Patho Exam #3 Pt. 2 (26 & 28, 27)

Arteries

Blood vessels that carry blood away from the heart to the body's tissues

Mostly oxygen rich

Have thick, elastic muscular walls

Veins

Blood vessels that carry blood toward the heart from the body's tissues

Usually oxygen-deprived blood

Have thinner walls

Capillaries

Smallest blood vessels

Responsible for exchange between blood and interstitial fluid

Interna, media, externa

Three layers of arteries and veins

Regulates thrombosis, transfer of substances, regulates blood flow

Three functions of vascular endothelium

Regulates thrombosis

Function of vascular endothelium

Releases tissue plasminogen activator (t-PA), which helps dissolve blood clots

Controls transfer of substances

Function of vascular endothelium

The movement of molecules between the blood and surrounding tissue

Regulates blood flow

Function of vascular endothelium

Releases nitric oxide, which relaxes vascular smooth muscle and causes vasodilation

SNS activation

How vascular smooth muscle regulates blood pressure

Release of NE, which binds to receptors on vascular smooth muscle which causes vasoconstriction and + BP

Systolic pressure

Exerted when blood is ejected from ventricles during contraction

Diastolic pressure

Sustained pressure when ventricles relax

Cardiac output, blood volume, blood vessel diameter

Three factors altering blood pressure

Cardiac output

Volume of blood pumped by one ventricle per minute

Parallel

Blood volume has a _____ affect on cardiac output and BP

Baroreceptor reflex

Primary neural mechanism for short-term blood pressure regulation

Negative feedback loop

Baroreceptors

Stretch-sensitive receptors located inwalls of carotid sinuses

Detect changes in BP and signal brain to adjust heart rate, cardiac output, blood vessel diameter

Hormonal regulation

Type of blood pressure regulation

Slow, long-term process that adjusts B>V and systemic vascular resistance

Associated with ADH and RAAS

Antidiuretic hormone (ADH)

Increases water reabsorption by the kidneys
Raises blood volume and blood pressure

Renin-angiotensin-aldosterone system (RAAS)

Activated when BP, blood volume, or kidney perfusion decreases

Vasoconstricts and increases water retention

Epinephrine

Hormone that increases heart rate and cardiac contractility

Fight or flight

Low blood pressure detected

Renin converts angiotensinogen to angiotensin I

ACE converts angiotensin I to angiotensin II
Angiotensin II causes vasoconstriction and aldosterone rlease

Aldosterone increases sodium and water retention by kidneys

Result: BP increases

RAAS steps (4 total)

Lipoproteins

Transport cholesterol and triglycerides through blood stream

Types: Chylomicrons, VLDLs, LDLs, HDLs

Chylomicrons

Type of lipoprotein

Transport dietary triglycerides

VLDLs

Type of lipoprotein

Transport triglyercides synthesized in liver

LDLs

Type of lipoprotein

Transport cholesterol from the liver to body cells

Bad cholesterol - Particles can build up in artery walls and contribute to plaque formation (atherosclerosis), raising the risk of heart attack and stroke.

HDLs

Type of lipoprotein

Transports excess cholesterol from peripheral tissues back to the liver

Good cholesterol - High levels associated with lower cardiovascular risk

Hypercholesterolemia

High level of cholesterol in the blood

240 mg/dL or higher

Contributes to cardiovascular event

Primary

Type of hypercholesterolemia

Caused by genetic factors

Secondary

Type of hypercholesterolemia

Caused by medical or lifestyle factors

Arteriosclerosis

Loss of elasticity in the arteries

Atherosclerosis

Type of arteriosclerosis

Buildup of fatty plaques called atheroma in the walls of large arteries

Artheromas

Fatty plaques containing cholesterol and other lipids, inflammatory cells, and fibrous tissue

Steps of atherosclerosis

Endothelial injury

LDLs accumulate in damaged wall

LDLs oxidize, promoting inflammation and free radical formation

Inflammatory chemicals are released to attract immune cells

Macrophages engulf oxidized LDL

Smooth muscle cells migrate to form a fibrous cap

Stable

Type of plaque

Grows slowly and narrows the artery over time

Causes reduced blood flow

Unstable

Type of plaque

More likely to rupture and erode
May block artery or become and embolus

Fatty streaks, fibrous atheromatous plaque, complicated lesion

Progression of atherosclerosis

Fatty streaks

Progressive stage of atherosclerosis

Appear as thin, flat, yellow discolorations in the intima that progressively enlarge

Fibrous atheromatous plaque

Progressive stage of atherosclerosis (2nd)

Develops as lipids accumulate and fibrous cap forms over lip core

Complicated lesion

Progressive stage of atherosclerosis

Advanced, more complicated atherosclerotic plaque

May rupture, cause ulceration, hemorrhage

Thrombus formation

Large artery complication

Vessel occlusion (ischemia, infarction)

Medium artery complication

Peripheral arterial disease (PAD)

Narrowing or blocking of arteries supplying the LOWER extremities due to atherosclerotic plaque buildup

Asymptomatic

PAD is initially _____

Classic symptom of PAD

Intermittent claudication: cramping, aching, or fatigue in the leg muscles (most often the calf, but also thigh or buttock) that comes on with walking or exercise and eases within a few minutes of rest.

Acute arterial occlusion

Sudden blockage of arterial blood flow caused by thrombus or embolus

Occurs with patients of pre-existing PAD

Pistol shot, pulselessness, paralysis, parethesia, pallor

5 Ps of acute arterial occlusion

Pistol shot

Manifestation of acute arterial occlusion

Acute, sudden severe pain

Paresthesia

Manifestation of acute arterial occlusion

Abnormal sensation of the skin without an obvious physical cause,

Pallor

Manifestation of acute arterial occlusion

Abnormal paleness of the skin and mucous membranes, caused by reduced blood flow or a decreased amount of hemoglobin

Thromboangitis Obliterans (TAO)

Rare, progressive, non-atherosclerotic inflammatory disease that affects small and medium sized blood vessels

Inflammation

Narrowing and occlusion

Reduced blood flow

Occlusion

Blockage or closing off of a hollow structure, such as a blood vessel, so that flow through it is reduced or stopped

Aneurysm

Localized dilation and weakening of arterial wall

Saccular, fusiform, dissecting

Three types of aneurysms

Saccular

Type of aneurysm

Localized, sac-like bulge on one side of arterial wall

Fusiform

Type of aneurysm

Circumferential dilation along a section of artery

Dissecting

Type of aneurysm

Hemorrhage into vessel wall forming a blood-filled channel

Occurs when a tear develops in the tunica intima allowing blood to enter and separate the layers of the arterial wall

Life threatening

Berry aneurysm

Type of aneurysm dictated by location

Commonly occur in the Circle of Willis in the brain

Consists of a small, spherical vessel dilation

Thoracic or abdominal aorta

Where do saccular and fusiform aneurysms occur

Abdominal aortic aneurysm

Type of aneurysm

Wall of aorta weakens and stretches

Frequently asymptomatic with increased risk of clotting, rupture, hemorrhage

Blowing sound

Pulsating abdominal mass

Varicose veins

Enlarged, dilated, and tortuous superficial veins

Faulty valves allow blood to flow backward and accumulate

Common in legs

Thrombophlebitis

Inflammation of a vein associated with the formation of a blood clot

Serious risk of pulmonary embolism - blockage of a pulmonary artery in the lungs

Virchow’s triad

Three major risk factors that increase chance of venous thrombosis

Venous stasis - sluggish, reduced blood flow

Endothelial inury

Increased blood coagulability

Venous stasis - sluggish, reduced blood flow

Endothelial inury

Increased blood coagulability

What are the three factors of virchow’s triad?

Hypertension

High blood pressure; 130.80 mmHg or higher

Primary (essential) hypertension

High blood pressure with no identifiable single cause

Develops gradually over many years

Increased SNS activity

Arteriolar vasoconstriction

SNS activity of primary hypertension

Increases total peripheral resistance - resistance or opposition to blood flow

(+) heart rate and cardiac contractility

SNS activity of primary hypertension

Increases cardiac output

Stimulation of RAAS

SNS activity of primary hypertension

Promotes sodium and water retention, increasing BP and B.V

Secondary hypertension

High BP caused by identifiable cause

Renal disease

Common cause of secondary hypertension

Kidney disorders that affect fluid balance and BP regulation

Endocrine disorders

Common cause of secondary hypertension

Hormonal imbalances that increase BP

Pheochromocytoma

Rare tumor of adrenal medulla that releases excess adrenaline and noradrenaline

Malignant hypertension

Type of hypertension

Severe, rapidly progressive form of hypertension that can cause acute damage to vital organs

Left ventricular hypertrophy

Complication of hypertension

Left ventricular wall thickens when heart needs to work harder to pump blood against increased vascular resistance

Leads to heart failure

Example of diastolic heart failure since heart cannot relax

Nephrosclerosis

Complication of hypertension

Damage and hardening of small renal blood vessels due to long-standing hypertension

Glomerular damage

Complication of hypertension

Reduced blood supply and injury to the glomeruli

Stroke

Complication of hypertension

Hypertension damages and weakens cerebral B.V

Increased risk of ischemic and hemorrhagic _____

Cardiac conduction system

Group of specialized cells that generate and transmit electrical impulses

SA node

Component of cardiac conduction system

Pacemaker - sets rate at risk to 60-100 BPM for adults

AV node

Component of cardiac conduction system

Briefly delays the impulse, allowing the ventricles to fill with blood before they contract

AV Bundle

Component of cardiac conduction system

Carries impulse from the AV node

Right and left bundle branches

Component of cardiac conduction system

Conduct electrical impulses down the interventricular septum

Purkinje fibers

Component of cardiac conduction system

Spreads impulse rapidly through ventricular muscle

P wave

Segment of normal ECG

Depolarization of atria

QRS wave

Segment of normal ECG

Depolarization of ventricles

T wave

Segment of normal ECG

Repolarization of ventricles

P-R interval

Segment of normal ECG

Beginning of atrial excitation to begining of ventricular excitation

S-T segment

Segment of normal ECG

Entire ventricular myocardium depolarized

Q-T interval

Segment of normal ECG

Beginning of ventricular depolarization through ventricular repolarization

Heart rate

Heart beats per minute

Distance between two consecutive R waves (RR interval)

Herat rhythm

Pattern and regularity of the heart’s electrical activity

Arrythmias

Deviations from normal cardiac rate of rhythm, caused by disturbances in the heart’s electrical conduction system

Can cause reduction of efficacy of heart’s pumping cycle

Sick sinus syndrome

SA node abnormality

Alternating episodes of fast and slow heart rhythms

Heart block

AV Node Abnormality

Electrical impulses blocked

First degree, second degree, third degree

First degree AV Block

Impulses delayed, but all impulses reach ventricles

PR interval longer than 0.2 seconds

Second degree AV Block

AV Node Abnormality

Every second to third atrial beat dropped at AV node causing slower rate or irregular heart rhythm - progressive long PR

Third degree AV block

AV Node Abnormality

No transmission of electrical signal from atria to ventricles

Ventricular tachycardia

Ventricular Conduction Abnormality

Ventricular rate 100-200 bpm

Reduces cardiac output due to reduced diastole

Ventricular fibrillation

Ventricular Conduction Abnormality

Muscle fibers contract independently and no rapid cardiac output

No identifiable ECG components - just a squiggly line

Serous pericardium

Thin membrane that encloses heart divided into two layers:

Parietal - Lines wall of body cavity

Visceral layer - Covers the surface of the organ