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UPPER GI > SPLEEN > Flashcards

SPLEEN Flashcards

1
Q

Causes of splenomegaly

A

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)
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2
Q

What organisms cause OPSI?

A
  • Streptococcus pneumoniae (responsible for over 50% of cases of OPSI)
  • Haemophilus influenzae type b
  • Neisseria meningitidis
  • Capnocytophaga canimorsus (acquired by dog or cat bites)
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3
Q

What/when vaccinations do you give to prevent OPSI?

A
  • Pneumococcal = Pneumovax23 (booster after 5 years)
  • Hib = Hiberix (no booster)
  • Meningococcus = Meningococcal C conjugate (Meningitec). No booster
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4
Q

antibiotic prophylaxis for OPSI

A

Amoxycillin 250-500 mg daily

  • Immunocompetent = 2 years
  • Immunocompromised = lifelong
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5
Q

What is the mechanism of OPSI?

A
  • loss of splenic opsonins (IgG and C3b) and splenic macrophages after splenectomy
  • encapsulated bacteria not able to under phagocytosis
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6
Q

Differentials for Virchow’s node

A

Cancer until proven otherwise

Supraclavicular

  • SCC (nasopharyngeal, tongue, laryngeal)
  • Thyroid
  • Melanoma, Merkel cell

Infraclavicular

  • Gastric (classic), oesophageal
  • Breast
  • Pancreatic
  • Testicular
  • Lymphoma
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7
Q

What is the pathological hallmark of GAVE?

A

“Watermelon stomach” ie Gastric Antral Vascular Ectasia

superficial fibromuscular hyperplasia of gastric antral mucosa with capillary ectasia and microvascular thrombosis in the lamina propria

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8
Q

What is a Dieulafoy’s lesion

A
  • 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%)‏
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9
Q

What is the Savary-Miller classification for GORD?

A

Type I - single erosion

Type II - multiple erosion

type III - Circumferential erosion

Type IV - complications (ulcer, stricture)

Type V - Barrett’s

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10
Q

How do PPIs work and what are some complications?

A

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)

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11
Q

How would you investigate GORD?

A

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.
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12
Q

What is the pathogenesis of achalasia?

A

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
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13
Q

what is the difference between traction and pulsion oesophageal diverticula?

A

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).
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14
Q

Oesophageal Cancer risk factors

A

Modifiable

  • smoking
  • alcohol
  • obesity
  • nutritional (N-nitroso compounds)

Non-modifable

  • white male
  • achalasia
  • tylosis
  • Barrett’s
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15
Q

Rationale for NACT

A

“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

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16
Q

Eponymous signs in gastric cancer

A

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
17
Q

What is the Spigelman criteria for duodenal polyps?

A

Based on 4 parameters.

  1. number
  2. size
  3. degree of dysplasia
  4. histology (villous, TV, tubular)
18
Q

What are the non-traumatic indications for performing a splenectomy?

A

Haematological disorders

  • ITP
  • TTP
  • Autoimmune hemolytic anaemia not responding to steroids

Neoplasms

  • CML, CLL
  • Lymphangiosarcoma

Benign

  • Splenic vein thrombosis
  • abscess
  • cyst
19
Q

What is the post-gastrectomy syndrome?

A

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
20
Q

How does dumping syndrome occur?

A

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.
21
Q

what are the causes of stomach cancer?

A

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
22
Q

What is the pathogenesis of stomach cancer?

A

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.
23
Q

What are the 3 features to look for on oesophageal manometry for achalasia?

A
  1. Failure of LES to relax (skeletal muscle)
  2. LES hypertension
  3. Failure of smooth muscle oesophagus to contract causing aperistalsis (smooth muscle)

UPPER GI (1 decks)

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