Exam 3- Path

arterial system

arterial system

•High amounts elastin. Smooth muscle drives blood through system

venous system

•low pressure system with valves (skeletal muscle pump)

capillary permeability

• Spacing between epithelial cells determines which molecules can pass.

lymphatics

•accessory route for fluid

tunica intima

•Single layer of endothelium, smooth interface with blood

tunica media

•Smooth muscle: controls vessel diameter

tunica externa

•Primarily collagen: protection

nitric oxide

causes vasodilation

endothelin and angiotensin II

causes vasoconstriction (through the RAA system)

resistance

•opposition to flow

•Related to diameter of blood vessel, and viscosity of blood

hematocrit

volume of blood

Norepinephrine

drug that causes vasoconstriction

Mean arterial pressure (MAP):

calculated average of overall pressure throughout the cardiac cycle. (when it's greater than 60, there is adequate tissue perfusion)

cardiac output

the amount of blood the heart pumps per minute.

parasympathetic

•controls resting state

•Primarily via vagus nerve

•HR and PVR decrease

BP = CO x PVR

blood pressure equation

Baroreceptors

receptors in the carotid artery that send messages to the cardiovascular center from the brain

sympathetic nervous system

•PVR increases (alpha adrenergic)

•HR increases (beta adrenergic)

natriuresis

•hormones cause fluid loss (beta naturetic hormone- BNP)

Birth control, cold meds, NSAIDS, and cocaine

meds that can increase BP

endothelial dysfunction

damage with a decrease in Nitric oxide release.

left ventricular hypertrophy

consequence of long-term hypertension

Target Organ Damage

damage occurring in major organs fed by the circulatory system due to uncontrolled hypertension (can be heart attack, kidney failure, etc)

HDL (High Density Lipoprotein)

"good cholesterol" - collect other forms of lipoproteins and bring them back to the liver for metabolism

LDL (low density lipoproteins)

"bad cholesterol"

atherosclerosis

1.Endothelial injury

2.Buildup of oxidized LDLs in intima

3.LDLs engulfed by macrophages and form foam cells

4.Buildup of fatty streak, to plaque over time

5.Stenosis of artery/potential for plaque rupture and clot formation

DM or smoking

etiology of peripheral arterial disease

a blood clot (thrombus)

acute PAD is due to?

atherosclerosis

chronic PAD is due to?

clinical manifestations of PAD

•Intermittent Claudication.

•Thin, shiny skin

•Pulses weak or absent

•Cool feet

•Ulceration and Necrosis

smoking ad hypertension (more common in males)

etiology of aneurysm

weakening of arterial wall

patho of aneurysm

aortic aneurysm rupture

Life threatening

Cardinal symptoms are severe chest, abdominal pain or back pain, can't obtain BP (one or both arms)

Rx: emergency surgery for repair.

vessel wall injury, stasis of blood, hypercoagulability

virchow's triad components

deep vein thrombosis

blood clot forms in a large vein, usually in a lower limb. Risk factors include post-op, hip knee replacement, trauma/fractures, and immobility

clinical manifestations of DVT

•Pain

•Redness

•Swelling

•Warmth

coronary arteries

arteries lay on the surface of the heart. They branch off from ascending aorta at the coronary ostia. Fill during diastole when ventricle has just pushed a large amount of blood into the aorta. hence, there is increased pressure in the aorta which in turn pushes blood into the coronary arteries.

left anterior descending artery

supplies anterior portion of Left ventricle and most of the septum and papillary muscles of the left ventricle. Circumflex supplies lateral wall of left ventricle. (the "widow maker"- where many people have their heart attacks)

right coronary artery

supplies posterior of heart along with SA/AV nodes and right ventricle.

Na+, K+, Ca++, Mg

electrolytes that affect cell change polarity and action potential

circumflex artery

Supplies blood to the left atrium and posterior walls of the left ventricle

SA node, AV node, Bundle of His, Purkinje fibers

order of how the action potential travels down the heart

fixed/stable plaque

type of atherosclerotic lesion with thick cap on top

vulnerable/unstable plaque

type of athersclerotic lesion seen with acute coronary syndromes (unstable angina and MI). -Thin cap, large lipid core

unstable angina

chest pain that occurs while a person is at rest and not exerting himself (not predictable)

angina

chest pain

Atherosclerosis (fixed or partial obstruction)

etiology of (unstable) angina

myocardial ischemia (blood flow cannot keep up with oxygen demand)

patho of (unstable) angina

chronic stable angina

–Predictable: same symptoms, relieved with rest and/or NTG.

–Transient myocardial ischemia

–Occurs with increase in cardiac workload

acute myocardial infarction

-Complete occlusion of artery = No blood supply or O2.

-Cell death by ischemic injury and necrosis

troponin I

Preferred biomarker for determining cardiac necrosis

non ST-elevation MI

-ST depression or T wave changes

-Rise in biomarkers

-1-2 layers of heart affected

unstable angina

-ST depression

-No muscle damage

STEMI

-All layers affected

-Biomarker elevation

-Loss of contractility (C.O.)

-Arrhythmias

325 mg

How much aspirin should you give for a MI?

6-7 weeks

How long does it take for scar tissue formation post-myocardial infarction?

arrhythmia

Problem with impulse generation or conduction of impulses through the heart

atrial fibrillation

Which type of arrhythmia has an increased risk for blood clots?

pericardial effusion

-Fluid or blood build up in pericardial cavity

cardiac tamponade

Rapid life threatening compression of the heart chambers

erythropoiesis

production of red blood cells

hypoxia

stimulus of erythropoiesis

reticulocytes

immature RBCs

adequate iron stores, vitamins b12, and folic acid

production of RBCs requires?

120 days

lifespan of RBC

bilirubin

orange-yellow pigment in bile; formed by the breakdown of hemoglobin when red blood cells are destroyed. conjugated in liver and excreted in bile, then eliminated in stool

jaundice

increase in RBC destruction (hemolytic anemia) =

hemoglobin

o2 carrying component of RBC

37-52% (females slightly lower)

normal hematocrit

12-18 g/dL (females slightly lower)

normal hemoglobin levels

150,000-400,000 cells/uL

normal platelet count

decrease/change in production, loss (bleeding), increase in destruction (hemolysis)

etiology for low hemoglobin

anemia

Decreased O2 carrying capacity and tissue hypoxia

common clinical manifestations of anemia

Fatigue

SoB, especially with activity

Weakness

Tachycardia/palpation

Oral manifestations

Pallor

Jaundice

severe clinical manifestations of anemia

Hypotension (starts as orthostatic)

N/V, pallor, dizzy, diaphoretic

Increasing HR

hemolytic anemia

Destruction of RBCs

Hypersensitivity

Type II blood transfusion reaction

Hemolytic disease of the newborn (see also p 270).

rH- mom and rH + baby

Clinical manifestations: Common s/sx of anemia with jaundice (CNS toxicity)

autosomal recessive

etiology of sickle cell disease

sickle cell disease

Genetic: High incidence in African Americans.

Hemoglobin S: RBCs change shape

stress and hypoxia

Etiology: Autosomal recessive

Vessel Occlusion, Acute pain

Anemia and jaundice, Organ failure: Acute chest syndrome, renal failure CVAs

loss of hemoglobin synthesis

patho of iron deficiency anemia

iron deficiency anemia

Most common worldwide.

Etiology: Low intake, or chronic blood loss.

Patho: loss of hemoglobin synthesis, small pale RBCs

Clinical manifestations: Asymptomatic or mild common symptoms. Oral manifestations, koilonychia, pica.

Rx: Stop loss, replacement

Vitamin B12 Deficiency Anemia

pernicious anemia

Etiology: lack of Intrinsic Factor and low intake

Pathogenesis: DNA synthesis altered resulting in BIG cells with short lifespan

cobalamin

another name for b12

Anemia of chronic disease

Etiology: Many.

Example: renal failure

Impaired erythropoietin production.

Patho: multifactorial

General symptoms.

RX: Erythropoietin SQ (Epogen/Procrit) administered according to HGB level.

Polycythemia:

High RBC counts, HCT > 50%

secondary polycythemia

1.In response to tissue hypoxia

High altitude

Chronic lung disease (COPD)

Smoking

1. Vessel spasm

2. Platelet (PLT) Plug formation:

3. Blood Coagulation: clotting cascade

three stages of hemostasis

platelets

Contain numerous substances that play an impt. role in PLT aggregation and initial phase of clotting and repair.

Fibrinolysis

Clot Dissolution:

Tissue Plasminogen Activator (TPA) and Plasmin

Fibrin degrades, clotting factors deactivated.

Clot dissolves

arterial

turbulent flow: PLT activation (atherosclerosis leading to MI or stroke)

venous

stasis of flow (deep vein thrombosis)

clinical manifestations of bleeding

Cutaneous manifestations: Petechiae, purpura and ecchymosis.

Blood in urine

Bleeding gums

Blood in sputa or emesis

Epistaxis

Bleeding from procedural sites

Abnormal menstrual bleeding

heparin

most common cause of drug induced thrombocytopenia

Immune Thrombocytopenic Purpura (ITP)

Autoimmune disease

Acute more common in children

disseminated intravascular coagulation

Etiology: sepsis, pregnancy/birth process (OB)

Patho: widespread clotting and bleeding

Massive activation of coagulation cascade

Coagulation factors and PLTs depleted

Clinical manifestations: Areas of thrombosis combined with bleeding

may occur at any site, sites of previous injury (venipuncture)

Rx: remove cause, support shock, replace clotting factors

preload

the volume work of the heart

afterload

resistance that opposes ejection of blood. Pressure work of the heart. Force heart must generate to push blood out.

cardiac contractility (inotropy)

the myocardium's ability to stretch and contract in response to the filling of the heart with blood

stroke volume

The amount of blood ejected from the ventricles with each beat

60-70%

regular ejection fraction

frank/starling mechanism

•Increased stretch = increased force of contraction

•Therefore, increased volume = increased force of contraction

Ability of heart to compensate for varying degrees of venous return