Pathological Effects of Hypertension Flashcards
Arteriosclerosis
Hardening of medium-large sized vessels
Atherosclerosis
Hardening of vessels due to the deposition of lipids/formation of atheromas
Atheroma
A fatty deposit within the wall of blood vessels
State the 4 stages in the formation of an atheroma
A DISEASE OF THE TUNICA INTIMIA
Fatty streak, lipid plaque, fibro-lipid plaque, complicated atheroma
Describe the formation of an atheroma
Damage to the endothelium of the vessel, leading to decreased production of NO, increased endothelial permeability and leukocyte adhesion. LDL particles accumulate within the tunica intima. Oxidised LDL particles are taken up by macrophagespresent within the tunica intima. The macrophages become foam cells. AFATTY STREAKis formed. The macrophages secrete cytokines which stimulate fibroblasts. Thefibroblasts secrete collagenand the fatty streak become fibrotic. ALIPID PLAQUEis formed. As the lesion develops it causespressure atrophy on the tunica media.More collagen is secreted causing the plaque to become harder and white in colour, aFIBROLIPID PLAQUEis formed. Collagenization affects the media, weakening the arterial wall. The endothelium is also weakened and often ulcerates, allowing thrombosis and platelet aggregation. This is aCOMPLICATED ATHEROMA.
Describe the histological structure of blood vessel walls and how each layer contributes to the function of the vessel
Tunica intimia: Formed from the endothelium, basement membrane and lamina propia CT
Internal elastic membrane
Tuncia media: A muscular layer. Contains elastin. Allows control of lumen diameter
External elastic membrane
Tunica adventica/externa: A fibrous CT. Contains nerves and vessels
Explain the differences in structure between and artery and a vein
Lumen: Lumen diameter is increased in veins
Smooth muscle: Veins contain less smooth muscle, as the vessels are under much less pressure (smaller tunica media layer)
Valves: Veins contain valves to prevent the back flow of blood
Muscle pump action: Help the flow of blood through veins back to the heart
Explain the role of each type of vessel in the circulatory system and how damage to vessel structure leads to pathological consequences
Veins: Allow the return of blood from the systemic circulation back to the heart
- Damage: Incorrect functioning of the valves leads to the formation of varicose veins
Arterioles: Responsible for the regulation of TPR and blood pressure
- Damage: Constant constriction (may be caused by hypertension) leads to s_mooth muscle hypertrophy_ and vessel wall thickening. Arteriolosclerosis results. This means they are no longer able to control their diameter effectively.
Arteries: Carry oxygenated blood to tissues
Capillaries: Form capillary beds - essential for the transfer of oxygen, nutrients, CO2 and waste products
From which renal cells is Renin excreted?
Juxtaglomerular cells - JGA
Released in response to decreases renal perfusion.
Define hypertension and explain the classification of hypertension.
Normal blood pressure = 120/80 mmHg
Hypertension: The level of blood pressure at which treatment does more good than harm. 140/90 mmHg
- May be primary or secondary. May also be benign or malignant
Provide potential mechanisms and risk factors for primary hypertension
MULTIFACTORIAL
- Increased SNS acivity (increased inotropy and chonotropy)
- Increased RAAS acivity
- Renal pathology (role in regulating BP)
- Age
- Gender
- Diet: High salt intake
- Obesity
- Excessive alcohol consumption
Explain the factors regulating hypertensive blood pressure
RAAS/Defects in renal sodium homeostasis
Physiological vasoconstriction
Abnormalities in vascular smooth muscle growth and structure
Identify the risk factors for hypertension
MULTIFACTORIAL
Genetic and environmental factors interplay.
Age, gender, ethnicity
Diet, obesity, medication (corticosteroids, contraceptive), excessive alcohol intake
Identify the common causes of secondary hypertension.
- Renal disease: Renal artery stenosis (leading to failure
- Decreases renal perfusion causing RAAS activation which increases BP
- Endocrine disoders: Cushing’s, hyperthyroidism (Grave’s)
- Tumours: Phaeochromocytoma (a tumour of the adrenal gland, causes increased production of catecholamines in the adrenal medulla)
- Aortic coarctation
- Medication: Oral contraception
Can often be cured by surgery or treatment
Describe the pathological changes in blood vessels due to hypertension (including atherosclerosis and arteriolosclerosis)
Atherosclerosis: Hardening of blood vessels due to the deposition of fat within the vessel wall (tunica intima). Hypertension is a major risk factor.
Ateriolosclerosis: Hardening of the small arteries and arterioles due to hyaline cartilage deposits
- Most commonly caused by high blood pressure. The vessels must consistently contract to control blood flow. Leads to hypertrophy of the smooth muscle layer (tunica media) and sclerosis of the vessels, through the recruitment of fibroblasts which deposit hyaline.
- Damage to the endothelium is also seen, allowing protein to leak from vessels
- Can be attributed to the increased levels of AGE (advanced glycosylation end products) which act to modify cellular proteins and receptors, disrupting their function.
Ateriosclerosis: Hardening of medium to large sized vessels
