Written Flashcards
(39 cards)
What is the mechanism of action of capitorpril
Inhibits angiotensins converting enzymes whihc prevents angiotensin I from becoming angeotensin II
How would captopril influence her cardiac condition
Decrease Both After & preload which improve cardiac performance and increase COP
Decrease secondary hyperaldosternism which decrease edema
What would be the effect of captopril on her blood pressure?
a- Mixed VD arterial > Venous
b. Art. VD which decrease TPR which decrease after load
c. Weak vein, VD. Decreases VR and Decreases EDV and decrease pre-load
What are the side effects of captopril?
Dry cough
First dose hypotension
Bilateral renal stenosis
Hyperkalemia
Although the patient was doing better on captopril, it was noticed that her heart rate is constantly above 100 bpm and this was viewed as a load on her heart.
In general, what drugs can possibly control the heart rate in a heart failure patient and their effects on heart rate?
Digoxin: -ve chronotropic, decrease AV conduction
Ivabradine: inhibits the cardiac pace maker funny current
Bisoprolol: beta blockade. Decrease HR, Decrease work of hear and O2 consumption. Decrease excitability
Which of the following could change the decision of using Ivabradine to control heart rate in patient with heart failure? Explain your answer on the basis of its mechanism of action
a) The heart rate is above 120
b) The patient has AF
c) The patient is diabetic
d) The patient is asthmatic
b) The patient has AF
Ivabradine acts by selective specific inhibition of funny currents in SA node requiring sinus rhythm which isn’t the case in AF.
What is the mechanism of action of this combination? (Sacubitril/valsartan)
Sacubitril inhibit the enzyme neprilysin which is responsible for degradation of natriuretic peptides causing their accumulation resulting in VD, Natriuresis and Diuresis, lowering BP and reducing aldosterone levels
What are the possible benefits of this medicine (Empagliflozin) to the patient?
Reduce the risk of CV death and worsening of HF by blocking SGLT2 protein in the nephron reducing the amount of reabsorbed glucose and sodium in to the blood. This inhibition results in natriuresis and net decrease in preload and afterload.
What is the mechanism of action of spironolactone? What are the side effects?
It is a direct antagonist of aldosterone receptor, thereby preventing salt retention and myocardial hypertrophy & remodeling
SE: gynecomastia, hyperkalemia, menstrual irregularities, decrease digitalis action
A patient with HFrEF is currently on sacubutril/valsartan, ivabradine, empagliflozin and Spironolactone Pt developed Atrial Fibrillation. The patient was still not well controlled with of the above medications and it was decided to add an inotropic agent. Which of the following is suitable?
a. Digoxin
b. Amrinone
c. Adrenaline
d. Levosimendan
Which drugs are we likely to remove when the selected drug is added and why?
a. Digoxin
Spironolactone should be stopped because it causes hyperkalemia and decreases digitalis activity
Ivabradine, because the patient has no sinus rythm
The mechanism of action of the chosen drug in the previous question (levosimendan)
Levosimendan is calcium sensitizers, increase the sensitivity of troponin C fibers to ionic calcium, improving my cordial contractility.
Which of the aforementioned anti-hypertensive drugs could be useful if the patient has osteoporosis?
Hydrochlorothiazide produce hypercalcemia by increasing calcium reabsorption from the luminal membrane of tubular cells into the interstitium in exchange of sodium and reducing urine calcium levels
The physician ask for serum level of potassium, what will you expect to find?
Hyperkalemia produced by lisinopril and spironolactone might be balanced by hypokalemia of thiazide diuretic
Why would the use of NSAIDs in this patient be considered inappropriate?
As NSAIDs inhibit production of vasodilator prostaglandin that mediate partially the anit-hypertensive effects of ACE inhibitors and hydrochlorothiazide
If the patient is intolerant to Lisinopril due to dry irritant cough, Indicate the alternative anti-hypertensive that devoid from this side effect
Lisinopril is an ACE inhibitor—> decrease the degradation of circulating bradykinin causing dry irritant cough
Any ARBS does not produce this effect because they have no effect on ACE
A 65 year old man with a 2 month history of progressive headache presented to the emergency department with nausea, vomiting, visual disturbance, and confusion for 1 day, his blood pressure was noted as 195/123 mm Hg, MRI of the brain was performed in the emergency department and demonstrated hypertensive encephalopathy.
Mention the other agents that can be prescribed to this patient and mention their mechanism of action
Nitroglycerin: nitro dilator release NO
Nifedipine: CCB
Na Nitroprusside: it is a nitro dilator
A 10 year old boy is brought to the emergency department after being stung by a bee. He had been well until he was stung on his right forearm, while playing in the yard. He initially complained of localized pain and swelling. Fifteen minutes later, he began to complain of shortness of breath. His parents brought him immediately to the local emergency department
Explain why epinephrine is the first line treatment in this case?
Bronchodilation (B2)
+ve iontropic & +chronotropic (B1)
inhibition activation of mast cells which decrease histamine and leukotriene release
Respiratory symptoms of the boy were not improved after IM epinephrine what will you do next?
Repeated IM adrenaline after 5 minutes
What are the advantages of the IM route of epinephrine over IV administration?
It is safer than IV route
It does not require IV access
IM route easier to learn
Diphenhydramine IV, Ranitidine IV, Methylprednisolone IV, were given to the boy. Mention mechanism of action of each drug
Methylprednisolone is down regulation of the late phase inflammatory response
Diphenhydramine IV, Ranitidine IV: anti histamines
Mention 4 drugs that my cause anaphylaxis
Penicillin
ACE inhibitors
NSAIDS
NMBs
What is the role of the vasopressor drug mentioned (norepinephrine) in treatment of cardiogenic shock?
a1 adrenergic agonist–> VC –> increase in both systolic and diastolic blood pressure–> increase coronary blood flow –> indirectly improving cardiac function
Mention TWO other vasopressors that can be used in the treatment of cardiogenic shock
epinephrine
vasopressin
What is the role of dopamine in the treatment of cardiogenic shock?
increase CO and increase BP