Patho exam 2 Vascular Disease

Blood Pressure

Arterial

 Propels blood to all other tissues of the body (i.e., systemic circulation)

 Arteries are muscular and have a higher blood pressure ~120/80 mmHg

 Venous

 Propels blood through the lungs (i.e., pulmonary circulation)

 Veins are thin-walled and have a much slower rate of flow and lower pressure—

 Blood pressure is push or force of blood in the blood vessels

 Highest in arteries, lowest in veins

 Blood pressure gradient causes blood to circulate—liquids can flow only from the

area where pressure is higher to where it is lower

 Pressure is highest when ventricles contract (systolic pressure)

 Is the measure of the force of ventricular contractions as blood is ejected into

the large arteries

 Pressure is lowest when ventricles relax (diastolic pressure)

 Is the measure of the rate of ‘run off’ of blood into the capillaries, which is

governed by the peripheral resistance caused by the small arterioles

 Blood volume, vessel size, and blood viscosity are main factors that produce blood pressure

 Blood pressure varies within normal range from time to time

cardiac output/peripheral resistance

Cardiac output: The amount of blood that the heart pumps in 1 minute--stroke volume (amount of

blood pumped out of ventricle) X heart rate

Peripheral resistance: regulated by neural and hormonal inputs to the arterioles

 Balance between vasodilators and vasoconstrictors

adjustments of blood pressure are governed by

Adjustments of blood pressure are governed by:

 Sympathetic nervous system (norepinephrine/epinephrine)-arterial constriction

(increase peripheral resistance) and increases heart rate/contractility

 Parasympathetic nervous system-(acetylcholine)-decreases peripheral resistance &

decreases HR and contractility

 Hormones:

Antidiuretic hormone: Increases water reabsorption in kidneys—increasing blood

volume

 Kidneys -controls blood volume and secretes renin—ultimately results in release of

aldosterone

 Renin is secreted in response to decreased blood pressure in afferent arterioles

of kidney

 Renin activates angiotensin

 causes arteriolar constriction, which increases blood pressure.

 Angiotensin also triggers the release of aldosterone, which causes the kidneys to

retain salt (sodium) and water, thus expanding blood volume and further

increasing blood pressure.

Dysfunction Blood Pressure Regulation

Hypotension: decrease in blood pressure

 results in inadequate perfusion of organs

 Perfusion means the amount of blood supplying an organ

 Hypertension: increase in blood pressure

Hypertension

High blood pressure is a common condition of long-term force of the blood against artery walls

 A sustained Systolic pressure> 130 mm Hg or higher

 Or A sustained Diastolic pressure of 80 mmHg or higher

 Clinical manifestations:

 Commonly silent and gradual onset with no symptoms

 Fatigue, dizziness, headache and malaise

 Symptoms/signs also depend on the target organ

Pathogenesis of hypertension**

 Increase cardiac output/increase in circulating volume

 Increase heart rate or increase stroke volume

 Increase peripheral resistance

 Increase blood viscosity

 Vasoconstriction of arterioles

types of hypertension

. Essential/Primary or Idiopathic

 Most common (90 – 95%)

 Usually begins insidiously, a chronic disease

 Mechanism of essential hypertension (multifactorial)

 Genetic factors

 Not totally known

 Influence of sodium reabsorption and renin-angiotensin-

aldosterone pathway--Important factor in increase BP

 Reduced renal sodium excretion

 Decreased sodium excretion leads to increase in fluid volume

 Vasoconstrictive influences: Nicotine in smoking

 Environmental factors: Age, obesity (increase atp demand increase

blood volume to meet this need), high sodium diet (fluid retention),

stress

2. Secondary Hypertension

 Related to systemic diseases that raise peripheral vascular resistance of cardiac

output

 Etiology of secondary hypertension: Chronic renal disease, Endocrine

diseases (Diabetes mellitus, cushing’s syndrome, for example)

 Appears suddenly

Hypertentive Heart Disease

This condition is caused by long-standing high blood pressure or hypertension.

 Increased peripheral resistance

 Cardiac effects: increased peripheral resistance → higher workload → heart enlarges by

hypertrophy → heart failure

 Enlarged left ventricle requires increased nutrients and oxygen

 Eventually coronary blood flow cannot keep up with demand from enlarged ventricular muscle

 Makes ventricle susceptible to ischemia, infarction, and heart failure

 Eventually the enlarged muscle protrudes into the chamber, which reduces the amount of blood

volume filled within, reduces cardiac output--heart fails to supply adequate body circulation

Atherosclerosis

A chronic inflammatory and healing response of the arterial wall to endothelial injury

 Predisposing factors: Increase Cholesterol level, smoking and hypertension, genetic

 Age: can begin to see changes early, clinical manifestations not seen until 40 – 60 years

 Most common vascular disease

Affects large arteries (abdominal aorta, common iliac arteries, coronaries, femoral, popliteal,

carotids, major brain vessels)

 Causes CAD, cerebrovascular disease, peripheral arterial disease

 Characteristic lesion is formation of atheroma or atheromatous plaque

 Consists of deposition of lipid and connective tissue within the vessel wall.

 Lipid deposits are from cholesterol in blood stream diffusing into the arteries

Unstable/stable plaque

Unstable plaque

 Irregular mass of yellow, mushy debris encroaching on lumen of artery and extending

into muscular and elastic tissues of arterial wall

 Initially can be reversible

Stable plaque

 Surrounded by fibrous tissue--harden

 Causes permanent narrowing of vessel

Atherosclerosis Etiology

Endothelial damage or dysfunction of endothelium is the initiating factor of the development of

atherosclerosis

 Caused by hypertension, smoking (contain oxygen free radicals), increase in low density

lipoproteins (LDL), decrease in HDL, hypercholesterolemia (seen in Diabetes mellitus),

immune mechanisms, high glucose levels

 The 2 most important factors: hypertension and hypercholesterolemia

 Lowering cholesterol by diet or meds slows progression

 Risk factors: increase age, male, post-menopausal women, genetics (familial

hypercholesterolemia)

LDL & HDL

 LDL and HDL transport cholesterol between liver and other tissues that metabolize

cholesterol

 LDL Can be taken up by arterial endothelial cells and accumulate in walls

 Bad cholesterol

 Deposits in areas of arterial damage

 HDL transports cholesterol to liver where it is lost to intestine in bile

 Good cholesterol because it is excreted

atherosclerosis Pathogenosis

: Endothelial injury/dysfunction → monocytes adhere and migrate into intima (inner

layer) and then media = are now called macrophages

 Cholesterol and lipids (LDL) accumulate in cytoplasm (unstable plaques) of macrophage

(foam cells) –reversible initially

 Foam cells accumulate, collect lipids and form plaque

 Prone to rupture and hemorrhaging results

 Can transmit cholesterol back to circulating HDL and be excreted

 High levels of LDL in blood is a stimulus that prevents cholesterol leaving

foam cell

 Results in narrow vessel lumen, which reduces blood flow to organ

 Predisposes to thrombus formation

 Caused by slowing and turbulence of blood flow and “rough” endothelial surface

 Initiates intrinsic clotting mechanism

 Pieces of plaque can break loose and suddenly block arteries (embolism)

 Fibrous plaque can break open leading to hemorrhage

 Weaken arterial wall leading to aneurysm (see below)

Atherosclerosis Diagnostic Test

Lipid profile

 Total cholesterol, LDL, HDL, and triglyceride

 C reactive protein

 Acute phase protein made by liver in response to system inflammation

 Atherosclerosis is an inflammatory process

 Used to predict CV disease/stroke

 CT scan, MRI , ultrasound, EKG

 Abnormal sounds heard over affected artery-usu. Large arteries or near skin

 Bruit sound- turbulence created by abnormal vessel

 Thrill- vibration sensation on palpation of vessel

 Angiography: radiopaque dye and x-rays

TREATMENT

 Diet, lifestyle changes (exercise) , lowering cholesterol

 Angioplasty: open occluded arteries, bypass procedures

 Laser to disintegrate the plaques

Aneurysm pathogenesis/clinical presentation/diagnostic tests/treatment

Aneurysm is a focal dilation of the wall of arteries, veins, or the heart.

 2 most important causes: hypertension and atherosclerosis

 causes degenerative changes in the walls—weakens wall

 Some other causes are as follows: syphilis, rheumatoid arthritis, genetics, and trauma.

PATHOGENESIS

 bulge in arterial wall caused by weakened vessel

 Results in turbulent blood flow- predisposes to clots

 Pieces of this clot can break off causing occlusion of smaller peripheral vessels

downstream (embolism).

 Weakened portion can rupture

CLINICAL PRESENTATION

 The clinical presentation is contingent upon which vessel and which segment of the vessel is

dilated

 Most cases of abdominal aortic aneurysms are asymptomatic and are discovered incidentally on

physical exam as an abdominal mass, which is often palpated as a pulsating mass.

 - Rupture into the peritoneal cavity or retroperitoneal space resulting in massive and possible

fatal hemorrhage.

DIAGNOSTIC TESTS AND TREATMENT

 X-ray of Ultrasound techniques can diagnose and measure aneurysms.

 A computed tomography or CT scan is accurate in determining the shape and size of an

aneurysm.

 Early detection prevents rupture.

 Surgical procedures have been very successful in repairing blood vessels affected by aneurysm

formation.

Peripheral Arterial Disease clinical presentation/what is it

Arterial occlusive disease that occurs when arteriosclerotic plaque or thrombus (clot)

blood flow to lower extremity

 Femoral artery is most common, but can occur in popliteal, iliac or tibial arteries

 Acute  sudden blockage leads to ischemia and necrosis

 Chronic (more common)  silent for years

CLINICAL PRESENTATION

 Intermittent cramping leg pain (lactic acid accumulation)

 Symptoms may ease after resting

 Weak or absent pulses in the legs or feet

 Sores or wounds on the toes, feet, or legs that heal slowly, poorly, or not at all

 A pale or bluish color to the skin

 A lower temperature in one leg compared to the other leg

 Poor nail growth on the toes and decreased hair growth on the legs

Varicose Veins

abnormal dilated superficial vein

 Superficial Leg veins most common because hold large amount of blood

 Caused by incompetence of valves from increase pressure over time

 Damaged valves become less competent at preventing backflow from one section of

vein into another segment

 Gravitation pull and prolonged standing promote pooling of blood in lower extremities

 Etiology: prolonged standing, sitting, pregnancy, and obesity, low activity, genetic

 Complications result from stasis of blood in the veins

 Poor nutrition to tissues (skin of distal leg) caused by chronic venous engorgement,

which can lead to skin ulcers

 Dilated veins can rupture

 Stasis of blood predisposes to repeated bouts of thrombophlebitis (an inflammatory

process that causes a blood clot to form and block one or more veins)

 Hemorrhoids are varices in the veins of the rectum and anal canal.

 They are also caused by increase in pressure and are commonly associated with chronic

constipation involving straining to defecate.

Deep venous Thromboembolism etiology/clinical presentation/sequila/what is it

Thrombus (blood clot) develops in deep leg vein accompanied by inflammation

 Deep venous thrombosis involving large leg veins (popliteal, femoral or iliac)

 Predisposition for thrombus development:

 venous stasis: slowing of blood allows platelet aggregation and clotting factors

adhere to wall

 vascular damage: attract platelets and stimulate clot formation

 hyper- coagulability: promote clot formation

 All these factors are known as Virchow’s Triad

ETIOLOGY: poor venous return associated with low activity or valve dysfunction in leg veins,

conditions that cause vascular damage (surgery or trauma), immobility, surgery, estrogen

(hypercoagulability), smoking

CLINICAL PRESENTATION: redness, tenderness and warmth over a vein, edema

 Often form silently and may be asymptomatic

DIAGNOSTIC TEST: angiography, CT or MRI

TREATMENT: increase mobility, hydration, antiembolism hosiery, compression devices, anti-

platelets/coagulants

SEQUELA: pulmonary embolism (PE)

 Venous thrombus travels from leg vein into inferior vena cava and into the

pulmonary arterial circulation and often results in fatal PE

 Embolism= a blockage in a blood vessel caused by a traveling mass

 Embolus: an unattached mass—such as a blood clot, fat globule, air

bubble, or piece of plaque that travels through circulatory system