Hypertension Flashcards

1
Q

What criteria determines the definition of hypertension?

A

HTN coincides with a level of BP above which the benefits of treatment outweigh side effects (this is a population definition; detecting and treating HTN will benefit individuals)

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2
Q

What polygenic factors influence risk of primary HTN?

A

Genes for sympathetic hyperactivity, renin activation and susceptibility to salt

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3
Q

What multi-environmental factors influence risk of primary HTN?

A

Obesity
Excess salt (especially in elderly)
Alcohol

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4
Q

How can salt be reduced in the diet?

A

Added salt
Processed foods
Prepared meals (i.e. fast food)

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5
Q

In what % of HTN is a specific cause identified?

A

5%

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6
Q

List 5 causes of secondary HTN

A

Kidney disease (acute or chronic)
Renovascular disease (e.g. renal artery stenosis)
Coarctation of the aorta
Endocrine causes (e.g. adrenal tumours secreting aldosterone/cortisol/catecholamines, OCP, HRT)
Sleep apnoea

OR ABCDE
Apnoea and aldosterone (Conn’s or secondary)
Bruit (renal artery stenosis) or bad kidneys (AKI or CKD)
Calcaemia (hyper), Cushings, Catecholamines, Coarctation
Drugs (NSAIDs, alcohol, steroids, lithium, cocaine, amphetamines, OCP, MAOIs)
Endocrine (hyperthyroid, hypothyroid, hyperPTH because of hypercalcaemia, etc)

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7
Q

When is a large arm cuff for measuring BP indicated?

A

If arm circumference >32cm (but don’t overestimate effect of using small cuff - should only elevate BP by a couple of mmHg)

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8
Q

What is the current criteria for diagnosis of HTN?

A

BP >140/90 mmHg (>135/85 mmHg if comorbidities e.g. DM, CKD, etc)
After 5 minutes seated rest
2 readings, 2 mins apart

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9
Q

How can an initial diagnosis of HTN be confirmed?

A

Additional visit in 1-4 weeks
Can also use 24-hour ambulatory measurements (in which case criteria is day-time >135/85 mmHg; you add 10mmHg for in-clinic BP) or home BP measures

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10
Q

When might isolated systolic HTN occur?

A

Generally reflects high pulse pressure (with relatively low DBP) seen in aged and stiff arteries

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11
Q

What routine tests should be ordered on diagnosis of HTN? Why?

A

FBE: associated anaemia of CKD
UEC: plasma K+ (high in renal disease, low in aldosteronism) and creatinine (high in renal disease)
Urine albumin/creatinine ratio: may be evidence of renal damage
LFTs: may be associated fatty liver or drug reaction
Fasting glucose: may be associated glucose intolerance
Fasting lipids: may be associated CV risk
MSU: clues as to causes of possible renal disease
ECG, echo: to detect coronary disease and cardiac hypertrophy

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12
Q

What % of patients in the general population have masked HTN?

A

10%

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13
Q

When should masked HTN be suspected?

A

In patients with evidence of end-organ damage but normal clinic BP readings

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14
Q

Define nocturnal nondipping

A

Decrease of less than 10% in average night-time SBP and/or DBP compared with day-time averages

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15
Q

What does nocturnal nondipping suggest mechanistically?

A

End-organ damage
Autonomic dysfunction
OSA

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16
Q

When might plasma K+ and creatinine be elevated in a case of HTN?

A

In the context of renal disease

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17
Q

When might plasma K+ and creatinine be low in a case of HTN?

A

In the setting of aldosteronism

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18
Q

6 Framingham CV risk factors

A
Age and gender
HTN
Smoking
DM
Hyperlipidaemia
Previous stroke/MI
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19
Q

What underlying secondary causes should be considered in the patient with HTN?

A

Pregnancy
OSA
Falls Hx and risks
Rx Hx

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20
Q

What is the relationship between blood pressure and risk of major CV and stroke events?

A

Above 115/75 mmHg, for each increase of 20 mmHg in SBP the risk of major CV and stroke events doubles

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21
Q

Give 5 examples of diseases high BP predisposes to

A
Coronary heart disease
Stroke
Cardiac hypertrophy
HF
Kidney failure
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22
Q

What is the prevention paradox?

A

Majority of deaths attributable to BP occur in people with “normal BP”. Modest risk in many with average BP accounts for more deaths than high risk in severe hypertensives

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23
Q

What is the public health prevention principal related to HTN?

A

Reducing the community average BP is good for the community

24
Q

What is the benefit of using a semiautomated manometer to measure BP?

A

Avoids observer error

25
When should a semiautomated manometer be used manually (with a stethoscope)?
If AF
26
Why might have some GPs complained that the new semiautomated manometers give a higher reading for SBP than the manual auscultatory method with a mercury manometer?
Possible explanations: doctor had hearing impairment, deflation too fast with mercury manometer, doctor tended to "round down" manual readings, doctor disregarded higher manual values which might have precipitated discussions about treatment
27
How can you distinguish between true HTN and "white coat" HTN?
24-hour ambulatory measurements
28
What considerations need to be made when assessing a patient for suspected HTN?
Diagnosis Secondary causes Target organ damage Management decisions
29
Why might fasting glucose and/or lipids be elevated with HTN?
If there is an associated glucose intolerance or CV risk
30
What aspects of Hx are important to elicit in a case of suspected HTN?
``` FHx Past coronary or cerebrovascular events HF symptoms Renal disease symptoms Smoking Diabetes High cholesterol ```
31
What aspects of examination are important when assessing a patient with HTN?
``` Vitals (esp BP, pulse rate/rhythm) Anthropometric measurements Full CV examination Fundal inspection Renal mass or bruits Stigmata of secondary causes ```
32
What factors should be considered when making a decision when to treat the hypertensive patient?
BP | CV risk
33
What are the guidelines for treating HTN based on BP?
SBP >180 mmHg DBP >110 mmHg SBP >160 mmHg and DBP
34
What are the guidelines for treating HTN based on BP and CV risk?
SBP >140 mmHg or DBP | With associated conditions (DM, existing CVD, renal disease) or high CV risk
35
What is the definition of high CV risk? What standard risk factors should be considered when assessing CV risk? What signs of end organ damage may indicate high CV risk?
>15% CV event risk over 5 years Standard RFs include age, SBP, total:HDL cholesterol ratio, smoking, DM End organ damage: microalbuminaemia or low eGFR with renal damage, LVH with cardiac damage, high pulse wave velocity with stiff large arteries, increased intima media thickness reflecting atherosclerosis
36
What is the "rule of halves" in HTN?
Only 1/2 detected Only 1/2 of detected are treated Only 1/2 of treated are controlled
37
What are the 5 pillars of non-pharmacological treatment for HTN?
``` Lose weight Improve fitness Avoid excess salt Moderate alcohol Stop smoking ```
38
Which is more important in pharmacological BP reduction: how or how much?
How much
39
What drug treatments are available for Mx of HTN?
``` ACEIs ARBs Ca2+ channel blockers Diuretics B blockers ```
40
Are most hypertensive patients managed with 1 drug or >1 drug?
Most require >1
41
How long after starting a new drug/new dose should you wait to add another?
2-3 weeks
42
What is better: using 2 different drugs to treat HTN or using a combination drug
Combination is similar
43
Drug treatment algorithm for HTN
Step 1: A, C or D Step 2: A+C or A+D Step 3: A+C+D Step 4 (for "resistant HTN"): consider adding spironolactone, B-blocker, centrally-acting agent, a-blocker or vasodilator
44
Considerations when deciding which Rx to use in step 1 of the HTN treatment algorithm
A: preferred step if
45
General considerations for each commonly used anti-hypertensive
A: useful in coronary disease and HF, renoprotective in DM, contra-indicated in pregnancy B: useful in coronary disease and HF C: avoid verapamil and diltiazam in HF D: thiazide-like drugs have less metabolic side effects
46
What is the most important cause of "resistant HTN"?
Poor compliance
47
What are some possible causes of "resistant HTN"?
Poor compliance Use of NSAIDs, cold remedies, anti-depressants, etc Consider secondary causes
48
Renal causes of secondary HTN
``` Intrinsic renal disease (GN, polyarteritis nodosa, systemic sclerosis, chronic pyelonephritis, PKD) Renovascular disease (atheromatous, fibromuscular dysplasia) ```
49
Endocrine causes of secondary HTN
``` Cushing's Conn's Phaeochromocytoma Acromegaly HyperPTH ```
50
Other causes of secondary HTN
Coarctation Pregnancy Drugs: steroids, MAOIs, OCP
51
Resistant HTN
Still not below target BP with maximum dose of triple therapy
52
ACEI SEs
Dry cough (at any time) Postural hypotension First dose hypotension (usually patients with existing renal disease or hyponatraemia) CIs: pregnancy, bilateral renal stenosis, hereditary angioedema, hyperkalaemia
53
ARB SEs
Postural hypotension First dose hypotension (usually patients with existing renal disease or hyponatraemia) CIs: pregnancy, bilateral renal stenosis, hyperkalaemia
54
2 classes of Ca2+ channel blockers
Dihydropyridine (vascular-selective, long-acting): "pines" | Non-dihydropyridine (cardiac and vascular): verapamil, dilitiazem
55
Ca2+ channel blocker SEs
Postural hypotension Peripheral oedema (especially dihydropyridines) Nausea Flushing Headaches CIs: diabetes (not recommended; increases insulin resistance)