Hypertension: Pathology review

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Case study0:00–1:31

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.

Pathology1:31–2:54

Now normal blood pressure is less than 120 systolic over 80 diastolic. According to the recent 2017 American Heart Association and American College of Cardiology guidelines, hypertension is currently defined as a blood pressure over 130 systolic and 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.
This is referred to as isolated systolic hypertension or isolated diastolic hypertension. Okay, just because you see an elevated blood pressure on the exam, it does not mean that individual has hypertension.
The blood pressure must be persistently elevated in order to define it as 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.

Primary Hypertension2:54–4:02

Reduced sodium excretion increases plasma volume, increasing the stroke volume, and as a result the systolic blood pressure.
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.
Additionally, decreased sodium excretion promotes vasoconstriction of the peripheral arterioles, increasing the systemic vascular resistance, which increases diastolic blood pressure.
Okay, so risk factors for primary hypertension include age, physical inactivity, obesity, diabetes mellitus, smoking, family history of hypertension, as well as excess salt or alcohol consumption.
It’s thought that in type II diabetes, high levels of insulin promote renal sodium retention.Okay, before diagnosing an individual with primary hypertension, the causes of secondary hypertension must be ruled out.

Secondary Hypertension4:02–9:48

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. Important causes include primary hyperaldosteronism, or Conn syndrome, Cushing syndrome and tumors like pheochromocytoma and neuroblastoma.
Clues in the question stem will help you identify which one it is. Hypokalemia, metabolic alkalosis and an increase in the aldosterone-to-renin ratio indicate Conn syndrome.
Abdominal striae, supraclavicular fat pads, truncal obesity, and hyperglycemia point towards Cushing syndrome. Paroxysmal hypertension, that is hypertension that comes and goes, associated with headaches, palpitations and sweating indicate a pheochromocytoma.
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.
So in response, the renin-angiotensin-aldosterone system, or RAAS, is activated, resulting in vasoconstriction and increased renal sodium and water reabsorption, and eventually hypertension.
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.
Okay, renal parenchymal diseases like diabetic nephropathy, glomerulonephritis or polycystic kidney disease can also cause hypertension by retaining sodium.
Moving on, Coarctation of the aorta is also an important cause of hypertension, especially in children. And the mechanism is quite similar to renal artery stenosis, since renal perfusion is decreased, just that the obstruction is more proximal.
Speaking of the aorta, aging causes the amount of elastin in the arterial wall to decrease, and the amount of collagen to increase, producing a stiff, non-compliant aorta.
This manifests in elderly adults as isolated systolic hypertension, which means an elevated systolic blood pressure, but a normal diastolic.
Moving on, both hyperthyroidism and hypothyroidism can cause hypertension. Hyperthyroidism increases the cardiac output, causing an elevated systolic blood pressure.
For some reason, hypothyroidism increases renal retention of sodium, and interestingly causes an isolated elevation of the diastolic blood pressure.
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-containing oral contraceptives are common causes of hypertension, especially in young women. Estrogen works by increasing the synthesis of angiotensinogen in the liver, which is ultimately converted to angiotensin one and two.
Cocaine is another potential drug that can cause hypertension by increasing sympathetic activity. Additionally, in people take monoamine-oxidase inhibitors, ingestion of tyramine-containing foods like cheese and wine may initiate an acute hypertension.
Remember that sometimes the exam might not mention the medication but simply state that the person has a history of atypical or drug-resistant depression, which is an indication for MAOIs.

Complications9:48–12:12

Alright, chronic hypertension can result in multiple complications affecting different organ systems. Let’s start with the heart.
Hypertension increases the afterload, that is the resistance the heart has to pump against. In response, the left ventricle hypertrophies to overcome that resistance.
Concentric hypertrophy increases the myocardial oxygen demand, which means the heart needs more coronary blood supply than usual.
Also, concentric hypertrophy makes the heart stiff, which limits diastolic relaxation. This is why heart failure from hypertension is a diastolic heart failure, so the ejection fraction will actually be normal.
Hypertension is also a risk factor for atherosclerosis, so there’s an increased risk of coronary artery disease, which is the most common cause of death from hypertension.
Aortic dissection is another important complication, and hypertension is the most important risk factor contributing to it.
Alright, onto the brain. Hypertension can weaken the walls of the small brain vessels, resulting in Charcot-Bouchard aneurysm, which can rupture and cause an intracerebral bleed.
Larger arteries can form berry aneurysm, which can rupture and cause a subarachnoid hemorrhage. Also, hyaline arteriosclerosis of the small blood vessels can occlude them, resulting in small lacunar infarcts.
In fact, properly managing hypertension has been shown to provide the greatest reduction in the risk of stroke. Okay, in the kidneys, hyaline arteriosclerosis of the afferent and efferent arterioles can lead to ischemia and atrophy of the renal tubules.
Over time, renal failure manifests. Finally we have to keep an eye on the eyes.
Remember for your exams that hypertensive retinopathy manifests as dot and flame-shaped hemorrhages that result from rupture of microaneurysms; arteriovenous nicking when enlarged arteries compress veins, as well as silver and copper-wiring which are occluded arteries that appear white or orange instead of red.
Alright, aside from the chronic complications, hypertension can also result in acute presentation. Both hypertensive urgency and emergency have a blood pressure greater than 180 over 120.

Hypertensive emergency12:12–13:14

The difference is that in hypertensive emergency, there is evidence of acute end-organ damage. Now both usually develop when someone is not consistently taking their antihypertensive medication.
Hypertensive urgency is usually found incidentally, so there’s no evidence of end-organ damage. In hypertensive emergency, end-organ damage can manifest in a variety of ways.
For example, CNS manifestations include headache, altered mental status seizures, papilledema, or stroke. Cardiac manifestations include myocardial infarction, acute left ventricular failure resulting in pulmonary edema, and aortic dissection.
Renal manifestations include acute kidney injury, presenting as an elevation in the BUN and creatinine, hematuria and microalbuminuria.Now, let’s switch gears and discuss treatment of hypertension.

Treatment13:14–16:20

The first choice of treatment is lifestyle changes, like low sodium diet, exercise, and stress reduction techniques. In some cases, antihypertensive medications can be given as well.
In general, for essential hypertension there are four main classes of medications that are used, Angiotensin-converting enzyme or ACE inhibitors, Angiotensin Receptor Blockers or ARBs, thiazide diuretics, and long-acting calcium channel blockers like dihydropyridine.
But what the examiners often do is try to clue you towards the medication you should choose based on the comorbidity of the patient.
So, if there’s hypertension with heart failure, it’s high yield to remember the treatment should include ACE inhibitors or ARBs, diuretics, aldosterone antagonists and beta blockers.
Bear in mind though that beta blockers must be used with caution in decompensated heart failure, which is when heart failure rapidly worsens.
That’s because of their ability to decrease heart rate and their negative inotropic effect, meaning that they decrease the force of heart contraction.
Moving on, if there’s hypertension with diabetes mellitus, the optimum treatment is ACE inhibitors or ARBs, thiazide diuretics, Calcium channel blockers, or beta blockers.
What’s important to remember is that ACE inhibitors or ARBs are protective against diabetic nephropathy. And when using beta blockers, hypoglycemia is the side effect to watch out for, as it may go unnoticed, since beta blockers blunt the counter- regulatory effects and symptoms of catecholamines, like tachycardia and tremors.
That’s particularly dangerous for people with diabetes, who already take a bunch of other hypoglycemic medications like insulin.
Next, hypertension in individuals with asthma should be treated with ARBs, thiazide diuretics, calcium channel blockers or cardioselective beta blockers.
What we should avoid here is ACE inhibitors, since their most common side effect is cough. And non-selective beta blockers, which also block beta2 receptors in the lungs, cause bronchoconstriction.
Finally, for hypertension in pregnancy, choose hydralazine, methyldopa, labetalol, or nifedipine. To remember this, you can use the mnemonic Hypertensive Moms Love Nifedipine.
Another thing to know is treatment of acute complications of hypertension. Hypertensive urgency just needs adjustment of oral antihypertensive medication, so there is no need to lower the blood pressure acutely.
On the flip side, in hypertensive emergency, it’s crucial to lower the blood pressure immediately with intravenous medications like nitroprusside or labetalol.All right, as a quick recap, Hypertension is defined as an elevation of blood pressure above 130 over 80 as per the AHA.

Review16:20–17:47

Hypertension can be classified into primary, or essential hypertension, and secondary hypertension. Risk factors for primary hypertension include age, obesity, diabetes mellitus, smoking, and family history.
Secondary hypertension causes are classified based on the organ of origin. Examples include Conn syndrome from the adrenals, renal artery stenosis in the kidney, or coarctation of the aorta.
Drugs like cocaine and oral contraceptives are also potential causes. Chronic complications of hypertension can affect a variety of organ systems, and include left ventricular hypertrophy, coronary artery disease, stroke and subarachnoid hemorrhage, renal failure and hypertensive retinopathy.
Hypertension can also present acutely as hypertensive urgency, which has a blood pressure greater than 180 over 120 without end-organ damage, or hypertensive emergency, which is with end-organ damage.
Treatment of hypertension varies depending on any concomitant conditions, like heart failure, diabetes, asthma or even pregnancy.Back to our cases.

Summary17:47–18:58

Anthony has multiple risk factors for primary hypertension, including a history of diabetes, obesity, lack of exercise and family history of hypertension.
After performing a physical exam to check for the chronic complications of hypertension, he’s given antihypertensive medication.
Alicia presented with hypertension and was placed on lisinopril, an ACE inhibitor. However, she developed oliguria and an elevated BUN and creatinine, signifying that her GFR declined after the initiation of lisinopril.
This is characteristic of renal artery stenosis. Labs showed elevation of renin and aldosterone levels, and an angiogram confirmed the stenosis.
Vikander is presenting with hypertensive emergency, as his blood pressure is above 180 over 120, and his symptoms include headache, altered mental status and papilledema, which means there’s end organ damage.
His probable history of medication non-compliance also supports this diagnosis. Intravenous esmolol is given to quickly lower his blood pressure
Hypertension: Pathology Review: Video and Causes | Osmosis