Metaplasia means away from the form. The developmental pattern of certain cells, like cervical cells, is straight and if the cells start to develop along a new pattern this is called Metaplasia.  Frequently, the move in pattern is due to insult and the cells that are moved are often more resistant to the insult.  For example, in yeast infections metaplasia occurs and the new cells are more resistant to yeast.

Dysplasia is an abnormality in differentiation and proliferation (cells are reproducing abnormally). Not only do we have cells that have moved from the original pattern of development but they have also increased their rate or reproduction. 

Generally, the younger the cell is, the worse it is. In the early life of the cell it is called acute malignancy and the older the cell gets, the less acute the malignancy.

When cells divide/reproduce to the point when all extra DNA is lost (telomeres), then you are actually losing your core DNA and the cell begins to age.

(Dr. Pennington depicted this with a drawing of a cell with a "tail" of DNA coming out of it. Here is a short video with a better visual http://www.youtube.com/watch?feature=player_detailpage&v=CCNuG2ejBuE).

Cancers are unique in that 90% of cancer cells have an enzyme called, Telomerase. This enzyme extends the telomeres every time the cell reproduces so that cancer cells are essentially immortal. Identifying this telomerase enzyme can be an early indicator of cancer because it only exists in cancer cells and stem cells.

The systolic pressure is the pressure on the arteries when the heart is contracting. Diastolic pressure is the resting pressure in the arteries between beats. The arteries are in a closed system so there is always pressure, even when the heart is not contracting. 

This could be that there is very little force operating to push the blood, there is very little blood to push, or the arteries are extremely dilated.

A paradoxical increase in venous pressure (jugular and abdominal veins) when a patient inspires. It tells you that there is an impediment (obstruction) in blood return to the right side of the heart.

What is probably going on is some degree of right side heart failure. The right side of the heart is not able to push the entire 70 mL of blood out so there is some blood left in there. When the blood cycles through the body and back to the right side of the heart again, it cannot fit the entire 70 mL back in so venous pressure goes up.

"Lub" (S1) is heard when the AV valves (bicuspid & tricuspid) close. This coincides with the beginning of ventricular systole (contraction). As the ventricle contracts and gets smaller, the ventricular pressure goes up. When it rises above the pressure of the atria, it closes the AV valves.

"Dub" is heard when the semilunar valves, in the aorta and pulmonary artery, close (caused by a backwash of blood). This coincides with the beginning of ventricular diastole (relaxation). Ventricle begins to relax and ventricular pressure goes down. When the pressure falls below the pressure of the aorta and pulmonary artery, it causes a backwash of blood that closes the semilunar valves.

Here is a link to a really helpful video online if you need a visual refresher on blood flow through the heart.

http://www.youtube.com/watch?feature=player_detailpage&v=Rj_qD0SEGGk

Heart murmurs are the result of turbulence of flow in the chambers of the heart and the blood vessels that lead into the chambers. This is turbulence that you don’t normally hear.

Analogy: Sitting by a stream, you hear water because of increased flow or because the water is going around rocks.  In the heart, we hear sounds because of quickness of blood flow or the blood is going over and around structural things that it doesn’t normally need to go around. 

P wave represents the depolarization of the atria (loses its charge which make is contract a little).

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The PR interval reflects the time the electrical impulse takes to travel from the SA node through the AV node where it enters the ventricles. There is a slight pause when the electrical impulse gets to the AV node to allow the ventricle to fill eith blood before it contracts. The PR interval is a good estimate of AV node function.

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If the PR interval was longer than normal it would indicate a possible heart block in the patient causing the conduction/delay time to be extended (a person can have 1st, 2nd, and 3rd (complete) heart block).

If the PR interval was shorter than normal it would indicate early activation of the ventricles.

QRS interval represents the depolarization of the ventricles, at which time the atria are repolarizing.

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The interval between S and T is the time between the ventricles depolarizing and repolarizing (isoelectric - time in which there is no electric variation and is on the baseline/how long it takes to repolarize).

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Occassionally, the impulse to the ventricles doesn't reach the ventricles at the same time, so they are not contracting simultaneously. You would see two QRS peaks (called rabbit ears). This shows damage to the conducting system leading into the ventricles, particularly damage to the left or right bundle branches or the bundle of His.

Rate: if heart rate goes up, we need more oxygen

Force: contracting more forcibility requires more oxygen

Muscle: the greater the amount of muscle, the more oxygen you need

Ventricle Wall Tension: it takes more oxygen to make ventricle wall tension go up

Age: susceptibility increases with age

Race: African Americans more susceptible partially due to endogenous cholesterol

Family: This does run in the family

Sex: Females are relatively immune until after menopause

The high blood pressure damages the vessel wall and in response to damage, the body causes inflammation (in the case of vessels it causes calcification or plaque). This now occludes the vessel and we need to increase the pressure even more which causes more plaque again and so on. It is a vicious circle. The problem is it damages the endothelial tissue and stimulates the inflammatory response that causes the plaque.

It is important to remember that if you add ten pounds of extra weight, you add a mile of extra blood vessels. So if someone is extremely overwheight, it takes A LOT more work to pump the blood through all that extra circulation and it causes extreme damage to the blood vessels which increases the production of plaque.

Transmural: goes completely through the myocardial muscle/tissue.

Subendocardial: goes about halfway through the myocardial tissue (from endocardium to about halfway through the myocardial tissue).

The surrounding vessels that feed the area. Example: This person had an infarction in the anterior wall of their left ventricle. What’s the major vessel that feeds the anterior wall of left ventricle? Anterior Descendent Artery.

24 hours after an infarction, the repair process is well underway and after three weeks the repair process is finished. Although repair has occured and scarring is done, the patient may not yet be adjusted since they have lost a portion of the muscle in their heart.

1. It is hard to find enzymes unique to just the tissue you are looking at

2. It is hard to know when to look for and measure these enzymes (Some enzymes are kicked out of the dead tissue quickly and the body metabolizes them immediately. Other enzymes are kicked out and metabolized much more slowly.)

1. CPK-1 (also called CPK-BB) is found mostly in the brain and lungs and goes up quickly/comes down quickly

2. CPK-2 (also called CPK-MB) is found mostly in the heart

3. CPK-3 (also called CPK-MM) is found mostly in skeletal muscle

These all collectively make up the total of CPKs.

Troponin is a muscular regulatory protein in cardiac muscle (also in skeletal muscle, but not smooth muscle) that is used as a marker in cardiac patients to determine if an MI has occured. Goes up 4-6 hours after an MI and takes the body about ten days to get rid of it.

This is not an enzyme.

Acute complications may include:

Heart failure if the damaged heart is no longer able to adequately pump blood around the body.

Cardiogenic Shock due to a huge loss of heart muscle mass

Ventricle Septal Defects leading to aneurysm or rupture of the myocardium

Mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle 

Dysrhythmias, such as bradycardia, tachycardia, ventricular fibrillation, ventricular tachycardia, atrial fibrillation, atrial tachycardia, and heart block.

Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second myocardial infarction.

Bradycardia is a heart rate less than 60 bpm (some people have normal heart rates below this, but extreme bradycardia can affect cardiace output). Tachycardia is a heart rate more than 100 bpm. Resting heart rate is normally between 60-100 bpm.

Cardiac Output = heart rate x stroke volume

Heart block is not actually a physical blockage in the heart, it is when the conduction system is blocked (can asses by looking at PR interval). Mostly seen in posterior MIs.

1st degree: all impulses are getting through the AV node, but the conduction time is a little prolonged (PR interval longer)

2nd degree: only some impulses coming from the SA node are getting through the AV node

3rd degree: none of the impulses that started at the SA node are getting through the AV node.

Chordae Tendineae look like strings anchored to the papillary muscle. The mitral valve is closed when the current causes the papillary muscle to contract and put tension on the Chordae Tendineae.

Two things that could disrupt this:

1. Chordae Tendineae are too long

2. Mitral valve has a mucopolysacharide that makes the valve weak and sloppy.

This is when there is a reflux from the Aorta into the left ventricle when the ventricle relaxes. The Aortic valve is letting too much blood back into the ventricle, so the ventricle will hypertrophy (get bigger).

About 50% of the time, Strep/Rheumatic Fever causes this because the protein from Strep is also found on the Aortic Valve. About 10% is the result of Syphilis.

If the mean arterial pressure or pulse pressure falls, stimulation of the baroreceptors in the carotid sinuses and aortic arch is reduced. This reduced baroreceptor activity removes inhibition from the vasomotor center in the medulla, resulting in increased adrenergic stimulation (increased adrenaline).

Note: If myocardial dysfunction progresses, cardiac output and systemic blood pressure ultimately fall. Myocardial ischemia then exacerbates myocardial dysfunction, and multisystem organ failure may result from persistent or severe organ ischemia.

When the heart is subjected to a lack of blood flow (lack of oxygen), you will see increased preload (means the ventricle stretches more to allow more blood in), heart rate, and stroke volume, and a reduced afterload—all contribute to increased cardiac output in an effort to maintain adequate oxygen delivery.

Note: Without timely interventions, cardiac compensatory mechanisms fail and precipitate the development of congestive heart failure.

Dyspnea: difficulty breathing (on a continuum)

Cough: non-productive (dry, no sputum/mucus)

Rales: crackling sounds due to congestion in lungs (fine, medium & coarse)

Liver: lack of liver perfusion (lack of blood flow)

Edema: pulmonary edema occurs in lungs (when left side of heart fails, there is fluid congestion in the lungs, which is why you feel short of breath)

Fever: low grade fevers

If cardiac output is insufficient: cannot maintain normal arterial pressure and cannot perfuse (due to low BP) the kidneys and other organs adequately, which causes cardiogenic shock. Cardiogenic shock characteristically develops if 40% or more of the left ventricular myocardium is infarcted.

Note:

mean arterial pressure = cardiac output x total peripheral resistance

1. Systolic < 90

2. Decreased blood flow to everything, including kidneys

3. Urine < 20 mL/hr - blood pressure is volume dependent

4. Vasocongestion - skin cold b/c blood going to vital areas

5. Decreased Mental Function - brain less perfused

6. Cardiac Index < 2.1 L/min - cardiac output in L/min

7. Left side of heart - this all indicates severe left side damage (mortality can be very high if patient has lost an extreme amount of cardiac muscle mass)

A thrombus (can be either arterial or venous) is a stationary clot attached to the vessel wall and an embolis is when the thrombus detaches from the vessel wall and is circulating in the blood (could be fat, clotted blood, air). Both have the possibility of blocking the vessels and creating a state of ischemia.

If in lungs, pulmonary embolis and in the brain, is a stroke.

Allergic: almost always in children - typically from some inhaled antigen

Idiopathic: usually in adults after 40 (NOT A GOOD SIGN)

Mixed: antigen or two that can be identified as well as some idiopathic stuff we cannot identify

Panlobular affects the alveoli ducts & sacs, as well as individual alveoli. This is a sensitive area because alveoli are only one cell thick and do not repair themselves, so they are gone forever when they die.

The CO2 receptors in your aorta and the great vessels in your neck will make the chest muscles fire, which will make you start breathing again in order to get rid of the CO2.

Note: this is what is happening when you try to hold your breath, but your body makes you breath again.

This means that the patient has no problems with the lungs themselves, but will die from pulmonary complications.

Examples are Extra Pulmonary (drugs & ALS), Thoracic Cage Disorders (pectus excavatum, pickwickian & sleep apneas), and Pleural disorders.

Drugs: if someone overdoses on depressants, it would supress the respiratory center (could not exchange oxygen and CO2)

ALS: difficulty breathing due to lack of muscle impulses

Pectus Excavatum: "caved in chest" decreases lung capacity (most severe - lower end of sternum fused to thoracic spine)

Pickwickian Syndrome: seen in EXTREMELY obese people due to the weight of their chest inhibiting gas exchange (always feel drowsy & sleepy from too much CO2)

Sleep Apneas: abnormal pauses or abnormally shallow breathing during sleep (seen in people who snore, overwheight, more common in males). Give them CPAPs (continuous positive air pressure) to force air into lungs.

Can have:

Fluid Effusion: excess fluid

Hemothorax: blood in pleural space

Pneumothorax: air in pleural space

Tension Pneumothorax: air in pleural space under pressure

It will create an increase in pressure. The more you put in there, the more pressure you create. This limits the ability of the lungs to expand/contract because it creates backpressure against the lungs.

This could NOT collapse an adult lung, but it COULD collapse a premature baby's lung because they have no surfactant.

You will put a chest tube in the pleural space to let out whatever is in there.

Note: if it is fluid you have to make sure you put the other end of the tube in water to prevent air from being sucked in

1. When you vomit, you bring up very acidic material. If this is sucked down into the lungs, the lungs have no way of fighting it off and lung tissue is killed.

2. Organisms can now go into the lungs as well and have a perfect place to grow with the dead and dying tissue from the acid.

THIS CAN BE AN EXTREMELY SEVERE TYPE OF PNEUMONIA