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CVS > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is the definition of hypertension?

A

That blood pressure above which the benefits of treatment outweigh the risks in term of morbidity and mortality

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2
Q

What is the difference between primary and secondary hypertension?

A

Primary - no cause for the hypertension can be found and is about 90% of all patients
Secondary - a cause for the hypertension can be found and is about 10% of all patients. Such as chronic renal failure, renal artery stenosis and endocrine diseases.

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3
Q

Blood pressure changes throughout the day, what causes this?

A

emotion
stress
exercise

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4
Q

What else can influence what your BP is?

A 
diet
obesity 
age 
medication on 
illicit drugs 
stresses
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5
Q

What are some of the main complications of high blood pressure?

A

End organ damage:

  • brain: stroke, haemorrhage, cognitive decline
  • kidney: renal failure, proteinuria
  • eye: retinopathy
  • heart: LVH, MI
  • blood vessels: peripheral vascular disease

Oedema

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6
Q

Is the clinic BP larger or smaller than the ABPM (Ambulatory Blood Pressure Monitoring)?

A

Clinical BP tends to be larger as the patient is sometimes more stressed in hospital and since its only one reading it isn’t a good representation of what the patients BP is like daily.
Whereas the ABPM is taken over 24 hours when the patients fluctuates their emotions and an average is taken.

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7
Q

How many stages of Hypertension is there?

A

3

stage 1
stage 2
severe hypertension

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8
Q

What are the blood pressure for the three stages of hypertension?

A
  1. Clinic BP >140/90 mmHg
    ABPM daytime average >135/85 mmHg
  2. Clinic BP >160/100 mmHg
    ABPM daytime average >150/95 mmHg

Severe >180/110 mmHg

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9
Q

What are some risk factors for high blood pressure?

A 
Cigarette smoking		
Diabetes mellitus		
Renal disease
Male				
Hyperlipidaemia		
Previous MI or stroke	
Left ventricular hypertrophy	  
Age 
Weight 
Alcohol intake 
Race 
Genetics

all of these are taken into account when calculating the risk of hypertension to a particular patient.
Assign Risk Calculator is used which takes into account their postcode.

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10
Q

Compare short and long term control of blood pressure.

A

Short term = arterial/carotid baroreceptors
• Vagus nerve and glossopharyngeal nerve respectively carry sensory fibers to medullary cardiovascular centres.
• This will trigger the vagus nerve or sympathetic nerves to decrease or increase the contractility of the heart and therefore affecting the heart rate and BP.

Long term = kidney permeability and plasma volume
• RAAS increases permeability of the conducting duct of the nephron by the release of renin from the juxtaglomerular.
• Therefore, more water is reabsorbed.
• Plasma volume increases
• Renin is released from the juxtaglomerular apparatus which converts angiotensinogen to angiotensin I which is then converted to angiotensin II by an ACE enzyme.
• Angiotensin II
- vasoconstrictor
- increases permeability of water in the conducting duct
- stimulates release of aldosterone which increases the reabsorption of Na+ back into the blood.
- Stimulates myocyte and smooth muscle hypertrophy – this is a poor prognosis indicator

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11
Q

Name some causes of secondary hypertension.

A

renal failure
drug induced - NSAIDS, oral contraception
pregnancy - preeclampsia
endocrine - cushings, Conns syndrome, acromegaly
coarctation of aorta
sleep apnoea

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12
Q

A true diagnosis of hypertension has to proven to ensure the patient will receive the correct treatment.
How is this done?

A

ABPM is used to measure their blood pressure over a long period of time.
While sleeping their should be a dip in BP as the parasympathetic system has been activated which reduces heart rate and hence BP. If this is not present and the BP remains high throughout the night then this shows a poor prognosis.

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13
Q

How can end organ damage be measured?

A

LVH - echocardiography, ECG
Proteinuria - albumin creatine ratio (ACR)
Kidney function - renal ultrasound, eGFR (glomerulus filtration rate)

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14
Q

After prescribing medication to a patient for hypertension, a target BP has to be set.
Why is this done and what is the target BP normally?

A

This is done to ensure the BP is controlled well.

Target BP normally =

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15
Q

What are the two ways hypertension is treated?

A
  • stepped approach

- low dosage of several drugs - to reduce side effects

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16
Q

What drug are young people with high renin prescribed for hypertension?

A

ACE inhibitors

  • to reduce the conversion of angiotensin I to angiotensin II
  • reduces the permeability of conducting duct
  • therefore less water is reabsorbed which decreases plasma volume and hence BP.
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17
Q

What drug are elderly people prescribed with low renin for hypertension?

A

Calcium channel blockers (CCB) - block Ca L type channels so it takes longer for the pace maker potential to be reached.

Thiazide- Type Diuretic - blocks reabsorption of Na so there is a higher conc of Na inside the conducting duct which pulls water into the conducting duct. This increases diuresis.

18
Q

State the stepped approach for treating hypertension and what drugs should be used at each stage.

A
  1. CCB (over 55, black/afrocarribean)
    Thiazide type diuretic (high risk heart disease/oedema/intolerance of CCB)
    ACEI/ARB (under 55/not afrocarribean/women of bearing age)
  2. Add thiazide type diuretic such as clortalidone or indapamide (so now have two drugs prescribed)
  3. Add CCB, ACEI, Diuretic together
  4. Consider treatment for resistant hypertension:
    Consider higher-dose thiazide-like diuretic treatment if the blood potassium level is higher than 4.5 mmol/l.
    If over 55 years
    - a calcium channel blocker
    If young
    - An ACEI or ARB
    - if a single agent doesn’t control BP then use the two together
19
Q

The following questions will be a description of the different antihypertensives.

A

…

20
Q

Angiotensin Converting Enzyme Inhibitors (ACEI)

  • mechanism
  • contradictions
  • adverse drug reactions
  • drug drug interactions
A
  1. prevent the conversion of angiotensin I to angiotensin II so reduces the permeability of the conducting duct so less water can be reabsorbed.
  2. renal failure, renal artery stenosis, hyperkaleamia
  3. cough, renal impairment, first dose can cause hypotension
  4. NSAIDs, potassium supplements, potassium sparing diuretics
21
Q

Give some examples of ACEIs

A

RAMIPRIL, Perindopril

22
Q

Angiotensin II Antagonists (ARB)

-mechanism

A
  1. Competitively block the actions of angiotensin II at the angiotensin AT1 receptor
23
Q

Give some examples of ARBs

A

LOSARTAN, VALSARTAN, CANDESARTAN, IRBESARTAN

24
Q

What is the benefit of ARBs compared to ACEIs

A

ARBs don’t give a cough

25
Q

Calcium Channel Blockers (CCB)

  • mechanism
  • prescribed to who?
  • contradictions
  • side effects
  • benefits
A
  1. blocking the L type calcium channels – pace maker potential takes longer to reach.
    selectivity between vascular and cardiac L type channels
  2. over 55 years
    women of child bearing age
  3. Acute MI, Heart failure, bradycardia
  4. Flushing, Headache, Ankle oedema, Indigestion and reflux oesophagitis, constipation
  5. Compliance is high
    Benefit in the elderly patient with systolic hypertension
    Rarely cause postural hypotension - reduction in systolic blood pressure of 20mmHg or more after standing for at least one minute
26
Q

Give some examples of CCB

A

Vasodilator
Amlodipine/Felodipine

Rate limiting
Verapamil/Diltiazem

27
Q

Thiazide Type Diuretics

  • mechanism
A
  1. prevents reabsorption of Na so water is pulled into the conducting duct and promotes diuresis.
28
Q

Name the three types of less commonly used antihypertensives and an example of each

A 
Alpha-adrenoceptor antagonists
	Doxazosin
Centrally acting agents
	Methyldopa
	Moxonidine 	
Vasodilators – cause very serious side effects. 
	Hydralazine – used IV in emergency consequences 
	Minoxidil
29
Q

Alpha-adrenoceptor antagonists

  • mechanism
  • adverse effects
A
  1. Selectively block post synaptic 1-adrenoceptors
    Oppose vascular smooth muscle contraction in arteries
  2. First dose hypotension
    Dizziness
    Dry mouth
    Headache
30
Q

Centrally Acting Agents

  • mechanism
  • side effects
A
  1. Converted to alpha-methylnoradrenaline which acts on CNS alpha adrenoceptors which decreases central sympathetic outflow
  2. Sedation and drowsiness
    Dry mouth and nasal congestion
    Orthostatic hypotension
31
Q

What is preeclampsia ?

A

a condition in pregnancy characterized by high blood pressure (>140/90mmHg), sometimes with fluid retention and proteinuria (>300mg/24h).

32
Q

does BP normally rise or fall during pregnancy ?

A

fall

33
Q

What should women be prescribed for hypertension before and after pregnancy ?

A

Before pregnancy
Nifedipine MR, Methyl dopa, Atenolol, Labetalol

During pregnancy
add thiazide diuretic and/or amlodipine

34
Q

What is accelerated hypertension ?

A

Increase in blood pressure to levels ≥180 mm Hg systolic and ≥110 mm Hg diastolic resulting in target organ damage such as neurological, cardiovascular or renal damage plus grade III retinal changes.

35
Q

What are the risk factors for accelerated hypertension ?

A

Existing diagnosis of HTN and prescribed antihypertensive agents.
Poor BP control prior to presentation.
A lack of a primary care contact. (healthcare contact)
Non Adherence to Medication.
Illicit drug use

36
Q

What is malignant hypertension?

A

The term malignant hypertension is usually reserved for cases where papilloedema grade IV fundal changes are present.

37
Q

Malignant and Accelerated hypertension are both hypertensive emergencies.
How would these be treated?

A

¥ Reducing mean arterial pressure by ≤25% for the first hour
¥ Then to 160/100-110 mmHg by 2-6 hours with subsequent gradual normalization over 24-48 hours.
¥ Best managed with a continuous infusion of a short acting, titratable antihypertensive agent.

38
Q

What is a hypertensive urgency?

A

Server hypertension without any target organ damage

39
Q

How NOT to treat hypertension !

A

¥ Do not reduce BP suddenly and excessively.
¥ Do not use sublingual and intramuscular medication.
¥ Do not use rapidly acting nifedipine or ACEI.
¥ Do not use intermittent as required therapy, oral or IV.
¥ Do not use IV hydralazine
5-20 minute lag before producing an erratic response
¥ Do not use sodium nitroprusside
(coronary steal syndrome and increased intracranial pressure, cyanide toxicity)

40
Q

what are two uncommon side effects of thiazide like diuretics ?

A

gout, impotence

CVS (20 decks)

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