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.