Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
|
What is Ascites (simply defined)? What is the most common cause of ascites?
What are other etiologies of ascites? |
Fluid filling in the peritoneal cavity (remember- peritoneal cavity is a potential space). CIRRHOSIS = most common cause of ascites.
Other Etiologies- 1. Other causes portal hypertension (ex: hepatic vein outflow obstruction) 2. R sided CHF 3. Constrictive pericarditis 4. peritoneal cancers, TB, infections, etc. |
|
|
What factors promote ascites formation?
|
- ↑ capillary hydrostatic pressure (ex: portal HTN)
- ↓ plasma oncotic pressure (↓ albumin, more albumin in third space) - ↑ capillary permeability (cytokines, endotoxins) - lymphatic obstruction/ ↓ fluid resorption - Peritoneal disease (cancer, infection, etc.) --> affects reabsorption capability of peritoneum |
|
|
What is the Underfill theory of ascites?
Describe the Overflow theory of ascites? |
UNDERFILL : Portal hypertension, causes increased hydrostatic pressure and loss of fluid from vascular space --> transient ↓ blood volume --> RAA activated and ↑ fluid retention.
OVERFLOW: Initial problem is excess Na retention (possibly from splenic vasodilation) --> leads to increase in ECF volume & ascites--> transient intravascular volume depletion--> more RAA activation & ↑ fluid retention |
|
|
What is the vasodilation theory of how ascites forms?
|
Increased presence of NO (vasodilator) --> causes splanchnic vasodilation --> kidneys sense this as underfilling and activate RAA --> ↑ fluid retention
|
|
|
What is the importance of the SAAG score and how does it get determined?
|
SAAG= Serum-ascites albumin gradient = Serum albumin - ascites albumin (take paracentesis sample)
If >1.1 g/dl = Portal HTN (because the fluid is more transudative and thus differs in protein content from serum)- ex: cardiac, cirrhosis, hepatic failure, liver mets, portal vein thrombosis If <1.1 g/dl= Non-portal HTN cause (since fluid more exudative, weeping, oozing) --> ex: peritoneal carcinomatosis, TB peritonitis, nephrotic syndrome, biliary leak |
|
|
What are the four stages of progression of portal hypertensive ascites development (hint: start from portal HTN).
What is the initial treatment of choice for stage 2? stage 3? |
1. Portal HTN (no ascites) --> 2. Uncomplicated ascites --> 3. Refractory ascites --> 4. HRS (hepatorenal syndrome)
Stage 1--> consider salt restriction (no specific therapy) Stage 2--> salt restrict and diuretics Stage 3--> Large volume paracentesis + albumin, TIPS and PVS (to ↓ sinusoidal pressure) |
|
|
How do you check if an ascitic patient has been compliant with their sodium restriction?
What is the function of diuretics in ascites? What diuretics would you use? |
24 hr urinary sodium (if Na excretion high --> not compliant, eating too much salt. If Na excretion low --> start diuretics to help them rid water).
Diuretics- aldosterone antagonist (amiloride), Loops (furosemide). They will deplete intravascular volume, hope is that body will compensate by reabsorbing some ascites fluid. (bbut can lead to renal HTN if excessive diuresis) |
|
|
How do you prevent activation of the RAA system when you perform large volume paracentesis in a person with diuretic-resistant/intractable ascites?
|
Give albumin simultaneously! This will cause water retention and not deplete intravascular volume too much.
|
|
|
Ascites:
A. Is always a result of portal HTN B. Can occur with normal portal pressures C. May be a result of excess fluid in the intracellular space D. Is always associated with renal Na retention |
B. Can occur with normal portal pressures
(for instance, any cause of Non-portal HTN ascites like peritoneal cancer, TB infection, nephrotic syndrome, protein loss ,etc.) |
|
|
Non-portal HTN ascites
A. Is caused by high hydrostatic forces B. Is associated with high SAAG C. May be caused by inflammatory disease of the peritoneum D. Is treated the same way as portal HTN forms of ascites |
C. May be caused by inflammatory diseases of the peritoneum
Remember, it is usually caused by low oncotic activity (not hydrostatic pressure), It is associated with a LOW SAAG <1.1, and to treat it, you get rid of the underlying disease process (TB, neoplasm, etc.) |
|
|
What is SBP? How do you evaluate a patient with Ascites who developed SBP?
Would your management change if they were non-neutrocytic vs. neutrocytic? |
Spontaneous Bacterial Peritonitis (occurs without trauma or precipitating event. Typically do blood cultures at the bedside, by drawing up ascitic fluid)
- non-neutrocytic = don't rush to treat - neutrocytic = treatment is indicated |
|
|
What antibiotics would be appropriate to treat SBP?
What would it mean if you cultured >1 pathogen from the peritoneal fluid? |
Anything that kills gram negative enterics (typically 3rd generation cephalosporin, augmentin, cipro)
If >1 pathogen is cultured --> this is a Secondary bacterial peritonitis (i.e. pt must have perforated, had infection, etc.) |
|
|
Type I vs. Type II Hepatorenal syndrome
|
Type I = occurs in advanced liver disease, sudden onset (grim prognosis)
Type II = occurs with preserved liver function, insidious onset (slow progression) |
|
|
In a nutshell, what is HRS (Hepatorenal syndrome)?
What is the BEST pharmacologic treatment for it? |
HRS = excessive renal vasoconstriction (as a result of splanchnic vasodilation and kidneys perceiving ↓ EABV), in the setting of cirrhosis but NO ACTUAL KIDNEY PROBLEM (no blood, no proteinuria, no infection).
Midodrine (selective a1 stimulator, vasoconstricts splanchnic vessels) + Octreotide (somatostatin inhibitor, inhibits release of endogenous vasodilators). Give with Albumin to expand plasma volume. |
|
|
How do you distinguish HRS from Pre-renal azotemia (both present with ↓ GFR, ↑ Cr, and Na avidity)?
What medications would you want to rule out when considering if a patient has Hepatorenal syndrome? |
With HRS, there is no improvement with volume expansion.
Vasodilators (like ACEi or ARBs- that might cause worsening sxs), or Vasoconstrictors (NSAIDs, and aminoglycosides, that might clamp down afferent arteriole). |
|
|
HRS...
A. Is associated with glomerular injury B. Is easily treated C. Is not related to the pathogenesis of ascites D. Is associated with marked renal vasoconstriction |
D. Is associated with marked renal vasoconstriction
It is difficult to treat and is linked to pathogenesis of ascites (from the increased RAA due to decreased perceived EABV) |
|
|
Treatment of Hepatorenal Syndrome involves...
A. Systemic vasodilation B. Albumin to increase plasma oncotic pressure C. Renal vasodilators D. Renal transplantation |
B. Albumin to increase plasma oncotic pressure
(This will help increase EABV and help the kidney's relax. Albumin is essentially a plasma volume expander). Remember- vasodilators do not help (they might even perpetuate the problem) |
|
|
Definitions- Platypnea and Orthodeoxia.
What condition are these found in? |
Platypnea - dyspnea when standing (from increased shunting at base of lungs)
Orthodeoxia- O2 sat decreases when standing (relieved when lie down). *both are seen in Hepatopulmonary syndrome (seen in chronic liver disease, <PaO2 without any cardiopulm conditoins). |
|
|
How do you diagnose Hepatopulmonary syndrome?
|
Bubble echocardiogram ( because there are shunts in pulmonary system- from vessel vasodilation-- the bubbles don't get cleared by lungs and cross to the left side and you see it in LA).
|
|
|
What is the etiology of Hepatic encephalopathy?
What are characteristic clinical findings in these patients? |
Thought to do with liver failure and inability to detoxify toxic metabolites (like NH3 and mercaptans). NH3 is produced by bacteria and absorbed in the colon.
Mild confusion --> tremor/poor coordination --> asterixes (liver flap) --> hyperreflexia and UMN lesions |
|
|
What is thought to be the etiology of neuromuscular decline in these patients?
What about the poor coordination and tremor? |
Ammonia can cause depleted glutamate stores (because it is converted to glutamine by ammonia, leading to decreased exciation).
It can also elevate GABA stores (inhibitory NT). This causes failure at the post-synaptic membrane --> asterixes. Extra-pyramidal signs have to do with deposition of NH3 in basal ganglia. |
|
|
What is the treatment for Hepatic encephalopathy?
In what patients would you consider a liver transplant? In what patients is it absolutely contraindicated? |
Treatment = lactulose (protonates NH3 to NH4 so it can't be absorbed), and neomycin (kills bacteria). Also restrict protein intake and maybe consider transplantation.
Transplant- acute liver failure, localized intrahepatic cancer, metabolic liver disease, cirrhosis w/ complication. If MELD is >17 --> more survival advantage! CONTRAINDICATION- active infection, metastatic liver disease, ongoing substance/EtOH abuse, comorbidity like CHF, COPD, Cholangiocarcinoma (doesn't seem to be fixed) |
