Is it worth listening to Goljan audio if I'm doing Pathoma? Filesharing is prohibited in this subreddit. These drugs also pr od uc e me th em og lo bin. Popular Posts This Week Sorry. I have heard that there are 'new' Goljan audio lectures since I took Step 1. Close Dialog Are you sure?
|Genre:||Health and Food|
|Published (Last):||4 July 2013|
|PDF File Size:||20.2 Mb|
|ePub File Size:||20.38 Mb|
|Price:||Free* [*Free Regsitration Required]|
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime. Goljan pathology audio transcripts. Upcoming SlideShare. Like this document? Why not share! Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode. Published in: Business , Technology. Full Name Comment goes here. Are you sure you want to Yes No.
Charity Gibson Over the past few days I've been telling you about a NEW 5-second "water hack" that crushes food cravings and melts 62lbs of fat I know the video is long and you probably don't have time to watch the whole thing, so Stacey Newton Without requiring much effort from your part, The Gout Diet guides you step-by-step on how to remove gout quickly and efficiently.
You'll be able to say goodbye to gout, and feel better than ever before, in just 7 days or less! Here's an all-natural gout relief method. Show More. Vemula Amulya. Amogh Tiwari. Mason Sifford. No Downloads. Views Total views. Actions Shares. Embeds 0 No embeds. No notes for slide. Goljan pathology audio transcripts 1. CopyrightedR Material. All Rights Reserved. Need O2 for oxidation phosphorylation pathway — where you get ATP from inner Mito membrane electron transport system, called oxidative phosphorylation.
The last rxn is O2 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 O2 cannot get through…ie fibrosis.
Best example—Sarcoidosis a restrictive lung disease ; O2 already have trouble getting through the membrane; with fibrosis it is worse. Another example—Pulmonary edema; O2 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 pO2. There is NO hypoxemia in anemia, there is normal gas exchange normal respiration , therefore normal pO2 and O2 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 O2 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 O2 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 O2, so it can release O2 to tissues. Problems related to problems related to oxidative pathway a.
Most imp: cytochrome oxidase last enzyme before it transfers the electrons to O2. 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 O2 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 O2 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 O2, and O2 can give free radicals. Water in tissues converted to hydroxyl free radicals, leading to mutations in tissues. Audio file 2: Cell Injury 2 3. Cytochrome P in liver metabolizes drugs, and can change drugs into free radicals. Drugs are often changed in the liver to the active metabolite — ie phenytoin.
Where in the liver does acetaminophen toxicity manifest itself? Treatment: n-acetylcysteine; how? Well, the free radicals can be neutralized.
Superoxide free radicals can be neutralized with supraoxide dismutase SOD. Main function is to neutralize free radicals esp drug free radicals, and free radicals derived from peroxide. Glutathione gets used up in neutralizing the acetaminophen free radicals.
Goljan Audio Transcript Notes PDF
Goljan - Audio Transcript