Endocrine disorder characterized by excess cortisol, central obesity, abdominal striae, and moon facies
Cushing's syndrome
*rare cause of resistant HTN but can screen w/ 23h urine cosrtisol, MN salivary cortisol or low dose dex suppression test if + cushingoid features
Diagnosing HTN: BP >= 130/80 averaged at least this many times over a period of weeks-months.
3
*single measurement okay if >= 160/100 and HTN related organ damage (high pre-rest prob in CKD, HF/LVH) OR BP >= 180/120
This medication is used as first line for primary hyperaldosteronism?
Spironolactone
*start low dose and CTM lytes closely in first months
*significant benefit regardless of pimary aldosteronism
You need to stop some medications when screening for primary hyperaldosteronism
You get the points no matter what :)
Do NOT need to stop ACE/ARBs. If possible, stop spironolactone x1m but can also test while on this. You may get a false negative but not many things that cause a false positive.
60 y/o with HTN, HLD, T2DM here for a f/u. His BP is 135/89 in clinic today. He is on max dose amlodipine, losartan, HCTZ. Is this resistant HTN?
a. no, he is w/in goal b. yes, BP is uncontrolled on 3 meds c. maybeeee
Will get points for a and c
BP still above goal 130/80 on 3 meds; make sure legs are uncrossed x 5m, empty bladder, no clothing over arm and correct cuff size! Confirm pt is taking meds (>80% of doses).
Kidney related cause of secondary HTN due to atherosclerosis in older folks or fibromuscular dysplasia in younger folks
RAS: renal artery stenosis
*suspect RAS in pts > 55 w/ atherosclerosis and new onset HTN
*suspect in young patients with HTN
Suggestive clinical features of RAS: elevated Cr (>= .5-1) after starting this medication(s)
ACEi or ARB
In a patient with aldosteronism producing adenoma, this is the definitive treatment to cure HTN
Adrenalectomy
*adrenal CT/MR if surgery is being considered, imaging has high false positive and false negative rate for active adrenal adenomas
You should be checking renin/aldosteronism levels in the PM
False; check in the AM (0800)
*both aldo and renin have a diurnal variation, peaking in the AM and declining in the day
*BP and therefore renin changes with position. When going from laying to sitting/standing, BP temp decreases so RAAS is activated.
42 y/o with BMI 40, chronic fatigue, and uncontrolled HTN on 2 antihypertensive agents who came in for a f/u appt. The partner tells you that the patient snores really loud. Next steps?
Sleep study; OSA is one of the most common causes of resistant HTN
Catecholamine secreting tumor that can cause secondary HTN
Pheochromocytoma
*rare, about 1/10,000, most common in middle-aged adults
*positive if metanephrines are >4x ULN
Pheochromocytoma triad
HA, sweating, palpiations
The ACC and AHA recommends considering revascularization for RAS in patients with:
a. resistant HTN b. rapidly declining renal fxn c. CHF d. all of the above
All of the above
*med management FIRST (ACE/ARB has mortality benefit)
*revasc second line if unable to tolerate meds/uncontrolled BP
*CORAL (2014 study) showed no difference in medical tx (ACE/ARB) vs stenting (not in FMD, flash pulm edema, AKI)
Majority of patients with primary hyperaldosteronism have an abnormal K
False -- 60% of patients with primary hyperaldosteronism have normal K so normal K does NOT r/o primary hyperaldosteronism
38 y/o who comes in for new PCP appointment. You notice their BP is controlled on 3 antihypertensive agents. They also take some OTC meds several times/week. Which OTC med might they be taking that could also be increasing their BP?
NSAIDs, decongestants (pseudoephedrine), OCPs, antidepressants (TCAs, SSRI), olanzapine, immunosupressants (tac), herbals (ginseng), prednisone; EtOH, cocaine
This adrenal disorder is the most common cause of secondary HTN in middle aged adults
Primary hyperaldosteronism (Conn's syndrome): excessive aldosterone
*about 8% of all pts w/ HTN and 20% of pts w/ resistant HTN
Best initial test for hyperaldosteronism?
aldosterone/renin
*positive if ARR >= 20, esp if aldosterone >15
*excellent sens/spec if ARR > 30 and PAC > 20 and hypoK
In CKD, thiazide diuretics lose efficacy at this eGFR
eGFR < 30
*switch to loop diuretics; salt restriction and diuretics are very effective
The severity of HTN correlates with severity of OSA in patients who have secondary HTN d/t OSA?
True
28 y/o with a PMH of MDD who was seen by another provider 3 weeks ago for a HA and palpitations. They ordered serum metanephrine which came back elevated (1xULN). Next steps?
False positives: venlafaxine, TCAs, adrenergic receptor agonists (decongestants, amphetamines)
Patient w/ upper extremity HTN, delayed or decreased femoral pulses
Coarctation of the aorta
*common cause in children but may not be detected until adulthood because asx
*classic figure 3 sign or rib notching


Indications for further w/u of possible secondary etiology:
1. early or late onset HTN 2. severe accelerated course 3. resistant HTN
Resistant HTN is defined as BP above goal 130/80 despite being on how many antihypertensive agents
3
*max dose, different classes, if tolerated one of the 3 should be a diuretic
*RH inc risk of CV events by 50%+ compared to primary HTN
The use of CPAP been shown to help:
a. reduce BP b. reduce strokes c. reduce MIs d. all of the above
a. reduce BP
RCTs have not shown that CPAP reduces CV events (mortality, MI, stroke)
Approximately 30% of adults w/ HTN have a secondary cause
FALSE - 5-10% (AAFP)
65 y/o with PMH of obesity, CAD with new HTN and an abdominal bruit on physical exam. Next steps?
MRA or CTA; MRI > CT since it can determine degree of stenosis, CTA more sensitive for FMD
if MRI and CT angiography are CI, you can use duplex US (takes 2 h, challenging if larger habitus)
*med management FIRST; c/f RAS in patients > 55 with new onset severe HTN