Tropical Pancreatitis

8/3/2019 Tropical Pancreatitis

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TROPICAL

PANCREATITIS

Dr.HARSHA VARDHAN E.V


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DEFINITION

Tropical chronic pancreatitis is a juvenileform of chronic calcific, non-alcoholicpancreatitis.

Prevalent almost exclusively in thedeveloping countries of the Tropical world.

Some of its distinctive features are -

Younger onset,

Presence of large intraductal calculi, Accelerated course of the disease,

High susceptibility to pancreatic cancer.


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CLINICALPRESENTATION

MC age : 10-30 yrs

The classical triad of clinical presentationin tropical chronic pancreatitis:

Abdominal pain. Steatorrhoea.

Diabetes (fibrocalculous pancreaticdiabetes).


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Abdominal pain

presenting complaint in 30%90%.

Severe, upper abdominal in location,

radiates to the back, and is relieved bystooping forward or lying in a proneposition.

Decrease and usually disappears withonset of exocrine insufficiency and/ordiabetes.


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PANCREATIC CALCULI

70 90% of patients have calculi bylater stages.

Intraductal in location. Mostly on the right side of first and

second lumbar vertebra on plainabdominal radiography.

Solitary or multiple, Large, dense, and rounded with well

defined edges.


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PANCREATIC CALCULI


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Maldigestion/steatorrhoea

With severe exocrine pancreaticinsufficiency, pass bulky, frothy, orfrankly oily stools.

Overt steatorrhoea present in 20%.


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DIABETES

Diabetes is an inevitable consequenceof TCP commonly occurring a decadeor two after the first episode ofabdominal pain.

Diabetes in TCP is calledFibrocalculous Pancreatic Diabetes(FCPD).

Characteristic is that despite requiringinsulin for control, patients rarelybecome ketotic on withdrawal of insulin.

This is attributed to the following

factors:


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This is attributed to the following factors:

1) Partial preservation of beta cell functionas shown by C-peptide studies.

2) Decreased glucagon reserve.3) Reduced supply of non-esterified fatty

acid (NEFA), the fuel needed forketogenesis, due to the loss ofsubcutaneous tissue

4) Resistance to subcutaneous adiposetissue lipolysis to epinephrine

5) Carnitine deficiency, affecting transfer ofNEFA across mitochondrial membrane.


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PATHOLOGY

Gross findings

The size of the pancreas variesinversely with the duration of thedisease.

The cut section of the pancreas showsthe presence of homogenous areaswith early to advanced fibrosis &intraductal calculi.


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PATHOLOGY

Pancreatic calculi are composed of 95.5%calcium carbonate and small amount ofcalcium phosphate.

Microscopic examination reveals a thickenedcapsule and extensive intralobular andinterlobular fibrosis not limited to any onezone or area.

The characteristic cellular infiltration of the

pancreas is composed of lymphocytes andplasma cells, distributed mainly around theducts.


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ETIOPATHOGENESIS

1) Malnutrition.

2) Role of cassava and other dietary toxins.

3) Familial and genetic factors.

4) Oxidant stress hypothesis and traceelement deficiency states.

5) Infections.

6) Genetics.


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ETIOPATHOGENESIS

MALNUTRITION

Most of the initially described patientswith TP were malnourished, and thedisease was common in poorercountries.

Malnutrition could have been a resultrather than the cause of TP.

Calcific pancreatitis does not occur inpatients with kwashiorkor, a classicform of protein-calorie malnutrition.


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ETIOPATHOGENESIS

Cassava Toxicity (Cyanogen Toxicity)

Cassava is 87.5% carbohydrate withnegligible (0.7%) protein content andessential amino acids (404 mg/100 g).

Contains cyanogenic glycosides,releasing cyanogens that are tissue toxins.

The process of detoxification of cyanogenutilizes and depletes the body of essentialamino acids, namely, methionine andcysteine, which are essential formaintaining the normal structure andfunction of the pancreas.


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ETIOPATHOGENESIS

Recent epidemiological and experimentalstudies further question the cassavahypothesis.

TCP is prevalent in many parts of Indiaand Africa where cassava is notconsumed.

A recent study on rats fed cassava dietsfor up to one year did not produce either

pancreatitis or diabetes.

Thus the cassava hypothesis lacksexperimental support.


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ETIOPATHOGENESIS


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ETIOPATHOGENESIS -IMMUNITY


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ETIOPATHOGENESIS

Gene Mutations The New Paradigm

SPINK 1 is a potent protease inhibitorand is considered to be a majorprotective mechanism in preventinginappropriate activation of pancreaticenzyme cascade by inhibiting up to20% of trypsin activity.

SPINK1 mutations have been

described in up to 45% of patients withTP, and 4% of the healthy subjects inIndia.


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NATURAL HISTORY

Abdominal pain usually is the first symptomto manifest in the natural history of TCP.

After prolonged periods varying from a fewmonths to several decades, pancreatic calculimay be diagnosed by routine abdominalradiography.

Until this point, both endocrine and exocrinepancreatic function of the subject may be

found to be normal.

After some months to years, glucoseintolerance and/or exocrine pancreaticdysfunction may set in.


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NATURAL HISTORY


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NATURAL HISTORY


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INVESTIGATIONS Tests of pancreatic structure

(A) Ultrasonography.

(B) Computed tomography.

(C) Endoscopic retrogradecholangiopancreatography.

(D) Endoscopic ultrasonography

Tests of pancreatic function

(A) Tests of exocrine pancreatic function.(B) Tests of endocrine pancreatic function


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MANAGEMENT


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REFERENCES

Postgrad Med J 2003;79:606615

Indian Journal of Gastroenterology 2006Vol 25 March - April 79


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Tropical Pancreatitis

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