Transcript GRAND ROUNDS

69yo female with h/o severe bitemporal
headache, nausea and vomiting for 3
days. Sudden onset
No h/o CAD, HTN
Past medical Hx:
MM s/p BMST & chemo
Orthostatic hypotension - chemo
Physical Examination:
Vitals: BP 238/102 HR: 68x’ RR: 20x’
Gen: acutely ill, uncomfortable.
HEART: RRR, no M/R/G, nl S1/S2
LUNGS:CTAB
ABDOMEN/EXTR: soft, NT/ND, BS present, no
bruits.
NEURO: AxOx3, photophobia
Labs: BUN:10 Creatinine:0.6 Na:138 K:2.6
CT head: no acute abnormalities
-US Renal & Arterial Doppler:
Elevated peak systolic velocity in the mid
right renal artery with suggestion of parvus
tardus wave form suspicious for moderate to
severe right renal artery arterial stenosis.
Probable mild left renal artery stenosis.
-Bilateral renal angiography: Successful
balloon dilatation of probable fibromuscular
dysplasia, right renal artery without obvious
complication.

Type of HTN with underlying and
potentially correctable cause.

5-10% of HTN cases are thought to result
from 2y causes.

Secondary etiology may be suggested
by symptoms, examination findings or
laboratory abnormalities.
Indications for further investigation:
 Resistant HTN (defined by the JNC 7 as blood
pressure that is above the patient's goal despite
the use of 3 or more antihypertensive agents from
different classes at optimal doses, one of which
should ideally be a diuretic)
Worsening of control in previously stable
hypertensive patient.
 Stage 3 HTN
 Early onset of HTN <20yo, or older >50yo
 Findings on exam (sings and symptoms)

General Approach to the patient:
1. Confirm appropriate measure of BP’s
2. Diet
3. Drugs
DRUG CLASS
EXAMPLES
ESTROGEN
Oral contraceptives
Herbal
Ephedra, ginseng, ma huang
Illicit
Amphetamines, Cocaine
NSAID’s
COX 2 inh, ibuprofen,
naproxen.
Psychiatry
Buspirone, carbamazepine,
clozapine, fluoxetine, lithium,
TCA’s.
Steroids
Methylprednisolone,
prednisone
Sympathomimetic
Decongestants, diet pills
Children and Adolescent (birth – 18years of
age)
Renal Parenchymal Disease:
 Glomerular and interstitial diseases,
congenital abnormalities, reflux
nephropathy.
 Sometime not apparent until young
adulthood.
 Initial evaluation: BUN, Creatinine, UA,
Renal US.
Coarctation of the aorta:

2nd most common cause
2-5 times more common
in boys
 Usually diagnosed
around 5 years of age
with the onset of HTN or murmur.
 Classic findings: HTN upper extremities,
diminished or delay in femoral pulses and low
or unobtainable arterial BP in the lower
extremities.

Classic findings: HTN upper extremities,
diminished or delay in femoral pulses and
low or unobtainable arterial BP in the lower
extremities.
 Initial testing : EKG, Chest x ray and
confirmation with Echo/MRI

Young adults (19-39 years of age)
Renal Artery Stenosis caused by
Fibromuscular dysplasia:
 10% of the cases.
 Unknown etiology
 Predominantly young
women.
 Bilateral arterial
involvement 60-70%

Suspected if hypertension occurs in patients
younger than 35 years of age or if transient
ischemic attacks, stroke, aneurysm, or
dissection occurs in young patients

Diagnostic test:
Angiography (gold standard)/MRI with
gadolinium/CTA (patients with normal
renal function) / Renal Doppler (high
sensitivities).
* MRI and CTA equally accurate in
visualizing stenosis.
Labs: creatinine rarely elevated
 Treatment: percutaneous transluminal
renal angioplasty

Thyroid Dysfunction:
 Thyroid hormones affect cardiac output
 Hypothyroidism
* Major CV changes: decrease in
cardiac output and contractility, ↓HR,
↑Peripheral vascular resistance.
*Symptoms and signs: exertional dyspnea
and exercise intolerance, bradycardia,
HTN, cardiac dysfunction, edema (non
pitting), pericardial effusions.
*Diagnosis: TSH
*Treatment: thyroid hormone
(levothyroxine)
Hyperthyroidism:
*Major CV changes: ↑HR, ↑cardiac
contractility, ↑cardiac output, ↑diastolic
relaxation, ↓systemic vascular resistance.
*Signs and Symptoms: tachycardia
(rest/sleep), palpitations, systolic HTN, DOE
& angina.
*Diagnosis: TSH
*Treatment: Radioactive iodine or antithyroid drug. Beta blockers (propranolol,
atenolol)

Middle-Aged Adults: (40-64 years of age)
Aldosteronism: overproduction of aldosterone
independent from its usual regulator, the reninangiotensin system.
 Most common causes:
*Unilateral aldosterone producing adenoma
(approx. 50%)
*Bilateral Idiopathic hyperaldosteronism.
 3-15% prevalence in patients with HTN.

Pathogenesis:
↑aldosterone→ disruption of normal renin angiotensin
system
Na+ retention→ Vol expansion→HTN
↑K excretion→Hypokalemia
↑H ion excretion→Metabolic alkalosis
Supression of plasma renin
Clinical Features:
-HTN often resistant to treatment
-Hypokalemia (inconsistent
finding)→Muscle weakness, fatigue,
constipation, irregular HR with arrhythmias

Diagnosis:
-Best initial test is Aldosterone/Renin ratio,
most sensitive test.
-Levels should be measured in the am at
least 2 hrs after waking.
-Aldosterone/Renin ratio >20 -40 ng/dL
and aldosterone level > 15 ng/dL→Refer
endocrinologist for confirmatory tests (oral
salt loading test, saline suppression test,
fludrocortisone suppression test).
-Imaging: CT→ unilateral macroadenomas
>1cm.

OSA:
 Repetitive episodes of apnea or
reduced inspiratory airflow due to upper
airway obstruction during sleep.
 Intermittent hypoxia with arousal
response
 Cause of 2y HTN particularly in 40-59 year
olds.
 Standard diagnostic test:
polysomnography but also the nighttime
pulsoxymeter can be used to diagnose
mod to severe OSA.
Pheochromocytoma:
 Responsible for approximately 0.5% of cases
of 2y HTN.
 Age 30-60 years of age.
 Not part of the initial evaluation for 2y HTN
unless specific symptoms are suggestive
 Clinical findings
paroxismal elevations BP
Triad: Headache, Palpitations
Sweating.
 Dx: plasma free metanephrines or 24 hr urine
Cushing Syndrome:
 Signs and symptoms associated with
long term exposure to inappropriately
high levels of Cortisol.
 The most common causes:
*Exogenous→(iatrogenic) steroids glucocorticoid drugs are #1
* Endogenous→ Cushing Disease/
Adrenal Adenoma / Ectopic
ACTH(paraneoplasic tumor)
Sings and Symptoms
HTN
Increase weight
Hyperglicemia
Moon fascies
Buffalo hump
Truncal obesity

Diagnosis:
Suggested by body changes/HTN/
Hyperglicemia.

24 urine free cortisol
Low dose dexamethasone supression
Late night salivary cortisol test.
Older Adults: (65 years and older)
Renal Artery Stenosis caused by
atherosclerosis:
>90% or RAS are atherosclerotic in nature.
 Higher risk in older patients
smokers, PAD
 Bilateral RAS should be suspected in
patients with h/o “flash” or episodic
pulmonary edema


Clinical Clues:
*Onset severe HTN >55yo
*Unexplained deterioration of kidney
function during antihypertensive tt x
(Sustained elevation in the serum Creatinine by
more than 50% within 1 week of ACEI or ARB)
* Severe HTN with an unexplained
kidney atrophy or asymmetry in renal
sizes >1,5cm.
 Radiologic testing: Doppler renal US,
CTA, MRA.
 Treatment: medical ttx/ PCTA/Vascular
Revascularization.
SIGNS / SYMPTOMS
POSSIBLE 2yHTN CAUSE
DIAGNOSTIC TEST OPT
Arm to leg SBP
difference >20mmHg.
Delayed or absent
femoral pulses.
Murmur
Coarctation of the
aorta
MRI (adults). TTE
(children)
↑Creatinine >0.51mg/dL after starting
ACEI or ARB’s.
Abdominal bruit.
Renal Artery Stenosis
CTA / Doppler US of
renal arteries / MRI
with gladolinium
contrast
Brady/Tachycardia,
Cold/Heat intolerance
Constipation/Diarrhea
Irregular, heavy or
absent menstrual
cycles.
Thyroid Disorders
TSH
Unexplained
hypokalemia
Aldosteronism
Renin and Aldosterone
levels to calculate
Aldosterone/Renin
ratio
SIGNS / SYMPTOMS
POSSIBLE 2yHTN CAUSE
DIAGNOSTIC TEST OPT
Obesity, Apneic
events during sleep.
Daytime sleepiness.
Snoring
OSA
Sleep study. Sleep
apnea clinical score
with night time pulse
oximetry
Pounding headache/
Palpitations/Sweating.
Paroxysmal elevations
in BP’s. Syncope,
flushing, Orthostatic
Hypotension
Pheochromocytoma
24-hr urinary
metanephreines.
Plasma free
metanephrines
Buffalo hump, central
obesity, moon facies,
striae
Cushing Syndrome
24 hr urinary cortisol
Low dose
dexamethasone
supression.
Literature






Diagnosing Secondary Hypertension EDWARD ONUSKO, M.D.,
Clinton Memorial Hospital, Wilmington, Ohio Am Fam
Physician. 2003 Jan 1;67(1):67-74.
Diagnosis of Secondary Hypertension: An Age-Based
Approach ANTHONY J. VIERA, MD, MPH, and DANA M.
NEUTZE, MD, PhD University of North Carolina at Chapel Hill
School of Medicine, Chapel Hill, North CarolinaAm Fam
Physician. 2010 Dec 15;82(12):1471-1478.
Evaluation of Secondary Hypertension E. Eugene Baillie, MD
JAMA. 1977;238(23):2494.
doi:10.1001/jama.1977.03280240040007.
http://hyper.ahajournals.org.
Up to date
DynaMed