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MD2 Cardio > Hypertension > Flashcards

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
Q

When should a semiautomated manometer be used manually (with a stethoscope)?

A

If AF

26
Q

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?

A

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
Q

How can you distinguish between true HTN and “white coat” HTN?

A

24-hour ambulatory measurements

28
Q

What considerations need to be made when assessing a patient for suspected HTN?

A

Diagnosis
Secondary causes
Target organ damage
Management decisions

29
Q

Why might fasting glucose and/or lipids be elevated with HTN?

A

If there is an associated glucose intolerance or CV risk

30
Q

What aspects of Hx are important to elicit in a case of suspected HTN?

A 
FHx
Past coronary or cerebrovascular events
HF symptoms
Renal disease symptoms
Smoking
Diabetes
High cholesterol
31
Q

What aspects of examination are important when assessing a patient with HTN?

A 
Vitals (esp BP, pulse rate/rhythm)
Anthropometric measurements
Full CV examination
Fundal inspection
Renal mass or bruits
Stigmata of secondary causes
32
Q

What factors should be considered when making a decision when to treat the hypertensive patient?

A

BP

CV risk

33
Q

What are the guidelines for treating HTN based on BP?

A

SBP >180 mmHg
DBP >110 mmHg
SBP >160 mmHg and DBP

34
Q

What are the guidelines for treating HTN based on BP and CV risk?

A

SBP >140 mmHg or DBP

With associated conditions (DM, existing CVD, renal disease) or high CV risk

35
Q

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?

A

> 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
Q

What is the “rule of halves” in HTN?

A

Only 1/2 detected
Only 1/2 of detected are treated
Only 1/2 of treated are controlled

37
Q

What are the 5 pillars of non-pharmacological treatment for HTN?

A 
Lose weight
Improve fitness
Avoid excess salt
Moderate alcohol
Stop smoking
38
Q

Which is more important in pharmacological BP reduction: how or how much?

A

How much

39
Q

What drug treatments are available for Mx of HTN?

A 
ACEIs
ARBs
Ca2+ channel blockers
Diuretics
B blockers
40
Q

Are most hypertensive patients managed with 1 drug or >1 drug?

A

Most require >1

41
Q

How long after starting a new drug/new dose should you wait to add another?

A

2-3 weeks

42
Q

What is better: using 2 different drugs to treat HTN or using a combination drug

A

Combination is similar

43
Q

Drug treatment algorithm for HTN

A

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
Q

Considerations when deciding which Rx to use in step 1 of the HTN treatment algorithm

A

A: preferred step if

45
Q

General considerations for each commonly used anti-hypertensive

A

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
Q

What is the most important cause of “resistant HTN”?

A

Poor compliance

47
Q

What are some possible causes of “resistant HTN”?

A

Poor compliance
Use of NSAIDs, cold remedies, anti-depressants, etc
Consider secondary causes

48
Q

Renal causes of secondary HTN

A 
Intrinsic renal disease (GN, polyarteritis nodosa, systemic sclerosis, chronic pyelonephritis, PKD)
Renovascular disease (atheromatous, fibromuscular dysplasia)
49
Q

Endocrine causes of secondary HTN

A 
Cushing's
Conn's
Phaeochromocytoma
Acromegaly
HyperPTH
50
Q

Other causes of secondary HTN

A

Coarctation
Pregnancy
Drugs: steroids, MAOIs, OCP

51
Q

Resistant HTN

A

Still not below target BP with maximum dose of triple therapy

52
Q

ACEI SEs

A

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
Q

ARB SEs

A

Postural hypotension
First dose hypotension (usually patients with existing renal disease or hyponatraemia)
CIs: pregnancy, bilateral renal stenosis, hyperkalaemia

54
Q

2 classes of Ca2+ channel blockers

A

Dihydropyridine (vascular-selective, long-acting): “pines”

Non-dihydropyridine (cardiac and vascular): verapamil, dilitiazem

55
Q

Ca2+ channel blocker SEs

A

Postural hypotension
Peripheral oedema (especially dihydropyridines)
Nausea
Flushing
Headaches
CIs: diabetes (not recommended; increases insulin resistance)

MD2 Cardio (11 decks)

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