SPLEEN Flashcards
Causes of splenomegaly
1. Increased function
- Removal of defective RBCs - thalasemia, sickle cell
- infective - acute (EBV, CMV, HIV, endocarditis), chronic (toxoplasmosis, malaria, schistomiasis)
- immunological - RA, SLE, sarcoid
2. Abnormal flow
- Portal HTN = cirrhosis, PVT/SVT
3. Infiltration
- leukemias
- lymphoma
- myeloproliferative disease
- metastatic tumour (melanoma)
What organisms cause OPSI?
- Streptococcus pneumoniae (responsible for over 50% of cases of OPSI)
- Haemophilus influenzae type b
- Neisseria meningitidis
- Capnocytophaga canimorsus (acquired by dog or cat bites)
What/when vaccinations do you give to prevent OPSI?
- Pneumococcal = Pneumovax23 (booster after 5 years)
- Hib = Hiberix (no booster)
- Meningococcus = Meningococcal C conjugate (Meningitec). No booster
antibiotic prophylaxis for OPSI
Amoxycillin 250-500 mg daily
- Immunocompetent = 2 years
- Immunocompromised = lifelong
What is the mechanism of OPSI?
- loss of splenic opsonins (IgG and C3b) and splenic macrophages after splenectomy
- encapsulated bacteria not able to under phagocytosis
Differentials for Virchow’s node
Cancer until proven otherwise
Supraclavicular
- SCC (nasopharyngeal, tongue, laryngeal)
- Thyroid
- Melanoma, Merkel cell
Infraclavicular
- Gastric (classic), oesophageal
- Breast
- Pancreatic
- Testicular
- Lymphoma
What is the pathological hallmark of GAVE?
“Watermelon stomach” ie Gastric Antral Vascular Ectasia
superficial fibromuscular hyperplasia of gastric antral mucosa with capillary ectasia and microvascular thrombosis in the lamina propria
What is a Dieulafoy’s lesion
- An abnormal tortuous artery that courses through the submucosal layer in the absence of an associated ulcer.
- 95% occur in the upper stomach within 6cm of GO junction commonly on the lesser curvature, however they can occur anywhere in the GI tract (duodenum 18%, colon 10%, jejunum 2%, oesophagus 2%)
What is the Savary-Miller classification for GORD?
Type I - single erosion
Type II - multiple erosion
type III - Circumferential erosion
Type IV - complications (ulcer, stricture)
Type V - Barrett’s
How do PPIs work and what are some complications?
Mechanism
- irreversibly binds to H-K+ pump in gastric parietal cells
- H+ ions not secreted into the gastric lumen
- therefore treats acid refulx only
Complications
Gastric - C diff colitis, microscopic colitis, fudal polyps
Nutritional - B12, Mg and Fe malabsorption, calcium (?oestoporosis)
How would you investigate GORD?
Endoscopy
Confirm diagnosis and define anatomy
- Objective evidence of GORD
- Assess grade of reflux using Savary-Miller classification
- Monitor and treat complications of reflux if present
- Strictures ® Dilatations
- Barrett’s
Anatomy
- hiatus hernia
- short oesophagus (caused by Barrett’s, cancer, achalasia)
Manometry
- Exclude motility disorder
- all patients pre-operatively
- Exclude motility disorder (e.g. achalasia, scleroderma/CREST)
Ambulatory pH monitoring
- selective
- Useful in cases if endoscopy is negative or in extra-oesophageal symptoms
- Can clarify whether symptoms are associated with reflux events.
What is the pathogenesis of achalasia?
Destruction of inhibitory neurons in myenteric plexus within the distal oesophagus leading to unopposed activation of excitatory neurons
Loss of inhibitory neurons effects
- Smooth muscle effects = aperistalsis (dilated proximal oesophagus)
- Skeletal muscle effects = LES incapable of relaxation causing increase in resting pressure
what is the difference between traction and pulsion oesophageal diverticula?
Pulsion diverticula (intra-luminal)
- form as a result of high intraluminal pressures against weaknesses in the GI tract wall.
- Zenker diverticulum occurs due to increased pressure in the oropharynx during swallowing against a closed upper esophageal sphincter
traction diverticula (extra-luminal)
- occur as a consequence of pulling forces on the outside of the esophagus from an adjacent inflammatory process
- (eg, involvement of inflamed mediastinal lymph nodes in tuberculosis or histoplasmosis).
Oesophageal Cancer risk factors
Modifiable
- smoking
- alcohol
- obesity
- nutritional (N-nitroso compounds)
Non-modifable
- white male
- achalasia
- tylosis
- Barrett’s
Rationale for NACT
“PRIME” the patient
P - increased pCR rates
R - tumour regression can improve resectability and R0 resection rates
I - investigate - research trials
M - micrometastatic disease reduced/eliminated
E - evolution - biological behaviour followed
Eponymous signs in gastric cancer
Mets
- Krukenberg - seeding to ovaries
Lymph Nodes
- Virhow’s - supraclavicular
- Irish’s - Left axillary
- Sister-Mary Joseph = per-umbilical
Skin
- Trousseou - migratory thrombophlebitis
- Leser-Trelat - multiple seborrhoeic keratosis
What is the Spigelman criteria for duodenal polyps?
Based on 4 parameters.
- number
- size
- degree of dysplasia
- histology (villous, TV, tubular)
What are the non-traumatic indications for performing a splenectomy?
Haematological disorders
- ITP
- TTP
- Autoimmune hemolytic anaemia not responding to steroids
Neoplasms
- CML, CLL
- Lymphangiosarcoma
Benign
- Splenic vein thrombosis
- abscess
- cyst
What is the post-gastrectomy syndrome?
problems with anastomosis, motility, malabsorption or remnant stomach
Anastomosis
- leak
- stricture
- obstruction (e.g. internal hernia)
- marginal ulcer
Motility
- rapid transit - dumping, post vagotomy diarrhoea
- slow transit - gastroparesis, biliary/alkaline gastritis
Malabsorption
- microcytic anemia - Iron absorbed in duodenum, bypassed in B II or R-Y. Also needs to be reduced by acidic environment to be absorbed.
- macrocytic anemia - Decreased parietal cell mass –> less intrinsic factor –> B12 deficiency. Acid facilitates bioavailability
- vit D - Fat malabsorbtion after gastric resection due to inefficient mixing of food, bile, pancreatic enzymes –> decreased a
Remnant stomach
- peptic ulcer
- remnant gastric cancer
How does dumping syndrome occur?
Early or vasomotor dumping.
- Rapid emptying of hyperosmolar chyme from the residual stomach into the intestine
- causes fluid shifts from the vascular compartment;
- causes a fall in plasma volume and vasomotor symptoms, such as weakness, dizziness, fainting, headache, palpitations, sweating and dyspnoea.
Late dumping or reactive hypoglycaemia.
- Rapid transit of high carbohydrate load into small intestine causes excessive insulin release
- later reactive hypoglycaemia 1–3 hours after eating.
what are the causes of stomach cancer?
GENETIC
- CHD-1 mutation = associated with lobular breast cancer and signet ring colonic malignancy)
- Lynch syndrome
- p53 mutation (Li-Fraumeni syndrome aka SBLA syndrome - Sarcoma, Breast, Leukemia, Adrenal gland)
- BRCA-2
ENVIROMENTAL
- previous gastric surgery
- H pylori (cagA +)
- chronic gastritis (Correa hypothesis)
- cigarette smokers
- high nitrates
What is the pathogenesis of stomach cancer?
The pathogenesis of gastric cancer is complex and multifactorial and involves
- a pathway of transformation from normal mucosa to gastritis to atrophic gastritis to metaplasia to dysplasia to cancer (Correa hypothesis).
- Continuation of cellular destruction results in chronic atrophic gastritis and intestinal metaplasia.
What are the 3 features to look for on oesophageal manometry for achalasia?
- Failure of LES to relax (skeletal muscle)
- LES hypertension
- Failure of smooth muscle oesophagus to contract causing aperistalsis (smooth muscle)
