EFFECT OF SUGAR ON INFLAMMATION

Inflammation is a response triggered by damage to living tissues (Encyclopedia Britannica, Inc, 2014), the inflammatory response is a defense mechanism that evolved in higher organisms to protect them from infection and injury.

The injury can be cause by chemical agents, physical forces, living microbes or many other physiologic or pathologic stimuli that disturb the normal steady state as defined by Damjanov (2012), who insists that inflammation occurs only in multicellular organisms that are capable of mountaing a neurovascular and cellular response to injury.

Recent research suggests tha inflammation inside the body plays a role in the development of Type 2 Diabetes. In this condition, the body can’t produce enough insuline or the bodies can’t use the insuline adequately due of insuline resistence (Tierney, McPhee, & Papadakis, 2005).

In a normal condition, when the blood sugar rise rapidly, after some food, the pancreas secretes insulin whose primary purpose is to drive sugar into each cells where it is stored for energy. If the cells is full, it is rejected, them blood sugar rise again producing more insuline and the glucose converts to stored fat, as Dr Lundell (2012) explain, the extra sugar molecules attach to a variety of proteins that in turn injure the blood vassels wall and set off the inflammation.

In the other hand, inflammation is induced by chemical mediator produced by damage host cells, such as Cytokines (Beck, 2014) and others, the bolus of blood sugar that accompanies a meals or snack of highly refined carbohydrates like bread, white rice, French fries, sugar laden soda, increases levels of this inflammatory messenger (President & Fellows of Harvard College, 2007). Researchers discovered that in people with type 2 diabetes, cytokine levels are elevated inside fat tissue, causing low levels of abnormal inflammation that alter the action of insulin and contribute to development of the disease (Nazario, 2012) the body becomes less sensitive to insulin and the resulting insulin resistance also leads to inflammation. A vicious cycle can result, with more inflammation causing more insulin resistance and vice versa.

Spranger, et al.(2002) evaluated the effects of various inflamatory cytokines on the risk of type 2 diabetes and they concluded supporting the concept that subclinical activation of the immune system is involved in the pathogenesis of type 2 diabetes, demonstrating in their study that a specific pattern of cytokines was associated with an increased risk of type 2 diabetes, rather than isolated elevation of the respective cytokines.

Finally, although there is no clearly in the pathogenic mechanism, several studies demonstrating the association between elevated blood sugar levels, inflammation and diabetes mellitus, we are only in the beginning to understand the role of this form of internal inflammation may play in the development of chronic diseases like diabetes and vice versa.

Bibliography

Beck, S. (2014, 11 10). hopkinsmedicine.org. Retrieved from Acute and Chronic inflamation: https://www.google.com/?gws_rd=ssl#q=sarah+beck+acute+inflammation

Danjanov, I. (2012). Pathologic fro the Health Professions. ELSEVIER.

Encyclopedia Britannica, Inc. (2014, April 11). www.britannica.com. Retrieved from Encyclopaedia Britannica: http://www.britannica.com/EBchecked/topic/287677/inflammation

Lundell, D. (2012, Mar 1). www.sott.net. Retrieved from Heart Surgeon speaks out on what really causes heart disease: http://www.sott.net/article/242516

Nazario, B. (2012, Aug 10). www.wedMD.com. Retrieved from http://www.wedmd.com/diabetes/guides/inflammation

President & Fellows of Harvard College. (2007, february). www.health.harvard.edu. Retrieved from The Harvard Medical School: http://www.health.harvard.edu/fhg/updates/What-you-eat-can-fuel-or-cool-inflammation-a-key-driver-of-heart-disease-diabetes-and-other-chronic-conditions.shtml

Spranger, J., Kroke, A., Mohlig, M., Hoffmann, K., Bergmann, M., Ristow, M., . . . Pfeiffer, A. (2002, Jul 26). www.diabetes.diabetesjournals.org. Retrieved from American Diabetes Association: http://diabetes.diabetesjournals.org/content/52/3/812.long

Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2005). CURRENT Medical Diagnosis & Treatment. McGraw Hill.

 

 

HEART SURGEON SPEAKS OUT ON WHAT REALLY CAUSES HEART DISEASE

Dr Dwight Lundell said, “I freely admit to being wrong…..today is my day to right the wrong with medical and scientific fact….insisted heart diseased resulted from the simple fact of elevated blood cholesterol….the only accepted therapy was prescribing medications to lower cholesterol and diet that severely restricted fat intake….It is not working”.

I think this is a statement with a dramatic picturesque approach, before at all, cardiovascular disease can refer to differents heart or blood vessel problems, the term is often used to mean damage to your heart or blood vessels by atherosclerosis, a buildup of fatty plaques in your arteries, it buildup thickens and stiffens artery walls, which can inhibit blood flow through your arteries to your organs and tissues (Mayo Clinic Foundation, 2014).

Atherosclerosis is the most common cause of cardiovascular disease, but it can be caused by others correctable problems such as unhealthy diet, sedentary, obesity and smoking. Hyperlipidemia, included the high blood cholesterol, constitutes one of the most important risk factors for atherosclerosis (Damjanov, 2012) and cardiovascular diseases.

The discovery a few years ago that inflammation as concept, in the artery wall is the real cause of heart disease like Dr Lundell mentions,  is really true, but a long time ago, the medical community in spite of an incompletely understood the interaction between the critical cellular elements in the atherosclerotic lesion, postulated theories related to atherosclerosis and cells injury, for example Rokitansky in 1851, suggested that atherosclerosis begins in the intima with deposition of thrombus and its subsequent organization by the infiltration of fibroblasts and secondary lipid deposition, few years later in 1856, Virchow proposed that atherosclerosis start with lipid transudation into the arterial wall and its interaction with cellular and extracellular elements, causing intimal proliferation (Boudi, 2014). In the 1990s, Ross and Fuster postulated that vascular injury starts the atherosclerotic process. (Ross, Fuster, & Topol, 1996).

The above explained that we were not wrong, but we were finding explanations based on studies and investigations that were conducted.

Finally, with the knowledge that we have today, the concept a little clearer about the inflammation and potential precursors, I agree with Dr Lundell, what we can do is choose whole foods that our grandmother served and not the manufactured foods that we found in the grocery today, because eliminating inflammatory foods and adding essential nutrients from fresh unprocessed food, we can reverse the damage in our arteries.

Bibliography

Boudi, F. B. (2014, May 12). www.emedicine.medscape.com. Retrieved from Coronary Artery Atherosclerosis: http://emedicine.medscape.com/article/153647-overview#aw2aab6b2b

Damjanov, I. (2012). Pathology for the Health Professions. ELSEVIER.

Mayo Clinic Foundation. (2014, Jul 29). www.mayoclinic.org. Retrieved from Heart Disease: http://www.mayoclinic.org/diseases-conditions/heart-disease/basics/causes/con-20034056

Ross, R., Fuster, V., & Topol, E. (1996). Atherosclerosis and Coronary Artery Disease. Philadelphia, PA: Lippincott-Raven.

 

 

Gorlin Sign

retrieve from:http://www.epocrates.com/e/docalertquiz/07_11?CID=EPULSE201410&et_cid=23532502&et_rid=6318891

CARDIAC ULTRASOUND

 

 

 

 

 

RECEPTORS-NERVOUS SYSTEM-ACCION

	Receptor	Major Functions
Sympathetic	α 1	↑ vascular smooth muscle contraction, ↑ pupillary dilator muscle contraction (mydriasis)
	α 2	↓ sympathetic outflow, ↓ insulin release
	β 1	↑ heart rate, ↑ contractibility, ↑ renin release, ↑ lipolysis
	β 2	Vasodilatation, bronchodilatation, ↑ heart rate, ↑ contractibility, ↑ lipolysis, ↑ glucagon release, ↓ uterine tone
Para-sympathetic	M 1 M 2 M 3	CNS, enteric nervous system ↓ heart rate and contractibility of atria ↑ exocrine gland secretions, ↑ gut peristalsis, ↑ bladder contraction, bronchoconstriction, ↑ pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation)
Dopamine	D 1	Relaxes renal vascular smooth muscle
	D 2	Modulates transmitter release, especially in brain
Histamine	H1	↑ nasal and bronchial mucus production, contraction of bronchioles, pruritus and pain
	H 2	↑ gastric acid secretion
Vasopressin	V 1	↑ vascular smooth muscle contraction
	V 2	↑ H2O permeability and reabsorption in the collecting tubules of the kidney

Bibliography

Le, T., Bhushan, V., & Grimm, L. (2009). First AID for the USMLE STEP 1. USA: McGraw Hill.

 

NORMAL PRESSURES OF THE CARDIAC CHAMBERS

retrieved from:

Le, T., Bhushan, V., & Grimm, L. (2009). First AID for the USMLE STEP 1. USA: McGraw Hill.

 

AUSCULTATION OF THE HEART

retrieved from:

Le, T., Bhushan, V., & Grimm, L. (2009). First AID for the USMLE STEP 1. USA: McGraw Hill.

 

CORONARY ARTERY ANATOMY

MEDICAL FACTS

“FAT, FEMALE, FORTY,AND FERTILE”	ACUTE CHOLECYSTITIS
FATTY LIVER	ALCOHOLISM
FERRUGINOUS BODIES	ASBESTOSIS
GARDNER’S SYNDROME	COLON POLYPS WITH OSTEOMAS AND SOFT TISSUE TUMORS
GAUCHER’S DISEASE	GLUCOCEREBROSIDASE DEFICIENCY
GHON FOCUS	1 ͦ TB
GILBERT’S SYNDROME	BENIGN CONGENITAL UNCONJUGATED HYPERBILIRUBINEMIA
GLANZMANN’S THROMBASTHEMIA	DEFECT IN PLATELET AGGREGATION
GOODPASTURE’S SYNDROME	AUTOANTIBODIES AGAINST ALVEOLAR AND GLOMERULAR BASEMENT MEMBRANE PROTEINS
GOWERS’ MANEUVER	DUCHENNE’S (USE OF PATIENT’S ARM TO HELP LEGS PICK SELF OFF THE FLOOR)
GUILLAIN-BARRE SYNDROME	IDIOPATHIC POLYNEURITIS
“HAIR-ON-END” (CREW-CUT) APPEARANCE ON X-RAY	β THALASSEMIA, SICKLE CELL ANEMIA (EXTRAMEDULLARY HEMATOPOIESIS)
HAND-SCHϋLLER-CHRISTIAN DISEASE	CHRONIC PROGRESSIVE HISTIOCYTOSIS
HbF	THALASSEMIA MAJOR
HbS	SICKLE CELL ANEMIA
hCG elevated	CHORIOCARCINOMA, HYDATIDIFORM MOLE (OCCUR WITH AND WITHOUT EMBRYO)
HEBERDEN’S NODES	OSTEOARTHRITIS (DIP SWELLING 2   ͦ TO OSTEOPHYTES)
HEINZ BODIES	G6PD DEFICIENCY
HENOCH-SCHӦNLEIN PURPURA	HYPERSENSITIVITY VASCULITIS ASSOCIATED WITH HEMORRHAGIC URTICARIA AND URIs
HETEROPHIL ANTIBODIES	INFECTIOUS MONONUCLEOSIS (EBV)
HIGH OUTPUT CARDIAC FAILURE (DILATED CARDIOMYOPATHY)	WET BERIBERI (THIAMINE, VITAMIN B1 EFICIENCY)

Bibliography

Le, T., Bhushan, V., & Grimm, L. (2009). First AID for the USMLE STEP 1. USA: McGraw Hill.

 

SCREENING FOR ABDOMINAL AORTIC ANEURYSM:U.S PREVENTIVE SERVICES TASK FORCE RECOMMENDATION STATEMENT

 

 

 

 

 

 

Recommendation:

Ø The USPSTF recommends 1-time screening for Abdominal Aortic Aneurysm (AAA) with ultrasonography in men aged 65 to 75 years who have ever smoked (B recommendation)

Ø The USPSTF recommends that clinicians selectively offers screening for AAA in men aged 65 to 75 years who have never smoked (C recommendation)

Ø The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for AAA in women aged 65 to 75 years who have ever smoked (I statement)

Ø The USPSTF recommends against routine screening for AAA in women who have never smoked (D recommendation)

Risk factor for AAA include older age, a positive smoking history, having a first-degree relative with an AAA; and having history of other vascular aneurysms, coronary artery disease, cerebrovascular disease, atherosclerosis, hypercholesterolemia, obesity, or hypertension.

Factor associated with a reduced risk for AAA include African American race, Hispanic ethnicity, and diabetes.

Abdominal duplex ultrasonography is the standard approach for AAA screening. Screening with ultrasonography is noninvasive and easy to perform and has high sensitivity (94 % t0 100%) and specificity (98 % to 100 %) for detection.

Patient with large AAA (> or = 5.5 cm) are referred for open surgical repair or endovascular aneurysm repair. Patient with smaller aneurysm (3.0 to 5.4 cm) are generally managed conservatively via surveillance (repeated ultrasonography every 3 to 12 mo).

Early open surgery for the treatment of smaller AAAs does not reduce AAA-specific or all-cause mortality. Surgical referral of smaller AAAs is typically reserved for rapid growth (>1.0 cm per year) or once the threshold of > 5.5 cm on repeated ultrasonography is reached.

Short-term treatment with antibiotics or B-blockers does not seem to reduce AAA growth.

Bibliography

LeFevre, M. L. (2014, Aug 18). Screening for Abdominal Aortic Aneurism: U.S. Preventive Services Task Force Recommendation Statement. Ann of Int Med, ;161(4):281-291. Retrieved from Annals of Internal Medicine: http://annals.org

 

 

 

 

FLESH-EATING BACTERIA: VIBRIO VULNIFICUS & NECROTIZING FASCIITIS

Recently we have been hearing news about the “flesh eating bacteria”, creating a panic in our community. While the existence of this bacterium is real, it would be important to know more details about the bacteria that are affecting the Florida coastal area of the Gulf of Mexico and the bacteria commonly known as "flesh-eating bacteria" which produce what is medically known as "necrotizing fasciitis".

VIBRIO VULNIFICUS:

The first documented case of a disease caused by the Vibrio Vulnificus was in 1979, it is a gram-negative bacillus that only affects humans and other primates, and is usually found in warm, shallow, coastal salt water in temperate climates throughout most of the world (Schwartz, 2012).

Vibrio Vulnificus is a bacterium in the same family as those that cause cholera, the Vibrionaceae family that includes the genera Vibrio, Plesiomonas, and Aeromonas. As we mentioned before, they are natural inhabitants of sea water but they can also be found in fresh water, and they are part of the group of vibrios that known as halophilic because they require salt for growth (Ho, 2011).

These bacteria can cause disease in those who eat contaminated seafood or have an open wound that is exposed to seawater. Among healthy people, ingestion of Vibrio Vulnificus can cause vomiting, diarrhea, and abdominal pain. In immuno-compromised persons, particularly those with chronic liver disease, it can infect the bloodstream, causing a severe and life-threatening illness characterized by fever and chills, decreased blood pressure, and blistering skin lesions. 50 % of the time the bloodstream infection of Vibrio Vulnificus can be fatal (CDC, 2013).

Vibrio Vulnificus, according to Centers for Disease Control and Prevention (2013), can cause an infection of the skin when open wounds are exposed to warm seawater; these infections may lead to skin breakdown and ulceration. Persons who are immuno-compromised are at higher risk for invasion of the organism into the bloodstream and potentially fatal complications.

Antibiotics are necessary to eradicate the infection because it improves survival. In case of wound infection, aggressive debridement is useful to remove necrotic tissue, amputation of the infected limb is sometimes necessary. Also in patients with shock, resuscitate interventions should be performed (Schwartz, 2012).

The CDC recommends:

ü Culture of wound or hemorrhagic bullae, all V. Vulnificus isolates should be forwarded to a public health laboratory.

ü Blood cultures are recommended if the patient is febrile, has hemorrhagic bullae, or has any signs of sepsis.

ü Antibiotic therapy:

·        Doxycycline (100 mg PO/IV twice a day for 7-14 days) and a third-generation cephalosporin (e.g. ceftazidime 1-2 g IV/IM every eight hours) are generally recommended.

·        A single agent regimen with a fluoroquinolone such as Levofloxacin, Ciprofloxacin or Gatifloxacin, has been reported to be at least as effective in animal model as combination drug regimens with Doxycycline and a Cephalosporin.

·        Children, in whom Doxycycline and Fluoroquinolones are contraindicated, can be treated with Trimethoprim-Sulfamethoxazole plus an Aminoglycoside.

·        Necrotic tissue should be debrided; severe cases may require fasciotomy or limb amputation.

 

V. Vulnificus septicemia is the most common cause of death from seafood consumption in the United Stated (Haq & Dayal, 2005).

Choi, et al., reported in 2005 that the first evidence of V. Vulnificus septicemia was in the skin as purpura fulminans, which can take a catastrophic course without inmediate and intensive empirical antibiotic treatment. Furthermore V. Vulnificus infection may be a rare cause of necrotizing fasciitis, but it can be fatal (Tajiri, et al., 2008).

NECROTIZING FASCIITIS:

Necrotizing Fasciitis, first discribed by Joseph Jones, a Conferate Army surgeon, during the US Civil War, is a serious bacterial infection that spreads rapidly and destroys the body’s soft tissue (Quirk & Sternbach, 1996). It is considered a life-threatening disease that is often difficult but crucial to diagnose as soon as possible in order to save a life (Swain, Hatcher, Azadian, Soni, & De Souza, 2013).

Commonly called a “flesh-eating infection”, Necrotizing Fasciitis is a rare disease with a rapidly progressive inflammatory infection of the facia and a secondary necrosis of the subcutaneous tissue.

The causative bacteria, as mentioned by Richard E Edlich (2013), may be aerobic, anaerobic, or mixed flora (Kihiczak, Schwartz, & Kapila, 2006). There are a few recognized distinct syndromes of this entity where the most important are:

·        Type I, or polymicrobial

·        Type II, or group A streptococcal

·        Type III gas gangrene, or Clostridial Myonecrosis

There are a variety of organisms capable to causing Necrotizing Fasciitis; these include group A Streptococcus, Klebsiella, Clostridium, E. Coli, Staphylococcus aureus, and Aeromonas hydrophila, among others (CDC, 2013). A variant of Necrotizing Fasciitis type I is a saltwater necrotizing fasciitis, in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species (Edlich, 2013).

In many cases of Necrotizing Fasciitis, antecedent trauma or surgery can be identified; the initial lesion is often trivial, such as an insect bite, minor abrasion, boil, or injection site. The hallmark symptom is intense pain and tenderness over the involved skin and underlying muscle (Olafsson, Zeni, & Wilkes, 2005). But also the symptoms may begin at a site distant from the initial traumatic insult.

Most people who get Necrotizing Fasciitis have other health problems that may lower their body’s ability to fight infection such as diabetes, kidney disease, cancer, or other chronic health conditions that weaken the immune system.

Beginning an immediate treatment is essential in Necrotizing Fasciitis once the diagnose is confirmed. Antibiotic therapy is a key consideration, including a combination of penicillin G and an Aminoglycoside, as well as Clindamycin. Keep in mind that Necrotizing fasciitis is a surgical emergency and the patient should be admitted immediately to a surgical intensive care unit, where the surgical staff is skilled in performing extensive debridement and reconstructive surgery (Edlich, 2013).

If you are healthy, have a strong immune system, and practice good hygiene and proper wound care, your chances of getting Necrotizing Fasciitis are extremely low, explains m the CDC.

 

Bibliography

 

CDC. (2013, Jun 28). cdc.gov. Retrieved from Necrotizing Fasciitis: A rare disease, especially for the healthy: http://www.cdc.gov/features/NecrotizingFasciitis/

CDC. (2013, Oct 21). Centers for Disease Control and Prevention. Retrieved from Vibrio Illness: http://www.cdc.gov/vibrio/vibriov.html

Choi, H., Lee, D., Lee, M., Choi, M., Moon, K., & Koh, J. (2005). Vibrio Vulnificus septicemia presenting as purpura fulminans. J Dermatol, ;32(1):48-51.

Edlich, R. F. (2013, Apr 29). medscape.com. Retrieved from Necrotizing Fasciitis: http://emedicine.medscape.com/article/2051157-overview#a0101

Haq, S., & Dayal, H. (2005). Chronic Liver diseaseand consumtion of raw oysters: a potentially lethal combination--a review of Vibrio vulnificus septicemia. Am J Gastroenterol, ;100(5):1195-9.

Ho, H. (2011, Aug 15). medscape.com. Retrieved from Vibrio Infection: http://emedicine.medscape.com/article/232038-overview#a0104

Kihiczak, G., Schwartz, R., & Kapila, R. (2006). Necrotizing Fasciitis: a deadly infection. J Eur Acad Dermatol Venereol, ;20(4):365-9.

Olafsson, E., Zeni, T., & Wilkes, D. (2005). A 46 year old man with excruciating shoulder pain. Chest, ;127(3):1039-44.

Quirk, W., & Sternbach, G. (1996). Joseph Jones: infection with flesh eating bacteria. J Emerg Med, ;14(6):747-53.

Schwartz, R. A. (2012, Sep 17). medscape.com. Retrieved from Vibrio Vulnificus Infection: http://emedicine.medscape.com/article/1055523-overview

Swain, R., Hatcher, J., Azadian, B., Soni, N., & De Souza, B. (2013). A five-year review of necrotizing fasciitis in a tertiary referral unit. Ann R Coll Surg Engl, ;95(1):57-60.

Tajiri, T., Tate, G., Akita, H., Ohike, N., Masunaga, A., Kunimura, T., . . . Morohoshi, T. (2008). Autopsy cases of fulminant-type bacterial infection with necrotizing fasciitis: group A (beta) hemolytic Streptococcus pyogenes versus Vibrio vulnificus infection. Pathol Int, ;58(3):196-202.