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Year 3 > Week 13 GI > Flashcards

Week 13 GI Flashcards

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1
Q

3 tests indicated for liver function

A

Bilirubin

Albumin

PT (extrinsic and common)

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2
Q

Chronic and acute liver injuiry investigations

A

Chronic liver disease:

US

Chronic viral hepatitis: HBV, HCV

Autoimmune:

Autoimmune hepatitis (AIH):

  • ANA (anti nuclear antibody)
  • SMA (anti smooth muscle antibody)
  • LKA (anti liver kidney antibody)

AMA (anti mitochondrial antibody) - Primary biliary cirrhosis/cholangitis

Immunoglobulins - Increased IgG(AIH), Increased IgM (PBC)

Metabolic:

Ferritin (Haematochromotosis) - high

Caeruloplasmin (Wilsons) - low

Acute liver injury

US

Acute viral hepatitis: HAV, HBV, HCV, HEV, CMV

Autoimmune: ANA/SMA/LKM (AIH)

Immunoglobulins

Paracetamol levels

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3
Q

Fatty liver disease: Alcholic liver disease vs Non alcoholic liver disease

A

Presnts as asymptomatic abnormal LFTs or acute/chronic hepatitis - jaundic, fever, malaise, dark urine

Causes: alcohol, NAFLD: metabolic syndrome, drug e.g. methotrexate

Alcoholic

  • Alcoholic steatosis (lipid vacuole filling heptocyte cytoplasm)
  • Alcoholic hepatitis (neutrophils and lymphocytes filling hepatocytes with mallory bodies (damaged intermediate filaments)
  • Alcoholic cirrhosis (periceullar fibrosis, bands of fibrous tracts between portal tracts)

Weight: variable

HbA1C: N

Alcohol intake: High

ALT: N/High

AST: High

AST/ALT ratio: High >1.5

GGT: very high

Triglycerides: variable

HDL: high

MCV: High

Non-alcoholic liver disease

  • Steatosis
  • Non alcoholic steatohepatitis
  • Non alcoholic liver disease/Cirrhosis

Weight: high

HbA1C: high

Alcohol intake: normal

AST: N

ALT: N

GGT: N/high

AST:ALT: <0.8

Triglycerides: High

HDL: Low

MCV: N

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4
Q

Alcoholic hepatitis (characteristic clinical features, microscopy, assessment)

A

Form of alcoholic liver disease, inflammatory liver injury due to alcohol. Excess alcohol within 2 months

Jaundice

Increased bilirubin

AST:ALT ratio >1.5

Characterisitc features:

Hepatomeagly, fever, leucocytosis, hepatic bruit

Microscopy: Swelling of hepatocytes, mallory bodies (damgaged intermediate filaments in hepatocytes)

Assessment:

Glasgow alcohol hepatitis score

WBCC, Urea, Bilrubin, PT,

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5
Q

Chronic liver disease: clinical features

A

Clinical features: Spider naevi, foetor hepaticus (foul smelling breathe), encepalopathy, clubbing, palmar erythema

Prolonged PT time, decreaesed albumin

Assess severity: Childs Turcotte Pugh Score

  • Encelopathy, ascites, bilirubin, albumin, PT
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6
Q

Portal hypetension (patho and clinical features)

A

Critical to manifestation of chronic liver disease:

  • cirrhosis
  • increased portal pressure (hypersplenism)
  • porto-systemic shunting (oesophageal varices, encelopathy)
  • vasodilation
  • increased RAAS, catecholamines to compensate (leads to inreased Na+ and water rentention (ascites))
  • renal vasoconstriction - leading to hepati-renal syndrome (renal failure)

Clinical features:

Caput madusae

Ascites

Splenomegaly (leads to thrombocytopenia)

Encelopathy

Hepatocellular carcinoma

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7
Q

Acute pancreatitis

A

Autodigestion of pancreas due to premature activation of pancreatic enzymes (commonly trypsin)

Causes:

Gallstones

Alcohol

Trauma

Infection - mumps

Clinical features: Epigastric pain radiates to back, nausea and vomiting, fever, increased WBCs

Diagnosis:

Requires 2 out of 3:

Pain

Increased serum amylase (3x ULN)

CT appearence

Severity

Mild - absence organ dysfunctin

Moderate - transient organ dysfunction

Severe - persistent organ dysfunction

Complications:

Pancreatic necrosis

Pancreatic abscess

Pancreatic psuedo cyst (no epithelial lining)

DIC

Investigations

US

MRCP (MRI cholangiopancreatography)

CT

Initial treatment:

ABCs, fluids, O2, Antibiotics? (Meropenem for pancreatitis with necrosis)

Management:

Early feeding

Treat cause

ERCP

Cholecystectomy (gallbladder removal)

Alcohol addictions service

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8
Q

Ascites (definition, investigations, treatment)

A

Build up of fluid in abdomen

Assessment:

Ascites tap (take fluid out) -

PMN (polymorphic nuclear) count

Increased WBC (>250 neutrophils) - indicates spontaneous bacterial peritonitis (infection of ascitic fluid)

  • Increased lymphocytes indicates TB

Increased SAAG (serum albumin ascites gradient) - indicates portal hypertension

Management

Low salt diet

  • Spironolactone (aldosterone antagonist)

SE: hyperkalaemia, hyponatraemia

  • Frusemide (Na/CL-/K+ symporter anatagonists)

SE: hyponatraemia

  • TIPSS (transjugular intrahepatic portosystemic shunt)
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9
Q

,Encepalopathy

A

Failure of cirrhotic liver to get rid of toxins which affects brain function

Due to GI bleeding, infection, electrolyte imbalance

Decreased hepatic/cerebral function, increased ammonia levels, inflammatory response

Assessed by Conns score (Grade 1-4)

Clinical sign: heptic flap

Treatment:

Lactulose

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10
Q

Most common cause of abnormal LFTs

A

Fatty liver (alcoholic, non-alcoholic)

Chronic hepatitis

Autoimmue - PBC, autoimmune hepatitis

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11
Q

Chronic pancreatitis

A

Repeated bouts of acute pancreatitis leading to fibrosis of parenchyma

Causes:

Alcohol, CF

Clinical features:

Epigastric pain radiating to back

Pancreatic insufficiency - malabsorption leading to stearrohea (fat in stool)

Secondary diabetes

Increased risk of pancreatic carcinoma

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12
Q

Differential acute pancreatisis

A

Ischaemic bowel disease

Peforated duodenum

Pancreatic cancer

Cholangitis

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13
Q

Pancreatic carcinoma

A

Adenocarcinoma arising from pancreatic ducts

Ductal adenocarcinoma - most common

Risk factors:

Smoking, chronic pancreatitis, BRCA gene

Clinical features:

Epigastric pain, weight loss, pancreatitis

Carcinoma in head of pancreas: painless obstructive jaundice, steatorrhea, palpable gallbladder (due to back up pressure of bile), new-onset diabetes, abdo pain (due to peri-neural invasion)

Premalignant stage: pancreatic intraepithelial neoplasia (PanIN)

Serum marker: CA 19-9

Treatment:

Whipple’s procedure: head of pancreas, duodenum, gallbladder, bile duct

Folforimox

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14
Q

Pancreatic tumours

A

Intraductal papillary mucious neoplasms

  • Dysplastic linining secreting mucin
  • Can become malignant

Mucinous cystic neoplasms

  • mucinous lining, “ovarian stroma”

Serous cystadenoma

  • benign
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15
Q

Gallstones

A

Gallstones can be made of cholesterol or bile. Due to increased cholesterol or decreased bile salts (solublises cholesterol in bile)

Risk factors:

Four Fs: Female, fat, fertile (oestrogen (due to increased HMG co-reductase, incresaased cholesterol synthesis)), forty’s

Also extravasuclar haemolysis (due to increased bilirubin so less soluble in bile), bilary tract infection e.g. E.coli

Complications:

Bilary colic:

Gallstone temporarily blocks cystic duct.

Acute cholecystitis:

Inflammation of gallbladder wall

Severe RUQ radiating to scapula, tenderness, fever

Increased WBCC, increased Alk phos

Can resolve by itself but also lead to empyema, gangrene, rupture

Chronic cholecystitis:

Chronic inflammation of gallbladder due to attacks of acute cholecystitis

  • Vauge RUQ pain esp. after eating

Complication: porcelain gallbladder on XR (due to dystrophic Ca2+)

Treatment:

Cholecystectomy

Ascending cholangitis:

Bacterial infection of bile ducts, due to ascending infection of gram neg bacteria

Presents as sepsis, jaundice

Gallbladder carcinoma

Adenocarcinoma arising from epithelium that lines gallbladder wall

Risk factor: Gallstones

Presents in new onset cholecystitis in elderly women

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16
Q

Mucocoele

A

Colletion of mucus in gallbladder leading to distention

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17
Q

2 causes of asterixis (flapping tremor)

A

Liver failure

Drugs e.g. lithium, phenytoin

Type 2 resp failure (due to too much CO2)

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18
Q

Coeliac disease

A

Autoimmune disease due to gliadin found in gluten (rye, wheat, barley) leading to villus atrophy, intraepithelial lymphocytes, crypt hyperplasia. Assoc. with HLA DQ2/8

Differentials: lymphocytic colitis, IBS

Pathophys: Gliadin leads to inflammatory reaction - activation of T helper cells - lymphocytic repsonse - epithelial damage - villus flattening - loss of SA - malabsorption

Symptoms:

IDA (most common), Diarrhoea, Abdo pain, Dermatitis herpitformis

Complications:

- OP (due to decreased Ca+ absorption)

  • Peripheral neuropathy (decreased B12)
  • Enteropathy associated T cell lymphoma,
  • Functional hyposplenism (due to folate deficiency. Shown by presence of Howell Jolly bodies)

Investigations

FBC, blood smear (microcytic and hypochromic RBCs)

-tissue transglutaminase (TTG)

Endomysial antibody (EMA) - more sensitive than TTG

Endoscopy

  • atrophy and scalloping of mucosal folds, nodularity, mosiac pattern of mucosa

Duodenal biopsy (4 biopsies from distal duodenum as changes may be patchy (and must be on GFD))

Marsh Classification:

Stage 1: intraepithelail lymphocytes

Stage 2: crypt hyperplasia

Stage 3: villous atropy

Treatment:

Gluten free diet

TTG can be used to assess compliance (will be positive with ongoing exposure)

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19
Q

Chron’s (symptoms, complications, histology, investigations)

A

Chron’s : type of IBD characterised by transmural granulomatous inflammation of GI, affecting mouth to anus

Symptoms:

Episodic mild diarrhoea, pain, fever, may be precipitated by stress

Complications: Malabsorption, strictures, toxic megacolon, colonic carcinoma (less than UC)

Histology:

Transmural inflamamation

Skip lesions

fistulas

granulomas

Investigations

FBC, CRP, UEs, LFTs, stool cultures + C.diff. toxin, faecal calprotectin

Colonoscopy (1st line), sigmoidoscopy

Treatment: Surgery

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20
Q

UC (symptoms, complications)

A

Type of IBD characterised by diffuse inflammation, starting at rectum and up to colon, in a relapsing course

Symptoms:

Relapsing and remitting bloody diarrhoea, pain releived with bowel movement

Extra-intestinal symptoms: Erythema nodosum, uveitis, alk spondylitis, Primary sclerosing cholangitis

Histological hallmark: crypt abscess with neutrophils

Complications: Toxic megacolon, perforation, colonic carcinoma

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21
Q

Chron’s vs UC

A

Chron’s:

Transmural mucosa

Involves mouth to anus (usually terminal ileum)

Skip lesions

Granulomas

Lymphocyte infiltration

More common in women

Smoking can increase risk

UC:

Limited to rectum and colon

inflammation limited to mucosa

Continuous inflammation

More common in men

Smoking can reduce risk

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22
Q

Acute and Chronic histological changes in IBD

A

Acute changes during active disease:

Cryptitis

Loss of goblet cells

Crypt abcess

Ulceration

Chronic changes due to regeneration after ulceration

Crypt distortion

Loss of crypts

Submucosal fibrosis

Paneth cell metaplasia

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23
Q

Polyps of the colon

A

Hyerplastic polyps (most common, benign no malignant potential)

Harmatomtous (tumour comprimised of tissue normally present but disorganised) polyps

Inflammatory polyps

Majority of adenomas (benign glandular neoplasm) are polyps (has portential to be malignant via adenoma-carcinoma sequence

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24
Q

Adenoma-carcinoma sequence

A

Leads to adenocarcinoma

Risk factors:

Increased size of polyps (>2cm)

Increased no. polyps

IBD (UC higher risk)

Family history

Polyposis syndromes e.g. FAP (APC gene), Lynch syndrome (mismatch repair defects)

Duke’s staging

Bowel screening

50-70 for feocal occult blood (if +ve - colonoscopy)

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25
Most common site of neuroendocrine tumour?
Appendix
26
Differential granulomas
TB Sarcoidosis Chron's Diverticular disease
27
Ischaemic damage
Superficial ulceration Congestion of mucosal vessels - oedema - decreaed blood flow - necrosis
28
Diverticular disease
Pouch of mucosa that has herniated through a weak point in the musuclar propria Due to increased luminal pressure assoc. with low fibre diets Complications: Perforation, Abscess
29
IBD treatments
IBD: Corticosteroids - Budesonide, prednisolone Side effects: OP, immunosuppresion, Cushingoid Thiopurine - Purine anti-metabolite e.g. Aziothioprine Side effects: N&V, leucopenia, pancreatitis Biologics - Anti TNF: Inflixumab, Adalilumab, Golimumab Anti adhesion: Vedolizimab Side effects: Increased risk of infection e.g. TB, Hep B, lymphoma risk UC: Aminosalicylates: Anti-inflammatry e.g. Mesalazine Side effects: renal impairment Chron's: Methotrexate Anti-folate Side effects: GI upset, immunosuppresion, hepatotoxicity
30
Acute severe colitis
Pts who fail to repsonsd to optimal treatment 5-ASA/prednisolone Investigations Daily FBC, CRP, UEs Stool cultures (inc C.diff) Daily AXR Treatment: IV hydrocortisone Prophylactic LMWH Infliximab Surgery
31
IBD - Which would NOT be an indication for starting azathioprine?
Acute severe colitis
32
What is highly sensitive in the detection of pneumoperitoneum?
Erect CXR
33
Classic presentation of head/neck cancer
Ulcer that will not heal
34
Colonic mucosa
35
Normal gastric body
36
SI
37
Duke's stage criteria
A: Invasion into bowel wall, not through B: Invasion through bowel wall but not lymph nodes C: involves LNs D: Widespread metastases
38
Oesophageal anatomy and pathology
Mucosa (NK stratified squamous) Muscularis mucosae Submucosa Muscularis propria Adventitia Infections: candidia, HSV Inflammation: GORD: reflux of acid Drugs: iron Diverticula
39
Candida albicans infection oesophagus
White plauqes in oesophagus Histology: Neutrophils infiltrated, congegrates at luminal aspect PSA stain confirms the spores and hyphae of candida albicans
40
Barrett's oeosphagus
Metaplasia from stratified squamous to non-ciliated columnar (glandular), normally intestinal, epithelium with goblet cells Assoc. development of benign strictures Can become dysplastic: "Indefinite for dysplasia", low grade, high grade Low grade: - Cells polarised High grade: - Nuclei lose polarity - Mitotic figures - Necrosis Can lead to adenocarcinoma (p53) Treatment: PPI Endoscopy radiofrequncy abalation
41
Oesophageal cancer
**Squamous cell carcinoma** Assoc. with alcohol and smoking Oesophageal injury Proximal (upper) oesoephagus Pts can present with hoarse voice, cough (as tumour in proximal oesophagus) **Adenocarcinoma** Assoc. with Barett's, obesity Lower 1/3 of oesophagus Presents as progressive dysphagia, weight loss, haematemesis
42
Acute and chronic causes that damages the stomach conditions
Acute: **B**urns (Curling's ulcers) **A**lcohol **N**SAIDs **T**rauma Chronic: **A**utoimmune **B**acterial (H.Pylori) **C**hemical
43
Autoimmune gastritis
Autoimmune destruction of parietal cells due to autoantibodies against IF and parietal cells Affects fundus/body Leads to loss of parietal cells and intestinal metaplasia Loss of HCL (achlorhydria) secretion - leading to bacterial overgrowth, leading to increased gastrin (to compensate) Megaloblastic (pernicous) anaemia Persistent inflammation leads to dysplasia which leads to gastric adenocarcinoma
44
H.pylori
Most common cause of gastritis H. pylori colonises mucosa leading to chronic inflammation IL-8 released from epithelial cells attracts neutrophils Antra-predominant gastritis: hypergastrinaemia, duodenal ulceration, pts with lower with IL-8 Pangastritis: hypochlorhydia, intestinal metapalsia, gastric adenocarcinoma. Assoc with increased IL-8 Consequences peptic ulcer: peforates, haemorrhage, fibrosis Investigations: Urea breathe test, stool H.Pylori antigen
45
Chemical: Gastritis
Acidic damage to mucosa (imbalance between too much acid, and decresed mucosal defences Few inflammatory cells Oedema and elongation of gastric pits, ulceration (loss of mucosal layer) Usually in antrum Causes: bile acid, NSAIDs, alcohol, iron
46
Gastric cancer
Adenocarcinoma: Malignant prolfieration of epithalial cells Symptoms: Acanthosis nigricans, leser trelat sign Due to autoimmune or H.Pylori Chronic inflammation - intestinal metaplasia - intestinal dysplasia Classified via Lauren classification into: - Intestinal - Diffuse **Diffuse gastric cancer:** Malignant cells with mucin vacuoles (**signet ring cells**) - Linitis plastica: invades extensively without being endoscopically obvious, leads to thickening of stomach wall Krukenberg - GI mets to ovaries Virchow's node - supraclavicular lymph node (first place gastric ca. metastasises to) Sister Joseph nodule - Umbilial metastasis **Intestinal:** Risk factors: Intestinal metaplasia
47
Upper GI bleed symptoms
Haematemesis (vomiting blood) Coffee ground vomit Malaena (black faeces) Source: oesophagus, stomach, duodenum
48
Causes of upper GI bleeding
Peptic ulcer (due to acid, NSAIDs, H.pylori) oesophagitis gastritis malignancy
49
Management of upper GI bleed
**Rescuitate**: Pulse, BP IV access for fluids/blood O2 **Risk assess:** Endoscopy: High risk: Emergency endoscopy Medium risk: Endoscopy next day Low risk: Outpatients Risk score: Rockall (Endoscope. Predicts mortality), Glasgow Blatchford (Clinical. Predicts risk and need for intervention) Once bleeding stopped: **Drug therapy** IV PPIs (only given after endoscopy) Aspirin Can restart clopidogrel/DOACs if needed Tranfuse blood only if Hb\<7 Transfuse platelets if actively bleeding FFP if INR \>1.5
50
Risk score for upper GI bleeding
Endoscopic: Rockall (predicts mortality) Clinical: Glasgow Blatchford (predicts need for intervention and death)
51
Varices
Dilated collateral blood vessels due to complication in portal hypertension, usually due to cirrhosis Cirrhosis - incrased hepatic resistance - portosystemic shunting - varices Causes: alcohol, cirrhosis, non-alcoholic liver fatty disease Treatment: Endoscopic banding, TIPS (trans jugular intra heptic shunt), B-blockers
52
Varices bleeding management
**Resus:** restore circulating voume, tranfuse Hb \<7 **Diagnosis:** Endoscopy Prophylaxis: Non cardiac B-blockers (carvedilol) or band ligation **Therapy:** Antibiotics and Terlipressin (vaspressor) Endoscopic banding 1st line for oesophageal varices TIPS for uncontrolled variceal bleeding, "resucue" procedure for failed endo Balloon tamponade (temporary salvage) Prevent re-bleeding: B-blocker + repeated band ligation
53
Risk factors for colon adenocarcinomas
No. and size of polyps IBD Family history Polyposis syndromes: - Familial adenomatous polyposis (APC gene) - Lynch syndrome (mismatch repair gene)
54
Bowel screening
50-74 yrs every 2 years Faecal-occult blood test If +ve, send for colonscopy
55
Diseases assoc. with HLA-B27
UC Ankylosing spondylitis Reactive arthritis Psoriatic arthritis
56
Neuroendocrine tumour
Carcinoid tumour Commonly at appendix, benign
57
Gastrointestinal stromal tumour
Spindle cell tumours from intestinal cells of Cajal Sarcomas Most have TK abnormalities so treated with Imatinib c-kit (CD117) stain identifies upregulation of TK receptors Symptoms: Dysphagia, blood in stool
58
Enteropathy associated T cell lymphoma (EATL)
Complication of coeliac - overstimulation of T cells leading to high risk
59
Diseases which have granulomas
Crohn's Sarcoidosis Infective colitis (e.g. TB, shigella) Diverticular disease
60
Viral infections in intestines
Adenovirus CMV - in immunosuppressed, viral inclusions in epithelial cells HSV - multi nucleate giant cells, nuclear inclusions
61
Drugs which cause liver injury (6)
Paracetamol Aspirin Simvastatin Ramipril Levothyroxine Metformin
62
What is a common symptom in PBC?
Pruritis (itching) due to accumulation of bile acids
63
Autoimmune hepatitis (defintion, symptoms, investigations, histology, treatment)
Chronic inflammatory disease if untreated, leads to cirrhosis, liver failiure and death. Characterised by increased autoantibodies, IgG and inflammatory changes on histology More common in women Symptoms: Hepatomegaly, jaundice, weight loss Diagnosis: Increased ALT and AST Increaesd auto-antibodies - anti-ANA, SMA, LKA (\> 1:40) Increased IgG Liver biopsy Histology: interface hepatitis: inflammatory hepatocytes at junction of portal tracts and liver parenchyma Treatment: Glucocorticooids +/- Azathioprine
64
Marker for HCC
Alpha-fetoprotein
65
Spontaenous bacterial peritonitis
\>250 neutrophils, no intra-abdominal infection Usually, gram -ve bacteria Trreatment: IV antibiotics + IV albumin
66
Refractory ascites
Large volume parencentesis TIPS (trans jugular intrahepatic shunt) - imporves renal function and Na+ excretion - concern with encephalopathy
67
Haemochromatosis
AR (C282Y mutation) Excess absorption of Fe Leads to iron overload in liver, heart, skin (bronzing of skin) Investigations: Transferrin (high) Ferritin (high) Biospy: Perl's stain - stains iron blue Treatment: venesection
68
Causes hyperamylasaemia
Pancreatitis Bilary conditions e.g. cholangitis Ischaemia Viral infection e.g. mumps Stone in parotid duct (as produces amylase)
69
LFTs and jaundice
Jaundice clinical features: Yellow sclera, skin, dark urine, pale stool, itching Pre-hepatic: Haemolysis or increased bilirubin e.g. sickle cell, malaria Hepatic: Hepatitis, Gilbert's syndrome - Dark urine Post-hepatic: Obstruction in bile duct e..g gallstone - Dark urine, pale stool
70
Most common cause of upper GI bleed in cirrhosis
Variceal bleeding
71
What does a porcelain gallbladder indicate?
Calficiation of gallbaldder due to inflammation. Increased risk of gallbladder cancer.
72
73
When can you see the small intestine on a XR?
When filled with gas
74
Chilaiditi syndrome
Loop of large intestine has moved in between diaphragm and liver
75
What imaging to use for inflammation, perforation, obstruction, ischaemia?
**Inflammation:** Abdo XR: useful for colitis US for cholecystitis CT first choice otherwise **Perforation:** CXR senstivie for free gas, CT confirm **Obstruction:** AXR, CT to look for cause **Ischaemia:** CT 1st choice
76
Chronic biliary/cholestatic disease: PBC and PSC
Presents as chronic liver disease e.g. itch (due to excess bile acids) or abnormal LFTs (Increased Alk Phos, GGT \> 6 months) Causes: PBC, PSC Histology: Both have focal, portal predominant inflammation and fibrosis of bile duct. **Primary biliary cholangitis:** Autoimmune granulotamous destruction of intrahepatic bile ducts Middle aged women Symptoms: obstructive jaundice, can lead to cirrhosis Labs: - autoimmune (anti-mitochondrial antibodies) and high IgM Treatment: Ursodeoxycholic acid, liver transplant **Primary sclerosing cholangitis:** - inflammation and sclerosis of intra-hepatic and extra-hepatic bile ducts leading to peri(around)ductal fibrosis and onion skin appearence **Assoc. with UC.** Presents with obstructive jaundice, cirrhosis, risk of chonalngiocarcinoma (cancer of bile duct)
77
4 types of chronic diffuse liver disease
Fatty liver - alcoholic, non-alcoholic Chronic hepatitis Chronic bilary/cholestatic disease Genetic/depositional - Wilson's, Haemachromotosis
78
2 types of diffuse acute liver disease
**Acute hepatitis** - Diffuse hepatocyte injury - Spotty necrosis **Acute cholestasis** - Bile pigment (brown)
79
Specific histology of Hep B
Ground glass cytoplasm in hepatocytes
80
81
Haemachromotosis
Symptoms: Cirrhosis, secondary diabetes, bronze skin, cardiac arrythmia, gonadal dysfunction (as iron can deposit in testicle and lead to testicle atrophy) **Labs:** - Increased ferritin (as tissues loaded with iron) - Low TIBC/transferrin (as body wants to make less transferrin so there is less iron binding and iron levels), - Increased serum iron - Increased saturation **Biopsy:** brown pigments in heptocytes (can be iron or lipofuscin (wear and tear pigment) but prussian blue stain turns iron blue)) Increased risk of HCC Treatment: phlemobotomy
82
Wilson's disease
AR Lack of copper transport in bile, and lack of copper binding to ceruloplasmin (carries copper in blood) Leads to build up of copper in hepatocytes which leaks into blood Presents in childhood, cirrhosis, neuro symptoms, increased risk of HCC Labs: Decreased ceruloplasmin
83
Reye syndrome
Liver failure and encelopathy in children with viral illness who take aspirin
84
Hepatic vascular disease
Due to obstruction of hepatic vein outflow Budd chiari syndrome: Thrombosis of hepatic vein Can be due to HCC Painful hepatomegaly, ascites
85
Acute hepatitis
Inflammtion of liver parenchyma Presents wtih RUQ tenderness, **jaundice** (due to increased CB, UB - as bile ducts destroyed so CB leaks out, and heptocytes destroyed so less UB), **dark urine, fever, malaise** **Causes:** Viral hepatitis (Hep viruses, EBV, CMV), autoimmune, drug (paracetamol) **ALT\>AST** **Patho:** Hepatocytes infected with virus will lead to cytoxic killing of heptocytes **Microscopy:** spotty necrosis, diffuse hepatocyte injury, inflammatory cell infiltrate inc. plasma cells \< 6 months If \>6 months - chornic hepatitis
86
Specfic feature of Hep B on microscopy?
Ground glass cytoplasm - due to accumulation of surface antigen
87
What can co-amxoiclav do to liver?
Acute cholestatic hepatitis
88
Chronic hepatitis
Liver inflammation/abnormal LFTs for at least 6 months Presentation: chronic hepatitis Causes: Hep B, C, autoimmune, genetic Investigations Biopsy: Grade (degree of inflammation) - guides treatment, stage( degree of fibrosis) - guides prognosis
89
Focal liver disease
Asymptomatic or heptomegaly, RUQ pain or jaundice Can be non-neoplastic or neoplastic Non-neoplastic: Cysts (Von Meyenberg complex - biliary harmatoma) Abscess (can arise from ascending cholangitis) Neoplastic: Benign e.g. **hepatic adenoma** (young women, assoc with hormon therapy), **bile duct adenoma, haemangioma** (benign blood vessel tumor) Malignant: **HCC** (arises in cirrhosis, elevated alpha feto protein), **cholangiocarcinoma** (adenocarcinoma of bile duct), **angiosarcoma**, **liver mets** (commonly adenocarcinoma from GI tract) Investigations US, CT, biopsy (Need to exclude malignancy)
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Lymphocytic colitis vs collagenous colitis
**Lymphocytic colitis** Chronic watery diarrhoea, normal endoscopy Assoc. with other autoimmune diseases e.g. myasthenia gravis, RA Microscopy: colonic epithelial lymphocytosis Increassed chronic inflammatory cells in lamina propria **Collagenous colitis (pic)** Chronic watery diarrhoea, with normal colonscopy Mostly elderly women, smokers May precede Crohn's Histology: patchy thickening of subepithelial basement membrane
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GORD
Retrograde movement of gastric acid into oesophagus Symptoms: heart burn, regurgitation, epigastric pain Due to weakness of lower oesophageal sphincter, hiatus hernia Microscopy: inflammtory infiltrate, basal zone of squamous epithelium is hyperplastic Complications: Barret's oesophagus
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Peptic uclers
Duodenal ulcer: usually due to H.pylori. Epigastric pain which improves with meal - Almost never malignant Gatric ulcer: NSAID and H.pylori. Epigastric pain which worsens with meals - Can be caused by gastric carcinoma

Year 3 (15 decks)

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