Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Definition of Crohn’s Disease

A

IBD which affects entire GIT mouth to anus, transmural inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors for Crohn’s

A 
GxE 
Genetic predisposition 
Family history
Smoking
Western lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Signs & Symptoms of Crohn’s

Potential differentials

A 
Diarrhoea +/- mucus
Weight loss
FTT
Fatigue
Maliase
Crampy abdo pain
Skin manifestations: pyoderma grangrenosum, erythema nodosum
Complications e.g. bowel obstruction

Differentials: IBS, IBD e.g. UC, gastroenteritis, C diff infection, malignancy, coeliac, acute appendicitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations into potential IBD

A 
• Bloods:
		○ FBC; anaemia (Hb), infection (WCC)
		○ U&Es
		○ LFTS; low albumin
		○ CRP/ESR; inflammation
		○ Fe studies; anaemia, B12 & folate; nutritional status
	• Stool:
		○ Culture; r/o infective process
		○ Calprotectin
	• Colonoscopy 
		○ Biopsies to confirm Crohn's vs UC
		○ R/O malignancy
Surveillance as well for CrCa risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Management of Crohn’s

A

Management: - aim to induce & maintain remission
Medical
• Steroids - used in acute exacerbations +/- 5-ASA analogues to reduce inflammation
• 5-ASA e.g. sulfasalazine, mesalazine - reduce relapses, anti-inflammatory agents
• Immunosuppressives e.g. azathioprine, methotrexate - reduce relapses, steroid sparing agents
• Anti-TNF agents e.g. infliximab - very affective in achieving & maintaining remission, usually reserved for refractory cases

Surgical
• Local resection of disease
• Stoma formation
• Treatment of complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Complications of Crohn’s

A 
GI complications
	• Haemorrhage e.g. PR bleeding 
	• Bowel strictures
	• Bowel obstructions
	• Fistula formation
	• Malabsorption
Colorectal carcinoma

Other complications
• Kidney stones
• Gallstones
Uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathology of Ulcerative Colitis

‘‘CLOSE UP’’

A

Continuous submucosal inflammation of large intestine

Continuous inflammation
Limited to colon & rectum
Only submuscoal 
Smoking - protective
Excrete blood/mucus
Use aminosalicytes
Primary sclerosing cholangitits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Risk factors for UC

A

Genetic predispositon

Ex-/non-smokers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

S&S of UC

A 
Diarrhoea
Constipation - when rectum becomes inflamed
Mucus
PR bleeding
Weight loss
Fever 
Skin manifestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management of UC

A

Medical - induce & maintain remission
• Mesalazine (topical anti-inflammatory) +/- steroids in acute flare ups
• Thiopurines (azathioprine and mercaptopurine): work through purine synthesis inhibition in lymphocytes leading to immunosuppression.
○ Must check TPMT enzyme activity before use.
○ Homozygous mutations in TPMT can lead to dangerous bone marrow suppression.
○ Major side-effects include pancreatitis and hepatotoxicity.
• Biologics: infliximab/adalimumab
○ tumour necrosis factor alpha inhibitors

Surgical
Panproctocolectomy; technically curative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Complications of UC

A 
• Hemorrhage
	• Toxic megacolon
	• Colorectal carcinoma
	• Fatty liver
Primary sclerosing cholangitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathology of colorectal carcinoma

A

Mostly adenocarcinoma
Tend to arise from adenoma-carcinoma sequence - due to damage & repair cycles
Common mutations inc APC - Kras - p53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Risk factors/aetiology - colorectal carcinoma

A

Environmental factors - diet, red meat, alcohol
Chronic inflammation or IBD
Hereditary syndromes - Lynch (MLH1 & MSH2), FAP (APC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Signs & Symptoms of Colorectal carcinoma (L vs R)

A

Left sided & rectum; CIBH, rectal bleeding, blood/mucus, tenesmus

Right sided (later presentation); IDA, signs of anaemia, weight loss, lower abdominal pain (rarer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2WW Criteria for CrCa

A

Aged 40 or over with unexplained weight loss AND abdominal pain

Aged 50 or over with unexplained rectal bleeding

Aged 60 or over with IDA or CIBH

Any +ve FIT tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigations into CrCa

A

Examination - PR & abdominal

Bloods - FBC (anaemia), Fe studies (anaemia), LFTs, CEA

Stool - culture, calprotectin, FIT or FOB test

Imaging - sigmoid/colonoscopy + biopsies, CT/MRI for staging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment for CrCA

A

Surgery - resection, stoma formation +/- chemotherapy

Palliative options inc stenting/bypass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Complications of CrCa

A

Bowel Obstruction

Perforations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathology of oesophageal ca

A

Upper - squamous cell, arises from mutational damage/repair cycles
Lower - adenocarcinoma, due to GORD/Barrett’s oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors for oesophageal ca

A

SCC - diet, smoking, HPV-16, HPV-18, alcohol

Aden - GORD, Barrett’s, reflux, obesity, ZE syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

S&S of oesophageal ca - potential differentials

A
  • Progressive dysphagia
    • Weight loss
    • Cachexia
    • Fever
    • Anaemia
    • Retrosternal pain
    • Hoarse voice

Differentials: any condition which may cause/contribute to dysphagia e.g. strictures, achalasia, myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Investigation - Oesophageal Ca

A

OGD + biopsy
CXR
Barium swallow
CT/PET for staging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

2WW Criteria for Oesophageal Ca

A

Any patient with dysphasia

Any patient >55yrs with w/l + upper abdominal pain/reflux/dyspepsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment options for oesophageal ca

A

surgery - oesophagectomy
chemo
RT
palliative options - stenting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Definition of lower GI bleeds

A

bleeding distal to ligament of Treitz (suspensory ligament of the duodenum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Causes of lower GI bleeds

A

Anatomical - anal fissures, fistulas, haemorrhoids, diverticulosis
Inflammation - IBD (UC, CD), infection
Vascular - ischaemic colitis, angiodysplasia
Neoplasia - colorectal carcinoma, polyps
Other - upper GI bleeds, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Investigations for lower GI bleeding

A

History + PR examination
Bedside - obs, ECG, blood glucose, lying/standing BP
Bloods - FBC, U&Es, LFTs, Clotting, X-match
Stool - culture, calprotectin
Imaging - erect CXR, CTAP, colonoscopy/OGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Management of lower GI bleeds

A

Initial A to E assessment & quantify state of shock
• Minor bleeds – conservative management
• Major – colonoscopy & treat lesion, interventional radiology options

Oakland Scoring - predicts readmission
https://www.mdcalc.com/oakland-score-safe-discharge-lower-gi-bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Oakland score - parameters & what’s it used for

A

Use in patients presenting with lower GI bleed (urgent, emergent, or primary care setting) to help determine if outpatient management is feasible.

Age, sex, previous GI bleed, HR, BP, Hb, DRE examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Definition of UGIB & common sources

A

Bleeding proximal to ligament of Treitz

Oesophagus, stomach, duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Causes of UGIB

A

Oesophagus - varices, oesophagitis, MW tear, malignancy
Stomach - varices, gastric ulcer, MW tear, malignancy
Duodenum - peptic ulcer, duodenitis, diverticulum, aortoduodenal fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Risk factors for UGIB

A 
Medication - NSAIDs, Steroids, anticoagulants
Advancing age 
Alcoholism/excess
CLD
CKD
PUD/prev PUD
Prev h.pylori infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Investigations for UGIB

A

Bedside - observations, BP, BM’s, ECG, monitor UO

Bloods - FBC, U&Es, LFTs, clotting, ABG/VBG, G&S, X-match

Imaging - erect CXR, endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Management of UGIB

A

Initial resuscitation & A to E - consider blood products
Non-variceal - PPI, adrenaline + clips/thermal coag
Variceal; terilpressin, prophylactic abx, adrenaline + bands/TIPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Scoring system for UGIB

A

Blatchford - primary assessment, - when to scope
0-2 – low risk
>2 – admit

Rockall - post endoscopy, ABCDE (age, BP & HR, co-morbidity, diagnosis, endoscopic findings)
Re-bleeding risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pathophysiology of Coeliac Disease

A

Autoimmune reaction to prolamin peptides in gluten, barley & rye
Immunological response leads to mucosal damage & villous atrophy in small intestine
Leads to malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

S&S of Coeliac Disease

A

V varied, can be asymptomatic

Diarrhoea
Bloating
Steatorrhoea
Abdo pain
Weight loss
FTT
Primary amenorrhea
Fatigue
Malaise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Investigations for Coeliac Disease

A

Examination - signs of anaemia, malnutrition, dermatitis herpetiformis

Bloods - FBC, Fe studies, B12, folate, Ca, Anti-TTG & anti EMA

Stool - culture, ?calprotectin

Endoscopy - visualisation & biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Management of Coeliac Disease

A

Gluten free diet
Education & dietary support
Vit & mineral supplements if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Pathophysiology of pancreatitis

A

Pancreatitis is caused by the abnormal release and activation of enzymes, which cause autodigestion of pancreatic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Aetiology of pancreatitis - I GET SMASHED

A 
Idiopathic
GALLSTONES - women & older patients
ETHANOL - men & younger patients
Trauma
Steroids
Mumps/EBV/CMV
Autoimmune
Scorpions
Hyperlipidemia 
ERCP, emboli
Drugs e.g. furosemide, thiazide diuretics, azathioprine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

S&S of Pancreatitis

A

Can be quite vague

Abdominal/epigastric pain - radiating to back, relieved by leaning forwards, worse on movement, a/w nausea & vomiting
Anorexia/LOA
Steatorrhoea

Abdominal tenderness/distension
Cullen’s (umbilical) & Turner’s (flank) signs - haemorrhagic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Investigations into pancreatitis

A

Bloods - FBC (WCC), U&Es (urea), LFTs (LDH, AST, albumin), Amylase, Lipase, ABG

Imaging - CXR (r/o GI perf), USS (gallstones & biliary dilatation), CT/MRI (assess for complications)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Glasgow Score - Pancreatitis

A

Severity Score; 0-1 mild, 2 moderate, 3 or more severe
‘‘PANCREAS’’

paO2 <8
age >55
neutrophils >15
calcium <2
renal function, urea >16
enzymes (LDH, AST)
albumin <32
sugar >10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Management of Pancreatitis

A 
Resuscitation & A-E assessment 
IV fluids
Analgesia 
NBM & NG tube 
ERCP & cholecystectomy - gallstones (if needed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Complications of Pancreatitis

A
  • Chronic pancreatitis
    • Malnutrition
    • QOL
    • Pseudocysts
    • Necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Pathophysiology of Cirrhosis

A

Chronic damage to liver leading to loss of hepatocytes
Hepatocytes replaced by fibrosis & nodules
Leads to portal HTN & liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Aetiology of Cirrhosis

A 
Alcoholism 
NAFLD
Viral hepatitis - B&C
Autoimmune hepatitis
Hereditary - haemochromatosis, Wilson's
Vascular - Budd Chiari syndrome
Drugs - MTX, amiodarone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

S&S of Cirrhosis

A

Early non-specific signs - anorexia, weight loss, fatigue, weakness, nausea

Loss of synthetic function - easy bruising, abdominal swelling, ankle oedema

Loss of detoxification - altered sleep, jaundice, personality changes, amenorrhea

PR bleeding/melena

Haematemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Signs of examination of chronic liver disease

A

'’ABCDE’’ - ascites & asterixis, bruises, clubbing, dupuytren’s contracture, erythema (palmar)

jaundice
spider navei
caput medusa
organomegaly - liver/spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Investigations for cirrhosis

A

Bloods - FBC (Hb, MCV, Plts), LFTs, Clotting, AI/serology screen, albumin, AFP
Ascitic tap - micro, C&S, biochem, cytology
Liver USS+ biopsy - gold std
Endoscopy?

52
Q

Child Pugh Score - Cirrhosis

A

Severity & prognosis
5 markers (3x max each)
Albumin, Ascites, Bilirubin, INR/PT, HE

53
Q

Management of Cirrhosis

A

Treat/reverse cause
Prevent further damage - alcohol, diet, avoid hepatotoxic drugs
Dietary support - high protein, low na diet
Monitor & treat complications

54
Q

Potential complications of Cirrhosis

A

Ascites - drain, diuretics
HE - laxatives
UGIB - ?TIPS
SBP - abs & prophylaxis

55
Q

Definition & causes of acute liver failure

A

Acute dysfunction w/o underlying liver disease

Causes: trauma, drug OD (paracetamol), alcohol excess, infection (Hep A/B/E), pregnancy related, Budd-Chiari syndrome

56
Q

Definition of autoimmune hepatitis

A

Chronic relapsing hepatitis with an unknown aetiology, characterised by the presence of autoimmune features, hyperglobulinaemia and autoantibodies

57
Q

Pathogenesis & Aetiology of Autoimmune hepatitis

A

Commonly affects women of all ages (type 1) & younger women/girls (type 2)
Thought to be genetic predisposition & environmental trigger (e.g. drugs, infection)
Auto-immune reaction causes chronic inflammation & damage, can lead to cirrhosis & failure

Type 1 (Classic): anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (SMA), anti-actin antibodies, anti-liver soluble antigen

Type 2: anti-LKM (liver kidney microsomes), antibodies to liver cytosol antigen

58
Q

‘Ways’ in which AIH can present

A

• Asymptomatic (25%) - persistently elevated LFTs
• Acute hepatitis (40%) - fever, RUQ pain, anorexia, hepatomegaly, N&V, diarrhoea, jaundice
• Chronic liver disease/cirrhosis
Acute liver failure (rare) - jaundice, confusion, coagulopathy

59
Q

Investigations for AIH

A 
Routine bloods
	• FBC - low Hb, Plts & WCC may be low in hypersplenism
	• U&Es
	• LFTs - deranged, AST/ALT esp in acute 
	• Clotting
Non invasive liver screen
	• Auto-antibodies; ANA, anti-SMA, anti-LKM
	• Immunoglobulins
Imaging
	• USS etc to r/o other causes
	• Not diagnostic
Biopsy
60
Q

Management of AIH

A

Immunosuppression - mainstay of management
• Steroids i.e. prednisolone
• Azathioprine

Follow up & monitoring - remission = normal AST/ALT

61
Q

Cholelithiasis vs Choledocholithiasis vs Cholecystitis

A

Cholelithiasis: refers to gallstones - solid deposits that develop in the gallbladder.
Choledocholithiasis: refers to gallstones within the biliary tree.

Cholecystitis - inflammation of gallbladder, commonly caused by gallstones

62
Q

Types of gallstones & risk factors for developing them

A

Mixed, cholesterol or pigment

Female
Age 
Diet - high fat
Medication - high oestrogen 
Obesity
Family hx/genetics
Crohn's
Haemolytic disorders
63
Q

Causes of cholecystitis

A

Gallstones (calculous)

Non-calculous cholescystitis (significant systemic upset or following major surgery)

64
Q

S&S of Gallstones

A

Asymptomatic

but can present with biliary colic (intermittent severe RUQ pain) or cholecystitis

65
Q

S&S of cholecystitis

A 
RUQ/epigastric severe pain, tenderness & guarding
N&V
Pyrexia
Tachycardia
can become hypotensive

Murphy’s sign - catching breath

66
Q

Investigations for cholecystitis

A

Bedside - observations, BM, urine dip, preg test
Bloods - FBC, cultures, U&Es, CRP, LFT, amylase
Imaging - USS

67
Q

Management of Cholecysitis

A

Medical - abx, fluids, analgesia

Surgical - cholecystectomy, ERCP or MRCP if CBD stones present

68
Q

Management of Gallstones

A

Conservative - fluids, anti-emetics, analgesia
Lifestyle advice - dietary, weight loss

Monitor & treat complications

69
Q

Definition & risk factors for cholangiocarcinoma

A

Cancer arising from bile ducts (can be intra or extrahepatic)

RFs: primary sclerosing cholangitis (UC pts), liver flukes (parasitic infections)

70
Q

Clinical features of cholangiocarcinoma

A 
Obstructive jaundice - pale stool, dark urine, generalised itching
W/L
RUQ pain
Palpable GB 
Hepatomegaly
71
Q

Investigation & Dx of Cholangiocarcinoma

A

Bloods - liver & jaundice screen, LFTs, bilirubin, albumin, serology, Ca19-9

Imaging (Dx) - CT or MRI + biopsy, ct staging
MRCP/ERCP can aid in dx or management

72
Q

Treatment of cholangiocarcinoma

A

Surgery - can be curative in early stages, combined with chemo/RT

Palliative options in majority of cases e.g. stents, bypass obstruction, sx control with chemo/RT

73
Q

Definition of Primary Sclerosing Cholangitis (PSC)

A

An autoimmune mediated disease characterised by cholestasis, bile duct strictures & hepatic fibrosis

Primary: refers to PSC. Absence of another identifiable cause.

Secondary: refers to any condition causing bile duct damage and biliary obstruction.

74
Q

Pathology of PSC

A

Autoimmune ‘attacks’ causing progressive inflammation & hepatic fibrosis as well as destruction of intra & extrahepatic ducts. This leads to reduction in flow of bile (cholestasis), narrowing of bile ducts (stricturing) and cirrhosis of liver

75
Q

Aetiology of PSC

A

Genetic predisposition x environmental trigger

Strong a/w IBD especially UC

76
Q

Clinical features of PSC

A

Can remain asymptomatic especially in early stages, can be incidental finding or symptoms tend to develop from cholestasis
• Incidental finding - persistently raised ALP
• Intermittent jaundice, itching, fatigue, RUQ pain
• Hepatomegaly, splenomegaly & stigmata of CLD

Can also present with cholangitis (Charcot’s Triad)
• Fever
• RUQ pain
Jaundice

77
Q

Diagnosis of PSC

A

PSC is characterised by a ‘cholestatic’ pattern on LFTs and absence of autoantibodies.

MRCP - gold std, visualise biliary strictures & dilatation

78
Q

Treatment options of PSC

A

Medical - aimed at managing complications
• Cholangitis - IV abx & fluids
• Bone disease - at increased risk of osteoporosis & osteopenia, Vit D supplements
• Itching - cholestyramine
ERCP - balloon dilatation & stents
• Help to manage disease
Liver transplant
• Only option which alters survival, recurrence is a risk

79
Q

Complications of PSC

A 
Cholangiocarcinoma
	• COD in majority of patients with PSC
	• Low threshold for imaging if suspected
Colorectal carcinoma
	• Due to a/w IBD, annual colonoscopies
Hepatic malignancy
Due to cirrhosis, 6mths USS +/- AFP
80
Q

Definition & pathophysiology of hepatocellular carcinoma

A

Primary malignancy of hepatocytes

Damage & repair cycles promoting mutations

81
Q

Risk factors/aetiology of HCC

A

Chronic liver disease - alcoholic liver disease, NAFLD, cirrhosis, hepatitis, AIH
Metabolic liver disease - haemochromatosis
Alfatoxins

82
Q

Clinical presentation of HCC

A 
Stigmata of chronic liver disease on examination 
Weight loss
Fatigue
Maliase
Weakness
LOA
Ascites/abdominal distension
Jaundice
83
Q

Investigations for HCC

A

Bloods - full liver screen e.g. FBC, U&Es, LFTs, AI, serology, AFP
Imaging - CT or MRI +/- biopsy, CT staging

84
Q

Treatment options for HCC

A 
Surgical resection
Local therapy e.g. ablation 
Transplant 
Chemo e.g.  multikinase inhibitors (e.g. Sorafenib)
RT or brachytherapy
85
Q

Definition of gastric carcinoma

A

Malignancy of stomach - adenocarcinoma (90%)

86
Q

Risk factors for gastric cancer

A 
Smoking 
Alcohol
Diet 
Obesity 
Atrophic gastritis 
H. pylori infection
87
Q

S&S of gastric cancer

A

Constitutional symptoms: fevers, anorexia, lethargy, weight loss
Dysphagia: if involvement of gastric cardia
Indigestion
Dyspepsia
Nausea/vomiting
Haematemesis/melaena
Post-prandial fullness

88
Q

Examination - suspected gastric cancer

A

Usually absent unless late presentation with distant spread

Pallor
Cachexia
Lymphadenopathy
Virchow node: left supraclavicular node
Metastatic lesions
Hepatomegaly
Sister Mary Joseph nodule: periumbilical metastasis
89
Q

2WW Criteria - gastric cancer

A

• Upper abdominal mass consistent with gastric cancer, OR
• Dysphagia, OR
• > 55 years with weight loss and one of the following:
○ Upper abdominal pain
○ Reflux
o Dyspepsia

90
Q

Dx of gastric cancer

A
  • OGD +/- biopsy
    • CT/MRI staging
    • Bone scan - mets
    • USS for lymph nodes
91
Q

Management of gastric cancer

A 
Medical
	• Chemo & radiotherapy - 5FU
	• Targeted monoclonal abs - HER2
Surgical
Gastrectomy - full or partial
92
Q

Pancreatitis cancer - most common type

A

Ductal adenocarcinoma (85%)

93
Q

Risk factors for pancreatic cancer

A

Age, smoking, alcohol, chronic pancreatitis, diabetes, hereditary syndromes (BRCA, FAMMM), genetics

94
Q

Clinical presentation of pancreatic cancer

A

Later presentation
Jaundice, abdo pain & unexplained weight loss

diarrhoea, steatorrhoea, dark urine, new onset diabetes, signs of metastasis

95
Q

2WW criteria for pancreatic cancer

A

New onset jaundice >40yrs
>60yrs w/ unexplained weight loss +: diarrhoea, constipation, back pain, abdominal pain, nausea, vomiting or new onset diabetes

96
Q

Investigations for pancreatic cancer

A

Bloods: FBC, U&Es, LFTs, clotting, Ca19-9. CEA

Imaging: USS, CT/MRI pancreas, CT-TAP, PET staging, ERCP

Biopsy

97
Q

Treatment of pancreatic cancer

A

Medical - chemo (pal), pain control, nutritional support

surgical - <20% suitable, Whipple’s (possibly) for HOP tumours with no vascular involvement or mets

98
Q

Definition of primary biliary cirrhosis

Typical patient?

A

Chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis and ultimately cirrhosis

Typical patient - female (9:1), around 50yrs old, may have a family hx

99
Q

Pathophysiology of PBC

A

Autoimmune attack of small intrahepatic bile ducts. Damage & destruction of these ducts causes obstruction of the outflow of bile (cholestasis). This leads to a backpressure into the liver which causes irritation leading to fibrosis, cirrhosis & liver failure.
Bile acids, bilirubin & cholesterol are no longer being excreted through bile ducts into intestines & so they build up in the blood - cause itching, jaundice, increased risk of CVD.

100
Q

Aetiology & Risk factors for PBC

A

unknown exact cause, most likely GxE
Possible environmental triggers
Infection, pollutants, bacteria
Female sex
Middle aged
Other AI conditions e.g. thyroid, coeliac
Rheumatoid conditions e.g. systemic sclerosis, Sjogren’s & RA

101
Q

Clinical features of PBC

A 
Can be incidental finding on blood tests - persistently raised ALP & cholesterol
	Fatigue 
	Pruritis
	GI disturbances
	Abdominal pain
	Jaundice 
	Pale stools
	Xanthoma/xanthelasma
Signs of CLD - ABCDE
102
Q

Investigations for PBC

A

Bloods
• FBC
• U&Es
• LFTS - raised ALP & GGT, bilirubin (can be normal or raised in later stages)
• Clotting - prolonged PTT
• Autoantibodies - anti-mitochondrial antibodies (most specific to PBC) & anti-nuclear antibodies
• ESR - raised
• Immunoglobulins - IgM raised
Imaging
• USS - excludes extrahepatic biliary obstruction e.g. gallstones, strictures
• Liver biopsy - diagnostic & used in staging

103
Q

Management of PBCMedical

A
  • Ursodeoxycholic acid - reduced intestinal absorption of cholesterol
    • Colestyramine - bile acid sequestrate, can help with pruritis
    • Immunosuppression is considered in some patients

Surgical
• Liver transplant - in end stage liver disease

Monitor & treat complications

104
Q

Aetiology of Bowel Obstruction

A

Mechanical: small (adhesions, hernia, malignancy, intussuspection), large (colorectal cancer, volvulus, diverticular strictures)

Non-mechanical: pan-intestinal (paralytic ileus), colonic (acute colonic psuedo-obstruction)

105
Q

Clinical features of bowel obstruction

A

Abdominal pain, distension, vomiting & obstipation
Anorexia
Small bowel diarrhoea
Complete constipation

Abdominal tenderness/peritonism
Rebound
Abdominal distension
Abdominal mass

106
Q

Investigations - bowel obstruction

A

Bedside - observations, ECG, fluid balance, catheter, PR examination, pregnancy test

Bloods - VBG/ABG (lactate), FBC (WCC), U&Es (electrolytes, dehydration), LFTs, clotting, CRP (high),
amylase, group & save

Imaging - erect CXR (free air), abdominal XR (dilated bowel loops), CTAP

107
Q

Bowel dilation limits on X-ray

A

Small - >3cm
Large - >6cm
Caecum - >9cm

108
Q

Management of Bowel Obstruction

A

Conservative/supportive - NBM, Drip & Suck, analgesia, anti-emetics, abx if needed, correction of electrolytes

Endoscopic - decompression, stenting

Surgery - resection, laparotomy/laparoscopy

109
Q

Pathophysiology behind appendicitis & aetiology

A

Obstruction of lumen of appendix
Stasis & bacterial overgrowth, increase in intraluminal pressure, venous congestion & ultimately arterial compromise leading to necrosis

Aetiology - faecoliths, lymphoid hyperplasia, carcinoid tumours, fibrous strictures

110
Q

Clinical Features - Appendicitis

A

Colicky abdominal pain migrated to RIF & becomes constant

Symptoms: Abdominal pain, RIF pain, nausea, anorexia, constipation

Signs: RIF tenderness, percussion tenderness, localised guarding, tachycardia & pyrexia

Rovsing’s Sign - palpation in LIF causes pain in RIF

111
Q

Investigations - Appendicitis

A

Bedside - examination, observations, urine dip & pregnancy test

Bloods - FBC, U&Es, LFTs, clotting, amylase, CRP, group & save

Imaging - USS (+ pelvic to r/o gynae) & CT can confirm dx in older patients

112
Q

Management of appendicitis

A

Conservative - for acute uncomplicated appendicitis (antibiotics - co amoxiclav)

Surgical - laparoscopic appendectomy/open if needed, pre-op co-amox & post op 7days abx if pus or perforation

113
Q

Definition & Pathophysiology of Acute/Ascending Cholangitis

A

Acute infection & inflammation of biliary tree

Usually occurs due to bacterial overgrowth after obstruction of biliary tree

114
Q

Aetiology - Acute Cholangitis

A 
• Choledolithasis - stones in biliary tree 
	• Benign Strictures
		• Chronic pancreatitis
		• Iatrogenic injury (e.g. during cholecystectomy)
		• Radio / chemo-therapy
		• Idiopathic
	• Malignant Strictures
		• Pancreatic cancer
		• Gallbladder cancer
Cholangiocarcinoma
115
Q

Clinical Presentation - Acute Cholangitis

A

• Charcot’s Triad - RUQ pain, jaundice & fever

Nausea & vomiting

116
Q

Investigations - Acute Cholangitis

A

Bedside
• Observations
• ECG
• Urine dip & cultures
• Pregnancy test - in female patients of child bearing age
Bloods
• FBC - WCC
• U&Es - dehydration
• CRP - inflammation
• LFTs
• Amylase
Imaging
• USS - useful in checking presence of stones
• CT - good visualisation of the biliary tree, evaluate for abnormal lesions/tumours or where other dx
MRCP - offers excellent visualisation of the biliary tree. Often used where CT/USS are inconclusive.

117
Q

Management of acute cholangitis

A

Antibiotics
Fluids
Analgesia
Biliary Drainage - ERCP/Percutaneous transhepatic cholangiography

118
Q

Definitions of diverticulosis, diverticular disease & diverticulitis

A

Diverticulosis - presence of diverticula (outpouching of colonic mucosa & submucosa through muscular wall of large bowel)
Diverticular disease - diverticulosis a/w complications e.g. haemorrhage
Diverticulitis - acute inflammation & infection of diverticula

119
Q

Risk factors for diverticulitis

A 
Diet - red meat, low fibre
Smoking
Obesity
Family history
Medications - NSAIDs increase risk of perforation
120
Q

Clinical presentation of diverticulitis

A 
Abdominal pain, fever & tenderness in LIF
Anorexia
Nausea
Guarding 
Tachycardia
121
Q

Investigations - Diverticulitis

A

CT abdomen pelvis is imaging modality of choice for diagnosis of diverticulitis
• Bedside: observations, urine dip & pregnancy test
• Bloods: FBC, U&Es, LFTs, CRP, amylase, clotting, G&S
• Imaging: CT abdo pelvis w/ contrast ideally

122
Q

Management - Diverticulitis

A

Very dependent on severity & this can range significantly
• Consider inpatient vs outpatient management
○ Outpatient - fit & healthy, younger patients w/ mild disease
○ Inpatient - older, more frail patients w/ more severe disease
• Antibiotics; Co-amoxiclav or ciprofloxacin (if penicillin allergic)
○ OP - 7 day course
○ IP - IV abx regime
• Analgesia; paracetamol
○ Avoid NSAIDs & opioids due to increase risk of perforation
• Follow-up
○ Patients managed in the community should be reassessed at 48 hours and given appropriate safety-net advice.
○ Outpatient colorectal follow-up and colonoscopy (if appropriate) should be arranged.

123
Q

Complications - Diverticulitis

A

Bowel strictures
Fistula
Diverticular Bleed

124
Q

Types & Aetiology - Jaundice

A

TYPES & CAUSES
1) Pre-hepatic; increased hemolysis, livers ability to conjugate is overwhelmed  hemolytic anaemia, Gilbert’s syndrome

2) Hepatic; dysfunction of liver, mixed picture  HCC, cirrhosis, iatrogenic, drugs, AIH
3) Post-hepatic; obstruction  intramural (gallstones), mural (cholangiocarcinoma), extramural (abdominal masses

125
Q

Jaundice - INTERPRETATING LFTs & URINE

A 
Pre-hepatic = normal LFTs, increased urobilinogen (urine), no bilirubin in urine
Hepatic = all round bad LFTs, mixed picture on bilirubin in urine
Post-hepatic = classic cholestatic LFTs (increased GGT, ALP), bilirubin+++ urine (dark), no sterco (pale stools)
126
Q

‘Types’ - Ascites

A

Transudate (little/no protein)
Exudate (protein)
SAAG; >1.1 = transudate

Transudate fluid - ultrafiltration of plasma due to raised portal pressure
Exudate tends to be leakage of whole contents of plasma due to inflammatory causes (normal portal pressure)

127
Q

Causes of Ascites

A 
Transudate:
Cirrhosis 
Congestive cardiac failure 
Acute liver failure (trauma, OD)
Liver metastasis
HVT or PVT	
Exudate:
Infection – bacterial, fungal, TB
Malignancy
Pancreatitis
Nephrotic Syndrome
Bowel Obstruction

Finals (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions