GIT Flashcards
1
Q
criteria for diagnosis of achlasia cardia
A
incomplete relaxation of LES
aperistalsis of esophagus
2
Q
most common cause of achlasia
A
in US adenocarcinoma of proximal stomach
worlswide chagas is most common
3
Q
symptoms of achlasia ♧
A
•dysphagia to both solid and liquids in contrast to esophageal carcinoma in which dysphagia starts for soilds but progresses to liquids
DYSPHAGIA IMPROVES ON STANDING as it increases pressure on esophagus
•regurgitation
•chest pain
•wht loss
•recurring pulmonary inf due to aspiration
4
Q
diagnosis of achlasia
A
barium bird beak appearence
manometery to confirm the diagnosis
5
Q
treatment of achlasia
A
medical
antimuscarinic
nitroglycerin
ccb
inj of botulinum toxin
pneumatic or balloon dilation
surgical
hellers myotomy
6
Q
wht is esophageal ring
A
An esophageal ring is defined as a concentric, smooth, thin (3-5 mm) extension of normal esophageal tissue consisting of 3 anatomic layers of mucosa, submucosa, and muscle.
Three types of esophageal rings exist, and they are classified alphabetically as A, B, and C,
A several cm above squamocolumnar junction
B or schtazki ring the Schatzki ring is a web because it is composed of only mucosa and submucosa. Typically, the Schatzki ring is located at the SQJ,
The C ring is a rare anatomic finding on radiographic studies referring to the indentation caused by the diaphragmatic crura. It is rarely symptomatic.
7
Q
wht is esophageal web
A
An esophageal web is a thin (2-3 mm), eccentric, smooth extension of normal esophageal tissue consisting of mucosa and submucosa
8
Q
two types of esophageal carcinoma
A
SCC
ADENOCARCINOMA
9
Q
most common location of SCC of esophagus
A
upper and mid esophagus Risk factors are alcohol and tobacco use, diet (nitrosamines, betel nuts, chronic ingestion of hot foods and beverages such as tea), human papillomavirus, achalasia , Plummer–Vinson syndrome, caustic ingestion, and nasopharyngeal carcinoma.
10
Q
most common location of adenocarcinoma of esophagus
A
distal third of the esophagus/gastroesophageal junction . •Riskfactors:
GERD and
Barrett esophagus
11
Q
wht is barrets esophagus
A
Barrett esophagus is a complication of longstanding acid reflux disease in which there is columnar metaplasia of the squamous epithelium. Patients with Barrett esophagus are at increased risk of developing adenocarcinoma of the esophagus. Monitor these patients with routine endoscopic surveillance
12
Q
is achlasia premalignant
A
yes
13
Q
corkscrew appearence in
A
DES
Nonperistaltic spontaneous contraction of the esophageal body—several segments of the esophagus contract simultaneously and prevent appropriate advancement of food bolus.
2. In contrast to achalasia, sphincter function is normal(normal LESpressure
14
Q
types of esophageal hiatal hernia
A
Type I hiatal hernia
is the most common type. It is also called a sliding hiatal hernia. . In this type of hernia, the gastroesophageal junction is herniated into the chestType II hiatal hernia is also called a paraesophageal hiatal hernia, in which the stomach herniates through the diaphragmatic esophageal hiatus alongside the esophagus.
type II or “pure” paraesophageal hernia,
the gastroesophageal junction remains below the hiatus and the stomach rotates in front of the esophagus and herniates into the chest . If more than 30 percent of the stomach herniates into the chest, the condition is also called a giant paraesophageal hernia.
Type III hiatal hernias are combined hernias
in which the gastroesophageal junction is herniated above the diaphragm and the stomach is herniated alongside the esophagus.
type IV hiatal hernias, o
ther organs in addition to the stomach (colon, small intestine, spleen) also herniate into the chest
15
Q
complications of esophageal hernia
A
Complications of sliding hiatal hernias include GERD(mostcommon)
,reflux esophagitis(with risk of Barrett esophagus/cancer),and aspiration.
- Complications of paraesophageal hernias are potentially life-threatening and include obstruction, hemorrhage, incarceration, and strangulation.
16
Q
difference between boerhaave and malory weiss syn
A
the tear is mucosal and at the gastroesophageal junction,it is referred to as mallory–Weiss syndrome.
•If a tear is transmural (causing esophageal perforation), it is referred to as Boerhaave syndrome.
17
Q
clinical manifestations of esophageal perforation
A
pain(severe retrosternal/chest/shoulder pain), tachycardia,hypotension, tachypnea, dyspnea, fever,
Hamman sign (“mediastinal crunch” produced by the heart beating against air-filled tissues), pneumothorax, or pleural effusion.
18
Q
hamman sign
A
Hamman’s sign(rarely,Hammond’s sign]orHammond’s crunch]) is a crunching, rasping sound, synchronous with the heartbeat,heard over theprecordiumin spontaneousmediastinal emphysema. It is felt to result from the heart beating against air-filled tissues.
This sound is heard best over the left lateral position.
]It has been described as a series of precordial crackles that correlate with theheart beat rather than respiration.
19
Q
upper gi bleed
A
bleeding from above ligament of treitz
20
Q
lower gi bleed
A
bleeding below the ligament of trietz
21
Q
causes of upper gi bleeding
A
Peptic ulcer disease(PUD)—duodenal ulcer ,gastric ulcer gastritis b.Reflux esophagitis •esophageal varices •gastric varices •gastric erosion •mallory weiss tear •hemobilia •dielafoys vascular malformation •aortoenteric fistulas •neoplasm
22
Q
lower gi bleed causes
A
diverticulosis angiodysplasia IBD colorectal cancer colorectal carcinoma colonic polyps ischemic coliitis hemorrhoids
23
Q
hematemesis
A
upper gi bleed
vomiting blood
moderate to severe bleeding tht may be ongoing
24
Q
cofee ground emesis
A
upper gi bleed
lower rate of bleeding
( enough time for vomitus to transform into coffee grounds )
25
melena
black tarry liquid foul smelling stool
caused by degradation of hb by bacteria in stool colon
90% upper gi bleed if colon then most commonly ascending colon
26
hematochezia
bright red blood per rectum
lower gi source typically left colon or rectum
can be upper if massive bleeding ususally pt has hemodynamic compromise if upper
27
best initial test for hematemiesis
upper Gi endoscopy
28
hematochezia best initial test
rule out anorectal cause like haemorroids
| colonoscopy should be the best initial test cause of colon cancer being the most imp cause un elderly
29
melena best initial test
upper endoscopy
| if no bleeding site found then lower gi source searched from colonoscopy
30
wht does elevation of BUN creatinine ratio in pt with no renal insufficiency indicates
upper gi bleed.
31
most accurate test for evaluation of upper gi bleed
upper gi endoscopy
both diagnostic and theurapeutic
coagulate bleeding vessel
32
first step in management of upper gi bleed
resuscitation with iv fliuds is the first step
33
test which definatively locates point of bleeding
arteriography
| also therapeutic as embolization or intraarterial vasopressin can be given
34
guidelines for screening of colon cancer
The American Cancer Society and the United States Preventive Services Task Force (USPSTF)
strongly encourage routine colon cancer screening in all patients age ~50
. Screening can be
performed using
1. high-sensitivity fecal occult blood testing (FOBT) annually, 2.flexible
sigmoidoscopy every 5 years + FOBT every 3 years, or 3.colonoscopy every 10 yrs
All 3 strategies decrease colon cancer mortality
Patients with a history of colon cancer in a first-degree relative should be
screened at age 40 or 10 years before the age of the relative's diagnosis
Colonoscopy is the most sensitive and
specific test, but it is also the most costly and expertise dependent
35
guidelines for screening of lung cancer
Low-dose chest CT is recommended yearly for lung
cancer screening in patients who are
age 55-80,
have a ~30-pack- year smoking history, and
are currently smoking or quit within the past 15 yrs
36
most common cause of acute pancreatitis
alcohal abuse
gall stones
other causes are
3 post ERCP
4 viral infections
5 Drugs—sulfonamides,thiazidediuretics,furosemide,estrogens,HIVmedications, and many other drugs have been implicated
6. Postoperative complications (high mortality rate) 7.Scorpion bites
8.Pancreas divisum
9. Pancreatic cancer
10. Hypertriglyceridemia, hyoercalcemia
11. Uremia
12. Blunt abdominal trauma (most common cause of pancreatitis in children)
37
most common cause of pancreatitis in children
blunt abdominal trauma
38
symptoms of acute pancreatitis
Abdominal pain, usually in the epigastric region
•May radiate to back
•Often steady, dull,and severe;worse when supine and after meals
b. Nausea and vomiting, anorexia
39
signs of acute pancreatitis
•Low-grade fever,
•tachycardia
,•hypotension,leukocytosis
• Decreased or absent bowel sounds indicate partial ileus d.The following signs are seen with hemorrhagic pancreatitisas blood tracks along fascial planes:
•Grey Turner sign(flank ecchymoses)
•Cullen sign (periumbilical ecchymoses)
•Fox sign (ecchymosis of inguinal ligament)
40
grey turner sign
flank echymosis
41
cullen sign
periumblical ecchymosis
42
fox sign
ecchymosis of inguinal ligament
43
diagnosis of acute pancreatitis
serum amylase
serum lipase more specific than amylase
LFT
abdominal radiograph
•sentinal loop -sentinel loop (area of air-filled bowel usually inLUQ,which is a sign of localized ileus) or a
•colon cut-off sign(air-filled segment of transverse colon abruptly ending or “cutting off” at the region of pancreatic inflammation )
abdominal usg to define cause of pancreatitis
CT SCAN
MOST ACCURATE TEST FOR DX OF DS AND COMPLICATIONS
ERCP
44
complications of acute pancreatitis
```
pancreatic necrosis
pancreatic pseudo cyst
hrgic pancreatitis
adult respiratory distress syn
pancreatic ascitis or pleural effusion
ascending cholangitis
pancreatic abscess
```
45
complications of pancreatic pseudocyst
* rupture,
* infection
* gastric outlet obstruction
* fistula
* hemorrhage into cyst, and
* pancreatic ascites.
* It may impinge on adjacent abdominal organs(e.g.,duodenum,stomach,transverse colon)
* if large enough;or if located in the head of the pancreas,it may cause compression of the CBD.
46
toxic megacolon
Risk factors
• lBD
• Clostridium difflcile infection
```
Systemic toxicity
fever, tachycardia, hypotension
Diagnosis
• Bloody diarrhea
• Abdominal distension/peritonitis
• Marked colonic distension on imaging
```
```
Management
•Bowel rest, NG suction, antibiotics
• +/- Corticosteroids if IBO-associated
• Surgery if unresponsive to
medical management
```
47
diagnostic triad of chronic pancreatitis
The classic triad of
steatorrhea,
diabetes mellitus, and
pancreatic calcification on plain films or CT scan is also diagnostic.
48
gold standard for chronic pancreatitis
ERCP not done as invasive diagnosis formed with the help of CT SCAN
49
diagnostic modalities of chronic pancreatitis ♧
CT scan initial study of choice.
abdominal radiograph
pressence of pancreatic calcification
ERCP is gold standard
serum amylase and lipase level are not elevated
50
complications of chronic pancreatitis
```
narcotic addiction
diabetes mellitua
malabsorption
pseudocyst
duct dilation
CBD obstruction
vitB12 malabsorption
effusion
pancreatic cancer
```
51
most common location of pancreatic carcinoma
pancreatic head
52
diagnostic modalities of pancreatic cancer
ERCP most sensitive test for diagnosis of pancreatic cancer
tumor markeres
CA19-9
CEA
53
chain of lakes appearence is seen in
typical finding on ERCP in chronic pancreatitis
| due to strictures and duct dilation throughout pancreatic duct
54
most common location of diverticulosis
sigmoid colon
55
difference between diverticulosis and diverticulitis
Diverticulosis (pouches in the colon wall) should be distinguished from
diverticulitis, which refers to inflammation or infection of the diverticula and is a complication of diverticulosis.
56
diagnostic test for diverticulosis
barium enema is test of choice
57
complications of diverticulitis
abscess formation
colovesical fistula
obstruction
free colonic perforation
58
test of choive for diverticulosis
barium enema
59
test of choice for diverticulitis ♧
CT scan
Findings suggestive of
diverticulitis include increased inflammation in pericolic fat, presence of diverticula, bowel wall
thickening, soft tissue masses (eg, phlegmons), and pericolic fluid collections suggesting absces
barium enema and colonoscopy is CONTRAINDICATED
60
treatment of complicated and uncomplicated diveticulitis
uncomplicated - IV antibiotics , bowel rest and IV fliuds
| complicated - surgery
61
causes of cirrhosis of liver
1. Alcoholic liver ds
2. Chronic hepatitis B and C infections—next most common causes
3. Drugs (e.g., acetaminophen toxicity, methotrexate) 4. 4Autoimmune hepatitis
5.Primary biliary cirrhosis(PBC) ,secondary biliary cirrhosis
Inherited metabolic diseases (e.g., hemochromatosis, Wilson disease)
7.Hepatic congestion secondary to right-sided heart failure,constrictive pericarditis
8.α1-Antitrypsin (AAT) deficienc
y 9. Hepatic venoocclusive disease—can occur after bone marrow transplantation
10. Nonalcoholic steatohepatitis (NASH)
62
complications of liver failure
Complications of liver Failure ( AC, 9H) mnemonic
```
•Ascites
•Coagulopathy
•Hypoalbuminemia
•Portal hypertension
•Hyperammonemi
a •Hepatic encephalopathy
•Hepato renal syndrome
•Hypoglycemia
•Hyperbilirubinemia/jaundice
•Hyperestrinism
•HCC
•lowers the total triiodothyronine (T3) and thyroxine (T4) in circulation; however,
free T3 and T4 levels are unchanged, and TSH will be normal, reflecting a euthyroid status.
```
63
diffrential diagnosis of ascitis
```
Cirrhosis,porta lHTN
•CHF
•Chronic renal disease
•Massive fluid overload
•Tuberculous peritonitis
•Malignancy
•Hypoalbuminemia
•Peripheral vasodilation secondary to endotoxin-induced release of nitrous oxide,which leads to increased renin secretion(and thus secondary hyperaldosteronism)
•Impaired liver inactivation of aldosterone
```
64
treatment of bleeding esophageal varices
```
variceal ligation
endoscopic sclerotherapy
iv vasopressin
iv octreotide first line therapy
balloon tamponade blakemore tube
```
65
most common cause of SBP
ecoli
66
SAAG
< 1.1 g/dl most likely due cause otherthan portal hypertension
>1.1g/dl most likely due to portal hypertension
67
precipating factors for hepatic encephalopathy
```
alkalosis
hypokalemia
drugs(narcotics,sleeping medications)
gi bleeding
systemic infection
hypovolemia
```
68
clinical features of hepatic encephalopathy
dec mental function
confusion
asterexis ( not specific )
fetor hepaticus
69
treatment of hepatic encephalopathy ♧
lactulose prevent absorption of ammonia
rifaximin kill bacterial flora dec ammonia formation
limit protein 30-40g/day
70
gold standard for diagnosis of cirrhosis is
liver biopsy
71
charcot triad ♧
Fever,
jaundice,
right upper quadrant pain (Charcot triad) of acute cholangitis
72
reynods pentad ♧
IS MEDICAL EMERGENCY can be rapidly fatal
in cholangitis
•Fever
• jaundice,
• right upper quadrant pain (Charcot triad)
• Mental status changes,
•hypotension (Reynolds pentad)
Charcot triad plus septic shock and altered mental status(CNS depression—e.g., coma, disorientation).
73
definative test for cholangitis
Cholangiography(PTC or ERCP).
a. This is the definitive test, but it should not be performed during the acute phase of illness.Once cholangitis resolves,proceed with PTC or ERCP to identify the underlying problem and plan treatment.
b. Perform PTC when the duct system is dilated (per ultrasound)and ERCP when the duct system is not dilated
74
treatment of acute cholangitis
IV ANTIBIOTICS +IV FLIUDS
| decompress CBD via PTC ERCP or laprotomy
75
most dreaded and serious complication of acute cholangitis
liver abscess has high mortality rate
76
porcelien gallbladder
intramural calcification of GB wall
| 50%progresses to cancer thus needs prophylactic cholecystectomy
77
wht does elevated alk and ggt means
ALK-P
is elevated when there is obstruction to bile flow (e.g.,cholestasis) in any part of the biliary tree.
Normal levels make cholestasis unlikely
. 2. If levels are very high(10-fold increase),think of extra hepatic biliary tract obstruction or intrahepatic cholestasis (e.g., PBC or drug-induced cirrhosis).
3. If levels are elevated,measure the gamma-glutamyl-transferase(GGT) level to make sure the elevation is hepatic in origin(rather than bone or intestinal).If the GGT level is also elevated,this strongly suggests a hepatic origin.If the GGT level is normal but ALK-P is elevated,consider pregnancy or bone ds
78
elevated ast alt means
1.ALT and AST levels are MILDLY elevated (low hundreds)
,think of chronic viral hepatitis
acute alcoholic hepatitis
.
2..If ALT and AST levels are MODERATELY elevated (high hundreds to thousands), think of
acute viral hepatitis.
3..If ALT and AST levels are SEVERLY elevated (>10,000), extensive hepatic necrosis has occurred.
Typical cases are: a.Ischemia,
b.shock liver(prolonged hypotension orcirculatory collapse)
b. Acetaminophen toxicity
c. Severe viral hepatitis
4. Note that liver transaminases are often NORMAL OR EVEN LOW in patients with
• cirrhosis (without any active cell necrosis) or •metastatic liver disease, because the number of healthy functioning hepatocytes is markedly reduced.
.5.The following can cause an ELEVATION in ALT or AST levels in ASYMPTOMATIC patients (note the mnemonic): ABCDE
a. Autoimmune hepatitis
b. Hepatitis B
c. Hepatitis C
d. Drugs or toxins
e. Ethanol
79
CHOLESTATIC MARKERS
Cholestatic LFTs:
markedly elevated alkaline phosphatase
GGT;
ALT and AST slightly elevated
80
HEPATOCELLULAR NECROSIS MARKER
Hepatocellular necrosis or inflammation:
normal or slightly elevated alkaline phosphatase
; markedly elevatedALT and AST
81
NASH mechanism in diabetes
mechanism in diabetes leading to nash
NAFLD can be due to increased transport of (FFA) from adipose tissue to the
liver, decreased oxidation of FFA in the liver, or decreased clearance of FFA from the liver (due
to decreased VLDL production) It is frequently related to peripheral insulin resistance leading
to
increased peripheral lipolysis,
triglyceride synthesis, and
hepatic uptake of fatty acids.
Hepatic FFA increases oxidative stress and production of proinflammatory cytokines (eg, tumor
necrosis factor-alpha
82
NASH defination
DEFINATION
•Hepatic steatosis on imaging or biopsy
• Exclusion of significant alcohol use
• Exclusion of other causes of fatty liver
CLINICAL FEATURES
• Mostly asymptomatic
• Metabolic syndrome
+/- Steatohepatitis (AST/AL T ratio <1)
• Hyperechoic texture on ultrasound
Treatment
• Diet & exercise
• Consider bariatric surgery if BMI ;::35
83
management of GERD
if alarm symptoms ☆ alarm symptoms
present absent
⬇️ ⬇️
upper gi endoscopy trial of PPI
☆( dysphagia
odynophagia, wht loss
anaemia ,gi bleed)
84
treatment of hepatic hydrothorax ♧
transudate
Hepatic hydrothorax is a cause of transudative pleural effusions in patients with cirrhosis who
have no underlying cardiac or pulmonary disease to account for development of such an
effusion. Hepatic hydrothorax usually results in a right-sided pleural effusion.
Initial treatment is
usually with salt restriction and diuretics.
TIPS placement is considered in patients with
refractory hepatic hydrothorax
85
ROME DIAGNOSTIC CRITERIA of irritable bowel syndrome ♧
Recurrent abdominal pain/discomfort 2:3 days/month for the
past 3 months & >2 of the following:
diagnostic
• Symptom improvement with bowel movement
criteria
• Change in frequency of stool
• Change in form of stool
86
most common gi diagnosis in north america
irritable bowel syndrome
87
gilbert syndrome ♧
Gilbert's syndrome is a familial disorder of bilirubin glucuronidation in which the production of
UDP glucuronyl transferases (enzymes that mediate glucuronidation of various substances) is
reduced.
The genetic defect is mapped to the promoter region of the UDP glucuronyl transferase gene
Clinical manifestations of Gilbert's syndrome include icterus secondary to a mild, predominantly
unconjugated hyperbilirubinemia (normal levels in these patients are < 3 mg/dl) Those patients
who are symptomatic tend to have nonspecific complaints, including malaise, fatigue, or
abdominal discomfort.
Certain events, such as hemolysis, fasting or consuming a fat-free diet,
physical exertion, febrile illness, stress, or fatigue are thought to be triggers for
hyperbilirubinemia in patients with Gilbert's syndrome
88
finding of alcoholic hepatitis
Alcoholic hepatitis (AH) best explains patients presentation with fever, jaundice, anorexia,
■tender hepatomegaly,
▪mild (<300 U/L)
■ elevation in aminotransferases (aspartate
aminotransferase [AST] and alanine aminotransferase [AL T]) with an AST:AL T ratio >2:1
■macrocytic anemia (mean corpuscular volume [MCV>1 OO , thrombocytopenia, and
mild
elevation in the INR.
Alcohol use should be confirmed and quantified
by first obtaining the patient's social history and discussing substance use. Patients with AH
commonly have a history of chronic, heavy alcohol use (>7 drinks/day) and sometimes develop
AH symptoms after an acute increase in consumption
89
treatment of gastric mucosa associated lymphoma
mostly caused by h pylori
pathogenesis of low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma
.
1. Such lymphomas may regress after the eradication of H. pylori using antibiotic therapy Although
some recent studies have shown certain pitfalls in this strategy, ANTIBIOTIC THERAPY still remains as
the most accepted and recommended management of gastric MALT lymphoma without any
metastasis.
Chemotherapy typically plays a role in the management of patients with MALT lymphoma if
eradication of H. Pylori fails to produce regression of the lymphoma Such therapeutic regimens
usually include
CHOP (cyclophosphamide, adriamycin, vincristine, and prednisone) or
CHOP+
Bleomycin
90
diagnosis of celiac ds
The diagnosis of
celiac disease is highly correlated with
positive results on serological studies, primarily lgA
anti-tissue transglutaminase and
lgA anti-endomysia! antibodies.
However, many patients
with biopsy-confirmed celiac disease will have negative results on lgA antibody testing due to an
associated selective lgA deficiency, which is common in celiac disease
. If lgA serology is
negative but the suspicion for celiac disease is high, total lgA should be measured (or lgG-based
serologic testing should be done)
91
chronic mesentric ischemia cause
The pathophysiology of the pain is most likely related to shunting of blood away from the
small intestine to meet the increased demand of the stomach. In patients with atherosclerosis,
the celiac or the superior mesenteric arteries may be narrowed and unable to dilate appropriately
to maintain adequate blood flow to the intestines.
92
symptoms of chronic mesentric ischemia
ABDOMINAL ANGINA
postprandial epigastric pain (intestinal angina),
food aversion, and
weight loss.
Patients may also report nausea, early satiety, and diarrhea.
The anginal pain frequently starts within the first hour of eating and slowly resolves over the next 2
hours
93
signs of chronic intestinal ischemia
physical examination may show signs of malnutrition and may reveal an abdominal bruit in
- 50% of patients, but can be otherwise unremarkable. Although abdominal x-ray and CT scans
may demonstrate calcified vessels, diagnosis requires better visualization of the vessels.
CT angiography is the preferred choice, although Doppler ultrasonography may also be helpful
Treatment involves risk reduction (eg, tobacco cessation), nutritional support, and
revascularization
94
clinical finding of primary sclerosing cholangitis
Laboratory tests typically show predominantly
• elevated alkaline phosphatase levels with smaller
•increases in serum aminotransferases (cholestatic pattern) •Other nonspecific findings may
include elevated inflammatory markers (eg, erythrocyte sedimentation rate),
• increased lgM, and
•positive perinuclear antineutrophil cytoplasmic antibodies. •Endoscopic retrograde or magnetic
resonance cholangiopancreatography confirms the diagnosis by showing multifocal narrowing
with intrahepatic and extrahepatic duct dilation
•Liver biopsy is typically not necessary but classically shows intrahepatic ductular obliteration with lymphocytic
infiltration and periductular "ONION SKIN " fibrosis
95
primary sclerosing cholangitis
intra and extrahepatic bile duct thickening and narrowing of their lumens leading to cirrhosis, portal hypertension, liver failure
strongly associated with UC
96
diagnostic study of choice for PSC
ERCP AND PTC
| bead like dilatation of intra and extra hepatic duct
97
primary biliary cirrhosis
destruction of intrahepatic bile duct with portal inflammation and scarring
more common in women
anti mitochondrial antibodies 98%specific
confirm diagnisis with biopsy
treatment with urodeoxycholic acid
98
causes of secondary biliary cirrhosis
long standing mechanical obstruction
sclerosing cholangitis
cystic fibrosis
biliary atresia
99
klatskin tumors
tumors of proximal third of CBD
| involve junction of rht and left hepatic duct
100
most consistent risk factor for pancreatic carcinoma
smoking
101
FAP FINDING
Autosomal dominant disease caused by hereditary mutations in the APC tumor suppressor gene.
•Characterized by hundreds of adenomatous polyps in the colon.
•The colon is always involved, and the duodenum is involved in 90% of cases.
Polyps may also form in the stomach, jejunum,and ileum. •The risk of CRC is 100% by the third or fourth decade of life(in100%of FAP cases)
. •Prophylactic colectomy is usually recommended.
102
gardner syndrome
variant of FAP
polyps +, osteomas , dental abnormality , benign soft tissue tumor
desmoid tumors
sebaceous cyst
risk of CRC is 100%
103
turcot syndrome
polyps + cerebellar medulloblastoma or glioblastoma multiforme
104
peutz jeghers
autosomal dominant
multiple hamartomas entire git most commonly small bowel
pigmented spots around lips , oral mucosa , lips face genitalia
105
hereditary nonpolyposis colorectal carcinoma
lynch syndrome 1
early onset CRC , absent antecedent multiple polyps
lynch syndrome 2
(cancer family syndrome )
all features of lynch 1 + inc number of other cancers ( female genital tract , skin, stomach, breast ,bilary tract )
106
synptoms of rht sided colon cancer
Right-sided tumors
•Obstruction is unusual because of the larger luminal diameter (the cecum has the largest luminal diameter of any part of the colon), allowing for large tumor growth to go undetected.
•Common findings
:occult blood in stool,iron deficiency anemia,and melena. •Change in bowel habits is uncommon
. •Triad of anemia,weakness,RLQ mass(occasionally) is present
107
clinical features of left sided tumors
. .Left-sided tumors
•Smaller luminal diameter—signs of obstruction more common
•Change in bowel habits more common—alternating constipation/diarrhea; narrowing of stools (“pencil stools”) •Hematochezia more common
108
ascitis fluid analysis
Ascites fluid characteristics
COLOR
• Bloody: Trauma, malignancy, TB (rarely)
• Milky: Chylous, pancreatic
• Turbid: Possible infection
• Straw color: Likely more benign causes
CELLS
Neutrophils <250/mm3 : No peritonitis
neutrophils: >250/mm3 Peritonitis (secondary or spontaneous bacterial)
Total PROTEIN
•>2:2.5 g/dl (high-protein ascites)
CHF, constrictive pericarditis, peritoneal carcinomatosis,
TB, Budd-Chiari syndrome, fungal (eg, coccidioidomycosis) protein
• <2.5 g/dl (low-protein ascites)
o Cirrhosis, nephrotic syndrome
SAAG
>1.1 g/dl (indicates portal hypertension)
Cardiac ascites, cirrhosis, Budd-Chiari syndrome
• <1 .1 g/dl (absence of portal hypertension)
TB, peritoneal carcinomatosis, pancreatic ascites,
nephrotic syndrome
109
types of hepatorenal syndrome and treatment
HRS is characterized by decreased
glomerular filtration in the absence of shock, proteinuria, or other clear cause of renal
dysfunction, and a failure to respond to a 1.5 L normal saline bolus. It is thought to result from
renal vasoconstriction in response to decreased total renal blood flow and vasodilatory substance
synthesis
There are 2 subtypes of HRS.
Type 1 is rapidly progressive; most patients die within
10 weeks without treatment
Type 2 progresses more slowly, with an average survival of 3-6
months. The most common causes of death are infection and hemorrhage Unfortunately, no
medication has consistently proven beneficial in HRS and the mortality for these patients placed
on dialysis is very high
Liver transplantation is the only intervention with established benefit
110
malabsorption test for celiac ds
D-xylose is a monosaccharide that can be absorbed in the proximal small intestine without
degradation by pancreatic or brush border enzymes It is subsequently excreted in the urine. In
the 0-xylose test, the patient is given an oral dose of 0-xylose, with subsequent assay of urine
and venous blood. Patients with proximal small intestinal mucosal disease (eg, celiac disease)
cannot absorb the 0-xylose in the intestine, and urinary and venous 0-xylose levels will be low.
By contrast, patients with malabsorption due to enzyme deficiencies (eg, chronic pancreatitis) will
have normal absorption of 0-xylose
A false-positive 0-xylose test (ie, decreased
urinary excretion of 0-xylose despite normal mucosal absorption) can be seen in patients with
delayed gastric emptying or impaired glomerular filtration. This patient has low urinary excretion
(ie, low mucosal absorption) of 0-xylose consistent with celiac disease
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difference of ast alt finding in alcoholic and NASH ♧
The hepatic steatosis in NAFLD resembles that found in alcoholic liver disease.
However, alcoholic liver disease is characterized by AST predominance (AST/AL T ratio 2:1) in
contrast to the parallel rise in NAFLD ast/alt <1
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diagnostic modality of choice for ca oc head and tail of pancreas
Cancers in the head of the pancreas (60%-70%) typically present with jaundice (common
bile duct obstruction, elevated alkaline phosphatase and bilirubin) and steatorrhea
(pancreatic exocrine insufficiency or pancreatic duct blockage). In patients with these
findings, abdominal ultrasound is preferred for detecting pancreatic head tumors and
excluding other potential causes of biliary obstruction (eg, choledocholithiasis)
•
Cancers in the body and tail usually do not present with obstructive jaundice. Abdominal
CT scan is preferred (more sensitive and specific) and helps exclude other conditions.
Ultrasound is less sensitive for visualizing the pancreatic body and tail (due to overlying
bowel gas) and for detecting smaller (<3 em) tumors.
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polyp with greatest risk of malignancy ♧♧♧
villous polyp
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most common polyp
hyperplastic polyp
