ILA Hypertension Flashcards

1
Q

What BP readings are classed as hypertension?

A

Clinic BP ≥ 140/90 mmHg
or
ABPM ≥135/85 mmHg

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2
Q

What are the important aspects of clinical examination for hypertension?

A
  • Fundoscopy - for hypertensive retinopathy
  • Signs of secondary hypertension - palpable kidneys, abdominal bruit, neurofibromas, radiofemoral delay
  • Signs of end organ damage - ECG (LVH), proteinuria
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3
Q

What investigations would you do for hypertension?

A

Clinic BP

And to confirm BP:

Ambulatory BPM - ABPM - At least 2 measurements per hour taken during waking hours and use the average value to confirm diagnosis

Home BPM - used if pt cannot tolerate ABPM, record BP 2 times twice a day when seated at least 1 min apart for 4-7 days, discard, Discard the measurements from the first day and use the average of all the remaining measurements

Urinalysis - for blood and protein (hypertensive nephropathy and GN can be a cause of secondary hypertension)

24 hour urine metanephrine: phaeochromocytoma

urinary free cortisol: Cushing’s

U+E: K+ reduces in Conn’s

renin and aldosterone levels: for Conn’s - hyperaldosteronism

Abdo USS - PKD

MRI aorta - for coarctation

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4
Q

What are the three stages of hypertension and what would the clinic and ABPM readings be for each of these?

A

clinic, ABPM
Stage 1 - ≥140/90, ≥135,85
Stage 2 - ≥160/100, ≥150/95
Stage 3 - >180/110

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5
Q

What do stages 1, 2 and 3 mean in terms of treatment?

A

Stage 1 - consider treatment
Stage 2 - treat
Stage 3 - Immediate treatment

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6
Q

What is essential hypertension?

A

Same as primary hypertension

aetiology unknown

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7
Q

Secondary hypertension is more common than primary hypertension. T or F?

A

False -primary hypertension is 95% of cases

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8
Q

When should you consider secondary hypertension?

A

In a younger pt
Resistant BP
When there are signs of an underlying cause

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9
Q

What are the main causes of secondary hypertension?

A
CHAPS 
Cushing's
Hyperaldosteronism (Conn's) 
Aortic coarctation 
Phaeochromocytoma 
Polycystic kidneys 
Stenosis of the renal arteries
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10
Q

Apart from CHAPS, what are the other possible causes of secondary hypertension?

A
OCP 
Cocaine and amphetamines 
Pregnancy 
Acromegaly 
Steroids
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11
Q

What findings on examination would you get for the main causes of secondary hypertension?

A

CHAPS
Cushings - central obesity, moon face, buffalo hump, red striae, hirsutism

Hyperaldosteronism (Conn’s) - arrythmia, hypokalaemia

Aortic coarctation: radio-femoral delay

Phaeochromocytoma - skin stigmata of neurofibromatosis: cafe au lait spots, neurofibromas

Polycystic kidneys - palpable kidneys

Stenosis of the renal arteries - abdominal bruit

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12
Q

What is the non-pharmacological treatment of essential hypertension?

A
  • diet - high fruit and veg and low fat
  • regular physical exercise
  • reduction of alcohol intake
  • reduction of dietary sodium intake (5-6g per day)
  • smoking cessation
  • weight reduction
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13
Q

When would you offer antihypertensives to someone with stage 1 hypertension?

A

If they are under the age of 80 and they have one of:

  • target organ dmanage - retinopathy, nephropathy
  • established CVD
  • renal disease
  • diabetes
  • 10 year CV risk as > 20%

If they are under 40, investigate for secondary hypertension

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14
Q

When would offer antihypertensives to someone with stage 2 hypertension?

A

You would offer antihypertensives to anyone with stage 2 hypertension

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15
Q

What are the BP targets for a patient under 80 yrs old?

A

Clinic BP ABPM

< 140/90 < 135/85

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16
Q

What are the BP targets for a patient over 80yrs old?

A

Clinic BP ABPM

< 150/90 < 145/85

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17
Q

What are the BP targets for a diabetic?

A

<130/80

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18
Q

Define the BP difference in the white coat effect

A

A discrepancy of more than 20/10 mmHg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis

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19
Q

How would you measure response to treatment in pts with white coat syndrome?

A

use ABPM or HBPM as an adjunct to clinic blood pressure measurements

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20
Q

How would you manage stage 3 hypertension?

A

start antihypertensives immediately before waiting for results of ABPH or HBPM and consider admission

Refer to specialist care on the same day if pt has:
• Accelerated (malignant) hypertension = this is a rapid rise in BP, BP > 180/110 mmHg and signs of papilledema and/or retinal haemorrhage. Pt may have symptoms of headache and/or visual disturbance. Requires urgent Tx
• Suspected pheochromocytoma

(I also put: Need to reduce BP slowly as may lead to cerebral, renal and retinal ischaemia or MI. BP response to therapy should be carefully monitored in a high dependency unit. Aim is to reduce the diastolic BP to 100mmHg over 24-48 hours, using oral meds such as amlodipine)

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21
Q

What are the antihypertensive treatment steps for hypertension?

A

Step 1:
under 55 - ACEI or ARB
over 55 or afrocarribean of any age - CCB

Step 2:
ACEI/ARB + CCB

Step 3:
ACEI/ARB + CCB + thiazide diuretic

Step 4 (resistant hypertension): 
Add spironolactone, high-dose thiazide, apha blocker, beta blocker
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22
Q

How do ACEIs work?

A

inhibit ACE (enzyme) which converts angiotensin I to angiotensin II

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23
Q

What does angiotensin II do?

A

5 roles:
1. Increases sympathetic activity

  1. Reabsorption of Na+ in the kidneys, result in in water retention
  2. Increases aldosterone production from the adrenal gland, which results in more reabsorption of Na+ in the kidneys, result in in water retention
  3. Arteriolar vasoconstriction and increase in BP
  4. Causes the posterior lobe of the pituitary to secrete ADH, which causes water reabsorption in the kidneys

(all acts in to increase perfusion of the juxtaglomerular apparatus)

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24
Q

What does renin do and where is it produced?

A

Secreted by the kidney to increase perfusion of the juxtaglomerular apparatus

Converts Angiotensinogen to Angiotensin I

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25
Q

Where is the enzyme ACE produced?

A

Surface of pulmonary and renal epithelium

Ie lungs and kidneys

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26
Q

What is the mechanism of action of spironolactone?

A

Aldosterone antagonist

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27
Q

what happens when there is less aldosterone?

A

More sodium and water excretion

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28
Q

What are ACEIs used for?

A

hypertension
heart failure
diabetic nephropathy

29
Q

Give examples of ACEIs

A

Ramipril

Enalapril

30
Q

Side effects of ACEIs

A

Hypotension
Hyperkalaemia - due to lower aldosterone (remeber Conn’s gives low K+)
Acute renal failure (in renal artery stenosis)
Rash
Cough
Anaphylactoid reaction

31
Q

Interactions of ACEIs

A

K+ elevating drugs

NSAIDs - increases risk of renal failure

32
Q

CIs of ACIs

A

Renal artery stenosis
AKI
CKD
Pregnancy (teratogenic)

33
Q

What are the uses of ARBs?

A

Same as ACEIs
hypertension
heart failure
diabetic nephropathy

34
Q

Examples of ARBs

A

Candesartan
Valsartan
Losartan

35
Q

Side effects of ARBs

A
Hypotension
Hyperkalaemia 
Angioedema 
Acute renal failure (in renal artery stenosis) 
Rash
36
Q

Interactions of ARBs

A

Potassium elevating drugs

NSAIDS- increases risk of renal failure

37
Q

CIs of ARBs

A

Renal artery stenosis
AKI
CKD
Pregnant, breastfeeding

38
Q

Indications of CCBs

A

hypertension
Angina
tachyarrythmias

39
Q

What are the two groups of CCBs and give examples within each group?

Where does each group act on?

A

Dihydropyridines – amlodipine and nifedipine, selective for vasculature
Non-dihydropyridines – verapamil (heart), diltiazem (mixed heart and vessels), selective for myocardium

Way to remember: When you get blocked blood vessels, you can Di

40
Q

How do CCBs work?

A

Decrease ca entry into vascular and cardiac cells causing:

  • arteriodilation
  • reduced myocardial contractility
41
Q

Side effects of CCBs - CAME UP IN EXAM

A
Ankle swelling 
Flushing - CAME UP IN EXAM 
Headache 
Palpitations 
Bradycardia
Heart block 
Heart failure
42
Q

Interactions of CCBs

A

Beta blockers - causes heart failure, bradycardia and asystole

43
Q

CIs of CCBs

A

Heart failure
AV nodal conduction delay
Severe aortic stenosis

44
Q

Indications of beta blockers

A

Hypertension
Heart failure
Angina
Arrythmias

45
Q

Examples of beta blockers

A

Bisoprolol
Atenolol
Metoprolol
Propranolol

46
Q

What are the mechanisms of action of beta blockers?

A

Negatively inotropic (reduce force of contraction) and chronotropic (reduce heart rate)

Reduce renin secretion from the kidneys

47
Q

Side effects of Beta blockers

A
Fatigue 
Headache 
Sleep disturbance 
Bradycardia 
Hypotension 
Cold peripheries 
Impotence 
Worsening of asthma, PVD (claudication or Raynauds), heart failure
48
Q

CI of beta blockers

A

Asthma

heart block

49
Q

Indications for thiazide diruretics

A

Hypertension

Oedema

50
Q

Examples of thiazide diureitcs

A

Bendroflumethazide

51
Q

Mechanism of action of thiazide diureitcs

A

Inhibit the Na/Cl co-transporter in the DCT
Prevents reabsorption of sodium
(Vasodilation in long term)

52
Q

Side effects of thiazide diureitcs

A

Hyponatraemia
Hypokalaemia, due to increased NA+ delivery to the distal tubule, causes cardiac arrhythmias
Impotence

53
Q

Interactions of thiazide diureitcs

A

Loop diuretics – as also cause hypokalaemia

NSAIDS – reduce efficacy of thiazides

54
Q

CIs of thiazide diureitcs

A

Hypokalaemia
Hyponatraemia
Gout – can precipitate attacks

55
Q

Indications of alpha blockers

A

BPH

Hypertension

56
Q

Give examples of alpha blockers

A

Doxazosin
Tamsulosin
Alfuzosin

57
Q

Mechanism of action of alpha blockers

A

alpha 1 adrenoceptors are found in smooth muscle in blood vessels (and the bladder neck and prostate)

cause vasodilation (and reduced resistance to bladder outflow)

58
Q

Side effects of alpha blockers

A

postural hypotension
dizziness
syncope

59
Q

Cautions/CIs of alpha blockers

A

postural hypotension

60
Q

Antihypertensive that causes flushing

A

CCB

61
Q

Antihypertensives that cause impotence

A

Beta blockers

Thiazides

62
Q

What long term monitoring would you do for hypertension?

A
  • Monitor BP
  • For safety check electrolytes and renal function before starting treatment and repeat 1-2 weeks into treatment and after increasing the dose
63
Q

How do you calculate pack years?

A

number of packs smoked per day x number of years smoked

20 cigs/day for 30 yrs = 30 pack years

64
Q

What is the cut off for an abnormal cholesterol: HDL ratio?

A

above 6 is high

65
Q

What does Qrisk 2 or 3 calculate?

A

risk of having a heart attack or stroke over the next 10 years

66
Q

What are the factors taken into consideration in the Qrisk3?

A
age 
sex 
postcode 
Smoking 
diabetes 
Angina or heart attack in a 1st degree relative <60 
CKD stage 3,4 or 5 
AF 
BP 
Migraines ------
RA 
SLE --------
Severe mental illness ------ 
Atypical antipsychotic ------- 
Regular steroids ------ 
Erectile dysfunction ------
Cholesterol/HDL ratio
Systolic BP 
Difference between two most recent readings of BP 
BMI 

——– added to Qrisk 3 from Qrisk 2

67
Q

How often should the Qrisk 2 score be assessed in an individual?

A

every 5 years when over 40
The NHS health check is every 5 years and includes the Qrisk 3

This is when the pt no history of CVD, familial hypercholesterolaemia, CKD or diabetes mellitus and who are not being treated to reduce blood pressure or lipids

68
Q

What is the main drug that would be prescribed if sb’s QRIsk was >10%?

A

statins

atorvastatin 20mg OD

69
Q

How would you manage a pt with a Qrisk <10%?

A

Lifestyle advice
Treat comorbidities
Reassess in 5 years