angiotensinogen, which is produced by the liver, into angiotensin I. This travels to the lungs, where ACE converts it into angiotensin II. Angiotensin II causes vasoconstriction (leading to increased BP) and stimulates the adrenals to release aldosterone, which also helps retain water and increase blood pressure.
T or F: Nitroglycerin should always be given in heart attack situations.
False! Right-sided myocardial infarctions are preload-dependent, meaning if you decrease the preload, there will not be enough blood making it to the left heart to meet the circulatory demands of the body.
What class of diuretics causes basically hypo - everything?
Loops!
What is the mnemonic to remember what GPCR is paired with each adrenergic receptor?
QISS - a1 is Gq, a2 is GI, B1 is Gs and B2 is Gs
Na/K pump inhibitor, increased vagal stimulation
If I give a patient lisinopril, what reactants would you expect to be elevated?
Renin, angiotensinogen, angiotensin I
Name an example of a PDE-5 inhibitor.
Sildenafil, tadalafil. Leads to increased cGMP in smooth muscle.
Thiazides
Constipation is a side effect of which drug?
Verapamil
Name digoxin's two mechanisms of action (in depth)
Normally, the Na/K pump pumps Na into the extracellular space and keeps potassium within the cell. Sodium is then brought back into the cell via the Na/Ca exchanger, and calcium is brought outside of the cell. If the Na/K pump is not functioning (due to inhibition by digoxin), Na does not accumulate outside of the cell as much, and the Na/Ca exchanger does not function as much. So, Ca remains inside of the cells, leading to inotropy. Also, it increases vagal stimulation, leading to decreased AV conduction and decreased HR.
Explain the function of aldosterone.
It retains sodium and bicarbonate and depletes potassium and hydrogen (So it causes a metabolic ___???)
A 56-year-old man is admitted to the intensive care unit for hypertensive emergency with a blood pressure of 240/130 mmHg and signs of acute pulmonary edema. He is started on an intravenous sodium nitroprusside infusion. After 24 hours of therapy, his mental status declines. He becomes confused, tachypneic, and develops metabolic acidosis with an elevated lactate. Despite adequate oxygen delivery, his venous oxygen saturation is abnormally high.
Which of the following best explains this patient’s findings?
Cyanide poisoning!
pH - 7.55
Ca2+ - elevated
Drug?
Thiazide!
What drugs can be used for Raynaud's phenomenon?
Dihydropyridine CCB's
Surprise! Name some side effects of lisinopril.
Hyperkalemia, renal insufficiency (if there is bilateral renal artery stenosis), dry cough, angioedema, hypotension
Explain the pathophysiology of renal insufficiency when giving a patient with bilateral renal artery stenosis an ACE/ARB.
Typically, angiotensin II constricts the efferent arteriole more than the afferent arteriole. (Remember prostaglandins cause dilation of the afferent arteriole!) This raises glomerular capillary pressure, helping preserve GFR when renal perfusion is low. If renal arteries are blocked, there is less flow to the kidneys --> RAAS is activated --> Ang II causes efferent arteriole constriction. If Ang II is blocked by an ACE/ARB, this compensatory effect cannot happen.
What is MOA of fenoldopam?
Postsynaptic D1-receptor agonist with minimal effect on adrenergic receptors; causes vasodilation