GI lecture 5 Flashcards
(96 cards)
1
Q
Metabolic Associated fatty liver disease (MAFLD):
What is the pathogenesis (which is uncertain)?
A
1) Insulin resistance is key mechanism
2) Gut dysbiosis & genetics play major role
2
Q
Metabolic Associated fatty liver disease (MAFLD):
1) How common is it?
2) What are 3 risk factors?
3) List 3 groups that are at an increased risk
4) What are 3 protective factors?
A
1) 20-45% US population (includes adolescents & young adults)
2) Obesity, diabetes, hypertriglyceridemia
3) Hispanics, soft drinks, high fat diet
4) Physical activity, strict control of DM, lipids and weight
3
Q
MAFLD:
1) What does it increase risk of?
2) What reduces the risk?
A
1) CV disease
2) Coffee consumption
4
Q
How do you manage MAFLD?
A
1) Abstinence from alcohol
2) Vaccination for hepatitis A & B, pneumococcal, influenza, DTP
3) Weight loss
4) Manage diabetes & insulin resistance-diet, exercise, meds
5) Manage dyslipidemia
5
Q
MAFLD vs alcoholic liver disease: What does the management of both have in common?
A
1) Abstinence from alcohol
2) Manage DM, insulin resistance and dyslipidemia
3) Need Immunizations
6
Q
What are some management differences between MAFLD and alcoholic fatty liver disease?
A
1) MAFLD patients do not typically become unstable or need admitted to the hospital
2) Alcoholic: replace micronutrients, avoid nephrotoxic drugs
-Methylprednisolone x 1 month in alcoholic hepatitis may reduce short-term mortality
7
Q
Methylprednisolone x 1 month in ___________________ may reduce short-term mortality
A
alcoholic hepatitis
8
Q
List the epidemiology for MAFLD and AFLD (alcoholic fatty liver disease)
A
1) MAFLD: Insulin resistant, hyperlipidemia, metabolic syndrome
2) AFLD: Excess alcohol intake; develops in women after shorter duration and with less intake
9
Q
List the pathogenesis for MAFLD and AFLD (alcoholic fatty liver disease)
A
1) MAFLD: Multifactorial but based on excess fatty acid accumulation in the liver
2) AFLD: Alcohol metabolism induces higher levels of fatty acids and FA signal liver cells to compound to glycerol to form triglycerides. TG accumulate.
10
Q
List the management for MAFLD and AFLD (alcoholic fatty liver disease)
A
1) MAFLD: No pharmacologic agents. Improve risk factors.
2) AFLD: Steroids only with severe disease
11
Q
Describe initial screening for hep A, B, and C
A
Most use the acute hepatitis panel:
1) HAV Ab (hepatitis A virus antibody)
2) H Bs Ag (hepatitis B surface antigen)
-H Bc Ab IgM (hepatitis B core antibody IgM)
3) HCV Ab (hepatitis C virus antibody)
12
Q
What are the routes of transmission for Hep A and hep B?
A
1) Hep A: Fecal-oral + shellfish
2) Hep B: Vertical, sexual, blood
13
Q
Hep B:
1) Is there a carrier state?
2) What is the incubation state?
A
1) Yes, common
2) 50-180 days (60-90)
14
Q
What is the one type of hepatitis without chronic infections?
A
Hep A
15
Q
1) What is the incubation period for Hep A?
2) What abt for Hep C?
A
1) 10-50 days (avg 25-30)
2) 40-120 days
16
Q
What does the HBV vaccine protect you against?
A
Hep D
17
Q
What type of hepatitis has no vaccine or Ig prophylaxis?
A
Hep C
18
Q
Describe Hep A
A
1) RNA hepatovirus
2) Incubation period averages 30 days
3) Transmitted by fecal-oral route (person-to-person or ingestion of contaminated food or water) or via raw or undercooked shellfish
-Spread by crowding & poor sanitation
4) Globally 15 million people infected annually
-72% manifest jaundice, 25% require hospitalization, 0.5% die
19
Q
Describe the lab values/ PE findings in Hep A
A
1) Possible cervical lymphadenopathy
2) WBC normal-low, mild proteinuria & bilirubinuria
3) Significant early elevation of ALT & AST, bilirubin & AlkPhos
20
Q
How are Hep C and Hep D spread?
A
Blood
21
Q
What are the Sx of Hep A?
A
1) Abrupt onset of symptoms: malaise, myalgia, arthralgia, URI symptoms, and anorexia
2) RUQ tenderness & mild hepatomegaly found on PE in 85% of patients
3) N/V frequent; C/D possible
4) Low-grade fever common
22
Q
Describe Hep B
A
1) Hepatovirus (dsDNA, core protein, surface coat)
-8 different genotypes (A-J) & 4 major serotypes (subtypes)
2) Incubation period 6 weeks-6 months (avg 12-14wks)
3) Found in most body fluids: saliva, semen & vaginal secretions
23
Q
Hep B: Vertical transmission from _________+ mother; risk of chronic infection in child is ~90%
need vaccine w/in 24 hrs of birth to prevent*
A
HBsAg
24
Q
Describe the epidemiology of Hep B
A
1) HBV accounts for <=1 million deaths worldwide each year from complications of ESLD, including HCC (Hepatocellular Carcinoma)
2) Other risk groups: patients & staff of dialysis centers, medical providers, dental providers, lab & blood bank staff
3) 25% of chronic HBV infections progress to HCC
25
Hep B: Describe the onset and course
1) Abrupt or insidious onset
2) Acute liver failure in <1% with up to 60% mortality
3) Acute symptoms subside over 2-3 weeks with recovery by 16 weeks
26
Describe the features of Hep B
1) Range of presentation from asymptomatic to acute liver failure with death within weeks
2) Clinical features similar to HAV- Anorexia, nausea, jaundice, & RUQ pain-> usually resolves in 1-3 months
27
Describe the following antigens/ antibodies of Hep B:
1) HBsAg
2) Anti-HBs
3) IgM anti-HBc
1) **HBsAg:** first evidence of infection; appears in serum 1-10 weeks after acute exposure; undetectable 4-6 months after clearance; chronic if persisting > 6 months.
2) **Anti-HBs (antibody to HBsAg):** appears after clearance of HBsAg & **with vaccination; most have for life conferring long-term immunity
3) **IgM anti-HBc (IgM antibody to HBcAg):** indicates acute HBV infection
28
Describe the following antigens/ antibodies of Hep B:
1) Anti-HBc
2) HBeAg
1) Anti-HBc (total antibody to HBcAg): indicates prior infection Not from vaccine
2) HBeAg: indicates viral replication and infectivity; persistence >3 months increases likelihood of chronic HBV
29
Describe the following antigens/ antibodies of Hep B:
1) Anti-HBeAg
2) HBV DNA
1) Anti-HBeAg (antibody to HBeAg): indicates seroconversion from positive to negative HBsAg
2) HBV DNA: more sensitive & precise marker of viral replication & infectivity (get qualitative test to determine observation vs treatment)
30
Describe the initial screening of Hep B / how to interpret results
HBsAg & HBcAb:
1) Negative HBsAg & HBcAb = absence of active infection
2) Positive HBsAg & HBcAb = active infection
3) Positive HBsAg & negative HBcAb = recovering from acute infection or presence of chronic infection
31
What should you do once an active Hep B infection is confirmed?
1) Send pt for quantitative HBV DNA, HBeAg, HIV, HAV Ab, HCV Ab, CBC, CMP, PT/INR, U/S liver
2) Provide pt education on precautions to prevent transmission
3) Refer to infectious disease specialist or gastroenterology
4) Caution to avoid EtoH
5) *Vaccinate for HAV*
32
Describe management of Hep B
1) Mainly supportive
2) Measures to prevent infection in exposed contacts
3) **Admission:** coagulopathy, significant jaundice, encephalopathy
4) **Consider admission:** older pts, significant comorbidities, unable to tolerate PO fluids, poor social support system
5) Treatment with antiviral therapy unsettled (<1% risk of fulminant hepatitis, <5% of chronic hepatitis B in adult acquired infections)
33
Chronic Hep B: How do you Tx?
(Just know oral for 12wks)
1) **Entecavir (baraclude):** daily PO 2 hrs before or after meal
2) **Tenofovir:** daily PO (dosage depends on brand)
3) **Interferon** (preferred is peginterferon alpha-2a weekly SC injection, but can not use in cirrhosis)
4) Things to consider for treatment: renal function, ALT (elevated x 3-6 mo) and DNA viral levels ( >20,000 IU/mL (105 copies/mL) and amount of liver fibrosis/cirrhosis
34
Describe Hep C (what it is, transmission, incubation, etc)
1) Single-stranded RNA virus, 6 genotypes
2) Transmission: IV drug use, body piercing, tattoos & hemodialysis, transfusions before 7/92 blood to blood
Low risk of sexual & vertical transmissions
3) Incubation period 6-16 weeks
35
What are some risk factors for Hep C?
1) High risk: transmitted blood to blood, MSM, multiple sexual partners, IVDU
2) Others: incarceration/tattoos, HIV, HBV,
3) LOW: household, accidental needlestick
36
Hep C:
1) How common is it?
2) What are the Sx?
1) 58 million infected worldwide, estimated 2.4 million infected in U.S.
-No longer the most frequent indication for liver transplantation in U.S. due to improved treatments
2) Usually asymptomatic; waxing & waning aminotransferases
-**Most frequent Sx**: fatigue, sleep disturbances, nausea, diarrhea, abdominal pain, anorexia, myalgia, arthralgia, weakness, weight loss
37
List the extrahepatic manifestations of Hep C
1) Hematologic diseases (mixed cryoglobulinemia, lymphoma)
2) *Renal disease (membranoproliferative glomerulonephritis)
3) Autoimmune disorders (thyroiditis)
4) Dermatologic conditions (porphyria cutanea tarda, lichen planus)
5) Diabetes mellitus
38
Hep C: How is active infection diagnosed?
Active infection diagnosed with reactive (+) HCV Ab & detectable HCV RNA
39
Hep C: What is needed to know if a pt has relapsed? Why?
HCV Ab is not protective (does not confer immunity,) however will remain positive after a patient has been treated, therefore in a treated/cured patient, a positive RNA is needed to know if the virus has relapsed, NOT a positive HCV Ab***
40
What should you do once a Hep C infection is confirmed?
1) Send pt for HIV, HAV Ab, HBsAg, HBcAb, CBC, CMP, PT/INR, U/S liver
2) Provide pt education on precautions to prevent transmission
3) Refer to infectious disease specialist or gastroenterology
4) Vaccinate to HAV & HBV
5) Chronic if persisting > 6 months
41
Describe initial screening for Hep C
Step 1) **HCV Ab**
a) Negative HCV Ab = absence of Hep C
b) Positive HCV Ab = active OR past infection NOT life-long immunity
Step 2) **Differentiate active vs past infection with quantitative HCV RNA**
a) Undetectable HCV RNA = past infection
b) Detectable HCV RNA = active infection
42
List 3 issues encountered with management of Hep C
1) Anti-seizure medication (usually contraindicated)
2) PPI therapy
3) Compliance/Follow-up
43
List important notes for primary care providers regarding hep C
1) Patients treated for hepatitis C who achieve SVR (cure) will always have a ***positive HCV Ab even after cure from active infection.
2) Antibody is NOT protective!! Patients cured from hepatitis C can be re-infected!
3) All future screening for hepatitis C in patients who have been previously treated should be performed using ***HCV RNA (qualitative or quantitative).
44
Cirrhosis:
1) What are some common causes in developed countries?
2) What is the survival rate?
1) Chronic viral hepatitis (B & C), alcoholic liver disease, hemochromatosis, metabolic associated steatohepatitis (MASH)
2) Compensated ( >12 yrs) vs decompensated < 2 yrs w/o transplant)
45
Cirrhosis:
1) List some non specific Sx
2) What may you see with Hepatic decompensation?
3) What may you see with Hepatic decompensation on PE?
1) Non-specific: anorexia, weight loss, weakness, fatigue, muscle cramps
2) Signs of UGIB/varices, abdominal distention from ascites, confusion due to HE
3) Splenomegaly, jaundice, spider angiomata, gynecomastia, ascites, digital clubbing, asterixis
46
Cirrhosis:
1) What are the lab abnormalities?
2) What may you see on imaging?
1) Elevated Sr bilirubin, elevated ALT/AST, elevated ALP, prolonged PT/INR, hyponatremia, hypoalbuminemia, thrombocytopenia
2) Liver nodularity, ascites, varices, splenomegaly, hepatic or portal vein thrombosis
47
List what you may see on a cirrhosis pts Hx
1) Fatigue, easy bruisability, lower extremity edema, weight loss (muscle wasting) or gain (ascites), pruritis, increasing abdominal girth, confusion, sleep disturbances
2) Hypogonadism in men (impotence, infertility, loss of sexual drive, testicular atrophy)
48
Asterixis is a sign of what on PE?
Cirrhosis
49
Who should you suspect cirrhosis in?
1) Stigmata of chronic liver disease found on PE
2) Evidence on labs, (isolated thrombocytopenia!) imaging, or direct visualization in surgery
3) Evidence of decompensated cirrhosis (variceal hemorrhage, ascites, SBP-spontaneous bacterial peritonitis, HE-hepatic encephalopathy)
50
Cirrhosis:
1) What imaging should you do? Which is preferred?
2) What is diagnostic? Is it needed?
3) What labs should you get? (5)
1) U/S (preferred initially), CT, elastography
2) Liver biopsy is diagnostic of cirrhosis, but not usually necessary
3) CBC, CMP, hepatitis panel, UA, PT/INR,
51
Cirrhosis:
1) What 2 vaccines should pts get?
2) Who should you refer to? (2 options)
1) HAV & HBV
2) Gastroenterology or hepatology
52
List the major goals of cirrhosis management
1) Slowing or reversing progression of liver disease (ie, cure hep C, alcohol abstinence)
2) Preventing superimposed insults to liver (get vaccinations, avoid hepatotoxins (meds, alcohol)
3) Identify medications for dose adjustments or avoidance
4) Managing symptoms & lab abnormalities (ie, muscle cramps, umbilical hernia, hyponatremia)
5) Preventing, identifying, & treating complications
6) Determining appropriateness & optimal timing for transplantation: complications (MELD score, CP score) refer to GI or hepatology
-Child-Pugh score (A-C) – HE, ascites, t bili, albumin, PT/INR
53
1) What is a MELD score for?
2) What is a Child-Pugh (CP) score for?
1) Tells who w cirrhosis should get a transplant
2) How bad off a pt w. cirrhosis is
54
Cirrhosis complications:
1) How do you manage ascites?
2) What abt esophageal varices?
1) Diuretics & sodium restriction (< 2G/day), paracentesis (therapeutic and/or diagnostic), TIPS
2) Beta blockers, banding, sclerotherapy, TIPS
55
Cirrhosis complications:
1) How do you manage HE (Hepatic encephalopathy)?
2) How do you manage Portal vein thrombosis (PVT)?
1) Lactulose and/or rifaximin (Xifaxan)
2) +/- anticoagulation
56
Cirrhosis complications:
1) How do you deal with ascites?
2) What do you have a high index of suspicion/low threshold early antibiotics for?
1) Diuretics & sodium restriction (< 2G/day), paracentesis (therapeutic and/or diagnostic), TIPS
2) SBP (Spontaneous Bacterial Peritonitis)
57
Cirrhosis complications: What should you do for HCC? How do you screen for this?
Refer to hepatology/liver transplant specialist
Q6mo abd u/s +AFP
58
Non-portal hypertensive cirrhosis complications; Hepatic encephalopathy (HE):
1) What is it?
2) What causes it?
1) A spectrum of potentially reversible neuropsychiatric abnormalities seen in patients with liver dysfunction
2) Build-up of ammonia (NH3)
59
Non-portal hypertensive cirrhosis complications; Hepatic encephalopathy (HE):
1) What is an early sign?
2) What are some advanced neurological features?
3) What should these pts not do?
1) Disturbance in diurnal sleep pattern (insomnia & hypersomnia)
2) Asterixis, hyperactive DTRs
3) Drive or fast
60
How many grades of HE are there?
Grade 1-4
61
Hepatocellular carcinoma (HCC):
1) When is risk increased?
2) Is it asymptomatic?
3) How should you follow it?
4) When should you Dx?
1) Significant increased risk with cirrhosis
2) Frequently asymptomatic early in course
3) Monitored for with q6 mo u/s, AFP
4) Suggestion of diagnosis by elevated (or rising) alpha-fetoprotein (AFP) or by imaging
62
Describe Portal/mesenteric Vein Thrombosis:
1) Can also contribute to development of portal hypertension
2) Likely related to unbalanced hemostasis & slowing of portal flow
3) Nausea, vomiting, diarrhea; >50% with occult blood in stool
4) Fever, abd distention, tenderness, dehydration, hypotension
5) ~15% with hematochezia (could indicate severe ischemia or infarction)
6) May be asymptomatic if chronic
63
Acute (secondary) peritonitis:
1) What is it?
2) What usually causes it?
1) Acute inflammation of the peritoneum
2) Usually due to infection resulting from perforated viscus (usually polymicrobial)
64
Acute (secondary) peritonitis:
1) What are the Sx of the initial injury?
1) How do you detect pneumoperitoneum?
1) Abdominal pain, tenderness, guarding, rigidity, distention, rebound, diminished bowel sounds, free peritoneal air (on imaging)
2) On CT + PO contrast
65
Acute (secondary) peritonitis:
1) What are the signs of systemic infection?
2) What should you always do?
1) Fever, chills or rigors, tachycardia, sweating, tachypnea, restlessness, dehydration, oliguria, disorientation, hypotensive, shock
2) Always consult a surgeon: usually requires surgery to repair leak
66
How do you manage Acute (secondary) peritonitis?
NPO, IVF, broad spectrum antibiotics
Generalized: rapid resuscitation & surgical exploration
67
Ascites complications: Spontaneous Bacterial Peritonitis (SBP)
1) What is it?
2) What is it assoc with?
3) What causes it?
1) Ascitic fluid infection without an evident intra-abdominal surgically treatable source
2) Chronic ascites
3) Cirrhosis (or nephrotic syndrome)
68
Ascites complications: Spontaneous Bacterial Peritonitis (SBP)
How do you Dx this?
1) Paracentesis (positive bacterial culture & absolute PMN ≥ 250 cells/mm3)
2) Aerobic & anaerobic cultures, cell count & differential, gram stain, albumin, protein, glucose, LDH, amylase, bilirubin (if fluid dark orange or brown)
69
Spontaneous Bacterial Peritonitis (SBP):
1) What usually causes it?
2) Which pts have a poor prognosis?
3) What is usually very advanced?
4) How do you Tx?
1) Usually monomicrobial (E. coli)
2) Pts with SBP & cirrhosis
3) Liver disease
4) Antibiotics, paracentesis, liver transplant referral
70
Hepatorenal syndrome (ascites complication)
1) What is it one of several causes of?
2) What is it usually assoc. with?
3) How is it diagnosed? What is the prognosis?
1) AKI in acute or chronic liver disease
2) Portal hypertension of cirrhosis, severe alcoholic hepatitis, or metastatic tumors (also with fulminant hepatic failure of any cause)
3) Diagnosis of exclusion with poor prognosis
71
List 2 aspects of the clinical presentation of Hepatorenal syndrome?
1) Progressive rise in Sr creatinine
2) Often normal urine sediment
72
Ascites complications: Hepatorenal syndrome
1) What will you see on labs?
2) What can precipitate it?
3) Who can it occur in?
1) Minimal proteinuria (< 500 mg/day)
Very low rate of sodium excretion
Oliguria (ie, <500 mL/24 h)(depending on severity)
2) Bacterial infection (ie, SBP) or GI bleeding
3) May occur without precipitants in end-stage liver disease
73
Ascites complications; Hepatorenal syndrome management:
What is the ideal therapy?
Ideal therapy is improvement in liver function via…
1) Recovery from alcoholic hepatitis
2) Treatment of decompensated hepatitis B (antiviral therapy)
3) Recovery from acute hepatic failure
4) Liver transplantation
74
Hepatorenal syndrome management: When improved liver function not possible (short term,) then what do you do?
1) Medical therapy to reverse AKI
ICU admission?
Liver transplant candidate?
2) Failure of medical therapy: dialysis vs TIPS
75
Describe liver transplants
1) Definitive treatment for decompensated cirrhosis
2) Major goal is improved quality of life
3) First liver transplant 1963
Initial 1-year survival 25%
Current 5-year survival 85-90%
4) United Network for Organ Sharing (UNOS)
76
List and describe the 2 scores relevant to liver transplants
1) Model for End-stage Liver Disease (MELD) score
-Range 6-40
-Score of 15 to be listed
2) Childs-Pugh score
77
Fulminant (sudden onset) Hepatic Failure:
1) Define it
2) What is the prognosis?
1) severe acute liver injury with encephalopathy and impaired synthetic function (INR of ≥1.5) in a patient ***without pre-existing liver disease ***
2) Poor prognosis, should be managed in ICU at a transplant center
Monitor for cerebral edema and renal failure
Need good PO nutrition with protein
78
Fulminant (sudden onset) Hepatic Failure
1) Who can recover?
2) Who has a better chance of spontaneous recovery?
1) ~40% will recover spontaneously- depends on stage of encephalopathy.
2) Lower grade of encephalopathy,
10-40 yo
T bili < 18
Often leads to liver transplant
79
Fulminant (sudden onset) Hepatic Failure
1) What is the most common cause in adults?
2) What is the most common cause in the US?
3) What is the most common toxin assoc w/FHF in U.S.?
1) Viral & drug induced hepatitis
2) DILI is most common cause in U.S.
3) Acetaminophen
80
FHF: List the Clinical features (including Sx and labs)
1) Signs of hepatic encephalopathy
2) Jaundice, hepatomegaly, RUQ tenderness
3) Some nonspecific initial symptoms: fatigue/malaise, lethargy, anorexia, nausea + vomiting, RUQ pain, pruritis, jaundice, abdominal distension (ascites)
4) Elevated aminotransferase levels (ALT & AST often > 10X ULN with elev INR)
5) Elevated bilirubin
81
FHF:
1) What imaging?
2) What are the findings of this imaging?
1) U/S with doppler: often study of choice (risk of renal failure with IV contrasted CT)
2) Hepatomegaly, ascites, evidence of malignant infiltration, or evidence of hepatic vein occlusion
-Massively necrotic liver may also appear nodular due to parenchymal collapse
82
PT and VIT K in cirrhosis:
1) Liver disease patients can have complications with both ___________ and ___________.
2) _______________ manufacture almost all numbered coagulation factors as well as proteins involved in inhibiting thrombolysis
1) coagulation and anticoagulation
2) Hepatocytes
83
Describe PT/INR and VIT K in cirrhosis
(one of our objectives)
1) Parenteral vit K is important in evaluating patients with liver disease and prolonged PT/INR because the patient's response to parenteral vit K can help differentiate the cause of the anticoagulopathy.
2) Patients with advanced parenchymal liver disease will not respond to exogenous vit K as the liver is also not manufacturing other proteins/factors needed to reverse the anticoagulopathy.
3) Ex/ a patient with jaundice – whether or not the patient responds to vit K supplementation can help guide your diagnosis of obstructive or synthetic disease as well as the degree of synthetic disease.
84
Jaundice:
1) What is it?
2) What is it secondary to?
3) What does it usually present with?
1) Yellow/orange skin, mucous membranes & sclera due accumulation of bilirubin in tissues
2) Unconjugated (indirect) or conjugated (direct) hyperbilirubinemia
3) Bilirubin > 3 mg/dL
85
1) Where is jaundice best seen?
2) What do you refer pts for?
3) Who do you admit?
1) Conjunctiva, under tongue, and hard palate
2) Diagnostic procedures
3) Hepatic failure
86
Bilirubin:
1) What is it?
2) What does it do?
3) What does it give color to?
1) Metabolite of heme
2) Serves to excrete unwanted heme (from heme-containing proteins: hemoglobin, myoglobin, CYP450 enzymes)
3) Bile, stool, +/- urine
87
Bilirubin:
1) Why must it be excreted?
2) What is it derived from?
3) What is its path?
1) Potentially toxic
2) 80% derived from heme from senescent RBCs
3) Bili production > hepatocyte uptake > conjugation > excretion into bile ducts > excretion into intestines
88
Unconjugated hyperbilirubinemia (indirect) may be due to what 3 things?
1) Increased bilirubin production
2) Decreased hepatic uptake
3) Impaired conjugation
89
Conjugated hyperbilirubinemia (direct) may be due to what 3 things?
1) Biliary obstruction (extra-hepatic)
2) Intra-hepatic cholestasis
3) Hepatocellular injury
90
List some Historical clues for hyperbilirubinemia
-Use of medications or recreational drugs
-Use of dietary supplements or herbal medications
-Use of alcohol
-Hepatitis risk factors
-H/o abdominal operations (including gallbladder surgery)
-H/o inherited disorders (including liver diseases & hemolytic disorders)
-HIV status
-Exposure to toxic substances
91
Unconjugated hyperbilirubinemia (indirect): What are 3 signs?
1) Stool & urine color are normal
2) Mild jaundice
3) No bilirubin in urine
92
Conjugated hyperbilirubinemia (direct): What are the S/Sx?
1) Possibly asymptomatic in mild disease
2) Often with pruritis, light-colored stools (acholic), & jaundice
3) Malaise, anorexia, RUQ pain with liver disease
4) Dark urine, jaundice, and, in women: amenorrhea may occur
5) Other possible signs: enlarged tender liver, spider telangiectasias (angiomas), palmar erythema, ascites, gynecomastia, sparse body hair, fetor hepaticus (terrible breath caused by liver disease,) & asterixis
93
List the Initial labs & imaging for hyperbilirubinemia
1) Order Sr total & unconjugated bilirubin, ALP, ALT & AST, PT/INR, albumin
2) Initial imaging options: US, CT, MRI
94
Hyperbilirubinemia:
1) What if ALP, AST, & ALT normal?
2) What if predominant ALP elevation?
3) What if predominant AST & ALT elevation
1) Not likely hepatic injury or biliary tract disease
2) Suggests biliary obstruction or intrahepatic cholestasis
3) Suggests jaundice caused by intrinsic hepatocellular disease
95
Hyperbilirubinemia:
1) What if elevated INR corrects with Vit. K
2) What if it does not correct with Vit. K?
1) Suggests obstructive jaundice
2) Suggests hepatocellular disease with impaired synthetic function
96
Describe Hep C Tx
1) Confirm active infection: ensure no spontaneous clearance (detectable HCV level over 6-month period)
2) Rule out concomitant HIV & HBV infections
3) Determine genotype (possible resistance to treatment)
4) Classify as treatment-naïve or treatment-experienced
5) Assess for cirrhosis via fibro-scan or blood test (affects management)
6) Treat with appropriate agent (pan-genotypic agent preferred) (Just know oral for 12wks)
7) Repeat HCV RNA at 12-weeks post-treatment to assess for sustained virologic response (SVR)/cure
