Hernias, Biliary dz, Hepatitis Flashcards
(133 cards)
1
Q
define hernia & name the types of hernias
A
protrusion, bulge, or projection of any organ or part of an organ through the body wall that contains it
- Groin Hernias - Inguinal-most common-80% (Indirect and Direct)
- Femoral- 10%
- Other
- Umbilical, incisional, etc
2
Q
si/sx of a hernia
A
Lump
- Often worse at the end of the day
- May resolve with lying flat
Abdominal fullness/discomfort
Pain with lifting or exertion
Constipation
3
Q
Conservative Tx for hernias
A
Conservative Who:
- Men: may use conservative treatment if small, reducible, minor discomfort
- Women: Not recommended to treat conservatively- go right to surgical repair
- Recurrent: not recommended
Conservative How:
- Heat and self reduction with lying flat
- Trusses and hernia belts - Associated problems
4
Q
indications for urgent surgicla repair of hernias
A
Surgery Urgent surgical repair
- For incarcerated or causing bowel obstruction
- Pain, fever, sometimes erythema, nausea, vomiting, signs of bowel obstruction
- Goal is within 6 hours of onset of incarceration
5
Q
dx hernias
A
Good clinical exam
- Use gloved finger into the scrotum and into the inguinal ring, ask patient to bear down and check for a palpable bulge
- Palpate groin and femoral area for lumps
Imaging if bad exam”
Start with ultrasound and then use MRI if suspicion still exists because MRI is more sensitive and specific (Herniography
6
Q
define loactions fo hernias
Indirect(most common)
Direct
Femoral
A
Indirect(most common)
- Follows spermatic cord into the scrotum
- Lateral to the inferior epigastric artery
- Originates in the deep inguinal ring and passes through the superficial inguinal ring
Direct
- Bulges through abdominal wall in area of weakness in inguinal canal
- Medial to inferior epigastric artery
- Only passes through the superficial inguinal ring
Femoral
- Bulges through abdominal wall
- Inferior to the Inguinal ligament
7
Q
women are most likely to get what kind of herna
A
femoral
8
Q
describe progression of pilonidial dz
A
- Starts as a small non-painful area in the skin above the coccyx/upper half of gluteal cleft called a Pilonidal sinus
- Fills up with pus and debris and develops a tract to the surface called a Pilonidal cyst
- Painful, red, swelling
9
Q
what is most common cause of rectal bleeding
A
Hemorrhoids
10
Q
decribe the 2 classifications of hemhorroids
A
Internal Hemorrhoids
- Above the dentate line
- Classified according to the degree of prolapse
- Present with painless bleeding
- Four degrees of classification
External Hemorrhoids
- Located in the distal third of anal canal
- Below the dentate line-very painful
- Can become thrombosed: clot in the hemorrhoid
- Easy to see on exam
11
Q
Cardinal Signs of internal hemorrhoids:
A
- painless bleeding
- rectal protrusion
12
Q
name the degrees of internal hemhorroids
A
First Degree -Bulge in lumen of canal on palpation
Second Degree - Protrusion with BM with spontaneous reduction after
Third Degree - Protrude spontaneously or with BM but requires manual reduction
Fourth Degree -Permanently prolapsed and irreducible
13
Q
Painless Bleeding after defecation-drops into bowl-BRBPR is what degree of hemhorroid
A
first
14
Q
degree of hemhorroid?
Anal mass with defecation
- feeling of incomplete evacuation
- mucus or fecal leakage
A
third
15
Q
what degree of hemhorroid
Irreducible anal mass
may have painful bleeding
A
fourth
16
Q
tx of first and second degree hemhoroids
A
Diet
Banding
Sclerotherapy
Infrared coagulation
17
Q
tx of third and fourth degree hemhorroids
A
Banding
Hemorrhoidectomy
Procedure for Prolapse and Hemorrhoids (PPH)
Transanal Hemorrhoidal dearterialization (THD
18
Q
hemhorroid tx modality:
Better for immunocompromised and those on anticoagulants
avoid in immunocompromised pts
A
Better for immunocompromised and those on anticoagulants - Sclerotherapy
avoid in immunocompromised pts - rubber band ligation
19
Q
complication most concerning for tx of hemhorroids
A
- Concern for incontinence since hemorrhoids provide up to 20% of anal resting pressure
- Removing them reduces resting pressure and can result in incontinence (what we worry about)
20
Q
medication options for hemhorroids
A
- Diltiazem 2% ointment
- Botox
- Liposomal bupivacaine
21
Q
define anal fissures
A
tear in the anoderm distal to the dentate line (PAIN)
Most commonly seen in midline posterior
22
Q
what are some primary and secondaery causes of anal fissures
A
Primary caused by overstretching of the anal canal
- Chronic constipation-hard stool
- Vaginal delivery
- Anal intercourse
Secondary Causes are the result of another medical cause
- IBD
- Previous Anal Surgery
- Granulomatous Diseases: TB, sarcoidosis
- Malignancy
- STDs
23
Q
differentiate b/w acute and chronic fissures
A
Acute Fissure - Heals within 6 weeks
- On exam, looks like a small laceration with vascularization
- Half will go on to become a chronic fissure
- Treat with conservative management
Chronic Fissure Lasts more than 6 weeks despite conservative management
- On exam, paler with raised edges
- Can cause a pile which is also sometimes called a skin tag
24
Q
conservative tx of anal fissures
A
Stool management
- Increase fiber (25-30g per day), Decrease fat intake, Increase water intake
- Stool softener, Sitz Baths
Botox
•Injected into sphincter to help relieve spasm by inhibiting acetylcholine-”chemical sphincterotomy”
more successful in women
25
name surgical tx for anal fissures and their pros and cons
_Lateral Internal Sphincterotomy:_ risk of incontinence
* Leave open to prevent abscess/infection
* Success 90%; permanent solution
_Endoanal V-Y Advancement Flap:_ no risk of incontinence
* Preserves internal and external sphincters
* May reoccur
26
If fissure does not heal after 6 weeks.....?
consider endoscopy to look for Crohns
27
causes of anal abscesses
Almost all abscesses are caused by infected anal crypt gland
Located along dentate line
28
what is the Crypto glandular hypothesis;
Crypto glandular hypothesis;
states that an infection begins in the anal canal glands and progresses into the muscular wall of the anal sphincters to cause an anorectal abscess
* Bacteria can get inside the crypt and then spread through the anal duct to the glands
* Infection spread anywhere from here in the area of “least resistance”
29
si/sx of anal abcesses
Severe pain with sitting
Fever and malaise
Sometimes pain with bowel movements but not always
Purulent Discharge
30
name deep and superficial anal abcesses
_Deep_
* Intersphinteric
* Supralevator
_Superficial_
* Subcutaneous/perianal
* Ischiorectal
31
dx of anal abcesses
* Lateral decubitus position
* Redness, fluctuance, induration
* Digital Rectal Exam
32
tx of anal abcesses
complications?
Incision and Drainage
Antibiotics
_Complications_
* Spread of infection
* Development of fistula
**•About half of patients develop anal-rectal fistulas**
33
# define anal-rectal fistula
most common type?
An abnormal connection between an anal abscess and the rectal canal caused by abscess (cryptoglandular infection)
•Most common is intersphincteric fistula
34
tx of Anal-Rectal Fistula
_Seton suture_
* keeps the tract open until it starts to heal
* If pus stops within 6-8 weeks then can glue or put in a fistula plug
_Fistula Plug_: Fibrin plug that Helps to heal fistula
_Endorectal advancement flap_: Extreme cases without healing require surgery
35
when draining anal-rectal fistula it is important to remember...
* Drain as close to the sphincter as possible
* Drain supralevator abscess into the rectum
36
# Define
Cholelithiasis
Choledocholithiasis
Biliary colic
* Cholelithiasis: The presence of gallstones.
* Choledocholithiasis: Gallstones in the bile ducts/common bile duct (CBD)
* Biliary colic: Intermittent, usually postprandial pain caused by temporary blockage of cystic duct, usually by a gallstone.
37
# define
Cholecystitis (Acute):
chronic
Acalculous cholecystitis
Cholangitis (Acute/Chronic):
* Cholecystitis (Acute): inflammation of the gallbladder, usually caused by build-up of bile when a stone lodges in the neck or cystic duct.
* Cholecystitis (Chronic): Recurring cholecystitis or mild, chronic inflammation that may be subclinical
* Acalculous cholecystitis: Inflammation of the gallbladder in the absence of cholelithiasis
* Cholangitis (Acute/Chronic): Infection/Inflammation of the CBD, usually due to either a gallstone, neoplasm, or stricture
38
si/sx of Cholelithiasis (Gallstones
Severe, intermittent, often post-prandial RUQ pain or epigastric pain – biliary colic
steady pain after eating
radiates to scapula
Patients usually have a history of similar, less severe episodes – be sure to ask about this!
Patient may report intermittent heartburn or reflux, nausea, vomiting, decreased appetite
39
imaging modality of Cholelithiasis (Gallstones
US is primary choice – very sensitive, even for small stones (~2mm)\*
•Obese patients - CT scan or MRCP if able to tolerate
40
tx of Cholelithiasis (Gallstones)
Asymptomatic – leave them be
Symptomatic cholelithiasis – refer to general surgery for lap CCY
41
Risk factors for Cholelithiasis (Gallstones)
Risk Factors:
* Fat --\> bariatric surgery or rapid weight loss
* Female
* Fertile (pregnancy)
* 40s
42
Most common complication of gallstone disease
Cholecystitis
43
Si/Sx of Cholecystitis
Biliary colic – post-prandial RUQ/epigastric pain that progressively worsens\* - does not go away w/ Pepcid
radiates to scapula
(+) Murphy’s sign (97% sensitive but only 48% in elderly)
44
physical exam findings in
## Footnote
Cholelithiasis (Gallstones) vs Cholecystitis
Cholecystitis (+) murphys sign
## Footnote
Cholelithiasis (Gallstones) - Patients usually have a history of similar, less severe episodes – be sure to ask about this!
45
US & HIDA findings in Cholecystitis
US : may show cholelithiasis, thickened GB wall/pericholecystic fluid. - imaging of choice
HIDA : failure of the gallbladder to fill, usually reserved for after an equivocal US
46
tx of Cholecystitis
_symptoms resolve_ (biliary colic): outpatient surgical referral w/instructions to return to ED if sx return, advise low-fat diet
_Persistent Symptoms:_ Admit or refer for hospital admission and surgical evaluation
_OR:_ Per surgery -\> Lap chole (preferably elective) or open if necessary
_not a surgical candidate,_ consider percutaneous cholecystostomy drain via IR
47
Cholelithiasis (Gallstones) lab findings are usually ??
unremarkable
48
Choledocholithiasis is due to ?
Most commonly due to passage of stones from the gallbladder through the cystic duct into the common bile duct
49
Si/Sx of Choledocholithiasis
RUQ pain, jaundice
dark urine
(+) Murphy’s sign
50
lab values in Choledocholithiasis
↑direct bili ( not indirect bilirubin),
↑ AST/ALT
↑alk phos (slow), Lipase
51
Best non-invasive test for Choledocholithiasis
MRCP
52
tx of Choledocholithiasis
ERCP (Endoscopic Retrograde Cholangiopancreatography) -\> remove stones
Laparoscopic CCY (typically AFTER ERCP) preferably prior to discharge
53
Clinical syndrome characterized by fever, jaundice, and abdominal pain that develops as a result of stasis and infection in the biliary tract – usually due to choledocholithiasis
Cholangitis
54
si/sx of cholangitis
_Charcot’s Triad_ – Fever, jaundice and RUQ pain( hx of biliary colic)\*
_Reynold’s Pentad_ – Fever, Jaundice, RUQ pain, + hypotension and AMS\*
Acutely sick – on verge of sepsis
55
pathogens for cholangitis
E. coli (25-50%)
Klebsiella (15-20%)
Enterobacter spp.(5-10%)
Enteroccoccus spp. (10-20%)
56
imaging modality for cholangitis
ERCP – stone extraction +/- biliary stent placement\*
57
tx of cholangitis
_ADMIT, may need ICU level management_
_ABCs_
_Broad-Spect Abx after 2 sets of Blood Cx_
* Zosyn , Ceftriaxone
* Levaquin with Flagyl IV
_Contact GI or Advanced Endoscopy_ – Patient needs an **urgent ERCP** with sphincterotomy, stone removal, and biliary drainage (Should be done within 24-48 hours)\*
58
Chronic progressive disorder of unknown etiology that is characterized by
inflammation, fibrosis, and stricturing of medium and large ducts in the intrahepatic and/or extrahepatic biliary tree
leads to complications of cholestasis and hepatic failure
Primary Sclerosing Cholangitis (PSC)
59
Primary Sclerosing Cholangitis (PSC) is associated w/ what diseases?
•Associated with IBD (Ulcerative Colitis)\*
60
si/sx of Primary Sclerosing Cholangitis (PSC)
Usually Asymptomatic (50% at time of diagnosis) – elevated Labs found on routine evaluation
Fatigue and pruritis
F/C; night sweats, RUQ pain, jaundice •
61
lab values and imaging seen in Primary Sclerosing Cholangitis (PSC)
Labs: **↑Alk Phos**, and ↑Total bilirub Cholestatic)
AST/ALT usually \<300
_MRCP_ - "beaded" appearance of the bile duct
62
tx of Primary Sclerosing Cholangitis (PSC)
ERCP and balloon dilation/stent placement
Liver transplantation is the treatment of choice for patients with advanced liver disease
63
medication options in Primary Sclerosing Cholangitis (PSC)
* Cholestyramine – pruritis
* Ursodiol (15 mg/kg) daily may be helpful for cholestasis, but not effective in prolonging survival
Steroids and immunosuppressant (Imuran, MTX
64
Primary Sclerosing Cholangitis (PSC) screening
yearly RUQ US
or MRCP every 6-12 months, monitor CA 19-9 every 6-12 months
65
lab value that is indicative of acute pancreatitis
Lipase \>3x upper limits of normal, but will generally be \>100 only cause making lipase this elevated
66
lab values seen in acute pancreatitis that show:
greater risk of mortality
severity
BUN \>20 = greater risk of mortality
CRP \>150 assoc w/ severe pancreatitis
67
most common causes of acute pancreatitis
* Gallstones – (40-70%)
* ETOH – (25-35%)
68
si/sx of acute pancreatitis
Sudden onset severe epigastric pain radiating to the mid-back
nausea, vomiting
Anorexia
Tachycardia
abdominal guarding, distention
hypotension(sometimes), fevers, tachypnea
ecchymosis in the periumbilical area (_Cullen’s Sign)_
along the flank (_Grey-Turner Sign)_
69
culllen and grey turner signs are seen w/ what dx?
Acute pancreatitis
70
si/sx of chronic pancreatitis
Abdominal pain – epigastric and radiates to the back
Pancreatic insufficiency – fat malabsorption causing steatorrhea, malabsorption of vitamins A,D,E,K and B-12
Glucose intolerance
71
risk factors for chronic pancreatitis
* ETOH
* Recurrent acute pancreatitis
72
lab and imaging values in chronic pancreatitis
Normal Lipase – not reliable
Calcifications on US
73
tx of acute pancreatitis
IV Fluid Replacement\*\*: Cornerstone of management
Repeat labs assessing BUN/Creatinine, HCT q8-12 hours
Monitor CRP at 48 hours
74
tx of chronic pancreatitis
Pancreatic enzymes - approximately 30,000 international units (IU) of lipase per meal
Fat restriction \<20 g per day
Vitamin supplementation
Celiac nerve block/neurolysis – via EUS or percutaneous
Glucose management
75
in acute pancreatitis Patient should have a follow-up _____ in ____ months to ensure healing and rule-out underlying pancreatic tumors
•Patient should have a follow-up MRCP in 2-3 months to ensure healing and rule-out underlying pancreatic tumors
76
85% of pancreatic cancers are due to ____ \_\_\_\_\_ of the pancreas
85% of pancreatic cancers are due to **ductal adenocarcinoma** of the pancreas
77
3rd leading cause of death from cancer in the United States
pancreatic cancer
78
si/sx of pancreatic cancer
**Painless jaundice**
Initially asymptomatic until advanced disease
Weight loss
Pruritis
Dark urine
Pale stools , Steatorrhea
Epigastric pain
Palpable gallbladder(Courvoisier’s sign)
Glucose abnormalities (new onset diabetes)
79
imaging modality for pancreatic cancer
if metastasis present?
Contrast-enhanced CT – pancreas protocol\*
Histological diagnosis – Endoscopic Ultrasound guided core needle biopsy of pancreatic tumor, or percutaneous liver biopsy if metastasis present
80
CA19-9 tumor marker is useful to identify
pancreatic cancer
81
tx of pancreatic cancer
_Resectable dz –modified whipple, pancreatectomy_
* Tumor in the head or uncinate process - Pylorus-sparing pancreaticoduodenectoy(modified Whipple procedure)
* Body and tail – distal pancreatectomy
_Locally Advanced Disease (30%)_: Radiation and Chemo – goal is to shrink tumor to a resectable size
_Advanced Metastatic Disease (60%)_ - Systemic chemo
82
major risk factors for gallstone formation
pregnancy
rapid weight loss
83
symptomatic cholithiasis may be confused with??
heartburn or indigestion
84
acquired diabetes and malabsorption of fat soluable vitamins make you think??
chronic pancreatitis
85
painless jaundice makes you think??
biliary or pancreatic malignancy
86
stages of Liver Cirrhosis
Compensated
Compensated w/ varices
Decompensated à Ascites, variceal bleeding, encephalopathy, jaundice
87
common causes of Liver Cirrhosis
* Hepatitis C (26%)
* Alcoholic liver disease (21%)
* Hepatitis C plus alcoholic liver disease (15%)
* NAFLD
88
major complication of Liver Cirrhosis
Ascites (60% within 10 yrs)
89
si/sx of liver cihrrosis
Symptoms are with LATE STAGE disease so most have NO SYMPTOMS
Appearance of chronic illness
Palpable/firm liver (hard sharp nodular edge) -70%
Splenomegaly – 35-50%
Abdominal and thoracic superficial veins are dilated (caput medusa)
Ascites
90
labs and imaging tests in liver cihrosis
Often absent or minimal abnormalities in early or compensated
U/S – liver size, ascites, nodular liver
FibroSure test - Predicts stage of fibrosis in HCV, ASH, NASH
Transient elastography (fibroscan) -US passes a vibratory wave through the liver and measure hepatic fibrosis or liver stiffness
91
what is the MELD Score
MELD Score - Prognostic scoring system for end stage liver disease +/-cirrhosis 3 mo survival in patients with end stage liver disease
92
tx of liver cihorrosis
liver transplant
93
pHTN is defined as
Increased hydrostatic mmhg w/in portal vein \>10- 12mmhg (collaterals begin to develop)
•As mmhg increases blood flow decreases and then mmhg transferred to portal vein tributaries w/ subsequent dilation = collateral formation
94
Sequelae of portal HTN
* Ascites
* Esophageal and gastric varices
* Hepatic encephalopathy
* Splenomegaly and thrombocytopenia
95
causes of pHTN
## Footnote
Pre-hepatic
Intra-hepatic
Post-hepatic
_Pre-hepatic_
**•Portal vein thrombosis**
* Splenic vein thrombosis
* Portal vein atresia/stenosis
_Intra-hepatic_
**•Cirrhosis\***\* - Etoh or chronic hepatitis
_Post-hepatic_
* Budd-Chiari
* Extrinsic tumor compression
**•Right heart failure**
96
screening in pHTN
Screening EGD for varices and then annually
97
tx of pHTN
Prophylactic treatment (reduce first variceal bleed liklihood by 50%)
* Nonselective beta-blockers (nadolol or propranolol)
* Reduce portal and collateral blood flow
* Mild decrease on portal pressure
98
Pathologic accumulation of excess fluid in the peritoneal cavity -\> Due to hepatic and nonhepatic causes
•cirrhosis (80% cause b/c of portal HTN)
ascites
99
si/sx of ascites
need abt 1500ml for PE dx so relatively inaccurate
Abdominal distension
Bulging flanks
Shifting dullness to percussion
Fluid wave
100
imaging and labs in ascites
U/S
Paracentesis
* SBP?
* Cell count - w/ elevated WBC
* Culture and gram stain
* Glucose, LDH, protein, albumin
Albumin and total protein
101
tx of ascites
First line – Na Restriction
Second line – diuretics (spiro / Furosemide)
Surgical
* Large volume paracentesis – symptomatic relief
* TIPS – relief of ascites
* Liver transplant
102
Late Cirrhosis induced MS changes (chronic cirrhosis)
•Up to 70% of patients w/ cihorrosis
Hepatic Encephalopathy
103
si/sx of Hepatic Encephalopathy
Symptoms range alert w/ minor impairment memory, coordination, cognition to coma
•asterixis, twitchines
104
lab and imaging findings in Hepatic Encephalopathy
Ammonia elevation
EEG findings high-amplitude low-frequency waves and triphasic waves
105
tx of Hepatic Encephalopathy
Lactulose
Antibiotics (xifaxan-nonabsorbable antibiotic which absorbs ammonia)
106
causes of Gastroesophageal Varices
Increased portal vein pressure causes varices
•Diversion of blood back to systemic veins d/t high mmhg through liver thus forming collaterals between IVC & SVC and portal venous system
107
si/sx of Gastroesophageal Varices
Hematemesis/melena/hematochezia
Pale, hypotensive, lightheaded, syncope, orthostatic, tachycardic
Liver disease/Cirrhosis signs
AMS (encephalopathy)
108
red whale sign is indicative of??
Gastroesophageal Varices
red marks on varices = red wale sign
109
tx of gastroesophageal varicies
Octreotide
Abx – 3rd gen ceph
Band ligation \*\* - prevention of rebleed
TIPS
Angiotherapy
Liver transplant
110
infectious and noninfectious causes of hepatitis
_Infectious_
* Viral (Hep A, B, or C)
* Fingal
* Bacterial
* Parasitic
_Non-infectious_
* Autoimmune
* Toxins/drugs (ex. Tylenol OD, IVDU)
* ETOH
* Metabolic diseases
111
lab value indicative of hepatitis
elevated out of proportion transaminases (AST/ALT)
Hyperbilirubinemia
112
ETOH Hepatitis
labs
tx?
* ETOH (AST/ALT ration 2:1 not greater then 300)
* US = ascites, fatty liver
Steroid - Methyl prednisone
Pentoxiphylline - if steroids CI
Liver transplant after 6 mo no ETOH
113
hepatitis spread Fecal-oral route transmission assoc w/ crowding and poor sanitation
Lab values?
Tx?
Hep A
## Footnote
Fecal-oral route transmission assoc w/ crowding and poor sanitation
Symptomatic treatment
Clinical recovery w/in 3 mo and no chronic liver disease
114
hepatitis Transmitted infected blood products, sexual contact, delivery by HBV+ mother
Hep B
115
dx tests for Hep B
* HBsAG - first evidence of infection and if persistent \>6mo after illness indicates chronic infection
* HBV DNA - active viral replication, = predictor of cirrhosis and HCC
* Anti-HBc - – IgM indicating acute hepatitis infection and IgG indicating chronic or recovered infection
* Anti-HBs - – after successful vaccination or recovery from HBV infection
116
tx of hep B
Chronic
•Entecavir, Tenofovir
117
Associated with extrahepatic manifestations what hepatitis?
what are these manifestations?
Hep B Glomerulonephritis (mostly children)
•Polyarteritis nodosa (diffuse vasculitis w/ 30% mortality w/in 5yr)
118
HBV Risk factors for progression to cirrhosis, liver failure, HCC
* Persistently elevated HBV DNA or ALT
* Older, male, FHx HCC
* AFP elevated
* Co-infection any hepatitis
119
ONLY associated w/ HBV infection and only when HBsAg present
testing?
prognosis?
Hep D
## Footnote
* Testing = anti-HDV
* In combination w/ chronic HBV carries worse short term prognosis w/ often rapid FHF or progression to cirrhosis
120
hepatitis See typically only in immunocompromised patients
## Footnote
•Uncommon in US but consider if travel to endemic areas i.e. Central and SE asia, Middle east, North Africa.
Hep E = fecal oral transmission (waterborne)
121
hep C dx tests
* Anti-HCV ELISA - moderate sensitivity and specificity
* HCV RNA – confirmatory
122
tx of hep C
Ledipasvir/sofosbuvir -Harvoni
•Clinical recovery in 3-6 mo w/ low overall mortality \<1%
Usually asymptomatic or mild clinical illness w/ 6-7 wk incubation but 85% develop chronic HCV
123
hepatitis in Usually young to middle aged women
Autoimmune
Often insidious onset but near 40% acute hepatitis presentation can be following viral illness or drug exposure
124
autoimmune hep lab values
* Transaminases \>1,000
* (+) ANA
* Elevated IgG
* Liver bx
125
tx of autoimmun hep
* Corticosteroids
* Mercaptopurine
* +/- azathioprine
126
HCV inreased risk of developing liver cihorrosis if
* Chronic alcohol ingestion
* Male
* HCV \>40yo
* Co-infection with HIV and/or HBV
127
complications fo hepatitis
* Encephalopathy ( ICP)
* Chronic hepatitis
* HCC
128
Hepatocellular carcinoma (HCC) is caused by
Underlying liver dz
* Cirrhosis
* NASH
* NAFLD
129
labs and imaging modalities inn HCC
* Labs (ex. alpha-fetoprotein)
* US- screen for hepatic nodules in high risk pts
* CT
* MRI
130
biospsy requirements for HCC
**Biopsy (based on size) – diagnostic!**
* \<1 CT/MRI and follow every 3 mo to assess for enlarging lesion
* 1-2cm lesions bx should be performed
* 2 cm, cirrhosis, characteristic imaging studies (arterial hypervascularity and delayed washout), and elevated AFP values can be managed without biopsy
131
tx of HCC
_Surgical_
* Resection
* Liver transplant
_Medical/palliative_
* Sorafenib (VEGF blocker – slows progression w/ advanced HCC
* TACE/TARE – tx via hepatic artery ois a bridge to transplant
Chemotherapy ineffective and radioinsensitive tumor
132
si/sx of hepatitis
* Constitutional Sx (ex. fatigue/malaise, anorexia, N/V, fever)
* Hepatomegaly
* Jaundice
133
AST/ALT ration 2:1 not greater then 300 is seen in ..?
ETOH Hepatitis
