GI Pathology Flashcards
Causes of Oesophagitis (5)
gastro-esophageal reflux. Bacterial Viral - HSV1 and CMV Fungal - candida Chemical - ingestion of corrosive substance
Risk Factors for Gastro reflux (4)
Hiatus hernia (overweight), defective lower esophageal sphincter, increased ab pressure (vomiting) increase ab contents (outflow obstruction)
Histology of Oesophagitis (4)
Squamous cell affected basal cell hyperplasia, papillae elongation, inflammatory cells in basal laminae
Symptoms of Oesophagitis (1)
heart burn - mistake with cardiac symptoms?
Complications of Oesophagitis (6)
ulceration –> hemorrhage –> perforation –> fibrosis –> stricture/narrowing –> Barretts Oesophagus
Barrett’s Oesophagus
Chronic Reflux. Squamous cell metaplasia to collumnar, goblet cells (muscus secreting) in the laminae propria
Barrett’s Disease Progression (4)
Barrets –> dysplasia –> high grade –> adenocarcinoma
Oesophageal Carcinoma type + risk facors (5)
Squamous cell Tobacco (chew), alcohol thermal damage, HPV, ?? ethnicity
Presentation of Carcinoma and Adenocarcinoma (4)
Dysphasia - occlusion due to polypoidal lumps –> stricture and ulceration
Causes of Acute Gastritis (aggression (3) vs. Defense (3))
Increased aggression: chemical injury (NSAIDs, alcohol, smoking) corrosive radiation.
Impaired defense: delayed emptying (occlusion), prostoglandin imbalance = uncontrolled emptying, ischemic shock
Causes of Chronic Gastritis (ABC)
A = autoiummune - antiparietal and anti intrinsic factor antibodies B = Bacterial infections (H. Pylori) C = Chemical injury (NSAIDs)
Gastritis
Inflammation the mucousa of the stomach
Peptic Ulcers (depth)
Localized defect at least as deep as submucosa (can perforate vessels and musculature).
AKA slightly more serious Gastritis
Causes of ulcers (5)
Autoimmune NSAIDs H.Pylori Hyperacidicity Duodenal- gastric relfux
Acute Vs Chronic ulcers (appearance)
Acute = full thickness, necrosis with slough/ debris (neutrophils and dead tissue), red if reach vessel
Chronic = clear cut edges, extensive granulation tissue and deep scaring into the musculature –> bleed to death
Stricturing, hemorrhage, perforation and penetration fistula
Complications of ulcers
Hemorrhage = aneamia and perforation = peritonitis
Gastric Cancers (4 examples)
adenocarcinomas, endocrine tumours, MALT lymphomas and stromal tumours
Macroscopic subtypes of gastric cancer (3)
1) Exophytic - protrude into lumen
2) Linitis plastica - spread all along mucosa (diffuse)
3) Excavated - concave lesion
Diffuse vs intestinal gastric cancers
Diffuse = high grade, less differentiated, scattered growth Intestinal = well differentiated, metaplasia, adenoma aspects
Coeliac disease: reaction to what, releases which cytokine and induces which immune cells to kill which body cells (name of pathogenesis)
Gliadin in Gluten –> IL-15 –> intraepithelial lymphocytes (IELs) –> enterocytes killed
Immune mediate enteropathy
Presentation of Ceoliac (4 types)
Atypical = non specific symptoms Silent = no symps but evident serology OR villous atrophy Latent = no symps positive serology BUT no villous atrophy Symptomatic = aneamia, diarrhoea, bloating, fatigue (+ positive results)
Serology test for Coeliac
BEFORE gluten free diet and biopsy. Non invasive. looks at: IgA antibodies to transglutaminases (TTG)
IgG antibodies deaminate gliadin
Histological signs of Coeliac (4)
villous atrophy, crypt elongation, increased IELs and laminae propria inflammation
Blind ended sacs of bowel and protrusions of mucosa and submucosa
Diverticular of the large bowel
Most common site for Diverticular
sigmoid colon inbetween the taemic coli
Risk factors for Diverticular?
Age (>60) and fiber content of diet
Causes of Diverticular (2)
1) Increased intralumen pressure - due to irregular/ unco-ordinated peristalsis
2) Points of weakness the bowel wall - changes in connective tissue with age
Symptoms of Diverticular and % Asymptomatic?
Cramps and alternating diarrhoea and constipation. 90%
Complications of Diverticular (acute and Chronic)
Acute = Diverticulitis (bacterial) --> abscesses --> sepsis or perforations --> perionealitis Chronic = Intestinal obstruction = vomiting, distension and pain. Fistulas and colitis (rectal bleeding)
Colitis Acute VS Chronic causes
Acute = Infective: Campylobactor, shigella, salmonella (stool cultures) OR antibiotic related
Chronic = idiopathic (unknown) OR Ischemic
IBD?
And prevalence
Idiopathic bowel disease. Age 20 - 40 peaks in urban areas and includes Ulcerative Colitis and Crohn’s disease
UC VS Crohns (site + appearance of ulcers)
UC = Rectum –> up, continuous.
Crohn’s = manly iliopathic, small bowel. Transmural (through wall), skip lesions (not continuous). ‘Cobble stone’ lateral and longitudinal ulcerations.
UC vs Crohns (Presentation)
Both?
differences
Both = diarrhoea, pain, anorexia and weight loss
UC = inc. urgency, diarrhoea and rectal bleeding, ab pain, Granular/ red tissue
Crohn’s = Relapsing diarrhoea with blood, colicky pain, palpable mass. Granulomas
UC vs Crohn’s (Complications)
UC = toxic mega colon, perforation (emergency), bleeding (ulcers), carcinoma Crohn's = Fistula, strictures, heamorrhage, large bowel cancer, short bowel syndrome (Malnutrition)
Ischemic Colitis - most common site?
Secondary to acute, chronic or intermittent reduction in blood flow.
Splenic flecture due to crossing over of blood supply (watershed)
3 types of Ischemic Colitis
Transient = sudden onset, urgency and rectal bleed. resolve in 2 days - 2 weeks
Chronic segmental ulceration
Acute gangrenous - 10-20% of cases = surgical emergency
Causes of Ischemic colitis (3)
1) arterial embolism following MI or AF = 50%
2) Arterial thrombosis of SMA OR heamorrhage infarction of thrombosis of the SMV 30%
3) Non-occlusive - due to low cardiac output + SMA vasoconstriction (post op)
Colorectal polyps - 3 morphologies
Mucosal protrusion - secondary to pathology or lesion in bowel
Pundulated - on a stem
Sessile - broad flat base
Flat
Neoplastic (benign vs malignant), haemartomatous, inflammatory or reactive - further divisions
Classification of polyps - epithelial of mesenchymal
Examples of Haemartomatous (2)
Peutz-jeghers: STK11 gene on chromosome 16 - autosomal dominant. Teens in 20s - ab pain, GI bleeds, aneamia. Multiple polyps in small bowel
Juvenile: sporadic, spherical pundulated in the colon and small bowel in children
Examples of benign neoplastic polyp
Adenomas = epithelial, polypoid and flat, recto-sigmoid and caecum. Precursor for CR cancer 80%
Adenoma –> adenocarcinoma over about 10 years
Either villous, tubular or both
Risk (7) and protection (4) for Colo-rectal cancer
Risk = fat, red meat and calcium, obesity, oral contraceptive, alcohol and IBD Protective = fiber, folate, NSAIDs and aspirin
Mutation in what gene = 100% lifetime risk of colon cancer
autosomal dominate
Mutation in APC Tumor suppressor gene –> multiple benign andenoma polyps
Which syndrome gives a 50% lifetime risk of colon cancer
autosomal dominate
Lynch syndrome - mutation in missmatch repair genes. Also ovarian, endometrial, gastric and urinary tract
Examples of Colo-rectal cancer (4)
adenocarcinoma (95%), squamous cell carcinoma, adenosquamous, neuroendocrine and undifferentiated
Grading of CR cancers
Duke’s A-D
A = bowel wall no nodes = highest 5 year survival
B = invasion of wall (peritoneal - transcoelomic)
C = Regional lymph mets (regardless of depth) highest frequency
D = distant mets (lung, liver)
Sterile Sites in the GI tract
Pancreas, peritoneal cavity, stomach, gall bladder and liver
Normal Flora of the oropharynx (7)
Viridans strept, strept pyogenes, candida, Staph, Neissuria and Haemophilus and anaerobes
Normal flora of the colon (4)
Candida, anaerobes (bacteriodes), Enterobacteriaceae (gram negative bacilli and coliforms), Gram positive enterococci
Most common Coliform in the colon
E.coli
Cause of Angular Celitus
Inflammation of the corners of the mouth by C.albicans
Oral candidiasis - presentation
Oral thrush - loss of taste and pain when eating
1) pseudomembrane plaques on buccal mucosal palate
2) Atropic = erythemia with no plaques
High Risk of Mucositis
Chemo induced - can last up to 2 weeks afterwards.
Bacteraemia (viridans strept)
Dental plaques (on the tooth) progression (3)
Carries - bacteria on surface of tooth
Pulpitis - erosion of bone by acid released from bacteria
periapical abcess - spread to base of the tooth (nerve)
Peridontal infections (in the gum) progression (3)
gingitvitis - inflammation
peridonitis - loss of soft tissue of tooth sockets
Vincents Angina - infection of soft tissue –> neck
Peritonsillar infection or Quinsy cause
S. Aureus = unilateral swelling of tonsil
Peritonsillar infection symptoms (4)
Sore throat, painful swallow, ear ache, deviation of uvula to affected side (airway compromised)
Complication of Parapharyngeal space infections
Carotid sheath infection –> supportive jugular thromboplebitis and Lemierre’s Syndrome
Cause of oesophageal rupture
increased interoesophageal pressure or negative interthoracic pressure
eg. straining and continuous vomiting
Complication of oesophageal rupture (5)
1) Gastric contents in medialstinum = chemical medialstinitis –> bacterial infection and medialstinal necrosis
2) Sternal pain, crepitations and crackles with every heart beat
3) Dysponea, sepsis, tachyponae, cyanosis, hypotension
4) Neck pain, difficulty swallowing and speaking
5) Epigastric pain that radiates to the shoulder, back pain
Treating a ruptured oesophagus
avoid oral intake, nutritional support, IV antiBs, PPI and drainage of fluid and necrotic tissue
H. Pylori mode of action
Uteruses hydrolyzes the acid in the stomach allowing other bacteria to penetrate the mucosal lining = ulceration
Testing for H. pylori (4)
Urease Breath test, faecal antigen, serology (IgG for chronic and IgM for acute), culturing and sensitivity testing
Cholangitis (bile duct): symptoms and test results
Fever, ab pain, jaundice.
Liver test = Inc phosphatases, GGT, and conjugated billirubin
Cause of Cholangitis
Enterobacterieae - secondary to stones, stenosis, stents and surgery
Cholecystitis (gall bladder) Test results
Elevated total serum billirubin and alkaline phosphatase.
Positive murphy’s sign and radiological image
Liver Abscess causes
Strephtocci or coliforms - Ascending biliary tract infection, post peritonitis or colonic perforation
Staph aureus - haematogenous from endocarditis
Entamoeba Histoltytica - parasite in amebic cyst in contaminated food or faecal matter –> Trophozoite stage (invasive disease)
Test results for Liver abscesses
Serum alkaline phosphatases and bilirubin elevated
Cause of bacterial overgrowth and consequences
Achorhydria (high acid states) eg. after surgery
Blind loops of bowel
impaired mobility and radiation damage
Results in malnutrition and chronic diarrhoea
Whipples Disease
Location, appearance cause and associated symptoms
Distal duodenum
White plagues
Tropheryma Whipplei found in sewage
Chronic malabsorption, ab pain, diarrhoea, weight loss
Gastroenteritis pathogenesis
Toxins - staph or shigella
Direct invasion of bacteria into mucosal wall
6 hours of Gastroenteritis symptoms
Straph Aureus or Bacillus cereus
8-16 hours of gastroenteritis
Costridium infection
16 + hours of GI symptoms
Viral or bacterial infection
Bacterial causes of Gastroenteritis in Small bowel (6)
Salmonella E.coli Clostridium Staph aureus Bacillus cereus Vibro cholerae
Bacterial Causes of gastroenteritis in colon (4)
Campylobacter
Shigella
C. Difficile
Enteroinvasive E. coli
Viral causes of GI in the small bowel (3)
rotavirus
norovirus
astrovirus
Viral cause of GI in the colon (3)
Cytomegalovirus
Adenovirus
Herpes simplex
Parasytic GI in the small intestines (4)
Cryptosporidium
Microsporidium
Cyclospora
Giardia lamblia
Bacterial Gastroenteritis worsened by AntiBs
Salmonella and Ecoli
Mycobacterium tuberculosis
Aspiration of TB = non healing ulcers, obstructed gastric outflow, fistulas
Can be confused with malignancy
Complications of intra-abdominal infections (4)
- treatment
+ For last one:
- symptoms
- causes
1) Diverticulitis - antiBs or abscess drainage surgery
2) Meckel’s Diverticulum = bleeding, obstruction, infections, perforation OR silent - surgically remove
3) Appendicitis - Surgical or AntiBs. CT difficult to diagnose
4) Intra-peritoneal abscess - Pus in localised areas = non specific sweating, anorexia, swinging fever, pain and swelling. Due to ulcers, diveriticula perforation, mesenteric ischemia, trauma, pancreatitis
Structures in close proximity to the pancreas
spleen, duodenum, common bile duct, aorta, IVC, splenic arteries, adrenal glands
Acute Pancreatitis Symptoms (3)
Ab pain –> back
N&V
Raised serum amylase and lipase
Causes of Acute Pancreatitis
Gallstones
Alcohol
Rare = vascular insufficiency, mumps, coxackie B, hypercalcaemia
Idiopathic
Pathogeneses of Acute pancreatitis
- Mild
- Severe
Leakage and activation of pancreatic enzymes
Mild = swollen and fat necrosis - chalky calcium deposits
Severe = Swollen, necrosis and haemorrhage in flanks, umbilicus signs and Pseudocytes/ abscess formation
Complications of Acute Pancreatitis
shock, intravascular coagulation, haemorrhage, psuedocytes with pancreatic secretion
Pathogenesis of Chronic Pancreatitis
Irregular involvement of gland
Atrophy - fibrosis occurs
Dilated and disordered ducts
Fatty replacement
Symptoms of Chronic Pancreatitis
Back pain, weight loss
Fiborous tissue mimics cancer histologically and radiologically
Causes of Chronic Pancreatitis - TIGARO
Toxic - alcohol and smoking Idiopathic Genetic - PRSS1 and SPINK1 genes = cleavage of trypsin and self digestion Obstruction to duct (cancer or scarring) Recurrent Acute Autoimmune
Complications of Chronic Pancreatitis
Malabsorption of Fat and fat sol vitamins –> steatorrhoea
Diabetes
Pseudocytes
Stenosis of common bile duct
Primary Pancreatic cancer
- age
- 5 year survival
- Male Vs Female
- Location
Pancreatic adenocarcinoma 60 - 80 years 4% 5 year M>F 60% in Head and 30% in body
Causes of pancreatic andeocarcinoma (4)
Smoking
Family history
Heavy alcohol and red meat
Chronic pancreatitis
Genes/ genetic conditions involved in Pancreatic Andenocarcinoma
HNPCC (mismatch repair)
BRACA2 (famillia)
Lynch syndrome
ATM (ataxia telangiectasia)
Presentation of
- Tumour
- Patient
in Pancreatic andenocarcinoma
Poorly defined, grey-white.
Associated with fibrosis (desmoplastic stroma)
Highly invasive and present in margins
Epigastric pain radiate to back Weight loss, purities, nausea Palpable gall bladder with no pain (Courvoisier's sign) Trousseau's syndrome (Migraines) Diabetes Jaundice
Pancreatic Neuroendocrine tumours
Most common type?
Endocrine tumour of the islets of Langerham
Insulinoma (benign) - increases hormone levels = hypoglycemia
Risk factors of Neuroendocrine tumours
age 20 - 60
Male = female
MEN - multiply endocrine neoplasia (eg. thyroid or pituitary tumours)
Functioning tumours
One that produces hormones
opo. Non- functioning
Results in the symptoms
P67
marker of speed of tumour growth and proliferating
High = poorly differentiated + sinister advance
Low = well differentiated, more common
Appearance of neuroendocrine tumours
Circumscribed or encapsulated
Solid
Multiple
Any where in the pancreas
Symotoms of Glucagonoma
Stomatitis, rash, diabetes, wight loss
Gastrinoma symptoms
Zollinger-Ellison syndrome:
Peptic ulcers and diarrhoea
Somatostatimona symptoms
Diabetes, cholelithiasis, hypochorhydria
VIPoma symptoms
Verner-Morrison syndrome:
Diarrhoea, hypoalkaemia and achlorydria
Threshold/ measure for Jaundice
> 40umol/L billirubin in blood
Pre hepatic Jaundice
Cause
Symptoms - type of billirubin
Signs
Too much billirubin produced
Haemolytic anaemia –> unconjugate billirubin in blood + not excreted
Yellow skin and eyes
Hepatic Jaundice
Cause
Type of billirubin
Signs
Too few functioning liver cells
- Acute diffuse live disease
- Chronic liver disease
- inborn errors
Conjugated billirubin = yellow eyes and dark urine
Post Hepatic (obstructive) Jaundice
Causes
Type of billirubin
Signs
Bile duct obstruction (stones, stricture, tumour)
Conjugated - soluble and excrete but not through gut
Yellow eyes, pale stools and dark urine
ALT
Alanine Transferase - released when liver cells die
AST
Aspartite Transfrase - released when liver, muscle and RBC death
ALP
When raised? (5)
Alkaline Phosphatases - produced in bile ducts
Raised in:
- cholestasis
- Infiltration disease
- Space occupying lesion
- cirrhosis (liver disease)
- Jaundice
Liver function test results for Jaundice
Raised AST and ALT and Alkaline phosphatases
Low Albumin and clotting factors
Test for Jaundice
Ultrasound - bile ducts
Biopsy
Cause of hepatic Jaundice
Heptatitis
Acute Vs Chronic Hepatitis
Acute = liver damage but the causes resides Chronic = balance between damage and repair and cause doesn't reside
Clinical spectrum of Hepatitis (6)
1) asympotatic
2) Malaise
3) Jaundice
4) Coagulopathy5
5) Encephalopathy
6) Death
Cause of hepatitis (5) Identified on biopsy
Viral, toxic, metabolic (fatty liver disease), Inherited and autoimmune
Parental Route of infection
Injected into blood stream
Feacal -oral Hepatitis
A
Paretnal Hepatitis
B (and D)
C
Water bourne zoonosis hepatitis
E
Highest risk to develope to chronic BUT least common Hep
Hep C
Viral Hepatitis with vaccines
A and B
Other virus that cause hepatitus as part of systemic disease
Epstein Barr (EBV), Cytomegalovirus (CMV), Herpes simplec (HSV)
Fatty liver diseases (2)
Alcoholic or non alcoholic fatty liver disease (NAFLD)
Pathogenesis of Alcoholic Fatty liver disease
High Alcoholic intake = overworked hepatocytes
Fatty change –> Alcoholic steatohepatocytes –> Cirrhosis
Cause of NAFLD
Type 2 diabetes
High blood sugar = over work hepatocytes = stress response:
- inflammation
- oxidative stress (mitochondria death)
Common Drugs that cause drug induced liver disease
Paracetamol and antiBs
DILI
Drug induced liver injury
Paracetamol induced hepatotoxicity - biopsy results
Uniform zonal necrosis
DILI causes what type of hepatitis
Acute Hepatitis - damage prevent if drug stoped
Inherited Cause of Hepatitis (3)
1) Haemochromatosis
2) Wilson’s Disease
3) Alpha 1 antitrypsin deficiency
Haemochromatosis or Bronzed diabetes Cause Symptoms Signs/ test results Treatment
Error of iron metabolism - abnormal HFE gene
Skin pigments, liver cirrhosis, carcinoma, diabetes, arthritis and cardiomyopathy
Perl’s stain on biospy = blue + high blood transferrin
Venesection (collect blood) - depletes iron stores
Wilson’s disease
Cause
Symptoms
Signs
Error of copper metabolism
Liver cirrhosis and aucte liver failure, brain ataxia
Low serum copper but high urinary copper
Alpha 1 antitrypsin deficiency
Causes
Signs
Symptoms
Abnormal enzyme = accumulates in globules of glycoprotein + insufficent levels in blood (cant neutralise proteolytic enzymes)
Positive PAD stain on liver biopsy
Liver cirrhosis and emphysema of lung
Autoimmune cause of hepatitis (+ one defining factor)
Autoimmune hepatitis -
Chronic billiary disease
Primary Biliary cholangitis (PBC) - anti-mitochondrial antibodies
Primary Sclerosing Cholangitis (PSC) - associated with Ulcerative Colitis
Diagnosis of Autoimmune hepatitis
Treatment?
Auto-antibodies, raised IgG and ALT.
Other autoimmune disease?
Plasma cells on biopsy
TREAT with immunosuppression
Liver Cirrhosis definition
Diffuse hepatic process of fibrosis.
Normal liver architecture –> abnormal nodules
End of chronic liver disease
Complications of fibrosis and liver disease
4
Portal hypertension = varices and splenomegaly, spider neavi, ascites
Liver cell failure = oedema, bruising, muscle wastage, hormone imbalance, ascites, poor fluid retention, jaundice and itching
Oestrogen XS = gynaecomastia, testicular atrophy
Vulnerable to infection
Hepatic Failure - acute and chronic?
Acute = rare but sever and rapid liver injury Chronic = end stage liver disease
Cause of Hepatic failure
Structure and function change due to cirrhosis
Signs of Hepatic failure
Ascites (accumulation of fluid in abdomen)
Muscle wasting, bruising, gynaecomastia,
(Portal hypertension=) spider neavi, caput medusa
Hepatic failure - biopsy?
NO - risk of haemorrhage
Other signs of liver disease
Clubbing and osteoporosis
LFT (liver function test) use?
Show diminishing Liver function
Specific Liver function tests (what function they measure)
Blood Albumin - synthesis function
Blood Bilirubin - excretion function
Prothrombin time - Storage function
Other non-specific LFT
glucose, urea, prothrombin, cholesterol, bile acids, steroid horomens, ferritin
imaging and biopsy
Liver damage tests - what the measure
Enzymes that are synthesised by cells in the bile canaliculi when they are damaged Include - Alkaline photphatase - GGT - Bilirubin - ALT - AST
GGT
Glutamyl transferase - elevated due to structural damage eg. alcohol, fatty liver, heart failure
Alpha fetoprotein is?
tumour marker for primary hepatocellular carcinoma
Elevation in Unconjugated bilirubin (3)
Pre hepatic and hepatic
Pre heptaic
- Heamolysis
- Inaffective erythropoiesis
Heptaic = inherited disorders of conjugation - Gilberts
Elevation of conjugated bilirubin (7)
Post hepatic and hepatic
Post hepatic
- Gallstones
- Biliray strictures
- Cancer of head of pancreas
- Cholangitis
Hepatic
- Intrahepatic obstruction
- Hepatitis
- Inherited disorders
AST/ALT ratio elevated + normal ALP
Hepatitis - take cultures and serology
AST/ALP normal and elevated ALP
Obstructive disease
Antibodies screen
Autoimmune
Urine tests to ID location of hepatic lesion
Prehepatic - no bilirubin in urine
Hepatic - variable
Post hepatic - Present in urine (dark) BUT no in stools (pale)
Most common malignant primary Liver tumour
hepatocellular carcinoma
Most common liver tumour
Secondary Mets from lung, breast, colon, pancreas and stomach
Adenoma of hepatocytes (benign) caused by?
Exogenous steroiuds eg. Anabolic steroids or oral contraceptive pill
Appearance of benign adenoma of the bile ducts
Macro and Micro
Macro - tiny white nodules (ductile cells) on surface of liver (mistaken for mets)
Micro - cuboidal, glandular - may contain bile
Risk factors for Hepatocellular Carcinoma
Cirrhosis, fatty liver disease, Hep C and B. Male> female
Diganosis of Hepatoceullar Carcinoma
Biopsy = poorly differentiated may produce bile (green)
Produce feto protein = raised levels in blood
Prognosis and Treatment (6) of Hepatocellular Carcinoma
<1 year Surveillance with ultrasound Resection - no cirrhosis, small or peripheral Transplant - <5cm or <3x <3cm (for non -ressectable) Ablation Embolization Chemo
Two types of Cholangiocarcinoma (adenocarcinoma)
1) Central - around the hilus = obstructive jaundice due to inflamation
2) Peripheral - intrahepatic = late presentation
Secondary liver tumours
Asymptomatice - many nodules before liver function impaired (large functional reserve)
Secondary liver tumours treatment
Surgical resection - avoiding bleeds as much as possible
Gall stones - causes
cholesterol, bile salts, bacterial growth = calcification = stone or calculus
Gall stones - risk factors
Female, middle age, overweight, diabetes
Types of gall stone (3)
Cholesterol = yellow opalescent Pigment = small and black + haemolytic anaemia Mixed = most common 10% contain calcium - visible on X-ray
Clinical features and complications (5) of Galls stones
Asymptomatic
Pain/ cramps - biliary colic
Jaundice Colorectal bleeds Localised pain as it moves Cholecysitis Carcinoma risk
Cholecystitis causes
Chemical or bacterial
Secondary to Stone
Cholecystitis Acute vs Chronic
Acute = large, swollen gallbaldder, painful at site
Chronic = thickening/ fibrosis of gallbladder
Pain and Jaundice
Courvoiser’s test
Palpable, non tender gallbladder + mild painless jaundice
= malignancy
Crohn’s Vs UC - risk and protective factors
UC = smoking is protective
Corhn’s = genetic more common in women, smoking = risk
