GIT Flashcards

(189 cards)

1
Q

Name the test which dx the cause of Oropharyngeal dysphagia

A

Videofluoroscopic modified barium swallow

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2
Q

Name the test which dx oesophageal dysphagia

A

Manometry if motility issue

Barium swallow

Endoscopy with biopsy

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3
Q

What are the causes of oropharyngeal dysphagia?

A

stroke
advanced dementia,

oropharyngeal malignancy

or

neuromuscular disorder like myasthenia gravis

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4
Q

Important point of Achalasia

A

Sx for >5 yrs before receiving diagnosis and mild weight loss

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5
Q

How to t/m achalasia?

A

laparoscopic myotomy and pneumatic balloon dilation treatment of choice in pts with low risk of surgery.

Pts with high risk of surgery botulinum toxin injection, nitrates and calcium channel blockers (but exclude malignancy 1st)

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6
Q

Name the cause of pseudoachalasia

A

Due to oesophageal cancer not due to denervation

With Rapid symptom onset (<6mo),

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7
Q

What are the dx findings of diffuse oesophageal spasm?

A

Endoscopy—> usually normal

Esophagram—> corkscrew pattern

Manometry—>intermittent persistalsis with multiple simultaneous contractions

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8
Q

How to approach patient with GERD without alarming symptoms?

A

trial of daily PPI—>refractory—>change PPI or ↑ use of PPI twice daily—>persistent—->endoscopy or esophageal pH monitoring

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9
Q

How to approach GERD with Alarming symptoms?

A

Endoscopy before trial—>esophagitis due to autoimmune or Barrett’s esophagus—>treat accordingly—not esophagitis—>further evaluation (e.g manometry)

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10
Q

What are the alarming symptoms with GERD?

A

alarm symptoms (dysphagia, odynophagia, weight loss, anemia, GI bleeding, recurrent vomiting)

or men >50 with chronic (>5 years) symptoms or cancer risk factors (eg tobacco use)

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11
Q

How to d/f oesophageal strictures from oesophageal cancer?

A

Stricture has symmetrical circumferential narrowing on barium swallow

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12
Q

Triad of Globus sensation (HYSTERICUS)

A

sensation of a foreign body in the throat.

worse when swallowing saliva and is frequently associated with anxiety

Pain, dysphagia, dysphonia, or systemic symptoms are not typical for globus and suggest another condition

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13
Q

Name the medication which causes pill induced oesophagitis

A

Tetracycline
Potassium chloride/iron

Aldrendronate/Risedronate

Aspirin and NSAIDs

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14
Q

What are the endoscopy findings of Pill induced oesophagitis?

A

discrete ulcers with normal- appearing surrounding mucosa

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15
Q

Name the causes of oesophageal perforation

A

Oesophageal ulcer/pill/caustic/infectious

Instrumentation viz endoscopy

Spontaneous rupture such as Boerhaave syndrome

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16
Q

How oesophageal perforation presents?

A

Chest or abdominal pain with fever

Crunching sound on chest auscultation (Hamman sign)

Subcutaneous emphysema in the neck

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17
Q

What will be seen in CT scan and CXR of oesophageal perforation?

A

Wide mediastinum with pneumothorax

Air around para spinal muscles with pleural effusions

Pneumomediastinum

Oesophageal wall thickening with mediastinal air fluid level

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18
Q

Important point of oesophageal wall rupture

A

Water-soluble contrast is preferred (less inflammatory to tissues)—>non-diagnostic—>barium study (higher sensitivity)

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19
Q

What are findings in d/f tests of boerhaave syndrome?

A

Pleural fluid analysis::
Exudative with low pH and very high amylase

Chest X Ray::
Pneumomadiastinum and pleural effusion

CT OR Oesophagraphy with gastrograffin confirm the diagnosis

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20
Q

Endoscopic finding of Mallory Weiss year

A

Longitudinal laceration on endoscopy

Mucosal tear in stomach Or esophagus

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21
Q

Important point::

A

BUN ↑ in upper GI bleeding and not lower GI bleeding

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22
Q

Important point

A

H.pylori is important cause of adenocarcinoma and eradication is recommended before cancer removal to avoid future adenoCA development

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23
Q

What are the causes of Gastric outlet obstruction?

A

gastric malignancy

peptic ulcer disease

Crohn disease

strictures (with pyloric stenosis) 2* to caustic acid ingestion

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24
Q

Triad of Gastric Outlet Obstruction

A

Post prandial pain

Vomiting with early satiety

Positive ABDOMINAL SUCCUSSION SPLASH test

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25
Important point of Celiac disease
If IgA serology is negative and suspicion is high—>measure total IgA or IgG based serologic testing should be done
26
Name the condition in which D-xylose test come true positive
proximal small intestinal mucosal disease—>most common celiac disease
27
Name the condition in which D-xylose test come false positive
delayed gastric emptying or impaired glomerular filtration. Small intestinal bacterial overgrowth—>fermentation of d-xylose before absorption—course of antibiotic (rifamixin) will improve d-xylose absorption
28
Name the condition in which D-xylose test comes negative
normal in pancreatic enzyme deficiency Crohn disease (due to involvement of distal small intestine) lactose intolerance
29
Name the test which dx steatorrhea
Fecal fat tests (eg, Sudan stain on spot stool specimen or 72-hour collection) confirm steatorrhea
30
What are the biopsy findings of tropical sprue?
Small intestinal biopsy—> blunting of villi, infiltration of chronic inflammatory cells, including plasma cells, lymphocytes and eosinophils
31
Important point of lactose intolerance
There is no steatorrhea
32
What are the protective mechanism which prevent the growth of bacteria in intestine?
The proximal small intestine normally contains relatively minimal bacterial colonization due to gastric acidity and peristalsis. Other protective mechanisms against SIBO include::: - bacterial degradation by proteolytic digestive enzymes - trapping of bacteria by intestinal mucus, and - an intact ileocecal valve preventing retrograde bacterial movement from the colon
33
Name the d/f test to dx Small intestine bacterial overgrowth And name the Abx to Rx the condition (ABx like Rifaximin or Neomycin )
1)Jejunum aspirate which show more than 10*5 organisms per mL But this test is invasive 2) Carbohydrate breath test (either using glucose Or lactulose) which shows peak in breath hydrogen /methane (as CHO metabolise by bacteria 3) low B12 but high Folate as bacteria produce it
34
How SIBO occur?
All Conditions which alter small bowel motility result bacteria come from colon into small intestine result SIBO
35
What are the risk factors for zinc deficiency?
TPN formulations that lack zinc, IBD pts are at risk because of impaired absorption
36
Triad of Zinc Deficiency
alopecia with abnormal taste bullous, with pustulous lesions surrounding body orifices and extremities impaired wound healing.
37
What is the important feature of selenium deficiency?
Cardiomyopathy
38
Triad of COLLAGENOUS COLITIS
chronic watery diarrhea in which colon is frequently involved colonoscopy shows normal mucosa. Biopsy shows mucosal subepithelial collagen deposition
39
Important point of Irritable bowel syndrome
Following signs/symptoms suggest other disorder than IBS::: Rectal bleeding Worsening abdominal pain /nocturnal Weight loss Abnormal lab findings
40
What are the complications of ulcerative colitis?
Toxic mega colon Primary sclerosing cholangitis CRC Erythema nodosum/ pyoderma gangrenosum Spondyloarthritis
41
Important point for toxic megacolon
Opioids are Avoided due to antimotility effect that can promote perforation. Discontinue other anti-motility drugs like loperamide and anticholinergic agents
42
Name the surgical method for Toxic mega colon
Emergency surgery (subtotal colectomy with end-ileostomy—treatment of choice) if colitis not resolved.
43
How to approach per rectum bleeding?
* if age >50 yrs Or Red flags = colonoscopy * If age 40-49 w/o red flags = sigmoidoscopy / colonoscopy * if age less than <40 yrs w/o red flags —> anascopy—>haemorrhoids Or no source identified then choose 2nd methods
44
Triad of Factitious diarrhoea
Excessive use of laxative Watery diarrhoea esp nocturnal biopsy findings: dark brown discoloration of colon with lymph nodes shining through as pale patches (melanosis coli)—esp. in those using/abusing anthraquinone containing laxatives
45
What is the alternative dx of factitious diarrhoea?
histological evidence of pigment in macrophages of lamina propria
46
Important feature of Diverticular diseases
Association with chronic constipation And bleeding is usually painless Alcohol—>↑ diverticula formation but not ↑ risk of diverticular complications Ct (oral & IV contrast) used for dx acute diverticulitis
47
Name the complications of Acute diverticulitis
Associated with abscess, perforation, obstruction or fistula formation
48
How to t/m abscess due to diverticulitis?
**Fluid collection <3 cm—> IV antibiotics and observation—>surgery for pts with worsening symptoms **fluid collection >3cm—>CT-guided percutaneous drainage—>if Sx not controlled by 5th day—>surgical drainage and debridement
49
Important point for acute diverticulitis
Barium enema, sigmoidoscopy and colonoscopy—>Not done in acute diverticulitis. Colonoscopy—>performed after resolution of acute diverticulitis to rule out CRC
50
What are the CT-findings of acute diverticulitis?
CT scan: inflammation in pericolic fat, presence of diverticula, bowel wall thickening, soft tissue masses (eg phlegmons), and pericolic fluid collection suggesting abscess (upright x-ray shows nonspecific findings
51
What are the causes of Colovesical Fistula?
Diverticular diseases (sigmoid MCC) Crohn diseases Malignancy viz colon/ bladder/ pelvic organs.
52
What are the clinical findings of Colovesical Fistula?
Air comes out at the end after passing urine Stool in urine Recurrent UTI due to mixed flora
53
What is the CT-scan finding of Colovesical Fistula?
Contrast in bladder with thicken colonic and bladder walls
54
Triad of acute mesenteric ischemia
Rapid onset of peri umbilical pain which is out of proportion Per rectal fresh bleeding Increase WBCs and amylase/phosphate
55
How to dx Acute mesenteric ischemia?
Ct scan preferred MR angiography If dx unclear then Mesenteric angiography
56
CT scan findings of Acute mesenteric ischemia
focal or segmental bowel wall thickening pneumatosis intestinalis small bowel dilation mesenteric stranding and mesenteric thrombi
57
Important point of acute mesenteric ischemia
There must be underlying thrombotic condition to develop this disorder
58
How to t/m Acute mesenteric ischemia?
open embolectomy with vascular bypass or endovascular thrombolysis
59
Triad of chronic mesenteric ischemia
Atherosclerosis as a cause Post prandial pain with food aversion result weight loss Signs of malnutrition and abdominal bruit
60
How to dx Chronic mesenteric ischemia?
CT angiography (preferred) Doppler U/S
61
At what site of abdomen “Ischemic colitis” is mc?
Splenic flexure
62
What are the findings in d/f imaging used to dx ISCHEMIC COLITIS?
CT scan—> Thickened bowel wall / double Halo sign / pneumatosis coli Colonoscopy—> mucosal pallor Or cyanosis/ petechia / haemorrhage
63
Important point of RETROPERITONEAL HEMATOMA
pt on anticoagulation (normal or supratherapeutic INR) —> raise suspicion for retroperitoneal hematoma CT findings—> isodense area in retroperitoneum
64
Name the causes/ risk factors increases the risk of Angiodysplasia
advanced renal disease and vW disease due to ↑ bleeding tendency Aortic stenosis al ↑ risk due to acquired vWF deficiency (from disruption of vW multimers as they traverse the turbulent valve space induced by AS—has been reported to remit after valve replacement
65
Features of Hyperplastic Polyp
Most common non-neoplastic polyps in the colon. Arise from hyperplastic mucosal proliferation. No further work-up needed
66
Features Of Hemartomatous polyp
Include juvenile polyp:: (a non-malignant lesion, generally removed due to the risk of bleeding) Peutz Jeghers polyp:: (generally non-malignant).
67
What is the MC type of polyp found in the colon?
Adenoma
68
What feature of polyp suggest the cancerous condition?
Sessile> stalked (pedunculated) tubular2.5 cm in size
69
Important point Cancer family syndrome or (Lynch syndrome II)
Lynch syndrome II is distinctly associated with a high risk of extracolonic tumors, the most common of which is endometrial carcinoma, which develops in up to 43% of females in affected families. Also associated with ovarian and skin cancers
70
When to do screening of CRC if there is positive family Hx of FAP?
Begin at age 10-12 yrs of age Colonoscopy every year
71
When to do screening of CRC if there is positive family Hx of Lynch syndrome?
Begin at age 20-25 Colonoscopy every 1-2 yrs
72
When to do screening of CRC if there is positive Hx of IBD?
Begin 8 yrs post diagnosis (12-15 yrs if disease only in left colon) Colonoscopy with biopsy every 1-2 yrs
73
When to do screening of CRC if there is positive family hx of adenomatous polyp Or CRC?
Colonoscopy at age 40 yrs OR 10 years before the age of diagnosis in the relative Repeat every 3-5 yrs
74
What to do if colonic dysplasia is diagnosed?
Colonic dysplasia—>↑ risk of adenocarcinoma—>prophylactic colectomy advised
75
What are the portal HTN sign in patient of Cirrhosis?
Oesophageal varices Splenomegaly Ascites Caput Medusa Haemorrhoids
76
What are the signs of Hyper estrinism in patient of cirrhosis?
Spider angiomata Gynecomastia Loss of pubic hair Palmar Erythema Testicular atrophy
77
Important of point of NAFLD
Usually there is increase ALT>AST ratio If AST>ALT ratio increases it suggests progression to advance fibrosis and cirrhosis
78
What are the peritoneal causes of Ascites?
Malignancy (Ovarian / Pancreatic) Infection (Tb / fungal)
79
What are the extra peritoneal causes of Ascites?
A = alcoholic hepatitis / acute liver failure ``` B = Budd chiari syndrome C = Cirrhosis ``` ``` H = hypo albuminemia / HF M = malnutrition ``` N = Nephrotic syndrome
80
What are the causes of ascites If total protein is less than “2.5g/dl””? (Low protein ascites)
Cirrhosis | Nephrotic syndrome
81
What are the causes of ascites If total protein is more than “2.5g/dl””? (High protein ascites)
CHF Constrictive pericarditis Peritoneal carcinomatosis Tb Budd chiari syndrome Fungal infection
82
What does it meant to be increase SAAG ratio?
Due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature.
83
What are the causes of Ascites if SAAG more than 1.1 g/dl (It indicates portal HTN)? 3Cs
Cardiac Ascites Cirrhosis Budd Chiari syndrome
84
What are the causes of ascites if SAAG ratio is less than 1.1 g/dl? Absence of portal HTN Remember TPN
Tb Peritoneal carcinomatosis Pancreatic associates Nephrotic syndrome
85
How to t/m ascites?
Start with sodium and water restriction Add diuretic therapy viz spironolactone if needed Add loop diuretic if spironolactone doesn’t respond If both diuretic therapy fails then slowly tapping the fluid but keep monitoring renal function
86
Important point of ascites
Aggressive diuresis (>1 L/day) —>not recommended b/c of risk of hepatorenal syndrome
87
Triad of HEPATIC HYDROTHORAX
Pleural effusion due to ascites—>defect in diaphragm Right sided more common Best option for treatment: liver transplant but Primary treatment: thoracocentesis followed by diuresis and salt restriction—>no response—>TIPS—>TIPS contraindicated—->pleurodesis
88
What is the prophylactic treatment of Esophageal varices?
1st line = non-selective β-blockers 2nd line = endoscopic variceal ligation in those with contraindication to β-blockers
89
what is the t/m of Esophageal varices?
Endoscopic sclerotherapy Octreotide- long-acting somatostatin analog
90
How to approach Esophageal varices?
- Stabilze the patient with IV Fluids / Abx / Octreotide or Terlipressin Then do urgent endoscopic therapy either sclerotherapy Or band ligation
91
What to do even if ""bleeding stop"" after doing urgent endoscopic therapy for Esophageal varices?
Initiate Secondary prophylaxis such as BB plus endoscopic band ligation 1-2 weeks later
92
What to do even if ""continued bleeding"" after doing urgent endoscopic therapy for Esophageal varices?
Balloon tamponade (temporary)--> Tips Or shunt surgery
93
What to do even if ""Early Rebleeding"" after doing urgent endoscopic therapy for Esophageal varices?
Repeat Endoscopic therapy———->Hemorrhage-->TIPS Or Shunt Surgery
94
Triad of Acute liver failure
Increase ALT/AST >1000U/L Signs of hepatic encephalopathy INR>1.5
95
What is the most important prognostic factor of Acute liver failure?
PT
96
Triad of ISCHEMIC HEPATOPATHY
Rapid and massive in AST and ALT, with modest ↑ in alkaline phosphatase. Increase total bilirubin Pts who survive underlying cause (eg septic shock or HF)--> LFTs return to normal within 1-2 wks.
97
Name the dose dependent drug induced HEPATITIS
carbon tetrachloride acetaminophen tetracycline and substances found in the Amanita phalloides mushroom.
98
Name the dose independent drug induced HEPATITIS
isoniazid chlorpromazine halothane and antiretroviral therapy.
99
Name the drug which cause fatty liver
tetracycline valproate and anti-retrovirals
100
Name the drug which cause Hepatitis
halothane phenytoin isoniazid and alpha-methyldopa
101
Name the drug which cause Cholestasis
chlorpromazine nitrofurantoin erythromycin and anabolic steroids
102
Name the drug which cause Toxic or fulminant liver failure
carbon tetrachloride and acetaminophen
103
Important point
OCPs cause changes in LFTs without evidence of necrosis or fatty change
104
Important point
While extrahepatic hypersensitivity manifestations like rash, arthralgias, fever, leukocytosis, and eosinophilia are common in patients with drug-induced liver injury they are characteristically absent in cases of isoniazid-induced hepatic cell injury—Histologic picture is similar to viral hepatitis
105
Important point
pts with AH have h/o chronic alcohol use (>7drinks/day or 100 g/day)—sometimes develop symptoms after acute ↑ in consumption. In addition, alcoholic liver disease is unlikely with light to moderate alcohol intake (<15 drinks/wk for men, <10/wk for women). A standard drink is equivalent to 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof spirits (1 oz = 30 ml)
106
How to managed Hepatic Encephalopathy?
Give Lactulose—-> If no response—-> rifaximin—-> Neomycin if patient Unable to take Rifaximin Protein free diet Keep hydrate the patient Diuretics for ascites
107
What are the diagnostic findings in lab test of SBP?
Paracentesis and PMN>250/mm3 are key diagnostic Protein less than 1g/dl SAAG >1.1g/dl
108
How to t/m SBP?
Third Generation cephalosporins as empiric t/m Quinolones for SBP prophylaxis
109
Name the bacteria can cause SBP
E. coli >> Klebsiella >> Streph species
110
Important point of cirrhosis
Pts with cirrhosis are normally hypothermic and >100 F warrants investigation
111
What are the solid liver masses?
Focal nodular hyperplasia Hepatic adenoma Regenerative nodules HCC Liver mets
112
What are the risk factors which increases the chances of hepatic adenoma formation?
Use of long term Contraceptives Pregnancy Anabolic steroid use
113
How focal nodular hyperplasia occur?
Due to hyper-perfusion from anomalous arteries Imaging will show arterial flow and central scar on imaging
114
Name the solid liver masses which has high chance of hemorrhagic or malignant transformation
Hepatic adenoma
115
What are the risk factors for hepatic angiosarcoma?
vinyl chloride inorganic arsenic compounds thorium dioxide
116
Name the cause of direct jaundice in which ALT/AST/ALP is normal
Dublin Johnson syndrome | Rotor syndrome
117
Name the cause of jaundice in which there is increase ALT/AST pre dominantly
HAT H hemochromatosis A autoimmune hepatitis /alcoholic T toxin/drug induced IV Ischemic Viral
118
Name the cause of jaundice in which increase in ALP pre dominantly
PSC PBC Malignancy Cholestasis of pregnancy Choledocholithasis
119
Triad of Gilbert syndrome
Decrease In enzyme activity with normal LFTs Increase in indirect jaundice with underlying stressors No apparent liver disease
120
Triad of CN syndrome 1
Indirect jaundice with neurological impairment (Jaundice level >20 or up to 50) Normal levels of enzymes in LFTs Not affected by IV phenobarbital
121
Triad of CN syndrome 2
Indirect jaundice with level <20 No neurological problem IV phenobarbital level normalised bilirubin level
122
What are the diagnostic test findings of Wilson disease?
old standard liver biopsy (copper >250mcg/gram dry weight), confirmatory: ↓ ceruloplasmin level (<20 mg/dl) ↑ urinary copper excretion + Keyser Fleisher ring
123
Name the test to be done if ALP and GGT both are increase plus US show dilated ducts
ERCP
124
Name the test to be done if ALP and GGT both are increase plus US RUQ and AMA ERCP both are normal
Consider liver biopsy / ERCP /observation
125
Name the test to be done if ALP and GGT both are increase plus US show abnormal hepatic parenchyma OR positive AMA
Liver biopsy
126
Triad of PBC
Direct jaundice SxS in female +Ve AMA autoimmune destruction of intrahepatic bile ducts
127
How ursodeoxycholic acid (UDCA) cure the indirect jaundice?
UDCA is hydrophilic bile acid--> ↓ biliary injury by more hydrophobic endogenous bile acids—also ↑ biliary secretion and has anti-inflammatory and immunomodulatory effects-->delays histologic progression and improve sx and possibly survival
128
What are the features of vanishing bile duct syndrome?
Progressive destruction of intrahepatic bile ducts Histologic hallmark: ductopenia
129
What are the causes of Ductopenia?
Most common cause of ductopenia: primary biliary cirrhosis. Other causes: failing liver transplantation, Hodgkin’s disease, graft-versus-host disease, sarcoid, CMV infection, HIV and medication toxicity
130
Triad of PSC
Direct jaundice with Extra/Intra hepatic dilation or stricturing Onion skin pattern on liver biopsy ERCP or MRCP--> Beading
131
What are the different mechanisms to develop Gallstones?
TPN Or Fasting:: no stimulus for CCK and gallbladder contraction--> gall bladder stasis -Ileal resection Or Crohn's disease so return of bile salt-->bile becomes supersaturated with cholesterol-->cholesterol gall stone formation due to ↑ concentration of bilirubin conjugates and total calcium in gall bladder Estrogen-->↑ in cholesterol secretion Progesterone--> ↓ bile acid secretion and slows gallbladder emptying
132
How to t/m Gallstones without symptoms?
No t/m necessary in most patients
133
How to t/m Gallstones with typical biliary colic symptoms?
Elective laparoscopic cholecystectomy Or Urodeoxycholic acid in pops surgical patients
134
How to t/m complicated Gallstones?
Cholecystectomy within 72hrs
135
What are the findings On CT scan of Gallstones ileus?
Gallbladder wall thickening pneumobilia and an obstructing stone
136
How to t/m Gallstones ileus?
surgical removal of stone and either simultaneous or delayed cholecystectomy.
137
Triad of Biliary colic
Pain occur when intake of meal and resolve within 4-6 hours Due to obstructive cystic duct No inflammatory SxS unlike cholecystitis
138
Triad of Acute cholecystitis
RUQ pain when intake of meal and last longer than 6 hours inflamed Gallbladder due to Obstructed cystic duct Presence of SxS of inflammation unlike bilaru colic
139
What is POSTCHOLECYSTECTOMY SYNDROME ?
PCS refers to persistent abdominal pain or dyspepsia (eg, nausea) that occurs either postoperatively (early) or months to years (late) after a cholecystectomy.
140
How to t/m POSTCHOLECYSTECTOMY SYNDROME?
Treatment for PCS is directed at the causative factor: ERCP with sphincterotomy is the treatment of choice for sphincter dysfunction
141
What are the risk factors for the Acalculous cholecystits?
Prolonged Fasting Or TPN Critical illness ( sepsis / ICU / On vent) Severe trauma Extensive burns Recent surgery
142
What are the image findings of acalculous cholecystits?
gallbladder wall thickening and distension and presence of pericholecystic fluid
143
How to t/m acalculous cholecystits?
immediate antibiotics followed by percutaneous cholecystostomy under radiologic guidance. Cholecystectomy with drainage of any associated abscesses—definitive treatment once pts condition improves
144
Triad of EMPHYSEMATOUS CHOLECYSTITIS
Immunosuppression patients Fever with RUQ pain and N/V Air fluid level in gallbladder with gas in gallbladder wall which result in crepitus in abdominal wall adjacent to gallbladder
145
Name the bacteria which cause EMPHYSEMATOUS CHOLECYSTITIS
Gas forming bacteria viz Clostridium and some strains of E.coli
146
How to t/m EMPHYSEMATOUS CHOLECYSTITIS?
Emergent cholecystectomy with use of broad spectrum ABx
147
What is Charcot triad in acute cholangitis?
Fever RUQ pain Jaundice
148
What would be seen on imaging on acute cholangitis?
Biliary dilation on U/S Or CT scan
149
How to t/m acute cholangitis?
ERCP with sphincterotomy Or Percutaneous trans hepatic cholangiography With USE of Broad spectrum ABx
150
What are the diagnostic findings of acute pancreatitis?
Epigastric pain radiates to back Increase amylase/lipase >3 times normal limit Imaging shows focal Or diffuse pancreatic enlargement with heterogeneous enhancement on CT. and if U/S diffusely enlarged and hypoechoic pancreas
151
How to dx pancreatitis due to Gallstones?
RUQ U/S—> if non-Dx—>ERCP HIDA Scan not use to dx pancreatitis rather used for cholecystits
152
Important point of pancreatitis
If ALT increases think of biliary induced pancreatitis
153
Important information of acute pancreatitis management
Pt should be NPO except essential medications like antiplatelet therapy in case of stent placement Prophylactic antibiotics are not routinely used in acute pancreatitis—unless there is evidence of necrotizing pancreatitis with local infection
154
Name the medication which causes acute pancreatitis
Valproate Furosemide/thiazides sulfasalazine, 5-ASA azathioprine didanosine, pentamidine metronidazole, tetracycline
155
What are the CT findings of drug induced Pancreatitis?
peripancreatic fluid and fat stranding
156
Important point of chronic pancreatitis
Stool elastase— marker for pancreatic exocrine function low levels in CP rather than acute pancreatitis
157
What does it meant by Severe Pancreatitis?
pancreatitis with involvement of at least one organ
158
What are the CT findings of PANCREATIC PSEUDOCYST?
round, well circumscribed, encapsulated fluid collection (usually no necrosis or solid material), thick fibrous capsule, containing enzyme-rich fluid, tissue and debris
159
How to t/m pancreatic pseudocyst?
Minimal or no symptoms and without complications (eg pseudoaneurysm)—>expectant management (eg symptomatic therapy and NPO)—preferred initially  Significant symptoms (abdominal pain, N/V), infected pseudocyst, evidence of pseudoaneurysm—>endoscopic drainage
160
What are the inherited Rx factors for pancreatic cancer?
1st Degree relative with pancreatic cancer Hereditary pancreatitis Germline mutations (BRCA 1 and 2)(PJ syndrome)
161
How to approach pancreatic head cancer?
U/S—> if non-Dx—>ERCP—>PTC
162
Why U/S is not useful in pancreatic cancer at tail and body?
less visibility of tail and body due to overlying bowel gas and also less sensitive for detecting smaller tumors (<3cm)
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How to t/m hepatic adenoma?
If less than 5cm and asymptomatic-->stop COCP If more than 5cm and symptomatic---> surgical resection
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How Hepatic hemangioma present on US?
NO CENTRAL SCAR centripetal enhancement (from periphery to central
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Triad of Bile acid Diarrhea
Secretory diarrhea occur after removal of gallbladder Persist even after fasting (unlike lactose intolerance) Negative blood and stool work up
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How to manage bile acid Diarrhea?
Bile acid resins-->cholestyramine colestipol colesevelam
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What are the signs of hyper estrogen in Cirrhosis patient?
Spider angiomata Breast formation Palmar erythema testicular atrophy Loss of sexual hair
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What factors increases the chance of C.difficle infection?
1) Abx like Quinolone, Cephalosporins, clindamycin, pencillin 2) Decrease Gastric acid 3) Hospitalisation 4) Advanced age more than 65 yrs
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How to treat IBS?
Reassurance and Dietary modification If constipation type--->fiber supplementation If diarrhea---->Antidiarrheal like loperamide
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Lab presentation of alcohol
CBC shows increase WBC and neutrophilia LFT shows increase AST ALT GGT AST TO ALT ratio more than 2 AST and ALT increase upto 500 Also increase Ferritin
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How to treat IBD induced Toxic megacolon?
IV steroid like methylpred Avoid invasive imaging like colonoscopy
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How Proctaglia fugax occur?
Due to spastic Contraction of anal sphincter Or Pudendal nerve compression
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Triad of Proctaglia fugax
recurrent rectal pain with pain free episodes Unrelated to defecation Normal physical Ex without lab abnormalities
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How to manage Proctaglia fugax?
Reassurance Nitroglycerin ± biofeedback therapy for recurrent sxs
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Important point of IBS
SxS like rectal bleeding Or weight loss Abnormal labs Worsen abdominal pain esp at night All above features of present—-> Exclude IBS as a dx
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How to approach dysphagia and odynophagia in patient with HIV? Note point —> neither HSV nor CMV treat empirically
First check oral thrush If present —>candida given fluconazole with no need of EGD If no thrush or fail to respond empiric t/m Then do EGD with biopsy
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Name the vaccine given in chronic liver disease | HABIT (B=P)
HA HAV / HBV P pneumococcal I flu T Tdap
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Triad of Spontaneous bacterial peritonitis
High grade fever with abdominal tenderness Low BP with Hypothermia Paralytics ileus with severe infection
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How to dx and t/m SBP?
Dx test shows Neutrophils >250mm3 - SAAG >1.1g/dl and total protein <1g/dl Rx---> Quinolones (as ppx) and 3rd generation cephalosporin as Empiric
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Name the med for wilson disease treatment
1) Chelators like trientine or D pencillamine | 2) zinc as it interfer absorption of copper.
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How PJ syndrome present?
Pigment macules on lips, buccal mucosa, palm / soles Due to hemartomatous polyp result Anemia due to polyp ruptured Obstructive sxs or Intussusception Rectal prolapse
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How to dx and manage Autosomal dominant PJ syndrome?
Dx -----> Genetic testing Manage----> annual anemia screening and cancer screening via Upper/lower EGD
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Red flags which need to be evaluated via colonoscopy
abdominal pain with change in bowel habit, | Wt loss, Iron deficiency anemia, Fx hx of colon cancer
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When to suspected Infected Pancreatic Necrosis and How to dx it?
Abdominal pain with signs of sepsis (after the onset of Acute necrotizing pancreatitis) Dx: - CT abdomen shows Gas within the necrotic collection - Aspiration and culture of necrotic material
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How to tx Infected Pancreatic Necrosis?
IV ABx onced stabilize --->do Debridement
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What are the 4As of Hepatic encephalopathy?
Ataxia Asterixis Altered mental status Altered sleep pattern
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What factors increases the risk of Hepatic encephalopathy? | H PRIDE
H hypovolemia D drugs like sedatives narcotics I infection like pneumonia UTI SBP Increase Nitrogen load to GIT bleeding P portosystematic shunting like TIPS E lytes changes like low potassium
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Triad of Budd chiari syndrome
Ascities Abdominal pain HSM
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Name the condition leads to Budd chiari syndrome and how to dx?
Myeloproliferative disorder (PV) Malignancy like HCC OCP and pregnancy Dx --->US Doppler abdominal (decrease hepatic vein flow)