Patho Week 2. Fluids.txt

When the products of pyknosis start to fragment and rupture

A cause of hypoxia where there are sufficient RBCs, however they are are defective in the delivery of oxygen

Intracellular clumping, the inside of the cells looks like a scrambled egg. This typically initiates apoptosis or can be caused by the lowering of intracellular pH, such as when a cell must switch from areobic to anaerobic metabolism due to hypoxia

Arising from an obsure or unknown cause

• Happens after karyorrhexis, it is when the nuclear material is dissoved and auto-digested
• We see this after a lowering of pH within a cell

Induced inadvertently from a physician, surgeon or by a medical treatment or diagnostic procedure

Low hemoglobin

• A crackling or grating sound or feeling; think "Crepitus Crackling:
• In soft tissue it is often due to gas, such as gas gangrene
• In joints it can be caused by joint wear

• 1. Coagulative: i.e. Gangrene
• 2 Liquefactive: i.e. stroke victim, we see this in the brain
• 3. Caseous: i.e. in the lungs, looks like bleu cheese

• 1. Disuse
• 2. Denervation
• 3. Loss of nutrients
• 4. Loss of trophic hormones

• Total Bilirubin: 0.2 - 1.5 ml/dl
• Direct (conjugated): 0.0 - 0.3 ml/dl
• Indirect (unconjugated): 0.2 - 0.8 ml/dl

• Permanent = Heart, no
• Labile = skin, GI, lungs, yes
• Stable = liver, yes

35 - 45 mmHg

9 - 11 mg/dl

• Normal Bicarbonate levels:
• 22 - 26 MEq/l

2(Na+) + (glucose/18) + (BUN/2.8)

134 - 136 mEq/l

3.5 - 5.1 mEq/l

275 - 295 mOsm/l

The cardiac output is less so the kineys/adrenal glands think the volume is low, even though it really isn't so it pumps up aldosterone which conrols sodium/water balance. When the sodium levels increase the water follows it. Now there is increased capillary hydrostatic pressure which forces fluid into the interstitial tissue and edema can result.

When the capillary membrane is disturbed, such as inflammation from a bee sting, it becomes more permeable to larger items, such as proteins. The proteins can then escape the capillary and get into the tissue. Since proteins control oncotic pressure, the oncotic pressure of the capillary will decrease and the oncotic pressure of the tissue will increase.

• Pitting edema is protein poor edema, when you press your thumb up against it, you can make a depression that will soon disappear.
• Causes could include: garter belt, tunicate, starvation (low protein), too tight socks

• Non-pitting edema is protein rich edema, you cannot make a depression with your finger when you push on it.
• Causes can include: disruption of the cell membrane permiability (bee sting)

During edema, the cells are pushed farther away from the capillaries increasing the length of space between them. This disrupts the amount of nutrients the cells receive. A common type of this is pulmonary edema.

Pericardial edema is when fluid accumulates in between the visceral and parietal pericardium. This can create Cardiac Tamponade, which is when the space fills up it puts pressure on the heart and the heart cannot relax out enough to fill with blood. Therefore a patient can have decreased cardiac output which could lead to the adrenal glands releasing aldosterone and then you will have sodium/water retention which could lead to more generalized edema.

Since the skull cannot exand, the brain is pushed downward. This means that the brain stem that controls breathing and heart functions will be smashed through the foramen magnum, this can cause death.

• Abnomal accumulation of fluid in the abdominal cavity. As the pressure builds up in can put pressure on the diaphragm; since the diaphragm can no longer flatten out, there could be respiratory problems.
• This is common in liver failure and cancer patients. The patients can sometimes look pregnant.

Liver failure causes ascites because teh portal vein that drains the liver gets backed up diue to cirrhosis. This increase in capillary hydrostatic pressure of the blood vessels pushes fluid out into the abdominal cavity tissue.

drugs, IV drip, heart failure (decreased output, adrenal cortex thinks volume, aldosterone...)

• Hyper/hypovolemia cannot be measured, we can only look at signs/symptoms. Remember, total body sodium cannot be measured.
• Hyper/hyponatermia can be measured by serium sodium levels and serum osmolarity.

Decreased, because the RBCs have not changed, however the dilution in the excess volume has.

Because the edema has pushed the capillaries farther away from the alveoli

DI is a disease that has a lack of ADH so the body does not reabsorb fluid. However, the body does reabsorb sodium still, so you have a decrease in water in relation to sodium = hypernatremia - too much sodium in relation to water

In hypernatremia the cell shrinks because there is more sodium outside of the cell so the water follows it. That means that the cellular potassium would increase because it trades place with the sodium.

In hyponatremia, the cell swells because there is not very much sodium in the ECF, so there is more in the cell. The water then follows into the cell. The hematocrit will go down, because the concentration is off, there is a lot more water and still the same RBCs. Keep in mind, hypernatremia probably occurred due to lack of water, hyponatermia probably occurred due to too much water.

• 120 - 125 = nausea, malaise
• 115 - 119 = headache, lethargy
• 110 - 114 = seizures, coma

The serum sodium and the serum osmolarity must decrease, not just one of them.

Renal failure, the kidneys are not excreting enough K+, this is why patients must go to dialysis

Tall Tented T-wave and no U wave

The amount of free calcium

Vit D deficiency, bone tumors, other tumors, cancer

decreased reflexes, dysrhythmias, renal caliculi, vomiting, urination, anorexia

Pancreatitis; the pancrease breaks down fat, a sick pancrease cannot do that - calcium binds with the unbrokend fat and you poop it out. Therefore, there is a lack of free calcium.

Hypoventilating causes respiratory acidosis because the patient is not venting enough CO2

The cell is trying to reduce the extra hydrogen ions from the the ECF so it takes them into the cell, but to do this it must excrete potassium.

As pH decreases, more of the serum calcium becomes ionized (released from protein bindings). It is the extra hydrogen ions that breaks the binds between the calcium and the proteins. Keep in mind, calcium likes to be bound to proteins.

There are no sphincters at the venous end of a capillary, so if you impede the venous return from the capillary to the heart the hydrostatic pressure on the venous end will build up. This forces fuid out of the capillary and into the surrounding tissue.

The liver is not producing the proteins needed to keep the plasma oncotic pressure strong, so it is not pulling enough fluid back to the vessel. Or, the portal vein is blocked which can cause ascites.

• Hyper: Tall-Tented T-wave and NO U wave
• Hypo: broad T-wave and could have a U wave

The DTRs in Hypernatremia are increased, the DTRs in Hypokalemia are reduced.

DI can cause HYPERnatremia

SIADH is the Syndrome of Inappropriate ADH, it causes and EXCESS of ADH so water is retained too much, that causes hyponatremia because there is an excess of water in relation to sodium.

ADH causes a retention of water. People with Diabetes Insipidus have a reduction of water, therefore they void too much of it. This loss of water in relation to sodium causes Hypernatermia.

Hypernatremia has hypo effects on the CNS.

True

unchecked IV line, heart/liver/renal failure, too much aldosterone, glucocorticoids

Retention

Ascites causes hypovolumia, even though there is still a lot of fluid it is in a third space.