Advanced Therapeutics Homework

AbdelRahman Omar
ID: 1710184

4/6/2020
 Chronic Heart Failure

Cases
• Case #1: Mr. CH, a 78 year old, regularly visits your pharmacy for his medication and
has moderately symptomatic heart failure (NYHA III). During a recent review with his
doctor, Mr. CH described worsening of his heart failure symptoms. His doctor has
said he could take an extra dose of furosemide 40 mg if required, but Mr. CH would
need to be referred back to the cardiology consultant before changing any other
medication. He is currently prescribed ramipril 5 mg daily, nebivolol 2.5mg daily and
furosemide 40mg daily. His blood pressure has been measured as 103/62 mmHg (HR
54 bpm) and he has an estimated creatinine clearance of 20ml/min.

Questions:

1. What is the rationale behind the decision to refer Mr. CH to the cardiology consultant?

Ans) Mr. CH was referred to the cardiology consultant because he has a creatinine
clearance of 20ml/min which is very low and worsening symptoms which might not be
controlled by that increase in dose so the cardiologist can increase it up to 160 mg if
he sees fit.

2. What other drug treatment options might be considered?

Ans) Patient could be switched from nebivolol to carvedilol , metoprolol, or bisoprolol

because they have been shown to reduce mortality and morbidity. If symptoms are
persistent after maxmimum dose of ARA, we can start him on hydralazine 75mg tid PO
and isosorbide dinitrate 40mg tid PO. Last option if uncontrolled would be digoxin.

• Case #2: Mrs. JM, 66 years old, presents with a new prescription for candesartan 4mg
daily. On checking her medication record you see that she has been prescribed
lisinopril 20mg daily, bisoprolol 10mg daily and furosemide 40mg daily for the last
6months to treat her heart failure. Her blood pressure was measured 2 weeks ago and
was 128/78mmHg.

Questions:

1. How do you respond to the new prescription?

Ans) The patient is given the candesartan with the sam dose of bisoprolol and
furosemide. Her medication was changed probably because of the side effect of
the ACE inhibitor lisinopril. Her BP was well controlled on the previous
medication.

2. Could an aldosterone antagonist be added to Mrs. JM’s heart failure medication at

a later date if symptoms persist?

Ans) Yes, but the dose should be low (12.5 mg PO OD of spironolocatone), and
the patient’s potassium levels should be checked before initiation of ARA therapy.
Homework: Angiotensin Receptor II and Covid-19

Cells that are targeted by SARS-CoV-2 bind through Angiotensin-2 converting enzyme, which is highly
expressed in patients treated with ARBs or ACEIs. There are also increased receptors in patients on
thiazolidinedione and ibuprofen. This could lead to higher infection rates with Covid-19 for patients on
these drugs.i

Assignment #1

Question: What are the consequences of CHF on different organs such as heart, liver,
kidneys, and respiratory system?

Ans)

1) Effect on Kidneys: The kidneys wear out in congestive heart failure because of
differences in neurohormonal activity and reduced renal blood flow and volume.
These reductions lead to an increase in sodium and water retention through
aldestrone and vasopressin which can result in oedema. Glomerular filtration also
decreases as the disease advances. ii

2) Effect on Liver: Liver abnormalities can occur in patients with CHF such as slightly
raised levels of alanine aminotransferase, aspartate aminotransferase, and lactate
dehydrogenase which can affect liver function. Hepatic blood flow is also
decreased while the hepatic venous pressure is increased which results in liver
dysfunction.iii

3) Effect on Respiratory System: CHF can increase the risk of sleep-disordered

breathing (SDB) which might be a result of cardiac dysfunction. Its prevalence in
HF patients is up to 70%. It is a result of dysynchronization of heart, lung and
brain. CHF can also lead to difficulties in breathing, decreased exercising capacity,
and many more.iv

4) Effect on heart: The heart goes through many changes in its size and shape
through a number of signals or events which cause cell apoptosis and necrosis,
cell dropout, myocyte hypertrophy, fibrosis, increased wall stress, and chamber
dysfunction.v
i
Fang, L., Karakiulakis, G., & Roth, M. (2020). Are patients with hypertension and diabetes mellitus at increased
risk for COVID-19 infection? The Lancet Respiratory Medicine. doi:10.1016/s2213-2600(20)30116-8

Ljungman, S., Laragh, J. H., & Cody, R. J. (1990). Role of the Kidney in Congestive Heart Failure. Drugs,
ii

39(Supplement 4), 10–21. doi:10.2165/00003495-199000394-00004 

Kubo, S. H. (1987). Liver Function Abnormalities in Chronic Heart Failure. Archives of Internal Medicine,
iii

147(7), 1227. doi:10.1001/archinte.1987.00370070041006

Oldenburg, O. (2012). Cheyne-Stokes Respiration in Chronic Heart Failure. Circulation Journal, 76(10), 2305–
iv

2317. doi:10.1253/circj.cj-12-0689 

v
Francis, G. S. (2001). Pathophysiology of chronic heart failure. The American Journal of Medicine, 110(7), 37–
46. doi:10.1016/s0002-9343(98)00385-4