MMC Mobile show

MMC Mobile

Summary: The Medical School Podcast has two major purposes: 1) to publish Mastermind Group recordings of experts in various medical education fields, and 2) to prevent physician burnout by teaching wellness in medical education from the peer-reviewed, scientific literature. Doctor Dan recruits the listener into an active role in order to increase awareness about medically underserved populations, sources of stress in medical students and residents, and efforts to remedy the imbalances.

Podcasts:

 Integrative Medicine | File Type: audio/mpeg | Duration: 40:24

Episode 62: What is the evidence for acupuncture, Yoga, and vitamin therapy? Doctor Dan interviews Dr. Ronald Stram, founder of the Center for Integrative Health and Healing. Integrative Medicine Training After becoming board certified in Emergency Medicine, Dr. Stram did a fellowship at the Arizona Center for Integrative Medicine. Evidenced-Based Holistic Medicine Here are two databases that organize research by the strength of their evidence: * The Natural Standard * Natural Medicine Database

 Motherhood In Medicine | File Type: audio/mpeg | Duration: 20:01

Episode 61: Doctor Dan interviews co-founder of MommyMDGuides.com, Jennifer Reich. Learn how women physicians balance motherhood with medical practice. Pregnant Physicians It is estimated that some 20,000 women have a child at some point in their medical education and as many as 50,00 men and women become parents during this process. Parenthood is clearly an epidemic! Medical Careers Having a child can definitely change your life priorities and, sometimes, cause you to want a different lifestyle. This can lead to a change in medical specialty. Once you look into the eyes of your newborn, your world will change. This is not something to fear, but to embrace! Best Time To Have A Child In Medical School There is no “right” time, which means that ANY time is the right time! See, the responsibilities and stress always seem less desirable when you’re talking about someone else’s child. When it’s yours, it’s entirely different. Is it tough? Sure, but you better listen to the podcast and let Jennifer answer that question from a women’s perspective. Special Mentions * Jennifer’s Posiblog * Dr. Kristie McNealy’s blog * Christy Valentine, MD

 Cancer Part 2: USMLE Step 1 Prep | File Type: audio/mpeg | Duration: 30:02

Episode 60: This is Part 2 of the very long Cancer Podcast. Dr. Dan covers Grade versus Stage, paraneoplastic syndromes, and a high-yield list of the most common causes of the various cancers. Cancers and Associated Diseases – Part II Xeroderma pigmentosa – sun exposed areas, auto recessive, can cause all skin cancers (BCC, SCC, and melanomas), and the defect is in DNA repair enzymes. Other DNA repair defects are associated with BRCA1 and BRCA2, p53, they splice out the defects, this group is called the chromosomal instability syndromes – Wiskott Aldrich, Blooms, Ataxia Telangiectasias, and Fanconi’s, all have probs with DNA repair. Basic rule of thumb for BCC and SCC: * Upper lip and up is basal cell carcinoma; * lower lip and down is squamous cell (therefore, lesion on lower lip = sq cell; lesion on upper lip = basal cell) Example: inside nose is BCC, b/c above the upper lip Example: keloid – sq cell carcinomas and 3rd degree burns and sq cell carcinoma developing in areas of drainage from the sinus and ulcer that doesn’t heal from antibiotics. So, wherever there is constant irritation, and division of cells related to irritation, there is an increase susceptibility to cancer. This does not hold true for scar cancer tissue related cancers of the lungs or adenocarcinoma (just applies to things on the skin – ie burns and draining of sinus tracts). Only bacteria assoc with cancer? H. pylori – adenocarcinoma and low grade malignant lymphomas. XII. Grade vs Stage A. Grade = what does it look like? The term well differentiated means that the tumor is making something like keratin or glands, and if it’s identifiable it’s called low grade. When the cells are anaplastic, poorly differentiated under the microscope, and if you cannot tell what it is, then it’s called high grade. Example: sq cell carcinoma can see keratin pearls; can ID it, so it’s a low grade cancer. Example: see gland like spaces, can ID so its low grade B. Stage = (TNM) MC staging system; goes from least imp to most imp (TNM) Example: breast cancer with axillary node involvement; therefore, the N=1, but the “M” is worse, b/c it indicates that cancer has spread to other organs like bone, etc. Just b/c it goes to lymph nodes doesn’t mean it is the most imp prognostic factor. T=size of tumor; if tumor is over 2 sonometers, it has a chance of mets N=nodes (next most imp for prognosis) M=mets outside of nodes (most imp prognostic factor) Stage is more important than grade for prognosis; and within staging, M is the most imp factor for prognosis. Example: pt with prostate cancer, which of following has it the worst? The answer choices were cancer limited to prostate, it went into seminal vesicles, it involved the wall of bladder, went to lymph nodes, or bone? Answer = bone (bone represents the “M” of the TNM system – this is stage 4 by definition=mets) Example: a slide of a colon cancer and a lymph node: what is most important – size of tumor or lymph node involvement? Lymph node. If it was also in the liver, what is most imp? Liver specimen is the most imp prognostic factor. XIII. Host defenses – most important is Cytotoxic CD8 T cell Others – NK cells, Ab’s, macrophages, type 2 HPY. In hospital, they look for altered MHC class I Ag’s in the cancer pt, b/c cancer wants to kill T cells; they do this by putting in perforins, which activate  caspasases, and this leads to apoptosis (the signal, from the perforins, activate the caspasases, which have proteases, which break down the nucleus and mitochondria, and cell dies, without any inflammatory infiltrate). XIV. Other diseases seen in malignancy: A. Cachexia – cause is TNF alpha; it is irreversible. Once you see a pt with disseminated cancer about to go into catabolic state, can give then total nutrition, but still won’t help.

 Plastic Surgery Specialty Options | File Type: audio/mpeg | Duration: 26:59

Episode 59: Doctor Dan interviews Dr. Fardad Forouzanpour, a Cosmetic Surgeon. Dr. Fardad is a Board-Certified surgeon and one of only three physicians authorized to run his own Surgical Fellowship in Southern California. He has trained surgeons from all over the world. Dr. Fardad is also the inventor of the Umbilical Locator which was designed to help plastic and cosmetic surgeons locate the umbilicus when performing abdominoplasties. Plastic Surgery Fellowships Traditional Plastic Surgery This is the most well-known. It covers a lot of burns and reconstructions, even trauma. Cosmetic Surgery As the name implies, this separate fellowship opportunity allows surgeons to focus on mostly elective, aesthetic surgeries and procedures. Most patients pay cash, are often quite needy, and aren’t affected by the Health Care Reform. Words to the Wise: * Choose a specialty that you feel comfortable with, even if you had previously wanted to do something else. * Don’t do procedures unless you’re fully trained to do them and deal with the complications. * Not all surgeons’ personalities fit well with the often wealthy clients that have elective cosmetic surgeries.

 Mind-Body Medicine and Alternative Health Approaches | File Type: audio/mpeg | Duration: 22:21

Episode 58: Doctor Dan interviews Oleg Reznik, M.D., author of The Secrets of Medical Decision Making. He is an expert in Mind-Body medicine and is currently faculty at The American Institute for Mental Imagery. Medical Decision Making When we seek medical advice we’re hoping that a physician will always offer us what is in our absolute best interest. Indeed many physicians attempt to do that and some actually do. It is my perception however that great many physicians are bound by what I would call the Four Corners of the Medical Box. Physician Pressures: * Fear of litigation * Financial and time pressures * Guidelines of Health Care Authorities * The current Medical Model What propels a physician to leave this box by going beyond the boundaries of personal security? The Medical Decision-Making Solution: * Genuine compassion * Desire to do what is in patient’s absolute best interest * Courage to take the necessary risks.

 Edema | File Type: audio/mpeg | Duration: 9:24

Episode 57: In this episode, Doctor Dan discusses types and causes of edema, Starlings forces of oncotic and hydrostatic pressure, and gives relevant clinical examples that demonstrate each type. Listen to the podcast here… Fluid and Hemodynamics I. Edema – excess fluid in the interstitial space, which is extracellular fluid (ECF); this is outside the vessel. A. Types of Edema 1. Non-Pitting edema Increased vessel permeability with pus in the interstitial space (pus=exudates). Lymphatic fluid is another type of non-pitting edema. Blockage of lymphatics leads to lymphatic fluid in the interstitial space. Pits early, but eventually becomes nonpitting. Exudates and lymphatic fluid does not pit. 2. Pitting edema Transudate with right heart failure, swelling of the lower extremities, fluid in the interstitial space. Transudate does pit. 3. Three causes of edema: Exudates, lymphedema, and transudate. Transudates are the only one that has pitting edema. B. Transudate/Pitting Edema Transudate deals with Starling forces: 1. What keeps fluid in our blood vessels? Albumin, and this is called oncotic pressure. 80% of our oncotic pressure is related to the serum albumin levels. Anytime there is hypoalbuminemia then we will have a leaking of a transudate (protein of less than 3 g/dL) leaking into interstial space via capillaries and venules (pitting edema). 2. Normally, hydrostatic pressure is trying to push fluid out. Therefore, in a normal person, oncotic pressure is winning. Therefore, a decrease in oncotic pressure and an increase in hydrostatic pressure will lead to transudate (pitting edema). 3. Albumin is made in the liver. With chronic liver dz (cirrhosis), have a decreased albumin level. Can you vomit it out? No. Can crap it out (malabsorption syndrome), or can pee it out (nephrotic syndrome), can come off our skin (3rd degree burn b/c losing plasma), another possibility of low protein ct (low-intake) is seen in kids – Kwashiorkor – kid has fatty liver and decreased protein intake, leading to low albumin level. 4. Examples of clinical edema: a. Person with MI MI 24 hrs ago and he died and he has fluid coming out– transudate b/c increased hydrostatic pressure and left HF due to MI so things backed up into the lungs. B/c the CO decreased, the EDV increases and pressure on left ventricle increases, and the pressure is transmitted into the left atrium, to the pul vein, keeps backing up, and the hydrostatic pressure in the lung approaches the oncotic pressure, and a transudate starts leaking into the interstitial space, which leads to activation of the J receptor, which will cause dyspnea. Leads to full blown in alveoli and pulmonary edema, which is what this is. b. Venom from bee sting On arm leads to exudate due to anaphylactic rxn (face swelled), with histamine being the propagator, and type one HPY, causing tissue swelling. Rx – airway, 1:1000 aqueous epinephrine subcutaneously c. Cirrhosis of liver With swelling of the legs: transudate, mechanism: decreased oncotic pressure b/c cannot syn albumin, and increased hydrostatic pressure b/c portal HTN; there is cirrhosis of the liver, and the portal vein empties into the liver; in this case, it cannot, and there is an increase in hydrostatic pressure, pushing the fluid out into the peripheral cavities (so there are 2 mechanisms for ascites). Pitting edema in legs: decreased in oncotic pressure. d. Right heart failure Pt with dependent pitting edema: pt has right heart failure, and therefore an increase in hydrostatic pressure; with right heart failure, the blood behind the failed right heart is in the venous system; cirrhosis of liver is due to decrease in oncotic pressure. e. Modified radical mastectomy With nonpitting edema: lymphedema. Other causes – w. bancrofti,

 U.T. Houston Medical School – Work Life Program | File Type: audio/mpeg | Duration: 13

Episode 56: Doctor Dan interviewed Sam Hester from the Work-Life Program at the University of Texas Medical School at Houston. Work Life Balance in Medical School VISIT THE UT WORK LIFE WEB SITE WorkLife Balance Free, confidential articles (3,000) and resources to assist employees with balance in their work and personal lives. Relocation Counseling Cross-country or across the street moves are made easier with a wealth of free information. Assistance for every phase of your move is just one call or click-of-the-mouse away. Child Care Research shows that if you have a break in your child-care provider, it takes about 17 hours to find a replacement, with much of that necessitated during the business day. The WorkLife Program can provide you with a number of licensed child care providers nationwide to mach your particular child’s needs. Elder Care In the next 5 years, about 50% of the working population will be involved with the care of an elderly person in their life in some way. The WorkLife Program provides free comprehensive and ongoing Elder Care Needs Assessment, Planning, and Resource Services information for any location in the United States. Wellness In an effort to keep your employees on the job and as productive as possible, along with the skyrocketing costs of health care, the WorkLife Program can tailor a specific wellness program to meet your company’s needs. We can provide on-site seminars in stress management, and smoking cessation, as well as establish an on-site fitness/coaching program.

 How to Share Your Faith in Medical Practice | File Type: audio/mpeg | Duration: 18:51

Episode 55: Doctor Dan was interviewed by the head of the Christian Medical and Dental Association, a strong organization that hosts meetings on most medical school campuses. CMDA’s Life Support Podcast I originally invited them to our podcast and they decided to air it on their own podcast series called Life Support. We talk about sharing your faith, staying nurtured, and being Christ’s light in the dark halls of training hospitals.

 Cell membrane defects, cell cycle, and cancer drugs | File Type: audio/mpeg | Duration: 18:19

Episode 54: Learn about the spectrin defect causing spherocytosis, the ubiquitination of damages intracellular constituents, different types of cells, regulation of the cell cycle, and cancer drugs. Listen to the full podcast here… I. Cell Membrane Defects A. RBC membrane defect: Spherocytosis is a defect in spectrin within RBC cell membrane; if you can’t see a central area of pallor (if you don’t see a donut) then it’s a spherocyte. Absence of spectrin with in the RBC does not allow the RBC to form a biconcave disk; it is defective, and therefore forms a sphere. B. Ubiquitin – stress protein. High ubiquitin levels are associated with high levels of stress. Some of the intermediate filaments (keratin, desmin, vimentin) are part of the superstructure of our cells (“frame of the cell”, upon which things are built). When these intermediate filaments get damaged, the ubiquitin marks then for destruction. The intermediate filaments have been tagged (ubiquinated) and marked for destruction. Some of these products have names, for example: there are open spaces within the liver tisse, these spaces are fat and they are probably due to alcohol. The ubiquinited products of the liver are called Mallory bodies. These are the result of ubiquinated filaments called keratin and these are seen in alcoholic hepatitis. Another example: Silver stain of neurofibilary tangles – Jacob crutzfelt and alzheimers dz. Tau protein is associated with neurofib tangles; this is an example of a ubiquinated neurofilament. Example: Substantia nigra in Parkinson’s Dz – include inclusions called Lewy bodies, neurotransmitter deficiency is dopamine. Lewy bodies are ubiquinated neurofilaments. Therefore, Mallory bodies, Lewy bodies, and neurofib tangles are all examples of ubiquintation. II. Cell Cycle– A. Different types of cells: 1. Labile cells – cell where the division is via a stem cell. Three tissues that has stem cells: bone marrow, basement membrane of skin, and the base of crypts in the intestine. These cells have the tendency of being in the cell cycle a lot. In pharm: there are cell cycle specific and cell cycle nonspecific drugs. The cells that are most affected by these drugs are the labile cells b/c they are in the cell cycle. Complications of these drugs are BM suppression, diarrhea, mucocidis, and rashes on the skin (there are stem cells in all these tissues!). 2. Stable cells – in resting phase, Go phase. Most of parenchymal organs (liver, spleen, and kidney) and smooth muscle are stable cells. Stable cells can ungo division, but most of the time they are resting, and something must stimulate them to get into the cell cycle and divide – ie a hormone or a growth factor. For example: estrogen in woman will help in the proliferative phase of the menstrual cycle. The endometrial cells are initially in the Go phase and then the estrogen stimulated the cells to go into the the cell cycle. Therefore, they can divide, but they have to be invited by a hormone or a growth factor. 3. Permanent cells – can no longer get into the cell cycle, and have been permanently differentiated. The other types of muscle cells: striated, cardiac and neuronal cells. Only muscle that is NOT a permanent tissue = smooth muscle; hyperplasia = increase in #, while hypertrophy = increase in size. Would a permanent cell be able to under hyperplasia? NO, b/c that means more copies of it. Can it go under hypertrophy? Yes. A smooth muscle cell can undergo hyperplasia AND hypertrophy. B. Different phases of cell cycle: 1. G1 phase: The most variable phase of cell cycle is the G1 phase. Compare with menstrual cycle: The most variable phase is the proliferative phase (not the secretory phase). The prolifertive phase varies with stress; however, once ovulation has occurred, it is 14 days. Therefore, proliferative phase is analogous to G1 phase of the cel...

 Interview with a Transplant Patient | File Type: audio/mpeg | Duration: 31:10

Episode 53: Meet Mark Black: double organ transplant recipient, marathon runner turned motivational speaker. Boy, does he ever have some insight directed towards medical students. Congenital Heart Defect Podcast Cardiac Surgeries His surgeries started at one day old for a congenital heart defect. Ventricular Arrhythmias By the age of 21 he had frequent ventricular tachycardia and was at risk for sudden cardiac arrest. He had a heart and two-lung transplant and ran his first half-marathon and 2.5 years until he ran his first full marathon. Now 3 are in his rear-view mirror. Patient Opinion of Medical Students Listen to the podcast to discover what advice he has for medical students! He spent a lot of time in hospitals, up to 6 months at a time growing up. Many places were teaching hospitals so his insights are very enlightening. He authored a book titled Live Life From The Heart. To support him and order his book, visit Mark Black Speaks.

 Chronic Fatigue Syndrome and Fybromyalgia | File Type: audio/mpeg | Duration: 56:51

Episode 52: In this episode, Doctor Dan interviews Dr. Jacob Teitelbaum, a physician who got Chronic Fatigue Syndrome as a result of a viral infection while in medical school. Chronic Fatigue Syndrome: CFS can  result from a variety of causes and is most commonly idiopathic. The condition can be devastating, as Dr. Teitelbaum describes in this interview how he went from Medical Student to homeless on a park bench, where he truly learned about Chronic Fatigue Syndrome. How to diagnose chronic fatigue syndrome: * Truly listen to your patient * Document insomnia despite extreme fatigue * More than 3 months in duration * Severe, disabling fatigue How to treat chronic fatigue syndrome: Use the SHINE protocol, shown to provide relief for 91% of patients: S – Sleep 7-8 hours per night using medication toward the goal of restorative sleep. H – Hormonal support I – Infections: diagnose and treat underlying or secondary infections during this immune-suppressed period N – Nutritional support E – Exercise as able. To learn more, visit www.Endfatigue.com.

 Tissue Repair from Cellular Injury | File Type: audio/mpeg | Duration: 14:53

Episode 51: Doctor Dan covers tissue repair and cellular response to injury in the kidney, lungs and nervous system. Also, get a quick review of inflammation in general to keep your memory fresh. Listen to the podcast here… I. Tissue Repair Scar tissue (b/c its permanent tissue); scar tissue (fibrous tissue) does not contract; therefore, if you have more scar tissue to free wall of left ventricle will lead to decreased Ejection Fraction, which is Stroke Volume divided by the End Diastolic Volume. EF = SV/EDV A. Response of Kidneys to Injury: Kidney will form scar tissue; medulla is most susceptible to ischemia (b/c least amount of blood supply). What part of nephron most susceptible to tissue hypoxia? 2 places: 1. Straight portion of prox tubule b/c most of oxidative metabolism is located there, with brush borders – this is where most of reabsorption of Na, and reclaiming of bicarb is there. 2. Medullary segment of thick ascending limb – where the Na/K-2Cl pump is – which is where loop diuretics block. The Na/K-2Cl pump generates free water. The two type of water in urine: obligated and free. If the water is obligated, then the water is obligated to go out with every Na, K, and Cl (concentrated urea). Basically 20 ml’s of obligated water for every Na, K, Cl (it’s obligated) via Na/K/2Cl pump. The ADH  hormone absorbs free water b/c the pump generates free water. Let’s say you absorb one Na, how much free water is left behind in the urine? – 20 mls; then reabsorbed another K, that is another 20, so its up to 40; another 2 Cl’s are reabsorbed which is another 40; therefore, for absorbing one Na, one K, and 2 Cl’s, you have taken 80 mls of free water from the urine – this is free water that is generated; its is this pump that loop diuretics block, which is in the thick ascending limb of the medullary segment. B. Response of Lungs to Injury: Lung repair cell is type II pneumocyte (can also repair type I pneumocytes); it also synthesizes surfactant. C. CNS Repair cell is the astrocyte; the astrocyte proliferates (b/c it’s a stable cell, not a neuron), that can proliferate and produces protoplasmic processes – called gliosis (rxn to injury in the brain, which is due to astrocyte proliferation); this is analogous to fibroblasts laying collagen type 3 in the wound. D. PNS Wallarian degeneration is the mech of axonal regeneration. In PNS, have Schwann cells, while in the CNS, have oligodendrocytes (both make myelin). Tumor Schwann cell = schwannoma; if it involves CN VIII it is called acoustic neuroma. What genetic dz that is auto dominant has association? Neurofibromatosis. II. Extra Side notes and Review of Inflammation: A. ESR Putting whole blood into cylinder and see when it settles. The higher the density, or weight, therefore settle pretty quick and therefore have a increased sedimentation rate. When stuck together and looks like coins = roulouex. When aggregated together = increased sed rate, which is increased IgG and fibrinogen (includes every acute and chronic inflammation there is. * What causes RBC’s to clump? – IgM, b/c the neg charge normally keeps RBC’s from stick to e/o. * IgM is a lot bigger; cold agglutinins are associated with IgM ab, leading to agglutinin. This is why in cold whether, you get Raynaud’s phenomenon (lips, nose, ears, toes, fingers turn blue). The IgM ab can cause cold agglutinins, leading to ischemia. * Another type of clumping of IgM are Cryoglobulins – Ig’s congeal in cold weather; IgM ab’s do the same thing. High assoc of hep C with cryoglobulins. * Multiple myleoma = increased esr b/c increased IgG; with waldenstroms, will see increased IgM (Waldenstrom’s Macroglobemia). B. Acute appendicitis Get CBC, and want to see absolute neutrophilic leukocytosis, meaning that you have an increase of neutrophils in the peripheral blood; a...

 Strategies for USMLE Exam Day | File Type: audio/mpeg | Duration: 24:46

Episode 50: This is the first guest series lecture targeted for residents, but these “Test Day” strategies apply for the USMLE, MCAT, and every shelf exam you’ll ever take. Test Taking Strategies For The Boards The United States Medical Licensing Examinations, ABIM, and ABFM focus their content for the general, undifferentiated medical practitioner (GUMP). Board exams are designed to separate out good from bad test takers. It is assumed that all are adequate clinicians. Study guides are better than reviewing recent literature (within the last 5 years). USE PRACTICE QUESTIONS and STUDY GROUPS – not text books. Rule based questions are thrown out of the test development pruning process. The questions have to be answerable from information contained within the question. Therefore, you’ll be selecting the “single best answer” practically all the time. The diagnosis, treatment, or risk factors are always pulled directly from the question stem and are needed to jive with the correct answer. Including images in the test is expensive and are, therefore, are very important for the correct answer. It may be a normal chest x-ray, but that information will be important in the thinking process required to arrive at the correct answer. Questions That Don’t Count Towards Your Score 15% – 20% of your questions are being “tested” and aren’t being considered for your score. They are being live tested to see if the question is a discriminative question. That is, does everyone get it right or wrong? If so, it will be thrown out. This process takes about 1,5 – 2 years to vet questions in this way, so very recent articles CAN’T be included. Repeated Questions Almost 20% of the test is repeated annually. Therefore, read remembered questions and get extra points. Anatomy of a Test Question Question Stem Most of it is unnecessary information. Lead-In The last sentence is the actual question. Correct Answer There is only one. Distracters Incorrect answers often have some truth in them. Putting all this together, if you get a question, look at the picture first. Then look at the Lead-In. Look for magic words: (download the complete list of “magic words”) * Ashkenazi Jews and Gaucher’s Disease * “Plop” on auscultation – myxoma * Tearing chest pain – dissection * Pt. works with animals – Tularemia * Demographics are always specific for the clinical pattern consistent with the correct answer. * http://medical-mastermind-community.com/pre-med/usmle-step-1 Absolutes are “always” wrong Words such as never, always, everyone, etc. These statements are way too broad to be true most of the time. Time Management * Spend 1-2 minutes on a question. Don’t waste your time. * Save calculations for the end, unless you are very quick with 2×2 tables in biostatistics. If you recognize nothing, guess. * Half of the test will have to answers that you’ll think about. The good distracter is partially correct. Examination Day Tips * Wear layered clothing, so you can peel them off. Don’t get cold! * Don’t study for 1-2 days before the test.

 Inflammation | File Type: audio/mpeg | Duration: 20:33

Episode 49: The original recording is very long for this topic because it covers, inflammatory mediators, phagocytosis and opsonization, complement and arachadonic acid, and cluster designations. Listen to the podcast here… I. Acute Inflammation A. Cardinal signs of inflammation In the scenario with a bee sting: you will see redness (Tubor). The king of vasodilators is histamine and it vasodilates the arterioles. Therefore, histamine is responsible for the redness of acute inflammation (i.e., bee sting), and is working on arterioles. Now if we felt the area, it will be warm (Calor = heat), this is due to vasodilating the arterioles, which is caused by histamine. For example in endotoxic and septic shock, the skin is warm b/c you are vasodilated. Tumor is a raised structure caused by histamine. Histamine can lead to increased vessel permeability in the venules; is arterial thicker than venules? Yes. The venules are very thin; they basically have an endothelial cell with a basement membrane, all you have to is drill a hole through the BM and you are out. Therefore, increased vessel permeability occurs at the venule level, not the arterial level. Histamine contracts the endothelial cells, and leaves the BM bare, leading to increased vessel permeability, producing an exudate, and swelling of tissue, hence tumor of acute  inflammation. The area may hurt (Dolor = pain) but histamine does not have anything to do with this. Bradykinin is part of the kininogen system between factor 11 and Hageman factor 12. So when you activate the intrinsic pathway, you automatically activate the kininogen system. When you activate factor 12 (Hageman factor), it will activate 11 and the whole kininogen system. The end product is bradykinin. ACE inhibits the degredation of bradykinin, therefore complicating the clinical condition with angioedema. Also inhibit metabolism of bradykinin, which increases vessel permeability, producing the angioedema (swelling of the tissues). How bradykinin produces cough is not really understood. Bradykinin and PGE2 cause pain (dolor) and is the only one out of the four Latin terms of acute inflammation that is not due to histamine release. B. Steps involved in Acute inflammation (this the normal sequence in acute inflammation): 1. Emigration: Includes margination, pavementing, rolling, adhesion, and transmigration Neutrophils in  circulation start to become sticky b/c of adhesion molecule synthesis. Endothelial cells begin to synthesize adhesion molecules. Eventually, neutrophils will stick to endothelial cells, these steps are called pavementing or margination. Then neutrophils look for bare basement membrane on the venules and then they drill a hole through it via type 4 collagenase. Cancer cells also have type 4 collagenase, that’s how they metastasize. Cancer cells attach to endothelial via adhesion molecules, usually against laminin in BM, and they have collagensae to get through the BM, therefore, cancer cells are pretty much like a neutrophil when invading tissue. 2. Chemotaxis: When they pass BM of small venules, they emigrate but they have to know what direction to go. They get directions in a process called directed chemotaxis. C5a and LT-B4 (leukotriene B4) are the chemotactic agents. These chemotactic agents are also involved in making adhesion molecules on neutrophils). Therefore, they make adhesion molecules AND give direction by acting like chemotactic agents. 3. Phagocytosis via opsonization: a) Example: in an acute inflammation with staph aureus, the bacteria are being processed by opsonins, which immobilize the particles on the surface of the phagocyte. The two main opsonins are IgG and C3b. They help with phagocytosis. b) Example of an opsonization defect: Brutons agammaglobinemia: an x-linked recessive dz, where all the immunoglobulins are missing, including IgG. Therefore,

 Interview with Napoleon Hill Foundation educator Judy Williamson | File Type: audio/mpeg | Duration: 54:21

Bonus Episode: Learn about Mastermind Groups from the Education Director for the Napoleon Hill Foundation World Learning Center. Napoleon Hill Foundation Podcast Judy Williamson – World Learning Center I’m very grateful that she donated some time and guidance to our Medical Mastermind Community. After all, I organized our community as a Mastermind organization after reading Napoleon Hill’s Think and Grow Rich, which I highly recommend, and at the behest of my mentors. Authentic Community Because you are an inquisitive type, here are the research articles I refer to in the interview regarding Authentic Community. * Healer’s Art Community This paper references the next one and renders their community less effective than a Mastermind: * The Healer’s Art’s ill-informed definition of what makes up the most effective Community. (page 139, 2nd paragraph says “shared expertise”, opposite of Napoleon Hill’s philosophy. Want to listen to a live Mastermind Meeting? Listen in to me on the next Medical Mastermind Community teleconference. You must first join the Community, then you can login to access the conference call instructions here. When is the next meeting? Add our Google Calendar to yours and receive automatic email reminders.

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