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GI Clin Med liver Flashcards

1
Q

Hepatitis

A

Inflammation of the liver

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2
Q

What can cause hepatitis

A

Hep A, B, C, D, E

Drugs and toxic agents

*clinical manifestations may be similar regardless of cause

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3
Q

True liver function tests

A

PT/INR
Albumin
Cholesterol

*alt/ast and alp and bilirubin ldh and get can come from other places “liver tests”

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4
Q

What causes mile elevations in ALT

A

Chronic hep b, c, d

Acute viral hep (A-E, EBV, CMV)

Steatosis/steatohepatitis

Hemochromatosis

Medications/toxins

Autoimmune hepatitis

Alpha-1 antitrypsin defiency

Wilson disease

Celiac disease

Glycogenic hepatopathy

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5
Q

Mild elevations AST

A

Alcohol related liver injury

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6
Q

Nonhepattic mild elevations

A

Strenuous exercise

Hemolysis
Myopathy
Thyroid disease
Macro-ast

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7
Q

Severe elevations ast/alt

A 
Acute viral hepatitis a-e
Medications/toxins
Ischemic hepatitis
Wilson
Acute bile duct obstruction
Acute budd chairi syndrome
Hepatic artery ligation
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8
Q

Non hepatic sources bilirubin

A

Rbc

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9
Q

Non hepatic sources ast

A

Skeletal msucles, cardiac muscle, rbc

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10
Q

Non hepatic sources alt

A

Skeletal muscle, cardiac muscle, kidney

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11
Q

Nonhepatic source led

A

Heart, rbc,

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12
Q

Non hepatic source alkaline phosphatase

A

Bone, first trimester placenta, intestines

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13
Q

Hepatocellular disease-primary injury to hepatocytes

A

Ast, alt higher than alkaline phosphatase

Elevated direct bilirubin

Elevated or normal indirect bilirubin

Associated liver enzymes often elevated

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14
Q

Cholestatic liver disease-injury to bile ducts

A

Alkaline phosphatase higher than AsT, ALT

Elevation of alkaline phosphatase with near normal ast, alt levels

Normal direct bilirubin

Elevated indirect

No abnormal liver tests; no anemia, onset in late adolescence, fasting makes bilirubin rise

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15
Q

Hemolysis

A

Normal direct bilirubin

Elevation represents more than 90% of total bilirubin

Anemia usual; increased reticulocyte count, normal liver enzyme levels (LDH may be up)

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16
Q

Overall hepatocellular

A

ALT >AST

Both up

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17
Q

Cholestasis

A 
ALP up(if isolated consider bone involvement)
Check get

Elevated alp
Failure of bile to reach duodenum
Jaundice and pruritus
Pure cholstatsis 
Oral contraceptives, anabolic steroids sex hormones
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18
Q

Non inflammatory drug induced cholestasis

A

Anabolic steroids, azathripine, cyclosporine, estrogens

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19
Q

Inflammatory drug induced cholestasis

A

Amoxicillin

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20
Q

Clinical presntation viral hepatitis

A

Malaise, nausea, vomiting, diarrhea, low grade fever followers by dark urging, jaundice and tender hepatomegaly; may be subclinical and detected on basis of elevated aspartate and alanine levels

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21
Q

Hep a

A

Ss RNA hepatovirus (picornavirus family0

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22
Q

Prodrome hep a

A

Anorexia, nausea, vomiting, malaise, aversion to smoking

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23
Q

Duration hep a

A

2-3 weeks

Complete clinical 9 weeks recovery 6-12 months no clinical sequelae

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24
Q

Risk factor hep a

A

1 international travel contaminated water or food, including inadequately cooked shellfish

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25
Symptoms hep a
Fever, malaise, myalgia, arthralgias, easy fatigability, upper respiratoy symptoms, anorexia, enlarged and tender liver, jaundice , nausea, vomiting, diarrhea or constipation More severe in adults Ab pain RUQ or epigastric Alcoholic stools
26
Transmission hep a
Fecal oral Poor sanitation crowding Excreted in feces for up to 2 weeks before clinical illness but rarely after the first week of illness
27
Labs hep a
Markedly elevated AST ALT Elevated bilirubin and ALP-cholestasis Anti hAC IgM early later IgG Acute hep-IgM diagnose igG-protective and previous exposure
28
Vaccine HAV
Yup
29
Hep with fulminant
ABD
30
Hep B
Hepadna virus partially dsDNA inner core and outer surface coat
31
Prodrome hep b
Anorexia, nausea, vomiting, malaise, aversion to smoking
32
Duration hep B
Acute illness usually subsides over 2-3 weeks->complete clinical laboratory recovery 16 weeks
33
Risk factors hep b
``` MSM Inject drugs HIV Hemodialysis Physicians, dentists, nurses, personnel working in clinical and pathology laboratories and blood bands Incarcerated STD Blood transfusion ```
34
Symptoms hep b
Fever low grade, enlarged and tender liver, jaundice Asymptomatic w/o jaundice->a fulminating disease and death Glomerulonephritis, serum sickness, and polyarthritis nodosa
35
Transmission hep b
Blood or blood products Sex Perinatal Asia africa HBsAg positive mothers 90% transmit to baby
36
Labs hep b
Markedly elevated ALT AST easily higher than HAV No cholestasis so ALP and bilirubin normal
37
Vaccine HBV
Ok
38
What percent of hep b is acute vs chronic
90% acute | 10% chronic
39
Mortality hep b
Fulminant hepatitis less than 1% with mortality 60%
40
Prevent hep b
Vaccine | HBIG if exposure in unvaccinated
41
HBc-AB IgG
Prior infx | Chronic infx
42
HBsAg
Surface antigen, first evidence, positive during acute and carrier (chronic) Before biochemical evidence of liver disease and persisting throughout the clinical illness Persistence of HBsAg more than 6 months after the acute illness
43
HBsAb
Surface antibody, immunity Appears after clearance of HBsAg and after successfulvaccination
44
HBcAg
Core antigen
45
HBcAb IgM
Appears shortly after HBsAg is detected, ONLY THING DETECTABLE DURING GAP WINDOW PERIOF->CONSIDERED ACUTE HBV Diagnose acute Reappear during flares of previously inactive chronic hep b IgG also persists but persists indefinitely
46
HBcAb IgG
Appears during late in acute phase and persists indefinitely, whether goes on to chronic infection or immunity (prior infx)
47
HBeAg
Viral proliferation and infect iv its + acute and active chronic Negative inactive chronic Secretory form of HBcAg ->viral rep and infectivity If persist beyond three months->chronic
48
HBV DNA
Detectable during current infection, typically parallels the presence of HBeAg, more sensitive and precise marker of viral replication More sensitive precise marker of viral replication
49
Hep D
Defective RNA virus needs HBV
50
Risk factor Hep D
HBV endemic Mediterranean basin ; spread predominantly by non percutaneous means Nonendemic areas-spread percutaneous lh in HBsAg IV drug users or hemophiliac transfusion
51
Labs HDV
Ani HDV
52
Vaccine hepD
Vaccinate against hep b
53
Mortality hep d
Enhances severity of HBV infection
54
Hep E
RNA hepevirus hepevirdae
55
Risk factors hep e
Epidemic form in Asia, the Middle East, and North Africa, Central America , India Pet
56
Tramsioson hep e
Enteric, cooked organ meat, spread by swine
57
Labs hep e
IgM anti HEV
58
Vaccine HEV
Approved in china
59
Acute HEV chronic
Acute But in transplant patients treated with tacrolimus instances of chronic with progression to cirrhosis have been reported
60
Mortality hep e
Pregnant
61
Hep c
Flavivirus ss RNA Chronic
62
Risk factors hep c
HIV Transfusion Body piercing and tattooed, hemodialysis Hospital and outpatient facility acquired transmission-re use syringes in caths Unsafe medical practices Bloody fisticuffs
63
Symptoms hep c
Mild and asymptomatic fluctuating elevations of serum ALT AST
64
Labs hep c
HCV RNA | Enzyme immunoassay that detects antibodies to HCV
65
What is someone has HCV ins drum, without HCV RNA in serum
Recovery from prior HCV infection
66
Vaccine hep c
No but chronic carriers should be vaccinated against HAV HBV
67
Complications HCV
Cirrhosis, hepatocellular carcinoma, HIV coinfection, cryoglobulinemia and membranoproliferative glomerulonephritis, lichen Plano’s, autoimmune thyroiditis, lymphocytes sialadentis, idiopathic pulmonary fibrosis, sporadic porphyria cutaneous tarda, monoclonal gammatopathies
68
Prevent HCV
Test donated blood Screen baby boomers Safe sex Don’t share razors of tooth brush
69
Treat hep c
Curable with proper treatment
70
Chronic hepatitis
At least 6 months
71
Etiology chronic hepatitis
Hepatitis B virus, hep C, hep D, drugs (methyldopanitrofurantoin, isoniazid, dantrolene), autoimmune hepatitis, Wilson’s, hemochromatosis, a1-antitrypsin defiency)
72
Chronic hepatitis grade
Histologic assessment of necrosis and inflammatory activity based on exam of liver
73
State chronic hepatitis
Reflects the level of disease progression and is based not he degree of fibrosis
74
Presentation chronic hepatitis
Asymptomatic ALT AST Elevations Acute fulminant Fatigue, malaise, anorexia, low grade fever, jaundice , ascites, varices bleeping, encephalopathy, coagulopathy, hypersplenium
75
When do people with chronic hepatitis get extrahepatic manifestations
HBV-urticaria, arthritis, polyarthritis nodosa, vasculitis, polyneuropathy, glomerulonephritis HCV-mixed cryoglobulinemia
76
How ID presence or absence of fibrosis in chronic hep
Serum fibrosure and/or US elastography
77
Toxic and drug induced hepatitis dose dependent
Onset in 48 hours, predictable , necrosis around terminal hepatic venue Mushroom poisoning, acetaminophen
78
Toxic and drug induced hepatitis idiosyncratic
Variable dose and time of onset Small number of exposed persons affected May be associated with fever, rash, arthralgias, eosinophilia Ioniazid
79
Treat toxic and drug induced hepatitis
Supportive -withdraw agent, gastric lovage and oral administration of charcoal Liver transplant Acetaminophen overdose, sulfhydryl compounds, use remark Matthew nomogram -start therapy in 8 hours if ingestion
80
Fulminant hepatitis
Massive hepatic necrosis with impaired consciousness occurring within 8 weeks of the onset of illness
81
Causes of fulminant hepatitis
``` ABCDE Drugs Ischemia Budd chiari syndrome Idiopathic chronic active hep Acute Wilson’s disease Reye’s syndrome acute fatty liver of pregnancy ```
82
Clinical fulminant hepatitis
Encephalopathy Rapidly shrinking liver side, raising bilirubin, prolongation PT, clinical signs of confusion, disorientation, somnolence, ascites and edema-hepatic failure with encephalopathy, ALT AST fall Cerebral edema,
83
Mortality fulminant hepatitis
Common
84
Treat fulminant hepatitis
Maintain fluid balance, support of circulation and respiration, control bleeding, correction of hypoglycemia, and tratment of other complications of the comatose state in anticipation of liver regeneration and repair Restrict protein intake Oral lactulose or neomycin Prophylactic antibiotics -improves survival Liver transplant
85
Alcoholic liver disease
80 mg a day men 30-40 mg a day women Often denied in exam
86
Men or women more susceptible to get advanced liver disease with less alcohol intake
Women
87
Cofactors in alcoholic liver disease
Hep B and B malnutrition
88
Fatty liver alcohol
Asymptomatic and goes away with stopping alcohol
89
Alcoholic hepatitis
Asymptomatic->severe liver failure with jaundice, ascites, GI bleeding and encephalopathy Anorexia, nausea, vomiting, fever, jaundice, tender hepatomegaly, RUQ pain
90
Alcoholic hepatitis AST ALT
AST ALT 2:1
91
Diagnosis alcoholic hepatitis
Biopsy hepatocyte swelling, mallory denk
92
Adverse prognosis alcoholic hepatitis
Critically ill A maddreys discriminates function (PT and serum bilirubin involved)-over 32 associated with poor prognosis MELD score of end stage liver disease->21 is also significant mortality Glasgow alcoholic hepatitis scare-predicts mortliaity based on age, serum bilirubin, BUN, prothrombin time, and WBC Over 9 who receive glucocorticoids had higher survival rates compared to those that didn’t Ascites, varices hemorrhage, encephalopathy, hepatorenal syndrome poor
93
Lab of alcoholic hepatitis
``` Mild liver enzymes Anemia Leukocytosis Leukopenia Thrombocytopenia ALP GGT up PT up Depressed albumin and gamma globulin up Increased transferrin saturation, hepatic iron stores, and sideroblastic anemia Folic acid defiency by ```
94
Imaging hepatic alcoholic
UD exclude biliary obstruction and identifies subclinical ascites CT IV MRI Serum fibrosure and or US elastography can identify presence or absence of fibrosis
95
Liver biopsy of alcoholic hepatitis is identical to what
Non alcoholic steatohepatitis
96
Treat alcoholic hepatitis
Abstinence is essential Multivitamin G;ucose administation increases thiamine requirement and can precipitate wernicke korsakoff syndrome if thiamine is not co administered
97
Wernicke encephalopathy
Confusion, ataxia, involuntary abnormal eye movements
98
Korsakoff syndrome
Severe memory issues | Confabulation/make up stories to fill in the gaps
99
Treat korsakoff
Correct K Mg and phosphate deficiencies Transfusions of packed rbc, plasma as necessary Monitor glucose Severe alcholic hepatitis(discrimination function>32 MELD >20) steroids Pentoxifylline increase survival Liver transplantation-but must obstinate from alcohol for 6 months to be considered
100
Non alcoholic fatty liver disease
Asymptomatic elevated ALT AST hepatomegaly Steatosis without fibrosis Common 20-45% of Americans
101
Causes oris factors non alcoholic fatty liver disease
Obesity, DM, hyper TG, insulin resistance Hispanic Vinyl chloride
102
Histology non alcoholic fatty liver
Focal infiltration by polymorphonuclear neutrophils and mallory hyaline similar to non alcoholic steatohepatitis
103
Symptoms NAFLD
Asymptomatic mild URQ discomfort | Hepatomegaly
104
Lab NALFLD
Milf elevation ALT AST | Maybe normal though
105
Imaging NAFLD
CT< US< MRU see macrovascular steatosis MRU-quantify fat content US elastography-assess liver stiffness can be used to estimate hepatic fibrosis
106
Primary biliary cirrhosis
Progressive non supportive destructive intrahepatic cholangitis Chronic Autoimmune destruction FEMALE over 50
107
Symptoms primary biliary cirrhosis
Asymptomatic isolated elevation in ALP or impaired bile excretion->liver failure and cirrhosis
108
Risk of primary biliary cirrhosis
UTI Smoking Hormone replacement therapy Hair dye
109
Clinical manifestations PBC
Pruritus, fatigue, jaundice, xanthelasma, osteoporosis, steatorrhea, skin hyperpig, portal hypertension
110
Associated disease PBC
Sjirgen autoimmune
111
Diagnose PBC
AMA 90% ALP GGT bilirubin, cholesterol IgM
112
Treat PBC
Ursodeoxycholic
113
Autoimmune hepatitis 1
More common Anti smooth msucle antinuclear Antibodies
114
Type II autoimmune hepatitis
Women | Antiliver.kidney microsomal antibodies anti LKM
115
Clinical manifestation autoimmune hepatitis type I
Women Abrupt onset 1.3 insidious 2/3 Progressive jaundice, anorexia, hepatomegaly, abdominal pain, epistaxis, ever, fatigue Healthy woman-spider telangiectasia, cutaneous striae, acne, hirstisum, hepatomegaly
116
Autoimmune hepatitis and cirrhosis
Leads to itwhich causes death if untreated risk of hepatocellular cancer
117
Extrahepatic manifestations autoimmune hepatitis
Rash, arthralgias, keratoconus TI is sicca, thyroiditis, hemolytic anemia, nephritis, UC
118
Treat autoimmune hepatitis
Glucocorticoids
119
Hemochromatosis
Elevated iron saturation or serum ferritin or a FH Most asymptomatic Recognized after 5th decade
120
What does hemochromatosis cause
Hepatic abnormalities, cirrhosis, heart failure, hypogonadism and arthritis
121
Genetics hemochromatosis
HFE gene mutation AR
122
Iron in hemochromatosis
Liver, pancreas, heart, adrenals, testes, pituitary, kidneys
123
Symptomsand signs of hemochromatosis
Earlier in men Early-fatigue Later-arthropathy, hepatomegaly, hepatic dysfunction, KSIN pigmentation, cardiac enlargement, DM
124
Hemochromatosis increased risk for infection with what
Y, LM, VV
125
Lab hemochromatosis
Milf ALT AST Elevated iron and transferrin saturation Elevated ferritin
126
Imaging hemochromatosis
MRI CCT overload iron | MRI quantitiate
127
Liver biopsy hemochromatosis
Homozygous C282Y | Serum ferritin less than 1000, serum AST normal, hepatomegaly absent
128
Risk factors hemochromatosis
Male sex, excess alcohol consumption and DM
129
Screen HFE
All first degree family members
130
Treat hemochromatosis
Avoid foods rich in iron such as red meat, alcohol, vitamin C, raw shellfish, and supplemental iron PHLEBOTOMIES every week Monitor hematocrit and serum iron Chelating agents deferoxamine for patients with hemochromatosis and anemia or secondary iron overload tue to thalassemia who cant tolerate phlebotomies
131
Complications hemochromatosis
Anthropathy, DM, heart disease, portal hypertension, fibrosis, cardiac conduction defects and insulin requirements
132
Wilson disease
AR under 40 | Excessive deposition of Copper in liver and brain
133
Serum ceruloplasmin urine copper wilson
Serum ceruloplasmin low | Urinary excretion high
134
Genetic wilson
ATP7B Heterozygous ok
135
Where is copper in wilson
Copper deposition, espicially in the liver, brain, cornea, and kidney
136
Who do we consider Wilson’s in
Liver disease in adolescents and neuropsychiatric disease in young adults Any young kid with hepatitis, splenomegaly with hypersplenism, Coombs negative hemolytic anemia, portal hypertensiona nd neurologic psychiatric abnormalities
137
Neuro wilson basal ganglia
Akinetic rigid Parkinsonism , tremor, ataxia , dystonia syndrome , dysarthria, dysphagia, migraines, seizures Behavior and personality changes
138
Diagnose wilson
Low ceruloplasmin, high urine copppper up Jayden flies her MRI brain increased basal ganglia and brainstem and cerebellar copper ATB 7B
139
Budd chiari
Tender, painful hepatic enlargement RUQ pain jaundice, splenomegaly, ascites, frequently complicated by hepatocellular carcinoma
140
Imaging budd chiari
Occlusion/absence of flow in hepatic vein or inferior vena cave
141
What predisposes a patient to budd chiari
Hereditary and acquired hypercoagulable states (Polycythemia very, specific mutation V617F) in gene of JAK2 Thrombosis-activated protein C resistance (factor V Leiden mutation, protein C or S or antithrombin defiency,
142
Liver and budd chiari
Canal webs->right sided heart failure->NUTMEG LIVER
143
In India china and South Africa, what is budd chiari syndrome associated with
Poor standard of living
144
Presentation budd chiari
Fulminant, acute, subacute or chronic Mainly subacute
145
With chronic disease what complications from budd c
Bleeding varices, hepatic encephalopathy, hepatopulmonary syndrome
146
Imaging budd chiari
Prominent caudate lobe Contrast enhanced CEUD Pulsed Doppler US MRI-see obstructed vein Direct venography-delineate canal webs and occluded hepatic veins (spider web pattern ) most precisely
147
Liver biopsy budd c
Percutaneous or transjugular | Nutmeg-ventricular congestion and fibrosis
148
Alpha 1 anti trypsin
AR | Accumulated in hepatocytes causing liver damage and decreased levels of protease inhibitors
149
PiM
Normal
150
PiS
Mildly recused
151
PIX
Homozygous severe reduction in enzyme
152
How does alpha 1 antitrypsin cause increased risk of HCC
Micronodular cirrhosis
153
Presentation a1 antitrypsin
Baby-liver fail-liver transplan Older-pulmonary emphysema at young age Don’t smoke and liver transplant
154
Ischemic hepatitis
Ischemic hepatopathy, hypoxichepatitis, shock. Liver, acute cardiogenic liver injury Acute fall in cardiac output due to MI, arrhythmia, septic or hemorrhagic shock, hypotension
155
Treat ischemic hepatitis
Statin
156
Hallmark ischemic hepatitis
ALT AST increased Greater than 5000 Early rapid rise in the serum lactate dehydrogenase Alp bilirubin mild Jaundice worse outcomes PPT prolonged, encephalopathy, or hepatopulmonary syndrome
157
Mortality ischemis hepatitis
High
158
Right heart failrue
Passive congestion liver nutmeg Serum bilirubin up alp normal ALT AST mild up HEPATOJUGULAR REFLUX PRESENT WITH TRICUSPID REGURGIATION THE LIVER MAY BE PULSATILE ASCITES(high SAAG serum ascites albumin gradient over 1) Increased N terminal proBNP
159
Causes of non cirrhosis portal hypertension
Portal vein thrombosis Splenic vein obstruction Schistomiasis
160
Risk factors non cirrhosis portal hypertension
OC, preg, treatment f thrombocytopenia with eltrombopag
161
Signs of non cirrhosis portal hypertension
Acute portal vein thrombosis causes abdominal pain Splenomegaly GI bleed
162
Lab noncirrhotic portal hypertension
Normal But hypercoagulable stage is found in many patients with portal vein thrombosis JAK stat factor V Leiden mutation, protein C and S defiency
163
Imaging non cirrhosis portal hypertension
Color Doppler US and contrast enhanced CT, MRA of portal system is generally confirmatory, EUS
164
Treatnon cirrhotic, portal hypertension
Splenectomy Anticoagulation particularly with low molecular weight heparin Anti helmets
165
Pyogenic hepatic abscess signs
Fever, RUQ pain, jaundice (charcots triad..) | Often ins eating of biliary disease
166
How can the liver be invaded by bacteria:pyogenic hepatic abscess
Bile duct, portal vein, hepatic artery, direct extension, traumatic implantation
167
Risk factors pyogenic hepatic abscess
Old males
168
Pyogenic liver abscess
Increased risk of GI malignancy
169
Ascending cholangitis
Resulting from biliary obstruction due to a stone , stricture, or neoplasm is most common identifiable cause of hepatic abscess in US
170
Appendicitis diverticulitis
10% of liver abscess
171
40% of liver abscesses
Dental source
172
Most common organisms of pyogenic hepatic abscess
E. coli, klebsiella, proteus vulgarisms, enterobacter aerogenes, microaerophilic and anaerobic species
173
Pyogenic hepatic abscess hepatocellular carcinoma
Rare can present as a pyogenic abscess because of tumor necrosis, biliary obstruction, and superimposed bacterial infection
174
What must always be considered with pyogenic liver abscess
Amebic
175
Pyogenic hepatic abscess symptoms and signs
Insidious Fever Pain Jaundice, tenderness RUQ,
176
Labs pyogenic hepatic abscess
Leukocytosis with shift left Normal liver test Blood culture positice
177
Imaging pyogenic hepatic abscess
Chest x ray-elevation diaphragm if abscess in right love US, CT< MRI intrahepatic lesions MRI-high signal intensity T2
178
Cavernous hemangioma
Incidental finding US CT MRI Enlarge in women on hormonal therapy Surgical resection of cavernous hemangiomas is rarely necessary
179
Focal nodular hyperplasia
All ages Not oc Asymptomatic Hypercascular mass central stellate scar on CT MRI Stain positive for glutamine synthetase with central stellate scare Not a neoplasm
180
Hepatocellular adenoma
Women 30-40 OC Acute ab pain if tumor undergoes necrosis or hemorrhage Occurs with glycogen storage disease and FAP Hypovascular
181
Hepatocellular Adelina microscopically
Consists of sheets of hepatocytes w/o portal tracts or central veins
182
Clinical benign liver neoplasms-cavernous hemangioma adenoma
Palpable mass Liver function normal Arterial phase helical CT and multiphase dynamic MRI with contrast can distinguish an adenoma from focal nodular hyperplasia in 80-90% of cases
183
Treat focal nodular hyperplasia
OC not discontinue Should do US every teat for 2-3 years to ensure the lesion is not enlarging Excellent prognosis
184
Treat hepatocellular adenoma
Bleeding, necrosis, rupture——hormone therapy, third trimester, men Resection is advised in all who is 5 cm Discontinue OC get regression Transarterial embolization is the initial treatment for adenomas complicated by hemorrhage
185
Cirrhosis
Development of liver fibrosis , regenerative nodules, decreased liver function Portal hypertension
186
Cirrhosis reversible
If remove cause
187
4 types of cirrhosis
Compensated, compensated with varices, decompensated
188
Symptoms cirrhosis
Anorexia, nausea, vomiting, diarrhea, vague RUQ pain, fatigue, weak, ab pain glisson capsule , ascites,
189
Signs cirrhosis
``` Spider telangiectasia, palmar erythema, dupuytren contractures Glossitis cheilosis (vitamin deficiencies) Weigh loss Jaundice Capture Medusa Ascites Encephalopathy Fecer ```
190
Labs cirrhosis
``` Anemia Pancytopenia PT up Hyponatremia, alkalosis Glucose disturbances, hypoalbuminemia ```
191
What decreases cirrhosis
Coffee tea
192
Most common causes of cirrhosis
Alcohol Chronic hepatitis C infection NAFLD Hepatitis B infection
193
Most common genetic disorder that causes cirrhosis
Hemochromatosis Also wilson, a1 antitrypsin, PBD, heart failure, autoimmune (SMA antiLKM)
194
Diagnostic cirrhosis
``` Viral hepatitis Hemochromatosis AMA primary biliary cirrhosis SMA anti LKM autoimmune Ceruloplasmin wilson A1 anti ``` US-liver size NEED BIOPSY
195
Complications cirrhosis
CMP or hepatic function panel | PE for ascites and encephalopathy
196
Problems with cirrhosis
DM and vitamin D defiency
197
Portal hypertension
Increased hydrostatic pressure Caused by increased intrahepatic resistance to the passage of blood flow through the liver together with increased splanchnic blood flow due to vasodilation within the splanchnic vascular bed
198
Consequences of portal hypertension
``` Varices with hemorrhage Ascites Hypersplanism Hepatic encephalopathy Spontaneous bacterial peritonitis Hepatorenal syndrome Hepatocellular carcinoma ```
199
EGD or capsule endoscopy
To determine whether varices are present
200
Treat portal hypertension
Beta adrenergic blockers to reduce risk of hemorrhage in patients with small varices who have varices red wale marks or advanced cirrhosis (B or C)
201
Symptoms esophageal varices
Bleeding, Retching or dyspepsia Varices DP not cause symptoms UGIB0life threatening, most common cause of GIB due to portal HTN
202
Risk of bleeding with esophageal varices
Size over 5 mm Presence at endoscopy or red wale markings Child score B or C Active alcohol cause
203
Diagnose esophageal varices
Upper endoscopy
204
Treat esophageal varices
60% recur Acute resuscitation in ICU Rapid rectus situation with fluids and blood products -give fresh frozen plasma or platelets be patients have coagulopathy duct to cirrhosis VK intravenous! For abnormal prothrombin time
205
Antibiotic prophylaxis esophageal varices
Don’t want gram negative infection-50% get Fluoroquinolone or IV third generation cephalosporins Reduce risk of serious infection in 10-20% as well as hospital mortality, espicially in patients with child Pugh C
206
Esophageal varices and somatostatin and octreotide
Infusions reduce portal pressures vasoactive drugs
207
Lactulose esophageal varices
Encephalopathy may complicate GIB in patients with severe liver disease
208
Prevent re bleed
Nonselective beta adrenergic blockers (propranolol, nadolol) reduce risk or rebleeding Long term treatment with band ligation reduces
209
Emergent endoscopy esophageal varices
Hemodynamically stable with active bleeding->endotracheal intubibation to protect against aspiration during endoscopy Preformed to exclude other or associated causes of UGIB -immediate banding
210
Complications emergent endoscopy
20-30% chest pain, fever, bacteremia, esophageal ulceration, stricture, perforation
211
Balloon tube tamponade esophageal varices
Mechanical tamponade with specially designed nasogastric tubes containing large gastric and esophageal balloons -Minnesota or sengstaken blkemore tubes
212
Balloon tube tamponade effectiveness
Initial control of active hemorrhage in 60-90% rebleeding in 50%
213
Complications balloon tube tamponade
Prolonged inflation Esophageal and oral ulceration , perforation, aspiration, airway obstruction
214
Why is balloon tube tamponade a temporary measure in patients not controlled with pharm or endoscopic technique
High rate of complications
215
What must be done before balloon tube tamponade
Endotracheal intubation
216
Transvenous intrahepatic portoystemic shunt
Over a wire that is passed through a catheter inserted in the jugular vein, an expandable wire mesh stent is passed through the liver parenchyma, creating a portosystemic shunt from the portal vein to the hepatic vein
217
TIPS effectiveness
Control acute hemorrhage in over 90% of patients Increased risk of encephalopathy Lowers risk of rebleeding but not mortality
218
Who gets TIPS
Recurrent episodes of varices bleeding that have failed endoscopic or pharm therapies
219
Liver transplant varices
Treat with band ligation or TIPS to control bleeding pre transplant
220
Hepatic encephalopathy
Altered mental status and cognitive function occurring in presence of liver failure Acute reversible, chronic and progressice
221
States of encephalopathy
Mild confusion, drowsiness, stupor, coma
222
Diagnose hepatic encephalopathy with clinical features
Confusion, slurred speech, change in personality, violent and hard to manage, sleepy and difficult to arouse, asterixis——coma Encephalapp-stoop test ask name color of written word
223
Pathophysiology hepatic encephalopathy
Gut derived neurotoxins ammonia elevated not removed by liver But severity not due to height of ammonia levels
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Precipitates hepatic encephalopathy
GI bleeding, azotemai, constipation, high protein diet
225
Treat hepatic encephalopathy
Remove precipitates and orrect electrolyte imbalances Lactulose -colonic acidification and diarrhea-WANT THIS want to increase stools Liver transplant
226
Ascites cirrhosis cause
Portal hypertension; hypoalbuminemia Urinary Na concentration low Free water excretion impaired->hyponatremia
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Two categories of ascites
``` Normal peritoneum Diseased peritoneum(More common with portal HTN and cirrhosis) ```
228
Signs and symptoms ascites
Increasing abdominal girth Elevated jugular venous pressure, right sided heart fail, large tender liver (budd, acute alcoholic hep), asterisks, anasarca, shifting dullness
229
Risk factors ascites
Alcohol transfusion tattoos, injection drug use, history or viral hep, jaundice, birth in endemic area of hepatitis
230
Diagnose ascites
US
231
Labs ascites
Abdominal paracentesis -new onset and has cirrhosis and ascites When patients deteriorate to exclude bacterial peritonitis
232
White cell in ascites
Spontaneous bacterial peritonitis Over 500 leukocytes Over 250 PMC TB or peritoneal carcinomatosis
233
Albumin and total protein in ascite
SAAG portal HTN 1.1 Non portal hypertension lesss than 1.1 Subtract ascites fluid albumin from serum albumin
234
Culture and gram stain ascites
Aerobic and anaerobic culture
235
imaging ascites
US distinguish ascites with portal and nonportal Doppler-budd c LAD- CT-see causes of portal and nonportal , see budd c, LAD
236
SAAG greater than or equal to 1.1
Portal hypertension -hepatic congestion (heart failure, constrictive pericarditis, tricuspid insuffiency, budd C, Venmo occlusive) or liver disease (cirrhosis, alcoholic hep, fulminant hepatic failure, fibrosis
237
SAAG less than 1.1
``` Diseased peritoneum (bacterial, TB, fungal, HIV) Infections, malignant (carcinomatosis, mesothelioma, pseudomyxoma, cancer) ```
238
SAAG less than 1.1 hypoalbuminemia
Nephrotic syndrome Protein losing enteropathy Severe malnutrition
239
Miscellaneous conditions SAAG less than 1.1
Myxedema greater than 1.1!! | Rest pancreatic, bile, nephrotoxicity, ovarian disease
240
Spontaneous (primarY0 bacterial peritonitis is common with what history
Chronic liver disease and ascites Absence of an apparent intra abdominal source of infection
241
Peritoneal signs and spontaneous bacterial peritonitis
No
242
Neutrophil in spontaneous bacterial peritonitis
Higher than 250
243
How get spontaneous bacterial peritonitis
Translocation of enteric bacteria across the gut wall or mesenteric lymphatics leads to seeding of the ascetic fluid Monomicrobial - e coli klebsiella (enteric gram -) - strep p, viridans, enterococcus(gram +) NO ANAROBIC
244
Signs and symptoms spontaneous bacterial peritonitis
Subtle Fever ab pain Change in mental status Worsening or renal function Chronic liver disease with ascites
245
Lab findings primary bacterial peritonitis
Abdominal paracentesis -PMN over 250
246
Secondary bacterial peritonitis
Secondary to intra abdominal infection | Appendicitis, diverticulitis, perforated peptic ulcer, gallbladder, multiple organisms,
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Prevent SBP
Oral once a day antibiotics
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Treat peritoneal infection
Third gen cephalosporin Beta lactam/beta lactamase agent -not aminoglycosides bc of nephrotoxicity
249
Major cause of death PB
Kidney injury give IV albumin
250
Treat SBP
Broad spectrum metronidazole or third gen cephalosporin
251
Most effective treatment for recurrent spontaneous bacterial peritonitis
Liver transplant
252
Prognosis spontaneous bacterial peritonitis
Over 30% mortliatiy | But if treated and seen early less than 10
253
Malignant ascites
Peritoneal carcinomas
254
What are the most common tumors causing carcinomatosis
Ovary, uterus, pancreas, stomach, colon, lung, breast
255
How do tumors metasticize to peritoneal
Lymphatic obstruction, hepatocellular carcinoma
256
Cytology malignant ascits
90%
257
Malignant ascites SAAG
Less than 1.1
258
Malignant ascites respond to diuretics
No
259
Familial Mediterranean fever SAAG <1.1
Rare AR in Mediterranean ancestry where they lack a protease in serosa fluids that inactivate interleukin 8 and the chemotactiv complement factor 5A
260
Symptoms familial Mediterranean fever
Before 20 Episodic bouts of acute peritonitis that may be associated with serositis involving the joints and pleura Sudden fever, ab pain, ab tender, guarding or rebound
261
Familial Mediterranean fever untreated
Resolve in 34-48 Horus
262
Why may someone with familial Mediterranean fever undergo laparotomy unnecessarily
Mimic surgical peritonitis
263
Colchicine
Decreased frequency of familial Mediterranean fever
264
Main cause of death familial Mediterranean fever
Secondary amyloidosis
265
Mesothelioma SAAG
Primary abdominal malignant mesothelioma | Asbestos
266
Signs of mesothelioma
Ab pain, bowel obstruction, increased abdominal girth, and small to moderate ascites
267
Chest radiograph mesothelioma
Pulmonary asbestosis
268
Ascites in mesothelioma
Hemorrhagic
269
Cytology mesothelioma
Negative
270
CT PET-CT mesothelioma
Sheet like masses involving the. Mesentery and omentum
271
Diagnosis mesothelioma
Laparotomy or laparoscopy
272
Chylothorax ascites SAAG<1.1
Lipid rich lymph in peritoneal cavity milky appearances TG greater 1000
273
Why get chylothorax ascites
Lymphatic obstruction or leakage caused by malignancy, espicially lymphoma Post op trauma, cirrhosis, TB, pancreatitis, filariasis
274
Pancreatic ascites
Accumulation of pancreatic secretions due to disruption of pancreatic duct or to a pancreatic pseudocyst in patients with chronic pancreatitis and complicates acute pancreatitis
275
Pain with pancreatic ascites
No be enxymes not active
276
Describe fluid of pancreatic ascites
High protein amylase high excess 1000
277
Bile ascites SAAG<1.1
From complications of biliary tract surgery, percutaneous lvier biopsy or abdominal trauma
278
Pain bile ascites
Unless infected no pain , fever, or leukocytosis
279
Paracentesis bile ascites
Yellow fluid
280
Ration of ascites bilirubin to serum bilirubin in bile ascites
Greater than 1
281
Most important treatment of cirrhosis
Abstinence from alcohol F
282
Other cirrhosis treatment
If HAV HBV get pneumococcal vaccines and a yearly flu vaccine Liver transplant Nonsteroidal anti inflammatory drugs contraindicated Don’t use angiotensin converting enzyme inhibitors and angiotensin II antagonists
283
Complication paracentesis
Bleeding, infection, bowel perforation
284
How treat ascites and edema
Dosing intake restricted Bed rest Fluid intake restricted Diuretics
285
What diuretic for ascites and edema
Spironolactone with furosemide
286
TIPS and ascites
Lower ascites recurrence and hepatorenal syndrome
287
What is associated with increased mortality with TIPS
Chronic kidney disease, diastolic cardiac dysfunction, refractory encephalopathy, hyperbilirubinemia
288
Complication fo TIPS
Hepatic encephalopathy, infection, shunt stenosis, shunt occlusion
289
Hepatorenal syndrome
Histology kidneys morale get acute decreased in cardiac output precipating event
290
Treat hepatorenal syndrome
``` Discontinue diuretics IV albumin Vasoconstrictor TIPS Liver ranspaotn ```
291
Acute liver failurefulmient or sub most common cause
Acetaminophen | Suicide or unintentional
292
Second most common cause of acute liver failure
Anti TB drugs, antiiepileptics, antibiotics
293
Characterization fulminant hepatic failure
Development of hepatic encephalopathy within 8 weeks and 6 months Acute onchronic liver failure too
294
Liver transplant
If irreversible Abstinent for 6 months Prioritzaion based on MELD and CHILD
295
What is given after liver transplant
Immunosuppressant
296
What order to calculate MELD
CMP (serum bilirubin, creatinine) and PT/INR
297
What MELD score is required for liver transplant
14 or over

► Med Notes (62 decks)

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