This document provides information about hypertension including its definition, causes, risk factors, presentation, evaluation, management of acute hypertension, and treatment approaches. It defines hypertension as a chronic medical condition where blood pressure is elevated. It notes the most common cause is primary or essential hypertension which has no identifiable secondary cause. It discusses risk factors like age, family history, obesity, smoking, high cholesterol and discusses secondary causes like renal disease. It outlines how to evaluate patients, potential complications, and treatment approaches including lifestyle modifications and drug therapies.

1. Hypertension
Ahmed A. Ajeebi
4’th Y, Faculty of Medicine, Jazan University

2. Qs.
What’s HTN ?!
Who at risk ?
How is’t occur ?
Pt. , How present ?
Emergency HTN !
How to approach ?
What about management ?

3. What’s HTN ?
Chronic medical condition in which blood pressure elevated.
Blood pressure is force which exerted by blood against the wall
of the blood vessels, which is adequate to maintain perfusion
during activity and rest.
Blood pressure;
A. Maximum systolic pressure in the artery when left ventricle
contract to force the blood into aorta & other arteries.
B. Minimum diastolic pressure in the artery when ventricle
relaxed & filling up, blood receiving from veins.

4. What’s HTN ?
Regulation of blood pressure;
A. Baroreceptor reflex in medulla “localization in Rt. & Lt. carotid
sinus and Aortic arch”
B. Renin angiotensin system “for long term”
• Kidney - composition
• Endogenous vasoconstriction - angiotensin I
C. Aldosterone release “adrenal cortex”
• Stimulate sodium retention & potassium execration by
kidney
• Increases fluid retention

5. What’s HTN ?
Arterial blood pressure maintained
by cardiac output and systemic
vascular resistance, so the relation
between systemic arterial pressure
and morbidity appear to be
quantitative rather than qualitative

6. What’s HTN ?
Background;
A. Hypertension is one of the most common worldwide diseases afflicting
humans and is a major risk factor for stroke, myocardial infarction,
vascular disease, and chronic kidney disease.
B. Despite extensive research over the past several decades, the etiology
of most cases of adult hypertension is still unknown, and control of
blood pressure is suboptimal in the general population.
C. Hypertension is the most important modifiable risk factor for coronary
heart disease (the leading cause of death in North America), stroke
(the third leading cause), congestive heart failure, end-stage renal
disease, and peripheral vascular disease, Therefore, health care
professionals must not only identify and treat patients with
hypertension but also promote a healthy lifestyle and preventive
strategies to decrease the prevalence of hypertension in the general
population.

7. What’s HTN ?
JNC-8 classification
The classification is based on the average
of 2 or more readings taken at each of 2
or more visits after initial screening.
Stage Systolic pressure Diastolic pressure
Normal < 120 mmHg < 80 mmHg
Pre - hypertensive 120 - 139 mmHg 80 - 89 mmHg
Grade I
hypertension
140 - 159 mmHg 90 - 99 mmHg
Grade II
hypertension
> 160 mmHg > 100 mmHg

8. What’s HTN ?
Prehypertension, emphasizes that
patients with prehypertension are
at risk for progression to
hypertension and that lifestyle
modifications are important
preventive strategies.
Hypertension may be categorized
as either essential “primary” or
secondary.

9. Who at risk ?
Tobacco use, particularly cigarettes, including chewing tobacco
Elevated LDL cholesterol (or total cholesterol ≥240 mg/dL) or low HDL
cholesterol: component of metabolic syndrome
Diabetes mellitus: component of metabolic syndrome
Obesity (BMI ≥30 kg/m2): component of metabolic syndrome
Age greater than 55 years for men or greater than 65 years for women: increased
risk begins at the respective ages; the Adult Treatment Panel III used earlier age
cut points to suggest the need for earlier action
Estimated glomerular filtration rate less than 60 mL/min
Microalbuminuria
Family history of premature cardiovascular disease (men < 55 years; women < 65
years)
Lack of exercise

10. How is’t occur ?
Hypertension may be primary, which may
develop as a result of environmental or genetic
causes, or secondary, which has multiple
etiologies, including renal, vascular, and
endocrine causes. Primary or essential
hypertension accounts for 90-95% of adult
cases, and a small percentage of patients (2-
10%) have a secondary cause. Hypertensive
emergencies are most often precipitated by
inadequate medication or poor compliance.

11. How is’t occur ?
Primary (essential) hypertension is diagnosed
in the absence of an identifiable secondary
cause. Risk factor family Hx. of HTN or heart
disease, a high sodium diet, smoking, obesity,
ethnicity “black>white”, and advanced age.
Pt. asymptomatic until complication develop,
so pt. should evaluated for end organ damage
to the brain”stroke, dementia”, eye “cotton wall
exudate, hemorrhage” , heart “LVH” and
kidney “chronic kidney disease, proteinuria &
artery stenosis”

12. How is’t occur ?
Secondary forms of hypertension, for identifiable causes, such as primary
hyperaldosteronism, account for 20% of resistant hypertension (hypertension
in which BP is >140/90 mm Hg despite the use of medications from 3 or more
drug classes, 1 of which is a thiazide diuretic).
other causes;
A. Renal causes 2.5-6% “Chronic renal disease, polycystic kidney disease,
urinary tract obstruction, renin producing tumor, liddl syndrome”
B. Renovascular hypertension “RVHT” causes .2-4% of cases.
C. Vascular causes “Coarctation of aorta, vasculitis, collagen vascular
disease”
D. Endocrine causes account for 1-2% include, exogenous causes include
administration of steroids. Another endocrine causes oral contraceptive
use oral contraceptive use in association with mild renal disease, family
Hx., female older than 35 year

13. How is’t occur ?
E. Exogenous administration of the other steroids used for
therapeutic purposes also increases blood pressure (BP),
especially in susceptible individuals, mainly by volume
expansion, they blocks both “COX-1” and “COX-2” which can
inhibit natriuretic effect, which in turn increase sodium retention,
also inhibit vasodilation of prostaglandins and produce
vasoconstriction enzyme endothelin-1
F. Endogenous hormonal causes;
1. Primary hyperaldosteronism
2. Cushing syndrome
3. Pheochromocytoma
4. Congenital adrenal hyperplasia

14. How is’t occur ?
G. Drugs and toxin;
1. Alcohol
2. cocaine
3. NSAIDs
H. Other causes;
1. Hyperthyroidism & hypothyroidism
2. Hypercalcemia
3. Hyperparathyroidism
4. Obstructive sleep apnea
5. Pregnancy induced hypertension

15. How is’t occur ?
I. Neurogenic causes, include;
1. Brain tumor
2. Bulbar poliomyelitis
3. Intrcranial hypertension

16. How is’t occur ?
Environmental and genetic/epigenetic causes;
A. Hypertension develops secondary to environmental
factors, as well as multiple genes, whose inheritance
appears to be complex. Furthermore, obesity, diabetes,
and heart disease also have genetic components and
contribute to hypertension.
B. In an attempt to elucidate the genetic components of
hypertension, multiple genome wide association studies
(GWAS) have been conducted, revealing multiple gene
loci in known pathways of hypertension as well as some
novel genes with no known link to hypertension as of yet

17. How is’t occur ?
C. Epigenetic phenomena, such as DNA methylation and
histone modification, have also been implicated in the
pathogenesis of hypertension. For example, a high salt
diet appears to unmask nephron development caused by
methylation.
D. Despite these genetic findings, targeted genetic therapy
seems to have little impact on hypertension. In the
general population, not only does it appear that
individual and joint genetic mutations have very small
effects on BP levels, but it has not been shown that any
of these genetic abnormalities are responsible for any
applicable percentage of cases of hypertension in the
general population

18. Pt. how present ?
Asymptomatic, pt. unaware they have HTN until complicate
Non-specific symptom, mild symptom
Headache
Confusion
Morning headache
Fatigue
SOB
Nausea

19. Pt. how present ?
Anxiety
Nose bleeding
Heart palpitation
Chest pain
Pale skin
Change of vision

20. • Complication
- Stroke
- Coronary artery disease
- Arterial Fibrillation
- Renal Failure.
- Erectile Dysfunction
- Renovascular HTN
- Pheochromocytoma

21. Emergency HTN
The most common hypertensive emergency is a rapid
unexplained rise in BP in a patient with chronic essential
hypertension, which lead to end organ damage
Most patients who develop hypertensive emergencies
have a history of inadequate hypertensive treatment or an
abrupt discontinuation of their medications
Other causes of hypertensive emergencies include the use
of recreational drugs, abrupt clonidine withdrawal, post
pheochromocytoma removal, and systemic sclerosis, as
well as causes of secondary HTN that listed before.

22. Emergency HTN
Pt. with end organ damage revealed by renal
disease, chest pain “MI or ischemia”, back pain
“aortic dissection”, or change in mental status
“hypertensive encephalopathy”

23. How to approach ?
Obtain a history of the patient’s use of over-the-counter
medications; herbal medicines such as herbal tea containing
licorice, ephedrine/ephedra, current and previous unsuccessful
antihypertensive medication trials; oral contraceptives; ethanol;
and illicit drugs such as cocaine
The patient’s lifestyle factors should also be included, such as
changes in weight, dietary intake of sodium and cholesterol,
exercise level, and psychosocial stressors
The historical and physical findings that suggest the possibility
of secondary hypertension are a history of known renal disease,
abdominal masses, anemia, and urochrome pigmentation

24. How to approach ?
A history of sweating, labile hypertension, and
palpitations suggests the diagnosis of
pheochromocytoma
A history of cold or heat tolerance, sweating, lack of
energy, and bradycardia or tachycardia may
indicate hypothyroidism or hyperthyroidism
A history of obstructive sleep apnea may be noted A
history of weakness suggests hyperaldosteronism.
Kidney stones raise the possibility of
hyperparathyroidism

25. How to approach ?
Physical examination revealed elevated blood pressure
Routine investigation of the HTN pt include;
A. ECG
B. Urine dipstick test for protein and blood
C. Fasting blood for lipids “total and HDL cholesterol” and
glucose
D. Serum urea, creatine and electrolyte

26. How to approach ?
If the urea or creatinine is elevated, more
specific are renal investigation are indicated
A low serum potassium may indicate an
endocrine disorder (primary hyperaldosteronism
or glucocorticoid excesses)

27. What about management ?
Drugs
1. ACEIs; arterial & venous vasodilation, has advantage in HTN pt. with CHF & diabetic
nephropathy.
2. beta-blocker; which decrease heart rate, cardiac out put, ideal in HTN pt. with angina.
3. CCBs; which cause arterial vasodilation.
4. alpha-blocker; cause relaxation of smooth muscle, which has advantage in pt. w/ BPH
5. ARBs; Has benefit of ACEs apart form side its effect “cough”.
6. Diuretics; decrease plasma volume, useful in CHF, smoker & chronic urinary disease.
Surgical intervention
Life style modification

28. What about management ?
Stage Systolic pressure Diastolic pressure
Life style
modification
Drug therapy
Normal < 120 mmHg < 80 mmHg Encourage -
Pre - hypertensive 120 - 139 mmHg 80 - 89 mmHg Yes No indication
Grade I
hypertension
140 - 159 mmHg 90 - 99 mmHg Yes
Thiazide Diuretic,
ACEIs, beta
blocker, CCBs
Grade II
hypertension
> 160 mmHg > 100 mmHg Yes
2 drugs
combination,
Diuretic + ACEIs,
ARB, CCBs, beta
blocker

29. What about management ?
Treatment of primary HTN
Population Agent
Uncomplicated Diuretics, beta-blocker, ACEIs
CHF
Diuretics, beta-blocker, ACEIs,
ARBs, Aldosteron antagonist
Diabetic
Diuretics, beta-blocker, ACEIs,
ARBs, CCBs
Post- MI
beta-blocker, ACEIs, ARBs,
aldosteron antagonist
Chronic kidney dosease ACEIs, ARBs

30. What about management ?
Etiology Management
1ْ Renal disease ACEIs
Renal artery stenosi May treated with angioplasty or stinting
OCP user Discontinue “may delayed”
Pheochromocytoma
alpha agonist & beta blocker, then
removal of tumor
Conn’s syndrome “hyper aldosteronism” Removal of tumor
Cushing’s syndrome Removal of tumor & exogenous steroids
Aortic Coarctation Surgical repair

31. What about management ?
Treatment of Emergency HTN
Status Management
Hypertensive urgency
oral hypertensive “beta blocker, clonidine,
ACEIs”, with goal lowering BP within 24h
Hypertensive emergency
IV medication “labetalol, nitroprusside,
nicardipine”, with goal lowering BP 25%
over first 2 hour to prevent cerebral hypo
perfusion or coronary insufficiency

32. hope it was helpful presentatio