GI Flashcards
1
Q
Liver Abscess or cyst
A
Liver infection resulting in a walled off collection of pus or cyst fluid
Pyogenic cause: E. Coli, Klebsiella, etc.
- > 60% caused by biliary tract disease (gallstones)
- > 60 yrs age, most common liver abscess in industrialised area
Amoebic cause: Entamoeba histolytica (most common worldwide)
Hydatid cyst cause: Tapeworm
(sheep rearing countries)
Other: TB
History: Fever, malaise, nausea, anorexia, night sweats, weight loss, RUQ or epigastric pain, jaundice, PUO, foreign travel
Exam: Fever, jaundice, tender hepatomegaly
Investigation:
Blood: FBC (mild anaemia, leukocytosis, increased eosinophils due to hydatid disease), LFTs (increased ALP and bilirubin), increased ESR, increased CRP
Stool MCS: For tapeworm
Ultrasound to detect mass
Aspiration and culture of abscess material
2
Q
Liver Failure
A
Severe liver dysfunction leading to jaundice, encephalopathy, and coagulopathy
3
Q
Liver Failure causes
A
- Viral (hepatitis a,b,d,e)
- Drugs (paracetamol overdose)
- Less common: Autoimmune hepatitis, budd-chiari syndrome, haemachromatosis, wilson’s disease
4
Q
Liver failure: Pathogenesis of manifestations
A
Jaundice: Decreased secretion of conjugated bilirubin
Encephalopathy: Increased delivery of gut-derived products into the systemic circulation and brain due to decrease in extraction of nitrogenous products by liver and portal systemic shunting
Ammonia may play a part
Coagulopathy: Decreased synthesis of clotting factors, decreased platelets (hypersplenism if chronic portal hypertension)
5
Q
Liver failure Epidemiology
A
Paracetamol overdose accounts for 50% of acute liver failure in the UK
6
Q
Liver failure symptoms
A
May be asymptomatic. Fever, nausea, jaundice.
7
Q
Liver failure examination
A
Jaundice
Encephalopathy
Liver asterixis
Fetor hepaticus (in portal hypertension where portosystemic shunting allows thiols to pass directly into the lungs -> sweet smelling breath)
Ascites and splenomegaly
Bruising
Look for secondary causes (kaiser Fleischer rings)
8
Q
Liver failure Investigation
A
Identify cause: Viral serology, paracetamol levels, autoantibodies (ASM, LKM), ferritin, caeruplasmin and urinary copper (decreased and increased respectively in Wilson’s disease)
Blood: FBC (Hb decreased in GI bleed, WCC increased in infection), U&E (may show hepatorenal failure), glucose, LFTs, ESR/CRP, coagulation screen, group and save, ABG
Ultra sound and CT scan liver
Ascitic fluid: MCS, check for spontaneous bacterial peritonitis
Doppler scan of hepatic or portal veins: to exclude budd- chiari syndrome
Electroencephalogram: to monitor encephalopathy
9
Q
Liver failure management
A
Resuscitation (according to airway, breathing, and circulation) ITU care
Treat the cause if possible: n-acetylcysteine for paracetamol overdose
Treatment/Prevention of complications:
- Invasive ventilatory and cardiovascular support often required
- Monitor: Vital signs, pH, creatinine, urine output, and encephalopathy
- Manage encephalopathy: Lactulose and phosphate enemas
- Antibiotic and anti-fungal prophylaxis
- Hypoglycaemia treatment
- Coagulopathy treatment: IV vitamin K, FFP
Renal failure: Haemofiltration and nutritional support
Surgical: transplantation
10
Q
Complications of liver failure
A
infection, coagulopathy , hypoglaecaemia,
hepatorenal syndrome, cerebral oedema
11
Q
Prognosis of liver failure
A
Childs Pugh score
12
Q
Mallory Weiss tear
A
Persistent vomiting/retching causes hematemesis via an oesophageal mucosal tear.
Vomiting ALWAYS precedes bleeding
13
Q
Mallory Weiss epidemiology
A
Account for around 10% of cases presenting with upper GI bleed
14
Q
Mallory Weiss Aetiology
A
Most occur after a sudden rise in intra-abdominal pressure or transmural pressure gradient across the gastro-esophageal junction. This induces a tear and subsequent GI bleeding.
Risk factors:
Alcohol
Hiatal hernia
Retching, vomiting, straining
15
Q
Mallory Weiss history and examination
A
Commonly presents with hematemesis after an episode of forceful or long-term vomiting, retching, coughing, or straining.
melena
light-headedness
syncope
abdominal pain
Examination is usually unremarkable (May have postural drop due to blood loss)
16
Q
Mallory Weiss Investigations
A
Blood:
- FBC (to evaluate the extent of blood loss)
- U&Es (to evaluate the degree of volume loss)
- Clotting screen if coagulopathy suspected
- Pregnancy test
- Endoscopy is diagnostic and can be therapeutic (shows linear laceration at the gastro-esophageal junction, perform within 24h to maximise diagnostic efficiency)
17
Q
Mallory Weiss Management
A
In 80-90% of patients, haemorrhage stops spontaneously and re-bleeding is rare.
Monitor intravascular volume and stabilize if significant hypovolaemia.
Correct coagulopathy if present.
Uncontrolled haemorrhage usually responds to endoscopic injection clipping, and electrocoagulation.
Surgery is rarely required in the case of a bleeding artery at the base of the tear.
18
Q
Nasogastric tube insertion
A
Tube that is passed through the nose and down through the nasopharynx and esophagus into the stomach.
19
Q
NG tube indications
A
- Aspiration of gastric contents for diagnostic (GI haemorrhage) or therapeutic purposes (Bowel obstruction, ileus, sepsis)
- Intra or postoperatively where ileus may be expected to occur, or to facilitate surgery in laparoscopic procedures where a decompressed stomach is needed
- Preoperatively to decompress the stomach to reduce risk of aspiration
- Administration of drugs, enteral feeding
20
Q
Ileus
A
Lack of movement somewhere in the intestine that leads to a build up and potential blockage of food material
21
Q
NG tube insertion complications
A
Trauma Bleeding Infection Vomiting Misplacement of tube Blockage of tube Aspiration of gastric contents risk
22
Q
Non-alcoholic Fatty Liver Disease (NAFLD)
A
Results from fat deposition in the liver.
The hepatic manifestation of the metabolic syndrome ->3 out 5 of obesity, hypertension, diabetes, hypertryglyceridemia, hyperlipidemia
Spectrum of disease ranging from: Steatosis (fatty liver), steatohepatitis,
Fibrosis, and Cirrhosis.
23
Q
NASH Epidemiology
A
Very common and increasing in incidence due to rising obesity rates.
24
Q
Aetiology of NASH
A
-Associations: Obesity and diabetes, parenteral nutrition, short bowel syndrome, hyperlipidemia, drugs (amiodarone, tamoxifen)
Insulin resistance plays a key role and is linked to obesity.
Insulin resistance causes the accumulation of fat and hepatocyte injury. Inflammation of the hepatocytes leads to fibrosis and eventually, cirrhosis in some individuals.
25
NASH history
Most cases are asymptomatic and discovered because of abnormal liver function tests
Occasionally cases present with complications related to cirrhosis
26
Cirrhosis History
Early non-specific symptoms: anorexia, nausea, fatigue, weakness, weight loss
Symptoms caused by decreased synthetic function of liver: easy bruising, abdominal swelling, ankle oedema, leukonychia
Symptoms caused by decreased metabolic (detoxification) function of liver: Jaundice, confusion, amenorrhea
Portal hypertension: abdominal swelling, haematemesis, PR bleeding or malaena
27
NASH Examination
```
Stigmata of chronic liver disease:
Asterixis (liver flap)
Bruises
Clubbing
Dupuytren's contracture
Erythema
```
Hepatomegaly
28
NASH Investigation
LFT:
Increase in liver enzymes
Generally in NASH:
Increase in ALT and sometimes AST
Generally in Alcoholic fatty liver disease:
Increased AST and AST:ALT >2
Imaging studies: USS, CT, MRI to look for fatty infiltrates
Biopsy: To diagnose and assess the severity of the disease (Liver with more than 5% fat content is abnormal)
Histopathologic changes: Mallory Denk bodies
29
NASH Prognosis
Steatosis has a very low risk of progression to chronic liver disease.
NASH progresses to cirrhosis in 10-15% of cases over 8 years.
Patients with cirrhosis due to NAFLD generally have a better survival rate than patients with cirrhosis due to alcoholic liver disease.
30
NASH Management
Aim of management is to reduce progression of NAFLD and to reduce risks of cardiac and liver related mortality.
- Reverse factors that contribute to insulin resistance: Healthy diet, active lifestyle, medication that controls blood glucose
- Advise on limiting alcohol intake
- currently no specific drug licensed for treatment
31
NASH complications
Portal hypertension with ascites
Encephalopathy
Variceal haemorrhage
Hepatocellular carcinoma
Hepatorenal syndrome
32
Acute Pancreatitis
Acute inflammatory process of the pancreas.
Mild- minimal organ dysfunction and uneventful recovery
Severe- Organ failure and complications such as necrosis, abscess or pseudocyst
33
Acute pancreatitis aetiology
Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation.
Causes: I GET SMASHED
```
Idiopathic
Gallstones
Ethanol
Steroids
Mumps virus
Autoimmune diseases
Scorpion bites
Hypertryglyceridemia and hypercalcaemia
ERCP
Drugs (azathioprine, valproate, thiazide, steroids)
```
34
Pancreatic acinar cells
Functional unit of the exocrine pancreas. Synthesizes, stores, and secretes digestive enzymes.
35
Acute pancreatitis history
Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement)
Anorexia, nausea, vomiting
May be history of gallstones or alcohol intake.
36
Acute pancreatitis epidemiology
Common
peak age 60
Males: alcohol
Females: Gallstones (fat, female, fertile, forty)
37
Acute Pancreatitis Examination
```
Epigastric tenderness
fever
shock
tachycardia
tachypnoea
Decreased bowel sounds due to ileus
```
If severe and hemorrhagic -> Turners sign and Cullen's sign
38
Acute Pancreatitis
| Investigation
```
BLOODS
Increased amylase
FBC (increased WCC)
Hypocalcaemia
LFT
```
USS: gallstones or biliary dilatation
AXR: Exclude other causes. Psoas shadow may be lost
CT scan: inflammation, necrosis, pseudocyst
39
Acute Pancreatitis Management
Medical:
- fluid and electrolyte resuscitation
- urinary catheter
- NG tube if vomiting
- analgesia and blood sugar control
- early HDU or intensive care support
- enteral feeding over parenteral
- antibiotics if infective pancreatic necrosis develops
ERCP and sphincterotomy:
For gallstone pancreatitis, cholangitis, jaundice, or dilated common bile duct, ideally within 72 hours
Early detection and treatment of complications
40
Acute Pancreatitis complications
Local: Pancreatic necrosis, pseudocyst, abscess
Systemic: Sepsis, ARDS, DIC
Long term: Chronic pancreatitis
41
Acute Pancreatitis
| Prognosis
80% run milder course (5% mortality)
20% run fulminating course with high mortality
(Infected pancreatic necrosis associated with 70% mortality)
42
Chronic Pancreatitis
Chronic inflammatory disease of the pancreas characterised by irreversible changes to structure (atrophy, fibrosis, calcification) leading to impaired endocrine and exocrine function.
43
Chronic pancreatitis aetiology
Alcohol 70%
Idiopathic 20%
Rare: Recurrent acute pancreatitis, cystic fibrosis
44
Chronic pancreatitis epidemiology
Mean age 40-50 in alcohol abuse
45
Chronic pancreatitis history and exam
- Recurrent severe epigastric pain
- radiating to back
- relieved by sitting forward
- can be exacerbated by drinking alcohol or eating
- weight loss, bloating, pale smelly stool (steatorrhea) due to pancreatic insufficiency (trouble absorbing food and fat)
Tenderness in epigastric region
weight loss
malnutrition (deficiency in fat soluble vitamins A,D,E,K)
46
Chronic pancreatitis Invesitgations
Bloods:
- increased glucose may indicate endocrine dysfunction
- amylase and lipase are usually normal
ERCP or MRCP:
Early changes-> main ductal dilatation and stumping of branches
Late changes-> chain of lake appearance
AXR: pancreatic calcification may be visible
CT: pancreatic cysts
Faecal elastase
47
Chronic pancreatitis management
General:
Treatment is symptomatic and supportive - dietary advice, abstinence from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacement (creon),
Chronic pain management
Endoscopic therapy: sphincterotomy, stone extraction, etc. (remove stones)
Surgical: Optional if medical treatment fails
48
Chronic pancreatitis complications
Local: pseudocyst, biliary duct stricture, pancreatic ascites, pancreatic carcinoma
Systemic: Diabetes, steatorrhea, reduced QOL, chronic pain syndromes, dependence on strong analgesics
49
Chronic pancreatitis prognosis
Difficult to predict as pain may improve, stabilise, or worsen
Surgery may improve symptoms in 60-70%
Life expectancy can be reduced by 10-20 years
50
Peptic ulcer disease
Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin.
51
Peptic ulcer disease aetiology
Imbalance between damaging action of acid and pepsin and mucosal protective mechanism.
Very strong association with H. pylori infection and NSAID use
Rare: Zollinger-Ellison syndrome (tumours form which secrete gastrin and lead to increase in acid)
52
Peptic ulcer disease epi.
Common
| more common in males
53
Peptic ulcer disease history and exam
Epigastric pain relieved by antacids
If worse soon after eating food, gastric
If worse several hours after eating food, duodenal
May present with haematemesis and malaena
May be no physical findings
Epigastric tenderness
Anaemia
54
Peptic ulcer disease Investigations
Bloods: FBC (anaemia), amylase (to exclude pancreatitis), cross match if actively bleeding
Secretin test (in patients suspected of Zollinger- Ellison syndrome: IV secretin causes a rise in serum gastrin in ZE patient but not controls)
Endoscopy:
-4 quadrant gastric ulcer biopsy to rule out malignancy (duodenal ulcer do not need biopsy)
Rockall scoring for severity after GI bleed (less than 3 has good prognosis, greater than 8 have a high mortality)
Testing for H. pylori:
C-Urea breath test
Stool antigen test
Serology
55
Peptic ulcer disease Management
Acute:
Resuscitation if perforated or bleeding (IV colloids/crystalloids), vital sign monitoring, endoscopic/surgical treatment
Endoscopy:
Haemostasis by injection sclerotherapy, laser, or electrocoagulation
Surgery:
If bleeding cannot be controlled
H. Pylori eradication
If not associated with H. pylori: PPi or H-2 antagonists + stop NSAID use
56
Patients with acute upper GI bleeding
Should be treated with IV PPI (omeprazole) at presentation until the cause of the bleeding is confirmed.
Patients with actively bleeding ulcers or ulcers with high-risk stigmata should continue IV PPI.
Switch to oral PPI if there is no rebleeding within 24 hours.
57
H. Pylori eradication
triple therapy for 1-2 weeks
```
One PPI (omeprazole)
2 antibiotics (clarithromycin and amoxicillin)
```
58
Peptic ulcer disease
| Complications and Prognosis
Rate of complication is 1% per year (haemorrhage, perforation, obstruction/pyloric stenosis)
Overall lifetime risk is 10%
generally good prognosis
59
Gastritis
Irritation and inflammation of the stomach lining
Most common causes: H. Pylori, NSAIDs, alcohol, stress, autoimmune
Investigation: Gastritis is suspected when people complain of pain and discomfort in the upper part of the abdomen. Biopsy and endoscopy.
Treatment depends on aetiology:
- H-pylori eradication therapy
- reduction in NSAIDs or alcohol exposure
- symptomatic therapy with h2 antagonists and PPIs
If untreated progression to gastric carcinoma and lymphoma
60
Features of upper GI malignancy that require urgent endoscopy
```
GI bleeding
anaemia
early satiety
unexplained weight loss
progressive dysphagia (difficulty)
odynophagia (pain)
persistent vomiting
```
61
Perianal abscess
Thought to arise due to obstruction and infection within an anal gland and subsequent spread of infection into the adjacent tissue space. (E. coli and enterococci are common)
History: severe, perianal pain, worse sitting, lying supine, or bowel motions
Sometimes perianal pus discharge
Examination: tachycardia may be present, exam of anus reveals tender, fluctuant swelling in the perianal region with redness of overlying skin, DRE is not possible cause of pain
Investigation: Inflammatory markers
Treatment: Surgical drainage
62
Perianal fistula
Most anal fistulae present initially as anorectal abscesses.
It is an abnormal tract or cavity communicating between the skin and the rectum or anus.
Surgical treatment, obliterate internal fistulous opening
63
Peritonitis
Inflammation of the peritoneum, the membrane that lines the abdominal cavity and its organs.
1. Primary
2. Secondary
64
Primary Peritonitis: Spontaneous bacterial peritonitis
Occurs in patients with ascites and is thought to be caused by bacterial translocation into the peritoneal cavity in the setting of:
1. immune system dysfunction
2. altered portal circulation
3. abnormal gut motility
- Patients are commonly minimally symptomatic but may present with abdominal pain, fever, vomiting, altered mental status, GI bleeding
- Investigation: Paracentesis, peritoneal lavage, abdominal imaging
- defined as ascitic fluid absolute neutrophil count >250 cells/mm^3
- treatment: antobiotics and albumin
- complication: renal dysfunction
65
Secondary Peritonitis
A clear site of origin is identified (perforated viscus, external penetrating injury, presence of foreign body)
66
Most frequent encountered bacterial infection in patients with cirrhosis
Spontaneous bacterial peritonitis
67
Pilonidal sinus
Small hole or tunnel in the skin, usually at the top of the cleft between the buttocks.
Most commonly occur in young adults, more men than women, and people with a lot of body hair and overweight
May be asymptomatic or may become infected. This will cause pain and swelling and abscess full of pus to develop.
Treatment:
Minimal disease-> hygiene, keep area hair free
Abscess-> drained
Surgery: Wide excision or excision and primary closure
68
Portal hypertension
Increased PB within the portal venous system and defined as an increase in the pressure gradient between the portal veins and the the hepatic veins (>5mmHg)
69
Portal Hypertension Pathophysiology
Portal pressure depends on portal blood flow and vascular resistance.
A rise in portal pressure leads to the development of collaterals to carry blood from the portal system to the systemic circulation.
Collaterals occur at specific sites:
1. Oesophagus (varices)
2. Anal canal (varices)
3. Falciform (umbilical varices)
4. Abdominal wall and retroperitoneum
Leads to dilated cutaneous veins, varices, splenomegaly, ascites, small intestine mucosal oedema (malabsorption)
70
Portal hypertension aetiology
Prehepatic cause: Portal vein occlusion
Intrahepatic: commonest cause -> cirrhosis from chronic liver disease
Posthepatic: Hepatic vein occlusion (budd-chiari)
71
Portal Hypertension Investigation
Bloods
FBC (anaemia, low platelets in hypersplenism)
Abdominal USS: splenomegaly, collateral veins
MRI: liver lesions
GI endoscopy: Varices
Liver biobsy
72
Management of portal hypertension
Emergency management of bleeding varices
-> variceal banding (endoscopic ligation technique)
Surgical portosystemic shunting
Liver transplantation
Primary prophylaxis: Beta blockers (splanchnic vasoconstriction and reduction of cardiac output)
73
Primary biliary cirrhosis
A chronic inflammatory liver disease involving progressive destruction of intra-hepatic bile ducts, leading to cholestasis and, ultimately, cirrhosis.
74
Cholestasis
Reduction or stoppage of bile flow
75
Primary biliary cirrhosis aetiology and epi.
unknown
autoimmune is likely
1-2 in 10,000
more women than men (9:1)
76
PBC history and exam
Incidental finding on blood test (increased alkphos & cholesterol)
Insidious onset
Fatigue, weight loss, pruritus
discomfort in RUQ
May present with complication of liver decompensation (jaundice, ascites, variceal bleeding)
Early: no signs
Late: Jaundice, sctrach marks, xanthomas, hepatomegaly, ascites, palmar eythema, clubbing, spider naevi
77
Associated conditions of PBS
Sjogrens syndrome (dry eyes and mouth)
athritis
raynaud phenomenon
autoimmune thyroid disease
78
PBC Investigations
Blood: LFT (+AlkPhos, +GGT, +AMA, +IgM, +cholesterol)
USS: Exclude extra-hepatic biliary obstruction
Liver biopsy: Chronic inflammatory cells and granulomas around intra-hepatic bile ducts, destruction of bile ducts, fibrosis, and regenerating nodules of hepatocytes.
79
Primary sclerosing cholangitis
Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intra-hepatic and extra-hepatic bile ducts.
80
Primary scleosing cholangitis aetiology and epi.
Unknown.
Close association with IBD, especially UC
2-7 in 100,000
Presents between 25-40
81
PSC History and exam
Asymptomatic
Diagnosed with persistently raised alkphos
Intermittent jaundice, RUQ pain, puritus, weight loss, fatigue
May have acute cholangitis: fever, rigors
No signs or evidence of jaundice, hepatospenomegaly ,etc.
82
PSC Investigations
Blood
LFT: (+alkPhos, +GGT)
Serology: Immunoglobulin levels (pANCA present in 70%)
ERCP: Stricturing and interspersed dilatation of intrahepatic and extrahepatic bile ducts
MRCP: non invasive
Liver biopsy: Confirms diagnosis and allows staging of disease
83
Rectal prolapse
Prolapse of the rectum through the anus.
Most often occurs in elderly females.
Presentation: Recurrent rectal prolapse on staining that this time fils to reduce spontaneously
Exam: Non-tender, oedematous, circumferential, full thickness rectal tissue protrudes through the anal canal
Unlike prolapsed piles, a rectal prolapse looks like a complete ring with a central orifice
May present with minor bleeding
Management: reduce rectal prolapse, stool softener, will probably happen again, avoid straining, operative repair
84
Ulcerative colitis
Relapsing and remitting inflammatory disorder of the large bowel.
Classification: Location
Mild, Moderate, Severe
Presents at age 15-30
85
Ulcerative Colitis
```
Mucosa and submucosa
Starts distally (rectum) and spreads proximally
Continuous inflammation
Pseudopolyps
BLOODY DIARRHOEA always present
Tenesmus
Pain diffuse/Lower abdominal pain
Relapse/remitting (well between attacks)
P-anca positive
Increased risk of PSC, CRC, cholangiocarcinoma -> surveillance colonoscopy
```
86
EXTRA GI features of IBD
```
Aphthous mouth ulceration
Erythema nodusum
Pyoderma gangrenosum
Episcleritis/scleritis/anterior uveitis
Arthritis
```
87
Crohns disease
Non-caseating granulomas
Transmural
Any part of the GI tract, esp. terminal ileum and AC
Skip lesions
Ulcers, strictures, perianal abscesses, fistulae
Diarrhoea (Not blood usually)
Pain diffuse/RLQ
Weight loss/ systemically unwell more likely
p-anca negative
88
Diagnosis of UC and Crohns
Stool sample
(Infectious? Faecal calprotectin - IBS?)
Bloods: FBC, iron studies, folate, B12, LFT, U and E, CRP, ESR, Auto-antibodies
Imaging: AXR, Ct abdomen, MRI abdo/pelvis, double contrast barium enema
Flexible sigmoidoscopy/colonoscopy and biopsy
89
Wilson's disease (hepatolenticular degeneration)
Autosomal recessive disorder characterized by decreased biliary excretion of copper and accumulation in liver and brain, especially basal ganglia.
90
Wilson's disease
| Aeti. and epi.
Mutation in gene coding for a copper transporting ATPase in hepatocytes.
Excess copper damages hepatocyte mitochondria, causing cell death and release of free copper into plasma, which is then deposited in other tissues.
prevalence 1 in 30,000
carrier 1 in 100
liver disease presents in kids >5 yrs
Neurology in adults
91
Wilson's disease
| History and exam
Liver: Hepatitis, liver failure or cirrhosis, jaundice, easy bruising
Neuro: Dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, ataxia
Psychiatry: Personality change, conduct disorder, psychosis
Liver: Jaundice, ascites, gynaecomestia
Neuro: as above
Eyes: Kayser- Fleischer ring and sunflower cataract
92
Wilson's Investigation
Blood
LFT (+AST, ALT, ALKPHOS)
Serum caeruloplasmin and copper (low, but may provide false negative as it is an acute phase protein)
24 Hour urinary copper level increased
Liver biopsy: Increased copper content
Genetic analysis: difficult
93
UC management
Acute Exacerbation:
IV rehydration, IV corticosteroids, antibiotics, bowel rest, parenteral feeding may be necessary, and DVT prophylaxis. Monitor vital signs and fluid balance.
Mild disease: Oral or rectal 5-aminosalicylic acid derivates
Moderate disease: Oral steroids and oral 5-asa. Immunosuppression with azathioprine, cyclosporine, inlfiximab, 5-mercaptopurine
Advice: Patient education and support. Treatment of complications. Regular colonoscopic surveillance.
Surgical: Indicated for failure of medical treatment, presence of complications , or to prevent cancer.
Proctocolectomy with ileostomy or an ileo-anal pouch formation.
94
UC Investigation
Bloods: FBC (-Hb, +WCC)
Increased CRP and ESR
Stool: Culture as infectious colitis is differential diagnosis.
AXR: Rule out toxic megacolon
Flexible sigmoidoscopy or colonoscopy: determines severity, histological confirmation , detection of dysplasia
Barium enema: Pseudocyst, colon has leadpipe appearance
95
UC Aetiology
Positive family history of IBD (15%)
| Associated with increase in serum pANCA and PSC
96
Viral Hepatitis
3 main symptoms apply to all hepatitis:
Fever
Jaundice
Raised ALT and AST
97
Hepatitis A
```
Fecal oral transmission
Travelers
Acute
vaccination
Management: Supportive and avoid alcohol
```
98
Hepatitis E
Faecal oral
epidemics
Very bad for pregnant women (fulminant hepatitis)
Supportive management
99
Hepatitis B
sexual contact, blood, vertical transmission
Prodrome: flu-like, rash, lymphadenopathy
Acute: Nausea, RUQ pain, anorexia, jaundice
Outcome: 90% completely recover 10% develop chronic infection
Management: Acute (symptom supportive) and chronic (peginterferon alpha and tonofovir)
100
Risk factor for hepatocellular carcinoma
Hepatitis B and C
101
Hep C
Parenteral route transmission
(sex and vertical transmission uncommon)
acute and chronic (80% develop chronic)
Acute management: supportive
Chronic management: Interferon and ribavarin
102
Hep D
Can only happen if infected with hep b
103
Volvulus
Twisting of the small or large bowel around its mesenteric axis.
104
Volvulus aetiology
Risk factors: chronic constipation and high fiber diet
Most common location: Sigmoid and Caecum (most mobile segments)
Can lead to obstruction and
torsion and occlusion of mesenteric vessels resulting in ischaemia and necrosis (emergency)
105
Sigmoid and caecal volvulus
Sudden onset abdominal pain, constipation, nausea, and vomiting
Pain is continuous with overlying colicky pain during peristalsis
Abdomen distended, tympanic, tender to palpation.
may have fever, tachycardia, hypotension
106
Sigmoid volvulus
Coffee bean sign
107
Caecal Volvulus
Presents with features of bowel obstruction.
Colicky abdominal pain, vomiting, and abdominal distension.
Looks like embryo
108
Sigmoid volvulus
No ischaemia -> endoscopic reduction -> if fails surgery
Usually occurs in institutionalised elderly
109
caecal volvulus
young population
| surgical
110
Bowel obstruction
Mechanical or functional obstruction of the intestines which prevents the normal movement of products of digestion.
111
Bowel obstruction symptoms
```
abdominal pain
distension
nausea
vomiting
fever
```
Complete obstruction or strangulation is a surgical emergency
Can present atypically in elderly
112
Bowel obstruction investigations
Blood count and lactate
Ct abdomen
Mri
113
Bowel obstruction management
```
IV fluids
Drip and suck
catheter
enemas
stents
surgery
```
