Arthrosclerosis

hardening of the gruel- Formation of fibro lesions in the intimal layers of arteries= hardening of arteries.

Liprotein

• ·         Cholesterol & Trigycerides- essential for all body functions- insoluable in plasma so they can’t get around in blood on their own.

• ·         Lipoprotiens- carry cholesterol & Triglyseride

1. §  The more protein the higher densisty= HDL

1. §  The more lipid the lower the densisty= LDL

High Density Lipoproteins=GOOD

• ·         Carry Cholesterol from peripheral circulation back to the liver

• o   When HDL is very high it can reabsorb some of the cholesterol out of the plaque and reverse some of atheroscolorsis

• o   HDL CHO returns to the liver and is excretes in bile rather then used to form more LDL

Regular exercise & moderate alcohol intake increase HDL

Low Density Lipoprotein

• ·         Main carrier of Cholesterol

• ·         We need it for everything – membranes/ hormones synthesis (70%) don’t want to get rid of all of it

Receptor dependent pathway

• o   - gets rid of 30%- has to go by cells that have receptors.

• §  HEPATOCYTES- Remove 75% LDL from circulation in liver

• §  NON- HEPATIC TISSUE- take rest (30%) (adrenals, sm muscle, lymph)

• §  SCAVENGER PATHWAY- Monocytes/macrophages ingest the rest (30%) LDL to get it out of circulation- excess cholesterol accumulates in tissues

Hyperlipidemia

• ·         Caused by high dietary intact

• ·         Caused by Genetic- autosomal dominant trait-

1. o   Causes defect in lipoprotein carriers

1. o   Lack of CHO receptors in the liver-

1. o   Defective CHO metabolism

Can’t carry them around

  Can’t hook up in liver

  Can’t use them in the cells

So we got these fatty streaks how do they get their? This is the process

• ·         Endothelial Cell injury- somewhere in cell there is injury could be due to blood flow, may have a lot of blood glucose= causes  turnaic blood flow = damage as soon as there is damage this causes

• ·         Migration of inflammatory cells- Macrophages move into vessels engulf LDL to get lipid out

• ·         Lipid Accumulates and smooth muscle cell proliferate- Macrophages have moved into tissue and absorbed as much lipid as they can, at this point they care called foam cells full of lipids cant move as they use to, still secreating inflame mediatory. Platelets form a patch over the top- muscle desinigrates in muscle

• ·         Plaque structure- collogen comes to try and heal fibrous cap formation, now have more turbulent blood flow. Now vessel is occluded vessel will eventually rupture. Will move down stream and clog a vessel any thing below this vessel will now no longer have blood flow.

Things that make a plaque more vulnerable=more easy to rupture?

·         Large lipid core

·         Thin fibrous cap- very easy to knock out

·         Fissured cap- cap with a bruise

·         Inflammation within cap

·         Superficial endotheial erosion- platelet aggregation.

Process of Athrosclerosis happens all over the body not just the heart.

·         A lot of turbulent B/F start vascular problems

Women C/0 Pain in LLE

·         Foot cool & Pale-

·         Reports often red/ warm when sitting-

·         Pain with walking- 

·         Skin on LLE shinier then RLE-

·         Foot cool & Pale- no B/f weak Pedal pulse

·         Reports often red/ warm when sitting- B/F decreased

·         Pain with walking- Prostoglandins

·         Skin on LLE shinier then RLE- lose fat layer under skin can’t maintain tissues

Aterial Structure Disorders: Aneurysms- blood gets inside lumen causes rupture/ hemmorage

·         Wall of artery weakens and stretches

·         Risk of rupture and hemorrhage

·         Risk of clot formation

·         Treatment- Stent Grafts-

o   Opens up like umbrella

Varicose Veins- veins wear out incompetent valves- harbers clots

• ·         Venous stasis

• ·         Valves become incomplete

• ·         Loss of Vascular Muscle tone

• ·         Vessels dilate causes

o   Stasis dermatitis- brown looking color RBC break down hemoglobin now in tissue

o   Ulcerations- d/t no blood flow

Venous Thrombus-

·         Thrombophelbitis- clots that gets loose and settles in a vessel= DVT, now will have injury, stasis blood flow, hyper-reactivity coagulation

·         Precursor to venous insufficiency & PE

·         When we have Venous stasis we are prown to thrombopheblitis & PE

Blood Pressure

·         Reflects rhythmic changes as blood moves through the heart

·         Systolic

o   Left ventricular contraction

·         Diastolic

o   Left Ventricular relaxation

·         Mean arterial pressure

o   60- Average of all pressure together, good indication of good tissue prefussion

·         Pulse pressure

o   Systolic-diastolic- 40- prepresents general compliance of major vessels if systolic is high indicates artherosclerosis

BP Regulation-

• o   Neural control- Lower pons and medulla cardiovascular center rapid, short-term regulation,

• o   Pheripheral control-Baroreceptors- in cartotid & Aortic arch respond to pressure changes SNS heart rate and Vasoconstriction

Renin Angiotension Aldosterone

• o   Decreased BP-renin release angiotensinogen- angiotensis 1 ace lungs (weak) Angiotension 2- vasoconstriction release aldosterone= Save sodium water excrete possium=increase blood volume. Angiotension 2= increase afterload.

ADH & ANP

•   ADH

·         Released from posterior Pituitary with increased serum osmolarity

·         Stops excretion of NA & water increase blood volume = increase bp

• o   Atrial Natriuretic Peptide

§  Released from over stretched Atria

§  Increase Na + water excretion vasodolation decrease Preload & afterload decrease BP.

HTN

o   Primary- unidentifiable cause

o   Secondary- with identified caused this is what we see more in clinical situation.

Classification of BP

o   Normal 120/80

o   Pre-hyp SP 120-139 0r DP 80-89

o   Hypertension stage 1 SBP 140-159 or DP 90-99

o   Hypternsion stage 2 SP >160 or DP >100

Isolated systolic hypertension

o   Greater risk for kidney heart disease stroke ex

Orthostatic Hypertention

o   BP medication will prevent us from being able to handle this

How will this effect your BP

• o   Vasodilation-

• o   Decrease stretch of baroreceptor

• o   Hypoxemia-

• o   Inhibit angitenstion enzyme-

• o   Beta Blocker-

• o   Calcium Blockers-
  

• o   Vasodilation- decrease BP

• o   Decrease stretch of baroreceptor- increase BP

• o   Hypoxemia- Increase BP

• o   Inhibit angitenstion enzyme- Decrease BP

• o   Beta Blocker- Decrease BP

• o   Calcium Blockers- Decrease Blockers