GIT Flashcards

1
Q

criteria for diagnosis of achlasia cardia

A

incomplete relaxation of LES

aperistalsis of esophagus

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2
Q

most common cause of achlasia

A

in US adenocarcinoma of proximal stomach

worlswide chagas is most common

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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

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4
Q

diagnosis of achlasia

A

barium bird beak appearence

manometery to confirm the diagnosis

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5
Q

treatment of achlasia

A
medical 
     antimuscarinic 
     nitroglycerin 
     ccb
inj of botulinum toxin 
pneumatic or balloon dilation 
surgical
     hellers myotomy
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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.

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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

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8
Q

two types of esophageal carcinoma

A

SCC

ADENOCARCINOMA

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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.
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10
Q

most common location of adenocarcinoma of esophagus

A

distal third of the esophagus/gastroesophageal junction . •Riskfactors:
GERD and
Barrett esophagus

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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

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12
Q

is achlasia premalignant

A

yes

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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

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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

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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.

  1. Complications of paraesophageal hernias are potentially life-threatening and include obstruction, hemorrhage, incarceration, and strangulation.
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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.

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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.

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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.

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19
Q

upper gi bleed

A

bleeding from above ligament of treitz

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20
Q

lower gi bleed

A

bleeding below the ligament of trietz

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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
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22
Q

lower gi bleed causes

A
diverticulosis 
angiodysplasia
IBD
colorectal cancer 
colorectal carcinoma
colonic polyps
ischemic coliitis
hemorrhoids
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23
Q

hematemesis

A

upper gi bleed
vomiting blood
moderate to severe bleeding tht may be ongoing

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24
Q

cofee ground emesis

A

upper gi bleed
lower rate of bleeding
( enough time for vomitus to transform into coffee grounds )

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25
Q

melena

A

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

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26
Q

hematochezia

A

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

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27
Q

best initial test for hematemiesis

A

upper Gi endoscopy

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28
Q

hematochezia best initial test

A

rule out anorectal cause like haemorroids

colonoscopy should be the best initial test cause of colon cancer being the most imp cause un elderly

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29
Q

melena best initial test

A

upper endoscopy

if no bleeding site found then lower gi source searched from colonoscopy

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30
Q

wht does elevation of BUN creatinine ratio in pt with no renal insufficiency indicates

A

upper gi bleed.

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31
Q

most accurate test for evaluation of upper gi bleed

A

upper gi endoscopy
both diagnostic and theurapeutic
coagulate bleeding vessel

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32
Q

first step in management of upper gi bleed

A

resuscitation with iv fliuds is the first step

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33
Q

test which definatively locates point of bleeding

A

arteriography

also therapeutic as embolization or intraarterial vasopressin can be given

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34
Q

guidelines for screening of colon cancer

A

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

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35
Q

guidelines for screening of lung cancer

A

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

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36
Q

most common cause of acute pancreatitis

A

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)

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37
Q

most common cause of pancreatitis in children

A

blunt abdominal trauma

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38
Q

symptoms of acute pancreatitis

A

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

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39
Q

signs of acute pancreatitis

A

•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)

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40
Q

grey turner sign

A

flank echymosis

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41
Q

cullen sign

A

periumblical ecchymosis

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42
Q

fox sign

A

ecchymosis of inguinal ligament

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43
Q

diagnosis of acute pancreatitis

A

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

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44
Q

complications of acute pancreatitis

A
pancreatic necrosis
pancreatic pseudo cyst
hrgic pancreatitis 
adult respiratory distress syn 
pancreatic ascitis or pleural effusion
ascending cholangitis
pancreatic abscess
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45
Q

complications of pancreatic pseudocyst

A
  • 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.
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46
Q

toxic megacolon

A

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
Q

diagnostic triad of chronic pancreatitis

A

The classic triad of
steatorrhea,
diabetes mellitus, and
pancreatic calcification on plain films or CT scan is also diagnostic.

48
Q

gold standard for chronic pancreatitis

A

ERCP not done as invasive diagnosis formed with the help of CT SCAN

49
Q

diagnostic modalities of chronic pancreatitis ♧

A

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
Q

complications of chronic pancreatitis

A
narcotic addiction 
diabetes mellitua
malabsorption 
pseudocyst 
duct dilation  
CBD obstruction 
vitB12 malabsorption 
effusion
pancreatic cancer
51
Q

most common location of pancreatic carcinoma

A

pancreatic head

52
Q

diagnostic modalities of pancreatic cancer

A

ERCP most sensitive test for diagnosis of pancreatic cancer
tumor markeres
CA19-9
CEA

53
Q

chain of lakes appearence is seen in

A

typical finding on ERCP in chronic pancreatitis

due to strictures and duct dilation throughout pancreatic duct

54
Q

most common location of diverticulosis

A

sigmoid colon

55
Q

difference between diverticulosis and diverticulitis

A

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
Q

diagnostic test for diverticulosis

A

barium enema is test of choice

57
Q

complications of diverticulitis

A

abscess formation
colovesical fistula
obstruction
free colonic perforation

58
Q

test of choive for diverticulosis

A

barium enema

59
Q

test of choice for diverticulitis ♧

A

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
Q

treatment of complicated and uncomplicated diveticulitis

A

uncomplicated - IV antibiotics , bowel rest and IV fliuds

complicated - surgery

61
Q

causes of cirrhosis of liver

A
  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
  4. Nonalcoholic steatohepatitis (NASH)
62
Q

complications of liver failure

A

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
Q

diffrential diagnosis of ascitis

A
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
Q

treatment of bleeding esophageal varices

A
variceal ligation 
endoscopic sclerotherapy
iv vasopressin 
iv octreotide first line therapy
balloon tamponade blakemore tube
65
Q

most common cause of SBP

A

ecoli

66
Q

SAAG

A

< 1.1 g/dl most likely due cause otherthan portal hypertension
>1.1g/dl most likely due to portal hypertension

67
Q

precipating factors for hepatic encephalopathy

A
alkalosis
hypokalemia 
drugs(narcotics,sleeping medications)
gi bleeding 
systemic infection 
hypovolemia
68
Q

clinical features of hepatic encephalopathy

A

dec mental function
confusion
asterexis ( not specific )
fetor hepaticus

69
Q

treatment of hepatic encephalopathy ♧

A

lactulose prevent absorption of ammonia
rifaximin kill bacterial flora dec ammonia formation
limit protein 30-40g/day

70
Q

gold standard for diagnosis of cirrhosis is

A

liver biopsy

71
Q

charcot triad ♧

A

Fever,
jaundice,
right upper quadrant pain (Charcot triad) of acute cholangitis

72
Q

reynods pentad ♧

A

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
Q

definative test for cholangitis

A

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
Q

treatment of acute cholangitis

A

IV ANTIBIOTICS +IV FLIUDS

decompress CBD via PTC ERCP or laprotomy

75
Q

most dreaded and serious complication of acute cholangitis

A

liver abscess has high mortality rate

76
Q

porcelien gallbladder

A

intramural calcification of GB wall

50%progresses to cancer thus needs prophylactic cholecystectomy

77
Q

wht does elevated alk and ggt means

A

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
Q

elevated ast alt means

A

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

  1. 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
Q

CHOLESTATIC MARKERS

A

Cholestatic LFTs:
markedly elevated alkaline phosphatase
GGT;
ALT and AST slightly elevated

80
Q

HEPATOCELLULAR NECROSIS MARKER

A

Hepatocellular necrosis or inflammation:
normal or slightly elevated alkaline phosphatase
; markedly elevatedALT and AST

81
Q

NASH mechanism in diabetes

A

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
Q

NASH defination

A

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
Q

management of GERD

A

if alarm symptoms ☆ alarm symptoms
present absent
⬇️ ⬇️
upper gi endoscopy trial of PPI

☆( dysphagia
odynophagia, wht loss
anaemia ,gi bleed)

84
Q

treatment of hepatic hydrothorax ♧

A

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
Q

ROME DIAGNOSTIC CRITERIA of irritable bowel syndrome ♧

A

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
Q

most common gi diagnosis in north america

A

irritable bowel syndrome

87
Q

gilbert syndrome ♧

A

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
Q

finding of alcoholic hepatitis

A

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
Q

treatment of gastric mucosa associated lymphoma

A

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
Q

diagnosis of celiac ds

A

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
Q

chronic mesentric ischemia cause

A

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
Q

symptoms of chronic mesentric ischemia

A

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
Q

signs of chronic intestinal ischemia

A

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
Q

clinical finding of primary sclerosing cholangitis

A

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
Q

primary sclerosing cholangitis

A

intra and extrahepatic bile duct thickening and narrowing of their lumens leading to cirrhosis, portal hypertension, liver failure

strongly associated with UC

96
Q

diagnostic study of choice for PSC

A

ERCP AND PTC

bead like dilatation of intra and extra hepatic duct

97
Q

primary biliary cirrhosis

A

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
Q

causes of secondary biliary cirrhosis

A

long standing mechanical obstruction
sclerosing cholangitis
cystic fibrosis
biliary atresia

99
Q

klatskin tumors

A

tumors of proximal third of CBD

involve junction of rht and left hepatic duct

100
Q

most consistent risk factor for pancreatic carcinoma

A

smoking

101
Q

FAP FINDING

A

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
Q

gardner syndrome

A

variant of FAP
polyps +, osteomas , dental abnormality , benign soft tissue tumor
desmoid tumors
sebaceous cyst

risk of CRC is 100%

103
Q

turcot syndrome

A

polyps + cerebellar medulloblastoma or glioblastoma multiforme

104
Q

peutz jeghers

A

autosomal dominant
multiple hamartomas entire git most commonly small bowel
pigmented spots around lips , oral mucosa , lips face genitalia

105
Q

hereditary nonpolyposis colorectal carcinoma

A

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
Q

synptoms of rht sided colon cancer

A

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
Q

clinical features of left sided tumors

A

. .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
Q

ascitis fluid analysis

A

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
Q

types of hepatorenal syndrome and treatment

A

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
Q

malabsorption test for celiac ds

A

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

111
Q

difference of ast alt finding in alcoholic and NASH ♧

A

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

112
Q

diagnostic modality of choice for ca oc head and tail of pancreas

A

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.

113
Q

polyp with greatest risk of malignancy ♧♧♧

A

villous polyp

114
Q

most common polyp

A

hyperplastic polyp