AssessmentsHypertension: Pathology review
USMLE® Step 1 style questions USMLE
A 55-year-old woman comes to the clinic for a hypertension follow up. She was diagnosed with hypertension 6 months ago and was prescribed a low-sodium diet and exercise. Medical history is significant for diabetes mellitus type 2 that is currently managed with metformin. She has been smoking 1 pack of cigarettes daily for 20 years. Family history is significant for osteoporosis in her mother and diabetes mellitus in her father. Temperature is 37.0 °C (98.6 °F), pulse is 80/min, and blood pressure is 152/95 mmHg. Urinalysis reveals microalbuminuria. DXA scan shows normal bone mineral density. A decision is made to add a pharmacological treatment to manage the hypertension. The first-line treatment for this patient’s condition works by which of the following mechanisms of action?
Anthony is a 40 year old male with a history of type 2 diabetes mellitus presenting to a family medicine clinic for his annual health check-up.
His blood pressure measurement is 145 over 95 millimeters of mercury, and his BMI is 32.
On further history, he explains that his job as a truck driver has prevented him from exercising regularly.
His father had a history of hypertension and passed away from a stroke.
A follow-up appointment showed a blood pressure of 150 over 90.
Alicia is a 30 year old female who came in because she’s concerned that she might be pregnant.
Her pregnancy test is negative, however, her blood pressure is 170 over 90.
On her second appointment, her blood pressure remains elevated.
She is placed on lisinopril.
A couple of days later, she presents with decreased urine output, and an elevated blood urea nitrogen and creatinine.
Finally, Vikander is a 62 year old-male with a history of hypertension.
He complains of headache, altered mental status, and visual changes.
On further history, he mentions he is “sick of all the medications he has to take”.
Fundoscopic examination reveals a swollen optic disk, and his blood pressure is 200 over 120.
Okay so all three people present with hypertension.
Now normal blood pressure is less than 120 systolic over 80 diastolic.
Now, typically, both systolic and diastolic pressures tend to rise or fall together, but that’s not always the case.
Sometimes, you can have systolic or diastolic hypertension.
So on your exam, remember that the diagnosis requires at least 2 separate readings on 2 separate visits.
The reason for this is because of the phenomenon of “white coat hypertension”.
This is hypertension on physical exam that occurs because of anxiety experienced by the individual.
Hypertension is classified into primary, or essential hypertension, and secondary hypertension.
Primary hypertension occurs without a known secondary cause, and accounts for 90 percent of cases.
The pathophysiology of primary hypertension is thought to be related to decreased renal sodium excretion.
Also, the increased plasma volume causes decreased renin release from the juxtaglomerular apparatus, producing what’s called low-renin hypertension, and this can be high yield.
Okay, before diagnosing an individual with primary hypertension, the causes of secondary hypertension must be ruled out.
Your exams will often try to clue you towards this by mentioning that the individuals were on multiple antihypertensives and they didn’t work, or by having a relatively young individual with hypertension.
The best approach is to look at different organ systems, starting with the adrenal gland.
Clues in the question stem will help you identify which one it is.
Abdominal striae, supraclavicular fat pads, truncal obesity, and hyperglycemia point towards Cushing syndrome.
Neuroblastomas are common in children, and present with an abdominal mass.
Next is the kidney.
Renal artery stenosis, also called renovascular disease is usually caused by an atherosclerotic plaque occluding the renal artery, especially in 60 to 70 year old males.
Less commonly, it can be caused by fibromuscular dysplasia, especially in 20 to 30 year old females.
This classically causes the “string of beads” appearance of the renal artery.
Regardless of the cause, renal artery stenosis decreases renal perfusion.
This makes your body think it’s in a hypotensive state.
Decreased renal perfusion causes the affected kidney to shrink, and histologically, there will be glomerular tubulointerstitial atrophy and fibrosis.
A high yield fact to remember for your exams is that unilateral renal artery stenosis does not cause CKD because the contralateral kidney is functioning normally, and in fact it hypertrophies to compensate.
However, bilateral renal artery stenosis results in CKD because both kidneys are affected.
Also, it’s important to not give ACE inhibitors to people with bilateral renal artery stenosis.
This is because angiotensin II constricts the efferent arteriole in the glomerulus, which maintains the GFR.
If an ACE inhibitor is given, the efferent arterioles dilate, causing a drop in the GFR.
And the mechanism is quite similar to renal artery stenosis, since renal perfusion is decreased, just that the obstruction is more proximal.
The adjacent parathyroid glands are also potential suspects, because primary hyperparathyroidism causes hypercalcemia which increases vasoconstriction of the peripheral arterioles, resulting in an increased total peripheral vascular resistance.
Alright, if the person presents with hypertension, bradycardia and an irregular respiratory pattern, think of an increased intracranial pressure, which triggers a reflex that results in the Cushing’s triad.
In pregnancy, it’s crucial to consider preeclampsia and eclampsia.
Finally, always be aware of what medications the individual is taking.
Estrogen works by increasing the synthesis of angiotensinogen in the liver, which is ultimately converted to angiotensin one and two.
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- "Fundamentals of Pathology" H.A. Sattar (2017)
- "Williams Textbook of Endocrinology" W B Saunders Company (2008)
- "Pharmacotherapy for hypertension in adults aged 18 to 59 years" Cochrane Database Syst Rev (2017)
- "Hypertensive crisis" Cardiol Rev (2010)