Page 1 of 1: clubbing of the fingers

shabana · Credits: 11520 My Scrapbook

please i want two things
first i want to know the Pathology or the reasons of the clubbing of the fingersin case of subacute infective endocarditis and
is this feature occurs in any other cases ?what are they?

second what is the effect of atrial septal defect on the left side of the heart as i know itis nothing ........ is it right ?

shabana · Credits: 11520 My Scrapbook

???????

shabana · Credits: 11520 My Scrapbook

where are you docotrs

MockTurtle · Credits: 5597 My Scrapbook

The pathophysiology of clubbings pretty confusing.I tried to understand it while reading Ca lung,firstly cause i wasnt makin much headway,and primarily cause understandin the mechanism of this phenomenon is a very low yield topic as far as the entrances are concerned.Anyway,if know u must,then read on from what e-medicine has to say,though it's not very interesting.Pathophysiology: The specific pathophysiologic mechanism of digital clubbing remains unknown. Many theories have been proposed, yet none have received widespread acceptance as a comprehensive explanation for the phenomenon of digital clubbing. As stated best by Samuel West in 1897, "Clubbing is one of those phenomena with which we are all so familiar that we appear to know more about it than we really do."

Alterations in size and configuration of the clubbed digit result from changes in the nail bed, beginning with increased interstitial edema early in the process. As clubbing progresses, the volume of the terminal portion of the digit may increase because of an increase in the vascular connective tissue and change in quality of the vascular connective tissue, although some cases have been associated with spurs of bone on the terminal phalanx.

Although clubbing is a common physical finding in many underlying pathological processes, surprisingly, the mechanism of clubbing remains unclear. Different pathological processes may follow different pathways to a common end. Many studies have shown increased blood flow in the clubbed portion of the finger. Most researchers agree that this results from an increase in distal digital vasodilation, the cause of which is unknown. Also unknown is the exact mechanism by which increased blood flow results in changes in the vascular connective tissue under the nail bed. Many researchers agree that the common factor in most types of clubbing is distal digital vasodilation, which results in increased blood flow to the distal portion of the digits. Whether the vasodilation results from a circulating or local vasodilator, neural mechanism, response to hypoxemia, genetic predisposition, or a combination of these or other mediators is not agreed on currently.

Evidence that favors the presence of a circulating vasodilator derives from the association of clubbing with cyanotic congenital heart disease. Many potential vasodilators, which usually are inactivated as blood passes through the lungs, bypass the inactivation process in patients with right-to-left shunts. Patients with tetralogy of Fallot with substantial shunting have a high incidence of clubbing. After surgical correction diminishes the shunt, the clubbing improves. Also previously observed is clubbing confined to the feet in patients with late untreated patent ductus arteriosus in whom blood from the pulmonary artery bypasses the lungs and is shunted into the descending aorta. In the absence of a shunt, the circulating vasodilator may be produced by the lung tissue, or, possibly, it passes through the pulmonary circulation without becoming inactivated. Proposed vasodilatory factors include ferritin, prostaglandins, bradykinin, adenine nucleotides, and 5-hydroxytryptamine.

A neural mechanism has been proposed with particular consideration of the vagal system. An increased incidence of digital clubbing has been associated with the Pathology and disease of vagally innervated organs. Furthermore, regression of clubbing after vagotomy has been reported. Although some factor related to the vagal system is a possible contributor to the development of clubbing, especially clubbing occurring with hypertrophic osteoarthropathy, the hypothesis of a neural mechanism has decreased in popularity because of the lack of evidence of clubbing in neurologic disorders and the presence of clubbing in diseases of organs not innervated by the vagal system.

Hypoxia has been proposed as an alternative explanation for clubbing in cyanotic heart disease and pulmonary diseases. An increase in hypoxia may activate local vasodilators, consequently increasing blood flow to the distal portion of the digits; however, in most cases, hypoxia is absent in the presence of clubbing, and many diseases with noted hypoxia are not associated with clubbing.

Genetic inheritance and predisposition also may play a role in digital clubbing. Hereditary clubbing is observed in 2 forms, including idiopathic hereditary clubbing and clubbing associated with pachydermoperiostosis. The 2 forms are believed to be separate entities. Both demonstrate autosomal dominant inheritance with incomplete penetrance.

More recently, platelet-derived growth factor released from fragments of platelet clumps or megakaryocytes has been proposed as the mechanism by which digital clubbing occurs. The fragments are large enough to lodge in the vascular beds of the fingertips, and, subsequently, they release platelet-derived growth factor. This factor has been shown to have general growth-promoting activity and causes increased capillary permeability and connective tissue hypertrophy.

wondergirl · Credits: 13247 My Scrapbook

to add more...

Hypertrophic osteoarthropathy (HOA) is a clinical syndrome characterized by digital clubbing, periostosis of tubular bones, and synovial effusion especially of large joints. Clubbing has been associated with various gastrointestinal disorders like inflammatory bowel disease, sprue, and bowel neoplasms. It has also been rarely associated with esophageal carcinoma, leiomyoma, Plummer-Vinson syndrome and achalasia cardia

shabana · Credits: 11520 My Scrapbook

thanks very much for your reply but i will ask you something can you summarize what you say dr mockturtle and wondergirl please

because i get confused after i read your reply

. ....do you want to say that the cause is increased vascular bed by unknwon mechanism and it may be due to release of chemical mediators

flowerchildn · Credits: 7753 My Scrapbook

shabana dear for clubbing read pj mehta med and harry has a small note in it
but pj gives the list which is nearly exhaustive
yes one of the mechan is unknown though there r more theories than that
i always believe search for the answers urself
ull remember btter much better

npshades · Credits: 809 My Scrapbook

hey shabana
many of our friends gave a extensive notes on clubbing u can go thru them
about ure second question
thats is about ASD
blood from left atrium goes into right atrium
so right atrium recieve blood from superior vena cava and inferior vena cava[as a part of venous return]+left atrium the whole blood goes into right ventricle causing mid diastolic murmur [MDM] in tricuspid area[because of extra volume of blood flowing thru the tricuspid valve] then thru the pulmonary valve causing ejection systolic murmur[ESM] at pulmonary area and then into left atrium
and the same viscious circle follows
so i think u may be clear now that there is no problem on left side of heart[but right side may enlarge because of volume overload.the more consistent finding here is WIDE AND FIXED SPLIT OF SECOND HEART SOUND

I AM GIVING THE ECG AND X-RAY FINDINGS OF ASD[i hope u will have no doubt after reading this concept]

In patients with an ostium secundum defect, the electrocardiogram (ECG) usually shows right axis deviation and an rSr' pattern in the right precordial leads representing delayed posterobasal activation of the ventricular septum and enlargement of the RV outflow tract. An ectopic atrial pacemaker or first-degree heart block occurs occasionally in patients with defects of the sinus venous type. In patients with an ostium primum defect, the RV conduction defect is characteristically accompanied by left axis deviation and by superior orientation and counterclockwise rotation of the QRS loop in the frontal plane. Varying degrees of RV and right atrial (RA) hypertrophy may occur with each type of defect, depending on the height of the pulmonary artery pressure. Chest roentgenograms reveal enlargement of the right atrium and right ventricle, dilatation of the pulmonary artery and its branches, and increased pulmonary vascular markings

THIS IS ECHO CRADIOGRAPHIC FINDING OF ASD

This test shows pulmonary arterial and RV dilatation, and anterior systolic (paradoxical) or flat interventricular septal motion if a significant RV volume overload is present. The defect may be visualized directly from subcostal, right parasternal, or apical echocardiographic windows.

THE CAUSE OF CLUBBING IN SIMPLE REASON IS
The cause of clubbing and hypertrophic osteoarthropathy is not known with certainty, but the disorder may reflect platelet clumping and local release of platelet-derived growth factor at the nail bed

HOPE U WILL BE CLEAR NOW
TAKE CARE AND HAVE A GREAT DAY

shabana · Credits: 11520 My Scrapbook

thank you very very very very very very very very very very much my good friend npshades for your clear summarized answer

ratnakar_potla · Credits: 5703 My Scrapbook My Reading List 2 Books

I just wanna say in short:
where ever it is clubbing always occurs secondary to hypoxia.
It may or may not denote breathlessness!!!

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