In my opinion, there is no one in the country who knows more about what student need to learn for Step 1 than Dr. There are currently a number of board prep materials available to medical students thanks to Dr. Goljan, let me discuss a few of them. Audio Lectures: Years ago Dr.

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Need O 2 for oxidation phosphorylation pathway — where you get ATP from inner Mito membrane electron transport system, called oxidative phosphorylation. The last rxn is O 2 to receive the electrons. Terms: 1. Causes of tissue hypoxia: 1.

Here are 4 causes of hypoxemia: a. Ventilation defects — best example is resp distress syndrome aka hyaline membrane dz in children.

In adults, this is called Adult RDS, and has a ventilation defect. Lost ventilation to the alveoli, but still have perfusion; therefore have created an intrapulmonary shunt. Stasis in veins of the deep veins, leads to propagation of a clot and days later an embolus develops and embolizes. In this case, you have ventilation, but no perfusion; therefore there is an increase in dead space. Therefore, perfusion defects because an increase in dead space, while ventilation defects cause intrapulmonary shunts.

Diffusion defect — something in the interphase that O 2 cannot get through…ie fibrosis. Best example—Sarcoidosis a restrictive lung disease ; O 2 already have trouble getting through the membrane; with fibrosis it is worse. Another example—Pulmonary edema; O 2 cannot cross; therefore there is a diffusion defect.

These are the four things that cause hypoxemia resp acidosis, ventilation defects, perfusion defects, and diffusion defects. Hemoglobin related hypoxia In the case of anemia, the classic misconception is a hypoxemia decrease in pO 2.

There is NO hypoxemia in anemia, there is normal gas exchange normal respiration , therefore normal pO 2 and O 2 saturation, but there is a decrease in Hb. That is what anemia is: decrease in Hb.

If you have 5 gm of Hb, there is not a whole lot of O 2 that gets to tissue, therefore get tissue hypoxia and the patient has exertional dyspnea with anemia, exercise intolerance. Carbon monoxide CO : classic — heater in winter; in a closed space with a heater heater have many combustable materials; automobile exhaust and house fire.

When theres heat, cyanide gas is given off; therefore pts from house fires commonly have CO and cyanide poisoning. Clue was that O 2 did not correct the cyanosis. Most recent drug, Dapsone used to Rx leprosy is a sulfa and nitryl drug.

Therefore does two things: 1 produce methemoglobin and 2 have potential in producing hemolytic anemia in glucose 6 phosphate dehydrogenase deficiencies. Therefore, hemolysis in G6PD def is referring to oxidizing agents, causing an increase in peroxide, which destroys the RBC; the same drugs that produce hemolysis in G6PD def are sulfa and nitryl drugs.

These drugs also produce methemoglobin. Therefore, potential complication of that therapy is methemoglobinemia. Curves: left and right shifts Want a right shifted curve — want Hb with a decreased affinity for O 2 , so it can release O 2 to tissues. Problems related to problems related to oxidative pathway a. Most imp: cytochrome oxidase last enzyme before it transfers the electrons to O 2. Uncoupling — ability for inner mito membrane to synthesize ATP.

Inner mito membrane is permeable to protons. Examples: dinitrylphenol chemical for preserving wood , alcohol, salicylates. Uncoupling agents causes protons to go right through the membrane; therefore you are draining all the protons, and very little ATP being made.

These are all the causes of tissue hypoxia ischemia, Hb related, cyto oxidase block, uncoupling agents. Absolute key things! What happens when there is: a. Decreased of ATP as a result of tissue hypoxia 1.

Why do we have to use anaerobic glycolysis with tissue hypoxia? Mitochondria are the one that makes ATP; however, with anaerobic glycolysis, you make 2 ATP without going into the mitochondria.

Mitochondrial system is totally shut down no O 2 at the end of the electron transport system — can only get 2 ATP with anaerobic glycolysis. Good news — get 2 ATP Bad news — build up of lactic acid in the cell and outside the cell increased anion-gap metabolic acidosis with tissue hypoxia due to lactic acidosis from anaerobic glycolysis.

Therefore, buildup of lactic acid within the cell will lead to Coagulation necrosis. With no ATP, Na into the cell and it brings H20, which leads to cellular swelling which is reversible. Cell without O 2 leads to irreversible changes. With decrease in ATP, Ca has easy access into the cell.

Within the cell, it activates many enzymes ie phospholipases in the cell membranes, enzymes in the nucleus, leading to nuclear pyknosis so the chromatin disappears , into goes into the mito and destroys it.

Therefore, with irreversible changes, Ca has a major role. Of the two that get damaged mito and cell membrane , cell membrane is damaged a lot worse, resulting in bad things from the outside to get into the cell.

Types of Free Radicals: 1. Oxygen: We are breathing O 2 , and O 2 can give free radicals.


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Goljan Pathology Lecture Notes (Typed Pathology Notes) PDF


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