Pharmacology -ACE inhibitors

Question 1

What do ACE Inhibitors actually do ?
(6)
what do they end with ?
-months

Answer 1

ACE = > CONVERTS ANG1—>ANG2
What does angiotensin 2 actually do ?
1- Vasconstriction
2-metabolism of Bradykinin ( vasodilator )
3-Aldosterone released from adrenal context of kidney , causing K+ levels to decrease, Na+ increases, water retention increases
4-Release of noradrenaline via
sympathetic NS—>vasoconstriction
5- Causes kidney to hold onto the water
6-Pituitary glands = releases ADH , which causes thirst , and water retention via kidney !

ALL OF THE ABOVE IS INHIBITED !

• so vasodilation is allowed =LOWERS BP
• More bradykinin ( as the break down of Bk is stopped)
• no aldosterone ( higher K+/H+ levels /less Na+ ,less water retention –>diuretic effect)
• noradrenaline not released = vasodilation
• cough

normally end with = “PRIL,”
examples include :
Captopril , Lisinopril , Ramipril ,Perindopril

Question 2

What is treated with ACE inhibitors?

5

Answer 2

1-Hypertension ( will reduce BV -water is released, hence BP reduced)
2-Heart Failure =systolic dysfunction ( less vasoconstriction , less growth of L.V ,cardiac work ,increased cardiac output )
3-renal indications ( efferent arterioles are dialated reducing the pressure , which will slow down the progression of renal damage )
4-Recovering after an MI - thickening of Ventricular wall is prevented , as remodelling is reduced due to decreased hypertension .
5-Atrial fibrillation -atrial remodelling Is reduced as BP is lower

Question 3

How can ACE inhibitors help renal function ?
(2)
*******

Answer 3

• kidney has increased blood flow Because of damaged vessels
• ACE inhibitor= dilation of efferent arterioles , lowers the pressure

Question 4

what are the potential side effects of ACE inhibitors?

6

Answer 4

1-bradykinin =causes dry cough and angiodema (Swellling of deeper layers of skin )
2-acute renal failure (when efferent arterioles are dialated =Glomelualr filtration is compromised = lack of pressure)
3-1st dose hypotension (low bP )
4-Hyperkalemia ( too much K+ , as aldosterone isn’t being made)
5-rash , taste disturbance
6-teratogenicity = harm to unborn child

Question 5

What precautions should be taken when introducing ACE inhibitor therapy ?
(5)

Answer 5

1- start Low dose and monitor to see If it really working
2-avoid in renal and vascular disease
3- Hyperkalemia ( monitor patients diet and other meds to avoid this ) = this is because aldesterone normally keeps Na+/K+ levels in balance by keeping Na+ in kidney and filtering K+ out , but when it isn’t present K+ levels in the kidney rise .
4- Vasodialators = aortic stenosis= narrowing of aortic valve opening !
5-DONT GIVE IN PREGNANCY

Question 6

Whats the main difference between the ACE inhibitor and Angiotensin receptor blocker ?
(2)

Answer 6

1- angiotensin receptor blockers don’t have any effect on bradykinin metabolism so you won’t get a dry cough
–> this could increase compliance but also reduce risk of angioedema ( swelling of deep layers of skin )

Question 7

what new research is there about dual drug ?

3

Answer 7

DUAL NEP enzyme + angiotensin receptor inhibitor
1-causes vasoconstriction
2-inhibits Neprilysin ( which makes vasodilators )
3- It is better at reducing morbidity , morality in heart failure

Question 8

what receptor do the Angiotensin receptor antagonist block ?

2

Answer 8

1-AT1
2-they end with "Sartan," examples include: 
-Azilsartan (Edarbi)
-Candesartan (Atacand)
-Eprosartan.

Question 9

where do the adrenoceptors act ?
(just name 3 )
(7 possible examples given )

Answer 9

1) B1 in the heart ( increases HR,conducitvity , force of contraction)
2) B1=kidney =increase renin production
3) B2=airways = causes relaxation , vasodilation
4) B2=LIVER , Skeletal muslce= causes production of glucose
5) A1=salivary glands = K+ release
6) A2=platelet clumps
7) A2=Brainstem = causes decrease in sympathetic outflow

Question 10

what do Beta blockers end with ?haha
What do alpha blockers end with ?trigonometry
(2)

Answer 10

1-beta blockers =-lol=atenolol

2-Alpha bockers =-osin =prazosin

Question 11

how does a beta blocker work ?

4

Answer 11

1- Beta receptor is blocked
2-this means G-protein won’t release alpha subunit to activate adenyl cyclase and make cAMP
3-cAMP can not go and activate Protein kinase A which is linked to a L-type ca2+ channel
4-this means ca2+ won’t flood in
=>contraction is less forceful (so cardiac work goes down, O2 demand also goes down , very useful when the heart is recovering from MI)
=>slower HR
=>cardiac conduction goes down

Question 12

what can B blockers treat and why ?

4

Answer 12

1-MI/atrial fibrillation=> secondary prevention , by reducing cardiac work, and reduces AV conduction = so ventricular dysarthymia goes down
2- Hypertension- Decrease BP , as they stop Noradrenaline from binding ( hence vasoconstriction is stopped)
3-Angina Pectoris(chest pain )=reduced rate of contraction , lowers O2 demand= reduces the frequency of MI)
4-Heart failure ( questionable research , but the beta blocker reduces Cardiac work , hence protects the heart= stops left ventricular hypertrophy , it also prolongs diastole allowing adequate filing )

Question 13

what are the adverse effects and precautions of Beta blockers?
(6)

Answer 13

1-Bradychardia ( HR too slow )
2-Lipid soluble Blockers =cross the BBB =fatigue. insomnia , depression and nightmares
3-Metabolic effects = less secretion of glucagon , interfers with autonomic and metabolic response
4-Can hurt unborn baby
5-Don’t withdraw suddenly =can cause RAPID UNMASKING OF receptors =HT , angina , MI
6-Don’t use with other drugs that slow down heart rate , they could cause cardiac dysfunction .

Question 14

what part of the action potential do Beta blockers effect in :
a) pacemaker cell
b)Non pacemaker cell
(2)

Answer 14

a) slows phase 4 /0 (less ca2+ intake )

b) Slows phase 2 (influence of ca2+ is slow- remember it is needed so the refractory period is longer)