Acute Pancreatitis Flashcards
What is Acute Pancreatitis?
AP is autolysis of pancreas caused by lipolytic and proteolytic enzymes with development of enzymatic toxemia, functional impairment of internal organs and formation of purulent and degenerative complications.
Etiology of A.P
It is a poly etiological disease that develops rapidly and phase like often recurrent and frequently involves organs and systems anatomically and functionally connected with pancreas in the pathological process
The causes of AP are divided into -mechanical
-neurohumoral
- toxic-allergic
Mechanical causes are ;
-all the block types of hepatopancreatic ampulla and common pancreatic duct due to biliary calculus, stricture ,tumor, edema of major duodenal papilla, -stable spasm of sphincter of hepatopanctreatic ampulla incase of recurrent colic and acute Cholecystitis
-duodenopanctreatic reflux due to duodenostasis as well as duodenal dyskinesia within ulcer , duodenitis and inadequate food load.
Traumatic causes are rare
Neurohumoral causes are
- disturbance of lipid exchange
- systemic vascular diseases
- gastric diseases
- secondary disturbances of blood circulation in pancreas
- hepatic diseases
- pregnancy
- puerperal diseases
Toxico -allergic causes
- food and drug allergy
- a focus of latent or acute infection
- alcohol
Another cause is damage of pancreacytes and setup of conditions of intratissue activation and self activation of enzymatic pancreatic system
Pathogenesis of A.P
Due to pathobiochemical theory that is two interrelated “cascade-like” pathobiochemical and mophofunctional reactions
-the initial factor causes the auto digestive process in pancreas is lipolytic enzymes -phospholipase A and lipase released in active state
If pancreatic secretion gets into interstitial tissue incase of rupture of ductoacinar commissure junctions due to acute intaduct hypertension under the influence of lolytic enzymes there can be necrobiosis of pancreacytes and interstitial fat tissue
Around the foci of adipose necrobisis there is formation of demarcation inflammatory reaction which character is regulated by involvement degree of local mediators of inflammation in the pathological process-histamine, serotonin, and cathecholamines as well as kallikrein , kinin, plasmid, thrombin systems of micro circulatory bloodstream
If then the process stops there is development of adipose pancreatonecrosis which tends to be abortive or slow-progressing (recurrent) course
-Development of the second pathobiochemical cascade occurs due to accumulation of free fatty acids in pancreacytes damaged by lipase
It leads to shift of pH cell up to 3,5-5,5 and only in such condition in the result of auto catalytic rxn intracellular tripsinogen can be transformed into tripsin
Tripsin brings about damaging influence on the cell and its structure that leads to release and activation of lysosomal enzymes in particular elastase and some other processes (chemotripsin , collagenase, etc)
Tripsin and other proteases cause proteolytic necrobiosis of pancreacytes
Under the influencer of elastase there is lysis of venule walls and interlobular connective intersection that leads to massive hemorrhage and facilitated rapid spreads of enzymatic autolysis in pancreasis and outside its boundaries
At the same in microcirculatory bloodstream of pancreas tripsin activates kalliren-kinin, plasmin, thrombin and lymph enlargement of plasma and hemorrhagic edema and formation of disseminated micro thrombosis .
In case of hemorrhagic pancreanecrosis there is simultaneous release of lipolytic enzymes that stimulates of release lypotic enzymes that stimulates activation of tripsin
That is the way cycles of interactive influence of lipolytic and lipolytic and proteolytic processes
Proteolytic necrobiosis of pancreacytes, destruction of micro vessels and micro circulation disturbances augment rapidly because perifocal inflammatory reaction is almost absent and hemorhagic pancreanecrosis inclined to have rapid progressing course
Entrance of toxicogenic polypeptides , lipids, and other products of enzymatic auto aggression , pancreatic enzymes and biogenic amines to blood and lymph , activation of kallikrein-kinin plasmin and thrombin systems of blood and lymph cause the development of toxemia which accompanied by disorder of central and peripheral hemodynamics, functional impairment of parenchmatous organs and toxic complications
So in general Pathogenesis develops coz of;
- lipolysis
- proteolysis
- demarcation inflammation with evident disturbances of micro, hemo, and lymph circulation
- pancreatogenic toxemia
Classification of A.P
Clinical anatomical forms
- Edematous pancreatitis(abortive pancreanecrosis)
- hemorrhagic pancreatitis
By prevalence
- local(focal) process
- subtotal process
By course
- abortive
- progressing
Disease stages
- hemodynamic disturbances and pancreatogenic shock(the 1-3rd days)
- functional deficiency of parenchymatous organs (5th-7th days)
- degenerative and purulent complications (the 14th to 30th days)
Complications of Acute Pancreatitis
- pancreatogenic shock
- pleural effusion, pancreatogenic pneumonitis, “pancreatic lung”
- pancreatogenic toxic renal degeneration and erosive hemorrhagic gastroenteritis
- pancreatogenic delirium syndrome
- pancreatogenic destruction of articuloskeletsl apparatus
- pancreatogenic coma
Postnecrotic complications
-degenerative
parapancreatic infiltration, pancreatic cyst
-purulent
abscess of pancreas or omental bursa , phlegmonous or apostematous pancreatitis, abscesses of retroperitoneal tissue spaces and abdomen (subdiaphragmatic , subhepatic, interintestitial)
Phlegmon of retroperitoneal tissue , greater omentum and mediastinum peritonitis
-Visceral
external and internal fistula(pancreatic, biliary , gastric , interstitial, gastropancreatic and duodenal, bronchopancreatic and pleural)
arrosive hemorrhage
Occlusive lesions(compression or thrombosis of branches of abdominal aorta , portal vein and its inflow)
Clinical picture of A.P
Clinical picture is determined by form and course of the disease
Incase of pancreatonecrosis it is less evident and tends to wave like course and incase of hemorrhagic one it is full blown with prevalence of hemodynamic disorders especially at the first clinical stage of the disease
The basis symptoms are
1.Pain is permanent and predominant
It is localised in epigastric region and spreads over the left hypochondrium
It irradiates to loin and it is girdle . Rarely the pain irradiates to shoulder girdle , behind the sternum, to the heart region
Intensity of pain syndrome as a rule corresponds to the severity of the disease
- Vomiting
It often preceded the pain, it is excruciating and does not cause relief
At first there is vomiting of gastric contents
