Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BRS > pharmacology hypertension > Flashcards

pharmacology hypertension Flashcards

1
Q

What is normal bp, stage 1 & 2 hypertension?

A

Normal < 135/85. stage 1: 135/85 - 149/94. stage 2: >150/95

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the Q risk?

A

risk of having CVD event in next 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is first line + 2nd line for adults with T2 diabetes (+ hypertension) or someone under 55 (not african)?

A

First line: ace inhibitor or ARB. 2nd line: calcium channel blocker or thiazide like diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is 1st + 2nd line for african people & people aged 55 or older?

A

1st line: calcium channel blocker. 2nd line: ARB, ACEi or thiazide like diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is plasma clearance?

A

How much blood an organ cleans of the drug per minute (total body clearance = liver (cl) + kidney (cl) + etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is elimination half life?

A

Time required for concentration of drug to decrease in half (greater clearance, shorter half life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is time-to-peak plasma levels?

A

Time for drug to reach its maximum concentration (faster absorption, shorter time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why do we prefer amlodipine over felodipine?

A

Blood pressure tends to increase most rapidly in early morning hours after waking up. Amlodipine has longer half life, mores stable plasma concentration curve, so able to cover difficult time in the morning better than felodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What angiotensin receptor mediates its actions and what are these?

A

Angiotensin receptor AT1: vasoconstriction, salt & water reabsorption, induces aldosterone secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do ACE inhibitors cause a cough?

A

Angiotensin II converts bradykinin to inactive metabolites stopping it from working, ACE inhibitors prevent bradykinin breakdown leading to spasm & cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why do ACE inhibitors cause hyperkalaemia?

A

Angiotensin induced aldosterone cause sodium to be reabsorbed and potassium excreted by principal cells, ace-inhibitors mean less aldosterone so less potassium is secreted causing hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What should you monitor after putting someone on ACE-inhibitors?

A

Renal function (eGFR), serum electrolytes (potassium) and blood pressure 1-2 weeks after starting treatmen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why can ACE inhibitor cause renal impairment?

A

Glomerulus requires sufficient perfusion pressure driven by flow from afferent arteriole. With ACEi less perfusion pressure so flow into afferent arteriole in narrowed/reduced, if pressure drops we rely on angiotensin to close tap on efferent arteriole to maintain pressure. So if flow of afferent arteriole impaired for whatever reason (unwell, renal stenosis) GFR will go down.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why do thiazide like diuretics cause hypokalaemia?

A

Block sodium-chloride co-transporter in DCT, so more sodium remaining in distal nephron. Normally this is reabsorbed in expense of potassium leading to hypokalaemia as more is drawn in. (more sodium in distal nephron so have to get rid of potassium - increased potassium excretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why do thiazide diuretics lose diuretic effects?

A

Diuretic effects lasts 1-2 weeks, kidney becomes tolerant to diuretic because there is rebound activation of renin-angiotensin system that counteracts diuretic effect by increasing sodium reabsorption. Continuing anti-hypertensive effects is due to further vasodilating action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are examples of ACE inhibitors?

A

Ramipril, lisinopril, perindopril

17
Q

What is mechanism of ACE inhibitors?

A

Inhibit angiotensin converting enzyme to prevent conversion of angiotensin I to angiotensin II by ACE

18
Q

What is target of ace inhibitor?

A

angiotensin converting enzyme ACE

19
Q

What are side effects of ace-inhibitor?

A

Cough, hyperkalaemia (care with K+ supplements or potassium sparing diuretics), foetal injury (avoid in pregnancy), renal failure in those with renal artery stenosis, urticaria/angioedema

20
Q

When are ACE inhibitors contraindicated?

A

pregnancy & renal artery stenosis

21
Q

What do most ACE inhibitors require?

A

Most (except lisinopril) are pro-drugs needing hepatic activation first for therapeutic effect

22
Q

What are examples of calcium channel blockers?

A

Amlodipine, felodipine

23
Q

What is mechanism of calcium channels blockers?

A

Block L-type calcium channels mainly on vascular smooth muscle decreasing calcium influx, downstream inhibition of myosin light chains and prevention of cross-bridge formation, cause vasodilation reducing peripheral resistance

24
Q

What is target of calcium channel blockers?

A

L-type calcium channels on vascular smooth muscle

25
Q

What are side effects of calcium channel blockers?

A

Ankle oedema, constipation, palpitations, flushing/headaches

26
Q

What type of calcium channels have higher degree of vascular selectivity?

A

Dihydropyridine type calcium channel blockers

27
Q

What are examples of thiazide-like diuretics?

A

Bendroflumethiazide & inapamide

28
Q

What is mechanism of thiazide-like diuretics?

A

Block sodium/chloride co-transporter in early DCT inhibiting sodium/chloride reasborption resulting in increased osmolarity of tubular fluid & thus less water reabsorbed in collecting duct

29
Q

What is target of thiazide-like diuretics?

A

Sodium/chloride co-transporter in DCT

30
Q

What are side effects of thiazide-like diuretics?

A

Hypokalaemia, hyponatremia, metabolic alkalosis (increaased H+ secretion), hypercalcaemia, hyperglycaemia (hyperpolarised pancreatic B cells), hyperuricemia

31
Q

What are examples of angiotensin receptor blockers ARBs?

A

Kisartan, candersartan, irebesartan, losartan

32
Q

What is mechanism of Angiotensin receptor blockers?

A

Act as non-competitive antagonists at AT1 receptor (on kidneys & vasculature)

33
Q

What is target of ARBs?

A

Angiotensin receptor AT1

34
Q

What are side effects of ARBS?

A

Hypotension, hyperkalaemia (care with supplements/potassium sparing diuretics), foetal injury in pregnancy, renal failure in renal artery stenosis

35
Q

When are ARBs contraindicated?

A

Pregnancy & renal artery stenosis

36
Q

Are ARBs as effective as ACEi?

A

no

37
Q

What do ARBs require?

A

Losartan & candesartan are pro-drugs requiring hepatic activation

BRS (81 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions