GIT Flashcards
Name the test which dx the cause of Oropharyngeal dysphagia
Videofluoroscopic modified barium swallow
Name the test which dx oesophageal dysphagia
Manometry if motility issue
Barium swallow
Endoscopy with biopsy
What are the causes of oropharyngeal dysphagia?
stroke
advanced dementia,
oropharyngeal malignancy
or
neuromuscular disorder like myasthenia gravis
Important point of Achalasia
Sx for >5 yrs before receiving diagnosis and mild weight loss
How to t/m achalasia?
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)
Name the cause of pseudoachalasia
Due to oesophageal cancer not due to denervation
With Rapid symptom onset (<6mo),
What are the dx findings of diffuse oesophageal spasm?
Endoscopy—> usually normal
Esophagram—> corkscrew pattern
Manometry—>intermittent persistalsis with multiple simultaneous contractions
How to approach patient with GERD without alarming symptoms?
trial of daily PPI—>refractory—>change PPI or ↑ use of PPI twice daily—>persistent—->endoscopy or esophageal pH monitoring
How to approach GERD with Alarming symptoms?
Endoscopy before trial—>esophagitis due to autoimmune or Barrett’s esophagus—>treat accordingly—not esophagitis—>further evaluation (e.g manometry)
What are the alarming symptoms with GERD?
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)
How to d/f oesophageal strictures from oesophageal cancer?
Stricture has symmetrical circumferential narrowing on barium swallow
Triad of Globus sensation (HYSTERICUS)
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
Name the medication which causes pill induced oesophagitis
Tetracycline
Potassium chloride/iron
Aldrendronate/Risedronate
Aspirin and NSAIDs
What are the endoscopy findings of Pill induced oesophagitis?
discrete ulcers with normal- appearing surrounding mucosa
Name the causes of oesophageal perforation
Oesophageal ulcer/pill/caustic/infectious
Instrumentation viz endoscopy
Spontaneous rupture such as Boerhaave syndrome
How oesophageal perforation presents?
Chest or abdominal pain with fever
Crunching sound on chest auscultation (Hamman sign)
Subcutaneous emphysema in the neck
What will be seen in CT scan and CXR of oesophageal perforation?
Wide mediastinum with pneumothorax
Air around para spinal muscles with pleural effusions
Pneumomediastinum
Oesophageal wall thickening with mediastinal air fluid level
Important point of oesophageal wall rupture
Water-soluble contrast is preferred (less inflammatory to tissues)—>non-diagnostic—>barium study (higher sensitivity)
What are findings in d/f tests of boerhaave syndrome?
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
Endoscopic finding of Mallory Weiss year
Longitudinal laceration on endoscopy
Mucosal tear in stomach Or esophagus
Important point::
BUN ↑ in upper GI bleeding and not lower GI bleeding
Important point
H.pylori is important cause of adenocarcinoma and eradication is recommended before cancer removal to avoid future adenoCA development
What are the causes of Gastric outlet obstruction?
gastric malignancy
peptic ulcer disease
Crohn disease
strictures (with pyloric stenosis) 2* to caustic acid ingestion
Triad of Gastric Outlet Obstruction
Post prandial pain
Vomiting with early satiety
Positive ABDOMINAL SUCCUSSION SPLASH test
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
Name the condition in which D-xylose test come true positive
proximal small intestinal mucosal disease—>most common celiac disease
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
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
Name the test which dx steatorrhea
Fecal fat tests (eg, Sudan stain on spot stool specimen or 72-hour collection) confirm steatorrhea
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
Important point of lactose intolerance
There is no steatorrhea
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
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
How SIBO occur?
All Conditions which alter small bowel motility result bacteria come from colon into small intestine result SIBO
What are the risk factors for zinc deficiency?
TPN formulations that lack zinc, IBD pts are at risk because of impaired absorption
Triad of Zinc Deficiency
alopecia with abnormal taste
bullous, with pustulous lesions surrounding body orifices and extremities
impaired wound healing.
What is the important feature of selenium deficiency?
Cardiomyopathy
Triad of COLLAGENOUS COLITIS
chronic watery diarrhea in which colon is frequently involved
colonoscopy shows normal mucosa.
Biopsy shows mucosal subepithelial collagen deposition
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
What are the complications of ulcerative colitis?
Toxic mega colon
Primary sclerosing cholangitis
CRC
Erythema nodosum/ pyoderma gangrenosum
Spondyloarthritis
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
Name the surgical method for Toxic mega colon
Emergency surgery (subtotal colectomy with end-ileostomy—treatment of choice) if colitis not resolved.
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
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
What is the alternative dx of factitious diarrhoea?
histological evidence of pigment in macrophages of lamina propria
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
Name the complications of Acute diverticulitis
Associated with
abscess,
perforation,
obstruction
or fistula formation
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
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
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
What are the causes of Colovesical Fistula?
Diverticular diseases (sigmoid MCC)
Crohn diseases
Malignancy viz colon/ bladder/ pelvic organs.
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
What is the CT-scan finding of Colovesical Fistula?
Contrast in bladder with thicken colonic and bladder walls
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
How to dx Acute mesenteric ischemia?
Ct scan preferred
MR angiography
If dx unclear then Mesenteric angiography
CT scan findings of Acute mesenteric ischemia
focal or segmental bowel wall thickening
pneumatosis intestinalis
small bowel dilation
mesenteric stranding and mesenteric thrombi
Important point of acute mesenteric ischemia
There must be underlying thrombotic condition to develop this disorder
How to t/m Acute mesenteric ischemia?
open embolectomy with vascular bypass or endovascular thrombolysis
Triad of chronic mesenteric ischemia
Atherosclerosis as a cause
Post prandial pain with food aversion result weight loss
Signs of malnutrition and abdominal bruit
How to dx Chronic mesenteric ischemia?
CT angiography (preferred)
Doppler U/S
At what site of abdomen “Ischemic colitis” is mc?
Splenic flexure
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
Important point of RETROPERITONEAL HEMATOMA
pt on anticoagulation (normal or supratherapeutic INR) —> raise suspicion for retroperitoneal hematoma
CT findings—> isodense area in retroperitoneum
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
Features of Hyperplastic Polyp
Most common non-neoplastic polyps in the colon.
Arise from hyperplastic mucosal proliferation.
No further work-up needed
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).
What is the MC type of polyp found in the colon?
Adenoma
What feature of polyp suggest the cancerous condition?
Sessile> stalked (pedunculated)
tubular2.5 cm in size
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
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
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
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
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
What to do if colonic dysplasia is diagnosed?
Colonic dysplasia—>↑ risk of adenocarcinoma—>prophylactic colectomy advised
What are the portal HTN sign in patient of Cirrhosis?
Oesophageal varices
Splenomegaly
Ascites
Caput Medusa
Haemorrhoids
What are the signs of Hyper estrinism in patient of cirrhosis?
Spider angiomata
Gynecomastia
Loss of pubic hair
Palmar Erythema
Testicular atrophy
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
What are the peritoneal causes of Ascites?
Malignancy (Ovarian / Pancreatic)
Infection (Tb / fungal)
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
What are the causes of ascites If total protein is less than “2.5g/dl””?
(Low protein ascites)
Cirrhosis
Nephrotic syndrome
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
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.
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
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
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
Important point of ascites
Aggressive diuresis (>1 L/day) —>not recommended b/c of risk of hepatorenal syndrome
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
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
what is the t/m of Esophageal varices?
Endoscopic sclerotherapy
Octreotide- long-acting somatostatin analog
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
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
What to do even if ““continued bleeding”” after doing urgent endoscopic therapy for Esophageal varices?
Balloon tamponade (temporary)–> Tips Or shunt surgery
What to do even if ““Early Rebleeding”” after doing urgent endoscopic therapy for Esophageal varices?
Repeat Endoscopic therapy———->Hemorrhage–>TIPS Or Shunt Surgery
Triad of Acute liver failure
Increase ALT/AST >1000U/L
Signs of hepatic encephalopathy
INR>1.5
What is the most important prognostic factor of Acute liver failure?
PT
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.
Name the dose dependent drug induced HEPATITIS
carbon tetrachloride
acetaminophen
tetracycline
and substances found in the Amanita phalloides mushroom.
Name the dose independent drug induced HEPATITIS
isoniazid
chlorpromazine
halothane
and antiretroviral therapy.
Name the drug which cause fatty liver
tetracycline
valproate
and anti-retrovirals
Name the drug which cause Hepatitis
halothane
phenytoin
isoniazid
and alpha-methyldopa
Name the drug which cause Cholestasis
chlorpromazine
nitrofurantoin
erythromycin
and anabolic steroids
Name the drug which cause Toxic or fulminant liver failure
carbon tetrachloride and acetaminophen
Important point
OCPs cause changes in LFTs without evidence of necrosis or fatty change
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
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)
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
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
How to t/m SBP?
Third Generation cephalosporins as empiric t/m
Quinolones for SBP prophylaxis
Name the bacteria can cause SBP
E. coli»_space; Klebsiella»_space; Streph species
Important point of cirrhosis
Pts with cirrhosis are normally hypothermic and >100 F warrants investigation
What are the solid liver masses?
Focal nodular hyperplasia
Hepatic adenoma
Regenerative nodules
HCC
Liver mets
What are the risk factors which increases the chances of hepatic adenoma formation?
Use of long term Contraceptives
Pregnancy
Anabolic steroid use
How focal nodular hyperplasia occur?
Due to hyper-perfusion from anomalous arteries
Imaging will show arterial flow and central scar on imaging
Name the solid liver masses which has high chance of hemorrhagic or malignant transformation
Hepatic adenoma
What are the risk factors for hepatic angiosarcoma?
vinyl chloride
inorganic arsenic compounds
thorium dioxide
Name the cause of direct jaundice in which ALT/AST/ALP is normal
Dublin Johnson syndrome
Rotor syndrome
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
Name the cause of jaundice in which increase in ALP pre dominantly
PSC
PBC
Malignancy
Cholestasis of pregnancy
Choledocholithasis
Triad of Gilbert syndrome
Decrease In enzyme activity with normal LFTs
Increase in indirect jaundice with underlying stressors
No apparent liver disease
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
Triad of CN syndrome 2
Indirect jaundice with level <20
No neurological problem
IV phenobarbital level normalised bilirubin level
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
Name the test to be done if ALP and GGT both are increase plus US show dilated ducts
ERCP
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
Name the test to be done if ALP and GGT both are increase plus US show abnormal hepatic parenchyma OR positive AMA
Liver biopsy
Triad of PBC
Direct jaundice SxS in female
+Ve AMA
autoimmune destruction of intrahepatic bile ducts
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
What are the features of vanishing bile duct syndrome?
Progressive destruction of intrahepatic bile ducts
Histologic hallmark: ductopenia
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
Triad of PSC
Direct jaundice with Extra/Intra hepatic dilation or stricturing
Onion skin pattern on liver biopsy
ERCP or MRCP–> Beading
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
How to t/m Gallstones without symptoms?
No t/m necessary in most patients
How to t/m Gallstones with typical biliary colic symptoms?
Elective laparoscopic cholecystectomy
Or Urodeoxycholic acid in pops surgical patients
How to t/m complicated Gallstones?
Cholecystectomy within 72hrs
What are the findings On CT scan of Gallstones ileus?
Gallbladder wall thickening
pneumobilia
and an obstructing stone
How to t/m Gallstones ileus?
surgical removal of stone and either simultaneous or delayed cholecystectomy.
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
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
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.
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
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
What are the image findings of acalculous cholecystits?
gallbladder wall thickening and distension and presence of pericholecystic fluid
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
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
Name the bacteria which cause EMPHYSEMATOUS CHOLECYSTITIS
Gas forming bacteria viz Clostridium and some strains of E.coli
How to t/m EMPHYSEMATOUS CHOLECYSTITIS?
Emergent cholecystectomy with use of broad spectrum ABx
What is Charcot triad in acute cholangitis?
Fever
RUQ pain
Jaundice
What would be seen on imaging on acute cholangitis?
Biliary dilation on U/S Or CT scan
How to t/m acute cholangitis?
ERCP with sphincterotomy
Or
Percutaneous trans hepatic cholangiography
With USE of Broad spectrum ABx
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
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
Important point of pancreatitis
If ALT increases think of biliary induced pancreatitis
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
Name the medication which causes acute pancreatitis
Valproate
Furosemide/thiazides
sulfasalazine, 5-ASA
azathioprine
didanosine, pentamidine
metronidazole, tetracycline
What are the CT findings of drug induced Pancreatitis?
peripancreatic fluid and fat stranding
Important point of chronic pancreatitis
Stool elastase—
marker for pancreatic exocrine function
low levels in CP rather than acute pancreatitis
What does it meant by Severe Pancreatitis?
pancreatitis with involvement of at least one organ
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
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
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)
How to approach pancreatic head cancer?
U/S—> if non-Dx—>ERCP—>PTC
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)
How to t/m hepatic adenoma?
If less than 5cm and asymptomatic–>stop COCP
If more than 5cm and symptomatic—> surgical resection
How Hepatic hemangioma present on US?
NO CENTRAL SCAR
centripetal enhancement (from periphery to central
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
How to manage bile acid Diarrhea?
Bile acid resins–>cholestyramine
colestipol
colesevelam
What are the signs of hyper estrogen in Cirrhosis patient?
Spider angiomata
Breast formation
Palmar erythema
testicular atrophy
Loss of sexual hair
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
How to treat IBS?
Reassurance and Dietary modification
If constipation type—>fiber supplementation
If diarrhea—->Antidiarrheal like loperamide
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
How to treat IBD induced Toxic megacolon?
IV steroid like methylpred
Avoid invasive imaging like colonoscopy
How Proctaglia fugax occur?
Due to spastic Contraction of anal sphincter
Or
Pudendal nerve compression
Triad of Proctaglia fugax
recurrent rectal pain with pain free episodes
Unrelated to defecation
Normal physical Ex without lab abnormalities
How to manage Proctaglia fugax?
Reassurance
Nitroglycerin ± biofeedback therapy for recurrent sxs
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
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
Name the vaccine given in chronic liver disease
HABIT (B=P)
HA HAV / HBV
P pneumococcal
I flu
T Tdap
Triad of Spontaneous bacterial peritonitis
High grade fever with abdominal tenderness
Low BP with Hypothermia
Paralytics ileus with severe infection
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
Name the med for wilson disease treatment
1) Chelators like trientine or D pencillamine
2) zinc as it interfer absorption of copper.
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
How to dx and manage Autosomal dominant PJ syndrome?
Dx —–> Genetic testing
Manage—-> annual anemia screening and cancer screening via Upper/lower EGD
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
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
How to tx Infected Pancreatic Necrosis?
IV ABx onced stabilize —>do Debridement
What are the 4As of Hepatic encephalopathy?
Ataxia
Asterixis
Altered mental status
Altered sleep pattern
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
Triad of Budd chiari syndrome
Ascities
Abdominal pain
HSM
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)
