GI and LFTs Flashcards
what is inculded in LFTs
AST(SGOT), ALT(SGPT)
Alkaline Phosphatase
Total Bilirubin
Albumin
Total Protein/Globulins
clinical application and shortcomings of LFTs
•Despite being called “Liver function tests”, they do not actually provide any information about the liver’s function
•Clinical Application:
- Non-invasive screen for possible liver disease
- Can be used to measure treatment efficacy in certain liver diseases
- Monitor progression of disease such as viral or alcoholic hepatitis
- Reflect severity of liver disease in patients who have cirrhosis, and be used to reflect prognosis (Usually in conjunction with albumin, PT/INR)
•Shortcomings:
- Abnormal values could also be from a non-hepatic source
- Labs can be normal in advanced liver disease and hepatic cancer
what are the 3 patterns of LFT abnormalities & how are they defined?
•1. Hepatocellular pattern: Disproportionate elevation in the transaminases (AST/ALT) compared with the alkaline phosphatase
•Serum bilirubin may be elevated
•2. Cholestatic pattern: Disproportionate elevation in the alkaline phosphatase compared with the transaminases (AST/ALT)
•Bilirubin may be elevated
•3. Isolated hyperbilirubinemia: Elevate bilirubin with normal transaminases and alkaline phosphatase
•Synthetic liver tests can be normal or abnormal in any of these
Diff Dx for hepatoceullar pattern
Acet Tox
DILI
Viral Hep A, B, C
ETOH hep
autoimmune Hep
NAFLD
Diff dx for cholestatic pattern
conditions where flow of bile from liver is reduced or blocked
choledocholithiasis
biliary obstruction
enzymes that reflect hepatocell vs cholestatic pattern
hepatocell - AST, ALT
chole - Alk phos, GGT, 5-nucleotidase
Tests that measure biosynthetic function of the liver
Albumin
globulins
coagulation (PT/INR)
define bilirubin and its 2 components
- a breakdown of the porphyrin ring of of heme-containing proteins
- Unconjugated – (indirect bili) fraction is insoluble in water and is bound to albumin in the blood
- Calculated as total-direct
- Conjugated – or direct bilirubin is water-soluble and can be excreted by the kidney
Lactate dehydrogenase is a marker for ______.
hemolysis
elevation in indirect bili could indicate
Elevation is rarely due to liver dz -> Requires hemolytic work-up
Isolated elevation is likely due to hemolytic disorders/ genetic conditions
elevation in direct bili could indiczte
Elevation almost ALWAYS implies liver or biliary tract dz -> seen in MANY types of liver dz
•Choledocholithiasis
define the transaminases
AST
•Found in liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs leukocytes and erythrocytes in decreasing order of concentration
ALT
•Found primarily in the liver -> more specific indicator of liver injury
define alk phos
•Found in or near bile canicular membrane of hepatocytes
Consists of many isoenzymes found in the liver, bone, placenta and less commonly in the small intestines
- Enzyme present in cells that join to form bile ducts
- Also found in bone, as well as other tissues – can be fractionated
- If elevated & it is the only elevated finding try and figure out source of excess isoenzymes -> measure GGT & 5-nuceotidase as they are rarely elevated in conditions other then liver disease
Transaminase ratio in
Viral hepatitis & NAFLD
VS
Alcoholic liver dz
HEP - AST:ALT <1 - ALT MORE elevated than AST
ETOH - AST:ALT >2:1 - AST MORE elevated
Tests that measure biosynthetic function of the liver
Serum Albumin
Serum Globulins
PT/INR
define albumin and when it can be normal or LOW
- Synthesized exclusively by hepatocytes -> long half-lives with a slow turnover
- Not great markers of liver injury due to to their long half-life and slow turnover times -> LATE finding
- NORMAL -> hepatitis, drug-related hepatoxicity and obstructive jaundice
- Changes are seen in acute liver conditions -> _abnormally low in chronic liver d_z
PT/INR in the setting of abnormal LFTs will help determine
if liver is working!
if it is normal then just hepatic inflammation
Choledocholithiasis shows what si/sx & lab values
RUQ pain*** radiates to back
jaundice, dark urine
(+) Murphy’s sign
↑direct bili ****
↑ AST/ALT
↑alk phos (slow)
7 and 11 rule in CBD
Normal CBD:
- <7mm w/ GB present
- <11mm – w/o GB (s/p cholecystectomy)
Imaging and Tx of Choledocholithiasis
RUQ US & CT show dilated ducts,
MRCP – Best non-invasive test*
ERCP – need to weigh the benefit/risks
Endoscopic ultrasound
Intra-operative cholangiogram at the time of CCY
TX:
ECRP to remove stone
THEN contact surgery to remove gallbladder (Cholecystectomy)
pt appears to ER w/
Nausea/vomiting
Abdominal pain
LABS: AST:ALT ratio of 2:1
Dx?? & Tx???
Acute ETOH Hepatitis
ETOH Withdrawal treatment/ CIWA protocol-> Phenobarbital & Lorazepam
IV fluids-> Include MV, thiamine and folate – Wernicke’s Encephalopathy coverage
Calculate Maddrey’s Discriminant Function
AST to ALT ratio is less then 1
RUQ US – increased echogenicity consistent with hepatic steatosis
DX??
NAFLD
Si/sx & tx of NAFLD
Jaundice
↑transaminases
Usually obese, HTN, T2D
Abstain from alcohol
Optimize glucose control, HTN management and cholesterol therapy
Weight loss of 1-2lbs per week , Nutritionist referral
Check LFT’s after 3 and 6 months to monitor for improvement
If no improvement, consider: Bariatric surgery
RUQ US – increased echogenicity consistent with hepatic steatosis
dx?
NAFLD
RUQ US & CT show dilated ducts,
Dx?
Choledocholithiasis
RUQ US: hepatomegaly
dx?
Hepatitis
Labs in Hep C
AST/ALT - normal - elevated
Tbili - mildly elevated
Alk Phos - normal
alk phos in NAFLD is ____
normal
elevated indirect bili in the setting of normal LFT
dx?
Gilbert Syndrome
Tx of Hep C
w/o cirrhosis
w cirrhosis
w/o cirrhosis
- Glecaprevir/pibrentasvir
- Sofosbuvir / velpatasvir
w/ cirrhosis
•Genotype 1-6: Glecaprevir / pibrentasvir
• Genotype 1, 2, 4, 5, or 6 Sofosbuvir/ velpatasvir
Upper GI vs Lower GI Bleeds are defined as:
Upper: Defines as bleeding derived from a source PROXIMAL to the Ligament of Treitz
Si/Sx of Upper GI Bleeds
Hematemesis “coffee-ground”
Melena – black tarry stool heme (+)
Hematochezia – dark red blood in stool
Hemodynamic instability(Hypotensive, tachycardia, orthostatic)
Hgb <10
Factors influencing outcome of upper GI Bleeds
CV compromise
Age >65
Co-existing cardio-respiratory dz
HgB <10
Hematemesis & melena
tx of upper GI Bleeds
Stabilize ABCs
Fluid resuscitation
Type and screen – transfuse 2 units
FFP
PLTs <50k and actively bleeding
Start on PPI – protonix (pantroprozole)
- omeprazole, esomeprazole, lansoprazole, pantoprazole
- PPIs are recommended for ALL patients with peptic ulcer bleeding
No H2-blockers due to tachyphylaxis
ONCE stable transfer for urgent endoscopy
common causes of upper GI Bleeds
Gastroduodenal Ulcer (20-50%)
Esophagitis, gastritis, duodenitis (~13%)
Angiodysplasia, telangiectasia (5-7%)
Mallory Weiss Tear (~5%)
Variceal Bleed (annual rate of 5-15% in patients with varices)
Tumor (<3%)
common causes of lower GI Bleeds
Diverticular Bleeding
Angioectasias(AVM)
Hemorrhoids
IBD
Neoplasm
Post-polypectomy
Ischemic Colitis/ Infectious Colitis
si/sx of lower Gi bleeds & imaging
Sudden onset rectal bleeding
Bright red blood per rectum
Stool dark brown-black
Tagged RBC Scan
CT angiography – identify bleed -> CI in kidney dz / contrast allergy
Risk Stratification - Predictors of severe LGIB
- HR >100
- SBP <115
- Syncope
- Nontender abdominal exam
- Bleeding during first 4 hrs of eval
- ASA use
- >3 active comorbid conditions
0 Factors = 9% risk
1-3 Factors = 43% risk
4-6 Factors = 84% risk
tx of lower GI Bleeds
Stabilize ABCs
Serial crit/hgb q 6 hrs
Check INR – stop anticoags??
Prep for colonoscopy – likely w/in 24hrs
Angiography (w/ transcatheter embolization)
tx of Acute Variceal Bleed
Combo of medication & endoscopic intervention
Stabilize ABCs
Abx prophylaxis: Ceftriaxone
Start IV Octreotide – reduce mortality
•reduces splanchnic blood flow and portal blood pressures – assoc w bleeding due to portal HTN
Urgent endoscopy
- Endoscopic variceal ligation – most common
- Endoscopic sclerotherapy
- Balloon tamponade
- TIPS – definitive therapy to refractory variceal bleeding, definitive Tx
discuss stages of acetametophen toxicity
Stage 1 (30min – 24 hrs) - anorexia, nausea, pallor, vomiting, diaphoresis, and malaise, though some may be asymptomatic
•Transaminitis may be seen at 8-12 hours after ingestion
Stage 2 (24-72 hrs) - “Paradox” - symptomatic improving and patient may appear to be improving clinically, but lab evidence of hepatotoxicity (and nephrotoxicity) become apparent,
- Significantly elevated transaminases, Prothrombin may be prolonged, Renal function may be deteriorating
- Patients then develop RUQ pain, hepatomegaly
Stage 3 (72-96 hours) - LFT abnormalities peak, jaundice, confusion(hepatic encephalopathy), marked transaminitis, coagulopathy, lactic acidosis (DEATH)
Stage 4 (4 days – 2 wks) – Patients who survive enter a recovery phase
protocol for drawing serum acetametophen
hepatotoxicity is best predicted by relating the time of ingestion to the serum acetaminophen concentration
•Drawn 4 hours post ingestion
•If timing unknown observe for 4hrs and then draw labs
what is The Modified Rumack-Matthew Treatment Nomogram
•Looks at acetaminophen concentration vs time post ingestion and tells you whether that person requires tx
tx of acetameophen tox
tx indications?
N-acetylcysteine(NAC)
- <8 hrs from time of ingestion
- Tx before onset of liver injury (↑ALT)
Tx indications:
- Serum acetatophen drawn 4 hrs or more is w/in tx line
- Single ingestion of at least 7.5g
- Unknown time of ingestion and serum acetaminophen concentration >10mcg/mL
- Any evidence of hepatotoxicity
- Delayed presentation (>24 hours after ingestion) with lab evidence of hepatotoxicity and history of acetaminophen ingestion
define Ascites
Pathological accumulation of fluid (usually protein-containing) in the peritoneal cavity
Most common complication of cirrhosis – is a result of portal HTN
si/sx of Ascites
Distended abdomen with shifting dullness
mild TTP diffusely
LE edema
Flank dullness
Shifting dullness- more specific but less sensitive
Fluid thrill or wave – tense ascites
Any new case of ascites requires:
- Abdominal US
- Dx Paracentesis
- Ascitic Fluid Analysis
- Calculate SAAG -(albumin inn ascites – albumin in serum)
SAAG helps determine ____??
calculated???
- SAAG >1.1 = ________
- SAAG <1 = _____, ___, ______
SAAG – (albumin inn ascites – albumin in serum)
- Helps determine cause of ascites
- SAAG >1.1 = portal HTN
- SAAG <1 = cancer, TB, malignancy
Ascites should always be ______???
this analysis should ALWAYS include?
Ascites should always be “tapped” and sent for fluid analysis! Need to rule out infections and malignancy
•Total protein
Protein <2.5 assoc w/ portal HTN & hypoalbuminemia
Protein >2.5 assoc w/ TB, malignancies, pancreatitis
•Albumin
•Cell count and diff
in ascites
Protein <2.5 assoc w/ ____ ____ & ______
Protein >2.5 assoc w/ T___, _____, _____
Protein <2.5 assoc w/ portal HTN & hypoalbuminemia
Protein >2.5 assoc w/ TB, malignancies, pancreatitis
tx of ascites
Tx underlying cause
Diuretics: spironolactone & furosemide
•Aldosterone antag more effective then loop diuretics
Spontaneous Bacterial Peritonitis most common pathogens:
•E. coli
streptococcal spp.
K. pneumoniae
Dx of Spontaneous Bacterial Peritonitis
- Ascites PMN count >250 , culture can be (-)
- Fluid cell count <250, but cultures indicate early SBP
- Pt known to have cirrhosis/ascites present w/ abdominal pain or AMS
Tx of Spontaneous Bacterial Peritonitis
Cefotaxime or ceftriaxone
Alt: cipro
•AVOID: quinolones in pts on SBP prophylaxis
drugs that can cause drug induced liver toxicity
Abx
psychiatric/seizure meds
diabetes
cardiac meds
misc
Transaminitis start to show in Acetaminophen Toxicity how long after ingestion??
•Transaminitis may be seen at 8-12 hours after ingestion
when do paradox sx occur in Acetaminophen Toxicity
Stage 2 (24-72 hrs)
“Paradox” - symptomatic improving and patient may appear to be improving clinically, but lab evidence of hepatotoxicity (and nephrotoxicity) become apparent,
when do LFT abnormalities peak in Acetaminophen Toxicity
Stage 3 (72-96 hours)
LFT abnormalities peak, jaundice, confusion(hepatic encephalopathy), marked transaminitis, coagulopathy, lactic acidosis (DEATH)
cetaminophen Toxicity cause liver damage at what doses?
Potential Liver damage
- Adults >150mg/kg in acute dose
- Adults 7.5grams in 24 hrs
- Children >200mg/kg
patterns of LFTs in common conditions:
AST, ALT, TBili, Alk Phos
ETOH liver dz
NAFLD
viral hep A or B
Hep C
Biliary Obstruction
DILI
Gilbert Syndrome
What diagnostic imaging tool doubles as a therapeutic intervention in a patient with a biliary obstruction?
ERCP
Recall drugs that would be pertinent in the management of patient with acute ETOH hepatitis and why.
Phenobarbital +/- lorazepam to reduce risk of delirium tremens
IV thiamine to cover for wernickes encephalopathy
Anti-emetics
Closely monitoring LFTs for improvement
Psychiatric/social services consult for substance abuse
What are the 2 categories of non-alcoholic fatty liver disease?
Non-alcoholic fatty liver & non-alcoholic steatohepatitis
What is the diagnostic imaging of choice for assessing biliary obstruction?
Magnetic resonance cholangiopancreatography (MRSP)
What is a common complication of NAFLD?
Crytogenic cirrhosis
What is the most common cause of an upper GI bleed?
Peptic ulcer disease
What are the most common causes of peptic ulcers?
NSAIDs and H. pylori
Recall risk factors for a poor prognosis a/w upper GI bleed.
- CV compromise/hemodynamic instability
- >65 yo
- Comorbid cardio-respiratory disease
- Hgb <10
- Hematemesis
- Melena
What is the first line treatment for esophageal varices bleeding?
Endoscopic variceal ligation (banding)
Why is endoscopic variceal ligation (banding) preferred to other forms of treatment for variceal bleeding?
Significantly reduces the risk of rebleeds, death, & stricture formation
What is the indication for an esophageal ballon?
Tamponade bleeding if endoscopic intervention fails and you need to buy time to figure out what to do next (temporizing measure, not a definitive tx)
Recall complications a/w the esophageal balloon technique.
- Rebleeding
- Esophageal rupture
- Necrosis
What are the indications for a TIPS procedure?
- Refractory variceal bleeding
- Refractory ascites
- Budd-chiari
- Hepatorenal syndrome
Recall contraindications for a TIPS procedure.
- CHF
- Severe tricuspid regurg
- Severe pulmonary HTN
- Hepatic cysts
- Sepsis
- Biliary obstruction
Describe risk factors for UGI Bleeding
i. Previous bleeds
ii. Anticoagulants/NSAIDs
iii. Glucocorticoids
iv. Liver disease
v. Severe vomiting
vi. Aortic surgery
What labs would be indicated on patient with an UGI bleed concern?
i. CBC
ii. BMP
iii. LFT’s
iv. Type & screen (blood transfusions may be indicated)
Describe the management of a patient w/ an upper GI bleed.
- ABCs
- Fluid resusitation
- IV pantoprazole
- Consult GI & admit to ICU
- Serial H&H x6 hours
Describe the management of a patient w/ an acute esophageal variceal bleed.
- ABCs
- Fluid resusitation
- IV octreotide
- Abx prophylaxis
- +/- thiamine
- Consult GI for urgent endoscopic intervention
What is the most common cause of lower GI bleeds?
Diverticulosis
What are the indications for a blood transfusion in a bleeding patient?
Hgb <7
Crit < 21%
Recall predictors for a severe LGI bleed.
- HR >100
- SBP <105
- Syncope
- Non-tender abdominal exam
- Bleeding during 1st 4 hours of eval
- ASA
- >3 active comorbidities
Discuss the management of a patient with a lower GI bleed.
. Admit to hospital (consider ICU admission)
ii. Stabilize patient
1. ABC’s
2. IV fluid +/- blood transfusion
3. Serial crit x6 hours
4. Consult GI (prep for colonoscopy)
5. Stop Warfarin (if applicable)
6. Reassess INR if blood products or antidote administered
iii. Tagged RBC scan &/or CT angiography +/- transcatheter embolization
Why would CT angiography be the preferred method for diagnosing a LGIB?
It is super selective and therefore has decreased risk of ischemia and increased hemostasis
Recall pathophysiology of hepatic injury from acetaminophen overdose
NAPQI accumulates in the liver when glutathione stores are deleted in the presence of high acetaminophen levels
What is the most common complication of liver cirrhosis?
Ascites
What serum-albumin ascites gradient level is indicative of portal HTN?
>1.1
What is a concerning and common complication of ascites?
Spontaneous bacterial peritonitis
