Case Presentation:

HYPERTENSION
Group 4
Case:
A 35 year old man presents with a blood pressure of
150/90 mmHg. He has been generally healthy, is sedentary,
drinks several cocktails per day and does not smoke cigarettes.
He has a family history of hypertension and his father died of
Myocardial Infarction at age 55. Physical examination is
remarkable only for moderate obesity. Total cholesterol is 220
and HDL cholesterol level is 40mg/dL. Fasting glucose
175mg/dL. Chest x-ray is normal. ECG shows LV
enlargement.
 📌Elevated blood
pressure

📌 Sedentary lifestyle

1.
📌 Alcohol intake

📌 Family history

📌 Obesity
What are the
📌 Increased
risk factors of cholesterol level

the disease? 📌 Comorbidities

Elevated Blood Pressure
Sedentary Lifestyle

▣ associated with other risk factors that may

contribute to the elevation of blood
pressure levels
▣ leads to the development of systemic arterial
hypertension (SAH).
▣ one of the major risk factors for cardiovascular
diseases
Alcohol Intake

▣ CNS Alcohol induced hypertension – alcohol

increases sympathetic outflow, secondary
to the release of corticotropin- releasing
hormone.
▣ Baroreceptor impairment
▣ Sympathetic nervous system in alcohol-
induced hypertension
▣ Contain calories and may contribute to
unwanted weight gain – a risk factor for
▣ Interfere with the effectiveness and increase
the side effects of some of the blood
pressure medications
Family History

▣ Family history is an important non-modifiable

risk factor for hypertension.
▣ The hereditary nature of hypertension is well
established by numerous family studies,
demonstrating associations of blood
pressure among siblings and between
parents and children.
Obesity

▣ Indicators for risk of hypertension include

obesity, abdominal obesity, weight gain,
and fat distribution
▣ measured by body mass index (BMI)
Normal BMI : 20-25
Overweight : 25-29.9
Obese : >30
▣Weigwas associated with increased risk of
developing hypertensionht gain
Increased Cholesterol Level

▣ If your cholesterol is high:

• excess oily stuff will stick to arterial walls
• over time, leads to fatty build up
• then hardens forming plaque
▣ Blood vessels become stiff and narrowed
• blood no longer flows through them as
easily as it once increase in the blood
pressure.
▣ Ultimate danger:
blood clot  block blood flow severe
cardiovascular event.
▣
Comorbidities

▣ Diabetes mellitus

▣ Left ventricular hypertrophy

 📌 Chest pain

📌 Difficulty of
breathing

2. 📌 Fatigue

📌 Vision problems
Signs and 📌 Severe headache
symptoms of
📌 Irregular
the disease? heartbeat
 3. A thorough
cardiovascular
assessment
What will you
find in the
physical exam? IAPePa
Physical Exam

▣ Assessment of the neck vessels – are the jugular veins

distended?
▣ Cardiovascular assessment- IAPePa
□Inspection: Visual assessment on the chest of the
patient. Note if there are any signs of swelling,
Pectus Excavatum or Carinatum
□Auscultation: Note for any murmurs, bruits, gallops
and (pulmonary) wheezes.
□Percussion: Note any dullness all over the area
could be suggestive of abnormal growth of a mass or
cardiomegaly.
□Palpation: Palpation allows you to assess the neck
for tenderness, abnormal temperature, excessive
moisture, pulsations, or masses.
▣ Edema
 4.
What is your
diagnosis? Hypertension
 📌 Urinalysis

📌 Blood chemistry

5. 📌 HbA1c

📌 Serum electrolyte

What are the 📌 Repeat FPG TEST

laboratories 📌 Thyroid function
that you will
📌 Echocardiogram/
request? 2D
 6.
Discuss
hypertension.
 Hypertension

Definition:

▣Systolic BP of >140 mm Hg
and/or
Diastolic BP of >90 mm Hg on
more than one occasion.

▣ HIGH BLOOD PRESSURE

.
Classification

▣ Essential (primary) hypertension - unknown

cause.
▣ Secondary hypertension - due to specific
causes such as:
renal disease
medications
adrenal disease
hypertension in pregnancy.
Risk factors
Increased
alcohol
intake Smoking

High
sodium,
cholesterol
and Psychologi
saturated fat cal and
intake environmen
tal stressors
Hypertension

Genetic
Old age
Clinical manifestation

▣ asymptomatic
▣ when symptoms appear, they usually indicate
vascular damage
▣ coronary artery disease with angina
▣ left ventricular hypertrophy
▣ left ventricular failure
▣ pathologic changes in the kidneys may be
manifested by nocturia.
▣ cerebral vascular involvement
Diagnostic evaluation

▣ Thorough history and physical examination

▣ Retinas are examined
▣ Laboratory studies are performed to detect
possible damage to organs as kidneys or
heart
▣ Electrocardiography
▣ Urine analysis
Management

GOAL:
To achieve and maintain an arterial blood pressure
below 140/90 mm Hg whenever possible.

Nonpharmacologic approaches:
▣ Weight reduction
▣ Restriction of sodium, tobacco and alcohol
▣ Exercise
▣ Relaxation
Management

▣ Medications
Diuretics
Beta blockers

▣ Hospital management:

Assessment Diagnosis Planning and

Monitor BP intervention
Nosebleeds Understanding the
Anginal pain disease process
Shortness of breath and its treatment,
Alteration in vision compliance with
Vertigo, headache the self-care
program, and
absence of
complication
Patient education for self-care

▣ Administer anti-hypertensive drug as

prescribed
▣ Restrict sodium and fat
▣ Control weight
▣ Follow an Exercise program
▣ Regular follow up
▣ Control smoking
▣ Self monitoring of blood pressure.
 7.
What drugs will
you prescribe and
📌 Thiazide
why? Explain the
mechanism of 📌 Captopril

action. 📌 Statins
Thiazide

□ diuretic, inexpensive, with relatively few side effects

□ effective in many mild hypertension

□ MOA
Inhibits sodium/Cl
symporter

(Acts on DCT)

Enhanced NaCl
excretion.
Captopril

□ useful for hypertension

□ MOA
Inhibits enzyme (ACE, increase in
kininase II, pedtidyl endogenous
dipeptidase) vasodilators (kinin)

BP is regulated
Statins

□ best used by people who have a family history of

cardiovascular disease and a high risk of heart
problems
□ the best option for someone who has not been able to
lower high blood pressure on their own.

□ MOA:
- competitively inhibiting HMG-CoA reductase
- mimic the natural substrate molecule, HMG-CoA, and
compete for binding to the HMGCR enzyme.

▣ Follow up after a month or 3 months

 8.
What are the side
effects or adverse
effects of the
drugs?
Side Effects

Thiazide Captopril (ACE Statins

• Sexual impotence Inhibitors) • Intermittent
• Severe elevations of serum
• Hypokalemia hypotension aminotransferase
• Acute renal failure activity
• Dyslipidemia • Hyperkalemia • Severe hepatic
• Dry cough (with toxicity
• Hyperuricemia wheezing)
• Angioedema • Myopathy and
• Hyperglycemia • Teratogenic rhabdomyolysis.
• Neutropenia or .
proteinuria
• Minor toxic effects
 9.
Explain the
RAAS system.