Arterial Hypertension Flashcards
Arterial hypertension _ definition
Arterial hypertension is progressive cardiovascular syndrome associated with target organ damage often present before high BP values are observed..
We seee persistent elevated BP in arteries…
BP considered high with the systolic pressure above 140mmHg and diastolic pressure above 90mmHg
Mechanism of action of patient with A.H
Resistance of peripheral action
Increase cardiac output
Increase amount of circulation blood
Provoking factors of A.H
Obesity
High sodium intake
Age
Family history
Smoking
Sedentary life style
Alcohol consumption
Stress calcium intake
Provoking factors of A.H and mechanism behind it/cause
.obesity -increases activity of SNS
.High Sodium intake -retain excess fluid which causes pressure on artery walls
.Smoking -elevates BP damages artery wall and narrows blood vessels
.sedentary lifestyle -lack of physical activity
.age -increase peripheral action as the arteries become less elastic…damage kidneys
.family history -genetic factors
.high alcohol consumption -increase BP …causes vasoconstriction increase peripheral resistance action
.stress -increase heart rate by increasing cardiac output and increasing total resistance of peripheral action
Calcium intake - calcium is important for contraction of heart…increases cardiac output
Pathogenesis of arterial Hypertension
Increase Activity of sympathetic nervous system
Hyper Activation of renin-angiotensin-aldosterone system (RAAS)
Imbalance between vasoconstrictors hormone and vasodilators hormone ps
Steps for RAAS
Renin release
Then reach acts on a protein called angiotensinogen
Converts to Angiotensin 1
AG1 is converted to angiotensin II by enzyme ACE( found in lungs
AG11 causes BP increase
AGIl stimulatesthe adrenal glands to secrete aldosterone
Aldosterone regulates sodiumand potassium balance in body
Ald promotes sodium reabsorption and potassium excretion in the kidney which leads to increased fluid retention and HBP
AG11 stimulates release of vasopressin
Effects of angiotensin two
Hypertrophy of heart
Vasoconstriction
Promote release of noerphinephineand epinephrine
Activates SNS
Activates fibrosis in heart and vessels
Hypertrophy of cardiomyocytes
Types of arterial hypertension
Primary- No identifiable cause
Secondary - due to underlying health conditions
Target organs of arterial hypertension and how to confirm damages
Heart- left ventricular hypertrophy(thickening of left ventricle)
sokolov Lyon criteria
. We look at lead 5 or 6 where R wave is high (R5/R6) +(Sv1/Sv2)=>35
Tests
ECG
Echocardiogram cardiacmarkers CT with contract
Kidney
Elevated creatine
Appearance of micro albumins
Proteinuria
Tests
glomerulus filtration rate (online )urine tests Biochem tests ultrasound
Blood vessels
Thicking of intima. presence atherosclerosis plaque . Aorta aneurysm(dilation of aorta )
Tests
ultrasound. CT of coronary Arteries
Aorta aneurysm -CT
Eyes
Hypertensive retinopathy
Sausage shaped veins hard exudates
Brain
Carotid artery
scanning brain and neck arteries and carotid ultrasound
Complains of patient with A.H
Headache-
Dizziness
Blurred vision
Chest pain-tightness
Shortness of breath
Fatigue
Treatment of A.H
First physical activity
Healthy diet -DASH
Medication
Ace inhibitors-amilopril
Aldosterone inhibitors-spironolactone eplerenone
Angiotensin blockers-losartan valsartan
CCB -amlodipine nifedipine
Diruetics-furosemide ,thiazide(chlorthalidone)
Imidiazole receptors -
Increase Alpha 2 agonist receptors -clonidine
Classification of Blood pressure by stage
Stage one
Characteristised by presence of on,y risk factors without change in target organs
Stage two
Presence of target organs affection
Stage three
Characterised by association with clinical disease eg diabetes Miletus stroke ischemic heart disease
Extra more detailed info
This is for informational purposes only. For medical advice or diagnosis, consult a professional.
The renin-angiotensin-aldosterone system (RAAS) is a complex hormonal system that plays a crucial role in regulating blood pressure, fluid balance, and electrolyte balance in the body. It’s a key player in the long-term maintenance of blood pressure. Here’s a simplified breakdown of how it works:
1. Renin Release:
* When blood pressure drops or blood flow to the kidneys decreases, the kidneys release an enzyme called renin.
2. Angiotensinogen Conversion:
* Renin converts angiotensinogen, a protein produced by the liver, into angiotensin I.
3. Angiotensin II Formation:
* Angiotensin I is converted into angiotensin II by an enzyme called angiotensin-converting enzyme (ACE), primarily in the lungs.
4. Angiotensin II Effects:
* Angiotensin II has several powerful effects on the body:
* Vasoconstriction: It narrows blood vessels, which increases blood pressure.
* Aldosterone Release: It stimulates the adrenal glands to release aldosterone.
* Sodium and Water Retention: Aldosterone increases sodium reabsorption in the kidneys, which leads to water retention, increasing blood volume and blood pressure.
* Other Effects: Angiotensin II also stimulates thirst, increases heart rate, and has other effects that contribute to raising blood pressure.
In Summary:
The RAAS is a feedback loop that helps maintain blood pressure. When blood pressure falls, the RAAS is activated to raise it. When blood pressure is high, the RAAS is suppressed.
Clinical Significance:
The RAAS plays a significant role in the development and progression of hypertension (high blood pressure). Many medications used to treat hypertension target different components of the RAAS, such as ACE inhibitors (which block the conversion of angiotensin I to angiotensin II) and angiotensin receptor blockers (ARBs), which block the effects of angiotensin II.
Important Note: This is a simplified explanation of the RAAS. It’s a complex system with many interacting components and feedback loops. If you have any concerns about your blood pressure or the RAAS, please consult with a healthcare professional.
