Cardiology Flashcards
(18 cards)
What is MOA of ACE inhibitors?
Low blood flow through kidneys -> renin released into blood stream -> cleaves angiotensinogen released by the liver -> angiotesnin 1 -> flows through the lungs -> ACE released in lungs converts ANG 1 to ANG 2 -> causes 3 effects to increase BP:
- vasoconstriction
- Acts on POSTERIOR PITUITARY to release ADH -> Acts on kidneys, causes water retention -> Increase in BP
- Acts on adrenal glands -> aldosterone -> water reabsorption in kidneys AND POTTASIUM EXCRETION -> Increase in BP.
So excessive aldosterone can cause hypokalemia and Hypernatremia.
- ACE inhibitors block above effects. Hence also can cause side effect of hyperkalemia and Hyponatremia.
What is the MOA of ARB?
Same as ACE but only blocks ANG 2 receptors and hence causing the effect.
What is reno-protective role of ACE inhibitors?
The reno-protective effects of ACE inhibitors are mediated through dilation of the glomerular efferent arteriole.
- Diabetic nephropathy is characterised by glomerular hyperfiltration, where increased intraglomerular pressure leads to progressive damage and worsening proteinuria.
- ACE inhibitors like ramipril are renoprotective because they inhibit angiotensin II, and dilate the efferent arteriole.
- ACE inhibitors reduce glomerular pressure, thereby reducing albuminuria and slowing the progression of kidney disease. This is especially beneficial in diabetic nephropathy, as lowering pressure in the glomeruli helps protect kidney function.
Side effects of ACE inhibitors?
- Hyperkalemia
- Angioedema
- Dry cough
- first-dose hypotension: more common in patients taking diuretics
Contraindications of ACE inhibitors
- C1estrase deficiency as can cause further release in Bradykinin leading to worsening of symptoms such as cough, angioedema.
- Pregnancy : teratogenic. Other alternatives Hydralazine, Methylodopa, Nifedipine, Labetalol.
- Bilateral Renal artery stenosis
- Severe CKD
- Aortic stenosis: may result in hypotension
- hereditary of idiopathic angioedema
How much rise in Creatinine and potassium is acceptable once patients are started on ACE inhibitors?
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
Most common cause of subacute endocarditis?
Streptococcus viridans infection.
often sensitive to penicillin, and the mortality rate associated with it is relatively low.
What are the 4 poor prognostic factors of Infective Endocarditis?
- Staphylococcus aureus infection.
- prosthetic valve (especially ‘early’, acquired during surgery).
- culture negative endocarditis, as not knowing organism can be hard to treat.
- low complement levels, due to immunodeficiency.
Initial blind therapy for IE for native valve, penicillin allergy and prosthetic valves?
- Native valve: Amoxicillin + low dose Gentamicin
- Penicillin allergy / MRSA/ Severe sepsis: Vancomycin + low dose Gent
- Prosthetic valve: Vancomycin + Rifampicin + Low dose Gentamicin
Treatment for S. aureus: native/prosthetic valve
- Native valve : IV Flucloxacillin.
Penicillin allergy: Vancomycin + Rifampicin - Prosthetic valve : Flucloxacillin + rifampicin + low-dose gentamicin.
Penicillin allergy: vancomycin + rifampicin + low-dose gentamicin.
Treatment for fully sensitive Strept
- Benzylpenicillin
- If penicillin allergic
vancomycin + low-dose gentamicin
Treatment for less sensitive Strept.
- Benzylpenicillin + low-dose gentamicin
- If penicillin allergic:
vancomycin + low-dose gentamicin
What are the indications for surgery in Infective Endocarditis?
Indications for surgery:
- severe valvular incompetence
- aortic abscess (often indicated by a lengthening PR interval)
- infections resistant to antibiotics/fungal infections
- cardiac failure refractory to standard medical treatment
- recurrent emboli after antibiotic therapy
What is the site on nephrons that Carbonic anhydrase inhibitors?
PCT in nephron.
Main site of sodium reabsorption (60%): PCT in nephron - this is blocked.
What site of the nephron does Loop diuretics act on?
Ascending loop of Henle.
Sodium (25%), potassium and chloride: thick ascending limb - this mechanism is blocked
What site of the nephron do Potassium sparing diuretics act on?
Late distal collecting duct or collecting duct
Sodium (1%) reabsorbed and potassium excreted: late
distal convoluted tubule or collecting duct.
- this mechanism is blocked.
What is the site that Thiazide diuretics act on?
Early distal convoluted tubule.
Sodium(5%) and chloride: early DCT - this mechanism is blocked.
What is the Anti-HTN flow chart?
