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.► ABORDAGEM SINDRÔMICA > Symptom To Diagnosis - Hypertension > Flashcards

Symptom To Diagnosis - Hypertension Flashcards

1
Q

5 endocrine causes of HTN:

A
  1. Primary hyperaldosteronism.
  2. Pheochromocytoma.
  3. Thyroid.
  4. Hyperparathyroidism.
  5. Cushing.
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2
Q

2 renal causes of HTN:

A
  1. Chronic kidney disease.

2. Acute renal failure.

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3
Q

2 vascular causes of HTN:

A
  1. Renovascular disease.

2. COTA.

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4
Q

Pulmonary cause of HTN:

A

Sleep apnea.

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5
Q

GI cause of HTN:

A

Obesity.

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6
Q

10 drugs that cause HTN:

A
  1. Prolonged steroids.
  2. NSAIDS.
  3. Cox-2.
  4. Cocaine.
  5. Alcohol.
  6. Sympathomimetics (decongestants, anorectics).
  7. OCPs.
  8. Cyclosporine and Tacrolimus.
  9. EPO.
  10. Stimulants (modafinil, amphetamines).
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7
Q

Secondary causes of HTN are quite rare in unselected populations:

A
  1. 18%-4.4% –> Renovascular HTN.
  2. 04-0.2% –> Pheochromocytoma.
  3. 01-0.4% –> Primary hyperaldosteronism.
  4. 3% –> Cushing.
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8
Q

Patients who are normotensive at age 55 have a …% lifetime risk of developing HTN.

A

90%.

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9
Q

Across the BP range of 115/75mmHg to 185/115mmHg, each increment of 20mmHg systolic BP or 10 mmHg diastolic BP … the risk of cardiovascular disease.

A

Doubles.

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10
Q

There are 3 objectives of testing in patients with HTN:

A

Objective 1: Assess presence or absence of target organ damage (TOD).
Objective 2: Assess presence or absence of other cardiovascular risk factors.
Objective 3: Identify secondary HTN.

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11
Q

Initial testing in a patient with HTN and no clinical clues should include:

A
  1. ECG.
  2. Electrolytes.
  3. BUN/Cr.
  4. Calcium.
  5. TSH.
  6. Urine albumin-creatinine ratio.
  7. Fasting glucose.
  8. Fasting lipid panel (total cholesterol, HDL, TGs, LDL).
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12
Q

Assessing TOD - Heart:

A
  1. LV Hypertrophy - Physical exam, ECG, echocardiography in selected patients.
  2. CAD - History, ECG, stress test in selected patients.
  3. Heart failure - History, physical exam, echo.
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13
Q

Assess TOD - Brain:

A
  1. Stroke.
  2. TIA
    - -> History, physical exam.
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14
Q

Assess TOD - Kidneys:

A
  1. Proteinuria.
  2. Chronic kidney disease.
    - -> Albumin/creatinine ratio, serum creatinine.
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15
Q

Assess TOD - Eyes:

A

Retinopathy –> Fundoscopic or ophthalmologic exam.

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16
Q

Assess TOD –> Peripheral vasculature:

A

Peripheral vascular disease –> History and physical exam, ABI measurements in selected patients.

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17
Q

Non pharmacologic approaches to managing HTN:

A

Weight reduction –> 5-20mmHg/10kg weight loss.
DASH diet –> 8-14mmHg.
Reduced sodium diet ( 2-8mmHg.
Aerobic exercise 30 min/day, several days/week –> 4-9mmHg.
Limitation of alcohol 2-4mmHg.

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18
Q

Atherosclerotic renal artery stenosis - Textbook presentation:

A
  1. Patients generally have either very abrupt HTN.
  2. HTN that worsens over 6 months.
  3. HTN refractory to treatment with 3 drugs.
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19
Q

About …% of patients with renal artery stenosis have renovascular disease.

A

50%.

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20
Q

Predictive value of abdominal Bruits in renovascular HTN:

A
  1. Should listen to all 4 abdominal quadrants and also spine and flanks between T12 and L2.
  2. Should be systolic + diastolic.
  3. Prevalence 6.5-31% in a healthy population; prevalence of 28% in patients with HTN.
  4. Prevalence of 78-87% in patients with proven renal stenosis.
  5. Sens 39-63%, spec 90-99%.
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21
Q

Bilateral Renal artery stenosis - Response to ACEI:

A

A reversible increase in serum creatinine can develop in some patients with bilateral RAS when starting ACEI therapy.

  • -> Peak creatinine somewhere between 4 days and 2 months.
  • -> Cr returns to baseline within 1 week of stopping the ACEI.
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22
Q

Gold standard for renal artery stenosis imaging:

A

INTRA-arterial digital substraction angiography (DSA).

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23
Q

Primary hyperaldosteronism - How does it present?

A

A patient with HTN has unexplained hypokalemia.

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24
Q

Etiology of primary hyperaldosteronism:

A
  1. 30-60% –> Adenoma (Conn).
  2. Idiopathic bilateral adrenal hyperplasia in most other patients.
  3. Rarer causes include micro adenomas, unilateral adrenal hyperplasia, and adrenal carcinoma.
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25
Q

Prevalence of primary hyperaldosteronism:

A

True prevalence is UNKNOWN but could be as high as 12-15% in selected populations with resistant HTN.

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26
Q

Volume expansion in primary hyperaldosteronism suppresses?

A

Plasma RENIN levels.

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27
Q

Primary hyperaldosteronism - Most patients have … K levels.

A

Normal K levels (50-60%).

A normal potassium level does not rule out hyperaldosteronism.

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28
Q

What is commonly used as screening for primary hyperaldosteronism?

A

Plasma aldosterone concentration/plasma renin activity (ARR). Elevated in primary hyperaldosteronism.

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29
Q

What should be done before measuring the plasma aldosterone/plasma renin activity ratio (ARR)?

A
  1. Hypokalemia must be corrected before testing.
  2. All antihypertensives should be stopped for 2 weeks, if possible.
    - CCBs, alpha-blockers and hydralazine –> Do not significantly change the results.
    - Aldosterone antagonists and beta-blockers must be stopped.
    - ACEI, ARBs, diuretics can cause FALSE(-) results.
30
Q

An ARR

A

23.6

31
Q

An ARR>… rules in primary hyperaldosteronism.

A

67.

32
Q

What is a hypertensive emergency?

A

Severe BP elevation and acute end organ involvement.

33
Q

What is a hypertensive urgency?

A

Severe BP elevation without any acute TOD.

34
Q

What is the cutoff of “severe BP elevation”?

A

> 180/100

35
Q

Bottom line about the hypertensive emergency:

A

It is defined by the presence of clinical symptoms, not by the degree of BP elevation.

36
Q

Hypertensive urgency - Steps in management:

A

Rule out TOD through history, physical exam, selected lab tests.

  1. Kidney –> Serum Cr and urinalysis.
  2. Heart, lung –> ECG, chest radiograph, and cardiac enzymes.
  3. Neurologic signs and symptoms –> Head CT scan, sometimes, brain MRI.
37
Q

Cerebral vasoconstriction limits hyperperfusion up to a MAP of …?

A

180mmHg.

Above a MAP of 180mmHg, Autoregulation is overwhelmed.

38
Q

The classic MRI finding in hypertensive encephalopathy is?

A

Subcortical vasogenic edema.

39
Q

Failure of autoregulation of cerebral blood flow is also called?

A

Reversible posterior leukoencephalopathy syndrome (RPLS).

40
Q

Symptoms in reversible posterior leukoencephalopathy syndrome (RPLS):

A

92% –> Encephalopathy.
39% –> Visual symptoms.
53% –> Headaches.
87% –> Seizures.

41
Q

Hypertensive emergencies and eclampsia?

A

68% –> Had HTN.
11% –> Eclampsia.
11% –> Immunosuppressive use.
11% –> Other causes.

42
Q

Hypertensive encephalopathy is primarily a … diagnosis.

A

Clinical.

43
Q

Hypertensive encephalopathy - CT or MRI?

A

BOTH:
CT –> Should be done to exclude intracranial hemorrhage (intracerebral or subarachnoid).
MRI –> Should be done to exclude acute ischemic stroke and to look for RPLS.

44
Q

MRI or CT for the diagnosis of acute ischemic stroke?

A

MRI much more sensitive than CT (83% vs 16% - Both have same specificity >95%) for the diagnosis of acute ischemic stroke.

45
Q

Tx of hypertensive emergency - Aortic dissection:

A 
Must use vasodilator + beta-blocker.
1. Labetalol.
2. Nicardipine + esmolol.
3. Nitroprusside + esmolol
or IV metoprolol.
46
Q

Tx of hypertensive emergency - Hypertensive encephalopathy:

A
  1. Nicardipine.
  2. Labetalol.
  3. Fenoldopam.
47
Q

Tx of hypertensive emergency - Cerebral infarction or hemorrhage:

A
  1. Nicardipine.
  2. Labetalol.
  3. Fenoldopam.
48
Q

Tx of hypertensive emergency - MI:

A

Labetalol OR esmolol + Nitroglycerin.

49
Q

Tx of hypertensive emergency - Acute pulm. edema/systolic dysfunction:

A

Nicardipine OR fenoldopam OR nitroprusside PLUS nitroglycerin PLUS diuretic.

50
Q

Tx of hypertensive emergency - Renal insufficiency:

A

Nicardipine and fenoldopam.

51
Q

Tx of hypertensive emergency - Eclampsia:

A

Labetalol OR nicardipine.

52
Q

Tx of hypertensive emergency - Acute postoperative hypertension:

A

Esmolol OR nicardipine OR labetalol.

53
Q

Treating a patient with a hypertensive encephalopathy:

A
  1. All patients should be admitted to the hospital; many will need to be treated in the ICU with IV medications.
  2. Little or no evidence to guide choice of specific drugs or rate of BP lowering in hypertensive encephalopathy.
  3. Guidelines recommend lowering the MAP by no more than 25% in the first 2 hrs and achieving a BP of 160/100mmHg (MAP=120mmHg) within 6hrs.
  4. Agents commonly used include labetalol, nicardipine, or fenoldopam, all of which are thought to maintain cerebral blood flow.
54
Q

Guidelines recommend treating HTN in acute ischemic stroke ONLY IF:

A
  1. The diastolic BP is >120 and/or the systolic is >220.
  2. Patient has noncerebral acute TOD.
  3. Thrombolysis is planned, in which case the target BP is 180/105 mmHg.
55
Q

Pheochromocytoma - Textbook presentation:

A
  1. Paroxysmal HTN, headache, palpitations, sweating.
  2. Occurring several times daily, weekly, or every few months.
  3. Patients generally have ORTHOSTATIC hypotension on physical exam.
56
Q

Familial pheochromocytomas:

A

10-15% –> VHL, MEN2, neurofibromatosis.

–> More often ASYMPTOMATIC (and normotensive) than sporadic cases.

57
Q

Symptoms of patients with pheo + PAROXYSMAL HTN:

A 
92% --> Severe headaches.
73% --> Palpitations and/or tachycardia.
65% --> Sweating.
60% --> Anxiety/panic.
51% --> Tremulousness.
48% --> Chest/abdominal pain.
43% --> Nausea +/- vomiting.
58
Q

Symptoms of patients with pheo + PERSISTENT HTN:

A

72% –> Severe headaches.
69% –> Sweating.
51% –> Palpitations and/or tachycardia.
28% –> Anxiety/panic - Chest or abdominal pain.
26% –> Tremulousness - Nausea +/- vomiting.

59
Q

Pretest probability of …% in hypertensive patients who have suggestive symptoms (pheo):

A

0.5%.

60
Q

Pretest probability of …% in patients with incidentally discover adrenal masses (for pheo).

A

4%.

61
Q

Single best test to rule out pheochromocytoma?

A

Plasma metanephrine.

62
Q

Plasma metanephrine measurement - What should be done?

A
  1. Patients should fast overnight and be supine for 20min prior to blood draw.
  2. Because caffeine and acetaminophen interfere with the assay, patients should avoid caffeine for 12 hrs and acetaminophen for 5 days prior to testing.
  3. Standard upper limit of normal for plasma metanephrines is 61 ng/L.
63
Q

Plasma metanephrine >236 is …% SPECIFIC for pheo.

A

100%.

64
Q

Patients with positive biochemical testing should undergo adrenal imaging. CT sens and spec:

A

Sens –> 93-100% for adrenal pheo. 90% for extra-adrenal tumors.
Spec –> 50-70%.

65
Q

Most specific test for pheo:

A
  1. 24h urine total metanephrines –> 89%.

2. 24h urine VMA –> 86%.

66
Q

MRI for detecting pheo:

A

Sens 90%.
Spec 50-70%.
Better than CT for identifying vascular invasion.

67
Q

When is I-MIBG or PET used in the diagnosis of pheo?

A

When the biochem is positive and BOTH CT and MRI are negative.

68
Q

Alpha and beta-blocker PRE-op for pheo:

A
  1. Alpha-blockers opposes catecholamine-induced vasoconstriction.
  2. Beta-blockers opposes the reflex tachycardia that occurs with alpha-blockade.
  3. Unopposed beta-blockade will cause inhibition of epinephrine induced vasodilation, leading to increased BP, left heart strain, and possibly HF.
69
Q

Bottom line about pre-op treatment for pheo:

A

Never give a patient with a pheochromocytoma a beta-blocker without first giving an alpha-blocker.

70
Q

…-…% of pheo patients have HTN after surgery.

A

27-38%.

71
Q

Definition of HTN:

A

Normal –> Systolic BP Systolic BP 120-139 OR diastolic BP 80-89.
Stage I –> Systolic 140-159 OR diastolic 90-99.
Stage II –> Systolic >160 OR diastolic >100.

.► ABORDAGEM SINDRÔMICA (41 decks)

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