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FINALS > GASTROENTEROLOGY > Flashcards

GASTROENTEROLOGY Flashcards

1
Q

What is Acute Pancreatitis?

A

Leakage of pancreatic enzymes that auto digest the pancreas

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2
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps virus (also Coxsackie B)
AI (e.g. polyarteritis nodosa)
Scorpion stings
Hypertryglyceridaemia/Hypercalcaemia/Hypothermia
ERCP
Drugs
Azothiprine
Mesalazine
Bendroflumethiazide
Furosemide
Valproate
GLP-1 agonists: -tides

OR

PANCREATITIS

Posterior peptic ulcer rupture
Alcohol
Neoplasm
Cholesthiasis,  cholecystectomy, increased calcium
Renal disease
ERCP
Anorexia
Toxins
Incineration
Trauma
Infections
Scorpion stings
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3
Q

What are the symptoms of Acute Pancreatitis?

A 
Severe epigastric pain:
Steady 
Boring
Radiates to back
Relieved by sitting forward
Nausea and vomiting
Weakness
Low-grade fever
Shock due to loss of fluid in peripancreatic third space
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4
Q

What are the signs of Acute Pancreatitis?

A

Low grade fever
Tachycardia
Hypovolaemia due to oedema and fluid shifting-shock
Abdominal tenderness (no guarding or rebound)
Diminished sounds from a localised ileus

Haemorrhage:
Grey turner’s: bleeding into the peritoneum
Cullen’s: methemalbumin formed from digested blood tracks around the abdomen from the inflamed pancreas

Jaundice is rare
Can rarely cause ischaemic (Purtscher) retinopathy causing temporary of permanent blindness

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5
Q

What is the sequalae of pancreatitis?

A
  • Pancreatic fluid collections
  • Psuedocysts
  • Pancreatic abscess
  • Pancreatic necrosis
  • Haemorrhage
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6
Q

What are pancreatic fluid collections?

A

Located on or near the pancreas and lack a wall of granulation or fibrous tissue
May resolve or develop into pseudocysts or abscesses
Aspiration should be avoided in case of infection

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7
Q

What are pancreatic psuedocysts?

A

Result from organisation of peripancreatic fluid collection, may or may not communicate with ductal system
Usually retrogastric
Walled by fibrous or granulation tissue
Within 4 weeks or more

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8
Q

What are pancreatic abscesses?

A

Intra abdominal collection of pus in the absence of necrosis

Result of an infected pseudocyst

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9
Q

What is pancreatic necrosis?

A

May involve parenchyma and surrounding fat
Complications directly linked to the extent
May degrade into vasculatur and cause haemorrhage

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10
Q

What are the investigations for Acute Pancreatitis?

A

Elevated (3x normal range or >1000u/ml) SERUM AMYLASE during first 24 hours
Initially increases 2-6 hours after onset of pain, does not correlate to disease severity
Elevated LIPASE is more specific and sensitive
Abdominal X-RAY
SENTINEL loop: isolated, dilated loop of bowel caused by irritation of the adjacent bowel
COLON CUTOFF: gaseous distention in proximal colon due to narrowing at the splenic fracture
Chest x-ray: left sided exudative pleural effusion
CT and USS: Peripancreatic fluid
Pancreatic calcifications

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11
Q

What is are the severity scores for Acute Pancreatitis?

A

Glasgow score:

PaO2: <8kPa
Age: >55yr
Nuetrophilia: >15x10’/L
Calcium (hypocalcaemia): <2mmol/L
Renal function: Urea >16 mmol/L
Enzymes: LDH >600, AST >200
Albumin: <32g/L
Sugar: Blood glucose >10mmol/L
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12
Q

How is Acute Pancreatitis managed?

A 
IV fluids
Bowel rest
?Parentral nutrition
NG decompression
Abx (controversial)
Analgesia
Surgical debridement if peripancreatic fluid
Surgery/ERCP for gallstones
If infected necrosis 
Radiological drainage
Surgical necrosectomy
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13
Q

What are the complications of acute pancreatitis?

A

Pulmonary complications:

  • Pleural effusions
  • Atelectasis
  • Mediastinal abscess
  • ARDS

Psuedocyst: circumscribed collection of fluid rich in pancreatic enzymes, blood and necrotic tissue located in the lesser sac of the abdomen.

Chronic pancreatitis

Splenic vein thrombosis

Pancreatic cancer if multiple episodes

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14
Q

What is Chronic Pancreatitis?

A

Chronic inflammation of the pancreas affecting endocrine and exocrine function

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15
Q

What causes Chronic Pancreatitis?

A

80% is alcoholism

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16
Q

What are the symptoms of Chronic Pancreatitis?

A
  • Recurrent epigastric pain
  • Constipation
  • Steatorrhoea (symptoms of pancreatic insufficiency usually develop 5-25 years after pain)
  • Flatulence
  • Weight loss
  • Vitamins ADEK deficiency
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17
Q

What are the investigations for Chronic Pancreatitis?

A 
Mildly elevated amylase and lipase (although can be normal)
STOOL ELASTASE (<200mcg/g)
Serum TRYPSINOGEN (<20ng/mL)
Glycosuria
Abdominal X-RAY
MRCP or endoscopic USS
CT for pancreatic calcification
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18
Q

How is Chronic Pancreatitis managed?

A 
Alcohol cessation
Low fat diet
Oral pancreatic enzymes: Lipase before, during and after meals
PPIs
Vitamins ADEK and B12 if alcoholic
Analgesia 
Steroids if AI
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19
Q

What are the complications of Chronic Pancreatitis?

A

Diabetes mellitus-usually after >20 years
Analgesia addiction
Exocrine and endocrine insufficiency
Ductal obstruction

Pseudocyst
Increased risk of pancreatic cancer
Gastric varices

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20
Q

What is the MC Pancreatic Cancer?

A

85% are pancreatic adenocarcinoma

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21
Q

What are the causes of Pancreatic Cancer?

A 
Age
Smoking
Diabetes
Chronic pancreatitis (not alcohol)
Hereditary non-polyposis colorectal carcinoma
MEN
BRCA 2 gene
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22
Q

What are the symptoms of Pancreatic Cancer?

A

Anorexia
Weight loss
VOMITING AFTER MEALS due to GASTRIC OUTLET OBSTRUCTION
Epigastric PAIN and atypical back pain-body and tail tumours
STEATORRHOEA (loss of exocrine function)

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23
Q

What are the signs of Pancreatic Cancer?

A 
Painless jaundice-Head of pancreas tumours
TROUSSEAU'S sign: migratory thrombophlebitis (vessel inflammation due to blood clot)
Diabetes
Palpable gallbladder
Epigastric mass
Hepatosplenomegaly
Lymphadenopathy
Ascites
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24
Q

What are the investigations for Pancreatic Cancer?

A

USS
High-res CT
show pancreatic pass with dilated biliary tree and hepatic metastases

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25
Q

How is Pancreatic Cancer managed?

A

<20% are suitable for surgery at diagnosis
Whipple’s resection: PANCREATICODUODENECTOMY is performed for resectable lesions in the head of the pancreas
Adjuvant chemotherapy
ERCP with stent palliative

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26
Q

What is an Insulinoma?

A

90% are benign pancreatic B islet cell tumours

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27
Q

What causes Insulinomas?

A

Sporadic

MEN-1

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28
Q

What are the signs of Insulinomas?

A

Whipple’s triad:

  • Symptoms associated with fasting or exercise
  • Recorded hypoglycaemia with symptoms
  • Symptoms relieved by glucose
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29
Q

What are the investigations for Insulinomas?

A

Screening test: HYPOGLYCAEMIA and INCREASED PLASMA INSULIN

Suppressive tests: give INSULIN and measure C-PEPTIDE, NO SUPPRESSION of c-peptide from exogenous insulin
CT/MRI + endoscopic USS

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30
Q

How are Insulinomas managed?

A

Excision

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31
Q

What are Glucagonomas?

A

Rare tumour of alpha cells of the pancreas, usually CANCEROUS and METASTATIC

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32
Q

What causes Glucagonomas?

A

Sporadic

MEN-1

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33
Q

What are the signs of Glucagonomas?

A
  • Overproduction of glucagon leading to INCREASED BLOOD GLUCOSE levels including gluconeogenesis and lipolysis
  • NECROLYTIC MIGRATORY ERYTHEMA (NME) is presenting problem in 70% of cases:
    Erythmatous blisters and swelling across friction areas (e.g. abdomen, buttocks, perineum and groin).
  • DIABETES MELLITUS
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34
Q

How are Glucagonomas managed?

A

Treat octerotide, somatostatin analog which inhibits glucagon release
Doxorubicin and streptozotocin (chemotherapies) selectively damage alpha cells
Surgical resection

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35
Q

What is Zollinger-Ellison syndrome?

A

Excessive levels of GASTRIN resulting from a gastrin secreting ADENOMA (GASTRINOMA) of the pancreas (or duodenum)
60% are malignant

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36
Q

What causes Zollinger-Ellison?

A

MEN-1

Sporadic

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37
Q

What are the signs of Zollinger-Ellison Syndrome?

A

Multiple gastroducodenal ulcers

  • Abdominal pain
  • Dyspepsia

Chronic diarrhoea due to inactivation of pancreatic enzymes

Malabsorption

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38
Q

What are the investigations for Zollinger-Ellison?

A

Fasting gastric levels

Secretin stimulation test

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39
Q

How is Zollinger-Ellison managed?

A

High-dose PPIs e.g. Omeprazole 60mg/d

Octreotide: synthetic somatostatin

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40
Q

What is Diverticulosis?

A

HERNIATION of colonic MUCOSA through the muscle wall at a TAENIA COLI (where vessels pierce the muscle to supply the mucosa) often due to LACK OF DIETRY FIBRE

95% are in the sigmoid colon and the rectum is spare as it doesn’t have Taenia Coli

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41
Q

What is Diverticular disease?

A

Symptomatic diverticulosis

  • Colicky L sided pain
  • Change in bowel habits
  • Bleeding

treat with high fibre

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42
Q

What is Diverticulitis?

A

When a diverticular becomes inflamed and infected

  • LIF pain and tenderness
  • Anorexia
  • N+V+D+Flatulence
  • Infection: pyrexia, raised CRP and WCC
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43
Q

How is Diverticulitis managed?

A

Mild: Oral Abx

Severe: IV Abx (Cephalosporin C. Dif and metronidazole)

Haartmann’s if perforated: temporary colonostomy and partial colectomy

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44
Q

What are the complications of Diverticulitis?

A

Haemorrhage

Fistula:

  • Enterocolic
  • Colovaginal
  • Colovesicle

Abscess: swinging fever, boggy rectal mass, drain rectally

Obstruction-strictures

Jejunal diverticulosis is a cause of malnutrition

Perforation: ileus, shock, peritonitis

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45
Q

What investigations should be done in suspected Diverticulitis?

A
  • Abdominal CT
  • Colonoscopy
  • Barium enema
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46
Q

What is the Hinchey Classification?

A

Describes colonic perforation due to diverticulitis

I- Para-colonic abscess
II- Pelvic abscess
III- Purulent peritonitis
IV- Faecal peritonitis

Laproscopic washout and drainage

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47
Q

What are the causes of Mallory-Weiss tears?

A 
Retching 
Vomiting
Coughing
Straining
Chronic hiccoughs 
Brunt 
NG tube

Increased abdominal pressure, large transient increase in transmural pressure across the gastro-oesophageal junction

Acute distention (non-distensible distal oesophagus)

Shearing forcs > transmural pressure gradient, M-W tear and rupture of SUBMUCOSAL ARTERIES

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48
Q

What are Mallory-Weiss tears?

A

Superficial mucosal tear at GOJ or proximal stomach causing RUPTURE OF SUBMUCOSAL ARTERIES

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49
Q

How do Mallory-Weiss tears present?

A

Blood oxidased:

  • Coffee-ground emesis
  • Malena

Systemic Blood loss:

  • Tachycardia
  • HoTN
  • Anaemia
  • Presyncope/syncooe

Rapid non-oxidised blood loss:

  • Haematemesis
  • Haemachetzia
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50
Q

What is Boorhaave’s syndrome?

A

Perforation: of full-thickness rupture posterolateral oesophagus just above the diagraphm

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51
Q

What are the causes of Boorhaave’s?

A

Iatrogenic from endoscopy

Severe vomiting

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52
Q

How does Boorhaave’s syndrome present?

A

Mackler’s triad:

  • Vomit
  • Subcutaneous emphesema
  • Chest pain

Severe retrosternal pain
Respiratory distress

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53
Q

How is Boorhaave’s syndrome managed?

A
  • Group and save
  • CXR- pneumomediastinum
  • CT will show contrast leaking into mediastinum

Surgery if unstable/spontaneous to decompress oesophagus, stop the leak and eradicate pleural and mediastinal contamination

  • Give Abx and antifungals
  • NBM 1-2 weeks insertion of NG tube, TPN or feeding jejunostomy
  • Large-bore chest pain
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54
Q

Where are bowel cancers found?

What surgical intervention is done for them?

A

15% Ascending colon and caecum
Right hemicolectomy with ileo-colic anastomosis

10% Transverse colon
R/L hemicolectomy

5% Descending colon
Left hemicolectomy
colo-colon anastamosis

30% Sigmod colon
High anterior resection + TME (Total Mucosal Excision)
Colorectal anastamosis

40% Rectum
Low anterior resection + low TME
Colorectal anastamosis

Anal Verge
abdominal-perianal excision of rectum with no anastamosis

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55
Q

What are the criteria to refer via the 2 week wait?

A

> 40 + unexplained weight loss + abdominal pain

<50 with rectal bleeding plus any of:

  • abdominal pain
  • change in bowel habits
  • weight loss
  • iron deficiency anaemia

> 50 unexplained rectal bleeding

> 60 iron deficiency anaemia + change in bowel habit

occult blood in faeces (screen everyone 60-74)

rectal abdominal mass

unexplained anal mass or ulcer

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56
Q

What is Duke’s staging?

A

A Tumour confined to mucosa
B Invaded bowel wall
C Lymph metastases
D Distant metastases

(T1+T2/N0 requires no radiation, T4 long corse of R+C)

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57
Q

What are the risk factors for Gastric Cancer?

A 
Blood group A
Gastric adenomatous POLYPS
HY. PYLORI Ulceration (-vely associated with duodenal ulcers)
PERNICIOUS anaemia
SMOKING
Diet: salt, spice, nitrates

M>F ~70-80y/o

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58
Q

How does Gastric Cancer present?

A
  • N&V
  • Dyspepsia
  • Anorexia and weight loss
  • Dysphagia
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59
Q

How is Gastric Cancer investigated?

A

U.GI endoscopy with Biopsy

MOST COMMONLY IN THE CARDIA

SIGNET RING CELLS- CONATIN LARGE VACUOLE OF MUCIN WHICH DISPLACES NUCLEUS TO ONE SIDE

CT to stage

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60
Q

What is Hepatic Encephalopathy?

A

Due to excess AMMONIA and GLUTAMINE in bacterial break down in the gut

Usually Acute

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61
Q

What are the causes of Hepatic Encephalopathy?

A

GI bleed

Infection (SBP)

Constipation

Renal failure

High protein

Low K+

Drugs:
- sedatives
DIURETICS

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62
Q

What are the features of Hepatic Encephalopathy?

A

Confusion, reduced GCS

Asterixis Flap (Arrhytmic -ve myoclonus 2-5Hz)

Constructional Apraxia (can’t draw 5pt star)

Triphasic slow waves EEG

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63
Q

What are the grades of Hepatic Encephalopathy?

A

I-Irratible
II-Confusion and inappropriate behaviour
III-Incoherence and restless
IV-Coma

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64
Q

How is Hepatic Encephalopathy managed?

A

Give Lactulose which increases ammonia secretion and metabolism

Liver transplant

Porto-systemic shunt

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65
Q

What can cause Small Bowel Obstruction?

A 
Adhesions from past surgery
Barbed structures
Hernias
Congenital issues
Gallstone ileus
Caecal volvulus
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66
Q

How does Small Bowel Obstruction present?

A

Vomiting then constipation
Central and mid abdominal pain
Shorter spasms of pain

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67
Q

What is seen on AXR in Small Bowel Obstruction?

A
  • Central gas shadows
  • Valvulae commitantes completely cross the lumen
  • Gas absent in large bowel

Oral gastrografin can detect partial obstructions

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68
Q

What can cause Small and Large Bowel Obstruction?

A

Foreign bodies
Intusseception
Crohn’s strictures
TB

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69
Q

How does Bowel Obstruction present?

A

Vomiting
- Faeculent

Colicky pain

Distention-progresses

Constipation

‘Tinkling’ bowel sounds

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70
Q

What can cause Large Bowel obstruction?

A

Colorectal carcinoma

Diverticular strictures

Constipation

Volvulus

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71
Q

How does Large Bowel Obstruction present?

A

Less likely to vomit, can be faecal

Lower abdominal pain with longer spasms that are more constant

Constipation starts earlier

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72
Q

What is seen on AXR in Large Bowel Obstruction?

A
  • Peripheral gas shadows proximal to the obstruction but none in the rectum
  • Hasutra do not completely cross the lumen
  • Large, dilated loop with air-fluid levels: coffee bean sign
73
Q

What is an Ileus?

A

FUNCTIONAL obstruction due to reduced motility

NO PAIN
NO BOWEL SOUNDS

74
Q

What is a volvulus?

A

TORSION of the colon around MESENTERIC axis

Can cause:
ISCHAEMIA
CLOSED-LOOP OBSTRUCTION

80% are in the sigmoid
Older, chronic, Chagas, Neuromuscular e.g. Parkinson’s or Duchenne’s
Large bowel: rigid sigmoidoscopy and rectul tube insertion

20% Caecum, failure of fixation of the proximal bowel in utero
All ages, adhesions, pregnancy
Small bowel: R hemicolectomy

75
Q

What are Simple Obstructions?

A

one obstructing point with no vascular compromise

76
Q

What are Closed-Loop Obstructions?

A

obstruction at two points (e.g. a sigmoid volvulus, distention with competent ileoceacal valve) forming a loop of grossly distended bowel

Risks perforating >12cm

77
Q

What are Strangualted Obstructions?

A

MESENTERIC ISCHAEMIA
blood supply is compromised and patient is very ill

Sharp, constant, localised pain: peritonism

78
Q

What is Paralytic Ileus?

A

adynamic bowel due to the absence of normal peristalsis

due to:

  • abdo surgery
  • pancreatitis
  • localised peritonitis
  • spinal injury
  • TCAs
79
Q

What is Psuedo Obstruction?

A

Presents as mechanical obstruction but with no cause found

Acute: Oglivie’s syndrome

After pelvic surgery, trama or carcinoma

Treat with neostagmine

80
Q

How is Bowel Obstruction Managed?

A 
Surgery:
- Strangulated
- Closed loop 
- Large bowel
Remove or stent

‘Drip and Suck’

  • NBM
  • Aspirate with NG tube
  • IV fluids
81
Q

What is Oesophagitis and what are the causes?

A

Inflammation of intraabdominal epithelia

GORD
Infection- Candida Albicans, Herpes, CMV
Drugs-Bisphosphonates
Radiotherapy 
Crohn's
Alcohol
82
Q

What is the gradning classification for Oesophagitis?

A

LA

A- One or more mucosal breaks < 5mm
B - Mucosal breaks > 5mm but no continuity across mucosal folds
C- spans across 2 folds but <75% of cicumference
D- mucosal breaks >75% of circumference

83
Q

What are the boundaries of the epiploic foramen of Wisnlow?

A

Communication between peritoneal pouches: opening of lesser sac inter greater sac

Anterior: free border of lesser omentum (with hepatic artery, portal vein and bile duct)

Posterior: IVC

Superior: Caudate process of Liver

Inferior: 1st part of duodenum

84
Q

What is Primary Sclerosing Cholangitis?

A

Progressive cholestasis with bile duct inflammation and strictures (fibrosis)

ASSOCIATED WITH UC: P-ANCA
HLA-DR3

  • Jaundice
  • Fatigue
  • Pruritis
  • RUQ pain

ERCP
Increased risk of cholangiocarcinoma and colorectal cancer

85
Q

What are the side effects of prophylactic antibiotics?

A

Diarrhoea
Psuedomembranous colitis
Thrombocytopaenia

86
Q

What is Primary Biliary Cirrhosis?

A

Interlobular bile ducts are damaged by chronic AI granulomatous inflammation causing obstruction

Progressive cholestasis -> fibrosis -> cirrhosis -> portal HTN

87
Q

How doe PBC present?

A 
Jaundice
Pruritis
Xanthelasma
Hepatosplenomegaly -> clubbing
Fatigue
Malabsorption
Bilirubin
ALP
IGM

Also have renal tubular acidosis -> hyperchloraemic metabolic acidosis

88
Q

What are the antibodies present in PBC?

A

AMA Anti-Mitochondrial Antibodies

SmM antibodies

89
Q

How is PBC managed?

A

Cholestyramine

Fat soluble vitamin supplements

Ursodeoxycolic acid

Liver transplant

90
Q

What are the 3 types of bowel polyp?

A

HAMARTOMATOUS: foetal malfomation resembling neoplasm in normal cells

  • Juvenile polyps
  • Peutx-Jeghers syndrome

NEOPLASTIC

  • Tubular
  • Villous Adenoma
  • Familial Adenomatous Polyposis and Gardner’s syndrome

INFLAMMATORY

  • UC - Psuedopolyps
  • Crohn;s
  • Lymphoid hyperplasia
91
Q

What is Peutz-Jegher’s syndrome?

A

AD mutation of tumour suppressor gene

GI Polyps in SI:

  • Obstruction
  • Intesusseption
  • Bleeds
  • 15x risk of GI cancer

Pigmented lesions:

  • Face
  • Lips
  • Oral mucosa
  • Palms of hands and soles of feet
92
Q

What is Villous Adeonma?

A

Have the potential for malignant transformation

Secrete large amounts of mucous:

  • Secretory diarrhoea
  • Microcytic Anaemia
  • Electrolyte imbalance-hypokalaemia
93
Q

What is FAD?

A

Familial Adenomatous Polyposis

AD- mutation of polyposis coli onco gene

Hundreds of polyps by 30-40 years

Inevitably develop carcinoma - 1% of carcinomas
Risk of duodenal ulcers

94
Q

What is Gardner’s syndrome?

A

FAD with

  • osteomas of skull and mandible
  • retinal pigmentation
  • thyroid carcinoma
  • epidermal cysts on skin
95
Q

What is Hereditary Non-Polyposis Colorectal Cancer?

A

AD 7 mutations in DNA mismatch repair genes

90% end up with colon cancer, usually proximal

Poorly differentiated and highly aggressive
Associated with endometrial caner

Amsterdam criteria:

  • at least 3 FHx
  • at least 3 generations
  • at least 1 <50 y/o
96
Q

What are the intestinal features of Crohn’s disease?

A
  • Non-bloody diarrhoea
  • Weight loss
  • Abdominal pain
  • Mouth to anus most commonly in termial ileum
  • Skip lesions
  • ‘Cobble-stone’
  • Abdominal mass in RIF
  • Megacolon - colonic dilation: proximal bowel dilation
  • ‘Kantor’s string sign’ - long narrowed ileum
  • Bowel obstruction and adhesion
  • Perianal disease: ulcers and fistulae
97
Q

What are the histologic features of Crohn’s disease?

A
  • Inflammation through all layers: mucosa to serosa
  • Increased goblet cells
  • Granulomas
  • Rose-thorn ulcers (barium enema)
98
Q

What are the extra-intestinal features of Crohn’s disease?

A
  • Gallstones secondary to reduced bile acid reabsorption
  • Oxalate renal stones as more Calcium lost in bile and it usually binds Oxalate
  • Arthritis
  • Erethema Nodosum on shins
  • Pyoderma Gangrenosum
  • Osteoporosis
99
Q

What is the antibody present in Crohn’s?

A

Anti-S Cerevisiae Antibody

ASCA

100
Q

What are the pharmacological options for Crohn’s?

A 
Aminosalicylates
Steroids
Immunosuppressants
TNF inhibitors
Abx
Supplements
101
Q

Surgery for Crohn’s

A

Not curative but symptom relief
Indications: fistuals abscesses and strictures
Careful of short bowel syndrome

102
Q

How are mild flare-ups of Crohn’s managed?

A

Symptomatic but systemically well

Prednosolone 30mg/d PO for 1 week then 20mg/d for 4 weeks

103
Q

How are severe flare-ups of Crohn’s managed?

A

IV steroids (Hydrocortisone) and NBM and fluids

Metronidazole

If improving put on oral prednisolone

If not infliximub or adalimumab

104
Q

What are the intestinal features of UC?

A
  • Ileocaecal valve to rectum
  • Bloody Diarrhoea
  • LLQ Pain
  • Tenesmus
  • Loss of haustra
  • Short and narrow colon: drain-pipe
  • Continuous disease
  • Toxic mega colon
105
Q

What are the histological features of UC?

A
  • Contained to submucosa
    Inflammatory cell infilitrate in lamino propria
  • Crypt abscesses formed by migrating neutrophils
  • Goblet cells depleted and reduced mucin
  • Psuedopolyps
  • Red, friable mucosa
106
Q

What are the extra-intestinal features of UC?

A
  • Primary sclerosing cholangitis
  • Uveitis
  • Arthritis
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Osteoporosis
107
Q

What is the antibody present in UC?

A

P-ANCA

108
Q

What are the complications of UC?

A

Higher risk of colorectal cancer

109
Q

How is UC managed?

A 
1st line:
Topical (suppository) aminosalicylate
Topical + oral aminosalicylate 
Oral aminosalicylate
- mesalazine
- sulfasalazine

2nd line:
Steroids: prednisolone
oral/topical

3rd line:
Infliximab-monoclonal antibody against TNF-a

110
Q

What is Hereditary Haemochromatosis?

A

A.R Increased intestinal absorption of iron which builds up in the body and is deposited in joints, the liver, heart, pancreas, adrenal glands and skin

111
Q

What are the features of Hereditary Haemochromatosis?

A

‘Bronze Diabetes’-hyperpigmentation due to melanin deposition

Grey skin

Cardiomyopathy

Diabetes Mellitus Type 2

Chronic liver disease: cirrhosis and hepatomegaly

Gonadal failure: erections, hypogynadism

Arthralgia: 2nd and 3rd MCP

Knee psuedogout: joint xrays show chondrocalcinosis

Hypoaldosteronism

112
Q

How is Hereditary Haemochromatosis managed?

A

Venesect ~1unit/1-3 weeks until ferritin <50ug

Low iron diet

113
Q

How is Hereditary Haemochromatosis investigated?

A

Transferrin saturation
>55% in males
>50% in females

114
Q

What is the HLA association in Hereditary Haemochromatosis?

A

HLA-A3

115
Q

What is Wilson’s disease?

A

A.R

Accumulation of Copper in Liver and Organs

Ceruloplasmin is low and so reduced excretion into bile

116
Q

What are the features of Wilson’s disease?

A
  • Liver disease
  • Kayser-Fleischer rigns-Cu ring in iris
  • Haemolysis -> haemolytic anaemia
  • Blue nails
  • Renal Tubular Acidosis-Faconi syndrome
117
Q

What are the neurological features of Wilson’s disease?

A 
Build up in Basal Ganglia:
- Tremor
- Dysarthia
- Dysphagia
- Dyskinesia
- Dystonias
Affects mood and cognition
118
Q

How is Wilson’s disease managed?

A

Penicillamin (may cause membranous nephropathy)

Trietine hydrochloride

119
Q

What is a-1 antitrypsin deficiency?

A

a-1 antitrypsin is protective against elastase (e.g. from neutrophils)

Affects lung and liver

120
Q

What are the features of a-1 antitrypsin deficiency?

A
  • Dyspnoea
  • Cirrhosis and hepatocellular CA
  • Cholestatic jaundice in children
121
Q

How is a-1 antitrypsin deficiency managed?

A

Transplant, volume reduction

IV a1-ATP concentrates
Physio and bronchodialtors

122
Q

What are the Pre-Hepatic causes of Jaundice?

A

Acquired
Inherited
Congenital

123
Q

What are the Acquired causes of Pre-Hepatic jaundice?

A
  • Mechanical
  • Immune
  • Drugs
  • Acquired membrane defects
  • Infection
  • Burns
124
Q

What are the Inherited causes of Pre-Hepatic jaundice?

A
  • Hb abnormalities
  • Metabolic defects
  • RBC membrane defects
    Spherocytosis
    Eliptocytosis
125
Q

What are the Congenital causes of Pre-Hepatic jaundice?

A

Dubin Johnson

Gilbert’s

Crigler-Najar

126
Q

What is Dubin Johnson syndrome?

A

A.R MRP2 defect resulting in defective hepatic extraction of blirubin

Black, glossy liver

127
Q

What is Gilbert’s syndrome?

A

A.R

UDP-Glucuronyl transferase deficiency leading to defective conjugation of bilirubin

Bilirubin increases on fasting

128
Q

What is Crigler Najar syndrome?

A

Type 1

Type 2

129
Q

What are the causes of Hepatocellular jaundice?

A 
Congenital (Gilbert's, Crigler Najar) 
Tumours: metastases/hepatocellular
Inflammation
Cirrhosis
Drugs
130
Q

What are the Congenital causes of Hepatocellular jaundice?

A

(Gilbert’s, Crigler Najar)
Rotor syndrome
A.R, defect in storage and uptake of bilirubin

131
Q

What are the Inflamamtory causes of Hepatocellular jaundice?

A 
AI Hepatitis
Viral:
- Hepatitis ABCDE
- EBV
Alcohol
Wilson's
Hereditary haemochromatosis
a1-antitrypsin deficiency
132
Q

What are the Cirrhotic causes of Hepatocellular jaundice?

A

Alcohol

Metabolic

133
Q

What are the causes of Post-Hepatic jaundice?

A

Intrahepatic

Extrahepatic

134
Q

What are the causes of Intrahepatic Post-Hepatic jaundice?

A

(Drugs, Cirrhosis, Hepatitis)

Primary Billiary Cirrhosis

135
Q

What are the causes of Entrahepatic Post-Hepatic jaundice?

A
  • Pancreatitis
  • Biliary stricture
  • Gallstones
  • Primary Sclerosing cholangitis
  • Carcinoma
    Head of pancreas, Liver mets, Porta-hepatic lymoh nodes, Cholangiocarcinoma, Ampulla
136
Q

What is Budd-Chiari syndrome?

A

Hepatic vein thrombosis due to underlying haematological/pro-coagulant condition

Severe abdominal pain of sudden onset with ascites and tender hepatomegaly

Polycythemia Rubra vera: bone marrow neoplasm

Thrombophilia: Protein C+S deficiency, protein C resistance, anti-thrombin II deficiency

Pregnancy
COCP

137
Q

What are the causes of Cirrhosis?

A 
V: Budd Chiari
I: Hep B and C
T
A: Hepatitis, PSC, PBC
M: Non-Alcoholic Fatty Liver
I: 
N
D
I
C
G: Hereditary Haemochromatosis, a1 anti, Wilson's
138
Q

What is Liver Cirrhosis?

A

Liver necrosis leading to nodular fibrosis and regeneration which is irreversible

139
Q

What are the 3 main impacts of Liver Cirrhosis?

A
  • Increased resistance to blood flow causing PORTAL HYPERTENSION
  • REDUCED liver FUNCTION
  • Hepatocellular CARCINOMA
140
Q

What is the impact of Portal Hypertension?

A

Blood backs up in the venous system

  • Oesophageal varices -> U GI BLEED
  • Enlarged Periumbilical veins -> CAPUT MEDUSAE
  • Congested and enlagred spleen -> SPLENOMEGALY -> PANCYTOPENIA
  • Increased hydrostatic pressure in the abdominal capillaries causes increase in vasodilators causing splanchnic vasodialtion which reduces effective volume in the kidneys activating RAAS further increasing the hydrostatic pressure (HEPATORENAL SYNDROME)
    This forces fluid out of the capillaries into the body (OEDEMA) and peritoneal cavity ASCITES
141
Q

What is the impact of Reduced Liver function?

A
  • Reduced albumin synthesis reduces oncotic pressure and fluid leaks into tissues causing ASCITES, ODEMA and LEUCONYCIA (white nails)
  • Reduced clotting factors leads to BRUISING
  • Reduced toxin removal causes NH3 build up causing ENCEPHALOPATHY
  • Reduced Bilirubin conjugation, reduced secretion into bile so bilirubin >40-50 causing JAUNDICE AND SCLERA ICTERUS
142
Q

What is the Child-Pugh score?

A

Prognosis of Cirrhosis

  • Bilirubin
  • Albumin
  • PTT
  • Ascites
  • Encephalopathy
143
Q

What is the Model for End-Stage Liver Disease?

A
  • Bilirubin
  • Creatinine
  • INR
144
Q

What are the two types of Hepatorenal syndrome?

A

Type 1:

  • Rapid
  • Poor prognosis (< 2 weeks)
  • Doubling of serum creatinine >221
  • Halving of Creatinine clearance

Give TERLIPRESSIN

Type 2:

  • Slow
  • Poor prognosis but live longer (<6 mo)

Make TRANSJUGUALAR INTRAHEPATIC PORTOSYSTEMIC SHUNT

145
Q

What is Non-Alcoholic Fatty Liver Disease?

A

Caused by obesity, hyperlipidaemia, DMT2, sudden starvation

Spectrum from STEATOSIS (fat in liver) to STEATOHEPATITIS (fat and inflammation) to FIBROSIS+CIRRHOSIS

Features are Hepatomegaly and ALT>AST but usually asymptomatic and found incidentally

To test for it to ENHANCED LIVER FIBROSIS BLOOD TEST

  • Hyaluronic acid
  • Procollagen III
  • Tissue inhibitor of metalloproteinase
146
Q

What is the fluid composition of Ascites?

A

TRANSUDATE

147
Q

What are the Primary Liver Tumours?

A

MALIGNANT:

  • Hepatocellular Carcinoma (most common)
  • Angiosarcoma
  • Hepatoblastoma

BENIGN:

  • Cysts
  • Haemangioma
  • Adenoma common in anabolic steroids, preg and ocp
  • Fibrma
148
Q

What are the causes of Hepatocellular Carcinoma?

A

Cirrhosis (causes of)
Male
Diabetes

149
Q

How does Hepatocellular Carcinoma present?

A
  • Jaundice
  • Ascites
  • RUQ pain
  • Hepatomegaly-irregular edge
  • Pruritis
  • Splenomegaly
  • Anorexia

USS

150
Q

What is the tumour marker for Hepatocellular Carcinoma?

A

Alpha-fetoprotein

151
Q

How is Hepatocellular Carcinoma managed?

A
  • Surgically resect

- Transplant

152
Q

What are the Secondary Liver Tumours?

A

90% of liver cancers

Metastasised from

  • Stomach
  • Lung
  • Colon
  • Breast
  • Uterus
153
Q

What is a Carcinoid Tumour of the Liver?

A

LIVER METS that release SEROTONIN (also lung)

  • Flushing
  • Diarrhoea
  • Bronchospasm
  • Hypotension
  • R valve stenosis
  • Niacin B3 deficiency: Pallagra

Also may secrete ACTH (Cushing’s) or GHRH

154
Q

What are the Liver Abscesses/Cysts?

A

Pyogenic
Amoebic

Cysts

155
Q

What are the causes and management of Pyogenic Liver Abscess?

A

Staph aureus in children

E. coli in adults

Give AMOC+CIPRO+METRON
(or CLIND if PA)

156
Q

What are the causes and management of Amoebic Liver Abscess?

A

Single mass in the R lobe - ANCHOVY SAUCE PUS

157
Q

How do Liver Abscesses present?

A
  • swinging fever
  • sweats
  • RUQ pain
  • increased WCC
  • USS/CT/Aspirate
158
Q

What causes Liver cysts?

A
  • Simple-sporadic
  • Polysistic Liver Disease

Hyatid cysts caused by Echinoccus Granulosus (tapweowrm parasite)

Outer capsule with multiple small daughter cysts
Causes Hypersensitivity Type I reaction

159
Q

Cholestasis

A

obstruction of bile flow along biliary tract from lvier to duodenum

160
Q

Cholelithiasis

A

Presence of gallstones in the gallbladder

PIGMENT <10%: small, friable and irregular due to haemolysis

CHOLSTEROL- large, solitary due to age and obesity

MIXED: CALCIUM slats +pigment + cholesterol

> 60% have 1 or more deranged LFT

161
Q

Choleodocholithiasis

A

Gallstones in the Billiary tract

162
Q

Biliary Colic

A

Intermittent obstruction of the cystic duct by gallstones causing steading, colicky, crescendoing, RUQ

Worse after eating fatty foods when CHOLECYSTOKININ levels are high

USS + LapChole

163
Q

Ascending Cholangitis

A

inflammation or infection of the biliary tree mostly due to gallstones obstructing the tract DISTAL to the cystic duct

Severely septic and unwell
CHARCOT’S TRIAD: Jaundiced, RUQ, Fever

Fluid resuss, BS Abx, Early ERCP

164
Q

Acute Cholecystitis

A

Inflammation of the gallbladder WALL due to GALLSTONE TRAUMA and BLOCKED CYSTIC DUCT

ESCHERICHIA

bile builds up and irritates

  • RUQ
  • Fever
  • Murphy’s sign
    Mildly deranged LFTs

USS + Lapchole

165
Q

Acalculous Cholecystits

A

Inflammation of the gallbladder with no gallstone obstruction

High fever
Systemic illness e.g. DM

Lapchole

166
Q

Gallstone Ileus

A

Obstruction of the small bowel by an impacted gallstone >2.5cm

Travelled through a CHOLEO-ENTERIC FISTULA

Known gallstones + small bowel obstruction

Laparotomy-remove the stone proximal to the obstruction

167
Q

Gallbladder abscess

A

Prodromal illness + RUQ
- Swinging pyrexia
- Systemically
NO generalised peritonism

Surgery with subtotal Chole if Calot’s triangle is hostile
Percutaneous drainage if unfit for surgery

168
Q

Mirizzi’s syndrome

A

Gallbladder presses on the common hepatic or common bile duct causing jaundice

May also cause fistula

169
Q

Mucocele/Empyema

A

overdistended gallbladder filled with mucoid or clear and watery content. Usually noninflammatory, it results from outlet obstruction of the gallbladder and is commonly caused by an impacted stone in the neck of the gallbladder or in the cystic duct

Infected: empyema

170
Q

Cholangiocarcinoma

A

Symptoms of biliary colic + jaundice

COURVOISIER’S SIGN; palpable mass in ruq

Periumbilical lymphadenopathy: SILVER MARY JOSEPH NODES
Virchow’s node

171
Q

What are the mechanical causes of Dysphagia?

A
  • Malignancy
  • Strictures
  • External compression
  • PHARYNGEAL POUCH
  • OESOPHAGEAL WEB
  • OESOPHAGITIS
  • CREST
  • Hypertensive LOS
  • Foreign body
172
Q

What are the Neuromuscular causes of Dysphagia?

A
  • ACHALASIA
  • DIFFUSE OESOPHAGEAL SPASM
  • Stroke liquids worse
  • Parkinson’s
  • MS liquids and solids
  • Myesthenia gravis
173
Q

What are Oesophageal webs?

A

Thin membranes covering along the oesophagus

SOLID>LIQUIDS

Plummer-vinsens syndrome: associated with iron deficiency aneamia

GLOSITIS
DYSPHAGIA
SPLENOMEGALY

Barium swallow
Endoscopic Dilation

174
Q

What is a Pharyngeal Pouch?

A

ZENICKER’S DIVERTICULUM

Posteriomedial diverricul through KILLIAN’S DEHISCIENCE (TRIANGLE) between the thyropharyngeus and cricpharyngeus muscles AT C5-C6

M>F

Dysphagia
Hallitosis
Regurgitation (risk of asp. pneumonia)
Aspirtion
Neckswelling gurgles on palpation
175
Q

What is Achalasia?

A

Primary motility disorder of the oesophagus where the smooth muscle fails to relax (progressive destruction of the ganglion cells in the myenteric plexus)
Oesophagus fails to relax and so does LOS, LOS pressure increases and food gets stuck leading to progressive dilation of the oesophagus

Progressive dysphagia ofsolid and liquid with regurgitation, chect pain and weight loss

Do Oesophageal manometry
Barium swallow shows bird beak

Baloon dilation
Laproscopic hellar myotomy

176
Q

What is Diffuse Oesophageal Spasm?

A

Multi focal high amplitude contractions of the oesophagus due to dysfunction of the inhibitory nerves

Severe dysphagia of solids and liquids
severe chest pain

Manometry shows repetative contractions
Cork screw on barium swallow

Relax SmM with nitrates or CCB
Pnuematic dilatation
Myotomy if severe

May progress to achalasia

177
Q

What is a hiatus hernia?

A

Protrusion of an organ (stomach) from abdo cavity into thorax via OESOPHAGEAL HIATUS

Sliding, whole thing goes up

Rolling/Para-oesophageal FUNDUS rises up to lie alongside lOS

178
Q

How are pepto-duodenal ulcers managed?

A

Trple therapy

PPI

Clarith

Metronidazole or Amoxicillin

FINALS (13 decks)

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