PO2 < 50 mm HG with/without PCO2 > 50 mm Hg.

Note: these are partial arterial blood gases that can only be measured by the amount of pressure the gas is contributing to the vascular system.

You are blowing off too much CO2 which leads to less carbonic acid, less hydrogen ions, so the patient is more alkaline (hypovolemic).

Lung cancers are categorized by where we find them and by what type of epithelial cells we see. What are the four most common Bronchiogenic Lung cancers from most common to least common?

These are really immature cells that have a quick doubling time and the five year survival rate is <5%.

Note: to figure out the doubling time you take ten cells and monitor how long it takes them to get to 20 cells.

Hematocrit is a percentage volume of RBCs. It should always be roughly three times the patient's hemoglobin.

Note: when drawing blood and putting the sample in a tube, the hematocrit is the portion of the tube that is RBCs.

The measurements are usually not used unless trying to figure out if a patient is anemic.

Mean Corpuscular Volume and Mean Corpuscular Hemoglobin Concentrations

PMNs (polymorphanuclear neutrophils) or "segs" make up to 38-70% of WBCs and are the primary cell for phagocytizing bacteria, which is why we have so many.

Note: Segs are made up of grainy segments which is what phagocytizes the bacteria using bleach and hydrogen peroxide.

Eosinophils have a segmented nucleus and a granulated cytoplasm. These granules have the ability to kill parasites and produce histamines because they have IgE receptors. This is why they are primarily involved in parasitic infections and allergic reactions.

The nucleus is bandlike with a grainy cytoplasm. These are young/adolescent segs that will eventually become a full grown seg. They think they can phagocytize as well as a full grown seg, but cannot yet.

Note: If seg numbers go up, so do stab numbers. In a few days they will become segs.

Monocytes are the largest WBC you have. They have an indented nucleus with only a few granules in the cytoplasm so they can sort of phagocytize.

Note: They have the ability to change themselves into Macrophages which eat up up bacteria and dead cells. This is why their number goes up in the repair process.

Lymphocytes are the second most common cell making up half of your cells. They have a big nucleus with a smooth cytoplasm and are extremely important because they kill viruses.

Note: If a patient has a high lymphocyte count, you would assume they have a virus.

Platelets are little pieces of the cytoplasm of a bigger cell called a Megakaryocyte that have broken off and are in the peripheral blood where they survive for four or five days in circulation and then are broken down while more are made. Since this cytoplasm is sticky, platelets are sticky.

Note: One Megakaryocyte can give us 50,000-70,000 platelets.

During RBC development, occurring in the bone marrow, red cells have a nucleus. Once they go through the stages of development, they eject the nucleus and we end up with a full fledged red cell.

A Reticulocyte is an immature RBC that has yet to eject its' nucleus remnants. This reticulocyte does not have the ability to carry oxygen until it gets rid of the nucleus remnants. A reticulocyte is to a RBC what a band is to a seg.

Morphological: size of cell/amount of hemoglobin

Etiology: Increased RBC loss/decreased RBC production

Normal amounts of color which relates to Hemoglobin.

Note: Color is more intense on the outer edges of RBCs because hemoglobin is on the outside but not in the center.

In aplastic anemia, the hemocytoblast shuts down so there are no RBCs or WBCs and platelets. This is a production problem.

This is called "pancytopenia" which means a lack of all cells.

Morphologically, aplastic anemia is normocytic/normochromic

Production problem

Lady comes into clinic after having worked all day and her main complaint is she is tired all the time. Her RBC count is in the basement, hemoglobin is 6 so her hematocrit is roughly 18. Her fingernails break easily, has a pale smooth tongue, hair looks frizzy, and she will complain of a lot of split ends. She would be admitted to find out what is wrong. What would be a good guess as to what could be wrong?

A decrease in B12 or Folic Acid Deficiency. Both are used in the construction of the cell wall of RBCs, so when you are deficient in either one, the walls are flimsy and big and can be broken down easily.

Note: you would first assume this is from pernicious anemia (B12 deficiency) since you need intrinsic factor to absorb B12 or maybe a tapeworm. Nothing special is needed to absorb folic acid.

All that sickle cell is is that two amino acids flipped spaces in the hemoglobin structure. An amino acid in the second position (Valine) changes places with an amino acid in the sixth postion from another chain (glutamic acid). This changes the protein and we now have Hgb S (sickle cell) instead of Hgb A (adult anemia). 

Red count and hemoglobin are normal, but the hematocrit is too high. This is because the patient is dehydrated which is making the blood volume go down since serum is made mostly of water.

Note: you would not know this by only looking at the hematocrit.

It begins with the promyelocyte (only one cell from stem cell) that does not differentiate into a myelocyte like it is meant to. This means that these immature promyelocytes will begin rapidly reproducing in the bone marrow which is bad.

Note: 80% of cases seen in ages 20-35.

Chemotherapy attacks rapidly producing cells in order shut them down. The goal is to get them to eventually turn back on and reproduce normally.

Note: Sometimes they do not turn back on and can cause Aplastic Anemia or will turn back on as if nothing happened.

The child has been lethargic and sleepy for a while, no appetite, flu-like symptoms, petechiae on legs and trunk, enlarged spleen and liver, extremely high WBC count (not as high as myelocytic, though).

Note: over 95% of these patients can be put into remission for the rest of their lives and 5% can be treated with bone marrow transplants.

WBCs gradually increasing over months

Note: 80% have abnormal gene on chromosome 22 and average survival time is about 3 years with or without treatment (usually die from pre-existing vulnerabilities).

WBC count gradually increasing over time, abdominal/bowel complaints due to enlarged spleen or liver. Average survival rate is 4-5 years and they generally die from pre-existing vulnerabilities as well.

Note: 50% of people will have an abnormal gene on chromosome 12.

A lump that developed weeks ago under the arm, in the groin area, or on neck that won't go away. The lump feels hard and rubbery.

Note: The other 25% of them have the same presentation but with night sweats since the lump showed up.

Stage One: one single node involved (all other clear)

Stage Two: two or more adjacent and two or more non-adjacent nodes on one side of the diaphragm.

Stage Three: Nodes above and below the diaphragm

Stage Four: Metastasis to other organs

Age (median in Non-Hodkins is 50) and the type of cell in the lymph node.

Note: With Non-Hodkins they have greater liklihood of nightsweats and survival is 8-10 years.

This is a proliferating disorder (similar to Leukemia) that causes them to produce malignant plasma cells and stop producing red cells, white cells, and platelets (this is pancytopenia).

Since plasma cells are precursors to B-lymphocytes, which are involved in antibody production, these people make abnormal antibodies as well.

They do not produce any bone

Note: Uncommon to see under age 40 and is treated with Chemo.

This is when there is an overproduction of IgM antibodies that cause increased volume and viscocity of the blood (causing hypertension and LV hypertrophy).

Note: Since IgM is extremely temperature sensative, these people will definitely have Reynaud's Disease.

This is when platelets are below the lower limit of 100,000.

Bleeding problems below 50,000.

Petechiae below 30,000.

Possibility of cranial bleeding below 20,000.

Intrinsic: Coagulation factors are in plasma

(8, 9, 11, 12)

Extrinsic: Coagulation factors are in tissue

(7)

Following the injury, local vessels constrict and the exposed collagen attracts platelets that will attach to this collagen and release serotonin (vasoconstrictor). This platelet mass "plugs" the vessel and the serotonin minimizes blood loss. Platelets form a lipoprotein surface on which coagulation proteins are activated. Thrombin (created in stage 2) encourages more platelet aggregation and Fibrinogen (converted to fribrin in stage 3) strengthens the platelet plug now attached to the vessel wall. The fibrolytic mechanism will effect the removal of the clot when it has served its purpose.

Correlated to some degree with cigarette smoking and genetics.

Note: 70% die withing a year and <10% within 5 years.

Acute Superficial Gastritis is an insult/inflammation to the gastric lining from lifestyle (like eating mexican food) and Chronic Atrophic Gastritis is a progressive atrophy of the glandular epithelium of the stomach and a decrease in chief cells which inhibits the production of glandular stuff (pepsin, intrinsic factor, hydrochloric acid).

Note: Chronic Atrophic Gastritis typically starts in mid-life and predisposes them to stomach cancer and stomach ulcers.

In the stomach and the duodenum.

Note: Stomach ulcers occur more commonly in the older population and duodenal ulcers occur more commonly in the younger population.

H. pylori grows in the epithelial lining and produces achlorhydrate which neutralizes hydrochloric acid, making it easier for it to get up to the mucosal lining.

Note: Ulcers are now treated with antibiotics.

The atrophy of villi in the small intestines which prevents them from being able to absorb gluten (vegetable albumin found in wheat, oats, barley, and most grains).

Note: we believe this has a genetic correlation and that it may be autoimmune since these people have an antibody to gluten.

Lactase is an enzyme that breaks Lactose down into glucose and galactose.

Note: Lactose is the principle carbohydrate found in milk and dairy products.

This patient has an inflammatory reaction that thickens the submucosal layer, which pushes it into the mucosal layer and causes a restriction of flow through the intestines.

Note: some will have skip lesions.

Rebound tenderness, low grade fever, elevated WBCs.

Note: if the appendix ruptures, peritonitis occurs.

Absess formations form from fibrous exudates to isolate things off.

Note: fibrous exudates also occur in the pleural cavity and the pericardium.

In the small intestines, since there is more surface area.

Note: the obstruction can be chronic, acute, partial, complete, or a variation of them.

Herniations (protrusions) of the mucosal lining through the muscular lining of the intestines that form a sacculus that becomes inflamed.

Note: occurs with age and rare under age 35.

Acute Fulminating - sudden abrupt onset with severe bloody diarrhea, nausea, vomiting, electrolyte/hydration disturbance, anemia. Poor Prognosis.

Chronic Intermittent- much slower onset with same symptoms, but will come back and forth

Chronic Continuous - most common with continuous diarrhea, bleeding and electrolyte problems (is very painful and must be taken care of).

Megacolon (also called toxic dilation). This is when they have lost peristalsis in the transverse colon, so the food being pushed into it by the ascending colon just sits there. This makes the transverse colon stretch and get thinner and eventually rupture. There will then be stuff flowing into the abdomen and peritonitis can occur. Must get immediate colostomy surgery. Mortality is 30% if rupture occurs.

Avoid nuts and alcohol.

Polyploid adenomas - Benign, are harmless and do not seem to be related to anything, but maybe diet.

Villous adenomas - a little larger than polyploids and both occur in the sigmoid and rectum. 25% become malignant over time.

Familial polyposis - Rare, 100% chance od becoming malignant around 40 years old and begin around puberty, are caused by a dominant gene.

Colon Rectal Cancer (recto sigmoid/easily accessed), then the 2nd most common is in the cecum (not accessible), followed by the ascending colon. Least common spot is the transverse colon.

Note: Colon Cancer is the 3rd most common spot in the entire body.

Increased destruction/hemolysis of RBCs would give you more unconjugated/indirect bilirubin, which means it is attached to albumin to go to the liver and could not be excreted through the urine.

Note: this person would have jaundice skin and sclera, but normal urine.

The liver normally separates the two and reuptakes the albumin, but some medications (antibiotics/contrast dies) can prevent this separation from happening.

Note: this person would have jaundice skin and sclera, but have normal urine because you are still dealing with unconjugated/indirect bilirubin.

This occurs when there is a decrease or total lack of the enzyme required to absorb bilirubin into the liver. At this point, the bilirubin is no longer attached to albumin and is called direct bilirubin. This person will have jaundice skin, sclera, and urine.

Will see sometimes in newborns (phylo-jaundice) and Gilbert's syndrome (child cannot make enzyme at all, usually dead by 3 months).

This is due to the fact that gallstones can block the entire system at the sphincter of Ode.

Note: Hepatic duct comes out of liver, Cystic duct comes out of gallbladder, Pancreatic duct comes out of pancreas and all attach to common bile duct which turns into the narrow vader area that leads to the spincter.

True. You will generally see metastatic cancers in the liver.

Note: Primary cancer of the pancreas is NOT unusual.

False. There are no early warning signs of Pancreatic cancer. These people usually die within the first year.

Note: We do not do well with transplanting the pancreas.