Last edited: 5/5/2022

4. HYPERTENSION | UPDATE
Hypertension | Updated Medical Editors: Sarah, Aldrich and May

OUTLINE
I) DEFINITION III) SECONDARY (2°) IV) COMPLICATIONS OF V) HYPERTENSIVE CRISIS II) TREATMENT OF
OTHER TYPES OF HYPERTENSION HYPERTENSION HYPERTENSION (A) HYPERTENSIVE URGENCY HYPERTENSION
II) ESSENTIAL (1°) (A) RENAL CAUSES OVERVIEW (B) HYPERTENSIVE EMERGENCY (A) LIFESTYLE MODIFICATIONS
HYPERTENSION (B) DRUG-RELATED CAUSES (A) CENTRAL NERVOUS SYSTEM I) DIAGNOSIS/WORKUP (B) MEDICAL MANAGEMENT
(C) ENDOCRINE CAUSES (B) RETINA FOR HYPERTENSION (C) PREGNANCY
(D) CARDIAC CAUSES (C) CARDIAC (A) ESSENTIAL HYPERTENSION WORKUP (D) HYPERTENSION EMERGENCY
(E) PULMONARY CAUSES (D) VASCULAR ISSUES (B) SECONDARY HYPERTENSION WORKUP III) APPENDEX
(F) NEUROLOGICAL CAUSES (E) RENAL SYSTEM (C) COMPLICATION WORKUP IV) REVIEW QUESTIONS
(G) PREGNANCY CAUSES
V) REFERENCES

I) DEFINITION II) ESSENTIAL (1°) HYPERTENSION

According to the American Heart Association, the average 95% of HTN patients
of 2 readings of blood pressure on 2 separate visits need to Most commonly affected groups:
be used to confirm hypertension. o Ages 25-50 y/o
When measuring bp, 2 parameters are used: o Family history of HTN (strong risk factor)

Systolic: pressure when ventricles are in systole (1) (↑) SNS activity
(contraction). (↑) NE/Epi → exert their effects on:
Diastolic: pressure when ventricles are in diastole
(relaxation). (i) Heart
o Beta receptors → HR (↑)
Table 1. Classification of Blood Pressure o Myocardial contractile cells → (↑) Contractility → (↑) SV
Stage SBP DBP ▪ (Remember; CO = HR x SV) → CO (↑)
Normal <120 AND <80 ▪ (Remember; MAP = CO x TPR) → BP (↑)
Essential 120-129 AND 80-89 (ii) Blood vessels
Stage 1 HTN 130-139 AND 80-89 o Alpha-1 receptors → Vasoconstriction → (↑)
Stage 2 HTN >140 AND >90 Resistance → BP (↑)

(iii) Kidneys
(A) OTHER TYPES OF HYPERTENSION
o Juxtaglomerular cells → (↑) Renin → A.T-II (↑) → BP (↑)
(i) Isolated Systolic Hypertension:
Patients can have isolated systolic hypertension, this is
when the systolic Bp is elevated but the diastolic is
normal.
o For example: 135/74 (SBP is stage 1).

(ii) Isolated Diastolic Hypertension:

Similarly, patients can have isolated diastolic
hypertension
o For example: 110/92 (DBP is stage 2).

(iii) White Coat Hypertension: Figure 1: Increased Sympathetic Nervous System Activity
Patients only have high blood pressure at the doctor’s
office, it is normal at home. Risk factors: (↑) ETOH, (↑) Stress, (↑) Smoking
(2) RAAS
▪ This measures the Bp throughout the day. Renin (↑) → A.T-II (↑) → BP (↑)

(iv) Masked Hypertension

This is the opposite of White Coat Hypertension.
Bp is normal at the doctor’s office but very high at home.

If the average of 2 readings of blood pressure on 2

separate visits is high, or the 24 hour Ambulatory Bp
Monitoring is high, next approach:
o Find out the underlying cause

Figure 2: RAAS mechanism to increase BP

Risk factors: (↑) Glucose/Insulin (DM)

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 (3) High Na+ retention (4) (↑) SVR
(↑) Blood volume → BP (↑) → (↓) Renin (from kidneys) (i) (↑) Weight
o This is called Low Renin Hypertension
o It is common in African-Americans o Length (↑) → (↑) SVR → BP (↑)
o Clinical pearl: these patients do not respond to ARBs
(ii) (↑) Age
or ACE-I drugs. Diuretics are used to lower their BP
o Compliance (↓) → (↑) SVR → BP (↑)

Figure 3: Sodium retention and Low Renin Hypertension

Risk factors: (↑) Na+ diet, Ethnicity Risk factors: (↑) Age, (↑) Weight
Other risk factors: (↓) Activity, (↑) LDL, TGs levels

III) SECONDARY (2°) HYPERTENSION

(A) RENAL CAUSES (B) DRUG-RELATED CAUSES
5% of HTN patients (1) Sympathomimetics
Most commonly affected groups:
o Young patients (<30 y/o) + sudden, severe, refractory Cocaine, NMDA, Amphetamines, Adderall (ADHD drug)
HTN (do not respond to antihypertensive drugs) (i) SNS
(1) Renovascular disorders o (↑) SNS activity → NE/Epi → (↑) HR and SV →
(↑) CO → (↑) BP
(i) Fibromuscular Dysplasia (ii) Renal Artery Stenosis
o Young women > Men o Plaque in the renal artery (ii) Blood Vessels
o Dysplasia of the vessels o Vasoconstriction → (↑) TPR → (↑) BP
Possible presented vignette: (↑) HR + Nosebleed +
Tremors + HTN → Secondary HTN due to use of cocaine

(2) OCPs (Oral Contraceptives)

Figure 4: Renovascular disorders mechanism
OCPs containing Estrogen (or if patient is pregnant)
o Estrogen works on the liver to (↑) Angiotensinogen →
A.T-I → A.T-II → BP (↑)
(3) NSAIDs
NSAIDs (used in pain and fever)
o Inhibits the enzyme COX-2 (which helps form PGI2)

(2) Renal Parenchymal disorders (Macula densa cells in the DCTs release PGI2
(prostacyclin) → causes vasodilation)
(i) Diabetic Nephropathy
o Therefore, there is vasoconstriction → (↓) blood flow
o Patient with uncontrolled
→ (↓) GFR →
diabetes + CKD
▪ (↑) Na retention (+H2O) → Blood volume →
(ii) Polycystic Kidney Disease BP (↑)
▪ (↑) Renin → A.T-II (↑) → BP (↑)
(PCKD)
(iii) Glomerulonephritis

Figure 5: Renal
Parenchymal disorders
mechanism

(↓) GFR → Renin (↑) (by JG cells)→ A.T-II (↑) → BP (↑)

Mechanism of Angiotensin-II
When it increases → it acts on:
o Blood vessels → vasoconstriction → (↑) TPR → (↑) BP
o Adrenal glands → Aldosterone (↑) → Kidneys → Na
+ H2O retention (+ K excretion) → (↑) Blood volume
→ (↑) BP

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 (C) ENDOCRINE CAUSES
Many endocrine disorders cause hypertension through various mechanisms e.g. via sympathetic system activation, Sodium
and Water retention, etc.
(1) Adrenal Gland Disorders (iii) Epinephrine/Norepinephrine:
The adrenal glands produce many hormones that regulate
In Pheochromocytoma (caused by a tumor in the adrenal
BP like aldosterone, cortisol, norepinephrine, and
medulla) that ↑ production of Epinephrine and
epinephrine.
Norepinephrine.
(i) Aldosterone: o (↑) NE/Epi → (↑) SNS activity
▪ (↑) HR, ↑ Contractility, ↑ Vasoconstriction = (↑) BP
In case of hyperaldosteronism (can be caused by tumor
of the adrenal cortex)
(↑) Aldosterone → (↑) Na+ + H2O Reabsorption Clinical Presentation:
• Paroxysmal episodes of ↑↑↑ BP
o Aldosterone also excretes potassium. • Severe headaches
▪ Results in: ↓ Potassium ↑ Sodium (↑) BP • Palpitations
• Aldosterone also decreases protons in the blood, • Hyperglycemia
this increases pH causing metabolic alkalosis.

(ii) Cortisol:
(2) Thyroid Gland Disorders
Hypercortisolism (Cushing’s Syndrome) causes hypertension.
o ↑ Cortisol → (↑) sensitivity of SNS Both hyperthyroidism and hypothyroidism can cause hypertension.
Thyroid hormones primarily increases heart activity,
especially beta receptors.
• This (↑) HR, ↑ Contractility of the heart, and ↑ ▪ Therefore, when Norepinephrine and Epinephrine
vasoconstriction bind to beta receptors, the activity is amplified due
o Results in: (↑) BP to the thyroid hormones.
• (↑) HR, ↑ Contractility, (↑) CO → (↑) BP
In hyperthyroidism, there is a ↓ tone of vessels
Remember: In case of hypothyroidism, there is an ↑ tone of vessels
Cushing’s Syndrome Clinical Manifestation o This leads to ↓ diameter of the vessels which ↑
▪ Buffalo Hump resistance of blood flow
▪ Abdominal Striae ▪ ↑ total peripheral resistance (TPR) = (↑) BP
▪ Moon Face
▪ Thin Bones (3) Parathyroid Gland Disorders
▪ Hyperglycemia
In case of hyperparathyroidism, there is ↑ ↑ ↑ parathyroid
hormone (PTH)
PTH ↑ calcium levels in the blood (hypercalcemia)
o The calcium can accumulate in the smooth muscle
cells of the vessels
▪ (↑) contraction of the vessels and (↑) vasoconstriction

Figure 6. Adrenal, Thyroid and Parathyroid disorders can all cause hypertension

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 3 of 22

 (D) CARDIAC CAUSES
The main cardiac cause is the coarctation of the aorta.
o This is seen mainly in adults.
This is when there is a stenosis/narrowing of the aorta.
So when the blood is pumped out of the left ventricle,
there would be ↓ blood flow down the descending aorta
o This (↑) BP proximal to the stenosis and (↓) BP in the
descending aorta.
▪ Results in: (↑) BP in upper extremities, head and
neck.
• AND (↓) BP in lower extremities
As there is ↓ blood flow distal to the stenosis, ↓ renal
perfusion
o Kidney’s interpret it as (↓) BP so they release Renin.
o ↑ Renin → ↑ formation of A.T-II (↑ )→ (↑) BP

Clinical Presentation:
o Strong pulses of brachial/radial arteries compared to
lower extremity pulse.
o Bp in upper extremities is (↑) than Bp in lower Figure 7. Coarctation of Aorta increases pressure proximal to
extremities. obstruction and decreases pressure distal to the obstruction

(E) PULMONARY CAUSES

In Obstructive Sleep Apnea, the patients go into a
hypopnic state where they don’t take in air or exhale air.
oWhen not inhaling = ↓ O2 levels in blood (hypoxemia)
oWhen not exhaling = ↑ CO2 levels in blood
(hypercapnia)
▪ This ↑ sympathetic activity → (↑) HR, ↑
Contractility, (↑) Tone of vessels → (↑) BP

Clinical Presentation:
▪ Obese Patient
▪ Snores at night
▪ Wakes up with headache
▪ Tired and Lethargic throughout the day
Figure 8. Obstruction Sleep Apnea can cause hypertension
through SNS activation

(F) NEUROLOGICAL CAUSES

Whenever there is ↑ Intracranial Pressure there is a
reflexive (↑) BP (mechanism is unknown), this is part of
the Cushing’s Triad.

Cushing’s Triad:
o Hypertension
o Bradycardia
o Irregular Respiratory Patterns

Possible causes of ↑ ICP:

↑ Blood in brain (hemorrhage)
Mass/Abscess
↑ Fluid / Edema

Figure 9. Increased Intracranial Pressure can cause

hypertension through unknown mechanisms

(G) PREGNANCY CAUSES

The mechanism is unknown but there are 2 conditions Table 2. Pre-eclampsia vs Eclampsia
associated with hypertension; pre-eclampsia and PRE-ECLAMPSIA ECLAMPSIA
eclampsia.
o There is a high risk in patients >20 weeks. Hypertension
The difference between pre-eclampsia and eclampsia is
Proteinuria
that in eclampsia there are seizures.
Seizures

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 IV) COMPLICATIONS OF HYPERTENSION

(A) OVERVIEW

The complications could be acute or chronic

Target organs
o Central nervous system
o Eye
o Cardiac
o Vascular
o Lungs
o Renal

(B) CENTRAL NERVOUS SYSTEM

(1) Subarachnoid hemorrhage (2) Intracerebral/intraparenchymal hemorrhage

High blood pressure → causes a lot of stress (shearing Vessels coming from MCA (middle cerebral artery) called
forces) on the vessels lenticulostriate vessels
o Causes the vessels to dilate and even potentially Whenever these vessels are under high pressure (lots of
rupture shearing forces)
We can get ballooning of the vessels → aneurysms o Can also form tiny aneurysm → Charcot Bouchard
o E.g., berry aneurysms aneurysm
o Forms kind of little saccular type of aneurysm o And rupture into the parenchyma of the brain →
▪ Can rupture and blood can leak into intracerebral/intraparenchymal hemorrhage (ICH)
subarachnoid space ▪ Affects basal ganglia
• Causes subarachnoid hemorrhage (SAH) • Caudate nucleus
o Look and see their actual initial or presenting blood • Putamen
pressure was • Globus pallidus

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(3) Posterior reversible encephalopathy syndrome Clinical vignette
(PRES)
Patient present with
Hypertension alters the capillaries o Super high blood pressure
o Lose the ability to maintain the balance of fluid o Neurodeficits
moving in and out of the blood vessel ▪ Weakness on one side
Fluid start leaking outside the actual capillaries and ▪ Sensory change on one side
causes vasogenic edema ▪ Facial droop
o Especially on the posterior portion of the brain → ▪ Seizure
posterior reversible encephalopathy syndrome ▪ Altered mental status
(PRES) • Confused
o *Sometimes it even causes hemorrhage as well • Obtunded

(4) Lacunar infarct

Especially found in chronic long-standing hypertension
The little vessels supply a lot of areas
o Basal ganglia
o Midbrain
o Pons
o Cerebellum
Sometimes the vessels can get really thick because of
the hypertension over a long period of time
o They have to accommodate because remember with
high pressure
▪ We’re increasing the risk of blood pressure
rupturing
Because they’re more thick-walled
o It actually kind of making the lumen really small
▪ It reduces the blood flow
o Can’t get good amount of O2 delivery into the
tissue of the brain
▪ Develop infarct or stroke → lacunar infarct
▪ Very tiny subcortical infarcts that involves
• Internal capsule
• Basal ganglia
(C) RETINA

Clinical vignette (3) Cotton wool spots

Patient present with Whenever we have exudates and hemorrhages
o Blurry vision o We can get infarction of the retinal tissue → cotton
o Decreased vision wool spots
Get fundoscopy and take a look at the retina
(1) Arteriovenous (AV) nicking
What happens is whenever we have high blood pressure
o These arteries can get thicker and compress
nearby veins
o Making them look blind-ended at one point
(2) Microaneurysms and exudates

Figure 11. Cotton wool spots & hemorrhages [Besenczi, Renátó et

al.,2016]

(4) Papilledema
Chronic high blood pressure also can cause swelling of
the optic disc
Figure 10. Microaneurysm and exudates [Besenczi, Renátó et al.,2016] o Blurs the margin → papilledema
Whenever these actual small vessels under high
pressure, they can
o Form little aneurysm
o Rupture
▪ Get microhemorrhages
o Have some of the fluid can leak out from the
vessels → exudates

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 (D) CARDIAC
(1) Atherosclerosis on coronary vessels
Increase the risk of atherosclerosis (plaques developing
within the vessels) due to chronic hypertension
o Concern: coronary vessels
(2) Demand ischemia
Whenever someone has hypertension
o The heart has to work harder because of reduction in
blood flow
▪ They can have demand type of ischemia
(3) Increased risk of thrombus formation
Also, we may actually have enough pressure that
ruptures or fissures the actual covering of the plaques
o This increases the risk of thrombus
(4) Blood flow reduction due to stable or unstable
plaque → ischemic
Whether there’s a stable or unstable plaque that ruptures
and clot forms
o There can be a reduction in blood flow
Reduction in blood flow to the myocardium
o Less O2 is delivered into myocardium → ischemic
▪ Can lead to infarction
Classic type of complication
Patient who presents with coronary artery disease
They can present with
o NSTEMI
o STEMI
o Unstable or stable angina
Hypertension | Update
(5) Left ventricle hypertrophy → diastolic heart failure
Whenever someone has chronic hypertension
o Imagine the pressure inside of the aorta is really high
→ high afterload
o It means that the pressure that the left ventricle
has to exert has to be higher than the pressure
within the aorta
▪ In order to push enough blood out
We know we need high pressure in the left ventricle and
low pressure in the aorta to push enough blood out
Because of the increase in afterload because of chronic
hypertension
o The left ventricle compensates the high pressure
by thicken up → hypertrophy
▪ Bigger and stronger and able to generate more
force to push blood out of the left ventricle
Subsequently, because the left ventricle is thicker
o The actual diameter of the cavity of the left
ventricle is smaller
o We don’t fill them really well → reduction in diastolic
filling
Reduction in diastolic filling
o Blood starts backing up into the lungs
▪ Patient present with fluid in the lungs →
pulmonary edema
▪ Dyspnea (shortness of breath)
In acute condition like hypertensive crisis
o They can present with flash pulmonary edema
o Very high pressure that can actually push blood back
into the lung
(6) Left atrium hypertrophy → increased risk of atrial
fibrillation
In normal condition
o We want blood to go from the atria into the ventricles
But whenever the left ventricle is super thick
o The pressure inside the left ventricle is higher
o So the left atrium is like
▪ “I got to push blood down into this high pressure
ventricle! How am I going to be able to do it!?”
▪ Exact same issue that the left ventricle had
with the aorta
So, the left atrium also undergoes hypertrophy
o Alters the electrical activity
Imagine electrical activity moving through the thick left
atrium
o It’s going to be a lot more difficult to move through the
thick left atrium
So, it Increases the risk of atrial arrhythmias → atrial
fibrillation
CARDIOVASCULAR PATHOLOGY: Note #4. 7 of 22
 (E) VASCULAR ISSUES
Complication that can come from chronic hypertension
(1) Aortic dissection
Hypertension weakens the vessel walls
o Causes medial degeneration of the vessel wall
The blood that’s actually rushing through the lumen can
rip through the tunica intima
o Remember tunica intima is the internal lining of the
vessel
When it does that, it forms a false lumen
o Where blood can actually track into another area
that’s not the lumen of the blood vessel → aortic
dissection
This can happen to patients with chronic hypertension
and brief acute rise in blood pressure
(3) Atherosclerosis → claudication (peripheral artery
disease)
Damage the vessel wall → increase the risk of causing
plaque formation
Imagine the reduction in blood flow and trying to supply
the muscles of the lower extremities
o If we’re exerting ourselves and start having less O 2
squeeze through the tiny blood vessel into the
extremities
o Causes severe pain and weakness of the lower
extremities → claudication
▪ Very common In patients who have peripheral
artery disease
(F) RENAL SYSTEM
Remember the complications from long-standing
hypertension
o Thicken the vessels → atherosclerosis
▪ Atherosclerosis of the small renal vessel
Remember renal arteries come off and give off capillaries
o Supply O2 to the kidney tubules themselves
o Determine the urine production
Imagine we have to be able to get blood flow right
through these thickened renal arteries
o We have less filtration
o Less O2 delivery to the kidney tubule cells →
ischemic
▪ If we don’t reverse the problem
• They start to die → undergo lots of fibrosis
and sclerosis
o They stop functioning → kidneys can start to atrophy
→ kidney starts to fail → worsen the secondary
hypertension
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(2) Aortic aneurysm
Remember very high blood pressure puts a lot of stress
(shearing forces) on vessel walls
o Causes vessel to dilate or expand in response to
that
o Also weakens the blood vessel
If we think about a thin-walled vessel
o As we stretch it out, it gets really thin → easy to
rupture
The increase in diameter of the vessel due to
o Direct force (shearing force) on the vessel
o Thickening of the vasa vasorum
▪ If we zoom out on the vessel wall
• There are tiny blood vessels that supply the
actual blood vessels → vessels on vessels
(vasa vasorum)
In patient with high blood pressure
o Causes the vasa vasorum to become thick and
sclerotic
o Imagine blood flow having to squeeze through the tiny
vessels
▪ Can’t deliver O2 to the actual wall of the vessel →
the vessels start to die → vessel gets weaker
• Unable to maintain their normal shape
• Causes the diameter of the vessel wall to get
bigger
Remember if kidney fails
o Their GFR goes down
→ Renin goes up
→ Angiotensin II goes up
→ Blood pressure goes up
▪ It worsens the hypertension
• It’s a vicious cycle
If people have a super transient acute rise in blood
pressure
o It might be enough to actually rupture some of these
smaller capillaries in the glomerulus
▪ Leak some of the components into the actual urine
→ red blood cells (hematuria)
As the kidneys start failing
o They actually lose the ability to regulate very
specific protein in urine → albumin
▪ We can lose them into the urine over time
(albuminuria)
Hypertension | Update
 V) HYPERTENSIVE CRISIS
Potential complications
o Someone doesn’t have their medication
▪ Not establishing good control
o They have very significant stress factor
▪ Causes their blood pressure to skyrocket

(A) HYPERTENSIVE URGENCY (B) HYPERTENSIVE EMERGENCY

Just the number ▪ Very important one
o Systolic blood pressure ≥ 180mmHg ▪ High blood pressure
o Diastolic blood pressure ≥ 120mmHg • Systolic blood pressure ≥ 180mmHg
• Diastolic blood pressure ≥ 120mmHg
No target organ damage
▪ Specifically, they have target organ damage associated
o Doesn’t damage the brain
with high blood pressure
▪ No ICH
▪ No Subarachnoid hemorrhage (1) Neurological
▪ No signs of PRES or lacunar infarcts
Intracerebral hemorrhage (ICH)
o Don’t have any particular damage to the heart
Subarachnoid hemorrhage (SAH)
▪ No types of coronary artery disease
Posterior related encephalopathy syndrome (PRES)
▪ No heart failure
The patients present in a ton of different ways
▪ No atrial fibrillation
o If they have a bleed or stroke
o No retinal injuries
o Look for any signs of neurodeficits
o No vascular issues like aortic dissection, aortic
▪ Weakness on one side
aneurysm, peripheral artery disease
▪ Sensory change
o No renal injury
▪ Ataxia
▪ Cranial nerve palsies
▪ Lethargic
▪ Altered mental status
▪ Delirious
▪ Confused
▪ Seizure
(2) Kidney
Bleed into the urine → hematuria on urinalysis
Acute kidney injury
o Deceased in urine output
o Increased BUN and creatine
(3) Cardiac
Left atrium and left ventricle hypertrophy
o Their heart has to work so hard
Plaques in vessel wall may
o Worsen demand ischemia
o Cause NSTEMI
Diastolic heart failure
o Pulmonary edema
▪ Shortness of breath
▪ Rales on auscultation
▪ Pulmonary edema on CXR
o If we see pulmonary edema
▪ Indicative of left sided heart failure
▪ Which can also be a result of high blood pressure
(4) Vascular
Different blood pressure in each arm
o Pain that radiates into their back
o Got a lot of deficits that come from aortic dissection
▪ Hypotensive
▪ Have palpable mass
▪ Lots of abdominal pain
(5) Retina
Fundoscopy
o Signs of AV nicking
o Cotton wool spots
o Microhemorrhages
o Exudates
o Papilledema
o Evidence of retinal damage

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 9 of 22

 VI) DIAGNOSIS/WORKUP FOR HYPERTENSION

(A) ESSENTIAL HYPERTENSION WORKUP

Look at their risk factors: Stages of hypertension
o Family History o Stage I Hypertension: > 130/80
o Old age o Stage II Hypertension: > 140/90
According to the AHA guidelines, diagnosis requires: o Hypertension Crisis: > 180/120
o Average of ≥ 2 readings on two separate visits, or
o Ambulatory blood pressure monitoring

(B) SECONDARY HYPERTENSION WORKUP

Can be seen in:
o Young patients
o Sudden and/or severe cases of hypertension
o Refractory hypertension in patients already taking multiple medications
Diagnostic tests can be done to rule out certain conditions
(1) Renal Vascular Diseases (4) Endocrine Diseases
Listen for bruits using a stethoscope Test for Aldosterone Level
▪ Bruits may cause reduced renal blood flow ▪ High aldosterone levels
Renal Ultrasound
▪ Can check for:
Test for Renin Level
▪ High aldosterone subsequently causes low renin
Doppler Study
▪ Can show reduced pulmonary blood flow
Basic Metabolic Panel
Basic Metabolic Panel (BMP)
▪ Aldosterone causes sodium to be absorbed and
▪ BUN and Creatinine
potassium to be excreted; aldosterone results in:
• Can be seen in Chronic Kidney Disease
o If there’s kidney damage, kidney tubules
aren’t as efficient in maintaining normal
▪ Elevated glucose levels
levels of BUN and creatinine
Urinalysis 24-hour Urine Cortisol
▪ Can show:
▪ Will indicate very high levels of cortisol
• Proteinuria
o Protein in urine ▪ The following signs may also be seen:
o Must be followed up with an albumin study
• Hematuria
o RBCs in urine
(2) Cardiac Conditions (i.e., Aortic Coarctation)

Compare BPs of extremities 24-hour Urine Metanephrine Test

▪ BP of Upper Extremities will be greater than BP of ▪ High metanephrine levels
Lower Extremities • Breakdown product of epinephrine and
norepinephrine
Check for brachial-femoral artery delay • Seen in Pheochromocytoma
▪ Pulses of the brachial radial artery will come way o Benign tumor that produces excess amounts of
before the femoral artery epinephrine and norepinephrine
o The following signs and symptoms may
Chest X-Ray also be observed in the patient:
▪ Can show rib notching
• Part of the rib is “chewed away”
▪ Can show the “Figure of 3 sign”
(3) Drug Use
Adrenal MRI
Ask Patient for the List of Drugs They’re Taking
▪ Can be done to check for a mass in the adrenal
▪ May include, but not limited to the following: medulla or in cases of hyperaldosteronism
TSH with Reflex
▪ Thyroid stimulating hormone (TSH) level can
Urine Toxicology Screen check for hyperthyroidism or hypothyroidism
Test for PTH and Calcium Levels
▪ Test for drugs if you suspect that the patient is
▪ Can check for hyperparathyroidism:
utilizing sympathomimetics that they shouldn’t be
• High levels of parathyroid hormone (PTH)
using (e.g., not prescribed to them)
• High levels of calcium (Ca2+)
• Patient may also show early signs of osteoporosis
▪ You can also test for the phosphate levels

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 (5) Pulmonary Diseases (7) Pregnancy

(i) Sleep Study (i) Pregnancy Test

▪ Can test for obstructive sleep apnea ▪ Check for presence of β-hCG

(ii) Urinalysis and/or 24-hour Urine Study

• Conduct if patient presents with the following: ▪ Done if patient is:

▪ To check for proteinuria

o Observe for evidence of seizures that

may progress in patients with eclampsia
(6) Neurological Diseases

(i) CT or MRI Imaging of the Brain

▪ To visualize the brain and check for:

▪ A severe neurological injury may cause a patient

to be obtunded, stuporous, or comatose
▪ Patient presents with neurological deficits
• Consider Cushing’s triad from a neurological
injury when you observe the following:

(C) COMPLICATION WORKUP

Essentially the same workup in secondary hypertension
(1) Neurological Complications (4) Vascular Complications
Consider if patient presents with a bleed, stroke, seizures, Consider if patient presents with:
PRES, any neurological deficits.
(i) CT or MRI Imaging
(2) Renal Complications (i) Abdominal Ultrasound
Consider if patient presents with urine output and bruits ▪ Can show abdominal aortic aneurysm
(i) Basic Metabolic Panel (BMP)
(ii) Echocardiogram
▪ BUN and Creatinine
(ii) Urinalysis ▪ Can show proximal aortic dissection
▪ Hematuria (iii) Computed Tomography Angiography (CTA)
(iii) Renal Ultrasound
▪ Can show aortic dissection
(3) Cardiac Complications
(5) Retinal Complications
Consider if patient presents with:
(i) Fundoscopy
▪ Observe the retina for any kinds of retinopathy

(i) EKG
▪ Can show ST segment elevation or depression
(ii) Echocardiogram
▪ Can check for evidence of heart failure (e.g.,
diastolic heart failure)
(iii) Chest X-Ray
▪ Can show pulmonary edema that occurs in
diastolic heart failure
(iv) Check for Troponin Level
▪ If EKG shows ischemic heart disease (e.g., STEMI)

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 11 of 22

 VII) TREATMENT OF HYPERTENSION

(A) LIFESTYLE MODIFICATIONS

Must always be advocated in all patients: (1) Weight Loss
o To reverse or stop hypertension from worsening o Most effective, especially in patients who:
o Even to patients without hypertension ▪ Are obese
▪ Have poor diet
(2) Exercise
(3) DASH Diet
(4) Low Sodium Diet
(5) Reduce Alcohol Consumption
Figure 12. Lifestyle Modifications
(6) Smoking Cessation

(B) MEDICAL MANAGEMENT

Start medications in patients whose BP is:
o > 140/90, or
o > 130/80 with many risk factors for cardiovascular
diseases

Monotherapy may not work if patient’s BP is really high.

o Systolic BP is at least 15-20mmHg greater than 140
o Use a combination therapy of 2 drugs

Figure 13. Pharmacologic Management of Hypertension

(1) First Line Medications

(i) Angiotensin-converting enzyme inhibitors (ACE-I)
(iii) Dihydropyridine Calcium Channel Blockers (CCBs)
▪ Drugs that end in “-pril”
▪ Drugs that end in “-dipine”

▪ Mechanism of action:
▪ Good in patients with the following conditions:
• Works on the vascular smooth muscle:
relaxes or dilates blood vessel

▪ May cause the following adverse reactions: ▪ Good in African-American patients who usually
have low-renin hypertension

(iv) Thiazide Diuretics

o Take caution in prescribing to patients with
asthma or COPD ▪ Examples:
▪ Mechanism of action:
• Works on the Renin-Angiotensin-Aldosterone
System (RAAS): Reduces production of ▪ Mechanism of action:
angiotensin II • Increases urine excretion of sodium and water
o Na+ in the blood  H2O in the blood 
blood volume  blood pressure

(ii) Angiotensin receptor blockers (ARBs) ▪ Useful in the following patients:

▪ Drugs that end in “-sartan” • African-Americans with low-renin
hypertension
o They have increased sodium retention
▪ Good in patients with the following conditions: • Patients with osteoporosis
o Thiazides help with calcium reabsorption
in the bloodstream
▪ Contraindications:
• Do not use in patients with gout: can increase
▪ Mechanism of action: uric acid concentration
• Also works on the RAAS: Blocks angiotensin
II at its receptor

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 (2) Second Line Medications

(i) Beta Blockers

▪ Drugs that end in “-lol”

▪ Good in patients with the following conditions:

▪ Contraindications:
• Be careful in prescribing beta blockers in
patients with the following conditions:
o COPD/Asthma
▪ Non-selective beta blockers can bind
onto the β2 receptors in the airways 
bronchoconstriction  worsen
▪ Not an absolute contraindication
o Bradycardia (HR)
▪ Beta blockers can lower the HR further
and may cause a syncopal event
o Decompensated Heart Failure
▪ Patients with acute heart failure may
already have heart contractility and
ejection fraction
• Beta blockers will further decrease
contractility  stroke volume 
cardiac output  BP
o Hypoglycemia
▪ Beta blockers blunt the sympathetic
signs of a hypoglycemic crisis:

(ii) Aldosterone Antagonists

▪ Example: Figure 14. Treatment of Hypertension with Comorbidities

▪ Good in patients with the following conditions

(reduces mortality):

▪ Mechanism of Action
• Blocks aldosterone
o Recall: aldosterone reabsorbs sodium and
excretes potassium

▪ Adverse Effect:
• Hyperkalemia

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 13 of 22

 (C) PREGNANCY

(1) Drugs Safe/Indicated for Use in Pregnancy (2) Unsafe Drugs During Pregnancy

(i) Hydralazine The following drugs are unsafe for use during pregnancy

▪ Direct vasodilator (i) ACE-I and ARBs

(ii) Methyl-DOPA ▪ Have been shown to be teratogenic

▪ Alpha-2 agonist (ii) Thiazides

(iii) Labetalol ▪ Not absolutely contraindicated, but generally
avoided
▪ Beta and alpha blocker • Thiazides decrease blood volume 
(iv) Nifedipine Decreases placental perfusion

▪ Calcium Channel Blocker

Mnemonic for Agents to Use in Pregnancy: Healthy

Moms Love Nifedipine
Hydralazine
Methyl-DOPA
Labetalol
Nifedipine

Figure 15. Treatment for Hypertension During Pregnancy

(D) HYPERTENSION EMERGENCY

Hypertensive urgency is treated with the previously discussed drugs under medical management
In cases of hypertensive emergency, their BP must be dropped immediately
o Medical management is not enough/too slow

(1) Dropping the Blood Pressure
(i) Assess patient for hypertension emergency
▪ Assess their initial BP
• BP must be > 180/120
▪ There is target organ damage
(ii) Decrease BP by 25% of initial BP in the 1st hour
▪ Proceed to next step if patient tolerates it
(2) Avoid Dropping the BP Too Quickly
Dropping the BP too fast can cause ischemic
complications
o May cause low/no perfusion to the brain  stroke
o May cause low/no perfusion to the coronaries 
myocardial infarction
o May cause low/no perfusion to the kidneys  acute
kidney injury

(iii) Decrease BP to < 160/100 over the next 2-6

hours
▪ If tolerated, proceed to next step

(iv) Slowly drop to patient’s baseline BP over the

next two days

Figure 17. Avoid Dropping the BP Too Quickly in Hypertensive

Emergencies

Figure 16. Guidelines in Management of Hypertension

Emergency

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 (3) Intravenous (IV Agents)

(i) Nicardipine
▪ Most common IV agent used for hypertensive
emergency

(ii) Labetalol
▪ Most common IV agent used for hypertensive
emergency

(iii) Hydralazine
(iv) Esmolol
▪ May be beneficial in patients with an aortic
dissection

(v) Nitroprusside
▪ Not commonly utilized

(vi) Nitroglycerin
▪ May be helpful in patients who have left heart
failure with pulmonary edema

Figure 18. IV Agents for Hypertensive Emergency

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 15 of 22

 VIII) APPENDEX

Table 3. Abbreviations
Abbreviations
HTN: Hypertension ARBs: Angiotensin Receptor Blockers
BP: Blood Pressure ACE-I: Angiotensin-converting enzyme Inhibitors
SNS: Sympathetic Nervous System Na+: Sodium
NE: Norepinephrine K+: Potassium
Epi: Epinephrine SVR: Systemic Vascular Resistance
HR: Heart Rate LDL: Low-density Lipoproteins
SV: Stroke Volume TGs: Triglycerides
CO: Cardiac Output CKD: Chronic Kidney Disease
MAP: Mean Arterial Pressure JG cells: Juxtaglomerular cells
TPR: Total Peripheral Resistance NMDA: N-methyl-D-aspartate
A.T-I: Angiotensin-I ADHD: Attention Deficit Hyperactivity Disorder
A.T-II: Angiotensin-II GFR: Glomerular Filtration Rate
RAAS: Renin-Angiotensin-Aldosterone System NSAIDs: Non-steroidal Anti-inflammatory Drugs
DM: Diabetes Mellitus ICP: Intracranial Pressure

Table 4. Summary of the Secondary Causes of Hypertension

Causes Disorder Mechanism

Renovascular Disorders
o Fibromuscular Dysplasia, Renal (↓) Renal blood flow → Renin (↑) → A.T-II (↑) → (↑) BP
RENAL Artery Stenosis

Renal Parenchymal Disorders

o Diabetic Nephropathy, PCKD, (↓) GFR → Renin (↑) (by JG cells)→ A.T-II (↑) → (↑) BP
Glomerulonephritis

Sympathomimetics (↑) SNS activity → NE/Epi → (↑) HR and SV →

o Cocaine, NMDA, (↑) CO → (↑) BP
Amphetamines, Adderall, etc. Vasoconstriction → (↑) TPR → (↑) BP
DRUGS Estrogen works on the liver to (↑) Angiotensinogen → A.T-I → A.T-II
OCPs → (↑) BP
Vasoconstriction → (↓) blood flow → (↓) GFR →
NSAIDs (↑) Na retention (+H2O) → Blood volume → (↑) BP
(↑) Renin → A.T-II (↑) → BP (↑)

(↑) Aldosterone → (↑) Na+ + H2O Reabsorption → (↑) Blood Volume

→ (↑) BP
Adrenal Gland
(↑) Cortisol→(↑) sensitivity of SNS → alpha & beta receptors have (↑)
o Hyperaldosteronism,
sensitivity to Epi and NE→(↑) HR, (↑) Heart Contractility and (↑)
Hypercortisolism,
vasoconstriction → (↑) BP
Pheochromocytoma
(↑) NE/Epi → (↑) SNS activity→ (↑) HR, (↑) Heart Contractility and (↑)
vasoconstriction → (↑) BP
ENDOCRINE
In hyperthyroidism, thyroid hormones primarily increases heart
activity, especially beta receptors.
Thyroid Gland ▪ NE/Epi bind to beta receptors, the activity is amplified due to
o Hyperthyroidism and the thyroid hormones.
hypothyroidism • (↑) HR, (↑) Contractility, (↑) CO → (↑) BP
In hypothyroidism, ↑ tone of vessels → (↓) diameter of vessels →
(↑) resistance of blood flow (↑) TPR → (↑) BP

Parathyroid Gland (↑) calcium → accumulate in the smooth muscle cells of the vessels →
o Hyperparathyroidism (↑) contraction of the vessels = (↑) vasoconstriction (↑) TPR → (↑) BP
(↑) BP proximal to the stenosis and (↓) BP in the descending aorta.
▪ Results in: (↑) BP in upper extremities, head and neck AND (↓)
BP in lower extremities
CARDIAC Coarctation of Aorta (↓) blood flow distal to the stenosis → (↓) renal perfusion
o Kidney’s interpret it as (↓) BP so they release Renin.
o (↑) Renin → (↑) formation of A.T-II (↑)→ (↑) BP

(↓) O2 levels (hypoxemia) + (↑) CO2 levels (hypercapnia) → (↑) SNS

PULMONARY Obstructive Sleep Apnea activity → (↑) HR, (↑) Contractility, (↑) Tone of vessels → (↑) BP

Anything that (↑) ICP(hemorrhage, (↑) ICP→ (↑) BP (mechanism is unknown), this is part of the Cushing’s
NEUROLOGIC Triad.
abscess, edema, etc.)

PREGNANCY Pre-eclampsia and Eclampsia o UNKNOWN, There is a high risk in patients >20 weeks.

16 of 22 CARDIOVASCULAR PATHOLOGY: Note #4. Hypertension | Update

 Table 5. Summary of Essential Hypertension
Causes Risk Factors MoA Diagram

Heart
(↑) SNS activity

Beta receptors → HR (↑)

Myocardial contractile cells → (↑) Contractility → (↑) SV
(Remember; CO = HR x SV) → CO (↑)
(↑) ETOH (Remember; MAP = CO x TPR) → BP (↑)
(↑) Stress
Blood vessels
(↑) Smoking
Alpha-1 receptors → Vasoconstriction → (↑) Resistance
→ (↑) BP

Kidneys
Juxtaglomerular cells → (↑) Renin → A.T-II (↑) → (↑) BP
RAAS

(↑) Glucose/ (↑) Renin → (↑) A.T-II → (↑) BP

Insulin (DM)
High Na+
retention

(↑) Na+ diet (↑) Blood volume → (↑) BP→ (↓) Renin (from kidneys)
Ethnicity o This is called Low Renin Hypertension

(↑) Weight
(↑) SVR

(↑) Age
(↑) Weight (↑) Length → (↑) SVR → (↑) BP
(↓) Activity
(↑) LDL, TGs (↑) Age
levels (↓) Compliance → (↑) SVR → (↑) BP

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 17 of 22

 Table 6. Complication of hypertension
Target Damage Clinical Presentation Diagram
Organ

(1) Subarachnoid hemorrhage

Ballooning of the vessels → aneurysms
o E.g., berry aneurysms
o Forms kind of little saccular type of aneurysm
▪ Can rupture and blood can leak into
subarachnoid space
• Causes subarachnoid hemorrhage
(SAH)
(2) Intracerebral/intraparenchymal hemorrhage
Lenticulostriate vessels are under high pressure
(lots of shearing forces)
o Can also form tiny aneurysm → Charcot
Bouchard aneurysm
o And rupture into the parenchyma of the brain →
intracerebral/intraparenchymal hemorrhage
(ICH) Super high blood
▪ Affects basal ganglia
NEUROLOGIC

pressure
• Caudate nucleus Neurodeficits
• Putamen o Weakness on one
• Globus pallidus side
o Sensory change on
(3) Posterior reversible encephalopathy syndrome
one side
(PRES)
o Facial droop
Hypertension alters the capillaries o Seizure
o Lose the ability to maintain the balance of fluid o Altered mental
moving in and out of the blood vessel status
Fluid start leaking outside the actual capillaries and ▪ Confused
causes vasogenic edema ▪ Obtunded
o Especially on the posterior portion of the brain
→ posterior reversible encephalopathy
syndrome (PRES)
o *Sometimes it even causes hemorrhage as well
(4) Lacunar infarct
Vessels can get really thick because of the chronic
hypertension
Because they’re more thick-walled
o Makes lumen really small
▪ It reduces the blood flow
o Can’t get good amount of O2 delivery into the
tissue of the brain
▪ Develop infarct or stroke → lacunar infarct
▪ Very tiny subcortical infarcts that involves
• Internal capsule
• Basal ganglia

(1) Arteriovenous (AV) nicking

High blood pressure → arteries can get thicker and
compress nearby veins
o Making them look blind-ended at one point
(2) Microaneurysms and exudates
Whenever these actual small vessels under high
pressure, they can
RETINA

o Form little aneurysm

o Rupture
▪ Get microhemorrhages Blurry vision
o Have some of the fluid can leak out from the Decreased vision
vessels → exudates
(3) Cotton wool spots
Whenever we have exudates and hemorrhages
o We can get infarction of the retinal tissue →
cotton wool spots
(4) Papilledema
Chronic high blood pressure also can cause swelling
of the optic disc
o Blurs the margin → papilledema

18 of 22 CARDIOVASCULAR PATHOLOGY: Note #4. Hypertension | Update

 (1) Atherosclerosis on coronary vessels
(2) Demand ischemia
The heart has to work harder because of reduction in
blood flow due to hypertension
(3) Increased risk of thrombus formation
Also, we may actually have enough pressure that
ruptures or fissures the actual covering of the plaques
o This increases the risk of thrombus
(4) Blood flow reduction due to stable or unstable
plaque → ischemic
Reduction in blood flow to the myocardium Patient who presents
o Less O2 is delivered into myocardium → ischemic with coronary artery
▪ Can lead to infarction disease
They can present with
(5) Left ventricle hypertrophy → diastolic heart o NSTEMI
o STEMI
Cardiac

failure
o Unstable or stable
Because of the increase in afterload because of angina
chronic hypertension Diastolic heart failure
o The left ventricle compensates the high o Pulmonary edema
pressure by thicken up → hypertrophy ▪ Shortness of
Subsequently, because the left ventricle is thicker breath
o The actual diameter of the cavity of the left ▪ Rales on
ventricle is smaller auscultation
o We don’t fill them really well → reduction in Atrial fibrillation
diastolic filling
Reduction in diastolic filling
o Blood starts backing up into the lungs
▪ Patient present with fluid in the lungs →
pulmonary edema
▪ Dyspnea (shortness of breath)

(6) Left atrium hypertrophy → increased risk of

atrial fibrillation
Left atrium also undergoes hypertrophy
o Alters the electrical activity
Increases the risk of atrial arrhythmias → atrial
fibrillation

(1) Aortic dissection

Hypertension weakens the vessel walls
o Causes medial degeneration of the vessel wall
The blood that’s actually rushing through the lumen
can rip through the tunica intima → forms a false
lumen
o Where blood can actually track into another
area that’s not the lumen of the blood vessel →
aortic dissection
VASCULAR

(2) Atherosclerosis → claudication (peripheral

artery disease) Different blood pressure
Damage the vessel wall → increase the risk of causing in each arm
plaque formation Claudication
Reduction in blood flow to lower extremities Tearing chest pain
o Causes severe pain and weakness of the lower Palpable mass
extremities → claudication Lots of abdominal pain

(3) Aortic aneurysm

Very high blood pressure puts a lot of stress (shearing
forces) on vessel walls
o Causes vessel to dilate or expand in response to
that
o Also weakens the blood vessel
o As we stretch it out, it gets really thin → easy to
rupture
The increase in diameter of the vessel due to
o Direct force (shearing force) on the vessel
o Thickening of the vasa vasorum

Hypertension | Update CARDIOVASCULAR PATHOLOGY: Note #4. 19 of 22

 Thickened renal arteries
o Less filtration
RENAL SYSTEM
o Less O2 delivery to the kidney tubule cells →
ischemic
Kidney starts to fail → worsen the secondary Hematuria
hypertension Albuminuria
Rupture some of these smaller capillaries in the Acute kidney injury
glomerulus o Decreased urine
o Leak some of the components into the actual urine output
→ red blood cells (hematuria) o Increased BUN and
As the kidneys start failing creatinine
o They actually lose the ability to regulate very
specific protein in urine → albumin
▪ We can lose them into the urine over time
(albuminuria)

20 of 22 CARDIOVASCULAR PATHOLOGY: Note #4. Hypertension | Update

 IX) REVIEW QUESTIONS
1) According to American Heart Association, which is
the most accurate way to measure blood pressure?
a) The average of 2 readings of blood pressure on a
visit
b) The average of 2 readings of blood pressure on 2
separate visits
c) The average of 3 readings of blood pressure on 2
separate visits
d) The average of 3 readings of blood pressure on 3
separate visits
2) A patient comes back to the doctor’s office for a
follow-up, their main complaint was severe
headaches and palpitations they claim that their bp
was 135/85 when they measured, you take their blood
pressure and it is 110/70, what is your next
approach?
a) Send them home because their bp is normal
b) Prescribe the patient Antihypertensive drugs
c) Put them under 24-hour ambulatory bp monitoring
d) Hospitalize the patient and observe
3) A patient presents with tachycardia and
hypertension, he’s having tremors and you observe
his nose bleeding, what is the diagnosis and cause of
his symptoms?
a) Essential tremor, Intake of propranolol
b) Secondary HTN, Intake of cocaine
c) Overactive thyroid gland
d) Heart attack
4) How do you treat patients who have hypertension
but the renin level is low?
a) ACE-Inhibitors
b) Angiotensin Receptor Blockers
c) Diuretics
d) High sodium diet
5) A 40 year old female patient comes to you presenting
with obesity, buffalo hump and moon face, you check
her glucose levels and they are high, she also has
hypertension. What is the most likely cause of that
high blood pressure?
a) Hyperaldosteronism
b) Obstructive Sleep Apnea
c) Hypercortisolism
d) Hyperthyroidism
6) In which weeks of gestation is preeclampsia and
eclampsia most likely?
a)>10 weeks
b)10-15 weeks
c)15-20 weeks
d)>20 weeks
7) Which mechanism leads to hypertension in patients
with hyperparathyroidism?
a) ↑ ICP → ↑ BP
b) ↑ TPR = ↑ BP
c) ↑ Na+ + H2O Reabsorption → ↑ BV → ↑BP
d) ↑ Renin → ↑ formation of AgII = ↑ Bp
8) In which pathology is the bp higher in the upper
extremities compared to lower extremities?
e) Hyperthyroidism
f) Cushing’s Triad
g) Coarctation of Aorta
h) Pheochromocytoma
Hypertension | Update
This scenario is used to answer question no. 9-12
A 60 y.o. male patient present with altered mental status
and dyspnea. Physical exam reveals blood pressure of
185/135mmHg and rales on lung auscultation. It was
revealed that the patient has hypertension over 15 years.
He was prescribed losartan to control the hypertension in
the past 10 years regularly. But he stopped taking the
medicine regularly a year ago. Chest X-Ray reveals
pulmonary edema and cardiomegaly. EKG was taken and
revealed atrial fibrillation with RBBB pattern. Urinalysis
shows hematuria and albuminuria.
9) The patient is most likely classified as
a) Grade I hypertension
b) Grade II hypertension
c) Hypertensive urgency
d) Hypertensive emergency
10) In response to number 9, why did you classify the
patient with the answer you chose? (May choose
more than 1)
a) The patient had super high blood pressure
b) The patient had chronic hypertension
c) The patient had evidence of organ failure shown by
urinalysis (hematuria and albuminuria)
d) The patient had possibly diastolic heart failure due to
having rales on lung auscultation
11) None of the damaged organs in this patient might
worsen the hypertension
a) True
b) False
12) What are other complications that could be found in
this patient related to the hypertension if left
uncontrolled?
a) Aortic dissection
b) Claudication
c) Left ventricle atrophy
d) Myocardial infarction
e) Papilledema
f) Sick sinus syndrome
g) Total heart block
13) Which of the following drugs is unsafe during
pregnancy?
a) Hydralazine
b) Methyl-DOPA
c) Lisinopril
d) Nifedipine
14) Which of the following drug classes are considered
first line medications in low-renin hypertension?
a) Angiotensin-Converting Enzyme Inhibitor
b) Angiotensin receptor blockers (ARBs)
c) Beta blockers
d) Thiazides
15) What is the mechanism of action of the drug class
that is contraindicated in patients with gout?
a) Relaxes or dilates blood vessel
b) Increases urine excretion of sodium and water
c) Blocks angiotensin II at its receptor
d) Reduces production of angiotensin II
16) Which of the following is a correct step in
management of a hypertensive emergency>
a) Decrease BP by 35% of initial BP in the 1st hour
b) Decrease BP to < 160/100 over the next 2-6
hours
c) Slowly drop to patient’s baseline BP over the next
three days
d) All steps are correct.
CARDIOVASCULAR PATHOLOGY: Note #4. 21 of 22
17) All of the following medications for hypertension
are also proven to be good for patients with coronary
artery disease and heart failure, EXCEPT:
a) Angiotensin-Converting Enzyme Inhibitor
b) Angiotensin receptor blockers (ARBs)
c) Beta blockers
d) Aldosterone antagonists
e) None of the above
X) REFERENCES
● Besenczi, Renátó & Tóth, János & Hajdu, András. (2016). A
Review on Automatic Analysis Techniques for Color Fundus
Photographs. Computational and Structural Biotechnology Journal.
14. 10.1016/j.csbj.2016.10.001.
● Le T. First Aid for the USMLE Step 1 2020. 30th anniversary
edition: McGraw Hill; 2020.
● Group A Streptococcal (GAS) Disease. (2021 Mar 22).
Retrieved from: https://www.cdc.gov/groupastrep/diseases-
public/post-streptococcal.html
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● Gupta-Malhotra et al.. Essential Hypertension vs. Secondary
Hypertension Among Children. American Journal of Hypertension
.2014.
● Papadakis MA, McPhee SJ, Rabow MW. Current Medical
Diagnosis &amp; Treatment 2018. New York: McGraw-Hill
Education; 2017.
● Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
Kluwer; 2020.
● Svetkey LP, McKeown SP, Wilson AF. Heritability of Salt
Sensitivity in Black Americans. Hypertension .1996.
● Unger T, Borghi C, Charchar F, et al. 2020. International Society
of Hypertension Global Hypertension Practice Guidelines..
Hypertension (Dallas, Tex. : 1979) .2020.
● Viera AJ, Neutze DM. Diagnosis of Secondary Hypertension: An
Age-Based Approach. Am Fam Physician .2010.
● Williams DA. Pance Prep Pearls. Middletown, DE: Kindle Direct
Publishing Platform; 2020.
Hypertension | Update