Saturday, October 25, 2014

raas system(renin angoitensin aldosterone )

RAAS systems is very important in our body because this control it is a part of homeostasis(control normality functioning of internal system).

RAAS can be divided into 2 parts:

  1. plasmatic endocrine cascade 
  2. local tissue RAAS- affecting heart , vessels, adrenal gland and brain) 
for plasmatic endocrine cascade , we can divided into 2 substances which are renin and angiotensin 1 (AT-1). renin synthesised as preprorenin in juxtaglomerular cells in kidney, then it will cleaved to prorenin which stiil inactive form and then finally to active renin. Renin is used to catalyze conversion of angiotensinogen produced by the liver into AT-1. Renin secretion will be secreted under certain condition which are:

  1. when blood pressure drop in vas afferens
  2. drop in sodium ion concentration detected by macula densa in distal tubule.
  3. when increased in sympathetic activity(when noradrenaline and adrenaline bind to B1 receptor)
AT1 only have small to none its own physiological effect because AT-1 will be converted to AT-2 by angiotensin converting enzyme (ACE). ACE also responsible for bradykinin breakdown( bradykinin has vasodilator effect), ACE maily bound to endothelial membrane especially in pulmonary circulation.AT -2 has very shot half life , maximum inly 1 minute, because hydrolyzed by plasmatic peptidases. AT -2 has certain effect:
  • cause vasoconstriction- increase peripheral vascular resistance.
  • increase aldosterone secretion- cause sodium ion retention which lead to water retention
  • tissue remodelling in vascular smooth muscle , fibroblast activation, collagen synthesis and cardiomyocyte hypertrophy and apoptosis.
  • effect central nervous system by activate thirst center activation, increased sympathetic tonus and ADH and ACTH secretion.

hence if activation of RAAS system occur in chronic condition it can lead to many problem for example:
  1. atherosclerosis
  2. vascular hypertrophy
  3. left ventricle hypertrophy fibrosis
  4. decrease glomerular filtration rate 
  5. protienuria 
  6. sodium retention
this will lead to hypertension, that can lead to stroke, heart failure and renal failure finally lead to death.

Wednesday, October 22, 2014

how to loss weight?

everyone will desired to have slim body to look beautiful or good, not only for that, the most important is to take care of our health.

why obese is so dangerous?

ok, here i will explain a bit why being obese is danger for us.Obese willlead you to have a lot of disease for example diabetes mellitus, hypertension,atherosclerosis, hormonal dysbalance , problem to have childs, liver problem and most important is heart probblem. for more explaination you can comment later and i will explain it

so , how can we loss our weight:

  1. first thing you need to keep in mind is, do not to try to loss weight more than 10kg in 6 months, because if you loss your weight to fast , it can lead to other problems.
  2. you need to take balance diet: refer here: http://healthncarelifestyle.blogspot.cz/2014/03/get-balanced-diet.html
  3. and also you need to make sure to reduce amount of food especially carbohydrate because carbohydrate if excess, it will change to fat in our bodies.
  4. drink a lot of water, because it can prevent us to feel hungry and also we need enough water for metabolism in our bodies.
  5. do exercise, 30 minutes everyday.
  6. stop smoking 
  7. the most important thing is to be motivated to do what you have planned.

Tuesday, October 21, 2014

how to change your car's tyres?

Instructions for changing a car tyre

Check out the gear in your car: make sure that your spare tyre and tools are in good condition. Do not attempt to change the tyre if they're not. Make sure that your personal safety will not be compromised. Be seen: safety clothing (if you have any) and turn on your hazard lights!
Right, here's how to change your car tyre:
  1. Block the wheels on the side not being lifted. Make sure no one's inside. Apply handbrake and put the vehicle in park (if automatic) or in gear (if it's a manual).
  2. Take off the wheel cover.
  3. Loosen the wheel nuts with the wheel wrench while the vehicle is on the ground. If the nuts are too tight to loosen by hand, you may need to apply pressure to the wheel wrench with your foot. If you do need to stand on the wrench, ensure it is in the horizontal position for your own safety.
  4. Put the jack together and place it on firm ground, as flat as possible. Every car is different and you can do a bit of damage if you put this in the wrong location - it needs to go in the reinforced area of the sill (if it's a sill jack). The sill is the body section below the base of the door openings.
  5. Slowly raise the vehicle.
  6. Remove the nuts and remove the wheel, pulling towards you with both hands.
  7. Lift the new wheel. Read the manufacturer's instructions if using a space saver. These are a temporary tyre and are not meant to be driven long distances or at speeds over 80km/h.
  8. Replace the wheel nuts, making sure these go on the right way, taper towards the wheel. Tighten snugly.
  9. Lower the car, then tighten them properly - standing on the wrench handle with it in the horizontal position to give a light bounce, if you had to stand on it to loosen them. If you over-tighten the nuts you can warp the brake components, but not to tighten them enough is dangerous.
  10. Replace the wheel cover or hubcap.
  11. Take the wheel to a tyre shop for repair or replacement.
When you've finished kneeling on your plastic sheet, use it to protect your boot from the dirty tyre. If you have a space saver, do not travel faster than 80 km/h and get the punctured tyre fixed as soon as possible.

Tuesday, July 15, 2014

having problem travel to Malaysia?

Having problem travel to Malaysia?

 Here some basic things you need to know about Malaysia.

First of all, when you arrived in Malaysia, you need to make sure you have cash in ringgit currency because in Malaysia, you cannot use your credit card in all shop not like European country. But don’t change the money in airport but you can change in KL central because the rate is much better than in airport.
When you arrived in airport, you can take ERL, which is direct train to KL central , cost RM 35. It takes time about 40 minutes, or you can take taxi, but much more expensive. From Kl central, you can take taxi, monorel or bus there  depend on your next station. The best way is before you arrive there, try to contact the apartment you rent, how you can go there.
In Malaysia, we have 14 states, 2 in borneo and 12 in peninsular Malaysia. In peninsular Malaysia I recommend you to go to capital city, Kuala Lumpur, because you can find everything there from foods, shooping, and culture. If you like to go to nature environment, I recommend you to go to Cameron Highland, there you can find a lot of fresh food from garden and environment colder than any other places in Malaysia. Next you must go to Langkawi, because there, the sea and beach are very beautiful and you can buy a lot of stuff without tax. Next you can go to Terengganu, on yhe East side, there you can find a lot more small island for scuba or diving, and you can eat tradisional food we called “keropok lekor”., and the beach also very beautiful. You also can go to Kelantan, they call tis place Serambi Mekah, because here 99% percent citizens are muslims. Here you can go to Khadijah Market, here you can find only women work here. In Kelantan there is also area with tax free, we called “Rantau Panjang”, border between Malaysia and Thailand.

Besides in peninsular Malaysia, you can go to Borneo because in Borneo, you can find more nature than in peninsular Malaysia.

In Malaysia, everything is cheaper if you compare in European countries. Even if oyu want to travel to those places that I already mention, you can go there by bus or by flight. We Have 3 different cheap flight which are AIR ASIA, MALINDO and FIRE FLY.


In you have any question, you can comment to this article or email me.

case study 1


A 63 years old man with a long history of alcohol use presents to his new primary care physician with a 6 months history of increasing abdominal girth. He has also noted easy bruisability and worsening fatique. He denies any history of GI bleeding. He continues to drink three to four coktails a night but says he is trying to cut down. Physical examination reveals a cachectic man who appears older than his stated age. Blood pressure is 108/70 mm Hg. His scleras are anicteric . his neck vein are flat, and chest examination demonstrates gynecomastia and multiple spider angiomas. Abdominal examination is significant for protuberant abdomen with a detectable fluid wave, shifting dullness, and an enlarged spleen. The liver edge is difficult to appreciate. He has trace pitting pedal edema. Laboratory evaluation shows anemia, mild thrombocytopenia, and elevated prothrombin time. Abdominal ultrasounogram confirms a shrunken , heterogenous liver consistent with cirrhosis, significant ascites and spenomegaly.

Question:

1)       Describe possible mechanisms for alcohol induced cirrhosis.
2)       What is the proposed mechanism of portal hypertension, and how does it affect ascites formation?
3)       Significant hematologic abnormalities exist. How might they be explained?

Answer:
1)       The exact mechanism of alcohol induced injury to the liver is unknown; however , it is thought that the marked distortion of hepatic architecture , fibrous tissue deposition and scarring , and regenerative nodule formation result from multiple processes. Chronic alcohol use has been associated with impaired protein synthesis, lipid peroxidation , and the formation of acetaldehyde, which may interfere with membrane lipid integritiy and disrupt cellular functios. Local hypoxia, as well as cell mediated and antibody- mediated cytotoxicity, have also been implicated.

2)       Portal hypertension is in part responsible for many of the complication of cirrhosis, including clinically apparent ascites , a sign of liver disease associated eith poor long term survival. Although no single hypothesis can explain its pathogenesis, portal hypertension and inappropriate renal retention of sodium are important elements of any theory. Portal hypertension changes the hepatocellular architecture, resulting in increased intrahepatic vascular resistance. This elevates the sinusoidal pressure transmitted to the portal vein and other vascular bed. Spenomegaly and portal to systemic shunting result. Vasodilator such as nitic oxide are shuntrd away from liver and not cleared from thr circulation , resulting in peripheral arteriolar vasodilation. Decreased renal artery perfusion from this vasodilation is perceived as an intravascular volume deficit by the kidney, activated raas system causing sodium and water resorption. By overwhelming oncotic pressure , increased hydrostatic pressure from fluid retention in the portal vein result in ascitrs formation. Exceeding lymphatic drainage capacity, ascites accumulates in the peritoneum.


3)       Splenomegaly and hyperslenism are a direct consequence of elevated portal venous pressure. Thrombocytopenia and haemolytic occur as a result of both sequestration and these formed elements by the spleen and depressive effect of alcohol on the bone marrow. The frequent bruising and the elevated prothrombin time in this patient highlight the coagulopathy seen ic cirrhosis and chronic liver disease. As a result of inadequate bile excretion, there is impaired absorption of the fat soluble vitamin K, a vitamin necessary for the activation of specific clotting factors. In addition, inadequate hepatic synthesis of other  clotting factors causes a coagulopathy.




Bleeding into gastrointestinal tract


Sometimes , we did not realise that we having problem with our gut, and actually our gut undergo bleeding problem. So here , I will share with you different types of bleeding in gut.

Types:
1.       Hematemesis: this is bleeding characterise by vomiting of blood. It can cause by esophageal varises( cause by portal hypertension), esophegeal ulcer, mallory weis syndrome gastric ulcer. Patients usually vomits up bright red, undigested blood. But in gastric bleeding, the vomited blood is digested by gastric juices and has appearance of “coffee ground”.

2.       Melena: appear in feces with tarry black , semisolid appearance, foul smell, usually originate from upper git(stomach, small intestine). But to appear as melena, blood must be at least 50 -100ml.

3.       Enterorrhagia: appear as fresh, bright red blood on the feces, originate from lower git. Usually appear in patients with haemorrhoids, ulcerative colitis.

4.       Occult bleeding: blood that cannot recognize by naked eye, but we can use benzidine test. Usually originate in the upper git, when chronically can lead to iron deficiency anemia.


ANGINA PECTORIS-CHEST PAIN

What is angina pectoris?
Angina pectoris is pain that occur in the chest because of heart muscle undergo lack supply of oxygen or we called it ischemia. This pain present with central chest tightness or heaviness and may radiate to upper extremities( more often to the left) , to the neck and jaw. This pain usually occur during exertion and relieved by rest.

This disease can cause by certain things, most common is atherosclerosis especially in obese people who taking diet rich in cholesterol and hypertension. This also can cause by anemia, tachyarythmias, polycythemia, myocardium hypertrophy.

Types of angina:
1.       Stable angina: which is induced by effort(physical activity) and relieved by rest and also relieved by nitrogylcerin(vasodilator). Relieved within 5 minutes
2.       Unstable angina: angina with increasing frequency and severity associated with myocardial infarction . this pain last longer, more tha 20 minutes and not relieved by nitroglycerin.
3.       Prinzmetal angina: caused by coronary arteries vasospasm.

How to diagnoses:
·         First by physical examination. Ask about the pain.
·         ECG test. May show ST depression. But if resting ECG normal, we should use exercise ECG, thalium scan, cardiac ct or coronary angiography

How to manage the problem:
1.       First of all, we need to change our lifestyle by stop smoking, do exercise, and weight loss. Controlour blood pressure, diabetes mellitus, cholesterol level.
2.       Give aspirin(vasodilator)
3.       B blocker-reduce heart work, hence reduce heart metabolism.
4.       Nitroglycerin(vasodilator)

5.       Long acting calcium antagonist- reduce heart contractility.

Sunday, March 23, 2014

sympathetic system: adrenergic receptors in human body

receptor for sympathetic system we called adrenergic receptors which are divided into 2 families: a receptors and b receptors.

a receptors:

  1. a1 receptors:
  • vasoconstriction : increase peripheral resistance and blood pressure
  • glycogenolysis, gluconeogenesis in liver
  • increase tone of sphincters in git and bladder
  • decrease tone oof motility of git
  • contraction of pregnanat uterus
  • mydriasis by contraction of dilator pupilla muscle.
    2. a2 receptors:
  • presynaptical localization: result in decrease release of noradrenaline
  • postsynaptical localization: decrease insulin release by b cell, decrease motility , tone and secretion in git
  • aggregation of platelets
  • vasoconstriction
  • inhibit acetylcholine release
b receptors:

1. b1 receptors:
  • positive effect on heart: increase heart rate, contractility, dromotropic effect(conductivity), bathmotropic(excitibility)
  • kidney-juxtaglomerular : increase renin secretion
2. b2 receptors :
  • vasodilation of blood vessels in skeletal muscles and coronary arteries.
  • bronchodilation
  • relaxation of visceral smooth muscle
  • increase muscle and liver glycogenolysis
  • increase insulin release by b cells
  • increase glucagon release
  • increase salivation-thick
  • decrease tone of bladder detrussor muscle
  • decrease tone of uterine smooth muscle
  • skeletal muscle tremor
3. b3 receptors
  • lipolysis

Saturday, March 15, 2014

grow new teeth using ultrasound transducer

20 minutes a day for four months to stimulate growth of a tooth’s root
Nanotechnology expert Dr. Jie Chen and his associate Dr. Ying Tsui from the Faculty of Engineering at the University of Alberta have developed a new ultrasound transducer to stimulate the growth of teeth and fix asymmetric jaw bones. The transducer utilizes LIPUS, which stands for “low-intensity pulsed ultrasound.” The miniature, wireless device does exactly what its name suggests: it sends pulses of ultrasound into biological matter, such as gums, muscles or bones to increase healing or stimulate growth of new tissue.
The transducer is a type of “system-on-a-chip,” which generally refers to an incredibly small system, like a microchip, that contains all the parts and electronic circuitry a system needs to run. Advances in system-on-a-chip technology allow scientists and researchers the opportunity to work on an increasingly smaller scale with computing power akin to computers from around a decade ago.
Perhaps the best part, other than growing new teeth, is the transducer doesn’t need to be surgically implanted. A patient need only apply the device topically for 20 minutes a day for four months to stimulate growth of a tooth’s root. So far it has been tested on 12 Canadian patients in the prototype stage. The team hopes to release a commercial form of the technology within the next two years.