Chapter 19 - Hypertension

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CLINICAL PHARMACY & Chapter 19: Hypertension

PHARMACOTHERAPY 1 Ms. Neri Margaret Fabillo


AY 2022-2023 MM/DD/YYYY
2nd Semester

OUTLINE
8. Alternative Treatment
1. Physiology
Strategies
2. Clinical Manifestation 9. Palliative Care
3. Differential Analysis 10. Goal of Therapy
4. Laboratory Tests 11. Possible Drug Interactions
5. Drug of Choice and MOA 12. Patient Education
6. Alternative Drug 13. Patient Assessment and
Treatment and MOA Monitoring
7. Other Drug Therapies and
MOA
.
I. PATHOPHYSIOLOGY
PPT: ● Absolute Risk
● Hypertension → highest in those who already have evidence of
→ blood pressure is elevated to an extent that clinical benefit is cardiovascular disease, such as previous myocardial
obtained from blood pressure lowering infarction, transient ischaemic attack or stroke, or who have
→ systolic and diastolic components are important in other evidence of cardiovascular dysfunction such as
determining an individual’s cardiovascular risk electrocardiogram (ECG) or echocardiograph abnormality

● Systolic ● Risk
→ pressure in arteries during contraction (systole) → increased in the elderly and in people with diabetes or renal
failure and is further enhanced by other risk factors such as
● Diastolic smoking, dyslipidaemia, obesity and sedentary lifestyle.
→ pressure in arteries during relaxation (diastole)
● Essential hypertension
→ no underlying medical illness to cause high blood pressure

● Hypertension is more common in black people of African


Caribbean origin.
● Hypertension is exacerbated by other factors, for example, high
salt or alcohol intake or obesity

BOOK:
● A figure of systolic/diastolic blood pressure of 140/90 mmHg is
considered the upper limit of ‘normal’.
● Hypertension
→ largely a condition of older individuals
● While diastolic pressure peaks at age 50, systolic pressure
continues to increase with advancing age, making isolated
systolic hypertension a common feature of old age.

● Stroke and Myocardial Infarction


→ most common and important cardiovascular complications

● An increase of 5mmHg in usual diastolic blood pressure is


associated with a 35–40% increased risk of stroke.

CLINPHARM Group 2 - 2A : Andres, Balando, Bucane, Canillas, Galangue,Gonzales, Llarenas, Mengote, Muncada, Pabia, Pazon, Rosales, Samante, Severino, Vierras, Yee 1 of 4
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II. CLINICAL MANIFESTATION
PPT & BOOK:
● Severe cases may present with headache, visual disturbances
or evidence of target organ damage (stroke, ischaemic heart
disease or renal failure)
● Malignant (accelerated) hypertension
→ uncommon condition characterized by greatly elevated blood
pressure (usually >220/120 mmHg) associated with evidence
of ongoing small vessel damage
→ may be associated with hypertensive encephalopathy
→ Clinical features:
▪ confusion
▪ headache
▪ visual loss
▪ seizures
▪ coma IV. LABORATORY TESTS
● A medical emergency that requires hospital admission and rapid
control of blood pressure over 12–24 h towards normal levels. AMBULATORY BLOOD PRESSURE MONITORING
PPT & BOOK:
III. DIFFERENTIAL ANALYSIS ● over 24 hours
● useful for patients who have unusual variability in blood
DIFFERENTIAL DIAGNOSIS I. PRIMARY pressure, resistant hypertension or symptoms suggesting
HYPERTENSION hypotension.

POTENTIALLY ASYMPTOMATIC HOME BLOOD PRESSURE MEASUREMENTS


● Dull to severe headache PPT & BOOK:
● Fatigue ● measurements are usually lower than clinic recordings, on
● Concentration difficulties average by 12/7 mmHg.
● Vision problems ● inexpensive but it is important to have a machine of validated
● Chest pain accuracy that the patient can use properly
● Difficulty breathing
● Irregular heartbeat SECONDARY CAUSES
● Pounding in chest, neck, or ears PPT & BOOK:
● Full blood count
DIFFERENTIAL DIAGNOSIS II. SECONDARY ● electrolytes
HYPERTENSION ● urea
● creatinine
● High blood pressure that does not respond to blood pressure ● urinalysis
medications (resistant hypertension) ● chest x-ray
● Very high blood pressure ● ECG
→ systolic blood pressure over 160 millimeters of mercury ● physical examination
(mmHg) or diastolic blood pressure over 100 mmHg
● A blood pressure medication or medications that previously ● Renin-angiotensin Ratio
controlled your blood pressure but no longer work → useful screening test to investigate for possible
● Sudden-onset high blood pressure before age 30 or after age hyperaldosterism
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● No family history of high blood pressure ● Serum Metanephrine & Urinary Catecholamines
● No obesity → may detect underlying pheochromocytoma

DIFFERENTIAL DIAGNOSIS III. COMPLICATED ● Conn’s Syndrome/Primary Hyperaldosterism


HYPERTENSION → very high aldosterone/renin ratio
→ usually caused by a benign adenoma or simple hyperplasia
within the zona glomerulosa of the adrenal gland

V. DRUG OF CHOICE AND MOA

Class Mechanism Adverse effects


of action

Proton pump inhibitors control diarrhea,


(omeprazole, gastric acid headaches,
lansoprazole, secretion by abdominal pain,
pantoprazole) inhibition of nausea, fatigue,
gastric H+, and dizziness
K+-ATPase

H2-receptor antagonists competitively diarrhea,

CLINPHARM 1 Hypertension 2 of 4
XI. POSSIBLE DRUG INTERACTION
block the headaches,
histamine abdominal pain,
B-ADRENOCEPTOR ANTAGONISTS
receptors in and confusion
gastric
parietal cells Phenothiazines

- increase in blood plasma levels


➔ increased levels of thioridazine could increase
VI. ALTERNATIVE DRUG TREATMENT AND MOA the risk of life- threatening cardiac arrhythmias.

Sucralfate
Verapamil
- has mucosal protective effects
MOA: forms a stick viscid gel that adheres to ulcer surface
providing physical protection - increase of blood plasma levels of either drug.

VII. OTHER DRUG THERAPIES AND MOA Clonidine

Bismuth Chelate - can cause life threatening increases in BP.


- has ulcer-healing properties
MOA: eradicates H. pylori which reduces ulcer recurrence Beta-agonists, levalbuterol, salmeterol

Antacids
- could affect the pulmonary organs and may cause
- can be aluminum- or magnesium- based antacids
bronchospasm.
MOA: neutralize existing stomach acid and provide rapid pain relief

VIII. ALTERNATIVE TREATMENT STRATEGIES Barbiturates

High fiber food - cause a reduction of blood plasma levels of the


- apples beta-blockers.
- pears
- oatmeal
DIURETICS
IX. PALLIATIVE CARE
Thiazide diuretics
Prevention and relief of suffering of any kind
- experience by adults and children living with - given concurrently with antidiabetic drugs causes a
life-limiting health problems decreased blood level of antidiabetic drugs.

Digoxin

- Hypokalemia

Lithium

- Decreased renal elimination of lithium; toxicity.

With ACE Inhibitors or NSAIDs

- Hyperkalemia

CALCIUM CHANNEL BLOCKER

Verapamil and diltiazem

- reduce the elimination and increase the blood levels of


carbamazepine, simvastatin, atorvastatin, and lovastatin.
➔ This can lead to toxicity from these drugs.

Increased Cyclosporine

X. GOAL OF THERAPY - toxicity.

1. Lower Blood Pressure Grapefruit juice


2. Educate Patients
3. Improve Diet & Exercise Habits - may elevate serum concentrations of verapamil,
felodipine, nifedipine, etc

CLINPHARM 1 Hypertension 3 of 4
infarction or stroke, angina or peripheral
vascular disease are at high risk of recurrent
XII. PATIENT EDUCATION event
➔ Type 2 diabetes over 40 years of age are also
● Patients need to be highly motivated to establish and at high risk and can be regarded as ‘coronary
maintain a healthy lifestyle and to take prescribed equivalents’
antihypertensive medications ➔ . A 10-year cardiovascular disease risk of 20%
● If diagnosis of hypertension is not made, measure the (equivalent to a 15% coronary heart disease
patient’s clinic BP at least annually thereafter Encourage risk) is regarded as an appropriate threshold for
measuring BP at home antihypertensive therapy in patients with
● Patients should be made aware that lowering BP can moderate hypertension, as well as for
decrease death from stroke, coronary events, HF, along lipid-lowering therapy.
with decreasing the progression of renal failure

REVIEW QUESTIONS (optional)

XIII. PATIENT ASSESSMENT AND MONITORING 1. Question 1


a. Answer 1
b. Answer 2
SECONDARY CAUSES c. Answer 3
d. Answer 4
1. History checking 2. Question 2
➔ Symptoms of renal disease, a. Answer 1
● Haematuria, polyuria, etc., b. Answer 2
paroxysmal symptoms that suggest c. Answer 3
the rare diagnosis of d. Answer 4
pheochromocytoma and include
headache, postural dizziness,
syncope. Aswers: a, b

1. Physical examination abdominal bruits


➔ Renal artery stenosis REFERENCES
2. Radiofemoral delay
➔ Coarctation of the aorta
3. Palpable kidneys
➔ Polycystic kidney disease
4. Laboratory analysis
➔ full blood count, electrolytes, urea, creatinine
and urinalysis.

CONTRIBUTING FACTORS

1. Obesity
2. Excess alcohol
3. Salt intake and lack of exercise use of drugs
(over-the-counter medicines used as cold and flu
remedies.)
4. smoking, diabetes and hyperlipidaemia
5. Family history of cardiovascular disease

EVIDENCE OF END-ORGAN DAMAGE

1. Examination of the optic fundi to detect retinal changes.


2. ECG to detect left ventricular hypertrophy or subclinical
ischaemic heart disease.
3. Check the renal function and test the urine for signs of
microalbuminutria which may be an indicator of a higher
risk of future end-stage renal disease and overall
vascular risk

DETERMINATION OF CARDIOVASCULAR RISK

- An accurate assessment of cardiovascular disease risk is


essential before recommending appropriate management
in hypertension.
➔ This is for patients with documented
atheromatous vascular disease eg. myocardial

CLINPHARM 1 Hypertension 4 of 4

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