Gastro Flashcards
1
Q
Management SBO
A
Initial
- analgesia
- nil by mouth
- gastric decompression
- dehydration
- > IV fluids
- metabolic alkalosis
- > electrolyte replacement
- ischaemia
- > WCC
- > CRP
- > lactate
- > CT abdo
- early surgical consult
Non operative
- adhesive
- > non op successful in approx 80%
- > higher rate of recurrence with non op
- > gastrograffin with xray 6-24 hours later (failure to reach colon after 24hrs predicts need for surgery)
- > trial of non op no longer than 5 days
- non adhesive
- > treat underlying cause
Operative
- indicated when evidence of bowel compromise
- indicated for surgically correctable causes
- > closed loop
- > volvulus
- > intussusception
- > tumour
- > hernia
2
Q
hep B management
A
acute
- usually supportive
- treatment for
- > protracted course (eg. >4 weeks)
- > severe course (eg. INR >1.5)
- antivirals
- > tenofovir or entecavir
chronic
- decompensated cirrhosis or fulminant hepatitis
- > treated with NRTI’s
- compensated cirrhosis
- > treated with NRTI’s since HCC risk reduced
- immune active phase
- > consider treatment if severe
- > do not treat all, as it may prevent spontaneous remission
- inactive carrier
- > treat immediately when HBeAg negative
- > prevents recurrence
- immunosuppression
- > treat with NRTI’s before immunosuppression
- pregnant women
- > high viral load = treat in 3rd trimester
- HCC
- > treat with NRTI
goals
- treatment usually >5 years
- without cirrhosis
- > HBeAg seroconversion on two tests months apart
- with cirrhosis
- > lifelong treatment
- consolidation period
- > 1 year extra therapy after HBeAg seroconversation
3
Q
microbio and pathogenesis of typhoid
A
Microbio
- classical
- > salmonella enterica serotype typhi
- also
- > salmonella enterica serotype paratyphi (ABC)
Inoculation
- typically contaminated
- > water for typhi
- > food for paratyphi
- humans only known resovoir
- > so infection = sick contact
GI infection
- survives acidic stomach and enters small bowel
- enters submucosa
- > via antigen sampling M cells
- > direct penetration into/around epithelial cells
- proliferate in sumucosa
- recruitment of immune cells
- > hypertrophy of peyers patches
- > subsequent perforation of submucosal tissue
- > abdo pain and possible ileal perforation
- release of typhoid toxin
- > causes many of enteric fever symptoms
Systemic spread
- dissemination from peyer’s patches via blood/lymph
- reaches reticuloendothelial system in
- > spleen
- > liver
- > bone marrow
Chronic carriage
- shedding organism in stool or urine >12 months
- gall bladder colonised
- > organism produces biofilm when exposed to bile
- > gall stones provide nidus for chronic infection
- immunological equilibrium
- > contagious
- > no symptoms
4
Q
Clinical features typhoid
A
Inoculation
- contaminated food or water
- travel to endemic areas
Incubation
- 1-3 weeks following ingestion
Signs/Symptoms
- first week
- > rising stepwise fever
- > chills
- second week
- > abdo pain
- > rose spots on trunk
- > bradycardia
- third week
- > hepatosplenomegaly
Other features
- diarrhoea/constipation equally common
- headache common
- neurological findings can occur
- typhoid encephalopathy
- > altered level of consciousness/delirium
- cough
- arthralgia/myalgia
Complications
- ileal perforation
- > peritonitis
- > intestinal bleeding
- sepsis/septic shock
5
Q
Diagnosis typhoid
A
FBC
- anaemia
- leukopaenia or leukocytosis
LFTS
-transaminitis
Stool culture
- least sensitive test
- > often negative by time of presentation
Blood culture
- slightly more sensitive than stool
- > still poor
- several culture tubes needed
Bone marrow
- high sensitivity
- > even after days of antibiotic treatment
6
Q
Risk factors and types of hernias
A
risks
- non modifiable
- > male
- > age
- > family history
- > connective tissue disease
- > chronic cough (COPD)
- > prematurity
types
- inguinal
- femoral
- egigastric
- umbilical/para
- incisional
- spigelion
- > between rectus and semi lunar line
- hiatus
7
Q
Investigation and management hernias
A
investigations
- FBC
- > WCC with necrosis
- EUCs
- > eGFR
- > electrolytes
- ultrasound
- CT for obstruction
- > transition point
- > aetiology
- Xray
- > less sensitive and specific
management
- incarcerated/strangulated
- > surgical repair (lap/mesh)
- small asympto
- > watchful waiting
- large or sympto
- > open or lap mesh
8
Q
X-ray small vs large bowel obstruction
A
3,6,9 rule
- 3 = small
- 6= colon
- 9 = caecum
small
- central
- <3cm
- mucosal folds (valvulae coniventes)
- > fully traverse
- > closely spaced
large
- peripheral
- <6cm
- <9cm for caecum
- haustra folds
- > dont fully traverse
- mottled appearance
- > due to faeces
obstruction
- dilated loops of bowel
- air fluid level
9
Q
cirrhosis pathology
A
cirrhosis
- chronic hepatic insult activates stellate cell
- > accumulation of collagen in parenchyma and space of disse
- in space of disse = capillarisation
- > lose of sinusoid fenestration
- capillarisation and stellate cell contraction
- > increases portal pressure
- overall, fibrosis with regenerative nodules
- > fibrosis may decrease with removal of insult/treatment
10
Q
alcoholic liver disease pathophys
A
alcoholic liver disease
- includes
- > steatosis
- > steatohepatitis
- > cirrhosis
- liver metabolism by ADH and ACDH
- > both reduce NAD to NADH
- > high NADH:NAD inhibits gluconeogenesis and increases
beta oxidation
- > accumulation of lipids
- CYP40
- > generates free radicals by NADPH to NADP
- > free radicals = inflammation, apoptosis and necrosis
- acetaldehyde creates antigenic adducts that drives inflamm
alcohol increases gut permeability to bacteria
- > taken up by portal vein
- > liver inflammation
11
Q
cirrhosis investigations
A
FBC -anaemia -thrombocytopenia EUC -hepatorenal LFTS -AST:ALT 2:1 in alcoholic -GGT induced by alcohol
Liver function:
Albumin
Coags
-PT
Causes:
- Hep
- > B surface antigen
- > C IgG
- autoimmune
- > ANA
- > anti-smooth muscle
- iron studies
- > haemochromotosis
- α 1 anti trypsin
Imaging
- upper endoscopy
- > varices
- ultrasound
- > small, nodular, hypertrophied caudate
- > splenomegaly, large portal vein
- CT/MRI following ultrasound
Biopsy
-usually unnecessary
Non invasive
- APRI
- > AST:platelet index
- transient elastography
12
Q
complications cirrhosis
A
portal HTN
- capillarisation/stellate contraction/nodules
- increased splanchnic blood flow due to vasodilation
- causes
- > splenomegaly
- > ascites
- > varices
splenomegaly
- due to portal HTN
- causes thrombotycopenia
ascites
- due to
- > portal HTN
- > splanchnic vasodilation from NO release
- > hypoalbuminaemia
- increases splanchnic lymph -> underfil of systemic arteries
- > activates RAS
- hyperaldosteronism
- > Na retention
- Na retention expands ECV
- > peripheral oedema
hepatorenal syndrome
- renal failure without renal pathology
- systemic hypotension with renal HTN
hepatic encephalopathy
- shunting of blood from liver
- > accumulation of toxins/metabolites
- FAM
- > false neurotransmitters
- > ammonia
- > mercaptam
other
- malnutrition
- > anorexia
- > poor gut absorption
- coagulation
- > factors, protein C/S, AT
- > thrombocytopenia
- > vitamin K
- osteoporosis
- > vitamin D absorption
death
-due to decompensation, above complications, variceal bleeding
13
Q
ddx dysphagia
A
solids only (constant)
- neoplasia
- > oesophageal
- > laryngeal
- strictures
- > GORD
- > radiation
- > caustic ingestion
- hiatus hernia
solids only (intermittent)
- eosinophilic oesophagitis
- rings
- webs
- vascular anomaly
liquids + solids
- neuromuscular
- > stroke
- > MS
- > myasthenia gravis
- motility disorder
- > achalasia
- > DES
- autoimmune
- > scleroderma
- > sjogrens
odynophagia +dysphagia
- pharyngitis
- > candida
- > strep
- pill induced
14
Q
upper GI ddx
A
UNACTED
- ulcer
- neoplasia/polyp
- angiodysplasia/AVM
- coagulopathy (medical/drugs)
- trauma (mallory weiss/buerharves)
- erosive esophagitis, gastritis, duodenitis
- deuilofoys lesion
15
Q
investigation upper GI bleed
A
ECG
FBC -anaemia (normocytic) Iron studies -suggests chronicity EUCs -urea:creatinine >100 LFTs -gastropathy/varices -coagulopathy Coags
Upper endoscopy with biopsy
- rapid urease test (with pH reagent –> colour change)
- histology with giemsia staining
- culture and sensitivity
Urea breath test -radiolabeled carbon isotope -split by urease -radiolabeled carbon dioxide breathed out Stool antigen
Consider
-fastig gastrin (zollinger ellison)
16
Q
ddx cirrhosis
A
All Viruses Are Nasty Bugs Causing Infections
- Alcohol
- Viral (B,C)
- Autoimmune
- NASH
- Biliary (primary sclerosing/biliary cholangitis)
- Cardiac
- Inherited (alpha 1 anti-trypsin deficiency, hereditary haemochromatosis, wilsons)
17
Q
ddx jaundice
A
unconjugated = glucorinic conjugation doesnt happen
- gilberts
- crigler najar I/II
- drugs
- haemolysis
intrahepatic = cirrhosis causes + “Ending In Sepsis, Morbidity, Death”
- excretory (dubin johnson, rotor, benign recurrent intrahepatic cholestasis, progressive familial intrahepatic cholestasis)
- infiltrative (sarcoid)
- sepsis
- malignancy (stauffers)
- drugs
obstructive =NIPS
- neoplasia
- infections (cholangitis)
- PSC
- stones (including mirizi syndrome)
18
Q
Gall stone types
A
Cholesterol (most common, >90%)
- usually mixed
- > cholesterol monohydrate
- > calcium salts of bilirubin and palminate
- > proteins and mucin
Pigment
- black
- > calcium bilirubinate
- brown
- > unconjugated bilirubin
- > chronic biliary infection
19
Q
Gall stone pathophys
A
Normal bile
- bile acids are detergents
- > form mixed micelles of cholesterol and phospholipids
Cholesterol supersaturation
- causes
- > high cholesterol diet
- > obesity/metabolic syndrome
- > gain of function mutations in hepatic cholesterol transporter
- > drugs (eg. fibrates)
- excess cholesterol
- > formation of mutlilamellar vesicles
Nucleation
- pronucleation factors
- > mucin
- > IgGs
- inhibit nucleation
- > apolipoprotein A 1 and 2
- within mucin gel layer
- > liquid crystals -> further saturation -> solid crystals -> biliary sludge
Gall bladder stasis
- required for sufficient nucleation to occur
- causes
- > pregnancy
- > OCP
- > infections
- > trauma
- > burns
- > fasting
- > spinal cord injury
20
Q
causes of acute pancreatitis
A
I GET SMASHED
- infection (mumps)
- gallstones
- ethanol
- trauma
- sludge
- malignancy
- sphincter of oddi dysfunction
- hypertriglyceridaemia/calcaemia
- ercp
- drugs (eg. valproate)
21
Q
pathophys pancreatitis
A
Occurs in three phases
- Initial phase
- > co location of lysosomal hydrolases with digestive enzymes
- > trypsin activiation -> acinar injury
- Second phase
- > activation and invasion of leuks/macrophages
- > intrahepatic inflammation
- > neutrophils activation of trypsin
- Third phase
- > widespread activation of digestive enyzmes
- > necrosis, oedema, haemorrhage
- > systemic release of inflamm mediators eg. bradykinin
- > SIRS/ARDS
22
Q
hx and exam acute pancreatitis and difference in chronic
A
hx
- risk factors
- epigastric pain
- > shooting to back
- > relieved by fetal position
- > worse with movement
- anorexia, nausea, vom
exam
- dehyrdration
- fever
- tachycardia
- tender epigastrium
- > rebound/percussion tenderness
- > guarding
- decreased bowel sounds
- > ileus
- decreased breath sounds
- > effusion
- haemorrhagic
- > cullens, grey turners, foxs
23
Q
investigations acute pancreatitis
A
Glucose
-elevated in chronicity
ABG
-ARDS
FBC -leukocytosis -raised haematocrit ->haemoconcentration in severe EUCs -raised urea/creatinine with dehydration LFTs -usually normal -transaminitis with gall stones Lipase -3 x upper limit CRP -severity scoring
CXR -pleural effusion Abdo xray -sentinal loop ->isolated dilatation of segment of bowel ->due to ileus -cut off sign ->distended colon stopping at splenic flexure ->inflammation Abdo ultrasound -fat stranding -inflammation -fluid collections -gall stones
if equivocal or persistent organ dysfunction
- CT abdo
- MRCP
- endoscopic ultrasound
24
Q
hx, exam and investigations chronic pancreatitis
A
hx
- > steatorrhea
- > malnutrition/weight loss
- > diabetes symptoms
exam
- > malnutrition
- > jaundice
investigations
- ultrasound/xray = calcification
- > lipase digestion of mesenteric fat
- > release of free fatty acids
- > complex with calcium to form salts
- ERCP
- > beading of ducts
- > biopsy for histology
- faecal elastase is low
25
Q
investigations cholecystitis
A
FBC -leukocytosis LFTs -cholestatic CRP
Ultrasound
- positive murphys
- gallstone
- thickening
- > gall bladder wall
- > cystic duct
Consider
- HIDA scan
- > hepatobiliary iminodiacetic acid
- > if ultrasound equivocal
- > delayed takeup into gallbladder >60mins
- MRCP
- > if raised LFTs
- > intra and extra hepatic ducts
- CT
- > if concern for local complications
26
Q
investigations appendicitis
A
HCG if female
Urinalysis
- genitourinary mimics
- > UTI
- can be abnormal in appendicitis
FBC
- leukocytosis
- lactate
CT -large, with wall thickening ->diameter >6mm -inflammed -appendicolith may be present Ultrasound -lower sensitivity and specificity ->avoids radiation in women and children -diameter >6mm
27
Q
complications appendicitis
A
complications
- perforation
- > usually after 12 hours with delayed medical treatment
- leads to
- > abscess and mass
- > peritonitis
- infective suppurative thrombosis of portal vein
- > hepatic abscess
28
Q
treatment appendicitis
A
treatment -antibiotics alone ->avoids surgery in approx 75% ->at risk of significant cost with failure -antibiotics alone is less effective than appendicectomy with or without antibiotics ->failure for antibiotics within 1 year = 30% ->failure for appendicectomy <2% -antibiotics (Gently Manage Appendicitis) ->gentamycin IV ->metronidazole IV ->amp/amoxicilin IV -additional ->nil by mouth ->IV fluids -surgery -open or laparoscopic
29
Q
appendicitis risk factors, aetiology and pathophys
A
risk factors -slight male to female -common in teenagers >predominately young adults -low fibre diet -smoking -<6 months of breast feeding
aetiology
- obstruction
- > faecolith
- > normal stool
- > lymphoid hyperplasia
pathophys
- closed loop obstruction
- > fills with mucous
- > intraluminal and intramural pressure
- pressure greater than venules but not arterioles
- > thrombosis of veins
- > engorgement of appendix
- distension
- > reflex anorexia
- > nausea, vom
- > visceral pain (T10)
- overgrowth of bacteria
- > bacterioides fragilis
- > e coli
- suppurative inflammation involves serosa
- > irritation of parietal pleura
- > localised RLQ pain
30
Q
aetiology and pathophys of cholecystitis
A
Aetiology
- almost always associated with gallstone in cystic duct
- 5% alcalculous
- > trauma, sepsis/infection, pregnancy, TPN
- > gall bladder stasis, biliary sludge
- > usually bacterial secondary infection
Pathophys
- gall stone lodged in cystic duct
- > leads to gall bladder inflammation by three means
- > release of prostaglandins drives local inflamm
- mechanical inflammation
- > increased pressure in lumen
- > resulting in ischaemia and necrosis of mucosa and wall
- chemical inflammation
- > conversion of lethicin to lysolethicin by phospholipase
- > lysolethicin acts as an irritant to mucosa
- bacterial inflammtion
- > secondary infection with gram negatives
- > E coli, klebsiella, enterococcus
31
Q
complications cholecystitis
A
- if left untreated, may resolve after 1 week
- gangrenous
- > abscess
- > perforation
- > peritonitis
- > sepsis
- emphysematous
- > gas forming organism (eg. clostridium)
- enteric fistula
- > adhesions
- > gall stone ileus
- > barnards = ileocaecal valve obstruction
- > bouveret = gastric outlet obstruction
- recurrent acute
- chronic
- > empyema
- > hydrops
- > porcelain gallbladder->carcinoma
32
Q
investigations for IBD
A
Blood: FBC -anaemia -leukocytosis -thrombocytosis EUC -hypokalaemia -high Na -high urea LFTs (primary scerlosing cholangitis) ESR, CRP (flare, degree of severity for CD) Anti-saccharomyces (CD) and pANCA (UC)
Stool studies:
- culture
- microscopy for ova and parasites
- histolytic antigen for amebiasis
- c diff toxin
- giadia antigen if travel
- if appropriate sexual hx, PCR for chlam/gon and dark field microsopy for treponema
- calprotecrin or lactoferrin for IBS
Colonoscopy with biopsy
Imaging
- abo xray (dilated loops with air fluid level, lead pipe)
- double contrast barium enema (in UC, granular appearance –> ulceration, thumbprinting with mucosal edema, narrowing/shortening of bowel)
33
Q
ddx for bloody diarrhoea
A
IBD
Infective colitis
- bacterial (salmona, shigella, camp, c diff, e coli [haemorrhagic, adhesive, invasive])
- viral (immunosuppressed, CMV, HIV, HSV)
- fungal (candida, asperigillus)
- protozoa (giardia, water)
- parasite (amebiasis, travel)
- STD
- > chlam, gon, syph
Inflammatory (DR AIDS)
- diverticular
- radiation colitis
- atypical colitides (collagenous, lymphacytic)
- ischaemic
- diversion
- solitary rectal ulcer syndrome
Neoplasm, carcinoma, polyps
Drugs
- NSAIDS
- mycophenolate mofetil
- ipilimumab
34
Q
natural hx and pathology of alcoholic liver disease
A
Steatosis
- macrovesicular
- intracellular displacing nucleus
- perivenular zone (3)
- 90% of alcoholics
- approx. 5% go on to cirrhosis
Alcoholic hepatitis:
- 10-20% of alcoholics
- approx 15% go on to cirrhosis
- inflammation with ballooning degeneration
- mallory-denk body (misfolded intermediate filaments or cytokeratin)
- perivenular fibrosis (sclerosing hyaline necrosis) –> bridging fribrosis
Alcoholic cirrhosis:
- classically micronodular cirrhosis
- fibrosis with regenerative nodules
35
Q
complications IBD
A
Toxic megacolon (both, mainly UC) Bleeding Perforation, abscess, peritonitis (mainly CD) Fistulae (CD) Colorectal cancer (UC) Adhesions (CD) Bowel obstruction (CD) Gallstones (CD) SIBO (CD) Gastric outlet obstruction (CD) Death
36
Q
extra-intestinal manifestations IBD
A
eyeBD Has Peripheral Manifestations
- Eye: episcleritis, uveitis
- Blood: venous and arterial thrombosis, autoimmune haemolytic anaemia
- Dermatological: pyoderma gangrenosum, erythema nodosum
- Hepatic: primary sclerosing cholangitis, steatosis, autoimmune hepatitis
- Pulmonary: interstitial, airway, parenchymal lung disease
- Musculoskeletal: arthritis (non-erosive), anklyosing spondylitis, osteoporosis/osteopaenia, osteonecrosis
37
Q
risk factors IBD
A
Young adult White/Jewish Family history Smoking increased CD, decreased UC Appendicectomy decreased UC OCP for UC (in smokers) Antibiotic use as child Previous infective gastroenteritis Diet high in animal protein/fat, sugar, fish and shellfish
38
Q
ddx for blood in stools
A
HAD bloody CRAPS
- Haemorrhoids
- Anal fissure
- Diverticulosis
- Colitis (ischaemic, inflammatory, infectious)
- Radiation induced telangectasia
- Angiodysplasia
- Polyps/neoplasia
- Solitary rectal ulcer syndrome
39
Q
viral hepatitis
A
jb
40
Q
bowel obstruction causes
A
m
