Obnoxious Tale

You see,I just kambek from library.I was hungry,lunch time.Grab Rm10 from my wardrobe/bank,went to my apartment cafetaria.I intend to eat at my room so must use the polystyrene.I fill the polystyrene container with white rice until full.Suddenly,I notice there is a ..............

 
.........strand of HAIR on the back of the senduk nasi...

WHAT THE FCUK FISH??! Nasi beriani i know... but,nasi bulu?? Lancauuu,spoil my appetie already.

  

Since I work  part-time  CSI during form 5,(after watching 20 episode of CSI,u are certified forensic-person)I. analyze the unidentified hair/bulu..I concluded that it is not arm pit hair(bulu ketiak) nor nasal hair..coz very long,16 cm..so must be..................PUBIC HAIR?? Just kidding,of coz la normal human hair..unless big-foot cooked the rice.

I feel sorry for those who eat lunch at that kafetaria.


To celebrate my 5th day blogging,I give you special bonus.Mr Muthu,drum role pulisss...

< insert drum role here >

INFECTIVE ENDOCARDITIS NOTE!!! I know my classmate/lazy-ass-person dont read about Infective Endocarditis. They never read before class....Luckyly,Dr Keough is here to make you a good doctor like him ..
your welcome..your welcome...oh no..puliss don't kiss me,i dont want your STD..
by the way,It took me 2 hours to complete typing this note,my finger's bone is breaking alrerady,arghhhh!! *jump off the building* 

Chill out. I'm Keough  and your BF like suprise-butt-seks.

(ladies ,pls don't thow slippers at me )

INFECTIVE ENDOCARDITIS (IE)

Braunwald's Heart Disease. Saunders Elsenvier 2008

Introduction

characteristic: Vegetation

vegetation
variable size amorphous mass of platelet and fibrin with abundant enmeshed mircroorganim and moderate inflammtory cell.

site
heart valve -most common
on septal defect
chordae tendinae
mural endocardium


Acute IE                                                                        Subacute IE
Typically by Staphylococcus aureus                      typically by viridan streptococcus
mark toxicity                                                                   mild toxicity
days to week                                                                weeks to month
metastasize infection                                                       rarely metastasize


Epidemiology

more common in man    2:1
median age: 47-69
risk factor
IV drug user
degeneratve valve desease in elderly
intracardiac device
hemodialysis
helath care related(nosocomial infection,central venous line,catheters) 5-29% of IE cases


ETIOLOGICAL MICROORGANISM

Staphylococcus aureus-major cause in all population
Viridans Streptococci- 30-65% of IE related to IV drug abuser
                                    -normal flora of oropharynx
                                     -susceptible to penicillin..Kill it with penicillin+gentamycin

Streptococcus bovis-normal flora20-40% cases of native valve IE (native valve=non-prosthetic valve)
Enterococci- not common-kill with penicillin+gentamycin or streptomycin
Fungi  - Candida albicans

PATHOGENESIS
  

microorganism gain acces to the blood 

          |

adhere to valve surface 

|

proliferate to cause local damage and vegetation growth

|

disseminate hematogenous;y with or without emboli

#Bacteremia is a common thing but only not all develop IE.IE is rare because intact epithelium is resistant to infection.Platelet-fibrin deposit only at 

1.abnormal valve

2.injured/inflammed cardiac epithelium

the place platelet-fibrin deposited is called NBTE

(Non Bacterial Thrombotic Endocarditis)

NBTE is coz by: 1) endothelial injury

                      2) hyperocagulable state

Endothelial injury is cause by 

1..blod flow across narrow orrifice,

2..high velocity jet striking epithelium 

3..flow from high pressure chamber to low pressure chamber

NBTE become IE as a result of BACTEREMIA 

fibronectin    

produce by endothelial cell in response to injury

receptor of fibronectin is available in surface of S aureus ,viridans,streptococci,enterococci,S.pneumoniae,Candida albicans.(so can adhere to endothelium)

PATHOPHYSIOLOGY

clinical manifestation is cause by

(1)  local destruction effect of intracardiac infection

(2) embolization of bland or septic fragment of vegetation resulting infarction or infestion

(3)  hematogenous seeding of bacteremia 

(4)   deposition of immune complex

Effect of local destruction

1. destroy valve

2. distortion or perforation of valve

3.  rupture of chordae tendinae

4. fistula between major vessel or chambers (causing progressive Chronic Heart Failure )

5. Abcess-causing purulent pericarditis

6.distrupt electrocardiograph condution-causing arrhythmia  .

Large vegetaion can cause valvular stenosis.

CLINICAL MANIFESTATION

Symptom                                                 Sign

fever                                                       fever

chill                                                        murmur

sweat                                                   regurgitation murmur

rigor                                                    embolic event

Anorexia                                                spleenomegaly

Weight loss                                              clubbing                       

malaise                                                     splinter hemorrhage

dysopnea

Cough

Stroke

headache

nausea-vomitting

Chest pain

myalgia/athralgia

DIAGNOSIS

LAB TEST

-anemia,normochromic normocytic RBC (maybe absent in acute IE)

-low serum iron

-leucocyt   -subacue IE-normal

                 -acute IE-elevated

-ESR increase (except if patient have CHF,DIVC and renal failure)

-urinalysis: 50% cases of IE have protienuria and microsopic hematuria

TREATMENT

Two objective

• remove infection-antibiotic
• correct destruction in heart-surgical