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44 Cards in this Set

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Normochromic, normocytic anemia

-Common causes are acute blood loss or diseases that are chronic (such as infections, liver disease, cancer, renal failure, endocrine disorders, protein malnutrition)


-can be d/t aplastic anemia

Signs and symptoms of anemia

-SOB, weakness, fatigue, chest pain, palpitation where the heart is beating rapidly, irritability, headaches, lightheadedness

Normochromic, macrocytic anemia

-Common causes are folic acid and B12 deficiency


-This is causes a major defect in delayed synthesis of DNA, causing the cell nucleus to take longer to mature.


-S/s: B12 deficiency will lead to parathesia, numbness, tingling, and loss of vibration and position sense associated with the demyelination of nerves


Hypochromic, microcytic anemia

-Common causes: decreased Hgb synthesis which the primary cause is iron deficiency


-Peptic ulcers with increased iron loss d/t bleeding can also cause this form of anemia.

Hemolytic anemia

Common causes: sickle cell, Glucose 6-phosphate dehydrogenase deficiency, ingestion of certain fava beans, autoimmune disorders and certain drugs

Aplastic anemia

Causes: exposure to chemical agents, drugs, chemo, infections, irradiation, bone marrow cancer


RBC range

Males: 4.8-6.0 x 10'6/mm'3


Females: 4.1-5.5

Hemoglobin range

Males: 14.0-18.0 g/dL


Females: 12.0-16.0 g/dL

Hematocrit range

Males: 40-52%


Females: 37-47%

Preload

-Degree of tension or distending forces on the ventricular muscle when it begins to contract or the volume of blood in each ventricle at the end of diastole

End-systolic volume

Volume that remains in the ventricle after contraction

Afterload

The pressure or resistance against which the ventricle has to pump


Stroke volume

Amount of blood ejected from the ventricles during contraction

Cardiac Output

CO= SV * HR

Frank-Starling mechanism

The greater the stretch on the muscle fibers, the stronger the contraction.

Sympathetic Nerves

-Supply both the atria and the ventricle


-Can increase cardiac output


-Increases rate and force of contractions


-Norepi released from sympathetic nerves


-Norepi and epi released from adrenal gland

Parasympathetic nerves

-Supply primarily the atria


-Acetylcholine released from the vagus nerve will slow the heart rate and decrease the force of contraction


-Ach slows the heart rate by increasing the membrane permeability to K+ and increasing polarization

Alpha adrenergic receptors

-Located mainly in the systemic blood vessels of the skin, abdominal viscera, and the skeletal muscle


-Dominant over beta receptors in the visceral organs


-Norepinephrine excites alpha > beta


-Causes vasoconstriction

Beta adrenergic receptors

-Located mainly in the lungs, heart, skeletal muscle and blood vessels of organs


-Dominant over alpha receptors in the heart


-Have a lower threshold the epinephrine increases the sensitivity


-Causes vasodilation in the heart.

Depolarization of the heart

-Starting RMP = -90mV


-Large increase in Na+ ions moving INTO the cell


-MP changes to +30mV


-Permeability of K+ decreases

Early Repolarization/Plateu

-Significantly longer and cells have a refractory period where then can not respond to a stimulus


-Ca+ ions move INTO the cell assisting with muscle contraction


-Repol levels plateu to give the heart adequate time to refill with blood

Repolarization

-K+ channels reopen, Na+ channels close


-K+ LEAVES the cells


-This returns the membrane potential to -90mV, but the ion distribution is still incorrect

Resting potential phase of heart

-Where the Na/K pump redistribute the ions to there appropriate compartments (Na ECF, K ICF)

Importance of Ca in heart contraction

-Calcium combines with troponin to form a cross bridge between actin and myosin enabling the muscle to contract

How to lower LDL and increase HDL

-Decrease SFA and cholesterol in diet


-Niacin decreases liver synthesis of VLDL


-Exercise


-Moderate alcohol intake


-Cholesterol lowering drugs

How to lower triglyceride levels

-Weight loss if overweight


-Exercise


-Decrease intake of SFAs


-Substitute MUFAs for SFAs without increasing caloric intake


-Limit CHO to 55% and make them complex


-Avoid alcohol


-Fish oil supplements


-Niacin

Recommended LDL value

<100 mg/dL

Recommended HDL value

>60 mg/dL

Recommended total cholesterol

< 200 mg/dL

Recommended triglyceride level

< 100 mg/dL

Recommended fasting plasma glucose

< 100 mg/dL

Pathophysiology of the atherosclerotic process

-Endothelial damage/inflammation


-Lipid infiltration


-The process begins with a slowly progressing atheromatous plaque with a thin, fibrous cap, which ultimately advances to a calcified plaque.

Lipid Infiltration

-Increased plasma LDL - Increased infiltration into the intima-


-LDLs (within intima) - peroxidation - modified LDL - taken up by scavenger receptor on macrophages- become foam cells- necrotic - deposit lipid and cholesterol within intima - fatty streak


Fatty streak lesion formation

-This is the initiating step of the atherosclerotic formation


-Oxidized LDLs are cytotoxic and thought to damage endothelial cells- swelling and proliferation- which results in fibrous plaque formation

Phase a plaque development most vulnerable to thrombus

-Generally the smaller ones, which occur in the early stages of inflammatory atherosclerotic evolution. Theory suggests that the activated foam cells secrete enzymes, capable of disrupting the integrity of the thin fibrous cap, making the plaque vulnerable to rupture.

"Event" that causes MI

-An MI occurs when the plaque is unstable, ruptures, and a thrombus is formed. The result is total obstruction of the arterial lumen at the affected site

Heart Failure

-HF occurs when the heart can no longer maintain an adequate cardiac output to meet the metabolic needs of the body. There is pump failure- the myocardium can no longer contract normally and therefore stroke volume decreases

Right-sided heart failure

-Increased venous pressure in systemic circulation


-Stasis of circulation


-Anoxemia of viscera


-Decreased liver function


-Hepatomegaly


-Ascites


Pedal edema

Left-sided heart failure

-Increased venous pressure and pulmonary circulation


-Pulmonary edema


-Decreased kidney function


-Sodium retention


-Water retention


-Increased blood pressure

Chylomicrons

-Produced in the intestines


-Primarily composed of triglycerides

VLDLs

-Produced in the liver and intestine


-Primarily composed of triglycerides and phospholipids

LDLs

-Produced in the liver and in circulation secondary to catabolism of other lipoproteins


-Primarily composed of cholesterol

HDLs

-Produced in the liver and intestines


-Primarily composed of protein

Guidelines for blood pressure

-Age > 60 years: BP goal < 150/90 mmHg


-Age < 60 years: BP goal < 140/90 mmHg