Hypertension: Types, Classification, Pathogens, Regulation & Treatment.

Hypertension:--


Definition-:

Abnormal elevation of Blood pressure in systemic arterial system is know an Hypertension,25% of population of USA is suffering from Hypertension.

•) Systolic Blood pressure is more dangerous in people > 50 years , because there is Right Ventricle Hypertrophy.

Normal Blood Pressure: 
SYSTOLIC BP- 120mmHg
DYSTOLIC BP- 80mmHg

Pulse Pressure= Systolic - Dystolic= 120 - 80 = 40 mmHg.

Mean Arterial Pressure = Diastolic +1/3Pulse pressure.
Normal valve of Mean Arterial Pressure = 93 to 100mmHg.

Factor effect on Blood pressure......

BP = CO × TPR (total peripheral resistance)
Increase Blood pressure will increase risk of stroke and Cardiac complain.

Cardiac output = stroke volume × 72 beats = 5 liters / minute
1) Systolic Blood pressure  depends on Cardiac output.
2) Diastolic Blood pressure depends on TPR (total peripheral resistance).

Classification of Hypertension

Normal = systolic(120), diastolic(80).
Pre Hypertension= systolic(120-129), diastolic(80).
Stage 1 Hypertension= systolic(130-139), diastolic(80-89).
Stage 2 Hypertension= systolic(140), diastolic(90).
Malignant Hypertension= over 180/120

How to prevent -:

Pre Hypertension-:
they need to take care, Diet(more foods and vegitables less lipids), Smoking, Increase Physical Activity, Rest him self.
Stage 1 hypertension-:
Need treatment but also recover by care.
Stage 2 Hypertension-
- Need treatment.
Melignent Hypertension-:
- It is very sevire type in which organs damage. If they are not treated 90% die in 1 year. Even with best treatment 30% die in 5 years.

Effect of Hypertension in CNS :-

When some has rapidly develop neurological defect due to vascular events. 
Transient Ischemic Attack - If defect is for less then 24 hours.
Stroke - If more then 24 hours or death occur with in 24 hours .

Types of Hypertension :-

Primary ( Essential ) Hypertension-:
1) Due to multiple genetic and environmental factors. Not due to single pathology.
Eg - If there is Congenital tendency to have increase smooth muscles in blood vessels se we can't remove all
 vessels.
2) Thats why this type is not curable.( Need antihypertensive drug throughout the life).

Secondary Hypertension-:
1) It is due to some well defined pathology and when such pathology is removed Hypertension is also removed.  
2) That is why this type is curable.

Pathogenesis Of Primary & Secondary Hypertension ??

Causes of Primary HTN:

•) Genetic predisposition.
•) Environmental factors.
•) Sympathetic system hyperactivity.
•) RAAS over active.
•) Defect of Nitriuresis (abnormal Na handling).
•) Due to increase intracellular Na+ and Ca+ ( in this patient Na+k+ ATPase is not functioning properly so Increase Na+ inside the cell , so this Na+ is exchange by Na+Ca+ exchanger so Ca+ level is increase inside the cell and increase contraction and result Hypertension).
•) Obesity.
•) Na intake.
•) Alcohol & Smoking.
•) Sedentary life style.
•) Polycythemia ( when RBC is more so blood is also more and cause Hypertension).
•) Increase Na intake and dincrease K intake.
•) NSADs.

Causes of Secondary HTN:

•) Renal and renal vascular causes.
•) Endocrine Abnormilities-
1) Acromegaly ( increase calcium ) cause hypertension.
2) Thyroid dysfunction.
3) Hyperparathyroidism (hypercalcemia).
4) Diabetic mellitus.
5) Cushing syndrome.
6) Exogenous harmone , eg - steroids and contraceptive pills.
7) Pregnancy produce Hypertension.
•) CVS complications-
1) Increase CO.
2) Increase TPR.
3) Polyarteritis Nodosa.
4) Coarctation of aorta.
•)  Neurological Conditions-
1) Phycological disorder.
2) Increase intra cranial pressure -> blood flow -> activate Sympathetic.
3) Sleep apnea.
4) Acute stress.

Blood Pressure Regulations::


1) Regulated by Baroreceptor Reflex- (It is Quick Reflex)-:


Baro® present on Arch of aorta & Internal Carotid Artery. If Increase Blood Pressure -- both area will effect.

•) If increase BP -> Strech Aorta - Also strech the Barrow® in aorta and send impulse to Vagus Nerve.
•) If increase BP -> Strech Internal carotid Artery - ® also stretched and send impulse to Glassopharengial  nerve.
•) Both Vagus and Glassopharengial Nerve activate nucleus on Medulla ( NTS Nucleus Tractus Soliterious).
•) NTS of medulla will Block the SYMPATHETIC system (Dincrease BP) and Activate PARASYMPATHETIC (Dincrease BP).

Baroreceptor Resetting--

Normally we have 120/80  mmHg BP at normal we have set point at 150 , BP increase more then 150 then our Barrow® will activate and manage the BP.
But In Chronic Hypertension BP is about 200/100 mmHg so if BP is increase more then 150mmHg also not activate the Barrow® because set point is increased so if BP is more then 240mmHg then only detectable by Baro®.


2) Regulation by RAAS system.( It is long term process)-:


•) In Nephron if BP dincrease ->JG cell which secrets -> Renin which convert -> Angiotensinogen into Angiotensin 1 -> In the presence of ACE (Angiotensin Converting Enzyme) it is converted into -> Angiotensin2.

•) Angiotensin 2 Functions:->
-> It it self direct Vasoconstriction and Increase BP.
-> Activate Poster Pitutiry to Increase ADH which act on Collecting Duct and Increase BP
-> Increase Aldosterone secretions which will increase tubular reabsorbed and increase BP.
-> Directly increase Sympathetic activity and increase BP.


Factors affect RAAS system-


∆)  JG cell tumer ( Renin producing tumer) -cause  Hypertension. Any renal disease which dincrease renal blood flow and increase renin secretions will cause Hypertension.

Eg:
 •)) Renal Artery Stenosis - dincrease  renal blood flow and increase renin secretions and cause Hypertension.
•)) Renal disease -> increase GFR -> so increase Na reabsorbed  and increase BP.
•)) Oral pills increase the secretion of Angiotensinogen by liver so cause Hypertension.
•)) Conn's syndrome will increase Aldosterone and cause Hypertension.
•)) Congenital Adrenal Hyperplasia.
•)) Gitelman syndrome - Hyperplasia in NaCl channel in DCT also cause Hypertension.

3) Others Reflex which also effect Blood Pressure-:


•} Bezold Jarish Reflex - it is reflex of heart,
when MI then serotonin activate Vagus Nerve and Dincrease BP.

•} Cushing Reflex - it is reflex in brain,
If Head injury -> increase ICT (intra cranial tension) -> trigger intra cranial vagus fiber and Dincrease BP.

•} Last Ditch Stand - It is CNS Ischemic Response,
When person is dieing, at that time if BP is less then 40mmHg so dincrease Brain blood flow and our body do one last try by increase BP so activate  Sympathetic system &-> BP rise about 250 mmHg
(And try to perfused blood all part of body).

Symptoms & why Hypertension called silent Disease?


High blood pressure for years without any symptoms. It is silent Disease until damage any organs.      

Eg- 
•} CVS(CCF, IHD ,MI).
•} CNS(stroke).
•} Vessels (atherosclerosis).
•} Kidney .
•} Eye (retina - Hypertensive retinopathy).

Hypersensitive retinopathy seen under melignent Hypertension. Thats why if patients comes with Distolic > 129   so we should do Opthalmoscopy.




Risk factors-:

High blood pressure has many risk factors, including:

Age. The risk of high blood pressure increases as you age. Until about age 64, high blood pressure is more common in men. Women are more likely to develop high blood pressure after age 65.

Race. High blood pressure is particularly common among people of African heritage, often developing at an earlier age than it does in whites. Serious complications, such as stroke, heart attack and kidney failure, also are more common in people of African heritage.

Family history. High blood pressure tends to run in families.

Being overweight or obese. The more you weigh the more blood you need to supply oxygen and nutrients to your tissues. As the volume of blood circulated through your blood vessels increases, so does the pressure on your artery walls.

Not being physically active. People who are inactive tend to have higher heart rates. The higher your heart rate, the harder your heart must work with each contraction and the stronger the force on your arteries. Lack of physical activity also increases the risk of being overweight.

Using tobacco. Not only does smoking or chewing tobacco immediately raise your blood pressure temporarily, but the chemicals in tobacco can damage the lining of your artery walls. This can cause your arteries to narrow and increase your risk of heart disease. Secondhand smoke also can increase your heart disease risk.

Too much salt (sodium) in your diet. Too much sodium in your diet can cause your body to retain fluid, which increases blood pressure.

Too little potassium in your diet. Potassium helps balance the amount of sodium in your cells. If you don't get enough potassium in your diet or retain enough potassium, you may accumulate too much sodium in your blood.

Drinking too much alcohol. Over time, heavy drinking can damage your heart. Having more than one drink a day for women and more than two drinks a day for men may affect your blood pressure.

If you drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and two drinks a day for men. One drink equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof liquor.

Stress. High levels of stress can lead to a temporary increase in blood pressure. If you try to relax by eating more, using tobacco or drinking alcohol, you may only increase problems with high blood pressure.

Certain chronic conditions. Certain chronic conditions also may increase your risk of high blood pressure, such as kidney disease, diabetes and sleep apnea.

SYSTOLIC Blood pressure :-


Pressure measure from major arteries when heart is at the peak of systole.

Increase CO - increase blood come in major vessels increase systolic BP. And Dincrease CO - dincrease blood come in major vessels dincrease Systolic BP.

DIASTOLIC Blood Pressure:-

During left ventricle diastole intra ventricular pressure decrease , so blood from aorta try to fall back but aorta valve is closed so there is cut of relation Between heart and vessels , so falling pressure of ventricle will not influence the major arteries.

It depends on how much blood is present in major arterial system this will depend on arterioles contract and relaxation.
If arterioles contraction-- more blood trap in large vessels so increase Diastolic Blood Pressure
If arterioles relaxation-- more blood leave the major arteries an decrease Diastolic BP.

Cardiac output :(CO)

Co= Stroke volume × Heart rate

i.e CO is amount of blood come out in per minute.
Normal value of Cardiac output = 5L/min.

Factor affecting Cardiac output :

* Increase Blood Volume-> increase vascular resistance-> increase Cardiac output.
* All factors which increase blood volume also increase SYSTOLIC Blood Pressure


T.P.R --- 

Sum of R affered by the arterioles to the blood flow from major arterial  system to venus side.

Factors affect T.R.P--

Humoral factors - 
1) Constrictors by (Angiotensin 2, Catecholamines,Thromboxine A2, Endothelin.
2) Dilator by NO, Prostaglandin ,Bradykin.
Nueronal Factors --
1) NonEpinephrin - work on ×1AR ® and do contraction and work on B2AR® and do dilation.

Factor effect on Blood Volume : 

1) Increase Na+ -- more Na+ in body retain more H2O in body and cause Increase Blood volume.
2) Mineralocorticoid ( increase retention of Na+ and H2O.)
3) ANP (arterial nitriuretic   peptide) increase blood to retainsion or reabsorbed.

 ANP Act on vessels cause vasodilation results Decrease Vascular resistance.
ANP Acts on last part of kidney and cause nitriuresis.

Treatment of Hypertension :

•} Angiotensin1®blocker- Losartan.
•} Angiotensin2®blocker- Tekmisartan.
•} ACE Inhibitor- Captopril, Enilopril.
•} diuretics-  including thiazides, chlorthalidone, and indapamide.
•} beta-blockers.
•} alpha-blockers.
•}calcium-channel blockers.
•}central agonists.
•}peripheral adrenergic inhibitor.
•}vasodilators.


Previous
Next Post »