Uremia refers to the retention of nitrogenous substances in the bloodstream/vascular system that should be excreted by the kidneys (kidneys usually excretes 99% of these nitrogens, which comes from protein intake).

This occurs when the patient has lost sufficient enough nephrons that they cannot maintain fluid and electrolyte balance.

Symptoms: fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes.

Assuming the diet is healthy, it will begin to be a problem when greater than 75% of the nephrons are lost.

Note: Each kidney contains about one million nephrons, so you can lose one kidney and still have half of your nephrons left. You can live this way until >75% is gone.

Glomerular Filtration Rate is compromised, which is the rate at which blood is filtered through the kidneys

(amount of plasma pushed through glomerulus/minute)

Infections (kidney or UTI)

Inflammatory diseases of kidney

Increases/Decreases in blood pressure & its result on GFR

Autoimmune disorders (SLE - Lupus)

Metabolic disorders (Diabetes)

Toxic substances (analgesic abuse, antifreeze & lead poisoning)

Pyelonephritis (a true UTI), which is pretty unusual.

Note: this is when we really start to watch for chronic renal damage.

80% are caused by E coli.

10% are caused by Proteus.

Both are gram negative rods.

Other: Pseudomonas

Progesterone levels go up, which relaxes the smooth muscle around the urethra. As the pregnancy continues, the urethra gets bigger and is more easily infected.

Nature compensates by making you pee more. The uterus gets bigger and pushes on the bladder so it cannot hold as much urine.

Hematuria and/or Proteinuria

(blood or protein in the urine)

Decrease in GFR (due to loss of nephrons)

Uremia/Azotemia (nitrogenous waste products in blood)

Edema (retain water due to inability to pee out sodium)

Increase in blood volume/pressure (due to water retention)

False, it is not from strep.

AKA Azotemia

It atrophies from the size of a fist weighing as much 250 grams to half the size of a fist and can weigh as little as 50 grams.

Note: everything in the nephron has atrophied and the tubular part has thickened. At this point, it is a non-functional nephron.

When there is a hardening of the renal artery by plaque that causes your blood pressure to go up. If you clean the plaque out of the renal artery, the problem is over.

Note: This is the reason for hypertension 10% of the time.

This antibody will also try to inactivate a protein in the glomeruli of the kidney, leading to non-functioning glomeruli. This means that the antibodies will occlude the glomeruli and destroy them.

It eventually gets to a point where there are not enough glomeruli to maintain hydration and electrolyte balance, resulting in the need for dialysis.

There are multiple bilateral cysts (like blisters) that develop on the outside and inside of the kidneys. These cysts are filled with clear, hemorrhagic tinged fluid.

The kidneys become enlarged and rapidly become non-functional and the patient will require dialysis.

It is caused by a dominant gene, so if someone has it they will pass it on to their offspring.

Note: these people usually only live to child-bearing age.

When there is a defect in the Hydrogen Ion excretion or Bicarb excretion, but the GFR is normal.

Note: this is a special circumstance, because usually it is an abnormal GFR that causes a defect in the Hydrogen Ion and Bicard excretion.

It is located in the distal tubule. This is where Hydrogen Ions are transferred back and forth.

Note: this is more common in females/children.

Since, they pee out all of their bicarb, they don't have any bicarb to buffer the hydrogen ions in the vascular system, so the blood pH goes does down and they become acidotic.

Note: remember that the damage is done here in the Proximal tubules.

A progressive kidney disease caused by diabetes-induced angiopathy of capillaries in the glomeruli that causes nodular glomerulosclerosis (hardening of the glomeruli).

Note: Angiopathy is a generic term for a disease of the blood vessels.

Since Type I Diabetics do not produce insulin, leaving an abundance of glucose in the vascular system, and glomeruli do not have insulin receptors, they have direct access to all of this glucose and become sclerotic (bigger, thick, hard).

Note: Cells that do have insulin receptors, would allow insulin to connect to the receptor and open up the cell to allow it to utilize glucose, but cells that do not have receptors are able to utilize glucose without needing a receptor.

Tubular part of the kidneys, retina, peripheral nerves, and blood vessels.

Note: this is why Diabetics, especially Type I, with extremely high blood glucose levels have problems in these areas.

Hyperuricemia, age (rare before age 30), genetic predisposition, excessive alcohol consumption, obesity, certain drugs (especially thiazides), and lead toxicity. All of these things interfere with the kidneys ability to filter out uric acid.

Note: If you see a very young child with high uric acid, you should suspect lead poisoning.

Metabolic Acidosis, which is the decreased ability to excrete hydrogen ions.

Note: Metabolic means that it is due to the urinary system instead of the lungs.

You will see a spiked T wave.

Note: T wave represents ventricular repolarization

They can become very anemic (normocytic, normochromic). This tells us that this is not a nutrition problem, but a production problem. They are producing red cells, but at a much slower rate because the bone marrow is not getting stimulus from erythropoietin.

Note: There is not enough erythropoietin because they lack kidney function.

Azotemia

Reminder: Uremia/Azotemia is an increase in notrogenous substances. Urea is very neurologically toxic.

As the BUN increases you will see a cascade of restlessness --> lethargy --> insomnia --> convulsions --> coma.

At the point of a coma, the nitrogenous substances in the blood will be through the roof.

Normally, when we go outside and expose our skin to UV light, we produce vitamin D from cholesterol and our kidneys then activate this vitamin D so we can absorb calcium. If the kidneys are not functioning, vitamin D cannot be activated, which means calcium cannot be absorbed.

This will lead to the bones becoming brittle, easily broken, and soft (osteodystrophy which is basically the same as osteoporosis).

A more accurate way of measuring renal function is creatine clearance because creatine is not diet or hydration influenced.

Note: you pee out 99% of creatine

Some examples of pre-renal conditions are burns, hemorrhages, MI, and embolism.

IN CLASS EXAMPLE: a patient has MI, has lost half of the left ventricle, blood pressure in the basement, and is not peeing. This has nothing to do with the kidneys and Acute Renal Failure is the least of this patients worries.

An oblique fracture proceeds at an angle across the bone.

This is the guy that comes into the ER after a car accident with a big piece of bone sticking out of his leg.

Stress fractures are usually seen in people involved in high activity such as runners. You usually cannot diagnose these and the only way to cure them is for the runner to quit running.

Note: Runners are addicted to running and if they quit running they are very crabby

Recognition- have the patient describe the event/what happend, find out the likelihood of a broken bone, and do an x-ray to confirm it.

Reduction- manipulation of the bone back to its approximate location. if its a transverse fracture they are closed reductions, so they dont have to cut the skin. If it's an Oblique fracture, you will have to have surgery to correct the fracture.

Retention- holding everything in place. If it is a closed reduction they will use a cast. Rule of thumb for casting is always go above and below the closest joint. If you dont do this, there will be movement and alignment will be altered.

Rehab- sometimes, sometimes not. If there has been malunion and the bone has not aligned properly then there might be some rehab.

Subluxation (touching) refers to the deviation from the normal relationship between articular cartilage and mating cartilage. In other words this is a SLIGHT dislocation.

Can you tense your deltoid (shoulder) muscle, no?

Then they have a torn axillary nerve.

Can you abduct and adduct your four fingers, no?

Then they have torn the ulnar nerve.

Osteomyelitis is an infection of the bone tissue

Note: often this occurs post surgery

Non-structural means that the reason for the scoliosis is not the spine, but is due to posture (like one leg significantly shorter than the other but the spine is fine)

Structural means that it is the spine that is the problem. It is not in the pelvic area, the legs or posture. Just the spine.

Rissner's sign is two little pieces of bone that develop at the base of the spine to anchor the spine. When the patient develops this, it stops the rotation of the spine.

Note: you may get more lateral curvature, but no more rotation.

It may be surgical removal of the limb, at which point they would radiate the area. They might also give some chemo. At this point, they will be thinking about prostetics.

Sometimes if the sarcoma is not too advanced, they will take the bone from the limb and replace it with an artificial bone

(there is a higher incidence of infection with an artificial limb)

They would have a 15,000-20,000 WBC count in the synovial fluid.

Note: the norm is 1-2

More common in females 3:1.

Note: They have developed fibrous growths in the connective tissue in the skin. It is very common to see Raynaud's Disease. May be autoimmune, but not sure.

it is unknown, but one correlation is excessive exposure to vinyl chloride, which is used to make plastic.

Note: you cannot get this from drinking out of plastic bottles. Think someone who works in a plastics factory.

Crystalize not just in the joint but in the ankle and the knee

NOTE~appears to crystalized razor appearance under a microscope

Prolactin is resposible for mammary gland production and milk production to an extent in females. Your prolactin levels are at the highest they will ever be during delivery(dont eat young) and the lowest they will ever be after delivery(maybe cause of post partem).

~NOTE~males have a small amount of prolactin from the anterior pituitary but it doesnt do anything.

They are both on the outside of the thyroid (not involved much in secreting cells of the thyroid) and are both treated with removal of the thyroid (thyroidectomy). Will need thyroid hormones for rest of life.

Note: slight chance removal would be followed up with isolated radiation if lymph node involvement is suspected.

True. When there is hypercalcemia (increase in serum calcium), there will be increased renal clearance of serum phosphorus (hypophosphorus).

Hypercalcemia = decreased serum phosphorus

Hypocalcemia = increased serum phosphorus

Serum calcium below 9.0

Norms for serum calcium are 9.0-10.5

ACTH dependent Cushing's and ACTH independent Cushing's.

ACTH stands for Adrenocorticotropic hormone.

1. stored protein is broken down into amino acids

2. fatty acids are released from adipose tissue

3. gluconeogenesis: liver stimulated to make glucose from non-carb source (combines amino acids & fatty acids to make carbs)

4. thymus gland functioning is decreased (t-cells, which are made in the thymus are not properly primed so cell to cell immunity isn't working)

5. can't filter sodium in kidneys, so you hold onto sodium and water, get edema, increase blood volume and increase blood pressure

Primary is when the adrenal glands are producing too much aldosterone and secondary is when the reninangiotensin system is set into motion as a protective response to increase blood pressure when kidneys are not perfused.

Both end in hypertension.

Hirsutism, which is excessive amounts of body hair. Seen often in women, since we consider androgens a male hormone.

Note: excessive androgen will inhibit estrogen.

What is Addisons’s disease?

Addison’s disease is hyposecretion from the adrenal cortex. This is the antithesis of Cushing’s disease.

What are some characteristics of Addison's disease?

Patient will have a decreased amount of cortisol, which increases cell sensitivity to insulin by increasing the cell receptors to insulin. Patients are hypoglycemic.

Who in particular would be in real danger if they had Addison's disease and why?

Insulin dependent diabetics because the insulin they have been using to control diabetes is now sending blood sugar to 200. This is really difficult to control.

What is another problem people with Addison’s face?

They have a decrease in aldosterone which means they urinate out sodium (NA), then lose water so they decrease blood volume and have a low BP.

What is yet another problem related to Addison's?

Since the patient is peeing out Sodium (NA) they hold onto potassium (increase reabsorbtion). This means blood PH goes down causing acidosis. So, People with Addison’s tend to become acidodic.

Patients with Addison's also have an a decrease in Androgens (coming from the adrenal glands). What population is most effected by this and what is a symptom they face?

Females see this problem most and they suffer from hair loss.

Why don’t you see the hair loss in men with Addison's?

They are not as affected by hair loss because of their testicular tissue.

What are people with Addison's routinely given and what is it made up of? Why are they getting this?

 They are getting vitamin shots made of cortisol, aldosterone, and androgens because they don’t have adrenal glands due to the Addison’s disease.

What happens to males if they are given to much androgen?

What is Diabetes Mellitus? What are the two types associated with diabetes?

True or False: Type I Diabetes is genetic?

True, but the gene has to be activated think viral infection, maybe aliens, but something has to trigger it. This is why you don’t see a one year old with type one diabetes.

What happens in insulin dependent diabetics (Type I)?

They begin to lose all of their beta cells (insulin producing cells). This is generally a gradual thing and this is why it takes a few years to manifest.

What percentage of beta cells does someone have to lose in order to develop Type I diabetes?

Assuming the diet is ok they have to lose greater than 90% of their beta cells.

Why did the Type I diabetes gene evolve?

Evolved in the Northern Climate because people living on ice burgs didn’t want there blood to freeze, so the body put more sugar in the blood to keep it from freezing.

Note: some frogs become diabetic in the winter and when it warms up they are not diabetic anymore

What is another term for Type I or Insulin Dependent Diabetes?

What causes non-insulin dependent (type II) diabetes?

This is not a problem with beta cells. The problem is in insulin action and even insulin receptors.

True or False: Type II Diabetics have a decrease in their insulin production?

False, often times type II diabetics have a increase in insulin production.

True or  false: 80% of type II diabetics are overweight?

When someone developes type II diabetes due to weight gain, what is it called?

What is the risk of having a fat two year old?

  They will develop type II diabetes in their 20’s

How do we diagnose diabetes?

Look for hyperglycemia by doing a blood test. You are looking for a fasting blood sugar greater than 126 on more than one occasion (never diagnose diabetes with just one blood test).

What is a glucose tolerance test?

Just as it sounds, the patient fasts all night then goes to the doctor and drinks a horrid sugar drink. The doctor will monitor the blood sugar levels over several hours to see how the body deals with this.

If the blood sugar is greater than 200 within a two hour interval and at one other time (maybe when fasting for instance) then they have diabetes.

For really accurate blood glucose levels to be seen, how long can this test take and what are we really wanting to see?

Can take 5-8 hours. We want to see two peaks and two valleys with the blood glucose.

What is impaired glucose intolerance?

When the person is showing a two hour blood glucose of 178 and a half hour of 170. They are pre-diabetic and within three months they will be diabetic.

What are two major complications of diabetes?

Ketoacidosis and Microangiopathy

What is ketoacidosis?

This is mostly with insulin dependent diabetics because they have the highest blood sugars. A person with type one diabetes is breaking down fat in order to produce insulin and fats contain ketones which are acids. This causes acid to be floating in the blood stream and lowers the blood PH.

Why does the body break down fats for glucose in relation to type I diabetes?

The cells think the body is starving, because they are not getting any insulin due to lack of beta cells, so they start to break down fat to try and get some nutrition.

What effect does Ketoacidosis have on the body?

Puts acid in blood

Lowers blood pH

Body converts some of the ketoacids to sodium

Hold onto water due to sodium

Increase in BP forces water to be peed out

Leaves patient feeling thirsty

What is the breathing like in a patient that is Ketoacidodic?

They are taking short, rapid inhales and long exhales (Kussmaul’s)

Why would someone that is Ketoacidodic be having Kussmaul’s? Why won't it work?

Doing this because blood pH is low and the body is trying to correct it. This will not work because the lung's only job is gas exchange and blood pH is a metabolic issue.

What is Microangiopathy and what patient normally suffers from this?

There are certain cells without insulin receptors (eye, glomerulus and peripheral nerves) and they are sucking up all the excess blood sugar therefore they are becoming bigger, fatter, and non-functional.

We will usually see this in a type I diabetic because their blood sugar can spike to 800. It would take years for a type II diabetic to develop this, because they will never hit a blood sugar level of 800. They just walk around with a blood sugar of 200 for years.