Dear friends and colleagues, Passing the MRCP UK is an important step in the medical career. PACES is the practical clinical exam and require a wide breadth of knowledge. This blog is a space to share materials, information and knowledge and I hope you find it useful. Am open for any ideas or suggestion and would value your contributions and comments. please visit my related pages on facebook and youtube. Best wishes, Dr Elmuhtady Said
PACES Stations
- General
- PACES station 1 abdomen
- PACES station 1 respiratory
- PACES station 2 history taking skills
- PACES station 3 cardiovascular
- PACES station 3 neurology
- PACES station 4 communication skill and ethics
- PACES station 5 (new station 5)
- PACES station 5 endocrinology
- PACES station 5 Fundus
- PACES station 5 rheumatology
- PACES station 5 skin
- record of PACES experience
Tuesday, 3 June 2008
ascites
exam question:
middle age male unwell with nausea and vomiting and abdominal distension,juandiced,ecchymoses,hepatosplenomegaly with ascites.had a urinary catheter.
asked to give various defferentials.
asked about investigation and management of ascites.
ascites is the pathological presence of fluid within the peritoneal cavity.
common causes:
1-liver cirrhosis with portal hypertension
2-malignacy
3-congestive cardiac failure
investigatons:
ascetic tab and send fluid for:
biochemstry
cytology
cell count,culture and gm stain
use the protein level to defferentiate between exudate and transudate.
exudate has protein content of 25g/L
serum-ascites albumin gradient correlate directly with the portal press.
SAAG gradient>11g/L indicate portal hypertension with transudate
SAAG gradeint<11g/L indicate exudate
lines of management:
1-bed rest ?of little value
2-soduim restriction
3-water restriction
4-diuretcs therapy
5-paracentesis
6-shunt
what are the complications of ascites?
what is the pathophysiology of ascites?
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PACES station 1 abdomen
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The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Three theories of ascites formation have been proposed:
ReplyDelete1-The underfilling theory: suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.
2-The overflow theory:
suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia.
3-the vasodilation theory:
is The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. According to the vasodilation theory, the underfilling theory is proposed to be operative early and the overflow theory is proposed to be operative late in the natural history of cirrhosis.
source:emedicine
complications of ascites:
ReplyDelete1-paraumblical hernia
2-hepatorenal syndrome
3-respiratory defficulties
4-hypercatabolic state
5-SBP
if you got ascites in your abdomen station ,it is a gift.observe the following:
ReplyDelete-the most likely cause is chronic liver disease.confirm that by looking for the prepheral stigmata.
-ascites is a sign of decompansation.is there any more markers of that?
-make sure your demonstrated shifting dullness when examining for the ascites.
-check for sacral odema and swallown ankles.
-now you need to present confidently...
try this one:
ReplyDeleteon examination of this patient,he has features of decompansated chronic liver disease with cirrohsis,portal hypertension and asites.there is no evidance of enchalopathy.
I would to investgate him to condirm cirrohsis and its aetiology,the severity of the CLD (child-pugh score)and the precipitanat factor for his decompansation.
can you suggest any other way for presentation?
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