Ward 13 Flashcards

1
Q

What is the most risk factor for premature death and CVD? How much of it is it responsible for?

A

Hypertension, causing 50% of all vascular death

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2
Q

At which blood pressure should we decide to treat?

A
  • All with BP ≥160/100 mmHg (or ABPM (ambulatory blood pressure monitoring) ≥150/95 mmHg).
  • For those ≥140/90, the decision depends on the risk of coronary events, presence of diabetes,
    or end-organ damage
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3
Q

BP in younger individuals

A

People—BP is on average lower in young people (eg 100–110/60–70 in 18-year olds)

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4
Q

What is white coat hypertension

A

Refers to an elevated clinic pressure, but normal ABPM (day average <135/85)

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5
Q

What is masked hypertension? Do you treat?

A
  • Opposite of white coat hypertension
  • NICE says don’t treat; but more likely to develop hypertension in future, and may have risk of CVD.
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6
Q

What is malignant hypertension also known as?

A

accelerated phase hypertension

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7
Q

What is malignant hypertension? What are things we observe in that situation?

A
  • A rapid rise in BP leading to vascular
    damage (pathological hallmark is fibrinoid necrosis)
  • Usually there is severe
    hypertension (eg systolic >200, diastolic>130mmHg) + bilateral retinal haemorrhages
    and exudates; papilloedema may or may not be present. Symptoms are common,
    eg headache ± visual disturbance
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8
Q

Does malignant hypertension require treatment? Why?

A
  • It requires urgent treatment, and may also precipitate acute kidney injury, heart failure, or encephalopathy, which are hypertensive
    emergencies.
  • Untreated, 90% die in 1yr; treated, 70% survive 5yrs.
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9
Q

What is primary hypertension also known as?

A

Essential hypertension

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10
Q

What is the cause of primary hypertension and how many cases of hypertension are caused by it?

A

Cause unknown, thought to be due to mutations in several genes.
- It is responsible for 95% of cases of hypertension

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11
Q

What is hypertension divided into?

A

Primary and secondary

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12
Q

What can the causes of secondary hypertension be divided into and which is most common?

A
  • Renal disease: Most common
  • Endocrine disorders: Most commonly treatable cause
  • Others
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13
Q

Renal diseases leading to hypertension

A
  • 75% are from intrinsic renal
    disease: glomerulonephritis, polyarteritis nodosa (PAN), systemic sclerosis, chronic
    pyelonephritis, or polycystic kidneys.
    -25% are due to renovascular disease, most frequently atheromatous (elderly male cigarette smokers, eg with peripheral vascular
    disease) or rarely fibromuscular dysplasia (young females).
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14
Q

Endocrine causes leading to hypertension

A

Cushing’s and Conn’s syndromes, phaeochromocytoma, acromegaly, hyperparathyroidism

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15
Q

What is crushing’s syndrome?

A

A syndrome caused caused by prolonged exposure to high circulating levels of cortisol

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16
Q

Causes of cushing’s syndrome

A
  • The most common cause of cushingoid features is iatrogenic corticosteroid use, while some herbal preparations can also increase circulating corticosteroid levels leading to Cushing syndrome.
  • ACTH-dependent cortisol excess due to a pituitary adenoma is called Cushing disease, and it is responsible for 80% of endogenous Cushing syndrome
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17
Q

What is conn’s syndrome?

A

Primary hyperaldosteronism

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18
Q

Causes of COnn’s syndrome

A

The syndrome may be secondary to adrenal hyperplasia, adrenal adenoma, aldosterone-secreting adrenal carcinoma (1%), or familial hyperaldosteronism

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19
Q

What is glomerulonephritis?

A

The term “glomerulonephritis” encompasses a subset of renal diseases characterized by immune-mediated damage to the basement membrane, the mesangium, or the capillary endothelium, resulting in hematuria, proteinuria, and azotemia

20
Q

Symptoms of hypertension

A
  • Most cases of hypertension are asymptomatic and are diagnosed incidentally on blood pressure recording or measurement.
  • Some cases present directly with symptoms of end-organ damage as stroke-like symptoms or hypertensive encephalopathy, chest pain, shortness of breath, and acute pulmonary edema
  • Headache is no more common than in the general population
21
Q

Signs of hypertension

A

Physical examination may be unyielding other than occasional pedal edema or raised blood pressure, but one needs to look for signs of precipitating disease:
- Coarctation of the aorta (radio-radial delay, radio-femoral delay, differences in left and right arm BP or upper and lower limb BP more than 20 mm Hg)
- Central obesity
- Aortic valve disease (systolic ejection murmur, 4th heart sound)
- Renovascular disease or fibromuscular dysplasia (FMD) - (renal bruit, carotid bruit)
- Polycystic kidneys (enlarged kidneys bilaterally)
- Endocrine disorders [hypercortisolism(thin skin, easy bruising, hyperglycemia), acromegaly)
- Thyroid disorders(palpable/ painful or enlarged thyroid, exopthalamus] make up the common treatable causes of secondary hypertension
- The presence of a 4th heart sound, which represents a stiff and non-compliant left ventricle, hints towards left ventricular hypertrophy and diastolic dysfunction.
- Tremors
- The presence of lung rales and/or peripheral edema suggests cardiac dysfunction and gives a clue to the chronicity of hypertension.

22
Q

Difference between cholecystitis vs cholelithiasis vs cholidocolithiasis vs cholangitis

A

1- Inflammation of the gallbladder
2- Stones in the gallbladder
3- Stones in the bile duct
4- Inflammation of the biliary tree

23
Q

Diagnosis of hypertension

A

The ACC recommends at least two office measurements on at least two separate occasions to diagnose hypertension.

The ESC/ESH recommends three office BP measurements at least 1 to 2 minutes apart and additional measurements only if the initial two readings differ by greater than or equal to 10 mm Hg. BP is then recorded as the average of the last two readings.

Both societies endorse the use of higher BP readings and putting patients into higher stages/grades for adequate medical therapy.

The patient should remain seated quietly for at least 5 minutes before taking the blood pressure, and proper technique is necessary. The blood pressure cuff should cover 80% of the arm circumference because larger or smaller pressure cuffs can falsely underestimate or overestimate blood pressure readings.

Ambulatory blood pressure measurement is the most accurate method to diagnose hypertension and also aids in identifying individuals with masked hypertension as well as the white coat effect.

24
Q

Evaluation of patients

A

The evaluation consists of looking for signs of end-organ damage and consists of the following,
- 12 lead ECG (to document left ventricular hypertrophy, cardiac rate, and rhythm)
- Fundoscopy to look for retinopathy/ maculopathy
- Blood workup
- Urine albumin to creatinine ratio
- Ankle-brachial pressure index - ABI (if symptoms suggestive of peripheral arterial disease)
- Imaging: including carotid Doppler ultrasound, echocardiography, and brain imaging (where clinically deemed feasible)
- Special tests: Renal ultrasound/arteriography (renal artery stenosis); 24h urinary meta-adrenaline; urinary free cortisol; renin; aldosterone; MR aorta (coarctation)

25
Q

Blood tests in a patient with hypertension

A
  • Including complete blood count, ESR, creatinine, eGFR, electrolytes, HbA1c, thyroid profile, blood cholesterol levels, and serum uric acid
  • To help quantify overall
    risk: Fasting glucose; cholesterol. To look for end-organ damage: ECG or echo (any
    LV hypertrophy? past MI?); urine analysis (protein, blood). To ‘exclude’ secondary
    causes: U&E (eg K+ in Conn’s); Ca2+ ( in hyperparathyroidism)
26
Q

Grading retinopathy and what is used

A

Fundoscopy
1 Tortuous arteries with thick shiny walls (silver or copper wiring).
2 AV nipping (narrowing where arteries cross veins, p560, fi g 12.19).
3 Flame haemorrhages and cotton-wool spots.
4 Papilloedema,

27
Q

Management of hypertension

A
  • Look for and treat underlying causes (eg renal disease, Increased alcohol)
  • The management of hypertension subdivides into pharmacological and nonpharmacological management.
28
Q

Non pharmacological management of hypertension

A

Reduce or control concomitant risk factors: stop smoking; low-fat diet. Reduce alcohol and salt intake and caffeine; increase exercise; reduce weight if obese, manage OSA.
- - Weight reduction alone can result in decreases of up to 5 to 20 mm Hg in systolic blood pressure
- Smoking may not have a direct effect on blood pressure but will help in reducing long-term sequelae if the patient quits smoking.
- Lifestyle changes alone can account for up to a 15% reduction in all cardiovascular-related events

29
Q

Should blood pressure be dropped rapidly?

A

Reduce blood pressure slowly; rapid reduction can be fatal, especially in the context of an acute stroke

30
Q

What is more important, adequate BP reduction or specific drug used?

A

= The ALLHAT study suggests that adequate BP reduction is more important than
the specific drug used
- However, beta-blockers seem to be less effective than other drugs at reducing major cardiovascular events, particularly stroke.
- Beta-blockers and thiazides may increase the risk of new-onset diabetes, Ca2+-channel blockers appear
neutral, and ACE-i or ARB may reduce the risk.

31
Q

What is a hypertensive crisis?

A

BP >200 systolic or diastolic 120

32
Q

What are symptoms of cushing’s syndrome?

A

Centripetal obesity (a condition where fat accumulates in the abdomen and around the center of the body, particularly in the form of visceral fat), skin thinning, weakness, weight gain, fatigue, weakness, round moon face, delayed wound healing, easy bruising, back pain, bone pain, loss of height, depression, mood swings, emotional reactivity, loss of libido, erectile dysfunction in males, irregular menstrual cycles in females, infertility, hyperhidrosis, hirsutism, biparietal visual loss if there is a large pituitary adenoma, recurrent fungal and bacterial infections due to impaired immunity, and difficulty in combing hair or rising from a sitting position

33
Q

What shoud be asked to a patient with hypertension?

A

FH- hypertension, endocrine disease, polycystic kideny disease, heart disease
DH- Cardiac and antihypertensive medications, steroids, contraceptive pill, levothyroxine/carbimazole, MAOI, antipsychotics, recreational drugs (cocaine, amphetamines)
SH- Exercise tolerance, smoking

34
Q

Worrying features of a patient with hypertension

A

Altered mentation, seizures, retinal hemorrhages, AKI, chest pain, arterial aneurysms

35
Q

Complications of hypertension

A

End organ damage, malignant HTN, CV disease

36
Q

Pharmacological therapy for hypertension

A
  • Monotherapy (1st line): If ≥55yrs, and in black patients of any age, 1st choice is a Ca2+-channel antagonist or thiazide. If <55, 1st choice is ACE-i (or ARB if ACE-i intolerant, eg cough).
    beta-blockers are not 1st line for hypertension, but consider in younger people, particularly
    if: intolerance or contraindication to ACE-i/ARB, she is a woman of child-bearing
    potential, or there is increased sympathetic drive.
  • Combination : ACE-i + Ca2+-channel antagonist or diuretic is logical, and has been commonly used in trials. There is little evidence on using 3 drugs but current recommendation
    is ACE-i, Ca2+-channel antagonist, and thiazide.
  • If BP still uncontrolled
    on adequate doses of 3 drugs, add a 4th—consider: spironolactone 25–50mg/24h or higher-dose thiazide, but monitor U&E. Alternatively, beta-blocker, or selective beta-blocker
    and get help.
37
Q

1st Choice of antihypertensive in patient with LVF

A

ACE inhibitor

38
Q

Hypertension crisis causese threatening causes of hypertensive crisis

A
39
Q

1st Choice of antihypertensive in patient with diabetes and why?

A

ACE inhibitor, beta blockers can aggravate or increase diabetes

40
Q

Management of hypertension crisis

A
  • Acute treatment: In the absence of end- organ damage, oral therapy with
    a calcium channel blocker or ACEi should be instigated.
    If end- organ damage is present, admit patient to a monitored area (HDU/ ICU), with close monitoring of BP (Box 7.7), ECG, neurological state, and fluid
    balance (consider arterial line, central line, catheterization).
    Rapid reduction in BP can be dangerous, resulting in cerebral hypoperfusion and
    is only necessary in an acute MI or aortic dissection. Otherwise, aim to
    reduce diastolic BP to 100mmHg or by 25% (whichever value is higher)
    over 24h
    Patients with early features of end- organ damage may be commenced on oral therapy, though more severe organ damage may require treatment with
    IV agents.
  • Chronic treatment BP needs checking regularly once discharged from hospital.
    Ensure GP knows what investigations have been undertaken, their
    results, and what the therapeutic plan/ target BP is
41
Q

Signs of end organ damage in hypertension

A
42
Q

Oral Pharmacotherapy for acute management of hypertensive crisis

A

If no evidence of LVF use labetalol; if LVF present commence
furosemide (20– 50mg IV) ±hydralazine.
- Consider ACEi to counteract
high circulating levels of renin.
- Nitroprusside and hydralazine are still used as adjuncts in severe crises under expert guidance

43
Q

IV pharmacotherapy for acute management of hypertensive crisis

A
44
Q

What is the drug in isoket

A

Isosorbide dinitrate

45
Q

When should senior help/ arrest team be called in bradycardia patient?

A

Drop in GCS or BP less than 90 systolic