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Clin mgt GI and Contraceptives > GI and LFTs > Flashcards

GI and LFTs Flashcards

1
Q

what is inculded in LFTs

A

AST(SGOT), ALT(SGPT)

Alkaline Phosphatase

Total Bilirubin

Albumin

Total Protein/Globulins

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2
Q

clinical application and shortcomings of LFTs

A

•Despite being called “Liver function tests”, they do not actually provide any information about the liver’s function

•Clinical Application:

    1. Non-invasive screen for possible liver disease
    1. Can be used to measure treatment efficacy in certain liver diseases
    1. Monitor progression of disease such as viral or alcoholic hepatitis
    1. Reflect severity of liver disease in patients who have cirrhosis, and be used to reflect prognosis (Usually in conjunction with albumin, PT/INR)

•Shortcomings:

    1. Abnormal values could also be from a non-hepatic source
    1. Labs can be normal in advanced liver disease and hepatic cancer
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3
Q

what are the 3 patterns of LFT abnormalities & how are they defined?

A

•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

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4
Q

Diff Dx for hepatoceullar pattern

A

Acet Tox

DILI

Viral Hep A, B, C

ETOH hep

autoimmune Hep

NAFLD

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5
Q

Diff dx for cholestatic pattern

A

conditions where flow of bile from liver is reduced or blocked

choledocholithiasis

biliary obstruction

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6
Q

enzymes that reflect hepatocell vs cholestatic pattern

A

hepatocell - AST, ALT

chole - Alk phos, GGT, 5-nucleotidase

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7
Q

Tests that measure biosynthetic function of the liver

A

Albumin

globulins

coagulation (PT/INR)

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8
Q

define bilirubin and its 2 components

A
  • 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
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9
Q

Lactate dehydrogenase is a marker for ______.

A

hemolysis

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10
Q

elevation in indirect bili could indicate

A

Elevation is rarely due to liver dz -> Requires hemolytic work-up

Isolated elevation is likely due to hemolytic disorders/ genetic conditions

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11
Q

elevation in direct bili could indiczte

A

Elevation almost ALWAYS implies liver or biliary tract dz -> seen in MANY types of liver dz

•Choledocholithiasis

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12
Q

define the transaminases

A

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

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13
Q

define alk phos

A

•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
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14
Q

Transaminase ratio in

Viral hepatitis & NAFLD

VS

Alcoholic liver dz

A

HEP - AST:ALT <1 - ALT MORE elevated than AST

ETOH - AST:ALT >2:1 - AST MORE elevated

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15
Q

Tests that measure biosynthetic function of the liver

A

Serum Albumin

Serum Globulins

PT/INR

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16
Q

define albumin and when it can be normal or LOW

A
  • 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
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17
Q

PT/INR in the setting of abnormal LFTs will help determine

A

if liver is working!

if it is normal then just hepatic inflammation

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18
Q

Choledocholithiasis shows what si/sx & lab values

A

RUQ pain*** radiates to back

jaundice, dark urine

(+) Murphy’s sign

↑direct bili ****

↑ AST/ALT

↑alk phos (slow)

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19
Q

7 and 11 rule in CBD

A

Normal CBD:

  • <7mm w/ GB present
  • <11mm – w/o GB (s/p cholecystectomy)
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20
Q

Imaging and Tx of Choledocholithiasis

A

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)

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21
Q

pt appears to ER w/

Nausea/vomiting

Abdominal pain

LABS: AST:ALT ratio of 2:1

Dx?? & Tx???

A

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

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22
Q

AST to ALT ratio is less then 1

RUQ US – increased echogenicity consistent with hepatic steatosis

DX??

A

NAFLD

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23
Q

Si/sx & tx of NAFLD

A

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

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24
Q

RUQ US – increased echogenicity consistent with hepatic steatosis

dx?

A

NAFLD

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25
RUQ US & CT show dilated ducts, Dx?
Choledocholithiasis
26
RUQ US: hepatomegaly dx?
Hepatitis
27
Labs in Hep C
AST/ALT - normal - elevated Tbili - mildly elevated Alk Phos - normal
28
alk phos in NAFLD is \_\_\_\_
normal
29
elevated indirect bili in the setting of normal LFT dx?
Gilbert Syndrome
30
Tx of Hep C ## Footnote 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
31
Upper GI vs Lower GI Bleeds are defined as:
_Upper_: Defines as bleeding derived from a source PROXIMAL to the Ligament of Treitz
32
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
33
Factors influencing outcome of upper GI Bleeds
CV compromise Age \>65 Co-existing cardio-respiratory dz HgB \<10 Hematemesis & melena
34
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_
35
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%)
36
common causes of lower GI Bleeds
Diverticular Bleeding Angioectasias(AVM) Hemorrhoids IBD Neoplasm Post-polypectomy Ischemic Colitis/ Infectious Colitis
37
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
38
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
39
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_)
40
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
41
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
42
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 la**bs
43
what is The Modified Rumack-Matthew Treatment Nomogram
•Looks at acetaminophen concentration vs time post ingestion and tells you whether that person requires tx
44
tx of acetameophen tox tx indications?
**N-acetylcysteine(NAC)** * \<8 hrs from time of ingestion * Tx before onset of liver injury (↑ALT) _Tx indications:_ 1. Serum acetatophen drawn 4 hrs or more is w/in tx line 2. Single ingestion of at least 7.5g 3. Unknown time of ingestion and serum acetaminophen concentration \>10mcg/mL 4. Any evidence of hepatotoxicity 5. Delayed presentation (\>24 hours after ingestion) with lab evidence of hepatotoxicity and history of acetaminophen ingestion
45
define Ascites
Pathological accumulation of fluid (usually protein-containing) in the peritoneal cavity Most common complication of cirrhosis – is a result of portal HTN
46
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
47
Any new case of ascites requires:
* Abdominal US * Dx Paracentesis * Ascitic Fluid Analysis * Calculate SAAG -(albumin inn ascites – albumin in serum)
48
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
49
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**
50
in ascites ## Footnote 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
51
tx of ascites
Tx underlying cause **Diuretics: spironolactone & furosemide** •Aldosterone antag more effective then loop diuretics
52
Spontaneous Bacterial Peritonitis most common pathogens:
•E. coli streptococcal spp. K. pneumoniae
53
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
54
Tx of Spontaneous Bacterial Peritonitis
Cefotaxime or ceftriaxone _Alt: cipro_ •AVOID: quinolones in pts on SBP prophylaxis
55
drugs that can cause drug induced liver toxicity
Abx psychiatric/seizure meds diabetes cardiac meds misc
56
Transaminitis start to show in Acetaminophen Toxicity how long after ingestion??
•Transaminitis may be seen at 8-12 hours after ingestion
57
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,
58
when do LFT abnormalities peak in Acetaminophen Toxicity
Stage 3 (72-96 hours) ## Footnote LFT abnormalities peak, jaundice, confusion(hepatic encephalopathy), marked transaminitis, coagulopathy, lactic acidosis (DEATH)
59
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
60
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
61
What diagnostic imaging tool doubles as a therapeutic intervention in a patient with a biliary obstruction?
ERCP
62
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
63
What are the 2 categories of non-alcoholic fatty liver disease?
Non-alcoholic fatty liver & non-alcoholic steatohepatitis
64
What is the diagnostic imaging of choice for assessing biliary obstruction?
Magnetic resonance cholangiopancreatography (MRSP)
65
What is a common complication of NAFLD?
Crytogenic cirrhosis
66
What is the most common cause of an upper GI bleed?
Peptic ulcer disease
67
What are the most common causes of peptic ulcers?
NSAIDs and H. pylori
68
Recall risk factors for a poor prognosis a/w upper GI bleed.
1. CV compromise/hemodynamic instability 2. \>65 yo 3. Comorbid cardio-respiratory disease 4. Hgb \<10 5. Hematemesis 5. Melena
69
What is the first line treatment for esophageal varices bleeding?
Endoscopic variceal ligation (banding)
70
Why is endoscopic variceal ligation (banding) preferred to other forms of treatment for variceal bleeding?
Significantly reduces the risk of rebleeds, death, & stricture formation
71
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)
72
Recall complications a/w the esophageal balloon technique.
1. Rebleeding 2. Esophageal rupture 3. Necrosis
73
What are the indications for a TIPS procedure?
1. Refractory variceal bleeding 2. Refractory ascites 3. Budd-chiari 4. Hepatorenal syndrome
74
Recall contraindications for a TIPS procedure.
1. CHF 2. Severe tricuspid regurg 3. Severe pulmonary HTN 4. Hepatic cysts 5. Sepsis 6. Biliary obstruction
75
Describe risk factors for UGI Bleeding
i. Previous bleeds ii. Anticoagulants/NSAIDs iii. Glucocorticoids iv. Liver disease v. Severe vomiting vi. Aortic surgery
76
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)
77
Describe the management of a patient w/ an upper GI bleed.
1. ABCs 2. Fluid resusitation 3. IV pantoprazole 4. Consult GI & admit to ICU 5. Serial H&H x6 hours
78
Describe the management of a patient w/ an acute esophageal variceal bleed.
1. ABCs 2. Fluid resusitation 3. IV octreotide 4. Abx prophylaxis 5. +/- thiamine 6. Consult GI for urgent endoscopic intervention
79
What is the most common cause of lower GI bleeds?
Diverticulosis
80
What are the indications for a blood transfusion in a bleeding patient?
Hgb \<7 Crit \< 21%
81
Recall predictors for a severe LGI bleed.
1. HR \>100 2. SBP \<105 3. Syncope 4. Non-tender abdominal exam 5. Bleeding during 1st 4 hours of eval 6. ASA 7. \>3 active comorbidities
82
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
83
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
84
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
85
What is the most common complication of liver cirrhosis?
Ascites
86
What serum-albumin ascites gradient level is indicative of portal HTN?
\>1.1
87
What is a concerning and common complication of ascites?
Spontaneous bacterial peritonitis

Clin mgt GI and Contraceptives (3 decks)

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