medicinethought-blog - Tumblr blog

medicinethought-blog · 8 years ago

Text

Systemic lupus erythematosus (Lupus)

Intro

Lupus is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body.

Symptoms

People with discoid lupus and subacute cutaneous lupus may exhibit thick, red scaly patches on the skin. Acute cutaneous lupus shows as a rash. Some have the classic “butterfly rash”. Hair loss, mouth and nasal ulcers, and lesions on the skin are also symptoms.

Joint pain is common. However, lupus arthritis does not cause severe destruction of the joints, unlike rheumatoid arthritis.

Anaemia is common, as well as antiphospholipid antibody syndrome

Inflammation of the fibrous sac surrounding the heart, heart muscle, and inner lining of the heart are common conditions.

Causes

Lupus runs in families, but a single gene hasn’t been identified. But, multiple genes influence a person's chance of developing lupus by environmental factors. But is quite poorly understood.

Pathophysiology

Germinal Centres

In healthy people, apoptotic lymphocytes are removed in germinal centres by specialised phagocytes, the tingible body macrophages (TBM), therefore no free apoptotic and potential autoantigenic material can be seen.

Cell Death Signalling

Apoptosis is increased in monocytes and keratinocytes

Expression of Fas by B cells and T cells is increased

There are correlations between the apoptotic rates of lymphocytes and disease activity.

Necrosis is increased in T lymphocytes.

TBM: large phagocytic cells in the germinal centres of secondary lymph nodes express a CD68 protein. These cells engulf B cells that have performed apoptosis after somatic hypermutation. Undigested apoptotic nuclei can be found on the outside of TBMs. This may present a threat to B cells and T cells. Dendritic cells in the germinal centre may endocytose antigenic material and present it to T cells, activating them. Apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells that may have self-specificity through somatic hypermutation. Necrosis (a pro-inflammatory form of cell death), is increased in T lymphocytes, due to mitochondrial dysfunction, oxidative stress, and reduction of ATP.

Diagnosis

Laboratory tests

Testing includes Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA). immunofluorescence is used to detect ANAs. The pattern of fluorescence shows the antibody present. Immunofluorescence can detect immunoglobulins.

Testing positive using ANA results in many connective tissue disorders and other autoimmune diseases. Antinuclear antibodies include anti-Smith and anti-double-stranded DNA (dsDNA) antibodies and anti-histone antibodies. Anti-dsDNA antibodies have a high affinity for SLE; The anti-dsDNA antibody titers also disease activity. Other ANA that may occur in people with SLE is anti-U1 RNP, SS-A (or anti-Ro) and SS-B (or anti-La). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.

Other tests are system level checks (low levels suggest consumption by the immune system), electrolytes and kidney function, liver enzymes, and complete blood count.

Treatment

Disease-modifying antirheumatic drugs

DMARDs reduce the incidence of flares (reoccurrence of disease), the progress of the disease, and the need for steroid use; flares are treated with corticosteroids. Hydroxychloroquine is an antimalarial medication and has few side effects, and improves survival. Cyclophosphamide is used for severe glomerulonephritis. Mycophenolic acid is also used for the treatment of lupus nephritis.

Immunosuppressive drugs

ID’s are used to control the disease and prevent flares. People who require steroids may develop Cushing's syndrome (obesity, puffy round face, diabetes mellitus, increased appetite, difficulty sleeping and osteoporosis). Which can diminish, but long-term use can elevate blood pressure and cataracts.

References

"Handout on Health: Systemic Lupus Erythematosus". www.niams.nih.gov. February 2015

Tebbe, B; Orfanos, CE (1997). "Epidemiology and socioeconomic impact of skin disease in lupus erythematosus". Lupus. 6 (2): 96–104

Gladman, Dafna (10 September 2015). "Overview of the clinical manifestations of systemic lupus erythematosus in adults".

Joint and Muscle Pain Lupus Foundation of America

Lam, SK; Quah, TC (1990). "Anemia in systemic lupus erythematosus.". The Journal of the Singapore Paediatric Society. 32 (3–4): 132–6

Syuto T, Shimizu A, Takeuchi Y, et al. (February 2009). "Association of anti-phosphatidylserine/prothrombin antibodies with neuropsychiatric systemic lupus erythematosus". Clin. Rheumatol. 28 (7): 841–5

Gaipl US, Kuhn A, Sheriff A, et al. (2006). "Clearance of apoptotic cells in human SLE". Curr. Dir. Autoimmun. Current Directions in Autoimmunity. 9: 173–87.

Gergely P Jr; Grossman C; Niland B; Puskas F; Neupane H; Allam F; Banki K; Phillips PE; Perl A. (January 2002). "Mitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosus.". Arthritis Rheum. 46: 175–90.

Ther Clin Risk Manag. 2011; 7: 27–32. The lupus band test in systemic lupus erythematosus patients. Adam Reich, Katarzyna Marcinow, and Rafal Bialynicki-Birula

Buyon JP, Clancy RM (December 2003). "Maternal autoantibodies and congenital heart block: mediators, markers, and therapeutic approach". Semin. Arthritis Rheum. 33 (3): 140–54.

Vasudevan AR, Ginzler EM (August 4, 2009). "Established and novel treatments for lupus". The Journal of Musculoskeletal Medicine. 26 (8)

0 notes

medicinethought-blog · 8 years ago

Text

GI Bleed

Intro

A Gi Bleed is the bleeding in the gastrointestinal tract, from the mouth to the rectum. When there is significant blood loss over a short time.

Diagnosis

Upper gastrointestinal bleeding is from somewhere between the pharynx and the ligament of Treitz. An upper source is known if the patient is vomiting up blood and has a tarry stool containing old blood. Many cases are due to peptic ulcer disease (gastric ulcers) and Esophageal inflammation and erosive disease are also common. People with liver cirrhosis are more susceptible to esophageal bleeds. Medications such as NSAIDs, COX-2, SSRIs, corticosteroids, and anticoagulants may also increase the risk of GI bleeds.

Lower gastrointestinal bleeding is from the colon, rectum or anus. Causes of lower gastrointestinal bleeding include hemorrhoids, cancer, angiodysplasia, ulcerative colitis, Crohn’s disease, and aortoenteric fistula. It may be indicated by fresh red blood in stool, Isolated melena may originate from anywhere between the stomach and the proximal colon.

Prevention

People with varices or cirrhosis β-blockers reduce the risk of future bleeding. Endoscopic band ligation (EBL) is also effective. Either B-blockers or EBL are recommended as initial preventative measures. In those who have had a previous bleed both treatments are recommended. With isosorbide mononitrate. Transjugular intrahepatic portosystemic shunting (TIPS) may be used to prevent bleeding in people who re-bleed despite other measures.

Treatment

Peptic ulcers

Crystalloid and colloids are used for peptic ulcer bleeding. Proton pump inhibitors (PPI) reduce mortality in those who are at the risk of re-bleeding and that need for surgery. Oral and intravenous formulations may also be used; however, the evidence to support this is not optimal. In those with less severe disease and where endoscopy is rapidly available, There tranexamic acid which inhibits clot breakdown. Somatostatin and octreotide, for varicial bleeding. After treatment of a high risk bleeding ulcer endoscopically giving a PPI once or a day is less expensive.

Variceal bleeding

Colloids or albumin is preferred in people with cirrhosis. Medications typically include octreotide, vasopressin, nitroglycerin to reduce portal venous pressures. This is in addition to endoscopic banding or sclerotherapy for the varices. If this is sufficient then beta blockers and nitrates may be used for the prevention of re-bleeding. If bleeding continues, balloon tamponade with a Sengstaken-Blakemore tube or Minnesota tube may be used in an attempt to mechanically compress the varices. This may then be followed by a transjugular intrahepatic portosystemic shunt. In patients with cirrhosis, antibiotics decrease the chance of bleeding again, shorten the length of time spent in hospital, and decrease mortality. Octreotide reduces the need for blood transfusions and may decrease mortality.

Procedures

The Blakemore oesophagal balloon used for stopping esophageal bleeds if other measures have failed

Endoscopy within 24 hours is recommended, A number of endoscopic treatments may be used, including: epinephrine injection, band ligation, sclerotherapy, and fibrin glue. Prokinetic agents such as erythromycin before endocopy can decrease the amount of blood in the stomach. They also decrease the amount of blood transfusions required. Early endoscopy decreases the amount of blood transfusions needed. A second endoscopy within a day is sometimes needed. If other measures fail or are not available, esophageal balloon tamponade may be attempted.

Colonoscopy is useful for the diagnosis and treatment of lower GI bleeding. Surgery, is still commonly used to manage lower GI bleeds by cutting out the part of the intestines that is causing the problem. Angiographic embolization may be used for both upper and lower GI bleeds. Transjugular intrahepatic portosystemic shunting (TIPS) may also be considered.

References

“Bleeding in the Digestive Tract”. The National Institute of Diabetes and Digestive and Kidney Diseases. September 17, 2014. Retrieved 6 March 2015.

Kim, BS; Li, BT; Engel, A; Samra, JS; Clarke, S; Norton, ID; Li, AE (15 November 2014). “Diagnosis of gastrointestinal bleeding: A practical guide for clinicians.”. World journal of gastrointestinal pathophysiology. 5 (4): 467–78.

Westhoff, John (March 2004). “Gastrointestinal Bleeding: An Evidence-Based ED Approach To Risk Stratification”. Emergency Medicine Practice. 6 (3).

Jairath, V; Barkun, AN (October 2011). “The overall approach to the management of upper gastrointestinal bleeding”. Gastrointestinal endoscopy clinics of North America. 21 (4): 657–70.

Cat, TB; Liu-DeRyke, X (September 2010). “Medical management of variceal hemorrhage”. Critical care nursing clinics of North America. 22 (3): 381–93. van Leerdam, ME (2008). “Epidemiology of acute upper gastrointestinal bleeding.”. Best practice & research. Clinical gastroenterology. 22 (2):

Palmer, K; Nairn, M; Guideline Development, Group (2008-10-10). “Management of acute gastrointestinal blood loss: summary of SIGN guidelines” (PDF). BMJ (Clinical research ed.).

Li, L; Yu, C; Li, Y (March 2011). “Endoscopic band ligation versus pharmacological therapy for variceal bleeding in cirrhosis: a meta-analysis”. Canadian journal of gastroenterology = Journal canadien de

Tsoi, KK; Hirai, HW; Sung, JJ (Aug 5, 2013). “Meta-analysis: comparison of oral vs. intravenous proton pump inhibitors in patients with peptic ulcer bleeding.”. Alimentary pharmacology & therapeutics. 38 (7): 721–8.

Sreedharan, A; Martin, J; Leontiadis, GI; Dorward, S; Howden, CW; Forman, D; Moayyedi, P (2010-07-07). Sreedharan, Aravamuthan, ed. “Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in upper gastrointestinal bleeding”. Cochrane database of systematic reviews (Online) (7):

Bennett, C; Klingenberg, SL; Langholz, E; Gluud, LL (21 November 2014). “Tranexamic acid for upper gastrointestinal bleeding.”. The Cochrane database of systematic reviews. 11:

Sachar, H; Vaidya, K; Laine, L (November 2014). “Intermittent vs continuous proton pump inhibitor therapy for high-risk bleeding ulcers: a systematic review and meta-analysis.”. JAMA internal medicine. 174 (11): 1755–62.

1 note · View note

medicinethought-blog · 8 years ago

Text

Bowel Cancer

Intro

Bowel cancer is the development of cancer from the bowel or colon. A cancer is the abnormal growth of cells that have the ability to invade or spread to other parts of the body. Signs and symptoms may include blood in the stool, a change in bowel movements, weight loss, and feeling tired all the time. Most diagnosis are due to old age and lifestyle factors with only a small number of cases due genetic disorders.

Cause

Most cases are caused by no link to genetic risk. Risk factors include older age, being male, high intake of fat, alcohol, red meat, processed meats, obesity, smoking, and a lack of physical exercise.

People with ulcerative colitis and Crohn’s disease are at increased risk the risk increases the longer a person has the disease, and the worse the severity of inflammation.

Genetic syndromes are also associated with higher rates of colorectal cancer such as: hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome), Gardner syndrome and familial adenomatous polyposis (FAP).

Diagnosis

PET, MRI and CT scans are usually used which then it used in partner with the TNM system which produces staging results using T stages:

Or Duke’s stages:

Surgery

If the cancer is found at a very early stage, small and localised it may be removed during a colonoscopy. , with the attempt of achieving a cure. This can either be done by an open laparotomy or sometimes laparoscopically. The colon may then be reconnected or a person may have a colostomy. Sometimes chemotherapy is used before surgery to shrink the cancer before attempting to remove it. The two most common sites of recurrence of colorectal cancer are the liver and lungs.

In both cancer of the colon, chemotherapy may be used in addition to surgery in certain cases. In Stage I colon cancer, no chemotherapy is offered, and surgery is the treatment. In Stage II colon cancer is and is usually not offered. For stage III and Stage IV colon cancer, chemotherapy is an integral part of treatment. If cancer has spread to the lymph nodes or distant organs, which is the case with stage III and stage IV colon cancer respectively, adding chemotherapy agents increases life expectancy. If the lymph nodes do not contain cancer, the benefits of chemotherapy are debatable. If the cancer is widely metastatic or unresectable, treatment is then palliative.

References

Cancer Research UK “http://creativecommons.org/licenses/by-sa/4.0”

“Colon Cancer Treatment (PDQ®)”. NCI. 2014-05-12. Retrieved 29 June 2014.

“Defining Cancer”. National Cancer Institute.

“General Information About Colon Cancer”. NCI. 2014-05-12.

World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 5.5.

“Colorectal Cancer Prevention (PDQ®)”. National Cancer Institute. 2014-02-27.

Bibbins-Domingo, Kirsten; Grossman, David C.; Curry, Susan J.; Davidson, Karina W.; Epling, John W.; García, Francisco A. R.; Gillman, Matthew W.; Harper, Diane M.; Kemper, Alex R.; Krist, Alex H.; Kurth, Ann E.; Landefeld, C. Seth; Mangione, Carol M.; Owens, Douglas K.; Phillips, William R.; Phipps, Maureen G.; Pignone, Michael P.; Siu, Albert L. (21 June 2016). “Screening for Colorectal Cancer”. JAMA. 315 (23): 2564–75.

Thorat, MA; Cuzick, J (Dec 2013). “Role of aspirin in cancer prevention.”. Current Oncology Reports. 15 (6): 533–40.

“Routine aspirin or nonsteroidal anti-inflammatory drugs for the primary prevention of colorectal cancer: recommendation statement.”. American Family Physician. 76 (1): 109–13.

“SEER Stat Fact Sheets: Colon and Rectum Cancer”. NCI.

World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 1.1.

Alpers, David H.; Kalloo, Anthony N.; Kaplowitz, Neil; Owyang, Chung; Powell, Don W. (2008). Yamada, Tadataka, ed. Principles of clinical gastroenterology. Chichester, West Sussex: Wiley-Blackwell. p. 381.

Astin M, Griffin, T, Neal, RD, Rose, P, Hamilton, W (May 2011). “The diagnostic value of symptoms for colorectal cancer in primary care: a systematic review”. The British Journal of General Practice. 61 (586): 231–43.

Adelstein BA, Macaskill, P, Chan, SF, Katelaris, PH, Irwig, L (2011). “Most bowel cancer symptoms do not indicate colorectal cancer and polyps: a systematic review”. BMC Gastroenterology. 11: 65.

Watson AJ, Collins, PD (2011). “Colon cancer: a civilization disorder”. Digestive Diseases. 29 (2): 222–8.

Cunningham D, Atkin W, Lenz HJ, Lynch HT, Minsky B, Nordlinger B, Starling N (2010). “Colorectal cancer”. Lancet. 375 (9719): 1030–47.

“Colorectal Cancer 2011 Report: Food, Nutrition, Physical Activity, and the Prevention of Colorectal Cancer” (PDF). World Cancer Research Fund & American Institute for Cancer Research. 2011.

Lee, I-Min; Shiroma, Eric J; Lobelo, Felipe; Puska, Pekka; Blair, Steven N; Katzmarzyk, Peter T (1 July 2012). “Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy”. The Lancet. 380 (9838): 219–29.

Fedirko V, Tramacere, I, Bagnardi, V, Rota, M, Scotti, L, Islami, F, Negri, E, Straif, K, Romieu, I, La Vecchia, C, Boffetta, P, Jenab, M (Sep 2011). “Alcohol drinking and colorectal cancer risk: an overall and dose-response meta-analysis of published studies”. Annals of Oncology. 22 (9): 1958–72.

Valtin, H (November 2002). “"Drink at least eight glasses of water a day.” Really? Is there scientific evidence for “8 x 8”?“. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 283 (5): R993–1004

Jawad N, Direkze, N, Leedham, SJ (2011). "Inflammatory bowel disease and colon cancer”. Recent Results in Cancer Research. Recent Results in Cancer Research. 185: 99–115.

Xie J, Itzkowitz, SH (2008). “Cancer in inflammatory bowel disease”. World Journal of Gastroenterology. 14 (3): 378–89.

Triantafillidis JK, Nasioulas, G, Kosmidis, PA (Jul 2009). “Colorectal cancer and inflammatory bowel disease: epidemiology, risk factors, mechanisms of carcinogenesis and prevention strategies”. Anticancer Research. 29 (7): 2727–37.

Juhn E, Khachemoune, A (2010). “Gardner syndrome: skin manifestations, differential diagnosis and management”. American Journal of Clinical Dermatology. 11 (2): 117–22.

Half E, Bercovich, D, Rozen, P (2009). “Familial adenomatous polyposis”. Orphanet Journal of Rare Diseases. 4: 22.

Möslein G, Pistorius S, Saeger H, Schackert HK (February 2003). “Preventive surgery for colon cancer in familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer syndrome”. Langenbecks Arch. Surg. 388 (1): 9–16.

Stein, Ulrike; Walther, Wolfgang; Arlt, Franziska; Schwabe, Holger; Smith, Janice; Fichtner, Iduna; Birchmeier, Walter; Schlag, Peter M (2008). “MACC1, a newly identified key regulator of HGF-MET signaling, predicts colon cancer metastasis”. Nature Medicine. 15 (1): 59–67.

Stein A, Atanackovic, D, Bokemeyer, C (Sep 2011). “Current standards and new trends in the primary treatment of colorectal cancer”. European Journal of Cancer. 47 (Suppl 3): S312–4. .

“Chemotherapy of metastatic colorectal cancer”. Prescrire International. 19 (109): 219–24. October 2010.

Akhtar R, Chandel S, Sarotra P, Medhi B (2014). “Current status of pharmacological treatment of colorectal cancer”. World J Gastrointest Oncol. 6 (6): 177–83.

Shaib, W; Mahajan, R; El-Rayes, B (2013). “Markers of resistance to anti-EGFR therapy in colorectal cancer”. Journal of Gastrointestinal Oncology. 4 (3): 308–18.

0 notes

medicinethought-blog · 8 years ago

Text

Bone Marrow

Intro

I recently had an assembly at school about stem cell transplants and due to there being a lot of stem cells differentiating into RBC in bone marrow I thought it would be a very interesting topic to research.

Bone Marrow

Bone marrow is the flexible tissue in the bones where red blood cells are produced known as hematopoiesis. The hematopoietic component of bone marrow produces billions of blood cells per day, which use the bone marrow vascular system to circulate the body’s systemic circulation. Bone marrow also produces the lymphocytes that support the body’s immune system.

Function

(Mesenchymal) stem cells: MSC’s (stromal cells) are multipotent can differentiate into osteoblasts, chondrocytes, myocytes, adipocytes and beta-pancreatic islets cells.

Bone Marrow barrier: The blood vessels form a barrier, inhibiting immature blood cells from leaving. Only mature blood cells contain the specific membrane proteins that are required to leave the area.

Lymphatic role: Plays a role in lymphatic system by being able to generate lymphocytes from immature hematopoietic progenitor cells (type of stem cell). Bone marrow performs as a valve to prevent the backflow of lymphatic fluid

Process of Hematopoiesis

Donation and Transplantation

Hematopoietic stem cells are removed from a person and infused into another person. These infused cells will then travel to the bone marrow and initiate blood cell production. Transplantation from one person to another is conducted for some patients, such patients with HIV. The patient’s own marrow is first killed off with drugs or radiation, and then the new stem cells are introduced. Sometimes before chemotherapy/radiation therapy the stem cells are harvested to be later infused.

The stem cells are taken directly from the red marrow in the iliac crest, often under general anesthesia. The procedure is minimally invasive and does not require stitches afterwards.

Or certain drugs that stimulate the release of stem cells from the bone marrow into circulating blood can be used. An intravenous catheter is inserted into the donor’s arm, and the stem cells are then filtered out of the blood. In adults, bone marrow may also be taken from the sternum, while the tibia is often used when taking samples from infants. In newborns, stem cells may be retrieved from the umbilical cord.

References

Birbrair, Alexander; Frenette, Paul S. (2016-03-01). “Niche heterogeneity in the bone marrow”. Annals of the New York Academy of Sciences. 1370: 82–96.

Vunjak-Novakovic, G.; Tandon, N.; Godier, A.; Maidhof, R.; Marsano, A.; Martens, T. P.; Radisic, M. (2010). “Challenges in Cardiac Tissue Engineering”. Tissue Engineering Part B: Reviews. 16 (2): 169–187.

The Lymphatic System. Allonhealth.com.

Raphael Rubin & David S. Strayer (2007). Rubin’s Pathology: Clinicopathologic Foundations of Medicine. Lippincott Williams & Wilkins. p. 90.

Appendix A:IV in Wintrobe’s clinical hematology (9th edition). Philadelphia: Lea & Febiger (1993).

“The Red Cell Membrane: structure and pathologies” (PDF). Australian Centre for Blood Diseases/Monash University.

The Lymphatic System. Allonhealth.com.

“Bone marrow transplantation”. UpToDate.com.

“Bone marrow ‘frees men of HIV drugs’”. BBC. 3 July 2013.

National Marrow Donor Program Donor Guide Archived 8 September 2008 at the Wayback Machine.. Marrow.org.

Bone marrow donation: What to expect when you donate. Mayo Clinic.

McGuckin, C. P.; Forraz, N.; Baradez, M. -O.; Navran, S.; Zhao, J.; Urban, R.; Tilton, R.; Denner, L. (2005). “Production of stem cells with embryonic characteristics from human umbilical cord blood”. Cell Proliferation. 38 (4): 245–255.

0 notes

medicinethought-blog · 8 years ago

Text

PE is a blockage of an artery in the lungs by a substance that has traveled through the bloodstream (embolism). PE usually results from a blood clot in the leg that travels to the lung.The risk of blood clots is increased by cancer, prolonged bed rest, smoking, stroke, certain genetic conditions, pregnancy, obesity, and after some types of surgery. And can sometimes be due to the embolization of air, fat, or amniotic fluid.

Symptoms

Syspnea (shortness of breath)

Tachypnea (rapid breathing),

Chest pain

Cough

Hemoptysis (coughing up blood).

Cyanosis (blue discoloration, usually of the lips and fingers),

Collapse,

Circulatory instability because of decreased blood flow through the lungs and into the heart

Sudden death

A pleural friction rub

A pleural effusion

Strain on the right ventricle

A fever

Risk factors

Alterations in blood flow due to injury, pregnancy,obesity cancer

Factors in the vessel wall due to surgery, endothelial injury

Factors affecting the properties of the blood due to estrogen-containing hormonal contraception

Cancer

Diagnosis

CT pulmonary angiography (CTPA) is a pulmonary angiogram obtained using CT with radiocontrast. its non-invasive, its larger accessibility, and you can identify other lung disorders from the differential diagnosis in case there is no pulmonary embolism. Assessing the accuracy of CT pulmonary angiography is lowered by the rapid changes in the number of rows of detectors available in multidetector CT (MDCT). CTPA is not inferior to VQ scanning, and identifies more.

A VQ shows that some areas of the lung are being ventilated but not supplied with blood, this type of examination is as accurate as CT, but is less used. It is particularly useful in people who have an allergy to iodinated contrast, impaired renal function, or are pregnant. The test can be performed with two-dimensional imaging, or single photon emission tomography (SPECT) which enables three-dimensional imaging. Hybrid devices combining SPECT and CT (SPECT/CT) further enables identification of abnormalities.

Low chance of PE, a normal D-dimer level (blood test) is enough to portray presence of PE, D-dimer is highly sensitive (positive implies patient doesn’t have PE and visa versa). Full blood count is done, clotting status (PT, aPTT, TT), and some screening tests (erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes).

Treatment

Anticoagulant Therapy

Anticoagulant therapy is the mainstay of treatment. Heparin or fondaparinux are given, while warfarin, acenocoumarol, or phenprocoumon therapy also starts within hospital. Low molecular weight heparin may reduce bleeding among people with pulmonary embolism. Warfarin therapy often requires an often adjustment and monitoring to dosage for up to 6 months. In cancer patients LMWH (low molecular weight heparin) is favored over warfarin and it is continued for six months and pregnant women are often placed on LMWH until at least six weeks after birth to avoid the teratogenic effects of warfarin. (Distort fetus)

Thrombolysis

PE causing hemodynamic instability (low blood pressure) is an indication for thrombolysis (the destruction of the clot with medication). Catheter-directed thrombolysis (CDT) is a new technique found to be relatively safe and effective for massive PEs. This involves accessing the venous system by placing a catheter into a vein in the groin and guiding it through the veins by using fluoroscopic imaging until it is located next to the PE in the plunomary circulation. Medication that breaks up blood clots is released through the catheter.

Inferior vena cava filter

An inferior vena cava filter is constructed if the person has undergone surgery (therefore, anticogulant therapy is contradicted), or a person has a pulmonary embolus after being anticoagulated. It may be implanted to prevent new or existing Deep vein thrombosis from entering the pulmonary artery and combining with an existing blockage. Inferior vena cava filters should be removed when starting anticoagulation.

(An ECG with someone with pulmonary embolism)

References

“What Is Pulmonary Embolism?”. NHLBI. July 1, 2011

“What Are the Signs and Symptoms of Pulmonary Embolism?”. NHLBI. July 1, 2011.

Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)) (7 ed.). New York: McGraw-Hill Companies. p. 432.

Goldhaber SZ (2005). “Pulmonary thromboembolism”. In Kasper DL, Braunwald E, Fauci AS, et al. Harrison’s Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 1561–65.

Lewis, S; Dirksen, S; Heitkemper, M; Bucher, L (2014). Medical-surgical nursing: Assessment and management of clinical problems (9 ed.). St. Louis, MO: Elsevier Mosby. p. 552

Stein PD, Sostman HD, Hull RD, Goodman LR, Leeper KV, Gottschalk A, Tapson VF, Woodard PK (March 2009). “Diagnosis of Pulmonary Embolism in the Coronary Care Unit”. Am. J. Cardiol. 103 (6): 881–6.

Pregerson DB, Quick Essentials: Emergency Medicine, 4th edition. EMresource.org

Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, Jenkins JS, Kline JA, Michaels AD, Thistlethwaite P, Vedantham S, White RJ, Zierler BK (Apr 26, 2011). American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation,American Heart Association Council on Peripheral Vascular Disease,American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. “Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association.”. Circulation. 123 (16): 1788–830.

Ferri, F (2012). Ferri’s Clinical Advisor. St. Louis: Mosby’s.

Carrier M, Righini M, Djurabi RK, Huisman MV, Perrier A, Wells PS, Rodger M, Wuillemin WA, Le Gal G (May 2009). “VIDAS D-dimer in combination with clinical pre-test probability to rule out pulmonary embolism. A systematic review of management outcome studies”. Thromb. Haemost. 101 (5): 886–92.

Schrecengost JE, LeGallo RD, Boyd JC, Moons KG, Gonias SL, Rose CE, Bruns DE (September 2003). “Comparison of diagnostic accuracies in outpatients and hospitalized patients of D-dimer testing for the evaluation of suspected pulmonary embolism”. Clin. Chem. 49 (9):

Schouten HJ, Geersing GJ, Koek HL, Zuithoff NP, Janssen KJ, Douma RA, van Delden JJ, Moons KG, Reitsma JB (May 3, 2013). “Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis.”. BMJ (Clinical research ed.).

van Es, N; van der Hulle, T; van Es, J; den Exter, PL; Douma, RA; Goekoop, RJ; Mos, IC; Galipienzo, J; Kamphuisen, PW; Huisman, MV; Klok, FA; Büller, HR; Bossuyt, PM (16 August 2016). “Wells Rule and d-Dimer Testing to Rule Out Pulmonary Embolism: A Systematic Review and Individual-Patient Data Meta-analysis.”. Annals of Internal Medicine. 165 (4): 253–61.

Söhne, Maaike; Ten Wolde, Marije; Büller, Harry R. (1 November 2004). “Biomarkers in pulmonary embolism”. Current Opinion in Cardiology. 19 (6): 558–562.

Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, Bengel F, Brady AJ, Ferreira D, Janssens U, Klepetko W, Mayer E, Remy-Jardin M, Bassand JP (2008). “Guidelines on the diagnosis and management of acute pulmonary embolism: The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)”. European Heart Journal. 29 (18): 2276–2315.

Stein PD, Freeman LM, Sostman HD, Goodman LR, Woodard PK, Naidich DP, Gottschalk A, Bailey DL, Matta F, Yaekoub AY, Hales CA, Hull RD, Leeper KV, Tapson VF, Weg JG (2009). “SPECT in acute pulmonary embolism”. J Nucl Med (Review). 50 (12): 1999–2007.

Konstantinides, S; Torbicki, A; Agnelli, G; Danchin, N; Fitzmaurice, D; Galiè, N; Gibbs, JSR; Huisman, M; Humbert, M; Kucher, N (14 November 2014). “2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism”. European Heart Journal. 35 (43): 3033–3069.

Da Costa Rodrigues, J; Alzuphar, S; Combescure, C; Le Gal, G; Perrier, A (5 July 2016). “Diagnostic characteristics of lower limb venous compression ultrasonography in suspected pulmonary embolism: a meta-analysis.”. Journal of thrombosis and haemostasis : JTH. 14: 1765–72.

Schaefer-Prokop C, Prokop M (2005). “MDCT for the diagnosis of acute pulmonary embolism”. European radiology.

Van Strijen MJ, De Monye W, Kieft GJ, Pattynama PM, Prins MH, Huisman MV (2005). “Accuracy of single-detector spiral CT in the diagnosis of pulmonary embolism: a prospective multicenter cohort study of consecutive patients with abnormal perfusion scintigraphy”. Journal of thrombosis and haemostasis : JTH. 3 (1): 17–25.

Stein PD, Fowler SE, Goodman LR, Gottschalk A, Hales CA, Hull RD, Leeper KV, Popovich J, Quinn DA, Sos TA, Sostman HD, Tapson VF, Wakefield TW, Weg JG, Woodard PK (2006). “Multidetector computed tomography for acute pulmonary embolism”. N. Engl. J. Med. 354 (22): 2317–27.Anderson DR, Kahn SR, Rodger MA, Kovacs MJ, Morris T, Hirsch A, Lang E, Stiell I, Kovacs G, Dreyer J, Dennie C, Cartier Y, Barnes D, Burton E, Pleasance S, Skedgel C, O'Rouke K, Wells PS (2007). “Computed tomographic pulmonary angiography vs ventilation-perfusion lung scanning in patients with suspected pulmonary embolism”. JAMA. 298 (23):

Scarsbrook AF, Gleeson FV (2007). “Investigating suspected pulmonary embolism in pregnancy”. BMJ. 334 (7590): 418–9.

Leung AN, Bull TM, Jaeschke R, Lockwood CJ, Boiselle PM, Hurwitz LM, James AH, McCullough LB, Menda Y, Paidas MJ, Royal HD, Tapson VF, Winer-Muram HT, Chervenak FA, Cody DD, McNitt-Gray MF, Stave CD, Tuttle BD (2011-11-15). “An official American Thoracic Society/Society of Thoracic Radiology clinical practice guideline: evaluation of suspected pulmonary embolism in pregnancy”. American Journal of Respiratory and Critical Care Medicine. 184 (10): 1200–8.

National Institute for Health and Clinical Excellence. Clinical guideline 144: Venous thromboembolic diseases: the management of venous thromboembolic diseases and the role of thrombophilia testing. London, 2012. Benson MD (October 2012). “Pulmonary embolism in pregnancy. Consensus and controversies.”. Minerva ginecologica. 64 (5): 387–98.

Palareti G, Cosmi B, Legnani C, Tosetto A, Brusi C, Iorio A, Pengo V, Ghirarduzzi A, Pattacini C, Testa S, Lensing AW, Tripodi A (2006). “D-dimer testing to determine the duration of anticoagulation therapy”. N. Engl. J. Med. 355 (17): 1780–9.

Yoo, HH; Queluz, TH; El Dib, R (Apr 28, 2014). “Anticoagulant treatment for subsegmental pulmonary embolism.”. The Cochrane database of systematic reviews. Hirsh J, Guyatt G, Albers GW, Harrington R, Schünemann HJ (June 2008). “Executive summary: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)”. Chest. 133 (6): 71–109

Lavonas, EJ; Drennan, IR; Gabrielli, A; Heffner, AC; Hoyte, CO; Orkin, AM; Sawyer, KN; Donnino, MW (3 November 2015). “Part 10: Special Circumstances of Resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.”. Circulation.

“References in Catheter-directed Therapy for the Treatment of Massive Pulmonary Embolism: Systematic Review and Meta-analysis of Modern Techniques - Journal of Vascular and Interventional Radiology”. www.jvir.org.

Hao, Q; Dong, BR; Yue, J; Wu, T; Liu, GJ (30 September 2015). “Thrombolytic therapy for pulmonary embolism.”. The Cochrane database of systematic reviews (9)

Nakamura, S; Takano, H; Kubota, Y; Asai, K; Shimizu, W (Jul 2014). “Impact of the efficacy of thrombolytic therapy on the mortality of patients with acute submassive pulmonary embolism: a meta-analysis.”. Journal of thrombosis and haemostasis : JTH. 12 (7): 1086–95.

Chatterjee, Saurav; Chakraborty, Anasua; Weinberg, Ido; Kadakia, Mitul; Wilensky, Robert L.; Sardar, Partha; Kumbhani, Dharam J.; Mukherjee, Debabrata; Jaff, Michael R.; Giri, Jay (18 June 2014). “Thrombolysis for Pulmonary Embolism and Risk of All-Cause Mortality, Major Bleeding, and Intracranial Hemorrhage”. JAMA. 311 (23): 2414.

Young, Tim; Tang, Hangwi; Hughes, Rodney (2010-02-17). Vena caval filters for the prevention of pulmonary embolism. John Wiley & Sons, Ltd.

1 note · View note

medicinethought-blog · 8 years ago

Text

CKD

Intro

CKD (not to be confused with CDK’s and cyclins), interested me when I was researching about nephrology, as the kidneys are so vital it would make sense to do a piece on the this specific renal disease.

CKD

CKD is a steady loss in kidney function over a period of time. This disease may also or only identified when it leads to one of its recognised complications, such as cardiovascular disease and anemia. CKD is a long-term form of kidney disease and is different from acute kidney disease in that the loss/reduction in kidney function must be present for over 3 months.

Symptoms/Signs

Blood pressure is high due to fluid overload and production of vasoactive hormones created by the kidney. increasing the risk of developing hypertension

Urea builds up, leading to azotemia (high level of nitrogen containing compounds in the blood and therefore ultimately uremia (urea in the blood).

Potassium builds in the blood (hyperkalemia) with a range of symptoms including discomfort and an irregular heart beat (cardiac arrhythmias).

Erythropoietin synthesis is decreased causing anemia.

Iron deficiency anemia, which arises as kidney function decreases andis especially prevalent in those requiring blood dialysis.

Causes

Diabetes.

High blood pressure.

Vascular disease including large and small vessel disease.

Congenital disease such as polycystic kidney disease.

Obstructive nephropathy caused by kidney stones and diseases of the prostate.

Pinworms.

Diagnosis

One way to measure the rate at which the kidney has deteriorated (into CKD) is a urine test. All individuals with a glomerular filtration rate (GFR) greater than 60 ml/min/1.73 m^2 for 3 months are classified as having CKD. Protein in the urine is regarded as an independent test for worsening of kidney function and also cardiovascular disease.

Stage 1 kidney damage with normal or relatively high GFR (greater than or equal to 90 ml/min/1.73 m^2). Kidney damage is said to be pathological abnormalities, including abnormalities in blood or urine tests or imaging.

Stage 2 mild reduction in GFR (60–89 ml/min/1.73 m^2) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.

Stage 3 moderate reduction in GFR (30–59 ml/min/1.73 m^2)

Stage 4 severe reduction in GFR (15–29 ml/min/1.73 m^2) Preparation for renal replacement therapy.

Stage 5 Established kidney failure (GFR <15 ml/min/1.73 m^2), permanent renal replacement therapy, or end-stage kidney disease.

Treatment

CKD increases the risk of cardiovascular disease and people with CKD often have other risk factors for heart disease such as high blood lipids. The most common cause of death is cardiovascular disease not kidney failure.

Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression of CKD to kidney failure. They have also been found to reduce the risk of myocardial infarction, stroke, heart failure, People progressively lose kidney function while on these medications, as seen in studies, which reported a decrease over time in estimated GFR in people. Erythropoietin and calcitriol, (two hormones processed by the kidney), is often necessary in people with advanced disease. Phosphate binders are also used to control the serum phosphate levels, which are usually high in advanced CKD.

At stage 5 CKD, renal replacement therapy is usually required, in the form of either dialysis or a transplant.

References

National Kidney Foundation (2002). “K/DOQI clinical practice guidelines for chronic kidney disease”.

KDIGO: Kidney Disease Improving Global Outcomes (August 2009). “KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)”(PDF). Kidney Int. 76 (Suppl 113).

Eknoyan G, Lameire N, Barsoum R, et al. (2004). “The burden of kidney disease: improving global outcomes”. Kidney Int. 66: 1310–4.

A Martínez-Castelao; JL. Górriz; J Bover; et al. (2014). “Consensus document for the detection and management of chronic kidney disease”. Nefrologia. 34 (2): 243–62.

Hruska KA, Mathew S, Lund R, Qiu P, Pratt R (2008). “Hyperphosphatemia of chronic kidney disease”. Kidney Int. 74 (2): 148–57.

Faul C, Amaral AP, Oskouei B, Hu MC, Sloan A, Isakova T, Gutiérrez OM, Aguillon-Prada R, Lincoln J, Hare JM, Mundel P, Morales A, Scialla J, Fischer M, Soliman EZ, Chen J, Go AS, Rosas SE, Nessel L, Townsend RR, Feldman HI, St John Sutton M, Ojo A, Gadegbeku C, Di Marco GS, Reuter S, Kentrup D, Tiemann K, Brand M, Hill JA, Moe OW, Kuro-O M, Kusek JW, Keane MG, Wolf M. (2011). “FGF23 induces left ventricular hypertrophy.”. J Clin Invest. 121 (11): 4393–408.

Gutiérrez OM, Mannstadt M, Isakova T, Rauh-Hain JA, Tamez H, Shah A, Smith K, Lee H, Thadhani R, Jüppner H, Wolf M (2008). “Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis”. N Engl J Med. 359 (6): 584–592.

Bacchetta J, Sea JL, Chun RF, Lisse TS, Wesseling-Perry K, Gales B, Adams JS, Salusky IB, Hewison M (August 2012). “FGF23 inhibits extra-renal synthesis of 1,25-dihydroxyvitamin D in human monocytes”. J Bone Miner Res. 28 (1): 46–55.

Bover J, Jara A, Trinidad P, Rodriguez M, Martin-Malo A, Felsenfeld AJ (1994). “The calcemic response to PTH in the rat: effect of elevated PTH levels and uremia.”. Kidney Int. 46 (2): 310–7.

Longo et al., Harrison’s Principles of Internal Medicine, 18th ed., p.3109

Brandenburg VM, Cozzolino M, Ketteler M (2011). “Calciphylaxis: a still unmet challenge”. J Nephrol. 24 (2): 142–8.

Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K, Ott S, Sprague S, Lameire N, Eknoyan G (2006). “Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO)”. Kidney Int. 69 (11): 1945–53.

“United States Renal Data System (USRDS)”.

Rahman, Mahboob; Smith, Michael C. (September 1998). “Chronic renal insufficiency: A diagnostic and therapeutic approach”. Archives of Internal medicine. 158: 1743–52.

Qaseem A, Hopkins RH, Sweet DE, Starkey M, Shekelle P (22 October 2013). “Screening, Monitoring, and Treatment of Stage 1 to 4 Chronic Kidney Disease: A Clinical Practice Guideline From the Clinical Guidelines Committee of the American College of Physicians.”. Annals of Internal Medicine. 159 (12): 835–47.

Johnson, David (2011-05-02). “Chapter 4: CKD Screening and Management: Overview”. In Daugirdas, John. Handbook of Chronic Kidney Disease

Chauhan V, Vaid M (November 2009). “Dyslipidemia in chronic kidney disease: managing a high-risk combination”. Postgrad Med. 121 (6): 54–61. doi:10.3810/pgm.2009.11.2077. PMID 19940417.

Xie, X; Liu, Y; Perkovic, V; Li, X; Ninomiya, T; Hou, W; Zhao, N; Liu, L; Lv, J; Zhang, H; Wang, H (November 2015). “Renin-Angiotensin System Inhibitors and Kidney and Cardiovascular Outcomes in Patients With CKD: A Bayesian Network Meta-analysis of Randomized Clinical Trials.”. American Journal of Kidney Diseases (Systematic Review & Meta-Analysis). S0272-6386

Lewis EJ, Hunsicker LG, Clarke WR, Berl T, Pohl MA, Lewis JB, Ritz E, Atkins RC, Rohde R, Raz I (2001). “Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes”. N Engl J Med. 345 (12): 851–60.

Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, Remuzzi G, Snapinn SM, Zhang Z, Shahinfar S (2001). “Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy”. N Engl J Med. 345 (12): 861–9.

“Anaemia management in people with chronic kidney disease (CG114)”. NICE Clinical Guideline. UK National Institute for Health and Care Excellence. February 2011.Jump up^ Locatelli F, Aljama P, Canaud B, Covic A, De Francisco A, Macdougall IC, Wiecek A, Vanholder R (September 2010). “Target haemoglobin to aim for with erythropoiesis-stimulating agents: a position statement by ERBP following publication of the Trial to reduce cardiovascular events with Aranesp therapy (TREAT) study”. Nephrol Dial Transplant. 25 (9): 2846–50.

Clement FM, Klarenbach S, Tonelli M, Johnson JA, Manns BJ (22 June 2009). “The impact of selecting a high hemoglobin target level on health-related quality of life for patients with chronic kidney disease: a systematic review and meta-analysis”. Archives of Internal Medicine. 169 (12): 1104–12.

Levin A, Hemmelgarn B, Culleton B, Tobe S, McFarlane P, Ruzicka M, Burns K, Manns B, White C, Madore F, Moist L, Klarenbach S, Barrett B, Foley R, Jindal K, Senior P, Pannu N, Shurraw S, Akbari A, Cohn A, Reslerova M, Deved V, Mendelssohn D, Nesrallah G, Kappel J, Tonelli M (November 2008). “Guidelines for the management of chronic kidney disease”. CMAJ. 179 (11): 1154–62.

Jump up^ Yang, Q; Abudou, M; Xie, XS; Wu, T (Oct 9, 2014). “Androgens for the anaemia of chronic kidney disease in adults.”. The Cochrane database of systematic reviews. 10: CD006881.

0 notes

medicinethought-blog · 8 years ago

Text

Nephrology

Intro

From my GCSE and A-Level studies, the kidneys have been a complex organ that has interested me a lot, it has a large significance in all of our lives.

Nephrology

Nephrology is related to kidney function, kidney problems, the treatment of kidney problems and renal replacement therapy (dialysis and kidney transplantation). Conditions that affect the kidneys (such as diabetes and autoimmune disease) and problems that occur as a result of kidney problems (such as renal osteodystrophy and hypertension). All of these are studied within nephrology.

Kidney Transplantation

Kidney transplantation is the transplant of a kidney into a patient with end-stage renal disease (chronic kidney disease: a progressive loss in kidney function over a period of time).

the donor and recipient should be the A, B or O blood group and be compatible with the HLA antigen. In most cases the barely functioning existing kidneys are not removed, as removal has been shown to increase the rates of diseases after they have been removed. Therefore, the kidney is usually placed in a location different from the original kidney, often in the iliac fossa (s a large, smooth, concave surface on the internal surface of the ilium (part of the 3 fused bones making the hip bone). so it is often necessary to use a different blood supply. Such as: The renal artery of the new kidney, previously branching from the abdominal aorta, is often connected to the external iliac artery in the recipient. The renal vein of the new kidney, previously draining to the inferior vena cava, is often connected to the external iliac vein in the recipient.

Sometimes, the kidney is transplanted together with the pancreas. This is done in patients with type 1 diabetes, where the diabetes is due to destruction of the beta cells of the pancreas (pancreatic islets) and the diabetes has caused renal failure. Transplanting just the islet cells from the pancreas is possible but is experimental. This involves taking a deceased donors pancreas’, breaking it down, and extracting the islet cells that make insulin. The cells are then injected through a thin tube into the recipient and they generally lodge in the liver. The recipient still needs to take immunosuppressants to avoid rejection, but no surgery is required.

Immunosuppressants are used to suppress the immune system from rejecting the new kidney. These medicines must be taken for the rest of the person’s life. The most common medication regimen today is a mixture of tacrolimus (achieves this by inhibiting the production of interleukin-2, a molecule that promotes the development and growth of a T-Lymphocyte-type of WBC), mycophenolate/mycophenolic acid (nhibits an enzyme needed for the growth of T-Lymphocytes and Beta cells), and prednisolone (steriod medication).

Complications

Transplant rejection (hyperacute, acute or chronic)

Infections and sepsis (when an infection injuries the organs) due to the immunosuppressant drugs that are required to decrease risk of rejection

Post-transplant lymphoproliferative disorder (a form of lymphoma (blood tumours) due to the immune suppressants)

Imbalances in electrolytes including calcium and phosphate which can lead to bone problems

Hypertension of heart

Ulceration of the stomach and esophagus (due to drugs)

Hirsutism (excessive hair growth in a male-pattern distribution) with ciclosporin,

Hair loss with tacrolimus,

Obesity, acne, diabetes type 2, hypercholesterolemia (high blood cholesterol), and osteoporosis (decreased bone strength). (due to drugs taken)

References

By BruceBlaus (Own work) [CC BY-SA 4.0 (http://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons

David E. R. Sutherland; Rainer W. G. Gruessner; David L. Dunn; Arthur J. Matas; Abhinav Humar; Raja Kandaswamy; S. Michael Mauer; William R. Kennedy; Frederick C. Goetz; R. Paul Robertson; Angelika C. Gruessner; John S. Najarian (April 2001). “Lessons Learned From More Than 1,000 Pancreas Transplants at a Single Institution”. Ann. Surg. NCBI, NLM, NIH. 233 (4): 463–501.

“Kidney transplant: MedlinePlus Medical Encyclopedia”. National Institutes of Health. June 22, 2009.

Haller, Maria C.; Royuela, Ana; Nagler, Evi V.; Pascual, Julio; Webster, Angela C. (2016-08-22). “Steroid avoidance or withdrawal for kidney transplant recipients”. The Cochrane Database of Systematic Reviews

Nankivell, B (2011). “Diagnosis and prevention of chronic kidney allograft loss.”. Lancet. 378: 1428–37.

Naesens (2015). “Proteinuria as a Noninvasive Marker for Renal Allograft Histology and Failure: An Observational Cohort Study.”. J Am Soc Nephrol.

Krumme, B; Hollenbeck, M (March 2007). “Doppler sonography in renal artery stenosis–does the Resistive Index predict the success of intervention?”. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 22 (3): 692–6.

“Transplant Medication Questions”. Piedmont Hospital. May 13, 2011.

“Kidney transplant”. www.webmd.com.

0 notes

medicinethought-blog · 8 years ago

Text

Blepharoplasty (ENT)

Intro

I have once been to an ENT consultant due to a benign mass in my neck and I thought that it would be a very interesting thing to research (apart from being such a tongue twister!), and I was quite interested in the sub speciality of reconstructive surgery.

Blepharoplasty

Blepharoplasty is reconstruction of the eyelids; and cosmetically modifying that region. With the removal, or the repositioning of excess tissues, such as skin and adipocyte fat (loose connective tissue), and the reinforcement of the corresponding muscle and tendon tissues, the operative goals are to restore function which are achieved by eliminating excess skin from the eyelids, smoothing the underlying eye muscles, tightening the supporting structures, and resecting and re-draping the excess fat of the retroseptal area of the eye, in order to produce a smooth transition from eyelid to the cheek.

Operation

An operation usually is performed through external surgical incisions made along the creases of the upper and the lower eyelids, which creases then hide the surgical scars from view, especially when effected in the skin creases below the eyelashes of the lower eyelid. The incisions can be made from the conjunctiva (the interior surface of the lower eyelid) if transconjunctival blepharoplasty is true.

Transconjunctival blepharoplasty technique is useful for patients with darker skin tones where standard external incision often leaves a visible white scar. Transconjunctival blepharoplasty technique uses the excision of the lower-eyelid adipose tissue without leaving a visible scar, but, the transconjunctival blepharoplasty technique does not allow the removal of excess eyelid-skin.

After the procedure, a type of stitch known as a canthopexy is placed near the outer corner of the lower eyelid, which is inside the tissue. This allows the eyelid’s position to remain stable and static during the healing process. The canthopexy is dissolved. For particular patients, a mid-face elevation may be required to restore and rejuvenate the lower eyelid and lower cheek area

Medical complications are determined by factors such as:

Dry-eye syndrome: which can form by the disruption of the natural, can occur due to the tear film of the eye

Palpebral skin laxity: looseness of the lower eyelid

Eyeball prominence: the protrusion of the eyeball in relation to the cheek.

References

“2014 Plastic Surgery Statistics Report” (PDF). American Society of Plastic Surgeons. p. 12. Retrieved 31 March 2016.

Jump up^ Sedghi, Ami (3 February 2014). “UK cosmetic surgery statistics 2013: which are the most popular?”. The Guardian. Retrieved 31 March 2016.

Pan, Brian S. Blepharoplasty, Lower Lid Subciliary (2006). http://www.emedicine.com/plastic/topic4.htm

University Of Chicago Medicine University Of Chicago Medicine Physician Bios (1998). http://www.uchospitals.edu/physicians/anthony-geroulis.html

JDr.Geroulis, Anthony J. Eyelid Surgery Chicago Transconjunctival Techniques (1998). http://www.geroulis.com/cosmetic-procedures/facial-rejuvenation-plastic-surgery/lower-eyelid-surgery-eye-lift-blepharoplasty-chicago

Steven Dresner, Los Angeles Blepharoplasty and Eyelid Surgery Procedures, (2010) http://www.eyesthetica.com/blepharoplasty/

McCurdy JA (February 2005). “Upper blepharoplasty in the Asian patient: the ‘double eyelid’ operation”. Facial Plastic Surgery Clinics of North America. 13 (1): 47–64.

0 notes

medicinethought-blog · 8 years ago

Text

Cervical Cancer

Intro

Cervical Cancer

Cervical cancer is a cancer from the cervix. It is due to the abnormal growth of cells that have the ability to invade or spread to other parts of the body. Early no symptoms are seen. Later symptoms may include abnormal vaginal bleeding, pelvic pain, or pain during sexual intercourse.

Cervical cancer typically develops from precancerous changes over 10 to 20 years. About 90% of cervical cancer cases are squamous cell carcinomas, 10% are adenocarcinoma, and a small number are other types. Diagnosis is typically by cervical screening followed by a biopsy. Medical imaging is then done to determine whether or not the cancer has spread.

HPV vaccines protect against between two and seven high-risk strains of this family of viruses. Regular Pap smears are also used as a mechanism to detect cancer. Other methods of prevention include: having few or no sexual partners and the use of condoms. Cervical cancer screening using the Pap smear or acetic acid can identify precancerous changes which when treated can prevent the development of cancer. Treatment of cervical cancer may consist of some combination of surgery, chemotherapy, and radiotherapy.

Causes

HPV

Smoking

Oral contraceptives

Multiple Pregnancies

Stages

1A, 1B, 2A, 2B, 3B, 4A, 4B.

Treatment

Microinvasive cancer (stage 1A) may be treated by hysterectomy (removal of the whole uterus including part of the vagina). For stage 1A2, the lymph nodes are removed, as well. Alternatives include local surgical procedures such as a loop electrical excision procedure or cone biopsy. For 1A1 disease, a cone biopsy (cervical conization) is also used.

If a cone biopsy does not produce clear margins, one more possible treatment option for women who want to preserve their fertility is a trachelectomy. This attempts to remove the cancer while preserving the ovaries and uterus. It is a viable option for those in stage 1 cervical cancer which has not spread. Due to the possible risk of cancer spread to the lymph nodes in stage 1b cancers and some stage 1a cancers, the surgeon may also need to remove some lymph nodes from around the uterus for evaluation.

A radical trachelectomy can be performed abdominally or vaginally. A radical abdominal trachelectomy with lymphadenectomy complications are uncommon. Recurrence in the residual cervix is very rare if the cancer has been cleared with the trachelectomy.

Early stages (IB1 and IIA less than 4 cm) can be treated with radical hysterectomy with removal of the lymph nodes or radiation therapy. Radiation therapy is given as external beam radiotherapy to the pelvis and brachytherapy (internal radiation). Women treated with surgery who have high-risk features found on pathologic examination are given radiation therapy with or without chemotherapy to reduce the risk of relapse.

Larger early-stage tumors (1B2 and 2A) may be treated with radiation therapy and cisplatin-based chemotherapy, hysterectomy (which then usually requires adjuvant radiation therapy), or cisplatin chemotherapy followed by hysterectomy.

Advanced-stage tumors (2B-4A) are treated with radiation therapy and cisplatin-based chemotherapy. Hycamtin and cisplatin, for women with late-stage (4B) cervical cancer treatment. Combination treatment has significant risk of neutropenia, anemia, and thrombocytopenia side effects.

References

“Cervical Cancer Treatment (PDQ®)”. NCI. 2014-03-14. Retrieved 24 June 2014.

“Defining Cancer”. National Cancer Institute.

Tarney, CM; Han, J (2014). “Postcoital bleeding: a review on etiology, diagnosis, and management.”. Obstetrics and Gynecology International.

Kumar V, Abbas AK, Fausto N, Mitchell RN (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier.

Kufe, Donald (2009). Holland-Frei cancer medicine. (8th ed.). New York: McGraw-Hill Medical.

World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 5.12.

Dunne, EF; Park, IU (Dec 2013). “HPV and HPV-associated diseases.”. Infectious Disease Clinics of North America. 27 (4): 765–78.

“Cervical Cancer Treatment (PDQ®)”. National Cancer Institute. 2014-03-14.

“FDA approves Gardasil 9 for prevention of certain cancers caused by five additional types of HPV”. U.S. Food and Drug Administration. 10 December 2014.

“Human Papillomavirus (HPV) Vaccines”. National Cancer Institute. 2011-12-29.

Tran, NP; Hung, CF; Roden, R; Wu, TC (2014). “Control of HPV infection and related cancer through vaccination.”. Recent Results in Cancer Research. 193: 149–71.

“Cervical Cancer Prevention (PDQ®)”. National Cancer Institute. 2014-02-27.

World Health Organization (February 2014). “Fact sheet No. 297: Cancer”.

“SEER Stat Fact Sheets: Cervix Uteri Cancer”. NCI.

World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 1.1.

Baalbergen, Astrid; Veenstra, Yerney; Stalpers, Lukas; Baalbergen, Astrid (2013). “Primary surgery versus primary radiotherapy with or without chemotherapy for early adenocarcinoma of the uterine cervix”. Reviews.

Erstad, Shannon (2007-01-12). “Cone biopsy (conization) for abnormal cervical cell changes”.

Jones WB, Mercer GO, Lewis JL, Rubin SC, Hoskins WJ (1993). “Early invasive carcinoma of the cervix”. Gynecol. Oncol. 51 (1): 26–32.

Dolson, Laura (2001). “Trachelectomy”.

Burnett AF (2006). “Radical trachelectomy with laparoscopic lymphadenectomy: review of oncologic and obstetrical outcomes”. Curr. Opin. Obstet. Gynecol. 18 (1): 8–13.

Cibula D, Ungár L, Svárovský J, Zivný J, Freitag P (2005). “[Abdominal radical trachelectomy–technique and experience]”. Ceska Gynekol (in Czech). 70 (2): 117–22.

Plante M, Renaud MC, Hoskins IA, Roy M (2005). “Vaginal radical trachelectomy: a valuable fertility-preserving option in the management of early-stage cervical cancer. A series of 50 pregnancies and review of the literature”. Gynecol. Oncol. 98 (1): 3–10.

Roy M, Plante M, Renaud MC, Têtu B (1996). “Vaginal radical hysterectomy versus abdominal radical hysterectomy in the treatment of early-stage cervical cancer”. Gynecol. Oncol. 62 (3): 336–9.

Dargent D, Martin X, Sacchetoni A, Mathevet P (2000). “Laparoscopic vaginal radical trachelectomy: a treatment to preserve the fertility of cervical carcinoma patients”. Cancer. 88 (8): 1877–82.

Schlaerth JB, Spirtos NM, Schlaerth AC (2003). “Radical trachelectomy and pelvic lymphadenectomy with uterine preservation in the treatment of cervical cancer”. Am. J. Obstet. Gynecol. 188 (1): 29–34.

Waggoner, Steven E (2003). “Cervical Cancer”. The Lancet. 361 (9376):

“FDA Approves First Drug Treatment for Late-Stage Cervical Cancer”. U.S. Food and Drug Administration. 2006-06-15.

Sardain, H; Lavoue, V; Redpath, M; Bertheuil, N; Foucher, F; Levêque, J (August 2015). “Curative pelvic exenteration for recurrent cervical carcinoma in the era of concurrent chemotherapy and radiation therapy. A systematic review.”. European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology. 41 (8): 975–85.

1 note · View note

medicinethought-blog · 8 years ago

Text

Mesentery

Intro

I decided to do a piece on the Mesentery simply because its status has been upgraded to “organ” instead of just a collection of tissues, and I thought it would be interesting to research about it

Structure

The mesenteric organ is composed of: mesocolon, mesoappendix, mesosigmoid and mesorectum. The mesentery in the small intestine stems from the mesenteric root and is connected with the front of the backbone; The duodenojejunal flexure (border between duodenum and jejunum-which are parts of the small intestine). is located at the left side of the second lumbar vertebra (part of the backbone) to the right sacroiliac articulation (joint in the pelvis); The root of the mesentery extends from the duodenojejunal flexure to the ileocaecal junction (separation of large and small intestine).

This section of the small intestine is located in the abdominal cavity and lies behind the colon and the greater omentum (section of the stomach). The mesentery is attached to the colon and continues to become the mesenteric organ. The parts of the mesocolon take their names from the part of the colon to which they attach. These are the transverse mesocolon, the sigmoid mesocolon, the mesoappendix and the mesorectum (all attaching to their corresponding colon, rectum and appendix). The mesocolon is continuous from the ileocaecal to the rectosigmoid level. It was also shown that a mesenteric conﬂuence (portal vein) occurs at the ileocaecal and rectosigmoid junctions.

Significance

An increased understanding of the mesentery has lead to an increase in the diseases related to it. E.g. Crohn’s disease (CD). In CD, the mesentery is thickened, making haemostasis challenging. In addition, “fat wrapping” involves extension of mesenteric fat over the circumference of gastrointestinal tract, and this may indicate increased plasticity. The relationship between derangements and mucosal manifestations in CD points to an overlap; and may be primarily a mesenteric disorder but includes GIT.

Suggestions

There should be more research on the diseases related to the mesenteric organ and the effect these have on the body as a whole.

References

Coffey, J Calvin; O'Leary, D Peter (2016). “The mesentery: structure, function, and role in disease”. The Lancet Gastroenterology & Hepatology. 1 (3): 238–247.

Guarino, Ben (4 January 2017). “Meet the mesentery: Irish scientists say this gut membrane should be upgraded to an organ”. Washington Post. Retrieved 4 January 2017.

The human body may have a new organ—the mesentery (arstechnica.com, 4 January 2017)

Coffey JC (August 2013). “Surgical anatomy and anatomic surgery – Clinical and scientific mutualism”. The Surgeon. 11 (4): 177–82.

Coffey JC, Sehgal R, Culligan K, et al. (June 2014). “Terminology and nomenclature in colonic surgery: universal application of a rule-based approach derived from updates on mesenteric anatomy”. Techniques in Coloproctology. 18: 789–94.

Zheng, MH; Zhang, S; Feng, B (15 March 2016). “Complete mesocolic excision: Lessons from anatomy translating to better oncologic outcome.”. World journal of gastrointestinal oncology. 8 (3): 235–9.

Culligan K, Coffey JC, Kiran RP, Kalady M, Lavery IC, Remzi FH (April 2012). “The mesocolon: a prospective observational study”. Colorectal Disease. 14 (4): 421–8; discussion 428–30.

Sahebally SM, Burke JP, Chang KH, Kiernan MG, O'Connell PR, Coffey JC (November 2013). “Circulating fibrocytes and Crohn’s disease”. The British Journal of Surgery. 100 (12): 1549–56.

0 notes

medicinethought-blog · 8 years ago

Text

Andrology & Cryptorchidism

Intro

I thought it would be very interesting to do some research regarding the male, reproductive system as it is less spoken about than gynaecology but is also sometimes avoided because its the reproductive organs and people tend to talk about less “taboo” topics.

Andrology

Andrology is the study of the male reproductive system and also urological problems that are to do with the male reproductive system (such as testicular cancer), andrology is a relatively new concept and has been around since the 1960′s. Therefore there is an understandable difference between gynaecology and andrology due to the time it has been around.

Cryptorchidism

Cryptorchidism is a condition where by one or both testes are absent from the scrotum and is actually the most common birth defect in males. In very rare cases this can also occur after infancy and even young adult hood.

The testicle may be located in a number of different areas such as: The inguinal canal (which is located on the right side around the crotch lymph nodes), moved to the upper thigh, opposite scrotum, femoral canal (opposite side to inguinal canal), undeveloped or may even be described as “missing” (anorchia).

Most of the time the testicle will move back by itself, but a process called orchiopexy is used to surgically move the testicle into the scrotum, these testicles are usually more prone to cancer and testicular torsion (which is when the spermatic chord twists and cuts off blood supply to the testicle). However testicles are retractile therefore can move back up and down the inguinal canal.

Causes

Most of the time there is no known cause with cryptorchidism therefore is called an idiopathic birth defect meaning it is spontaneous-however, there are some things that can be linked with this birth defect: Endocrine disruptors (hormone disruptors) that interfere with normal foetal hormone balance; exposure to regular alcohol consumption during pregnancy; cigarette smoking is also a known risk factor; occurs at a much higher rate in babies with congenital malformation syndromes (birth defects) such as Down syndrome, Noonan syndrome; if the mother has diabetes or is obese and the use of IVF has also been seen to play a part in cryptorchidism.

Cancer

without orchiopexy the chance of testicular cancer is greatly increased, even without the surgery the chance of having testicular cancer is still relatively high which the most common type of testicular cancer being seminoma. Seminoma is a type of germ cell tumour (a tumour of the cells that produce gametes), which is mainly based within the testicle. If the origination was in the testicle the germ cell tumour is located in the germinal epithelium of the seminiferous tubes.

This tumour is not always malignant but can also be benign and if malignant patients have a >95% survival rate, by the removal of a testicle-however, this doesn’t effect the males fertility.

Treatment

Orchiopexy is usually the main surgical procedure to move the testicles back to the scrotum. If the testicle is within the inguinal canal sometimes hormone therapy is used, the most common being HCG (human chorionic gonadotropin), and is a hormone present from the placenta after implantation and is used to detect pregnancy in some antibody pregnancy tests.

It is given in the form of injections over a 5 week period, but the success rate varies from 5% to 50%, However it does have some benefits such as allowing confirmation of Leydig cell (adjacent to seminiferous tubules and produce testosterone) responsiveness shown by a rise in testosterone or inducing additional growth of a small penis.

A lot of the time HCG hormone therapy is used in partnership with a gonadotropin-releasing hormone analogue (GnRH analog), a GnRH analogue is designed to interact with the GnRH receptor and modify the release of pituitary gonadotropins (glycoprotein polypeptide hormones such as FSH and LH). An example of an GnRH analog would be nafarelin, this procedure has been able to increase the likely hood of bringing down undescended testicles into the scrotum.

Suggestions

More research into the cause of Cryptorchidism.

More research into the treatment excluding surgery.

Research into 3 hormonal procedure as treatment.

Research into a procedure thats stops retractile nature of undescended testicles.

Endocrine enhancers to counteract the endocrine disruption before birth

Chemotherapy vs Surgery effectiveness on seminoma

References

Social Studies of Science (1990) 20, p. 32

“Testicular cancer”. Medline Plus

“Seminoma” at Dorland’s Medical Dictionary

Stacey E. Mills (2009). Sternberg’s Diagnostic Surgical Pathology. LWW

Wood, HM; Elder, JS (February 2009). “Cryptorchidism and testicular cancer: separating fact from fiction.”. The Journal of Urology: 452–61.

Tamparo, Carol. Diseases of the Human Body (Fifth ed.). Philadelphia, PA. p. 125.

The A.D.A.M. Medical Encyclopedia

Dähnert, Wolfgang (2011). Radiology Review Manual. 995.

Pettersson, Andreas; Lorenzo Richiardi; Agneta Nordenskjold; Magnus Kaijser; Olof Akre (May 3, 2007). “Age at Surgery for Undescended Testis and Risk of Testicular Cancer”. NEJM.: 1835–41.

Brouwers, Marijn M.; de Bruijne, Leonie M.; de Gier, Robert P.E.; Zielhuis, Gerhard A.; Feitz, Wouter F.J.; Roeleveld, Nel (2012). “Risk factors for undescended testis”. Journal of Pediatric Urology. : 59–66.

Gregory JJ, Finlay JL (April 1999). “Alpha-fetoprotein and beta-human chorionic gonadotropin: their clinical significance as tumour markers”. Drugs. 57 (4): 463–7

Parhar, Ishwar S. (2002). Gonadotropin-releasing Hormone: Molecules and Receptors. Amsterdam: Elsevier

0 notes

medicinethought-blog · 8 years ago

Text

PET & F-18

Intro

During my GCSE physics course I became interested particle physics and I became highly interested in medical physics-which is initially a reason why I got interested in medicine in the first place, I thought it was amazing to be able to explain to my family what medicinal procedures they were having done.

PET Scanners

Positron emission tomography (PET) is a form of imaging that observes the metabolic activity of cells within the body. It does this by injecting an isotope (such as F-18) that emits positrons but also is able to be metabolised by cells. Cancer (wether it is malignant or benign) is caused by a mutation in your DNA from external sources 90-95% (UV, diet) or hereditary 5%, if the mutation was to occur during interphase or mitosis at the metaphase it will be extracted at G0-However, if the original DNA is mutated and copied and this is then continuously copied and the cells obtain their own blood supply it therefore needs to metabolise chemicals and isotopes such as F-18 so it is able to divide further. Isotopes like F-18 are used, as positrons (beta positive decay) produce gamma rays when colliding with electrons-which are used in imaging.

FDG-PET

PET scanning with the tracer fluorodeoxyglucose (FDG), called FDG-PET, and is used in oncology it is injected into the patient as a liquid, or used in a gas or crystal form and the isotope used in FDG (F-18) can be created within a cyclotron.

Cyclotron production of F-18 may be accomplished by collision of Ne-20 with A heavy isotope of Hydrogen H-2, this isotope is sometimes deuterium and the particles are called deuterons, but usually is done by proton bombardment of O18-enriched water, causing a proton + neutron reaction in the water. This produces dissolved F18-fluoride (18-F minus) ions in the water.

This tracer is a positron emitter as it is unstable due to a proton rich nucleus it has able to undergo beta positive decay, therefore, releasing positrons (positive electrons) and an electron neutrino. The tracer also has glucose, and is therefore metabolised by cells and also phosphorylated (adding a phosphate group) by an enzyme called hexokinase. Because the O-18 atom is replaced by F-18 to generate FDG is required for the next step in glucose metabolism in all cells, it means that FDG is no longer metabolised by the cells. Furthermore, most tissues cannot remove the phosphate added by hexokinase.

This means that FDG is trapped in any cell that takes it up until it decays (as ionic phosphorylated sugars cannot exit the cell), during decay it expels positrons and therefore gamma rays (100 minutes is the approx half life of F-18). This results in intense labelling of tissues with high glucose uptake, such cancer cells. As cancer cells have higher metabolism than normal cells due to the constant division-the uptake is extremely high-therefore, are highly metabolically active and on a PET are bright red, the redness is due to the concentration of gamma rays which correlates to to the number of electrons which is proportional to the constant division of these cells. This intense labelling is due to the production of gamma rays which are detected due to the collision between electrons and positrons. The collisions occur between positrons and electrons at opposite directions, opposite momentums, a conserved mass and opposite velocity and due to the law of conservation it means that the product will also have to have these attributes. Therefore, 2 gamma rays are produced with the same mass, opposite velocities and momentum resulting in a spot which is blue/yellow/red depending on metabolism.

FDG-PET can be used for diagnosis, staging, and monitoring treatment of cancers and are useful as a 3D image is produced, this 3D image is detected usually by a method of triangulation which maps 3 gamma rays and then determines the location of these

Recommendations/Research

C-13 as better substitute in glucose labelling rather than F-18

Prolongation and Modification of the half life of isotopes for PET scanners and in general

Smaller subatomic particles in the collision and production of particles increasing detail

Differences in O-18 and Ne-20 procedures and the effect they have on F-18

Research into mechanisms of instant de-phosphorylation or hydrolysis

Larger range of qualitative and quantitative range of metabolic activity

Other enzymes as a phosphorylation mechanism that is reversible

References

O'Leary, Dan (2012). “The deeds to deuterium”. Nature Chemistry. 4: 236

Bailey, D.L; D.W. Townsend; P.E. Valk; M.N. Maisey (2005). Positron Emission Tomography: Basic Sciences. Secaucus, NJ: Springer-Verlag

Carlson, Neil (January 22, 2012). Physiology of Behavior. Methods and Strategies of Research. 11th edition. Pearson. p. 151.

Khan TS; Sundin A; Juhlin C; Långström B; et al. (2003). “11C-metomidate PET imaging of adrenocortical cancer”. European Journal of Nuclear Medicine and Molecular Imaging. 30 (3): 403–410

Minn H; Salonen A; Friberg J; Roivainen A; et al. (June 2004). “Imaging of adrenal incidentalomas with PET using (11)C-metomidate and (18)F-FDG”. J. Nucl. Med. 45 (6): 972–9

“Cancer Fact sheet N°297”. World Health Organization. February 2014

Josef Pacák, Zdeněk Točík, Miloslav Černý: “Synthesis of 2-Deoxy-2-fluoro-D-glucose”; Journal of the Chemical Society D: Chemical Communication, 1969, p. 77–77

Newberg A, Alavi A, Reivich M (2002). “Determination of regional cerebral function with FDG-PET imaging in neuropsychiatric disorders”. Semin Nucl Med. 32 (1): 13–14

Som P, Atkins HL, Bandoypadhyay D, Fowler JS, MacGregor RR, Matsui K, Oster ZH, Sacker DF, Shiue CY, Turner H, Wan CN, Wolf AP, Zabinski SV (1980). “A fluorinated glucose analog, 2-fluoro-2-deoxy-D-glucose (F-18): Nontoxic tracer for rapid tumor detection”. J Nucl Med. 21 (7): 670–675

0 notes

medicinethought-blog · 8 years ago

Text

Cardiology (Circulation & Myopathy)

Intro

The heart is such an incredibly intricate muscular organ with so many different complexities and now more than ever it is becoming even more researched simply due to MEDC’s continually increasing year upon year the death toll of heart related illnesses.

Coronary Circulation

Heart tissues continually needs to be supplied with oxygen (via the reversible interaction between oxygen and haemoglobin) to get rid of metabolic wastes such as Carbon Dioxide. As even though the heart pumps blood around the body-for the heart to function it self it still must have a source of oxidative measure to get rid of waste products otherwise will simply become inefficient. The circulation includes arteries, veins, and lymphatic vessels, Blood flow through the coronary vessels occurs relative to the hearts contraction and relaxation (seen on an ECG).

The heart tissue receives blood from two arteries which are located just above the aortic valve (the aortic valve is between the left ventricle and the aorta). These are known as the left main coronary artery and the right coronary artery respectively. The left main coronary artery splits after leaving the aorta into two vessels, the left anterior descending and the left circumflex artery. The left anterior descending artery supplies blood to the heart tissue at the front, outer sides, and the ventricular septal defect (a septum at which connects the right and left ventricles together). It does this by branching into smaller arteries-diagonal and septal branches. The left circumflex supplies blood to the back and underneath of the left ventricle. The right coronary artery supplies blood to the right atrium, right ventricle, and lower hind sections of the left ventricle.

The right coronary artery also supplies blood to the (AV) atrioventricular node (which is located inside the right atrium however has a very good blood supply to the outer surface of the heart tissue) and the (SA) sinoatrial node (which is located deeper inside the right atrium and is more central than the AV node however, still has a good blood supply). The right coronary artery runs in a heart indentation at the back of the heart and the left anterior descending artery runs in an indentation at the front of the heart. The coronary sinus is also a large aspect of blood flow and is a large vein that drains blood into the right atrium, and receives most of the drainage from veins of the heart. It receives blood from the great cardiac vein, the posterior cardiac vein, the middle cardiac vein, and small cardiac veins.

(Takosubo) Cardiomyopathy

Cardiomyopathy is a group of diseases that affect heart muscle. Cardiomyopathy is a significant deterioration of the heart muscle’s ability to contract-this deterioration can be examined and it extremely noticeable. Cardiomyopathy can lead to heart failure. Dilated Cardiomyopathy is inadequately understood and researched but some causes include alcohol, toxins, sarcoidosis (small patches of red and swollen tissues called granulomas which develop on organs), HOCM (and other congenital disorders) and in restrictive cardiomyopathy even some cancer treatments. Dilated and hypertrophic can also both be inherited from parents.

Types of cardiomyopathy: Hypertrophic cardiomyopathy (when the heart muscles are enlarged); restrictive cardiomyopathy (constrict the outflow tracts of the heart); dilated cardiomyopathy (causing the heart to dilate and impact the efficiency of its beating); Broken heart syndrome (Takosubo cardiomyopathy) which is caused by extreme emotional and physical stress and causes the muscles to weaken over a short or long period of time. A physical stress which might cause takosubo cardiomyopathy are transient vasospasms (many simultaneous spasms of coronary arteries could cause enough loss of blood flow to cause transient stunning of the myocardium)-these can happen over a long period of time to weaken the heart muscles to form it into this type of cardiomyopathy. However, a vasospasm could be caused by emotional stress or failure of the microvasculature (smaller blood vessels in body, responsible for microcirculation), and an abnormal response to catecholamines (chemicals that are made by nerve tissue such as epinephrine and norepinephrine, released in response to stress).

Treatment recommendations include intra-aortic balloon pump, an IABP is is a mechanical device that increases myocardial (cardiac muscle) oxygen delivery while at the same time increasing cardiac output. Increasing cardiac output increases blood flow and therefore oxygen delivery. It consists of a cylindrical polyethylene balloon that sits in the aorta, next to the left subclavian artery (major artery in the upper thorax) and counter pulsates. That is, it actively deflates when the ventricles contract (systole), increasing forward blood flow by reducing after load through an effect which is similar to a vacuum. It actively inflates as the muscle relaxes (diastole), increasing blood flow to the coronary arteries.

Recommendations

Carbon Nanotubes as a progressive alternative due to its altering structure, instead of using intra-aortic balloons

Research into anti-inflamatory drugs on people with cardiomyopathy

Research into cognitive behavioural therapy on cardiomyopathy

Beta-blockers/pacemaker to try and eradicate an irregular heart beat

Edoxaban as a anti-blood clotting technique to improve cardiomyopathy.

References

Intra-aortic balloon pumping Department of Anaesthesia and Intensive Care of The Chinese University of Hong Kong

Intra Aortic Balloon Pump (IABP) Counterpulsation mirror with better quality by P. J Overwalder, M.D., Department of Surgery, Division of Cardiac Surgery, University Hospital Graz, The Internet Journal of Thoracic and Cardiovascular Surgery. 1999. Volume 2 Number 2.

Intensive Care Medicine by Irwin and Rippe

“Intra-aortic Balloon Pump”. Texas Heart Institute.

Zamir, M (2005). The Physics of Coronary Blood Flow. Springer Science and Business Media. p. 387.

“Mayo Clinic Research Reveals ‘Broken Heart Syndrome’ Recurs In 1 Of 10 Patients”. Medical News Today, MediLexicon International Ltd.

Akashi YJ, Nef HM, Möllmann H, Ueyama T (2010). “Stress cardiomyopathy”. Annu. Rev. Med.

Kurisu S, Sato H, Kawagoe T, et al. (2002). “Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction”. American Heart Journal.

Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I (July 2001). “Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan”. Journal of the American College of Cardiology.

Kawai et al. JPJ 2000

Desmet, WJ; Adriaenssens, BF; Dens, JA (September 2003). “Apical ballooning of the left ventricle: first series in white patients”. Heart (British Cardiac Society).

Abe, Y; Kondo, M; Matsuoka, R; Araki, M; Dohyama, K; Tanio, H (2003-03-05). “Assessment of clinical features in transient left ventricular apical ballooning”. Journal of the American College of Cardiology.

“What Is Sudden Cardiac Arrest?”. NHLBI. 22 June 2016. Retrieved 16 August 2016.

“What Are the Signs and Symptoms of Cardiomyopathy?”. NHLBI. 22 June 2016. Retrieved 31 August 2016.

“Who Is at Risk for Cardiomyopathy?”. NHLBI. 22 June 2016. Retrieved 31 August 2016.

“Types of Cardiomyopathy”. NHLBI. 22 June 2016. Retrieved 31 August 2016

“What Causes Cardiomyopathy?”. NHLBI. 22 June 2016. Retrieved 31 August 2016.

“How Is Cardiomyopathy Treated?”. NHLBI. 22 June 2016. Retrieved 31 August 2016.

Betts, J. Gordon (2013). Anatomy & physiology. pp. 787–846. ISBN 1-938168-13-5. Retrieved 11 August 2014.

Davidson’s 2010, p. 525.

Gray’s Anatomy 2008, p. 981.

0 notes

medicinethought-blog · 8 years ago

Text

Dermatology (Acne Scarring & Treatment)

Intro

For a long time now I have been extremely interested in the world of dermatology and knew a relatively fair bit about skin and specifically medical advances with skin (Benzoyl Peroxide, Salicylic acid, Glycolic acid.. The list honestly goes on). My own problems with acne created this love for dermatology and the love I have for organic chemistry ties very well in with skin and its treatment.

Scarring

Scarring is large factor of having Acne and the scarring comes in 3 forms, there is also a very strong misconception between actual scarring and PIH (Post Inflammatory Hyper-pigmentation), PIH is a form of hyper pigmentation and is caused by inflammation (fundamentally the starting points for all these scars is in fact inflammation)-however, the inflammation which is involved in PIH doesn’t lead to a reduction or an increase in collagen production. PIH simply leaves behind a red mark. Collagen variation (which is from the abnormal healing process) is the source of what actually leads to different scarring-an increase in collagen production after this initial inflammation and abnormal healing leads to hypertrophic (raised scar) scarring a decrease in collagen production after the abnormal healing actually leads to atrophic (indented scar) scarring-these two types of scarring will stay within the areas at which the damage to the skin was done. (E.g. if a burn was 5 centimetres squared, the scar would stay bound to this region).

However, Keloid Scars are much different and will not stay bound to the specific area at which the damage to the skin was done-but will in fact “grow”, there is in fact an overgrowth of collagen which causes this. There are many ways that these can be reduced which I shall discuss in greater detail later.

Scarring Treatments

Glycolic Acid (2-Hydroxyethanoic acid)

Glycolic acid is part of the alpha-hydroxy acid family and is the smallest compound within it-glycolic acid is arguably the most effective alpha-hydroxy acid at diminishing scars and PIH as it is able to very successfully penetrate layers of the skin. Glycolic acid is extremely useful as a compound as it can help the appearance of PIH and also: Hypertrophic, Keloid and Atrophic scarring.

Glycolic acid can successfully achieve this as it able to stimulate collagen production (which is a benefit to atrophic and PIH but may be a danger to Hypertrophic and Keloid scarring); keratolyse the epidermis (peeling effect)-the keratolysis is able to weaken the bonds between the lipids in the epidermis which hold the dead skin cells together which exfoliates the stratum corneum. Over time this will reduce the appearance of scarring however, skin will be very volatile to UV rays which increases the chance of skin cancer. And if care is not taken can cause minor burns (Which are not nice! I’ve experienced them myself).

For the price these will be relatively successful on PIH and also atrophic scarring due to the peeling mechanism will decrease the indentation of the scars-however, the effect on very raised scars such as keloid will be relatively minimal due to the fact the collagen production is so extreme.

Carbon Dioxide Laser

Carbon Dioxide lasers have many uses and at first glance wouldn’t be thought of as something which could reduce the appearance of scarring. It works by essentially resurfacing the skin by vaporising skin to promote collagen production and as water is able to absorb specific frequencies of light extremely well it allows this to become a very effective process at eradicating scars. It eradicates scars more specifically by absorbing the beam which causes heat damage to cells therefore destroying them.

A beam can either be focused or defocused, if the beam is focused it is able to cut and seal bleeding vessels. However, if the beam is defocused it acts as a scattering effect which causes the vaporisation (more widely used in the treatment of scars). Keloid scars specifically will work very well with this treatment due to the excessive nodule like scars above skin it can destroy them relatively easily. For the price, it may not be worth using carbon dioxide laser surgery on PIH or atrophic scarring as it is usually better for an excess of collagen; therefore is better for hypertrophic and keloid.

Suggestions for Advancements (Treatment and Studies etc)

The effect of Glycolic acid as a collagen stimulator on Hypertrophic and Keloid Scarring.

The comparisons between alpha, beta and gamma hydroxy acids and their relation to scarring.

Carry out independent research on the true effect of “Bio-oil” on scars (as the research carried out has been within the company itself so may be bias).

More research on the validity of Vitamin E on the effect of PIH as an affordable option

Research of the oxidative effects on scarring (Oxygen Laser-in the destruction of free radicals?).

Research into the mixture of Lavender, Helichrysum, Neroli, Rosehip, Niaouli, Rosemary, Cistus and Frankincense are cicatrisant as essential oils that may offer a better alternative to increasing the appearance of scars.

Research into Vasoconstrictors and their role within acne

References

https://www.guysandstthomas.nhs.uk/resources/patient-information/dermatology/carbon-dioxide-laser-treatment.pdf

Levy, L.L.; Zeichner, J.A. (October 2012). “Management of acne scarring, part II: a comparative review of non-laser-based, minimally invasive approaches”. American Journal of Clinical Dermatology(Review). 13 (5): 331–40.

Sobanko, J.F.; Alster, T.S. (October 2012). “Management of acne scarring, part I: a comparative review of laser surgical approaches”. American Journal of Clinical Dermatology (Review). 13 (5): 319–30.

Yin, NC; McMichael, AJ (February 2014). “Acne in patients with skin of color: practical management”. American Journal of Clinical Dermatology (Review). 15 (1): 7–16

Callender, V.D.; St. Surin-Lord, S.; Davis, E.C.; Maclin, M. (April 2011). “Postinflammatory hyperpigmentation: etiologic and therapeutic considerations”. American Journal of Clinical Dermatology (Review). 12 (2): 87–99.

United States National Library of Medicine “Hydroxyacetic Acid” in TOXNET Hazardous Substances Data Bank (HSDB), citing Gerhartz, W. (exec ed.), Ullmann’s Encyclopedia of Industrial Chemistry. 5th ed.Vol A1: Deerfield Beach, FL: VCH Publishers, 1985 to Present., p. VA13 509.

Barton, Fritz (2014). “Skin Resurfacing”. In Charles Thorne. Grabb and Smith’s Plastic Surgery (7 ed.). Philadelphia: Lippincott Williams & Wilkins. p. 455.

Benninger, Michael S. (2000). “Microdissection or Microspot CO2 Laser for Limited Vocal Fold Benign Lesions: A Prospective Randomized Trial”. The Laryngoscope. 110(S92): 1–1.

0 notes