Hypertension Flashcards

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1
Q

the diagnosis and classification of hypertension includes 3 things, what are they?

A

The diagnosis and classification of hypertension includes

(1) establishing blood pressure (BP) levels…diagnosis should be based on multiple BP readings

(2) identifying
secondary causes of hypertension if present and

(3) evaluating the overall CV risk (SCORE) and extent, if any, of BP-related target organ damage

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2
Q

describe the classification of hypertension,

optimal, normal, high normal, grade 1, 2, 3, isolated systolic hypertension

A

Optimal

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3
Q

what happens is a patients DBP and SBP fall into 2 different categories?

A

you should apply the higher category

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4
Q

describe the methods of measuring blood pressure?

A

——-Brachial cuff and manual auscultation of the brachial artery

——-Ambulatory BP monitoring (ABPM) involves the subject
wearing an appropriately sized cuff connected to electronic sensors which enables 24-hour evaluation of SBP and diastolic
BP (DBP)

---------Home
BP monitoring (HBPM) also provides multiple BP measurements and is useful in measuring the subject’s true BP levels.
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5
Q

why are ABPM and HBPM particularily useful compared to readings in the GP practice/hospital?

A

—————–avoids white coat hypertension. normotensive individuals
whose BP appears elevated or those whose hypertension appears worse than it actually is, when measured by a healthcare
professional.

———-HBPM may also improve medication adherence in some patients

—————A recent review of
relative effectiveness of all 3 modalities of BP monitoring suggested that more widespread use of ABPM for the diagnosis
of hypertension would result in more appropriately targeted treatment.

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6
Q

what are the cut off levels for treatment of hypertension with ABPM and HBPM?

A

an average of 135/85mmHg with ABPM / HBPM equates to an average
of 140/90mmHg from multiple BP readings

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7
Q

what is the difference betwen primary and secondary hypertension?

A

essential hypertension—-90-95% (alcohol or obesity may play a role)

Up to 90% of patients have primary hypertension, for which no identifiable cause is found. For
the remainder, there is an underlying cause

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8
Q

list some causes of secondary hyptertension?

A

most common:
chronic kidney disease
hyperaldosteronism (conns)
obstructive sleep apnea—common in obese men

less common: 
phaeochromocytoma
medication
cushings
thyroid disorders
acromegaly
chemotherapeutic agents
coarctation (delayed or weak femoral pulses)
pregnancy
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9
Q

comment on the hyperaldosteronism as a cuase of hypertension?

A

Leads to Na+ retention; decreased K+ may be present.

Thought to be associated with 10-20% of resistant hypertension

↑ Na+ channel and Na+/K+ pump insertion in principal cells; enhances K+ and H+ excretion (upregulates principal cell K+ channels and intercalated cell H+ ATPases)

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10
Q

comment on the phaeochromocytoma as a cuase of hypertension?

A

Pheochromocytoma—most common tumor of the adrenal medulla in adults.

Episodic hyperadrenergic symptoms (5 P’s): 
Pressure (increased BP)
Pain (headache)
Perspiration
Palpitations (tachycardia) 
Pallor

Most tumors secrete epinephrine, norepinephrine, and dopamine, which can cause episodic hypertension.

Facial flushing, increased HR, sweating, increased glucose.

Due to massive release of
catecholamines from adrenal gland

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11
Q

comment on the medication as a cuase of hypertension?

A
Includes NSAIDs, 
MAOIs, 
mineralocorticoids, 
anti-Parkinson drugs, 
OCP,
licorice (???)
sympathomimetics (cold cures)
stimulants (e.g. cocaine).
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12
Q

comment on the cushings as a cuase of hypertension?

A

increased cortisol due to exogenous use of steroids, Adrenal tumour, ACTH tumour…

features:
Sudden increase weight; increase glucose; moon face; central obesity.
buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression.
proximal muscle weakness

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13
Q

comment on the thyroid
acromegaly
ob sleep apnea as a cuase of hypertension?

A

hyperthroidism- heat intolerance, weight loss, increase appetite hyperactive diarrhoea, increased reflexes, pretibial myexedema, periorbital edema, warm moist skin, fine hair, chest pain, palpitations,

sleep apnea- snoring, obesity, daytime fatigue

acromegaly—

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14
Q

what are the commest causes of secondary hypertension

A

The commonest
causes of secondary hypertension are

———renal parenchymal disease followed by

——-renovascular hypertension (caused by the kidneys’ hormonal response to narrowing of the arteries supplying the kidneys (renal artery stenosis)

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15
Q

give examples of renal parenchymal disease?

Acute

A

ACUTE——

ATN, which typically occurs in hospitalized patients.

Other entities include acute interstitial nephritis (which is often drug induced)

and cast nephropathy in multiple myeloma.

tumor lysis syndrome (acute urate nephropathy), which occurs among patients with high tumor burden lymphoma or following chemotherapy,

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16
Q

describe the linear relationship between increases in DBP and SBP and the risk of CV disease?

A

——–It is estimated that there is a doubling of the risk of CV
disease for every 10 point increase in DBP or every 20 point increase in SBP.

Therefore, the threshold for a diagnosis of hypertension requiring pharmacotherapy should be considered as flexible, based on the overall CV risk

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17
Q

what are the risk factors for CVD?

categorise into modifiable and non-modifiable…

A

modifiable——Hypertension, abnormal blood lipids, obesity and smoking are regarded as the key risk factors for CV disease.16

Othermodifiable risk factors include lifestyle choices (e.g. diet, physical inactivity) psychosocial factors (e.g. social isolation,
stress, low socio-economic status) and diabetes mellitus.

Non-modifiable risk factors include 
age, 
gender, 
ethnicity, 
family
history
18
Q

what are the signs of organ damage in hypertension?

heart?
kidneys?
arterial system?

A

—-ECG- LAE, left atrial enlargement—-(the terminal portion of the P wave has a duration of 0.04 seconds and a depth of 1 mm or more or their product is ≥ -0.04 mm x sec )

  • —-urinalysis for evidence of microalbuminuria
  • —-physical examination,
  • —-fundoscopy
19
Q

what is the drawback of automated devices for measureing BP?

A

may not measure BP accurately is there is a pulse irregularity.

check radial or brachial pulse before checking BP and measure BP manually using direct ausculatation

20
Q

what to do if BP is greater than 140/90?

in primary care practice

A

• Take a second measurement—if that measurement is substantially
different from the first measurement, take a third measurement;
record the lower of these measurements as the BP

• If BP on repeat testing is ≥140/90mmHg and not known to be
hypertensive, offer ambulatory BP monitoring (ABPM) or home BP monitoring (HBPM) to confirm the diagnosis; consider ABPM or HBPM monitoring (HBPM) for people on antihypertensive medication who are known to have ‘white coat’ hypertension

• If hypertension is not confirmed on ABPM/HBPM, measure BP every 5y or more frequently if close to 140/90 mmHg

21
Q

what to do if If the person has severe hypertension (systolic BP ≥180mmHg or diastolic BP ≥110mmHg?

A

——consider starting antihypertensive treatment immediately without waiting for the result of ABPM/HBPM.
Refer for same day specialist assessment if suspected:

  • Accelerated hypertension (BP >180/110mmHg ± papilloedema ± retinal haemorrhage) or
  • Phaeochromocytoma (labile/postural hypotension, headache, palpitations, pallor, and excessive sweating)
22
Q

presentationof hypertension?

asymptomatic/symptomatic….

A

Usually asymptomatic and found during routine BP screening or incidentally.

Occasionally headache or visual disturbance

• May be symptoms of end-organ damage—LVH, TIAs, previous CVA/ MI, angina, renal impairment, PVD

23
Q

what are the further assessments/investigations that you can do to identify end organ damage?

A

• Examination Check heart size, heart sounds, and for heart failure; examine the fundi, looking for silver wiring, AV nipping, flame
haemorrhages, and cotton wool spots

• Blood tests Creatinine, electrolytes, eGFR, glucose/HbA1c, lipid
profile; consider GGT if excess alcohol is a possibility

  • Urine Dipstick for RBCs and protein; laboratory sample for albumin:creatinine ratio
  • Cardiovascular risk estimation
  • ECG ± echo (if left ventricular hypertrophy is suspected)
24
Q

give some causes of microalbuminuria?

the range of microalbuminuria?

A

Causes:

  • –DM
  • —Arteriopathy- in pt with CCF, inc BP.
  • —-Presence of microalbuminuria predicts increased risk of MI, CVA, CCF
  • –other chronic illness- COPD, malignancy
  • —-acute illness: IBD, MI, acute pancreatitis, trauma, burns, meningitis
25
Q

describe the reccomended care pathyway for initiation of hypertension treatment, the NICE guidelines:

A

Offer antihypertensive drug treatment to people aged under 80 years with stage 1 hypertension who have one or more of the following:

—-target organ damage

—-established cardiovascular disease

—–renal disease

——diabetes

———a 10-year cardiovascular risk equivalent to 20% or greater. [new 2011]

  1. 5.2 Offer antihypertensive drug treatment to people of any age with stage 2 hypertension. [new 2011]
  2. 5.3 For people aged under 40 years with stage 1 hypertension and no evidence of target organ damage, cardiovascular disease, renal disease or diabetes, consider seeking specialist evaluation of secondary causes of hypertension and a more detailed assessment of potential target organ damage. This is because 10-year cardiovascular risk assessments can underestimate the lifetime risk of cardiovascular events in these people. [new 2011]
    http: //www.nice.org.uk/guidance/cg127/chapter/1-recommendations
26
Q

describe the guidelines for monitoring BP?

A
  1. 5.4 Use clinic blood pressure measurements to monitor the response to antihypertensive treatment with lifestyle modifications or drugs. [new 2011]
  2. 5.5 Aim for a target clinic blood pressure below 140/90 mmHg in people aged under 80 years with treated hypertension. [new 2011]
  3. 5.6 Aim for a target clinic blood pressure below 150/90 mmHg in people aged 80 years and over, with treated hypertension. [new 2011]
  4. 5.7 For people identified as having a ‘white-coat effect’[5], consider ABPM or HBPM as an adjunct to clinic blood pressure measurements to monitor the response to antihypertensive treatment with lifestyle modification or drugs. [new 2011]
27
Q

name the drug classes used in hypertension treatment?

A

ACEI (Angiotensin Converting Enzyme Inhibitor)

ARB(Angiotensin II ReceptorBlocker)

CCB(Calcium Channel Blocker)

DIURETICS

28
Q

what do the main classes of drugs nomenclature end in?

ARB’s, ACE, CCB, Diuretics

PDE5I, A1antagonist

Bblockers

A

B blockers -olol

ARB -sartan

ACE -pril

CCB -dipine

thiazide Diuretics

PDE5 inhibitor -afil

alpha 1 antagonist -zosin

29
Q
describe the MOA of all of the 
ARB's, 
ACE, 
CCB, 
Diuretics

PDE5I,
A1antagonists?

Beta blockers….

A

bbbbb…………..

30
Q

describe step 1 treatment? (hypertension)

A

Step 1 treatment

  1. 6.6 Offer people aged under 55 years step 1 antihypertensive treatment with an angiotensin-converting enzyme (ACE) inhibitor or a low-cost angiotensin-II receptor blocker (ARB). If an ACE inhibitor is prescribed and is not tolerated (for example, because of cough), offer a low-cost ARB. [new 2011]
  2. 6.7 Do not combine an ACE inhibitor with an ARB to treat hypertension. [new 2011]
  3. 6.8 Offer step 1 antihypertensive treatment with a calcium-channel blocker (CCB) to people aged over 55 years and to black people of African or Caribbean family origin of any age. If a CCB is not suitable, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. [new 2011]
  4. 6.9 If diuretic treatment is to be initiated or changed, offer a thiazide‑like diuretic, such as chlortalidone (12.5–25.0 mg once daily) or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide or hydrochlorothiazide. [new 2011]
  5. 6.10 For people who are already having treatment with bendroflumethiazide or hydrochlorothiazide and whose blood pressure is stable and well controlled, continue treatment with the bendroflumethiazide or hydrochlorothiazide. [new 2011]
  6. 6.11 Beta-blockers are not a preferred initial therapy for hypertension. However, beta-blockers may be considered in younger people, particularly:

those with an intolerance or contraindication to ACE inhibitors and angiotensin II receptor antagonists or

——–women of child-bearing potential or

———people with evidence of increased sympathetic drive. [2006]

1.6.12 If therapy is initiated with a beta-blocker and a second drug is required, add a calcium-channel blocker rather than a thiazide-like diuretic to reduce the person’s risk of developing diabetes. [2006]

31
Q

describe the toxicity/SA of ACEI’s?

A

captoprils catchh

Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations),􏰄Creatinine (􏰆GFR), Hyperkalemia, and Hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further􏰆GFR􏰃renal failure

Caution with renal dysfunction. Rarely angiooedema.
Not to be used during pregnancy

32
Q

describe the toxicity/SA of CCB’s?

and the moa?

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation.

MOA:Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reduce muscle contractility.

33
Q

why are Beta bloclers not really used in hTN?

A

ADRs include bradycardia, bronchospasm, fatigue and cold extremities

34
Q

what can be used in resistant htn?

A

Diuretics, such as spironolactone, which act as aldosterone antagonists have a role as add-on therapy in resistant
hypertension.
——- Care must be taken to monitor potassium as they can induce hyperkalaemia, especially in the presence of
renal dysfunction.

Alpha receptor blockers (such as doxazosin) act at the alpha 1 receptor to cause vasodilatation. They may be considered as add-on therapy in resistant hypertension.
——ADRs include postural hypotension, headache, flushing and ankle oedema.

35
Q

what combinations should not be used?

A

CCB + Beta blocker

ACEI + ARB

36
Q

Diabetes and HTN? reccomendations?

A

Management should aim to achieve a BP of

37
Q

elderly and TN, reccomendations in prescribing?

A

Since elderly patients may be particularly susceptible to postural hypotension and falls, (especially in the first weeks of treatment), dosages should be titrated slowly.

For those aged >80 years optimal control is defined as BP

38
Q

when would you start therapy with a beta blocker?

A

Beta-blockers are not a preferred initial therapy for hypertension. However, beta-blockers may be considered in younger people, particularly:

those with an intolerance or contraindication to ACE inhibitors and angiotensin II receptor antagonists or

women of child-bearing potential or

people with evidence of increased sympathetic drive. [2006]

1.6.12 If therapy is initiated with a beta-blocker and a second drug is required, add a calcium-channel blocker rather than a thiazide-like diuretic to reduce the person’s risk of developing diabetes. [2006]

39
Q

what are the symptoms of HTN

A

normally asymptomatic—-silent killer

except in the case of hypertensive crisis

40
Q

what are the symptoms of hypertensive crisis

A

In addition to extreme BP readings, a person in hypertensive crisis may experience:

Severe headaches
Severe anxiety
Shortness of breath
Nosebleeds

41
Q

why would you avoid using a beta blocker and a diuretic ?

why would you not combine insulin/sulfonylurea and a beta blocker?

A

increases chances of developing NOD (type 2)—-These drugs may not only increase blood sugar levels in those who don’t have diabetes, but may worsen sugar control in those with diabetes and also blunt warning symptoms when low sugar occurs.”

Many people know that it is a bad idea for anyone who takes insulin or a sulfonylurea drug to take a beta blocker. This is because it has long been known that these drugs block the counter-regulatory response that prevents a dangerous hypo or–if it cannot prevent the hypo–at least gives the victim some warning that one is coming by causing shakes and pounding pulse.