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Cardiovascular Nafisa > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is the Step 1 treatment for HYPERTENSION WITH TYPE 2 DIABETES

A

ACEi or ARB

(if not tolerated then beta- blocker)

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2
Q

What is the Step 1 treatment for HYPERTENSION WITHOUT TYPE 2 DIABETES
Age <55 and not of black African or African- Caribbean family origin?

A

ACEi or ARB

(if not tolerated then beta- blocker)

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3
Q

What is the Step 1 treatment for HYPERTENSION WITHOUT TYPE 2 DIABETES
Age 55 or over

A

CCB

if high risk of heart failure or CBB not tolerated: give thiazaide like diuretc TLD

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4
Q

What is the Step 1 treatment for HYPERTENSION WITHOUT TYPE 2 DIABETES
Black African or African- Carribean family origin

A

CCB

if high risk of heart failure or CBB not tolerated: give thiazaide like diuretc TLD

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5
Q

What is the Step 2 treatment for a patient already recieving CCB?

A

Give ACEi or ARB or thiazide like diuretic

*if patient is African/ Carribean, ARB is preferred in their second line treatment

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6
Q

What is the Step 3 treatment for someone who needs antihypertensive drug

A

ACEi or ARB
+CCB
+ thiazide like diuretic

(give a low dose spironaloctone as the TLD. However, you can give a higher dose TLD if their K+ levels > 4.5)

If other diuretics are ineffective. ADD ALPHA or BETA- BLOCKER

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7
Q

What is the Step 4 treatment for someone who needs antihypertensive drug

A

confirm resistant hypertension
confirm elevated BP with ABPM or HBPM
check for postural hypotension and discuss adherence

Consider seeking expert advice or adding a:
- low dose spironolactone if blood potassium level is ≤4.5mmol/L
- alpha blocker or beta blocker if blood potassium level is >4.5mmol/L

seek expert advice if BP is uncontrolled on optimal tolerated doses of 4 drugs

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8
Q

Why should you avoid TLD and beta- blocker together ESPECIALLY in diabetes or high risk of diabetes?

A

both drugs cause hypoglycaemia

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9
Q

CCB

A

calcium channel blocker

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10
Q

TLD

A

thiazide like diuretic

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11
Q

ACEi

A

Ace inhibitor

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12
Q

ARB

A

Angiotensin II receptor blocker

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13
Q

What is normal hypertension

A

120/ 80 mmHg

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14
Q

What should you do if a patient has blood pressure of 140/90?

When would you treat such a patient?

A

OFFER LIFESTYLE ADVICE

ONLY TREAT IF UNDER 80 with:
- target organ damage (left ventricular hypertrophy, CKD, retinopathy)#
- CVD or 10 year CVD risk >20%, renal disease, diabetes

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15
Q

What should you do if a patient has a blood pressure of 160/90?

A

ALL patients with such a blood pressure SHOULD be treated

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16
Q

What should you do if a patient has a blood pressure of >180 as their SYSTOLIC and >110 as their DIASTOLIC?

A

This is a HYPERTENSIVE CRISES.
It can be either a HYPERTENSIVE EMERGENCY or a HYPERTENSIVE URGENCY

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17
Q

What is hypertensive emergency

A

HYPERTENSIVE EMERGENCY:
- in a hypertensive emergency, the blood pressure is so high that it is causing immediate and severe damage to one or more critical organs. This is a life-threatening situation that requires rapid medical intervention, typically in a hospital setting, to lower the blood pressure and prevent further organ damage or complications.
-Treatment involves IV medications to lower blood pressure rapidly. Otherwise can have: reduced organ perfusion= blindess, MI, cerebral infarcation and severe renal impairment

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18
Q

What is hypertensive urgency

A

blood pressure is significantly elevated but does not currently exhibit acute or immediate target organ damage. Unlike a hypertensive emergency, where there is evidence of acute organ damage, hypertensive urgency is characterized by the high blood pressure itself without other acute symptoms or complications.

Treatment: Oral medications to reduce blood pressure slowly over 24- 48 hours.

(gradually and safely lower the blood pressure over a period of hours to days to reduce the risk of complications over the long term)

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19
Q

what is reduced organ perfusion

A

inadequate perfusion (blood flow) to vital organs

can result in organ damage

hypertensive emergency can cause reduced organ perfusion

(Chronic high blood pressure can cause the arteries and arterioles (smaller blood vessels) to constrict or narrow. When blood vessels narrow, it increases resistance to blood flow, making it harder for blood to move through these vessels. As a result, blood flow to organs and tissues can be compromised, reducing perfusion.)

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20
Q

why can high blood pressure lead to retinopathy?

A

Extremely high blood pressure can damage the blood vessels in the eyes, leading to retinopathy. Rapid reduction of blood pressure can help prevent or minimize this eye damage and reduce the risk of blindness.

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21
Q

why can severe high blood pressure lead to myocardial infarction (heart attack)

A

Severe hypertension can place excessive strain on the heart, increasing the risk of a heart attack (myocardial infarction). Lowering blood pressure quickly can reduce this strain and minimize the risk of cardiac events.

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22
Q

why can high blood pressure cause kidney damage?

A

reduced organ perfusion

Impaired blood flow to the kidneys can lead to kidney dysfunction or failure.

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23
Q

What are clinical blood pressure targets in: UNDER 80 YEARS?

A

IF they have atherosclerotic CVD* or diabetes with kidney, eye or cerebrovascular disease**
130/80

For EVERYONE ELSE
<140/90

  • a condition in which fatty deposits (plaques) build up on the inner walls of arteries.

** a group of medical conditions that affect the blood vessels and blood supply to the brain

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24
Q

What are clinical blood pressure targets in: OVER 80 YEARS?

A

<150 /90

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25
Q

What are clinical blood pressure targets in: pts with RENAL DISEASE

A

IF CKD, Diabetes, proteinuria > 1g in 24 hours:

< 130/ 80

(consider ACEi/ ARB if proteinuria present)

FOR EVERYONE ELSE:
<140/90

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26
Q

what are clinical blood pressure targets in: pts with DIABETES?

A

IF have complications with their diabetes such as: EYE, KIDNEY or CEREBROVASCULAR DISEASE
<130/80

FOR EVERYONE ELSE
<140/80

(THIS IS NOT A TYPO, IT ACTUALLY IS 80 AND NOT 90!)

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27
Q

What are clinical blood pressure targets in: pregnant pts?

A

CHRONIC HYPERTENSION
<140/90

CHRONIC HYPERTENSION & if target organ damage or have already given birth

<140/90

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28
Q

What drug is widely used as first choice in gestational hypertension?

A

Labetalol

(this drug is hepatotoxic- remember that

Other drugs include:
methyldopa (stop 2 days after birth)

nifedipine MR (unlicensed)

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29
Q

What is the mechanism of action of angiotensin- converting enzyme inhibitors?

A

Inhibits the conversion of angiotensin I to angiotensin II

Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels, leading to increased blood pressure. It also stimulates the release of aldosterone, which promotes sodium and water retention by the kidneys, further raising blood pressure.

Therefore ACEi inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to dilate or relax. This dilation reduces peripheral vascular resistance, which is the resistance that the heart must overcome to pump blood through the circulatory system. As a result, blood pressure decreases, and the workload on the heart is reduced.

ACE inhibitors also lead to a decrease in the production of aldosterone, a hormone that acts on the kidneys to increase the reabsorption of sodium and water. By reducing aldosterone levels, ACE inhibitors promote the excretion of sodium and water by the kidneys, which helps lower blood pressure and reduce fluid retention.

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30
Q

Give examples of ACE inhibitors?

A

Captopril (BD)
ENALAPRIL
Fosinopril
Imidapril
LISINOPRIL
Moexipril
PERINDROPIL (30- 60 minutes before food)
Quinapril
RAMPIRIL
Trandolapril

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31
Q

All ACEi inhibitors should be done once a take except for one of them. What is this and what is its dosing?

A

CATOPRIL

should be taken BD

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32
Q

When should a patient take their first dose of ACEi

A

At bedtime

(could be to mitigate side effects, as individuals may sleep through the initial period when side effects are most likely to occur)

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33
Q

What are examples of Angiotensin II receptor blockers (ARB)?

A

Azilsartan
CANDERSARTAN
eprosartan
Irbersartan
LOSARTAN
Olmesartan
Telmisartan
VALSARTAN

34
Q

What are side effects of ACEi?

A

persistent dry cough: give ARB as alternative

hyperkalaemia: higher risk in renal impairment and diabetes mellitus

anaphylactoid reactions* e.g. angioedema**

OTHER SIDE EFEFCTS:
oral ulcer, taste disturbance and hypOglycaemia

*non-allergic anaphylaxis but are not caused by the immune system’s production of IgE antibodies.

**condition characterized by the sudden and often rapid swelling of deeper layers of the skin, usually in areas such as the face, lips, tongue, throat

35
Q

What is anaphylaxis

A

a severe and potentially life-threatening allergic reaction that can occur rapidly and affect multiple organ systems in the body. It is characterized by a sudden and systemic release of chemical mediators, including histamines, that lead to a wide range of symptoms.

Allergic Anaphylaxis: This type of anaphylaxis occurs when the immune system recognizes a specific allergen as harmful and mounts an exaggerated immune response. The immune system produces IgE antibodies in response to the allergen, and upon re-exposure, these antibodies trigger the release of histamines and other chemicals

Non- allergic anaphylaxis: does not involve IgE-mediated immune responses. Instead, non-allergic anaphylaxis occurs when certain substances, such as some medications (e.g., radiocontrast dye, certain opioids), directly trigger the release of histamines and other mediators, leading to similar severe symptoms. The key difference is that non-allergic anaphylaxis does not involve the production of IgE antibodies or prior sensitization to an allergen.

(basically in allergic its the IgE antibodies that stimulate the release of the histamines BUT in non-allergic the thing thats irritating is releasing the histamine all by itself)

36
Q

Out of ACEi and ARBs, which one is renoprotective in renal disease such as CKD?

A

ARB

37
Q

Some drugs are NEPHROTOXIC and should be avoided in AKI. DAMN is the acronym to describe these drugs.

Spell out the DAMN acronym

A

D= diuretics
A= ace inhibitors/ arbs
M= metformin
N= Nsaids

38
Q

Why should ARBs be avoided in renovascular disease?

A

reduces eGFR via efferent arteriole dilation

May give in unilateral renal artery stenosis* BUT not severe bilateral stenosis

*Unilateral renal artery stenosis is a medical condition characterized by the narrowing or constriction of one of the renal arteries, which are the blood vessels that supply blood to the kidneys. “Unilateral” means that only one of the renal arteries is affected, while the other remains normal.

39
Q

What is renovascular disease

A

Renovascular disease refers to conditions that affect the blood vessels supplying the kidneys. It often involves the narrowing or blockage of these blood vessels, which can reduce blood flow to the kidneys and potentially lead to high blood pressure and kidney dysfunction.

40
Q

What are the hepatic effects of ARBs?

A

cholestatic jaundice

hepatic failure

*s a type of jaundice that occurs when there is an interruption in the normal flow of bile from the liver to the small intestine.

41
Q

In relation the the hepatic effects of ARBs, when must we stop ARBs?

A

if liver transamines 3x normal

or

jaundice occurs

42
Q

What is the advice for ACEi and pregnancy?

A

AVOID

43
Q

What are drug interactions of ACEi?

A

HYPERKALAEMIA if given with: aliskeren, ARB, K+ sparing diuretics/ aldosterone antagonists

Nephrotoxicity and reduced eGFR if given with: NSAIDs (afferent arteriole constriction)

HYPOTENSION: if given with diuretics (volume depletion= low blood pressure)

RENAL IMPAIRMENT, HYPERKALAEMIA and HYPOTENSION if given with renin- angiotensin system drugs i.e ACEi/ ARB, renin inhibitor

(avoid concomitant ACEi + ARB in diabetic neuropathy)

44
Q

Why are angiotensin- II receptor blockers an alternative to an ace inhibitor if a persistent dry cough occurs?

A

they do not inhibit the breakdown of bradykinin

(ACE inhibitors work by inhibiting the enzyme ACE, which is responsible for breaking down bradykinin. When ACE is inhibited, bradykinin levels in the body increase= It’s thought that the accumulation of bradykinin in the respiratory tract may stimulate the cough reflex= lead to dry cough)

45
Q

What are examples of centrally acting anti- hypertensives?

A
  • methyldopa
  • clonidine
  • moxonidine

“Centrally acting hypertensive” typically refers to a class of antihypertensive medications that work in the central nervous system (CNS) to lower blood pressure. These drugs act on specific receptors or pathways in the brain to reduce the signals that cause blood vessels to constrict, ultimately leading to a decrease in blood pressure.

46
Q

What is a side effect of methyldopa

A

drowsiness (so can affect driving)

47
Q

What is a side effect of clonidine

A

flushing

48
Q

what are examples of vasodilator antihypertensives?

A
  • hydralazine
  • minoxidil

a type of medication or substance that causes blood vessels to relax and dilate (widen). When blood vessels dilate, their diameter increases, allowing blood to flow more easily and reducing blood pressure.

49
Q

what are the side effects of hydralazine

A

fluid retention
tachycardia

50
Q

what are the side effects of minoxidil

A

tachycardia
fluid retention
& increase cardiac output

51
Q

what are examples of alpha- blockers?

A

prazosin
terazosin
indoramin

52
Q

what is the mechanism of action of alpha blockers

A

Alpha-1 receptors are found in the smooth muscle of blood vessels, particularly in the walls of arteries and arterioles. When these receptors are stimulated by the neurotransmitter norepinephrine, they cause the smooth muscle to contract, leading to vasoconstriction (narrowing of blood vessels). This vasoconstriction increases blood pressure.

Alpha blockers are antagonists of alpha-1 adrenergic receptors. This means that they bind to these receptors and prevent norepinephrine from activating them. By doing so, alpha blockers inhibit the vasoconstrictive effect of norepinephrine.

When alpha-1 receptors are blocked by alpha blockers, the smooth muscle in the blood vessel walls relaxes, leading to vasodilation (widening of blood vessels). This dilation reduces the resistance to blood flow, which, in turn, decreases blood pressure.

The net result of alpha blockade is a reduction in systemic vascular resistance and a decrease in blood pressure. By reducing the work the heart has to do to pump blood against high resistance, alpha blockers can help lower blood pressure and improve blood flow to various organs and tissues.

53
Q

What is the mechanism of action of beta- adrenoreceptor blockers (BETA- BLOCKERS)

A

In the body, there are beta-adreceptors located in various tissues, including the heart, blood vessels, and lungs. These receptors are activated by the stress hormones adrenaline and norepinephrine, which are released by the adrenal glands in response to stress or other stimuli.

When adrenaline or norepinephrine binds to beta-adreceptors, it triggers various physiological responses, including increased heart rate, increased force of heart contraction, and vasoconstriction (narrowing of blood vessels). These responses can result in increased blood pressure and a faster heart rate.

Beta-blockers work by binding to and blocking beta-adreceptors. By doing so, they prevent the binding of adrenaline and norepinephrine to these receptors, effectively reducing or blocking their stimulatory effects.

Cardiovascular Effects:

Heart Rate Reduction: By blocking beta-1 receptors primarily found in the heart, beta-blockers slow down the heart rate (negative chronotropic effect).

Decreased Force of Contraction: Beta-blockers also reduce the force of contraction of the heart muscle (negative inotropic effect), which can help lower blood pressure and reduce the heart’s workload.

Vasodilation: Some beta-blockers have additional effects on blood vessels. They can lead to vasodilation (widening of blood vessels), which reduces peripheral vascular resistance, helping to lower blood pressure.

54
Q

What are examples of beta- adrenoreceptor blockers (BETA- BLOCKERS)

A

acebutol
atenolol
bisoprolol
carvedilol
esmolol
labetalol
metoprolol
nadolol
nebivolol
oxprenolol
pindolol
propranolol
sotalol
timolol

55
Q

What is esmolol used to treat?

A

hypertension in PERIO OPERATIVE period

has short half life

56
Q

which betablocker is used for hypertension in pregnancy

A

labetalol

but this is HEPATOXIC

57
Q

what class is sotalol and what is a side effect

A

class 3 anti- arrhythmic

side effect: torsade de pointes

58
Q

what are the four different types of beta blockers and their acronyms?

A

Intrinsic sympathomimetic activity (ice PACO)

Water soluble, less likely to cross blood- brain barrier ( water CANS)

Cardio selective= less bronchospasm (Be A MAN)

Once daily dosing (BACoN)

59
Q

Describe ice PACO

‘intrinsic sympathomimetic activity’ beta blockers

A

intrinsic sympathomimetic activity: Intrinsic sympathomimetic activity (ISA) is a characteristic of some beta-blockers, particularly selective ones. Beta-blockers with ISA have a unique property in that they not only block beta-receptors but also have partial agonist activity at these receptors. In other words, they partially stimulate or activate the beta-receptors even as they are blocking them.

these beta blockers HAVE:
- less bradycardia
- less coldness of extremities

EXAMPLES (PACO):

  • pindolol
  • acebutolol
  • celiprolol
  • oxprenolol
60
Q

Describe water CANS beta blockers

‘water- soluble, less likely to cross- blood- brain barrier’

A

as they are less- likely to cross the blood- brain barrier

means LESS nightmares and sleep disturbances

make sure to REDUCE their dose though in renal impairment as these beta blockers are RENALLY CLEARED

Examples are (CANS):
- celiprolol
- atenolol
- nadolol
- sotalol

61
Q

Describe Be A MAN beta blockers

‘cardio- selective= less bronchospasm’

A

well- controlled asthma under a specialist if no other choice

Examples are (B A MAN)

Bisoprolol

Atenolol

Metoprolol
Acebutol
Nebivolol

62
Q

Describe BACoN beta blockers?

A

once daily dosing

intrinsically long duration of action

Examples are (BACN)

Bisoprolol
Atenolol
Celiprolol
Nadolol

63
Q

What are side effects of beta- blockers?

A

bradycardia, hypotension

hypErglycaemia OR hypOglycaemia

(beta- blockers mask symptoms of hypOglycaemia e.g. tachycardia)

64
Q

What are contra- indications of beta- blockers?

A

ASTHMA
(as beta- blockers cause bronchospasm. This includes B blocker eye drops e.g. timolol)

WORSENING UNSTABLE HEART FAILURE

SECOND/ THIRD DEGREE HEART BLOCK*

SEVERE HYPOTENSION AND BRADYCARDIA

*heart rhythm disturbances that occur when the electrical signals in the heart don’t flow properly.

65
Q

What are some interactions of beta- blockers

A

VERAPAMIL* INJECTION
(asystole** and hypotension)

THIAZIDE- LIKE DIURETIC
(causes hyperglycaemia: avoid in diabetes, high risk of diabetes)

*type of CCB
**Asystole is when your heart’s electrical system fails entirely, which causes your heart to stop pumping.

66
Q

what is the mechanism of action of calcium channel blockers?

A

Calcium channels are proteins on the cell membranes of these muscle cells and neurons that control the entry of calcium ions into the cells when activated.

Voltage-gated calcium channels open in response to changes in the electrical membrane potential (voltage) of the cell. When they open, calcium ions flow into the cell.

In cardiac muscle cells, calcium ions are essential for the generation of an action potential—the electrical signal that triggers muscle contraction. Calcium influx during the action potential allows the heart to contract and pump blood effectively.

In smooth muscle cells found in the walls of blood vessels, calcium ions also play a crucial role in muscle contraction. An increase in calcium levels in these cells leads to vasoconstriction (narrowing of blood vessels), which can increase blood pressure.

Calcium channel blockers work by binding to and blocking the voltage-gated calcium channels on the cell membranes of cardiac and smooth muscle cells.

By blocking these channels, calcium channel blockers prevent or reduce the entry of calcium ions into the cells. This leads to the following effects:

Cardiac Effects: In the heart, CCBs reduce the influx of calcium ions during the action potential, resulting in a decreased force of contraction (negative inotropic effect) and a slower heart rate (negative chronotropic effect). This helps reduce the heart’s workload and oxygen demand.

Vasodilation: In smooth muscle cells of blood vessels, CCBs inhibit calcium entry, leading to relaxation and dilation of the blood vessels. This reduces peripheral vascular resistance and lowers blood pressure.

The combined effects of reduced cardiac contractility and vasodilation make calcium channel blockers effective in lowering blood pressure and relieving angina by decreasing the heart’s workload and improving blood flow to the heart muscle.

67
Q

What are the two different types of calcium channel blockers?

A

DIHYDROPYRIDINE CBBS

RATE LIMITING CCB

68
Q

what are dihydropyridine CCBS?

A

Dihydropyridine CCBs primarily target the L-type calcium channels in vascular SMOOTH MUSCLE CELLS By blocking these channels, they inhibit calcium influx, leading to vasodilation (widening of blood vessels). This results in reduced peripheral vascular resistance and lower blood pressure.

69
Q

what are rate limiting CCBs

A

Rate-limiting CCBs, also known as non-dihydropyridine CCBs, primarily target the L-type calcium channels in the HEART, particularly in the atrioventricular (AV) node. By blocking these channels, they slow down the conduction of electrical impulses through the AV node, which results in a reduction in heart rate and a decrease in the force of atrial contraction.

70
Q

What are examples of dihydropyridine CCBs?

A

AMLODIPINE
FELODIPINE
Lacidipine
Lercanidipine
Nifedipine (maintain the same modified release brand)

71
Q

What are examples of rate- limiting CCBs?

A

verapamil and diltiazem

note: if pt. is on diltiazem make sure to maintain on same brand when doses > 60mg

72
Q

what are side effects of calcium channel blockers?

A

headaches (common)
ankle swelling flushing

73
Q

who should rate- limiting CCBs be avoided in?

A

those with heart failure

74
Q

what can verapamil cause

A

constipation

75
Q

what is the only CCB licensed for arrhythmia?

A

verapamil

76
Q

what is an interaction of CCBs?

A

GRAPEFRUIT JUICE

is an enzyme inhibitor- leads to increased CCB concentration

77
Q

What is a phaechromocytoma and why can it cause high blood pressure?

A

A phaeochromocytoma is a rare tumour of the adrenal glands, which sit above the kidneys.

A phaeochromocytoma can cause the adrenal glands to produce too much adrenaline and noradrenaline which often results in problems such as heart palpitations and high blood pressure.

78
Q

How to treat phaechromocytoma induced hypertension?

A

beta blocker + alpha- blocker (phenoxybenzamine)

refer to BNF

79
Q
A
80
Q

What is the Step 2 treatment for a patient already recieving ACEi or ARB?

A

Give CCB or thiazide like diuretic

Cardiovascular Nafisa (9 decks)

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