Gastro Flashcards
(40 cards)
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
investigations cholecystitis
```
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
investigations appendicitis
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
complications appendicitis
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
treatment appendicitis
```
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
appendicitis risk factors, aetiology and pathophys
```
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
aetiology and pathophys of cholecystitis
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
complications cholecystitis
- 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
investigations for IBD
```
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
ddx for bloody diarrhoea
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
natural hx and pathology of alcoholic liver disease
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
complications IBD
```
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
extra-intestinal manifestations IBD
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
risk factors IBD
```
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
ddx for blood in stools
HAD bloody CRAPS
- Haemorrhoids
- Anal fissure
- Diverticulosis
- Colitis (ischaemic, inflammatory, infectious)
- Radiation induced telangectasia
- Angiodysplasia
- Polyps/neoplasia
- Solitary rectal ulcer syndrome
39
viral hepatitis
jb
40
bowel obstruction causes
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