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Treatment of acalculous cholecystitis
Emergent cholecystectomy is the treatment of choice - patients who are too ill for surgery, perform percutaneous drainage of he GB with cholecystostomy
What are the complications of acute pancreatitis?
Complications of pancreatitis (ACUTE):
1. Pancreatic necrosis - can be sterile or infected
a. sterile heals on own
b. infected has high mortlatlity rate 2/2 multiple organ failure in 50% of causes; surgical debridement and antibodics indicated
2. Pancreatic pseudocyst
a. encapsulated fluid collection that appears 2-3 weeks after an acute attack - unlieke a true cyst, it lacks an epitheliel lining.
b. complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (duodenum, stomach, transverse colon) if large enough; or if located at the head of the pancreas, can cause comepression of the CBD
c. diagnosis by CT
d. IF cysts < 5cm then observe, if > 5cm then drain
Clostridium difficile presents with which hypervirulent features?
marked leukocytosis (15k-50k)
severe metaboli acidosis with elevated LACTATE levels
Increased need for colectomy
Cirrhosis of the liver v. Hepatitis of the liver
Cirrhoses - chronic liver dz characterised by fibrosis, disruption of the liver architecture and widespread nodules in the liver (the fibrous tissue replaces damaged or dead hepatocytes)
Hepatitis - inflammation of the liver hepatocytes.
Coagulopathy occurs 2/2 synthesis of clotting factors being decreased:
1. Prolonged PT; PTT may be prolonged with severe disease
2. Vitamin K is ineffective because it cannot be used by diseased liver
3. Treatment of coag is FFP
Adenocarcinoma of the esophagus is one of two types of esophageal CA that affects what population?
Most common in white males
most common in distal 1/3 of esophagus @ GE junction
RF: GERD and Barretts esophagus are main risk facors; alcohol and tobacco may not be as important as in SCC
IF a PEPTIC ULCER is uncomplicated, then a _____ _____ or ______ is not needed initially. Initiate empiric therapy. If you suspect any complications of PUD, order confirmatory testss
barium swallow, endoscopy
Patients with UC may have ______ ____ at first with eventual progression to bloody diarrhea
Murphys sign v. BOAS sign
Murphy's sign: RUQ pain, inspiratory arrest during deep palpation of RUQ, not present in many causes) - fever and leukocytosis - cholecystitis
BOAS sign - right should pain 2/2 that of gall stone - cholelithiasis
What is the most common location for liver abscesses (both pyogenic and amebic)?
Right lobe of the liver
What is the diagnosis of jaundice?
Serum levels of unconjugated v. conjugated BR.
-if unconjugated, then there must have been an issue prior to hepatic uptake and thus check CBC, reticulocyte count, haptoglobin, and LDH (with peripheral smear) to r/o hemolytic anemia
-if conjugated hyperbilirubinemia, then there must have been an issue after the bilirubin-albumin complex formed and after hepatic uptake either within or after the hepatic ducts. LFTS may points to cause
-get US/CT to assess biliary tract for obstruction or anatomic changes
-additional tests ERCP if conj with obstruction 2/2 US/CT
-liver biopsy is the last resort and indicated in some cases to determine cause of HCC injury
Clinical features of SBO?
Cramping abdominal pain (if continuous and severe then expect strangulanous activity.
-n/v may be feculent
-obstipation (LACK OF STOOL and FLATUS)
Radiation therapy is indicated in patients with ____ cancer but NOT indicated in patients with >>>>
Can use for patients with rectal cancer
Cannot use for patients with colon CA
Treatment of hemochromatosis? Diagnosis?
1. Marked elevation in serum iron and serum ferritin
2. Elevation of iron saturation (transferritin sat)
3. Decreased TIBC
4. Liver biopsy (determines hepatic iron concentration)
5. Genetic testing for chromosomal abnormality
TREATMENT: perform phlebotomies to removes excessive serum iron
-treat any complications (CHF. DM. hypothyroidism, arthritis) and consider liver transplantation if late stage hemacrhomatosos
Diseases of the appendix:
Lumen of the appendix is obstructed by:
1. Hyperplasia of lymphoid tissues (60%) of cases
2. Fecalith (35% of cases)
3. Foreign body
4. PARASITE/CARCINOID TUMOR (other rare causes)
Skin and soft tissue infections (SSTI's) are the most common of all infections
What are the categories?
Superficial uncomplicated infections
Infections associated with bites and animal contact
surgical site infections
infections of the immunocompromised host
Most patients with acute pancreatitis have mild to moderate disease, but to up 25% have severe disease
What are the causes of acute pancreatitis:
1. Alcohol abuse (40%)
2. gallstones (40%) - galllstone passes into the bile duct and blocks the ampulla of vater
3. post ERCP - pancreatitis occurs in up to 10% of patients undergoing ERCP
4. VIral infections (mumps or COXSACKIEBVIRUS)
5. Drugs (sulfonamides), HCTZ, ferusemide, estrogens, HIV medications, and many other drugs have been implicated
6. Post operative complications (HIGH MORTALITY RATE)
7. Scoprion bites
8. Pncreas divisum
9. Pacnreatic CA
10. HyperTG hyperCa
12. blunt abdominal trauma (most common cause of pancreatitis in children)
What are the clinical features of pseudomembranous colitis?
1. Profuse watery diarrhea
2. Crampy abdominal pain
3. Toxic megacolon with risk of perforation
Choledocholithiasis clinical presentation:
ASymptomatic for years
-RUQ pain/epigastric pain and jaundice
Autosomal recessive - Polyps plus cerebellar medulloblastoma or glioblastoma multiforme?
PERSISTANT OR CONTINUING INFFLAMMATION OF THE PANCREAS WITH FIBROTIC TISSUE REPLACEMENT OF PANCREATIC PARENCHYMA AND ALTERATION OF PANCREATIC DUCTS (AREAS OF STRICTURE/DILATION); EVENTUALLY RESULTS IN IRREVERSIBLE DESTRUCTION OF THE PANCREAS
CHRONIC PANCREATITIS - BOTH ENDOCRINE (INSULIN) AND EXOCRINE (ENZYMES) ARE AFFECTED
Albumin as a liver function test:
Albumin is decreased in chronic liver disease, nephrotic syndrome, malnutrition and inflammatory states *burns/sepsis/trauma
Clinical features of PANCREATIC CA
Very nonspecific - thus by the time dx is made, often too late and incurable.
1. Abdominal pain
2. Painless jaundice bc @ head of pancreas
3. Weight loss
4. Onset of glucose intolerance but the GM is mild
6. Migratory thrombophelbitis - develops in 10% of cases
7. Courvoisier's sign (palpable GB) present in 30% of patients involved head of pancreas - presents without pain
RISK FACTOR FOR CHOLANGIOCARCINOMA:
1. PSC major RF
3. CHoleochal cysts
4. Clonorchis sinensis infestation (Hong kong)
Treatment for patients with achalasia
1. Adaptive measures: chew food to consistency of pea soup b4 swallowing; sleep with trunk elevated, avoid eating before sleeping
2. Medical therapy
a. antimuscarinics (DICYCLOMINE) usually unsatisfactory
b. sublingual nitroglycerine - long acting nitrates, CCB
3. injection of outlimun toxin into the LES during endoscopy
-blocks cholinergic activity in the LES
-can be effective in up to 65% of cases; however, repeat procedure needs to be performed every 2 hrs
Tests to order in patients with GI bleeding and hematochezia:
first rule out anorectal cause (hemorrhoids). Colonoscopy is the intial test bc colon cancer is the main concern in patients > 50YO
Acute infectious diarrhea - top cases are what organisms?
1. Salmonella (14.6 cases)
2. Campylobacter (12.7 cases)
3. Shigella (4.7 cases)
4. E. Coli O157H7 (1.1)
5. Crptosporidia (3.0 cases)
What is alreay present (symptomatically) in a MW syndrome
Hematemesis is always present - it varies from steaks of blood in vomitus to massive bright red blood.
As many as 25% of patients with bleeding AV malformations have aortic stenosis however, no ____ and _____ relationship has been noted.
cause and effect (AVM and AVS)
Clinical features of esophageal cancer:
-dysphagia (MOST COMMON - to solids only then to liquids!)
-weight loss (second most common symptom)
-odynophasia (pain with swallowing)-late finding that suggests extraesophageal involvement (mediastinal invasion)
-hematemesis, hoarseness of voice, recurrent laryngeal nerve involvement
-aspiration pneumonia, respiratory symptoms due to involvement of traceobronchial tree
If ALT and AST levels are mildly elevated (low hundreds), think of what diagnosis?
Chronic viral hepatitis or acute alcoholic hepatitis (AST < 500) and (ALT < 300)
ORGANS effected by Wilsons dz v. Hemochromatosis
Kidney, liver, cornea = wilsons
liver (primary), pancreas, heart, joints, skin, thyroid, gonads, hypothalamus = hemo
Pigmented stones are the second type of GB stones that occur 2/2?
Black stones found in the GB associated with HEMOLYSIS, SCA, THALASSEMIA, HEREDITARY SPHEROCYTOSIS, ARTIFICIAL VALVES, ALCOHOLIC CIRRHOSIS
BROWN stones are usually found in BILE ducts and are associated with a BILIARY tract infection
bright red blood per rectum
-represents lower GI source (LEFT COLON OR RECTUM)
-consider diverticulosis, arteriovenous malformations, hemorrhoids, and colon CA
What is a bleeding scan?
radionucleotide scanning that reveals bleeding even with a low rate of blood loss. It does not localize the lesion; it only identifies continued bleeding. Role is controversial but it may help determine where arteriography is needed
Clinical features of cirrhosis?
-asymptomatic in early dz
-portal HTN, varices, ASCITES, hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, hyperestrinism
How do signs and symptoms change in relation to the effected side of colon (right v. left)
Right sided colon tumors:
-obstruction is unusual because of the larger luminal diameter (the cecum has the largest luminal diameter of any part of the colon that often allows for tumor growth to go undetected.
-common finding is occult blood in stool , iron deficiency anemia and MELENA (BLACK STOOL)
-change in bowel habits is uncommon
-triad of anemia, weakness, RLQ mass (occasionally) is present
Metastasis of GASTRIC carcinoma
1. Krukenberg's tumor: metastasis to ovary
2. Blumer's shelf: metastasis to rectum
3. Sister Mary Josephs node: met to periunbilival lymph node
4. Virchows node - metastasis to the supraclavicular fossa nodes
5. Irish's node (metastasis to the left axillary adenompathy
Acute uncomplicated UTI prevention of precurrences
Some supportive evdience
-cranberry juice (200-750 mL/d) or cranverryo concentrate tablets (12-20% reduction)
-topical estrogen creams
-avoid exposure to vaginal spermicides
No supportive evidence
-"enhanced" urinary hygiene
-oral estrogen replacement
Hypersensitivity to gluten
-weight loss, abdominal distention, bloating diarrhea
-biopsy in prximal small bowel reveals flattenng of villi which causes malabsorption
-strict adherence to gluten free diet
What are the majority of cases regarding PUD related to?
1. Helicobactor pylori infection
2. NSAIDS-inhibit prostaglandin production which leads to impaired mucosal defenses.
3. Acid hypersecretory states like ZE syndrome (excessive production of gastrin)
Considerations with acute bacterial sinusitis that recurs?
1. Inadequate course of therapy
2. Concurrrent allergic rhinitis
3. Anatomic abnormalities that block ostia
4. undiagnosed immundeficiency states
-common variable immunodeficiency
-immotile cilia syndrome (karteganer's)
The level of either _____ or _______ in acute pancreatitis does not reliably predict the severity of disease.
What are the clinical feature of budd-chiari syndrome:
Hepatomegaly, ascites, abdominal pain RUQ; jaundice, variceal bleeding
Complication to ACUTE PANCREATITIS:
Ascending cholangitis and be 2/2 ______ obstruction in the ampulla of Vater, leading to infection of the biliary tract.
The higher the AST-ALT ratio the greater the likelihood that ------ is contributing to the abnormal LFTs
What patients should not be treated if acute infections diarrhea is clinically present?
Pts with mild disease without systemic toxicity or dehydration
pts with spontaneously remitting sxs
pts with suspected shiga toxin-producing e. coli infection (O157H7) --> bloody diarrhea in an afebrile pt with a h/o eating raw hamburger or seed sprouts or visiting a petting zoo
Paraesophageal hernias tend to enlarge with time, and the entire stomach may ultimately move into the _____. Type 3 hernias (combination of type 1 and 3) are treated as type _____ surgically.
Complication of diverticulosis versus diverticulitis
Diverticulosis: painless rectal bleeding and diverticulitis
Diverticulitis: includes bowel obstruction, abscess and fistulas
How are CIRRHOTIC patients managed LONGTERM?
1. Periodic lab values 3-4 months (CBC, CMP, RFTs, LFTs, coagulation tests)
2. Perform an endoscopy to determine the presense of varices
3. If hepatocellular carcinoma is suspected then perform a CT guided biopsy for diagnosis
Treatment of pancreatic CA
1. Whipples procedure is the only hope for cure; only a minority of tumors resectable. Pronosis post resection with 5 year survival rate of 10% - grim.
2. If the tumor is unresectable and biliary obstruction is present , perform PTC or ERCP with stent placement across the obstruction for palliation.
What exacerbates GILBERTS syndrome?
fasting (crash diets); fever, alcohol, and infection. Asymptomatic in most cases, but occasionally jaundice is seen.
Clinical geatures of HCC
-weiht loss, anorexia, fatigue
-signs and symptoms of CLD; portal HTN, ascites, jaundice, splenomegaly
D. CARCINOID SYNDROME
E. HYPERTROPHIC PULMONARY OSTEODYSTROPHY
80% of episodes of upper GI bleeding stop spontaneously and only need supportive therapy - T OR F?
The development of a palpable mass in the epigastrium four weeks after the onset of acute pancreatitis is HIGHLY suggestive of a ______ _______ formation
Pancreatic pseudocyst formation
What is ACUTE GASTRITIS?
inflammation of the gastric mucosa 2/2 NSAIDS/ASA, H. pylori, alcohol, heavy cigarette use, smoking, caffeinel extreme physiologic stress (eg shock, sepsis, burns). It can either be asymptomatic or cause epigastric pain. The relationship between eating and pain is NOT consistent.
IF LOW PAIN or MODERATE and not worrisome, empiric therapy + acid suppress is good treatment with the stopping of NSAIDs
CHRONIC INFLAMMATORY DISEASE of colon or rectal mucosa that occurs at any age but usually young adulthood.
-distribution os UC involves to rectum in all caes and can involve the colon paritally or entirely
a. rectum along (10%)
b. rectum and left colon (40%)
c. rectum, left colon, right colon *30%)
unpredictable course and variable
Acute cholecystitis without stones that obstruct the cystic duct (up to 10% of patients with acute cholecystitis)
-idiopathic in patienst with underlying illness associated to dehydration ischemia burns trauma and a postoperative state
-signs and symptoms are the same as for acute cholecystits
COMPLICATIONS WITH CROHNS!
1. fistula between colon and other segments of intestine (enteroenteral), bladder, and vagina and skin.
-anorectal dz in 30% pateints - fissues, abscesses, perianal fistulas
What are the signs of appendiceal rupture 2/2 untreated acute appendicitis?
Complications -20% of cases
RF: delay in treatment (>24 hours) and extremes of age
-signs of appendiceal rupture (high fever, tachycardia, marked leukocytosis, peritoneal signs, toxic appearance)
HNPPCRC - without adenomatous polyposis
Lynch I v. Lynch II
Lynch syndrome I: site specific CRC - early onset CRC without multiple polyposis
Lynch syndrome II: cancer family syndrome - all features of lunch 1 plus increased number and early occurrence of other cancers (female genital tract, skin, stomach, pancrea, brain, breast, biliary tract).
Causes of hepatic encephalopathy:
1. Toxic metabolites
2. occurs in 50% of all cirrhosis cases
3. Hypokalemia and alkalosis (2/2 diuretics), dedating drugs (narcotics, sleeping meds), GI bleeding, systemic infection, and hypovolemia
4. Clinical features: confusion, asterixis, rigidity and fetor hepaticus
Rectal cancer versus CRC
20-30% of all CRC are rectal
1. Hematochezia is the most common symptom
3. Rectal mass, feelin of incomplete evacuation of stool due to mass
What indicates a non-neoplastic polyp?
A benign lesions with no malignant potential
-hyperplastic (metaplastic polyp) most common (90%); generally remain small and asymptomatic
-no specific therapy required but difficult to distinguish from neoplastic polyps
-juvenile polyps are highly vascular and common (if younger than 10) so remove
-inflammatory polyps (pseudopolyps) are associated with UC
What is the treatment of patients with suspected ascending cholangitis?
1. Blood cultures
2. IV fluids
3. Empiric antibiotics with good anaerobe and gram - coverage -
4. Decompress the CBD when patient becomes hemodynaicmally stable.
Signs of intestinal infarction:
hypotension, tachypnea, lactic acidosis, fever and AMS
-CHECK THE LACTATE LEVEL IF ACUTE MESENTERIC ISCHEMIA IS SUSPECTED
What is the prognosis of acute pancreatitis?
WHAT IS RANSON'S CRITERIA?
RANSON'S CRITERIA is used to determine the prognosis and mortality rates:
*pts with more than 3 or 4 Ranson's criteria should be monitored in ICU
1. (GALAW) Admission criteria:
2. Initial 48 hours criteria (C HOBBS)
Ca2+ < 8 mg/dL
Decrease in Hematocrit (>10%)
PaO2 < 60 mm Hg
BUN increase >8mg/dL
Base deficit > 4 mg/dL
Fluid sequestration > 6L
<3 criteria - 1%
3-4 criteria - 15%
5-6 criteria - 40%
>7 criteria - 100%
Arteriography is used for which reason in GI BLEEDING?
DEFINITIVELY LOCATES THE POINT OF BLEEDING
-mostly used in pts with lower GI bleeding
-should be performed during active bleeding
-potentially therapeutic (embolization or intra-arterial vasopressin infusion)
Pateint with a history of AORTIC GRAFT SURGERY who has a small bleed of GI involving the duodenum before massive, fatal hemorrhage hours to weeks later.
Performing an endoscopy or surgery during this small window of opportunity to prevent death is quinticential to survivial.
CA-P duration of therapy
1. ID society:
- s pneumona treat until afebrile for >72 hr
- s aureus< GNRS, anaerobes, atpicals, > 2 weeks
SCHATZKIS RING (Distal esophageal web)
circumferential ring in the lower esophagus that is always accompanied by a sliding hiatial hernia.
What are the clinical symptoms of primary biliary cirrhosis of the intrahepatic bile ducts?
Xanthomata and xanthelasmata
Portal HTN with resultant sequelae
Treatment for ESOPHAGEAL CA
Palliation is the goal in most patients becase the disease is usually advanced at presentation HOWEVER PERFORMATION OF AN ESOPHAGECTOMY MAY BE CURATIVE IF STAGE 0,1,2A.
-CHEMO + RADIATION B4 SURGERY PROLONGS SURVIVAL
Complications of hemachromatosis:
#CIRRHOSIS INCREASES RISK OF HCC BY 200; PRESENSE OF LIVER DISEASE IS ESSNTIAL FOR PROGNOSIS OF DZ
#Cardiomyopathy - CHF, arrhythmias
#DM - due to iron deposition in the pancreas
#Arthritis-most common sites are the 2nd and 3rd metacarpelphysial joints HIPs and KNEES
#Hypogonadism - loss of labido, mensus, impotence
#hyperpigmentation of skin
WHAT ARE THE CLINICAL FEATURES OF WILSONS DISEASE
1. Liver disease with acute hepatitis, cirrhosis or fulminant hepatic failure
2. KAYSER-FLEISCHER RINGS (yellow rings in the cornea representative of cu2+ accumulation and deposition in cornea...do not interfere with vision.
3. CNS findings:
-extrapyramidal signs= parkinsonian symptoms with resting tremor, rigitity, radykinesia, chorea, drooling, incoordination due to copper depostition in BG
-psychiatric distrubances - depression, neuroses, peraonlity changes, psychosis
4. Renal involvment
Symptoms of SCHATZKIs RING v. PV SYNDROME
SR: moderate dysphagia may be present; 2/2 alkali, acids, bleach, detergents (suicide attempts). Stricture formation indicates inc risk for esophageal cancer
Treatment: esophagectomy i full thickness necrosis has occurred. Pt should avoid vomiting, gastric lavage and all orgal intake which cnan compound the original injury. Give the pt steroids and AB its well
PVS: Anemia, oral mucosa, upper GI esophageal webbing causing dysphagia
Major differential points of SSTI's (skin and soft tissue infections)
Community v. Hospital acquired
-community: s aureus >>> group A streptococci and GBS
-hospital: s aureus, GNRs, enterococci
Erythema only v. pus &/or open wound
-erythema only: strept
-pus/open wound: s aureus
What is a flexible sigmoidoscopy?
Can be used to reach the area where approximately 50-70% of polyps and CA occur
Can be diagnostic in about 2/3 of all CRCs
How is hepatic functional reserve assessed?
-estimates hepatic reserve in liver failure; it is used to measure disease severity and is a predictor of morbidity and mortality.
-childs class C is the most severe disease and childs class A is the least severe disease.
MOST COMMON CAUSE = H PYLORI (>80%) cases
-autoimmune gastritis lads to chornic atrophic gastritis with serum antipareital and anti-intrinsic factor antiboide (possible dvelopment of pernicious anemia)
-most pts are asymptomatic and never develop complications - manifests as epigastric pain similar to PUD
complications: gastritis, carcinoma, mucosa-associated lymphoid tissue lymphoma (MALT)
-UPPER GI ENDOSCOPY WITH BIOPSY IS THE TEST OF CHOICE FOR Dx OF CHRONIC GASTRITIS
Acute UTI uncomplicated diagnosis:
Consistent symptoms + positive dipstick (U/A) = UTI (culture NOT NEEDED)
Pathophysiology of SBO
Dehydration is a key event in SBO
-intesntinal distention causes reflex vomiting, increased intesinal secretion proimal to point of obstruction and decreased absorption. This leads to hypochloremia, hypokalemia and metabolic alkalosis
WHAT IS THE TREATMENT FOR BILE DUCT STRICTURE
ENDOSCOPING STENTING IS PREFERRED OR SURGICAL BYPASS IF OBSTRUCTION IS COMPLETE OR IF ENDOSCOPIC SPINCTEROTOMY
Reynolds pentad is associated with ____ _ and is a highly toxic state that requires emergency treatment and can be rapidly fatal
COMPLICATIONS OF CBD stones
Diagnosis of HCC
Liver biopsy - required for definitive diagnosis
-lab tests (hepatitis B and C serology, LFTs, coagulation tests
-imaging studies: US, CT scan (chest abdomen pelvis; MRI/MRA if surgery is an options because they provide more detail about anatomy.
-tumor marker elevation of AFP is useful as a screening tool. AFP level may be elevated in 40-70% of patients with HCC and is also helpful in monitoring response to therapy.
What is the general characteristic of diverticulosis?
1. Increased intraluminal pressure-inner layer of colon bulges through focal area of weakness in colon wall (usually an area of blood vessel penetration)
2. LOW FIBER diets: contipation cause sintraluminal pressures to increase with a positive family history increases the risk
3. Most common location is the sigmoid colon however diverticula may occur anywhere in the colon.
Hemorrhagic pancreatitis is another complication of acute pancreatitis:
Cullen's sign (periumbilical bleeding)
Grays sign (flank ecchymoses)
Fox's sign (inguinal ecchymoses)
CT scan with TV contrast is the study of choice
Alkaline phosphatase (ALK-P) is elevated in which clinical scenarios?
1. ALK-P is elevated when obstruction to bile flow(cholestasis); in any part or biliary tree. If normal, unlikely biliary obstruction
2. IF EXCESSIVELY high (10 fold) think of extrahepatic hiliary tree obstruction or intrhepatic cholestass (PBC or DI-cirrhosis)
3. If level are elevated, measure the GGT (gamma-glutamyl transferase) level to make sure the elevation is HEPATIC origin (rather than bone or intestinal). If GGT is also elevated, then strongly suggests hepatic origin. If GGT level is normal but ALP elevated - think bone or pregnancy issue
What are the clinical features of achalasia:
1. Dysphagia (odynophgia less common) - both solids and liquids
3. Chest pain
4. Recurrent pulmonary complications secondary to aspiration, which may cause lung abscess, bronchiectasis, hemoptysis
What is the LAB TEST that diagnosis for GI bleeding?
-stool guiac for occult blood
-Hgb/hct level (may not be decreased in acute bleeds)
-A hgb level >7-8 acceptable in young health patients without active bleeds
-A hgb level in most elderly patients should have hgb level ?10 g/dL
-low MCV is suggestive of iron deficiency anemia and chronic blood loss
-coag profile (plt ct, PT, PTT, INR)
-LFTs, renal function
-the BUN-creatinine ratio is elevated with upper GI bleeding. This is suggestive of upper GI bleeding if patient has no renal insufficiency
What is the TREATMENT of PBC?
1. Cholestyramine for the pruritis
2. Vitamin D, Calcium, Bisphosphonates for osteoporosis
3. Ursodeoxycholic acid (hydrophilic bile acid) has been shown to slow progression
4. Liver transplantation is only curative therapy.
AUTOIMMUNE AB: (+) antimitochondrial antibodies
What medication should be avoided in patients with mesenteric ischemia?
Vasopressors because it worsens the ischemia.
Treatment of GALLSTONES
symptomatic v. asymptomatic
SYmptomatic-elective cholecustectomy for patients with recurrent bouts of biliary colic
asymptomatic - no treatment
NASH histologically is identical to patients with ____ liver disease, but these patients do not usually have a history of substance abuse.
Treatment of SBP:
spontaneous bacterial peritonitis
1. Broad spec therapy then give specific once identify bacteria.
-clinical improvement should be seen within 24-48 hours. Repreat paraventesis in 2-3 days to document a decrease in ascitis fluid PMN < 250
What risks can exacerbate PUD?
2. Alcohol and coffee
3. Emotional stress and type A personality
Signs of acute liver failure:
2. Elevated LFTs
4. Hypoglycemia(liver stones glycogen)
5. Hepatice encephalopathy 2/2 ammonia intoxication
In acute pancreatitis:
1. Serum amylase:
2. Serum lipase:
5. Order the following for assessment of prognosis:
1. Amylase = most common tests but many conditions cause hyperamylasemia and its absense doesnt rule out acute pancreatitis. If levels are >5x NL then highly specific for acute pancreas.
2. Lipase = more specific for pancreatitis than amylase
3. LFTs - to identify cause (gallstone pancreatitis)
4. Glucose, Ca@+. hct, BUN, ABG, LDH, WBC count
Treatment for PUD: Medical
1. d/c nsaids/asa
2. rstrict -OH use but not foods
3. Stop smoking/dec emotional stress
4. Avoid eating before bedtime and dec coffee intake
1. H2 blockers, PPIs, antacids
ERATICATE H. PYLORI with tripple therapy regimen
CYTOPROTECTION - sucralfate and MISOPROSTOL
Surgical: Rarely needed - required for ocmplication of PUD(bleeding performation gastric outlet obstruction
Barium enema are good for?
Evaluates the entire colon, completmentary to fleximble signmoidocopy - disadvantage is that any abnormal finding needs to be evaluated by colonoscopy
Complications of UC
3. Lytes and h20
4. Structures, benign, malignant usally malignant
5. Colon ca- increas risk
6. Cholangiocarcinoa (half of all biles duct CA are associated with UC)
7. Sclerosing cholngitis
8. Toxic mega
Diagnosis of crohns
-malabsorption and weight loss
-abdominal pain RLQ n/v
-extraintestinal manifestiations in 15% - uveitis, arthritis, anklosing SpA, erythema nodosum, pyoderma gangrenosum, aphthough oral ulcers cholelithiasis and neprholithiasis
If a patient with GERD also has a diatal hernia, the hernia often wrosens the symptoms of GERD - T or F
Types of varices 2/2 liver disease:
4. Caput medusae (distention of abdominal wall veins)
In cholelthiasis, biliary colic can lead to acute ________.
In choledocholithiasis, onset of symptoms leads to _____ and/or ______ which are life threatening causes.
Acute cholecystitis (obstruction of the GB leading to inflammation - not due to infection).
Acute pancreatitis or CHOLANGITIS
The distortion of the liver anatomy in CIRRHOSIS causes which two major events:
1. Decreased blood flow through the liver and thus causing PORTAL HTN (therefore associated ascites, esophageal varices, splenomegaly, peripheral edema, variscosity of veins "back stream" in circulation, hemorrhoids)
2. Hepatocellular failure that leads to impairment of biochemical functions such as decreased albumin synthesis and decreased clotting factor synthesis (thus can no longer carry Ca2+ or protein and will have increased bleeding 2/2 decreased coag.
Complications with CHRONIC pancreatitis:
1. Narcotic addiction - most common complication
2. DM/impaired glucose tolerance
4. Pseudocyst formation
5. Pancreatic ductal dilitation
6. CBD obstruction (2/2 to fibrosed portion in head of gland)
7. VItamin B12 malabsorption
8. Effusions (pleural, pericardial, peritoneal)
9. Pancreatic carcinoma (increased risk)
Porcelain gallbladder is defined as:
intramural calcification of the gallbladder wall
-prophylactic cholecystectomy is recommended bc 50% becomes malignant
SCC is most commonly seen in which patients regarding esophageal CA?
most commonly located in upper thoacic and mid thoacic esophagus
1/3 in distal 10 cm of esophagus
RF: alcohol and tobacco use, nitrosamines (diet), achlasia, PV syndrome, caustic ingestion, nasopharyngeal carcinoma
A lower GI bleed or positive occult blood test in stool in patients > 40YO is ___ ___ until proven otherwise
COmplication of cholecystitis: (inflammation of the GB)
1. Gangrenous cholecystitis
2. Perforation of GB
3. Emphysematous cholecystitis
4. CHolecystenteric fistula with gallstone ileus
5. Empyema of the GB
How should JAUNDICE be evaluated?
--> Hx, PE, LABS: ALT, AST, Bilirubin, ALKPHOS, ALBUMIN, PT
If normal LFTs (ALT, AST, ALKPHOS, albumin, PT)
-DJ syndrome/rotors syndrome
-see test for differential; hemolysis and gilberts syndrome most common
If abnormal LFTS (intrahepatic issue)
-->suspected intrahepatic disease based on LFT
-consider liver bx
-consider CT scan to r/o structureal dz
-medical management v. observation
-ducts will be normal
-->suspected extrahepatic obstruction
-noninvasive imaging (US/CT)
a. Normal ducts
b. Normal ducts but suspecte extrahepatic cholestasis
c. Dilated ducts
i. Direct duct visulaization - ERCP or PTC
--> if seen, then relieve obstruction
(surgically, endoscopicallly, percutaneously)
Hundreds of adenomatous polyps in the clon, the colon is always involved and the duodenum is involved in 90% of cases . Polyps may also form in the stomach, jejunum and ileum. This is an autosomal dominant d/o
AR disorder with increased skin pigmentation, DM, cirrosis and arthralgia in late stages
Clinical features of cholelithiasis?
1. MAJORITY ARE ASYMPTOMATIC - if found incidentally - dont touch it no need to remove
2. Biliary colic is due to temporary obstruction of the cystic duct by a gallstone.
3. Pain is 2/2 the gallbladder contractng AGAINST the obstruction
4. RUQ or epigastrium and mild-severe pain
5. BOAS SIGN - riht subscapular pain of biliary colic
Sulfasalazine is metabolized by bacteria to 5-ASA and sulfapyridine. 5ASA is the _____ _______ of the drug
-Antibiotic associated colitis because many patients do not have grossly visible pseudomembranes
a. AB rx kills organisms that normally inhibit the growth of Cdiff.
b. Overgrowth of C. diff and toxin production
c. almost all antibiotics have been associated but the most common include;
Symptoms usually begin during first week of antibiotic therapy but can continue 6 weeks after stopping AB.
HOW does CRC spread?
Direct extension - circumferencially and then through the bowel wall to invade other abdominal organs.
-portal circulation to the liver, liver is the most common site of distant spread
-lumbar/vertebral veins to lungs
-transperitoneal and intraluminal
Decreased liver syntheic function will cause a decrease in serum albumin concentration and an increase in INR (why?) Hypoalbuminemia can contribute to edemain end stage liver disease.
because the liver produces albumin and clotting factors. If clotting factors are low, then PT and PTT times will take longer and the INR will be hypercoaguable because there are minimal being produced
Multiple hamartomas that may be scattered through the GI tract that cause pigmented spots around the lips, oral mucosa, face, genitalia and palmar surfaces. These are very low malignant potential. Intussesception or GI bleeding may occur.
Diagnosis of ACHALASIA
Dx: barium swallow ("birds beak") beak-like narrowing of distal esophagus and a alrge, dilated esophgus proximal to the narrowing
dx: UPPER GI endoscopy to r/o secondary causes of achalasia (gastric carcinoma) and retention esophagitis or esophageal CANCER
dx: manometry to confirm the dz; reveals failure of LES relaxation and aperistalsis of esophageal body
When is discharge appropriate for CA-P?
When VS are stable for 24hr (temp <100; RR<24; HR<100, SBP >90, sat 90%)
-able to take ATB po
-able to maintain hydration and nutrition
-MS is normal or at baseline
-no other active clinical or psychosocial issues requireing ongoing hositalization
Treatment of MW syndrome/tear
upper endoscopy is diagnostic, most causes stop bleeding without any treatment but if treatment is required it is surgical (overing the tear) or angiographic embolization if bleeding continues, but this is raraely necessary. Acid suppression is used to promote healing.
Clinical features of PSC:
1. Begin insidiously
2. Chronic cholestasis include jaundive, pruritis; all patients eventually present with chronic obstructive jaundice.
3. Other symptoms include: fatigue, malaise, weight loss
Acute versus Chronic Mesenteric Ischemia
1. Results from a compromised blood supply, usually to the superior mesenteric vessels
2. Four types of acute mesenteric ischemia:
a. Arterial emboli (50% of cases) - cardiac origin (afibb, MI, valvular)
b. Arterial thrombi (25% of cases) - CAD, PVD, STROKE (atherosclerotic)
c. Nonocclusive mesenteric ischemic - splanchnic vasocontriction 2/2 CO dec
d. Venous thrombus - many predisposing factors - eg infection, hypercoag states, OCP, portal HTN, malig, pacreatitis
3. Mortality rate for all types is about 60-70% - if bowel infarct occurred, rate >90%
1. Caused by atherosclerotic occlusive disease of main mesenteric vessels (celiac artery, superior and inferior mesenteric articles)
-abdominal angina, dull pain, typically postprandial (when there is increased demand for spanchnic blood flow); analogous to anginal pain of CAD
-weight loss 2/2 abdominal angina
-mesenteric arteriography confirms the diagnosis
-surgical revascularization is definitive treatment and leads to pain relief in 90% of cases
How is wilsons disease dx? How is it treated?
Dx: Hepatic dz w/ elevated ALT>AST with impaired syn of clotthing factors
-decreased serum ceruloplasmin levels although ranges within normal dont exclude dx
-liver biopsy (elevated Cu2+)
-if dx, then warn first degree relatives
Rx: chelating agents - penicillamine that removes nad detoxifies the excess Cu2+ deposits.
-ZINC - prevent uptake of Cu2+
=liver transplantation if unresponsive to chelation + zinc
-montior Cu2+ levels, urinary copper excretion, ceruloplasmin and liver function: phsycial examination for isgns of liver or nerologic disease - psychological health
Treatment for DES?
-nitrates and CCB which decreases contractions but not curative
What is the most common causes of cirrhosis?
What is the primary method of diagnosis?
1. Alcoholic liver disease
2. Hepatitis C
Dx by liver biopsy (gold standard)
Nasogastric tube and diagnosis of GI bleeding>
Initial procedure for determining whether GI bleeding is an upper or lower GI source
-use the NG tube to empty the stomach to prevent aspiration
-false negative findings are possible if upper GI bleeding is intermittent or from lesion in the duodenum
-evaluation of aspirate
-bile but no blood --> UPPER GI BLEED UNLIKELY; source probable distal to lig of trietz
-BRIGHT red blood or "coffee" grounds appearance - upper GI bleeding
-nonbloody aspirate (clear gastric fluid) - upper GI bleeding unlikely but cannot be ruled out definitively (source may possibly be in the duodenum)
Complications associated with diverticulosis?
1. Painless rectal bleeding (up to 40% of patients)
-bleeding is usually clinically insignificant and stops spontaneously. No further treatment is necessary in these patients.
-if bleeding beomes severe (5%) a colonoscopy may be performed to locate the site of bleeding. If doesnt stop, segmental colectomy may be required
PATIENTS with colonic distention that exceeds that of 10cm increases the risk of bowel ruptures leading to either peritonitis and even death - treatment?
Complications of cholelithiasis?
2. Choledocholithiasis with assoicated symptoms
3. Gallstone ileus
NHL in stomach with features similar to those of adenocarcinoma of the stomach however includes bleeding, obstruction and perforation.
-EGD is standard diagnosis - same as adenocarcinoma of stomach.
-treatment depends upon the stage of the disease and complications
Complication of diverticulitis:
1. Abscess formation: drined either percutaneously under CT guidance or sugically
2. Colovesicular fistula (50% of fistulsa secondary to diverticulitis)
3. 50% close spontaneously
4. Obstruction-due to chronic inflammation and thickening of bowel wall
5. Free COLONIC PERFORATION - uncommon but catacstrophic and leads to peritonitis
Treatment for SBO
1. If incomplete - nonoperative management
2. IV fluids establish urine output; add K+ to correct hypokalemia
3. NG tube to empty stomach (gastric decompresion)
5. Surgery is indicated for complete obstruction, for patial obstruction that s persistent and or associated with constant pain or if strnagulation is suspected. Perform an exploratory laparomty with lysis of adhesions and resection of necrotic bowel.
Clinical features associated with esophageal perforation?
-PAIN (severe/retrosternal/chest/shoulder pain),
-hamman's sign ("mediastinal crunch") produced by the heart beating against airfilled tissues, pneumothorax or pleural effusion
Antibiotics for acute bacterial sinusitis that is uncomplicated?
If complicated (severe sinusitis)
Trial of symptomatic rx for 7days, if no better than treat with amox, doxy or TSX for 10days
consider CT scanning at baseline
treatment with azithro, FQs, or amox/clav for 10-14d - if no better after 3 days then change treatment
Incidence of CRC at 20 years with UC is?
At 30 years?
CRC + UC at 20 years - 5-10%
CRC + UC at 30 years -12-20%
Adults respiratory distress syndrome is a secondary complication to acute pancreatitis in what way?
LIFE THREATENING with high mortality rate
Acute infectious diarrhea options for empirical therapy
Ciprofloxacin 500 mg bid x 1-5d
Levofloxacin 500 mg daily x 1-5d
Erythromycin or azithromycin should be added in the immunocompromised host with increased risk for possible FQ resistant campylobactor infection
What type of hernia (esophageal) accounts for 90% of cases. Both the gastroesophageal juntion and portion of the stomach herniates into the thorax through the esophageal hiatus (so that the GE junction is above the diaphragm)
This is also the most common and benign finding that is assocated with GERD
Complication of liver failure (AC, 9H)
What are the common comorbitidies associated with NASH?
3. DM (some patients have none of these)
4. Usually asymptomatic and a benign course (but cirrhosis develops in 10% to 15%)
5. Typically discovered on routine laboratory tests (mild elevation in ALT and AST)
6. Treatment is not clearly established
Hepatic abscess is the most serious complication of acute cholangitis with a HIGH _____ _____
What is the treatment regimen for H PYLORI
Triple therapy: PPI + 2 AB --> take 2x daily --> more exp than bismuth-based
Quadruple therapy: PPI + BISMUTH + 2 AB --> dalf the time as triple therapy (1-week program opposed t 2 weeks for triple) --> expensive of PPI
-If H. pylori test positive then begin eradication therapy with triple or quad therapy. BEGIN ACID SUPPRESSION WITH ANTACIDES OR A PPI
-if ACTIVE NSAID induecd ulcer - stop NSAID USE. Also begin with either PPI or misoprostol. Continue 4-8 weeks depending on severity - treat the H. Pylori infection
Pathology of UC
1. Uinterupted involvement of the rectum and the colon without skip lesions
-inflammation is not transmural like CROHNS - here it is only mucosal and submucosa
Treatment of two possible causes of liver cysts:
1. Polycystic kidney disease: no treatment necessary
2. Hyadatid cysts: surgical resection without spilling + mebendazole
Treatment of acute cholecystitis?
Conservative meausres: (1) hydration with IV fluids (2) NPO (3) IV antibiotics (4) analgesics
Surgery: cholecystectomy is indicated in most patients with symptomatic gallstones. Early cholecystectomy is preferred (first 24-48 hours)
Focal nodular hyperplasia
benign liver tumor without malignant potential that occurs in women of childbearing years with NO assciaation with oral contraceptives
-usually asymptomatic. Hepatomeg present
Treatment of CRC
1. Surgical resection of tumor containing bowel as well as redection of regional lymphatics
2. CEA level should be obtained before surgery
3. Adjuvant therapy:
-Dukes C colon ca: postoperative chemo (5FU and leucovorin) but no radiation
-Dukes B2/C rectal: both chemo (5FU) and radiation therapy postoperatively
4. F/u is important and caries among physicians
-stool guiac test
-annual CT scan of abdomen/pelvis/CXR for up to 5 years
-colonoscopy 1 year then every 3 years
-CEA levels are checked periodically (3-6 mo)
i. Postop CEA <2-3 good prognosis
ii. Subsquent increase in CEA is marker for recurrance
iii. often, second look operations are based on HIGH CEA levels post resection
iv. VERY HIGH ELEVATIONS OF CEA suggest liver involvment
Crohns disease has a chroni, indolent course characterized by unpredictable flares and remissions. The effectiveness of medical treatment will ____ with advaning disease and complications eventually develop requiring surgery.
Clinical symptoms of appendicitis:
1. abdominal pain - starts in epigastrium, moves toward umbilicus, then to RLQ with distention of the appendix - the parietal peritoneam may become irritated leading to sharp pain
2. anorexia always present
3. nausea, vomiting (typically following pain)
Zenker's Diverticula v. Traction Diverticula v. Epiphrenic diverticula
Zenkers - most common type; found in upper 1/3 of the esophagus: failure of the cricopharyngeal muscle to relax during swallowing leads to increased intraluminal pressure. This causes outpouching of mucosa through an area of weakness in the pharyngral constrictors.
CLINICALLY: dysphagia, regurgitation, halitosis (BAD BREATH), weight loss, chronic cough
Traction diverticula: located in the midpoint of the esophagus near tracheal bifurcation. Due to traction from continguous medistinal inflammation and adenopathy (pulmonary tuberculosis). Tb causes hilar node scaring which causes retraction of the esophagus...it is usually asym and causes no treatment
Epiphrenic diverticula: found in the lower third of the esophagus. It is usually associated with spastic esophageal dysmotility or achalasia. Symptoms of dysphasia are more often realted to the udnerlying motility disorder unless the diverticulum is very large.
Acites is defined as the accumulation of fluid into the peritoneal cavity 2/2 portal HTN (increased hydrostatic pressure) and ________ (reduced oncotic pressure)
Ascited = portal HTN (increased hydrostatic pressure) and hypoalbuminemia (reduced oncotic pressure). Thus will also have abdominal distenstion, shifting dullness and fluid wave.
Abdominal ultrasound can detect >30mL fluid
Diagnostic = paracentesis to determine whether ascites 2/2 portal HTN or another cause. Looks at cell count, ascites albumin, gram stain, culture to r/o SBP (spontaneous bacterial pneumonitis)
-meausre the serum ascites albumen gradient. If >1.1g/DL, portal HTN likely. If <1.1 then portal HTN is unlikely and other cause.
1. Bed rest; low sodium diet; diuretics (furosemide and spironolactone)
2. Perform paracentesis if tense ascites, SOB or earlysatiety.
3. Peritoneovencous shunt or TIPS to reduce HTN
When should a CULTURE be drawn on a skin and soft tissue infection:
abscess or draining pus
DO NOT ATTEMPT TO CULTURE CELLULITIS IN PTS WITH INTACT SKIN
Carcinoid tumor v. Carcinoid syndrome
Carcinoid tumors originate from neuroendocrine cells and secrete serotonin
-the most common site for these tumors is the appendix, but they can be found in a variety of locations (small bowel, rectum, bronchus, kidney, pancreas)
syndrome results in 10% or patients with c. tumors.
-excess serotonin secretion can lead to carcinoid syndrome which is manifested by cutaneous flushing, diarrhea, sweating, wheezing, abdominal pain, heart valve dysfunctoin
-risk factors for mets increase with size of tumor - rare with appendiceal tumors however ilieal tumors have greatest likelihood for malignancy - surgival resection is tretament of choice.
Adenomatough polyps differ from inherited polyposis syndromes in what way?
Benign lesions that have significant malignant potential that are precursors of adenocarcinoma
What is CHOLANGITIS?
INFECTIOn of the biliary tract 2/2 to obstruction which leads to biliary stasis and bacterial overgrowth.
RIsk factors for CRC
1. Over 50yo
2. Adenomatous polyps (premalignant lesions but most do not become CA)
-villous adenomas have higher malignant potential than tubular ademona
-the larger the size the greater the number of polyps the higher the risk of malignancy
3. Personal history or prior CRC
5. Family Hx
6. Dietary factors
7. Major polyposis syndromes
How is spontaneous bacterial peritonitis diagnosed?
Estalished by paracentesis and examination of ascitic fluid for WBCs *especially PMNs) gram stain with culture and sensitivies.
=+ ascites culture - culture neg CBP is common
What is diagnostic for CHRONIC PANCREATITIS?
1. COMBINATION OF: CHRONIC EPIGASTRIC PAIN
2. CALCIFICATION OF PANCREAS ON PLAIN ABDOMINAL FILMS
Triad of symptoms:
3. Pancreatic calcification of plain films or CT
It can be difficult to distinguish the CHEST pain of DES from cardiac chest pain - thus what work up must be done?
Cardiac catheterizaton to r/o ischemic causes of chest pain, before an esophageal cause is investigated
-then perform ESOPHAGEAL MANOMETRY IS DIAGNOSTIC
-then perform upper GI barium swallow
Pancreatic cancer - what are the general characteristics?
Elderly (75% > 60YO); rare before 40YO; common to AA
Location: Pancreatic head (75%); pancreatic body (20%); pancreatic tail (5-10%)
When should a patient be hospitalized for CA-pnemonia?
CAP The CURB-65 score
1. Confusion (1 point)
2. BUN >19 (1 point)
3. RR >/= 30 (1 point)
4. SBP <90 or DBP </= 60 (1 point)
5. Age >/= 65 (1 point)
CURB score: 0-1 low risk, outpt rx; 2 short inpatient stay or closely monitored supervised outpt treatment; 3-5 severe pneumonia, inpt managment
What are the key features of the plummer vinson syndrome?
UPPER ESOPHAGEAL WEB + IRONDEF ANEMIA + ATROPHIC ORAL MUCOSA
-also KIOLONYCHIA (spoon shaped fingernails)
-10% develop SCC of the oral cavity, hypopharynx or esophagus
-treatment: ESOPHAGEAL DILITATION - CORRECT NUTRITIONAL DEFICIENCY
What imaging studies can be performed in patients with acute pancreatitis that will lead to its diagnosis?
1. Abdominal radiograph - has a limited role in dx of acute pancreatitis; instead rules out that of other diagnosis such as intestinal perforation (free air)l presense of calcification suggests CHRONIC, not acute PANCREATITIS.
2. Abdominal ultrasound - helps identify the cause of pancreatitis (gallstone) and useful for pancreatic abscesses or pseudocysts
3. CT scan of the abdomen - most accurate test for dx of acute pancreatitis and for identifying complications of the disease
4. ERCP - severe gallstone pancreatitis with biliary obstruction; identidy uncommon causes of acute pancreatitis if the disease is recurrent
Etiology of biliary cirrhosis - this disease occurs in response to chornic biliary obstruction from the following:
1. Long-standing mechanical obstruction
2. Sclerosing cholangitis
3. Cystic fibrosis
4. Biliary atresia
Diverticulitis recurs in about --% of pateints treated medically, usually within the first 5 years. Lower GI bleeding is RARE in diverticulitis but common in diverticulosis.
aquired motor d/o of the esophageal smooth muscle in which the lower esophageal sphinctor fails to completely relax with swallowing and abnormal peristalsis of esophgeal body replaces normal peristalsis of the esophageal body
How might colonic volvulus be diagnosed? What are the two types?
Colonic volvulus can most commonely be in the sigmoid colon 75% or the cecum 25%.
-cecal volvulus most commonly occurs in younger population. Cecal due to lack of right colonic fixation to retroperitoneam.
1. Plain abdominal film: sigmoid looks like an omega loop; cecal looks like coffee bean.
2. Sigmoidoscopy preferred diagnosetic and therapeutic test for sigmoid volvulus (NOT SECAL!); leads to successful treatment in many cases.
What is the prognosis of HCC?
If it is unresectable then the prognosis is less than 1 year
-if it is RESECTABLE then 25% of patients can live > 5 years
What is cholelithiasis? What are the three types of GB stones?
stones in the gallbladder
1. Cholesterol stones
2. Pigmented stones
3. Mixed stones (cholesterol and pigment) - most common
"Coffee grounds" emesis
suggests upper GI bleeding as well as lower rate of bleeding (enough time for vomitus to tranform into "coffee ground"
nonfibrolamella carcinoma of the liver:
(most common HCC) - usually associated with hepatitis B or C and cirrhosis. Unresectable with very short survival time (months)
Fibrolamellar - usually not associated with hepa B and C; is resectable; relatively llonger survival timel seen most commonly in adolescenets and young adults.
Treatment options for acute uncomplicated UTI
1. TMP-SMX 1 DS po bid x3day
-success rate 94%
-first line unless local resistance >15-20%
2. FQ (NOT moxi) x 3d
use when rx with TSX is contrandicated
3. Nitrofurantoin (***can instigate G6PD/exacerbate it!) 100mg po bid x 7d
4. Fosfomycin 3 gm po x 1 dose
Symptoms of acute cholecystitis:
-Pain is always present and is located in RUQ or epigastrium; it may radiate to the right schould or scapula (BOAS SIGN)
Closed loop versus open loop obstruction in SBO
Closed loop, the lumen is occlused at two poitns by an adheive band or hernia ring. This can compromise blood supple requiring emergent surgery
For diverticulosis - test of choice?
For diverticulitis - test of choice?
1. Barium enema
2. CT scan (barium enema is contraindicated 2/2 to acute bleeding)
What are CHOLEDOCHAL CYSTS
Cystic dilitations of biliary tree involving either the extrahepatice or intrhepatic duct or both; more common in women (4:1)
-EPIGASTRIC PAIN, jaundice, fever, and RUQ mass
-complications: CHOLANGIOCARCINOMA (MOST FEARED); HEPATIC ABSCESS< RECURRENT cholangitis/pacreatitis, rupture, biliary obstruction, cirrhosis, and portal HTN
-US is the best noninvasive tests, and ERCP is definitieve diagnosis
Treatment is surgery: complete resection of the CYST with a biliary-enteris anastomosis to restore continuity of biliary system with bowels
How might PUD be diagnosed?
Endoscopy is the most accurate. Essnetial in diagnosis of gastric ulcers because a BIOPSY is req to rule out melignancy of duodenal ulcers do not require biopsy bc dec likelihood.
-preferred when severe or acute bleeding is present (can perform electrocautery of bleeding ulcers) - biopsy can also be taken for H. pylori test if gastric also.
Diagnosis of acute cholangitis versus other biliary tract issues?
1. RUQ US is the initial study
2. Lab: hyperbilirubinemia, leukocytosis, mild elevation in ALT/AST
3. Cholangiography (PTC or ERCP) - definitive test but not perfrmed during the acute phase of illness. Once resolved, then proceed with PTC or ERCP.
PTC before ERCP when the duct system is dilated (per US) and use ERCP when the duct system is normal
Cholelithiasis v. Choledocholithiasis
Cholelithiasis (A) and Choledocholithiasis (B)
I. Abnormality (A) - gallstone in gallbladder
(B) - stone in the COMMON BILE DUCT
II. Features (A) - asymptomatic + biliary colic if obstructed stone 2/2 contracting GB
(B) - asymptomatic + RUQ pain/jaundice/eipgastric pain
III. Diagnostic (A) - US or CT
(B) - ERCP is the test of choice for RUQ US not sensitive
IV. Treatment (A) - resection if symptomatic (GB)
(B) - removal of stone via ERCP and spincterotomy
What are the clinical features of diverticulosis?
-Asymptomatic and dsicovered incidentally on barium enema or colonoscopy done for another reason.
-Vague LLQ discomfort, bloating, constipation/diarrhea may be present
-only 10-20% become symptomatic (develop complications)
Pancreatic necrosis is a complication of ACUTE pancreatitis. What are the two main types of necrosis:
1. Sterile pancreatic necrosis and infected pancreatic necrosis differ by a CT GUIDED PERCUTANEOUS ASPIRATION WITH A GRAM STAIN/CULTURE OF ASPIRATE
1. Cholestatis LFTS:
2. Hepatocellular necrosis/inflammation
1. markedly elevated ALK-P and GGT; slightly elevated AST and ALT
2. normal or slightly elevated ALK-P and markedly elevated ALT and AST
How does cholangiocarcinoma differ from carcinoma of the gallbladder?
This is a tumor of the intrahepatic or extrahepatic bile ducts: most adenocarcinomas
-7th decade diagnosis
-located in three regions: (1) proxmial 1/3 of CBD, (2) distal extrahepatic, (3) intrahepatic)
-most likely to be resected is distal and least likely is intrahepatic.
When might an upper GI bleed result in hematochezia?
If the bleeding is very briskand doesnt remain in colon to turn into melena
-this indicated heavy bleeding and patient often has some degree of hemodynamic instability
-an upper GI leed source is present in 5% of patients with hematochezia
What is the "best" rx for C. diff acute diarrhea in 2011?
-d/c the offending ATB (if possible)
-avoid narcotics and anti-motility agents
-oral metronidazole >>> oral vanc
-treatment based on dz classification: mild, moderate, severe, severe complicated
-increase role for po vanc
Treatment of esophageal hiatal herniation
1. Sliding: medically with antacids, small meals, and elevation of head post meals; 15% requires a nissens fundoplication
2. Paraesophageal: treatd with elevtice surgery due to risk of above complications
Treatment of hepatic encephalopathy?
Lactulose prevents absorption of amonia. Metabolism of lactulose by bacteria in colon favors the formation of NH4+ which is poorly absorbed from GI tract, thereby promoting excretion of ammonia.
-NEOMYCIN (AB) kills the bowel flora, so decreases the ammonia production by intestinal bacteria
-DIET: limit protein to 30-40 mg/day
Characteristics of jaundice:
1. Yellow coloration of skin, sclera, mucous membranes, sclerae due to over production or dec clearence of bilirubin
2. Clinical jaundice usually becomes evident when total bilirubin is > 2mg/dL
3. Conjugated v. unconjugated bilirubin
a. Conjugated (direct) -
loosely bound to albumin and therefore water soluble
when in excess, excreted in urine and is dark (only dark if conj br)
b. Unconjugated (indirect) -
tightly bound to albumin and therefore not water soluble
cannot be excreted in the urine even if blood levels are high
toxic, unbound form can cross BBB and cause neurologic deficits
EMPIRIC THERAPY FOR SKIN AND SOFT TISSUE INFECTION (SSTI)
Depending upon clinical setting/features
-risk of CA-MRSA: TSX, clinda or minocycline
-Cat bite: augmentin
-DM foot ulcer: cipro/clinda
-noncholera vibrio: doxy
-erysipelas: PCN or amoxicillin
If hospitalized (IV)
-MRSA: Vanc (or linezolid or dapto)
-Cat bite: Unasyn
-DM infectoin: ERTAPENAM
Laboratory testing (NOT IMAGING OR BIOPSY) for PUD?
REQUIRED to diagnose H. pylori
1. Biopsy by endoscopy: histologic ecal of endoscopic biopsy is gold standard.
2. UREASE detectoin via urea breathe test is the most convenient test (Sensitivity and Specificity > 95%)
3. Serology - presense of AB to H. pyloris doesnt indicate a CURRENT infection bc AB to H pylori can remain levated for mo-yrs post eradication of infection.
Diagnosis of UC (perform these studies)
1. Stool cultures for cdiff, oca, parasites to rule out infection
Diagnosis of SBO
1. Abdominal plain films (DILATED LOOPS OF SMALL BOWEL WITH AIR DLUID LEVELS PROIMAL TO POINT OF OBSTRUCTION ON UPRIGHT FILM AND MINIMAL GAS IN COLON *if complete SBO
What 2 other tests?
1. Barium ENEMA - to rule out colonic obstruction if plain film do not distinguish small from large bowel obstruction; barium enema identifies sites of obstruction
2. Upper GI series with small bowel follow-through if above are not diagnosed
1. chornic TRANSMURAL inflammatory dz that affects any parrt of GI mouth to ANUS ubt most commonly involves small bowel at terminal ileum
2. three major patterns: 1-40% have disease at ileum and cecum. 2-30% of patients have disease confined to small intestine. *3 25% patients have disease at colon ONLY
Acute appendicitis with obstruction leads to _____ of fluid and mucus, which promotoes ________ growth leading to inflammation. Distention of the appendix can compromise ______ supply resulting in ischemia and necrosis if untreated. Necrosis results in perforation and peritonitis.
Diagnosis of pseudomembranous colitis
C. diff toxins in stool is diagnostic but results take at least 24 hours (95%) sensitivity
-flexible sigmoidoscopy is most rapid test and is diagnostic but not frequently done
-abdominal radiograph to r/o toxic megacolon and perforation
Diagnosis of choledocholithiasis:
Order CMP with LFTS:
1. Labs: total and direct bilirubin levels are elevated and ALK-P
2. RUQ ultrasound usually intial study but will perform ERCP as the gold standard
3. PTC is an alternative to ERCP
Treatment of colonic volvulus
Sigmoid volvulus: nonoperative reduction (decompression) is successful in 70% of cases. The recurrent rate is HIGH so elective sigmoid colon resection is recommended
Cecal volvulus: emergent surgery
What are the clinical features of CHRONIC pancreatitis?
1. Epigastric pain
2. Recurrent abdominal pain
3. May be aggravated bya a drinking episode or by eating
4. Radiates to the back (in 50% of cases)
5. WEIGHT lOSS 2/2 malabsorption, alcohol abuse, DM; steatorrhea 2/2 to malabsorption
Cholestasis referes to obstruction of ____ _ from ANY cause. If LFTs reveal cholestasis (markedly elevated ALKPHOS), then obtain?
abdominal or RUQ ultrasound
Forceful dilation and what other surgical methods can treat but NOT CURE achalasia?
Forceful dilatation - mechanical, pneumatic, or hydrostatis
a. pneumatic balloon dilatation is most effective
b. Lowers basal LES tone by distrupting the muscular ring
c. Can be effective but there is a 5% risk of performation
a. "HELLER MYOTOMY" - circular muscle layer of LES is incised
b. usually reserved for patients who do not respond to dilation therapy
Clinical features of cholangiocarcinoma
Obstructive jauntice and associated symptoms - dark urine, clay colored stool, pruritis
Which esophageal cancer is the most common in the USA?
Used to be SCC > 90% cases but not the incidence of adenocarcinoma has increased dramatically in the US
Tests to order in patients with GI bleeding and MELENA
UPPER ENDOSCOPY intitial test bc the most likely bleeding site is in the upper GI tract.
ORDER COLONOSCOPY if no bleeding site is identified from the endoscopy
Acute infectious diarrhea (stool cultures: indications)
-acutely ill patients with fever and fecal WBCs
-diasease in very young and very old
-common source outbreaks
-persistent diarrhea after foreign travel
Carcinoma of the CB
Most are adenocarcinomas and occur in the elderly
-associated with gallstones in most cases but include cholescystemeric fisutla and porceliain gallbladder
-clinical features are nonspecific and suggest extrahepatic bile duct obstruction: jaundice: biliary colic: weight loss: anorexia: and RUQ mass
-difficult to remove with surgery: cholecystecotmy versus radical cholecystectomy with wedge resection of the liver and lymph node dissection - depending on depth of underlying condition
-pronosis is POOR bc disease underdetected until it is advanced.
What are the two etiologies of a LIVER ABSCESS?
1. Pyogenic liver abscess: most common cause is biliary tract obstruction - obstruction of bile flow allows baterial proliferation. Other causes include GI infection (diverticulitis, appendicitis) with spread by the portal veonous system and penetating liver trauma (GUNSHOT WOUND, SURGERY)
-causative organisms: E. coli, klebsiella, proteus, eneterococcus, anaerobes
-features: fever, malaise, anorexia, weight loss, nausea, comiting, RUQ pain, jaundice.
diagnosis by US or CT scan: elevated LFTs
-treatment: FATAL if untreated *treatment with IVAB and percutaneous drainage of the abscess. which reduces the mortality to about 5-20%. Surgical drainage is sometimes considered
2. Amebic liver abscess: most common in men (9:1); homosexual. Fecal oral contact transmission. Caused by intestinal amebiasis (e. histolytica) - the amebae reach the liver via the hepatic portal vein.
-clinical features: fever, RUQ pain, n/v, hepatosplenomegay, diarrhea
-seriological testing (immunoglobulin G enzyme immunoassay) will estbolish diagnosis. Elevated LFTs; E. histolytica stool antigen test *detects protozoe in the stool). Imagine studies (US/CT) identifies the abscess but it is difficult to distinguish from a pyogenic abscess.
-IV metronidazole is effective treatment in most cases. Therapeutic aspiration of the abscesss (IMAGE_GUIDED percutaneous aspiratoin causses. Therapeutic aspiration of the abscess may be necessary if the abscess is larger (HIGH RISK OF RUPTURE) or if there is no response to medical therapy
SIGNS OF ACUTE CHOLECYSTITIS
RUQ tenderness, rebound tenderness in RUQ
-murphys sign is pathogmonic (inspiratory arrest during deep palpation of the RUQ; not present in many cases)
-hypoactive bowel sounds
-lowgrade fever with leukocytosis
What is cholestasis?
Blocking of bile either intrahepatically or extrahepatically with increased conjugated bilirubin levels.
symptoms: jaundice, gray stools, darkened urine, bile salt deposition in skin causing pruritis, elevated serum alkphos, elevated serum cholesterol (impaired excretion), skin xanthomas (local accumulation of cholesterol), malbsorption of fats and fat soluble vitamins.
Treatment for acute primary biliary cholangitis: (PSC)
1. No curative treatment other than liver transplantation
2. When dominant stricture causes cholestasis, ERCP with stent placement for biliary drainage and bile duct dilatation may relieve symptoms
3. use cholestyramine for symptomatic relive to decrease pruritis
Diagnosis regarding esophageal CA
Barium swallow - useful for dysphagia
-UPPER endoscopy with biiopsy and brush cytology is required for deinitive diagnosis. It confirms the diagnosis in 95% if cases
-TEE US to determine the depth of penetratoin of the tumor *most reliable to test staging of local CA
-full metastatic workup (CT scan of chest/abdomen, CXR, bone scan)
Primary hemochromatosis verus secondary hemachromatosis?
Primary - early diasnogsis and treatment before development of complications (primary cirrhosis ut also heart dz and diabetes) imrpoves survival.
Secondary - iron overload 2/2 multiple blood transfusions or in CHRONIC HEMOLYTIC ANEMIA!
Screening for CRC
Fecal occult blood testing annually (poor sensitivity/specificity)
Colonoscopy every 10 years
(over the age of 50 OR 10 years prior to the diagnosisof CRC in family member)
CROHNS v. UC
CHRONS: involves transmural wall from mucosa to serosa; discontinous with skips
UC: mucosa and submucosa
CD: termianl ileum most commmon but can involved any part of GI
UC: colon and rectum - starts at rectum nd goes up
CD: fistula and abscesses
UC: SC and colorectal CA
What is acute pancreatitis:
inflammation fo the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pacreatic tissue autodigestion
A non-alcoholic patient has an asymptomatic elevation of serum transaminases (ALT/AST) and increased serum iron and feritin levels, and a family history of non-alcoholic liver cirrhosis. This diagnosis is strongly suggestive of?
Childs classification system to assess severity of LIVER DISEASE
1. Ascites: NONE
2. Bilirubin: <2.0
3. Nutrtional status: excellent
4. albumin: > 3.5
1. Ascites: controlled
2. Bilirubin: 2-2.5
3. Nutritional status: good
4. Encephalopathy: minimal
5. Albumin: 3-3.5
1. Ascites: uncontrolled
2. Bilirubin: >3
3. Nutritional status: poor
4. Encephalopathy: severe
5. Albumin: <3
Left sided colonic tumors and symptoms:
1. Smaller luminal diameter, signs of obstruction are more common - change in bowel habits more common - alternating constipation/diarrhea narrowing of stools ("pencil stools")
2. Hematochezia more common
What are the clinical features of gastric cancer
abdominal pai and unexplained weight loss are most common symptoms; reduced appetitie, anorexia, dyspepsia, early satiety, nausea and vomiting, anemia, melena, guiac positive stool
Peritoneal fluid (third space) can develop due to many causes - one of which being portal HTN, trauma, pancreatitis and malignancy.
How might one distinguish a diagnosis amongst the above as the causitive agent of the abdominal distention?
1. distinguish exudative from transudative fluid accumulation
-use SAAG which (serum ascites albumin gradient) is calculated bysubtracting the ascites albumin concentration from the serum albumin concentration.
-A difference of 1.1 g/dL or greater is 95% accurate in diagnosing a transudative process consistent with portal hypertension.
Where are most polyps found?
rectosigmoid region and most patients are assymptomatic
-#1 symptoms is rectal bleeding
TREATMENT OF CROHNS
a. Sulfasalazine (useful if colon involved bc is a 5-ASA *mesalamine) as tha active compound released in colon that is more useful in uS than in Crohns, 5-ASA compounds bock PGE release and serve to decrease inflammation
-there are preparations of 5ASA that are more useful in distal small bowel disease.
c. corticosteroids *prenisone for exacerbations and if no repsonse to metronidazome)
d. immunosuppressants AZA 6MP) with steroid if patients doesnt responseto above agents
e. BA sequetrants (cholestyramine or colestipol) pts with severe ileal disease who cannot absorb bile acids
Mallory Weiss syndrome
MUCOSAL tear at the GE jundtion as a result of forceful vomiting or restching. It usually occurs after repeated episodes of vomiting but it may occur after one episode
-most commonly associated with binge drinking in alcoholics but any isorder that causes vomiting can induce the musocal tear
Angiodysplasia of the colon (arteriovenous malformations, vascular ectasia)
-tortous, dilated veins in submuscosa of the colon (usually proximal) wall
-a common cause of lower GI bleeding in patients over age 60YO
-bleeding usually low grade but 15% of patients may have massive hemorrhage if veins rupture
-diagnosed by colonoscopy (preferred over angiography)
-in 90% of patients, bleeding stops spontaneously
-treated by colonoscopic coagulation of the lesion.
-if bleeding persists, a right hemicolectomy should be considered
ALT and AST usually have a similar increase, however in alcoholics, we expect an elevation in which enzyme?
elevation is AST>>>>ALT
Esophageal manometry is diagnostic -
simultaneous, multiphasic, repetitive contraction that occur after a swallow; spinhicter response is normal
HOw long might it take a pancreatic abscess to form in acute pancreatitis?
Although RARE< will occur 4-6 weeks post acute pancreatitis
-black tarry lquid foul smelling stool
-caused by depradation of hgb by bacteria in teh colon; presense of melena indicates that blood has remained in the GI tract for several horus
-the further the bleeding site fom retum, the more likely melena will occur
-note that dark stools can also result from BISMUTH, IRON, SPINACH, CHARCOAL, LICORICE
-melena sugests upper GI bleeding (esophagus, stomach, duodenum) - occasionally the jejunum or ielum is source but usualy if caused but colonic lesions - but if so then the ASCENDING COLON is the most common colonic location
In patients with CIRRHOSIS (fibrosis of liver tissue), the ALT/ASTs are ____ or ______ or meatstatic liver disease because the number of ealthy functioning hepatocytes are markedly decreased.
normal to low
Diagnostic test of choice for diverticulosis (LLQ, painless rectal bleeding, constip/diarrhea) and bloating)
Barium enema is the test of choice
-abdominal xrays are usually normal and are not diagnostic for diverticulosis
Pain in acute cholecystitis is 2/2 gallbladder wall inflammation whereas pain in biliary colic is 2/2?
contraction of the gallbladder against the obstructed cystic duct. ALso the pain of acute cholecytitis persists for several days whereas the pain of biliary colic lasts only a few hours.
Treatment for gastric CA
Surgical resection with wide (>5cm) margins (total or subtotal gastructomy) with extended lymph node dissection
-chemotherpay may be appropriate in some causes
What is hemobilia?
When blood fraining into the duodenum via the common bild duct. Soundce of bleeding can be anywhere along the biliary tract, the liver, or the ampullary region.
Causes: TRAUMA (MOST COMMON); PAPILLARY THYROID CARCINOMA; SURGERY 2/2 CHOLESCYSTECOMY
Diagnostic: Arteriogram is diagnostic - upper GI endoscopy shows blood coming our of the ampulla of vater
Treatment: resuscitation (+/- transfusoin) If bleeding is severe, surgery is necessary (options include ligation of hepatic arteries or arteriogram with emnolization of vessel).
peristalsis is decresd or absent without mechanical obstruction
-resolves with time or when the cause is adddresed medically - surgery is not usually needed.
CAuses: medications (narcotics, anticholinerguc effects) post operative state, spnal cord injury, shock, metabolic disorders (espcially hypokalemia) and eritonitis
-abdominal plain filmss show a unifrom distribution of gas in small bowel, colon and rectum
-failure to pass contrast medium byuond fized point is diagnostic.
RX: FLUIDS - NPO, correcton of electrolytes; NG suction if necessary and placeebt if long tube if ileus persists postoperatively
What is the DEFINITIVE DIAGNOSTIC STUDY to diagnose esophageal perforation?
CONTRAST ESOPHAGRAM = soluble gastrografin swallow preferred
-then a CXR shows air in the mediastinum
-if stable and perforation is small, medical management is appropriate (IV FLUIDS< NPO, AB, H2 blockers)
-if patient is ILL and perforation is large (or communication into the cavity, surgery should be performed within 24 hours of presentation = success rate is higher)
Indication for sinus aspiration 2/2 bacterial sinusitis (acute)
-associated with intracranial complications (empyema, meningitis, brain abscess)
-sinusitis in the immuncompromised host
-sinusitis that fails to respond to a "readonable course" of "appropriate" ATB reaction
The diagnosis of acute pancreatitis is normally made by:
1. Clinical presentation.
2. Lab studeies are supportive (amylase/lipase)
3. and CT scan is confirmatory
Causes of BUDD-CHIARI syndrome
myeloproliferative d/o (polycythemia vera)
chronic inflammatory diseases, infection
-CONDITON is idiopathy in 40% of cases
Presentation of a young, non-obese and on-blacnk patient with HTN should rasie suspician for ______ _______. FUrther, lab values with severe HTN, and elevated HR with serum chemistry levels revealing normal glucose, and normal serum creatinine, elevated sodium and low potassium, and a CT scan with a 2cm mass on left adrenal gland should be indicative of?
What would plasma renin be? what would serum aldosterone be? What would serum bicarbonate be?
-primary hyperaldosteronism causes HTN, hypernatremia, hypokalemia, and metabolic alkalosis
-excess aldosterone promotes distal tubular reabsorptin of sodum which results in volume expansion and secretion of poassium and ydroge ions. he mass on pt CT likelt to be adrenal adenoma. Likewise, Conn's syndrome should have aldosterone levels and renin levels checked. Aldosterone release is regulated by renin and therefore while aldosterone levels are increased, renin levels will be decreased 2/2 feedback inhibition. Muscle weakness and exercise intolerance are the result of hypokalemia
-the HIGH levels of serum bicarb are what will be present 2/2 the effect of aldosterone on intercalated B cells. decreased K+ causes deposition of intersitial cells and uptake of H+ ions which further increases the serum pH
Acute gastritis is best assessed by which method?
UPPER GI Endoscopy is the best test for evaluating a pt with epigastric pain. It can diagnose PUD, gastritis, esophagitis and can r/o CA of esophagus and stomach and H. pylori with BIOPSY
When should therapy be considered in acute infectious diarrhea?
Treatment for febrile, CA-diarrhea should be considered for the pt with:
1. sig systemic tox and dehydration esp in ver young and very old (>70)
2. bloody diarrhea or dysentery
3. fecal WBCs or lactoferrin
4. immunocompromising conidtions
5. suspected complicating bacteremia
What are the clinical findings in patients with hepatic encephalopathy?
Decreased mental function, confusion, poor concentration, stupor, coma
Asterixis (hand flapping tremor)
Rigidity and hyperreflexia
Fetor hepaticus (MUSTY ODOR OF BREATH)
Paraesophageal hiatal hernia accounts for <5% of cases. Describe dx
The stomach herniates into thorax through the esophgeal hiatus but the GE junction doesnt, it remains below the diaphragm. THis uncommon hearnia can become strangled and should be repaired surgically
What is hepatorenal syndrome?
progressive renal failur in advanced liver disease, 2/2 enal hypoperfusion resulting from vasoconstriction of the renal vessels that is precipitates by infection or diuretics.
-functional renal failure where the kidneys are normal in terms of morphology and no specific causes of renal dysfunction are eventend. The condition doesnt responde to volume expansion and thus asotemia, oliguria, hypoantrmia, hypotension and lo urine sodium results.
Treatment is by liver transplantation ONLY
Boas sign v. Murphys sign v. Chargot's triad
Boas sign - cholelithisis - gallstone - right should/scapular pain
Murphy's sign - RUQ pain/tenderness on inspiration and palpation
Chargots triad - RUQ pain, jaundice, fever (seen in 70% of patients with this disease)
Diagnosis of PANCREATIC CA:
ERCP most sensitive test to distinguis CA of head of pancreas from tumors of the ampulla and lymphomas.
CT scan is the perferred test for diagnosis and assessment of DISEASE SPREAD
tumor markers: CA19-9 (83 sensitivity nd 82 specificity) CEA (sensitivity of 56% and specificity 75%)
Risk factors associated with HCC
Cirrhosis-especially in associated alcohol or hepB/C; forms in 10% or cirrhostic pts
Carcinogens (aflatoxin, vinyl chloride, thorotrast)
Hemocrhomatosis, Wilsons dz
hepatic adenoma (10% risk of malignant transformation
Most common cause of LOWER GI BLEED IN PATIENTS < 60YO?
Most COMMON cause of LOWER GI BLEED in PATIENTS > 60YO?
Angiodysplasia if >60YO
Diverticulosis if <60YO
What is the treatment for GI bleeding:
1. If the patient is hemodynamically unstable, resuscitation is always TOP priority
-remember CABs - once the patient is stabilized , obtain a diagnosis
A. supplemental O2
B. place two large bore IV lines. Give IV fluids or blood if pateint is volume dep
C. draw blood for hgb, hct, PT, pTT, plt, INR; monitor hgb Q4Q8
D. Continue to monitor until 24 hours of stable hgb
E. type and crossmatch adequate blood (PRBCs). Transfuse as the clinical condition demands *shock, patients with cardiopulmonary DZ
2. Treatment depends on the CAUSE/SOURCE
A. UPPER GI BLEED
i. EGD with coag of bleeding vessel. If bleeding cont, repeast endoscopic therapy or proceed with ligation therapy
B. LOWER GI BLEED -
i. colonoscopy - polyp excision, injection, laser, cautery
ii. arteriogrphic vasoconstrictor infusion
iii. surgical resection of involved area - last resort
3. Indications for surgery
-hemodynamically unstable patients who have not responded to IV fluid, transfusion, endoscopic intervention or correction of coags
-severe initial bleed or recurrence of bleed post treatment
-continued bleeding for more than 24 hours
-visible vessel at base of ulcer (30-50%) chance of rebleed
-ongoing transfusion requirement (5U within first 4-6 hours)
Portal HTN as a complication of cirrhosis (severe liver disease)
-bleeding/hematemesis, melen, hematochezia) 2/2 esophagogastric varices is the most life-threaning complication of portal HTN.
-diagnose based upon clincial presense of about. paracentesis can help dx
-use transjugular intrahepatic portal-systemic shunt (TIPS) to lower portal pressure
Surgical intervention in CROHNS
1. reseve for complication of crohns dz. Sedmental resection of involved bowel. Recurence rate after surgery byyt up to 50%
2. Indications: SBO, fistula, diabling disase, performation of abscess...
What is GALLSTONE ILEUS?
Gallstone enters the bowel lumen via cholecystenteric fistula and gets stuck in the terminal ileum and causes obstruction at the ileocecal valve - causes obstruction and accounts for 1-2 % of bowel obstructions
Large bowel obstruction:
1. Causes: volvulus, adhesions, hernias, COLON CANCER (#1)
2. LBO v. SBO: LBO has less fluid and lyte loss
benign liver tumor seen in females 15-40YO 2/2 OCP use, anaboli steroid use with RUQ pain or fullness.
diagnose with CT scan, US
Treatment: d/c OCP; surgically remove tumors >5cm that do not regress s/p OCP d/c
What is the peak incidence of appendicitis?
Peaks in the teens and mid-20s - prognosis worse in infants and elderly 2/2 higher rates of perforation
IDSA/SHEA Tretment recommendations for C. Diff Acute Diarrhea (CDAD)
-(WBC<15k, crt WNL/unchanged)
-drugs: metronidazole 500 po 10-14d
-(WBC >/= 15K or inc serum creat; >50% baseline preCDAD
-drugs: Vancomycin 125mg po or via NGT qid 10-14day
-(WBC>above criteria with dec BP or shock, megacolon, perforation or severe colitis on CT)
-if NO ILEUS: Vancomycin 500mg po qid + metronidazole 500-750mg IV Q8hr
-if ILEUD: Vancomycin 500 mg via NGT or po + Metronidazole 500-750 IV Q8 + Vanc enema
First recurrance: same as initial episode
Second or further: PO vanc taper or pulse
Most esophagel diverticula are caused by an underling motility disorder of the esophagus:
1. Zenkers diverticulum
2. Traction diverticulum
3. EPiphrenic diverticula
Special associations during skin and soft tissue infections
1. Recurrent boils
4. Bite wounds (human, cat, dog, eikenella, pasturella multiocida, capnocytophaga)
5. Water exposure
7. S aureus, GBS, others
8. P aeruginosa, GNRs
9. Vibrios, Aeromonas, M,marinum
Diagnosis of appendicitis:
acute appendicitis is a clinical diagnosis
-imaging: CT scan (lowers false postivie rate significantly)
Polyposis PLUS osteomas, dental abnormalities, benighn soft tissue tumors, desomis tumors, sebaceous cysts. The risk of CRC is ____% by approximately age 40.
Treatment for acute pancreatitis?
Bowel rest (go NPO) - goal to REST THE PANCREAS
-IV FLUIDS - may have severe intravascular volume depletion
-Pain control - be cautious with narcotic
-Nasogastric tube if severe nausea/vomiting or ileus present; routine use is controversal
Risk factors regarding pancreatic cancer:
1. CIGARETTE SMOKING
2. Chronic pancreatitis increases risk
4. Heavy alcohol use
5. Exposure to chemicals-benzidine and b-naphthlyamine
How does DES (diffuse esophageal spasm) differ from achalasia?
DES - nonperistaltic sponaneous contraction of the esophageal body - several segments of the esophagus contract simultaneously and prevent appropriate advancement of food bolus
ACHALASIA - spincter function is normal (normal LES pressure)
1. Upper GI bleeding v. Lower GI bleeding
UPPER GI bleeding: source of bleeding above the ligament of trietz
LOWER GI BLEED: source of bleeding below the ligament of trietz
Initial empirical therapy for CA-P
Outpatient: if healthy without recent ATB: treat with macrolide or doxy; if recent ATB then use FQ or macrolide+amox
Comoribitidies - no recent ATB : adv macrolide or FQ; recent ATB treatment FQ or Adv macrolife + b-lactam
Inpatient: 3rd gen ceph + FQ or macrolide; at risk for pseudomonas then used antipseudomonal B lactam +AMG+FQ or macrolide or antipsydomonary b-lactam + cipro
How does PRIMARY BILIARY CIRRHOSIS differ from PRIMARY SCLEROSING CHOLANGITIS?
1. Chronic/progressive/ cholestatic LD/characterised by destruction of intrahepatic bile ducts with PORTAL inflammation and scarring - INTRAHEPATIC DUCT SPECIFIC
2. SLOWLY progressive dz with variable course can progress to cirrhosis and End stage liver dz
3. THIS IS AUTOIMMUNE WITH ANTI-MITOCHONDIAL AB, CARDIOLOPIN - and is often associated with other autoimmune disorders.
4. It is most common in middle-aged women
biliary cirrhosis, often abbreviated PBC, is an autoimmune disease of the liver marked by the slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. When these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the tissue. This can lead to scarring, fibrosis and cirrhosis. It was previously thought to be a rare disease, but more recent studies have shown that it may affect up to 1 in 3-4,000 people; the sex ratio is at least 9:1
An autosomal RECESSIVE disease that is 2/2 copper metabolism. This normal excess usually excreted by the liver however whene the patients liver has a deficiency in ++++++++, copper will accumulated in the liver cells (hepatocytes). What happens to the hepatocytes?
-as the hepatocytes die 2/2 to Cu2+ accumulation; the copper leaks into plasma and accumulates in various organs (kidneys, cornea, brain0
-most occurs during childhood/adolescence (5YO)
-diagnosis within 5-35YO
If there is not hemolysis, isolated hyperbilirubinemia (unconjugated) may indicate _______ syndome which is assymptomatic and requires no rx.
Treatment of HCC
1. Liver resectoin (in the 10% of patients who have resectable tumors)
2. Liver transplantation if diagnosis is made early
Bleeding from small bowel::
Bleeding from the colon::
-occult blood, hematochezia
Staging for CRC using Dukes' staging
Performed cia CT scan of abdomen and CXR
Stage A - stage I limited to muscularis mucosa
Stage B - stage II that goes past mm without node involvement
B1 - into submucosa/muscularis propria
B2 - through entire bowel wall
B3 - through bowel wall into adjacent structures
Stage C - positive regional lymph nodes
Stage D - stage IV goes to distant metastasis
What imaging can be done for upper GI bleeds:
Anoscopy or proctosignmoidoscopy
Exploratory laparatomy - last resory
GI bleeding is a complication associated with PUD:
bleeding may be slow (anemic symptoms) or rapid and severe (leading to shock)
Dx studies: STOOL GUIAC, UPPER GI ENDOSCOPY
Resuscitation: daignose site of bleed via endoscopy and test: performatm surgery for acute bleeds that require transfusion of >6U
-most common cause of upper GI bleeding is 2/2
CAuses of acute uncomplicated UTI in women/males
75-90% of cases E. coli
5-15% is S. saprophyticus
Probability of cystitis >90% in woman with dysuria and frequency w/o vaginal d/c
What is the treatment for acute mesenteric ischemia?
Supportive: IV fluids, broad-spec antibiotics
-direct intr-arterial infusion of papaverine (vasodilator) into the superior mesenteric system during arteriography is the therapy of choice for all arterial causes of acute mesenteric ischemia
-direct intra-arterial infusions of thrombolytics or embolectomy inficated in pations with embolic acute mesenteric ischemia
-heparin anticoagulation is the treatment of choice for venous thrombosis
-surgery (resection if nonviable bowel) may be needed in all types of acute mesenteric ischemia if signs of peritonitiis develops
Signs of biliary tract obstruction
INC alk-phos and inc GGT
elevated conjugated BR
Proximal v. distal SBO
Distal obstruction causes distention of proximal bowel segments, making the diagnosis easier on plain radiograph
Treatment of diverticulitis:
1. If initial episode of diverticulitis (fever, LLQ pain, leukocytosis)
a. Use of IV antibiotics, bowel rest (NPO), IV fluids.
b. Mild episodes can be treated outpatient basis if patient is reliable and has few or no comorbiditie.
c. IF persists > 3-4 days then require surgery
2. If second or subsequent episodes of diverticulitis:
a. surgery is recommended (resectionof involved segment) once acute inflammation resolves
3. Low-residue diet (eg: no nuts, seeds)
What are the causes of CONJUGATED hyperbilirubinemia?
-Urine positive for bilirubin
1. Decreased intrahepatic excretion of bilirubin
-hepatocellulr disease (viral, or alcoholic hepatitis, cirrhosis)
-inherited disorders (DUBIN-JOHNSON syndrome, Rotor's syndrome)
2. Extrahepatic biliary obstruction
-carcinoma of head of pacreas
-extrahepatic biliary atresis
How does hyperestrinism result in patients with CIRRHOSIS of the lIVER?
1. SPinder angiomas-dilated cutaneous arteriold with central red spot and reddish extensions that radiate ourward like a spiders web.
2. Palmer erythema
3. Testicular atrophy
Bowel duct stricture is 2/2 an _______ injury (like that of biliary surgery or cholecystectomy, liver transplantation); other causes include recurring choldocholithiasis, chornic pancreatitis, and PSC.
Clinical features: OBSTRUCTIVE JAUNDICE
EPIGASTRIC PAIN that is aching/gnawing in nature with NOCTURNAL SYMPTOMS and the EFFECT OF FOOD ON SYMPTOMS is present.
+/- Upper GI bleeding
Acute bacterial sinusitis
most common health problem in the US
-develops subsequent to viral rhinosinusitis in 0.5-2% of all cases
-should be suspected in pts with symptoms of virl rhinosinusitis that persis for more than 10d or worsen after 5-7
Hypo or hypercalcemia results from acute pancreatitis?
HYPOcalcification is due to fat saponification: fat necrosis binds to calcium
What is REYNOLDS PENTAD?
Charcots triad (fever, jaundice, RUQ pain) + septic shock + AMS (CNS depression - coma-disorientation)
WHat is choledocholithiasis?
Gallstones that are found in the CBD
-primary v. secondary causes;
primary-originate in the CBD (usually will be pigmented)
secondary - originate in the GB and then pass into the CBD (usually cholesterol/mixed) - 95% of all cases
What is CEA?
Tumor marker for pancreatic cancer, not useful for screenin; useful for baseline and recurrence surveillence
How might one determine whether or not a polyp is malignant?
1. Size (the larger the polyp, the greater the malignant potential)
2. Histologic type
3. Atypia of cells
4. Shape (sessile-flat, more likely to be malignant) versus pedunculated (on a stalk)
PSEUDOCYSTS may be present at sites distant to the ______ but are still 2/2 acute pancreatitis.
What causes the elevation in ALT or AST levels in asymptomatic patients (ABCDEFGHI)
Drugs or toxins
Fatty liver (TG)
Hemodynamic disorders (CHF)
Iron (hemachromatosis), copper (wilsons), AAT deficiency
Diagnosis of PBCirrhosis:
1. Laboratory findings - cholestatic LFTs (elevated ALKphos)
-positive antimitochondrial antibodies (AMAs) found i n90% to 95% of patients
-this is hallmark of the disease (specificity) of 98%; if serum is positive for AMAs, perform liver biopsy to confirm diagnosis
-elevated cholesterol, HDL
-elevated immunoglobulin M
2. Liver biopsy - percutaneous or laparacopic to confirm ddx
2. Abdominal US or CT scan to rule out biliary obstruction
What are the clinical features of Esophageal Hiatal Hernias?
asymptomatic, incidentally found
-heartburn, chest pain, dysphagia
Treatment of cirrhosis of the liver:
1. Treatment of underlying cause (alcohol, interferons for hepC/B)
2. Once cirrhosis develops aim to treat via managment the complicatoin. Most serious complication is the esophageal varices that are actively bleeding and hepatic encephalopathy
3. Liver transplant is the only hope for a cure. Abstinence from alcohol for more than 6 months is requiredbefore a patient is eligile for transplantation
Primary sclerosing cholangitis (PSC)
-general characteristics include:
1. Chronic/idiopathhic/progressive intrehepatic or extrahepatic duct disease
2. Thickened bile duct walls ad narrowing of their lumens; leads to cirrhosis, portal hypertension and liver failure.
Strong associates with UC (less with that of Crohns) - UC is present in 50-70% of patients with PSC; often the UC dominates the clinical picture. The course of PSC is unaffected by a colectomy done for UC
is a complication of longstanding acid reflux disease in which thre is columnar metaplasia of the squamous epithelium. Patients with Barretts esophagus are at increased risk of developing adenocarcinoma of the esophagus.
Why might a serum gastrin level be used in the dx of PUD?
If potential for ZE syndrome as a diagosis
Diagnosis for UC
1. Stool culture for cdiff ova parasits
2. fecal leukocytosis
-WBCs can appear in UC ischemic colitis or infectious disease
How is acute cholecystitis diagnosed?
RUQ ultrasound is the test of choice
a. HIGH sensitivity and specificity
b. Findings include thickened gallblasdder wall, pericholecystic fluid, distended gallbladder and presnse of stone(s).
CT Scan is as accurate as ultrasound but is more sensitive in identifying complicatons of acute cholecystitis (performation, abscess, pancreatitis)
RADIONUCLEOTIDE scan (HIDA-hepatoiminodiacetic acid)
-used when US is inconclusive-its sensitivity and specificity paralel that of ultrasound. If HIDA scan is normalthen acute cholecystitis can be ruled out
-positive HIDA scan means the gallbladder is not visualized
-if GB not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed
What is Budd-chiari syndrome?
Liver disease caused by the occlusion of the hepatic venous OUTLFLOW which leads to hepatic congestions and microvascular ischemia.
-variable vourse - indoent, gradual development of portal HT and progressive deterioration of Liver FUNC
-can lead to acute liver failure, which can be fatal without immediate therapy
Causes of SBO?
1. Adhesions from prior abdominal surgery
2. Incaercerated hernias
3. Malignancy, intussusception, Crohns disease, carcinomatosis and superior mesenteric artery syndrome (compression of third part of duodenum)
Pathology of Crohns
terminal ileum is hallmark location but other sites of GT tract may also be seen
-transmural thicknening and infalmation *full thickness wasll involvement)
Mesenteric: fat creeping" onto antimesenteric border of small bowel
What is the biliary dyskinesia?
Motor dysfunction of the sphincter of Oddi which leads to recurrent episodes of biliary colic without any evidence of gallstones on diagnostic studies such as ultrasound, CT scan, ERCP
Dx: made by HIDA scan - once the gallbladder is filled with labeled radionuclide; give CCK IV then determine the ejection fraction of the GB. If low then dyskinesia likely
Treatment: laparoscopic cholecystectomy and endoscopic spincterotomy
An underlying motility d/o is the cause of both proximal (ZENKERS) and distal (EPIPHRENIC) diverticula. Surgical treatment is aimed at correcting the motility d/o via ______.
A ______ is of 2ndary inportance in both cases
Esophageal/gastric varices are a complication of cirrhosis. What are the clinical findings? How is it diagnosed and how is it treated?
1. Massive hematemesis, melena, exacerbation of hepatic encephalopathy; esophageal >90% and gastric >10%.
2. Diagnosis emergeent upper GI endoscopy once patient is stabilitys if patient presents with hematemesis.
3. Initial treatment: FLUIDS to maintain BP and get hemodynamically stable
4. 2/2: administer BB as LT therapy to prevent rebleeding.
What is the risk of CRC in patients with FAP?
100% by age 30 or 40 thus requires prophylactice colectomy for treatment
EPIGASTRIC abdominal pain that radiates to the back in 50% of patients that is often steady, dull, and severe that gets WORSE WHEN SUPINE and POSTPRANDIALLY.
What are the complications of severe pseudomembranous colitis?
Anasarca, electrolyte disturbances
Treatment of choledocholithiasis
ERCP with sphincteromtomy and stone extracton with stent placement (successful in 90%) of patients with it.
-laparoscoptic choledocholithiotomy in select cases
Diagnosis of chronic pancreatitis:
CT scan is the initial study of choice - shows calcifications not seen on plain film. Mild to moderate cases may not be detectable, so a normal CT scan doesnt rule out chronic pancreatitis.
Abdominal radiographs: pacreatic calcification = 99% specific but only found in 30% of cases
ERCP is the GOLD STANDARD but not done routinely because of its invasiveness
Lab studies not helpful because serum amylase and lipase levels arent elevated in CHRONIC pancreatitis
Prothrombin time as a LFT describes?
THe liver synthesizes clotting factors I, II, V, VII, IX, X, XII, XIII, the function of which is reflected by PT
PT is not prolonged until most of the liver's synthetic capacity is lost which corresponds to advanced liver disease.
diagnosis of cholangiocarcinoma
1. PTC/ERCP for diagnosis and assesssment of resectability
2. IF patient has an unresectable tumor (more likely the case with proximal than distal bile duct tumors) - stent placement is an option during PTC or ERCP to relieve the obstruction
Performance of surveillance _______ in patients with known achalasia has been shown to detect the tumor at an early stage.
Acute Infectious Diarrhea is defined as:
increased frquency of defecation (>/= stools/day) lasting <14days
-accounts for 900k hospitalizations and 6k deaths annually
Tests to order in patients with GI bleeding and OCCULT BLOOD
colonoscopy is the initial test in most cases (colon CA is the main concern) Order and upper endoscop if no bleeding site identified from the colonoscopy
What are the causes of unconjugated hyperbilirubinemia?
(Urine negative for bilirubin)
1. Excess production of BR - hemolytic anemias
2. reduced heaptic uptake of BR or impaired conjugation
-drugs (sulfas, penicillin, rifampin, radiocontrast agents
-criggler najjar syndrome types I/II
-physiologic jaundice of newborn (immature conjugating system)
-diffuse liver dz (cirrhosis/hepatits)
Staging esophageal cancer that have invaded the muscularis propria and has positive regional nodes:
Stage 1: tumor invades lamina propria or submucosa; nodes negative
Stage 2a: tumor invades muscularis proprai or adventitia; nodes negative
Stage 2B: tumor invases up to muc propria with positive regional nodes
Stage 3: tumor invades adventitia (positive reional nodes) or tumor invades adjacent structures (positive or negative nodes)
Satge 4: distant mets
Clinical features of acute mesenteric ischemia versus chronic mesenteric ischemia
Acute: severe abdominal pain disproportionate to the physical findings. Pain is due to ischemia or possibly infarction of intestines analogous to MI in CAD. Abdomen may appear benign even when there is severe schemia. This can lead t a delay in dx. Acutesness and the severity of pain vary depending on the type of acute mesenteris ischemia
-GI bleeding (mild)
-peritonitis, sepsis, shock may be present in adv disease
Chronic: results in weight loss, abdominal angina postprandially.
Autosomal recessive disease of iron absorption-
-escessive iron absorption in the intestine leads to ncreased assumulation of inro (as ferritin and HEMOSIDERIN) in varous organs. Over years, fibrosis isn involved organs will occur seoncdary to OH free radials generated by excess iron
Hemochromatosis v. Hemosiderosis?
Hemochromatosis: common AR disease in US homozygous for C282Y on chromosome 6. Causes increase intestinal iron absorptino with elevated accumulation of iron in the liver, pancreas, heart adrenals tests pituitary kidneys joints and skin. Disease onset is after age 50 with nonspecific symptoms in early stages. Later signs include arthropathy, hepatomegatly, skin pigmentation and cardiac enlargement, DM and impotention. Patients WILL DEVELOP HEPATIC AND PACNREATIC INDUFFICIENCY with possibly CIRRHOSIS and HCC, CHF, and hypogonadism.
Lab findings will be elevated LFTs with elevated plasma iron and increase 50% sat of TIBC and elevated ferritin.
Hemosiderosis is the deposition of excessive iron in the tissues. This is caused by a variety of inherited metabolis disorders or by environmental exposures to iron containing substances and is therefore NOT considered to be a distinct disease entitiy.
Treatment of UC:
medical: corticosteroids for acute exacerbaton
-SULFASALAZINE is he mainstay of treatment - it is effective
surgical - curative (UNLIKE CROHNS disease) involves total colestomy
Factors increasing mortality of GI bleeding
>65YO, severity of initial bleed
extensive comorbid illnesses
onset or recurrency of bleeding while hospitalize for another condition
need for emergency surgery
diagnosis (esophageal varices have a 30% mortality rate)
endoscopic stigmata of recent hemorrhage
Causes of cirrhosis?
1. Alcoholic liver disease (most common cause)
-range of conditions from fatty liver (reversible due to acute ingestions) to cirrhosis (irreversible).
-15-20% of heavy drinkings develop alcoholic cirrhosis
2. Chronic hepatitis B and C infections
3. Drug toxicity: acetaminophen toxicity, MTX
4. AI hepatitis
5. Primary biliary cirrhosis (PBC); secondary biliary cirrhosis
6. Hereditary metabolic diseases (Hemachromatosis, Wilson's disease (deposition of iron or copper)
7. Hepatic congestion 2/2 RHF or constrictive pericarditis
9. Hepato veno-occlusive disease can occur after bone marrow transplantation
Diagnosis of gastric CA
Endoscopy with multiple biopsies is the most accurate!
-barium upper GI series less accurate but can completment upper endoscopy biopsy findings
-abdominal CT scan to stage and detect mets
if a patient presents with peritoneal fluid excess with exertional dyspnea. What is likely the cause of the patients distended abdomen and edema if a paracentesis shows an albumen level of 2.5 and a blood study shows an albumin of 3.8?
SAAG - serum albumen ascites gradient
serum albumin - ascites albumin = 1.3 therefore because it is greater than 1.1, we can denote his cause to portal HTN
SBO (small bowel obstruction): Three points to differentiate between:
1. Partial v. complete obstruction
2. Closed loop v. open loop obstruction
3. Proximal v/ distal loop obstruction
Treatment for BUDD-CHIARI syndrome
1. Medical therapy is uaually unsatisfoatory (anticoag, thrombolytics, diuretics)
2. Surgery is eventually necessary in most cases (balloon angioplasty with stent placement in IVC, portocaval shunts)
3. LIVERTRANSPLANT if cirrhosis is present!
ALT is primarily found in the ____
AST is primarily found in the ____
ALT - LIVER
AST - more nonspecific: kidney, heart, brain, skeletal muscle
What diagnosis does an upper GI barium swallow show ("corkscrew esophagus") - in 50% which represents multiple simultaneous contractions?
Pacnreatic ascites/pleural effusion is the MOST COMMON CAUSE OF INFLAMMATION of the PERITONEAL SURFACE.
IF AST and ALT are severely elevated (>10,000) extensive hepatic necrosis has occured. This includes:
2. Shock liver (prolonged hypotension or circulatory collapse)
3. Acetominophen toxicity
4. Severe viral hepatitis
What are the risk factors for acquisition of clostridium difficile?
Hospitalization or residence in a chronic care facility
-AB exposure - nearly all AB implicated however the big three (CLINDA, CEPHS, FQ)
-Advanced age (esp >65)
SBP: SPONTANEOUS BACTERIAL PERITONITIS is indicative of?
Infection ascites fluid that occurs in up to 20% of patients hospitalized for ascites
1. occurs in patients with ascites caused by chronic liver disease with HIGH mortality rate 20-30%
2. high recurrence rate (70%)
3. E. Coli, Klebsiella, Streptococus penumoniae
4. CLinical features: abdominal pain, fever, vomiting, rebound tenderness. SBP can lead to SEPSIS
****REBOUND TENDERNESS! = SBP!
47YO DM female presents with onset of tremors. Undergone both pancreatic and renal transplantation 2/2 ESRD and DM. Takes medications including that of immunosuppressants. BP 152/90 and pulse and RR WNL. Examination shows gum hypertrophy and labs show an increased BUN and inc CREATININE. Which immunosuppressant is likely to be responsible for the presentation of patient?
(Tacrolimbus, cyclosporine, AZA, Mycophenolate)
most commonly used and acts by inhibiting the trancription of IL-2 and severeal other cytokines (mainly the THELPER LYMPHOCYTES
-malignancy of SQCC of skin and lymphoproliferative D/O
-gingival hyperplasia and hirsuitism
What is OGILVIE'S SYNDROME
Signs, symptoms, radiographic evidence of large bowel obstruction are present but no mechanical obstruction.
-causes: surgery, trauma, serious medical illness (sepsis, malignancy) and medications (narcotics, psychotrpoic drugs, anticholinergics)
-diagnosis: not confirmed until mechanical obstruction of colon is exluded
-treatment: stop offending agent (narcotic) or supportive measures (IV fluids/electrolyte repletion)
-decompression with gentle enemas or NG suctions may be helpful
-colonoscopic decompression is usually successful
-surgical decompression with cecostomy or colostomy is LAST result
What is the treatment for diverticulosis?
1. High fiber foods (bran) increase the stool bulk
2. Psyllium *if the patient cannot tolerate bran)
Occurs in 7% of population-autosomal dominant condition in which there is decreased activity of hepatic uridine diphosphate flucuronyl transferase activity (UDP transferase);
DIAGNOSIS: MOST COMMON CAUSE OF ISOLATED ELEVATION IN UNCONJUGATED BILIRUBIN. +/- jaundice
NO TREATMENT NECESSARY AND LIVER BIOPSY RESULTS ARE OFTEN NORMAL.
Term used to describe esophageal perforation:
2/2: BLUNT TRAUMA, MEDICAL TUBES, INSTRUMENTS, FORCEFUL VOMITING ASSOCIATED WITH THAT OF ALCOHOLISM OR BULIMIA
Manifestations of strangulated bowel in SBO includdes fever, severe and continuous pain, hematemesis, schock, gas in bowel wall or PV, adbominal free air, peritoneal signs and _____. Will check _____ _____ to see if gut ischemia present
acidosis, lactice acid increased
Clinical indicators of Acute bacterial sinusitis
pain above or below the eyes on leaning forward
purulent rhinorrhea by hx
poor response to decongestants
0-1 = no treatment
2-3 = XR
4+ = ATB treatment
What are the signs associated with acute pancreatitis?
1. Low grade fever, tachycardia, hypotension, leukocytosis
2. Epigastric tenderness, abdomial distention
3. Decreased or absent bowel sounds indicate patial ileus
4. The following signs are seen with hemorrhagic pancreatitis as blood tracks along fascial planes:
-Grey turners sign (flank ecchymoses)
-Cullen's sign (periumbilical ecchymoses)
-Fox's sign (ecchymosis of inguinal ligament
Increased glomerular filtration pressure will increase glomerular _____ rate and decrease the serum ______ concentration. This will NOT cause ascites
Acid suppression therapy for pts with PUD includes:
H2 blockers; ranitidine; famotidine; cimetidine; PPI; esmoprezole; omeprazole; lansoprazole; pantoprazole, rabeprazole
Diagnosis of crohns
endoscopy (sigmoidoscopy or colonoscopy) with BIOPSY - typical findings are apthous ulcers, cobblestone appearance, pseudopolyps, patchy skip lesions
upper GI with SBfollow through
Familial juvenile polyposis coli
RARE = in childhood; only small risk of CRC
-more than 10 and up to hundred of juvenile colon polyps.
CLinical signs of appendicitis:
1. Mcburneys point (tenderness)
2. Rebound tenderness, guarding, diminished bowel sounds
3. Low-grade fever
4. Rovsings sign: deep palpation is LLQ causes referred pain in RLQ
5. Psoas sign: RLQ pain when right thigh is extended as patient lies on the L side
6. Obturator sign: pain in RLQ when flexed right thigh is internally rotated when pt is supine.
Treatment of bleeding esophageal VARICES:
1. VARICEAL LIGATION/BANDING
-initial endoscopic treatment of choice; effective control of ACTIVE BLEEDING
-lower rate of rebleeding than scleotherapy
2. ENDOSCOPIC SCLEROTHERAPY:
-sclerosing substance is injected into varices during endoscopy
-this controls acute bleeding in 80-90% of cases with 50% haveing rebleeds
3. IV vasopressin
-alternative to octraotide but LESS POPULAR due to risk of complication.
-vasoconstriction of mesenteric vessels reduces portal pressure
-NG is admin to prevent side effects of vasopressin (coronary vasoconstrict/MI, decreased CO/HTN)
3. IV octreotide
-now replacing vasopressin as firstline therapy; causes splanchnic vasoconstriction and reduces portal pressure
-fewer side effects
Rectal CA v. Colon CA
Rectal CA has a higher recurrence rate and a lower 5 year survival rate than colon CA
Three types of adenomatous polyps:
*tubular is the most common type in up to 60-80% of cases
*tubulovillous has an intermediate risk of malignancy
*villous is the GREATEST risk of becoming malignant
Two types of liver cysts and causes:
1. Polycystic liver cysts: AD usualy associated with ADPKD. Results in renal failure and is the main determinant of the prognosis whereas the liver cysts RARELY lead to hepatic fibrosis and liver failure.
-usually asymptomatic; some patients have absominal pain and upper abdominal masses
2. Hyadatid liver cysts: caused by infection from the tapeworm ECHINOCOCCUS GRANULOSUS or ECHINOCOCCUS MULTIOCULARIS. Cysts most commonly occur in the RL of the liver.
-small cysts are asymptomatic; larger cysts may cause RUQ pain and RUPTURE into the peritoneal cavity, causing fatal anaphylactic shock.
-treatment: SURGICAL resection (caustion to avoid spilling contents of the cysts into the peritoneal cavity). Mebendazole is given after surgery
How might HIDA diagnose that of acute cholecystitis? When is it superior to an US?
HIDA - radionuclide scan - hepatoiminodiacetic acid) is used to diagnose inflammation of the GB when US is inconclusive. If the scan is normal, then acute cholecystitis can be ruled out. If the test is positive then the GB cannot be visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed
Vascular tumor that are small, asymptomatic and most commony type of BENIGN liver tumor.
size increases 2/2 pregnancy or OCP use
complications: rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF seondary to a large AV shunt and gastric outlet obstruction
Dx with US or CT with IV contrast - no biopsy indicated
1. emergence is nationwide
2. both children and adults in variety of settings affected --> contact sports (wrestling, football and fencing), correctional facilities, native american communities, MSM
3. Transmission is person to person or by fomites
4. Strains causing MRSA (community) appear distinct --> unique resistance cassette (SCC mec IV) & broader susceptibility
Cholesterol stones are one of three major types of GB stones that are _____ - _____ in coloration and are associated with the following:
4. multiple pregnancies
5. Crohns dz
6. Native american ancestry
8. Cystic fibrosis
Treatment of appendicitis:
APPENDECTOMY - usually laparoscopic. Up to 20% of patients who are dx with acute appendicitis are found to have a normal appendix during surgary. Because illness is potentially life threatening, acceptable risk even during pregnancy.
RISK FACTORS of gastric CA:
1. atrophic gastritis
2. adenomatoush gastric polps
3. H pylori infecction -3-6x inc
4. Postantrectomy - many causes post billroth II anastomosis (15-20yrs post surgery)
5. PERNICIOUS ANEMIA
6. Menetriers disease
7. High intake preseved foods
8. Blood type A
Management of uncomplicated UTI (acute)
1-2 recurrences per year
-intermittent self treatment (educable, typical sxs)
-TSX, TMP, FQ x 3 days
>2 recurrences/yr associated with coitus
-TSX, NTF, or FQ after intercourse
>2 recurrentces without coitus
-continuous prophylaxis (95% reduction)
-TSX, TMP, NTF, F! qhs x 6 mo
What is the treatment for chronic pancreatitis?
Nonoperative management: narcotic analgesics for pain; bowel rest (NPO); pancreatic enzymes inhibit CCK release and thus decrease pancreatic secretions after meals; H2 blockers inhibit gastric acid secretion, preventing degradation of the pacnreatic enzyme supplements by gastric acid; INSULIN may be necessary if SEVERE pancreatitis; alcohol abstinence; small volume low fat meals - may improve abdominal pain.
Surgical managment on chronic pancreatitis: main goal is relief of incapacitating abdominal pain.
1. pancreaticojejunostomy (Pancreatic duct drainage procedure to decompress the dilated pancreatic duct - most common)
2. Pancreatic resection (distal pancreatectomy, Whipples procedure)
Typical symptoms: cough, SOB, sputum, pleuritic chest pain
Infiltrate on CXR is gold standard for dx
How is ACUTE CHOLANGITIS treated:
1. IV AB and IV fluids
-close monitoring of hemodynamics, BP and urine OUTPUT is important
-most patients respont rapidly. Once patient stabilized - ERCP or PTC performed for evaluation of underlying condition.
2. Decompress the CBD via PTC (catheder drain); ERCP (spincterectomy or laparotomy) - (T tube insertion) once the patient is stabilized, or emergently if the condition doesnt respond to the antibiotics.
Treatment for C diff colitis:
d/c offending agent
-metronidazole is the drug of choice (cannot be used if infant/preg)
-oral vanc used if patient resistance to met or cannot tolerate it
-redarless of choice of AB, recurrence may occur within 2-8 weeks after stopping the AB
-CHOLESTYRAINE MAY BE USED AS ADJUVANT TO IMPROVE DIARRHEA.
What is diverticulosis?
pouches in the colon wall that should be distinguished from diverticulitis, which refers to inflammations or infections of the diverticula and is a complication of diverticulosis.
What are the clinical features of CRC?
Abdominal pain is that most common feature - where CRC is the most common cause of large bowel obstruction in adults
-blood in stool
-colonic perforation is the most life threatening
Hepatocellular CA accounts for > 80% of primary liver CA and although rare in US, accounts for most deaths 2/2 cancers world wide. Highest in Africa and asia.
What are the two pathologic types?
Most common type of tumor within the intra/extra hepatic bile ducts
-tumors in proximal third of the CBD - involve the junction of the right and left hepatic ducts with very POOR prognosisbecausethey are unresectable.
What is ACUTE CHOLECYSTITIS
Obstruction of the cystic duct (not infection) induceing acute inflammation of the gallbldder wall
-chronic forms when recurent bouts of acute cholecystitis
-10 percent of patients with gallstones develop acute cholecystitis
Partial v. complete obstruction
Partial: with partial obstruction, patients are able to pass gas or have bowel mvmts as opposed to complete obstruction however patients with complete obstruction may occasionally be able to pass gas or stool because they may have residual stool or gas in the colon
Diverticulitis can occur in 15-25% of all patients with diverticulosis however this is not always a precedent of diverticulitis.
Pathophysiology of diverticulitis?
1. Occurs when the feces become impacted in the diverticulum, leading to erosion and microperforation
2. Clinical features; fever, LLQ pain, leukocytosis (elevated WBC); alteration in bowel habits, vomiting, sometimes a painful mass on rectal exam if inflammation is near the rectum.
Diagnostic tests for diverticulitis:
1. CT scan of abdomen and pelvis with ORAL and IV contrast is the test of choice
-reveals a swollen, edematous bowel wall or an abscess.
2. Abdominal radiographs help in excluding other potential causes of LLQ pain that can rule out obstruction or ileus.
3. Barium enema and colonoscopy are contraindicated in ACUTE DIVERTICULITIS due to the risk of perforation
What is the metabolism of BILIRUBIN
-80% of BR is derived from hemoglobin (RBC breakdown). The rest comes from myoglobin breakdown and liver enzymes
-hemoglobin is coverted to BR in the spleen. This unconjugated BR circulates in plasma, bound to albumin. This BI-albumin complex is not water soluble; therefore it is not excreted in the urine.
-in the liver, it dissciates from albumin and the BR is conjugated and excreted into the intestine, where bacteria act on it to produce urobilinogen and urobilin
-therefore, unconjugated hyperbilirubinemia results when there is a defect BEFORE hepatic uptake. Conjugated hyperbilirubinemia results when there is a defect AFTER hepatic uptake
Treatment for cholangiocarcinoma:
1. most patients do not have resectable tumors at diagnosis
2. survival rate low despite aggressive therapy and stenting or biliary drainage
Duodenal ulcer differs from gastric ulcer in what ways?
1. Duodenal: by an increase in offensive factors (higher rates of basal and stimulated gastric acid secretion). H. pylori in 70-90% of patients. LOW MALIGNANCY; majority are located within 1-2cm distal to pylorus usually on posterior wall. Age is YOUNGER (<40). BLOOD TYPE O. Risk factors includes NSAID use. Other - eating usually relieves pain and NOCTURNAL pain is more common than in gastric ulcers.
2. Gastric ulcers - caused by decrease in defensive factors (gastric acid level is normal) low unless ulcer is pyloric or prepyloric. H. pylori infection in 60-70%. HIGH LEVEL MALIGNANCY - must undergo biopsy to rule out malignancy). Location:
Type I: most common - 70% on lesser curvature
Type II: gastric and duodenal ulcer
Type III: Prepyloric (within 2 cm of pyloris)
Type IV: near esophagogastric juntion
Age distribution occurs in older patients (>40). BLOOD TYPE A. RIsk factors smoking. Eating does not usually relieve pain. Complication rates are higher than those of duodenal ulcers. There is a higher recurrence rate with medical therapy alone.
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