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.

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.

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.

anaphylactic shock

Anaphylactic shock: life threatening allergic reaction

Anaphylactic shock is a type 1 hypersensitive reaction (IgE mediated) which occur systematically which life threatening while asthma also in the same group but only occur locally. When you exposed to allergen for the first time , IgE will produced and bind to mast cells. When you reexposed to the same allergen, especially via injury or food, this cause release of histamine from mast cells to all body regions causing capillary leaks, bronchopspasm, wheeze, cyanosis, edema, hypotension because of loss of fluid by formation of edema, tachycardia and urticaria.

Example of precipitants are drugs for example penicillin, latex, stings, eggs, peanuts and pollens.

How we manage anaphylaxis:

First of all, we need to secure the airways and give 100% O2 intubation if respiratory obstruction. The next step is we need to remove the cause and raising the feet to help restore blood circulation. Then we give adrenaline to restore blood pressure and for brochodilation. For further detail you can refer Wikipedia.

Problem during diving in the sea: nitrogen narcosis & Caisson disease

When you diving into deep sea, this 2 problems will come out, but there are solutions for you.

1. Nitrogen narcosis occur when you diving more tha 80m, nitrogen gas will dissolve into body tissue especially in fat and also nervous tissue. This cause interference in transfer of signal across the neural synapses.this effect mental, physical and finally cause unconsciousness. But if you want to diving more deeper, you can replace nitrogen with helium, but its still has limitation until 150m. if you go deeper, another complication will occur which is neuromuscular disorder called high-pressure nervous syndrome (HPVS): tremors, vertigo and nausea.
2. Caisson disease is a decompression disease which occur when you rapid come out from deep water. When you diving for every 10 m, air pressure will increase 100kPa causing increase nitrogen gas dissolves especially in fat. Nitrogen gas metabolize slower than other gases that why when you rapid coming out from deep water, nitrogen bubbles will formed

fainting: first aid-CPR

If a person is unresponsive and not breathing you need to start cardio pulmonary resuscitation (CPR) right away. Gasping is not breathing!  By unresponsive I mean appears lifeless, doesn't move or respond when shoulder is tapped. Yell for someone to call Emergency Medical Services (EMS) and get an an automated external defibrillator (AED).  An AED applied fast may restart the heart. Don't worry, AEDs are user friendly.

Understand that when a victim's heart has stopped pumping blood (cardiac arrest), permanent brain damage can begin in four to six minutes, so you must act fast.

Cardiac arrest can strike at any age and may be caused by many conditions, including heart attack, suffocation, allergic reaction, drowning, choking, or electric shock.

Here's How:

1. Attempt to wake victim. If the victim is not breathing (or is just gasping for breath), call 911 immediately and go to step 2. If someone else is there to help, one of you call 911 while the other moves on to step 2.
2. Begin chest compressions. If the victim is not breathing, place the heel of your hand in the middle of his chest. Put your other hand on top of the first with your fingers interlaced. Compress the chest at least 2 inches (4-5 cm). Allow the chest to completely recoil before the next compression. Compress the chest at a rate of at least 100 pushes per minute. Perform 30 compressions at this rate (should take you about 18 seconds).If you are not trained in CPR, continue to do chest compressions until help arrives or the victim wakes up.It's normal to feel pops and snaps when you first begin chest compressions - DON'T STOP! You're not going to make the victim worse.
3.  Begin rescue breathing. If you have been trained in CPR, after 30 compressions, open the victim's airway using the head-tilt, chin-lift method. Pinch the victim's nose and make a seal over the victim's mouth with yours. Use a CPR mask if available. Give the victim a breath big enough to make the chest rise. Let the chest fall, then repeat the rescue breath once more. If the chest doesn't rise on the first breath, reposition the head and try again. Whether it works on the second try or not, go to step 4.If you don't feel comfortable with this step, just continue to do chest compressions at a rate of at least 100/minute.
4.  Repeat chest compressions. Do 30 more chest compressions just like you did the first time.
5. Repeat rescue breaths. Give 2 more breaths just like you did in step 3 (unless you're skipping the rescue breaths).
6. Keep going. Repeat steps 4 and 5 for about two minutes (about 5 cycles of 30 compressions and 2 rescue breaths).If you have access to an automated external defibrillator (AED), continue to do CPR until you can attach it to the victim and turn it on. If you saw the victim collapse, put the AED on right away. If not, attach it after approximately one minute of CPR (chest compressions and rescue breaths).
7. After 2 minutes of chest compressions and rescue breaths, stop compressions and recheck victim for breathing. If the victim is still not breathing, continue CPR starting with chest compressions.
8. Repeat the process, checking for breathing every 2 minutes (5 cycles or so), until help arrives. If the victim wakes up, you can stop CPR.