Hypertension

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HYPERTENSION

DR. P. TEJASWI
OBJECTIVES

• DEFINITION
• TYPES
• PATHOPHYSIOLOGY
• CLINICAL PRESENTATION
• TREATMENT
DEFINITION

• Hypertension is a long term complication in which blood pressure in the


arteries is persistently elevated.
• The SBP will be more than or equal of 140mm of Hg and DBP will be
more than or equal of 90mmof Hg
TYPES
• PRE HYPERTESION : SBP : 120-139 mm of Hg
DBP : 80-89 mm OF Hg
• HYPERTENSION stage 1 : SBP : 140-159 mm of Hg
DBP : 90-99 mm of Hg
• HYPERTENSION stage 2 : SBP : more or equal to 160 mm of Hg
DBP : moreor equal to 100 mm of Hg
• Pregnancy induced HTN : because of increased production of hormones
and enzymes during pregnancy
ETIOLOGY
• PRIMARY HTN : it is the elevation in BP without an identified cause
• SECONDARY HTN : it is the elevation in BP with an exact cause. This
type accounts for 5-10% of total cases
• The causes of secondary HTN includes
1. congenital narrowing of aorta.
2. renal disease.
3. endocrine disorders like brain tumors and head injury.
4. neurological disorders like brain tumors and head injury
• Sleep apnea
• Medications like oral contraceptive pills, NSAIDS and cocaine.
• Cirrhosis of liver
RISK FACTORS
• AGE : chance of CAD after 50 yrs of age
• Alcohol, smoking and DM
• Excessive dietary intake of sodium
• Gender
• Family history
• Obesity
• Sedentary life style
• stress
PATHOPHYSIOLOGY

In secondary forms of hypertension, the underlying pathways are well


understood:
• In renovascular hypertension, renal artery stenosis causes decreased
glomerular flow and pressure in afferent arteriole. this induces
renin secretion, increase vascular tone and blood volume via the RAA
pathway.
• Single gene disorders cause severe but rare forms of hypertension :
1. gene defects affecting enzymes involved in aldosterone metabolism
(e.galdosterone synthetase, 11 beta hydroxylase, 17 alpha
hydroxylase): this leads to increase in aldosterone , increased salt and
water resorption, plasma volume expansion and hypertension

2. Mutation affecting proteins that influence sodium reabsorption


(e.g.,liddle syndrome caused by gain of function mutation in epithelial
Na+ channel protein that increase distal tubular reabsorption of Na+
MECHANISM OF ESSENTIAL HYPERTENSION

1. GENETIC FACTORS :

single gene disorders


polymorphisms in several genes that affect BP ( Angiotensinogen and
angiotensin receptor genes

2. Reduced renal sodium excretion: - increase in fluid volume, increased


cardiac output, and peripheral vasoconstriction thereby increasing BP
3. Vasoconstrictive influences : structural changes in vessel wall, increase
in PR
4. Environmental factors such as stress, obesity, smoking, physical
activity and heavy salt consumption
CLINICAL PRESENTATION
• Severe headache
• Blurred vision
• Dizziness
• Nausea
• Vomiting
• Fatigue
• Confusion
• Epistaxis
• Chest pain
• Shortness of breadth
VASULAR PATHOLOGY IN HTN

• Hyaline arteriosclerosis:
Injured endothelial vessels
Increased smooth muscle cell matrix
• Hyperplastic arteriosclerosis:
Laminations show smooth muscle cells
Thick duplicated basement membrane
Fibrinoid necrosis
Vessel wall necrosis
TREATMENT

• LIFE STYLE MODIFICATION :


weight reduction
DASH (Dietary approaches to stop hypertension)
Dietary sodium reduction
reduction of alcohol consumption
exercise
stress management
PHARMACOLOGICAL THERAPY

• Various groups of drugs are used for the treatment of hypertension


which includes
DIURETICS
BETA BLOCKERS
ALPHA BLOCKERS
CALCIUM BLOCKERS
REFERENCES

ROBBINS AND COTRAN PATHOLOGIC BASIS OF DISEASE


SOUTH EAST EDITION VOLUME I

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