chronic pancreatitis Flashcards

1
Q

definition

A

Chronic relapsing, aggressive, polyetiological inflammatory destructive disease manifested with obstructn of ducts, sclerosis, irreversible loss of exocrine & endocrine func & deterioration of pancreatic struc.

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2
Q

etiology

A
  1. Alcohol intoxication
  2. Prob. Wit flow of bile
    - Disease of biliary tract and liver: infection in lymphatic tracts, cholelithiasis, tumors, parasites, cholecystitis: regurgitation of bile to pancrease and activate enzyme and digest parencyme
    - Disease of duodenum: Duodeno-pancreatatic reflux, oedema, duodenal ulcer, duodenitis, peptic ulcer below duodenal capillary
  3. Obstruction pancreatic duct (stenosis, stones, carcinoma)
  4. Alimentary factors – Vit insuff & ↓protein in meals, chronic disease of gastrointestinal tract
  5. Drugs – Corticosteroids, Sulfanamides, NSAIDs, diuretics, cytostatics, glucocorticosteroids, immunosuppressive, a/coagulants, indomethacin, paracetamol, estrogens, tetracyclines
  6. Trauma of the pancreas
  7. Toxic chem. – mercury, arsenic
  8. Infectn – herpes, measles, parasites of GIT
  9. Allergy – food allergy
  10. Hormonal disorder- calcification due to ↑Ca (hyperparathyroidism)
  11. Hereditary -insuff of alpha-antitripsin, metabolic disorders in Wilson disease
  12. Hyperlipidemia, hypertriglyceride (deposition of fat under glands)
  13. Idiopathic
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3
Q

pathogenesis

A
  1. Obstruction pancreatic duct - spasm in sphincter Odi (↓bicarbonate secretion, ↑protein concentration)
    - Protein precipitation in tissue of pancreas leads to prob of flow of enz thus obstrucn of small ducts→ ↑P in pancreatic duct→oedema of pancreas→autodigestion by enz→fibrosis
  2. ↓ inhibitory enz → Activation of enz in pancreas production → autodigestion
    - abn production of juice - H2O , HCO3 , proton , lipase , tripsin , amylase
    - abnormal drainage through lymph – edema of pancrease
  3. Alcohol consumption
    - prodn of pancreatic enz. cause deposition of protein plugs
    - Obstrucn of small ducts→ ↑pressure in pancreatic duct→oedema of pancreas→autodigestion
    - Decrease proteins and increase enzyme juice concentration, enzyme start digesting pancreas
  4. Biliary tract disease → temporary gallstone → obstructn of Sphincter Odi/ ↑pancreatic duct P → inflamn → sclerosis-fibrosis
  5. Common bile duct - increase pressure in common bile duct - disturbance in the flow of juice of panc - stagnation of the enz containing juice cause destruction of panc tissue – autolysis - place of destruction, appear sclerosis and fibrosis development.
  6. Duodenitis/dystrophy or atrophy of duodenal mucosa → ↑secretin, cholecystokinin, pancreozitin prodn → ↑duodenum P → spasm of Sphincter Odi→↑P pancreatic duct →c-on of pancreatic juice→ deposition of prot plug formn → sclerosis-fibrosis
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4
Q

classification

A
  1. acc to clinical stage : Relapsing, Algesia(pain), Latent
  2. acc to phase: Recurrent/relapse, Remission
  3. acc. to dev :
    - 1st stage- no prob in endo&exocrine func
    - 2nd stage – present endo&exocrine dysfunc
    - 3rd stage- Diarrhea, LOW, Vit insuff
  4. Rome classification
    - Chronic calcifying pancreatitis (alcohol intoxication)
    - Chronic obstructive pancreatitis (obstrucn of bile duct)
    - Chronic fibrous in duration
    - Fibrotic-sclerotic
    - Chronic cystosis & pseudocystosis
  5. According to pathophysiology:
    - Chr obstructive pancreatitis
    - Chr calcifying pancreatitis
    - Infiltrative fibrotic /inflammatory
    - Fibrotic sclerotic form
    - Cyst type
    - Retrograde flow
  6. Primary / secondary
    - Primary – inflammation of the panc tissue
    - Secondary – result of other GIT diseases.
  7. according clinical form and pancreatic function
    - chronic relapsing pancreatitis
    - chronic pancreatitis with permanent pain (algesia) syndrome
    - chronic latent pancreatitis
    - pseudotumour of the pancreas
    - Sclerotic
  8. Acc etiology

Primary:
- alcohol
- chronic obstruction of main pancreatic duct (stenosis,stones,carcinoma)
- infection
- drug-induced
- idiopathic
- hereditary
- Trophic - result of Kwashiorkor

Secondary:
- diseases of biliary tract
- hyperparathyroidism
- chronic disease of gastrointestinal tract
- hyperlipidemia, hypertriglyceride

  1. Acc morphology
    - obstructive
    - sclerotic arounds glands (calcified, alcoholic)
    - atrophic (parenchymatous, inflammatory)
    - Oedematous, Fibrous, Pseudo-cystic
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5
Q

main syndrome

A
  1. Pain
    - epigastric region, sharp spastic pain, belt like pain, 30-40 min after meal, hrs to days
    - trigger factor - fatty food, alcohol, ice-cream, stress, physical exhaustion, when lie flat
    - relieving factor - lie on R side wit leg pulled towards abdmn, avoid eating, cold application on epigastric region, spasmolytics, antacids, cholinolytics
  2. Dyspeptic
    - Gastric dyspepsia: nausea, vomiting, hypersalivation, belching, weight loss
    - Intestinal dyspepsia: Diarrhea, constipation, meteorism, loss of apptte & weight, jaundice, dry skin
  3. Inflammatory – Fever, lymphadenopathy, arthalgia, vasculitis
  4. Asthenic – weakness,↓activity to work, restless, malaise
  5. Malabsorpn (Q30 f, page 77)
    - Hypoproteinaemia, hypoglycaemia, hypolipidaemia, electrolyte disorders, dehydration
    - disturbed digestion by panc juice
  6. Endocrinal insuff- hyperglycemia, glucose intolerance
  7. Exocrine insufficiency (destructn of pancreatic cells, obstructn of ducts)
    - Pancreatic triad (Calcification, Steatorrhea, Exocrine pancreatic insuff)
  8. Jaundice
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6
Q

investigation

A

Objective examination
- Skin grey, dry, dirty color, red spot; enlarged nails, loss weight, muscle guarding, coated tongue, painful palpation on epigastric, weakness and fear of eating.
- Mayo-Robson‘s sign – Tenderness at L costovertebral triangle
- Kach‘s sign – Tenderness at L rectus abdominis, 5cm above umbilicus
- Shaffar zone (Degarden‘s point)
- Kerte‘s sign – muscular resistance of epigastric area.

Laboratory
- Blood – Leucocytosis L shift, ↑ESR, Normochromatic / hypochromic anemia, ↑enz in blood and urine: amylase, tripsin, lipase; ↑transaminase & urine amylase, hypercalcemia, glucosuria, bilirubin in blood
- Corprology : Steatorrhea, Amylorrhea, Creatorrhea
- Pancreatic juice examination
- Biochem - C-Reactive protein increase with mucoid, dysproteinemia

Instrumental:
1. U/sound - enlargement, form, density, edematous, fibrosis, cyst(stones) in the panc duct

  1. X-ray:
    - Enlargement/deformed duodenum, ↑duodenal papilla, dislocation
    - calcification (stones) in pancreas
    - ↑ retrogastric space
    - dilated ducts, central loop of small bowel, dilatation of transverse colon
    - In contrast, double line seen.
  2. Fibroduodenogastroscopy – stones, changes in Sphincter Odi, large papilla sphincter in tumor
  3. Endoscopic-pancreato-cholangiography- stones, stenosis of tracts
  4. Angiography- deformn+dilatation of arteries, abnorm distribution, disappearance of small arteries
  5. CT scan- size of organ, edema, calcification of pancreas, cyst, fibrosis, obstructn of biliary tract: stones, dilated vessels, differentiate wit tumor
  6. retrograde cholangiography
  7. ECG- tachycardia
  8. laproscopy and laparotomy – acute pancreatitis
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7
Q

treatment

A
  1. Diet N.5, no triggering food (hot, cold, spicy, gassy, alcohol, fatty)
  2. Pain
    Spasmolytics – Analgin, Baralgin , Noshpa, Atropine, Papaverin Analgesics –Pramidol, Meperidine Lidocaine/Novocaine Cold compression Cytostatic eg. 5-uracil
  3. Treatment of maldigestion & malabsorpn - avoid eating 2-3 days
  4. insulin therapy
  5. substitution therapy to restore normal flow of bowel
  6. Etiological: due to infectn- A/biotics: Penicillin, cephalosporin, erythromycin, amoxicillin
  7. Pathogenetic:
    - Antacids: almagel & pratop (salts-hydroxide of Al & Mg); phosphotical
    - H2-antagonists: Famotidine,Ranitidine,Cimetidine - ↓ gastric & pancreatic secretion
    - Proton pump inhibitor: Omeprazole
    - M-cholinorcp blocker: atropine
  8. Enzyme: (contains trypsin: Pancreatin, pancreamexin, Mezim, pancitrate, Festal); (lipase containing – Krion) - pancreatine, pancreatoazemine
  9. enzyme inhibitors: Contrical, Gardox, Tricivil, Aprotinin, Trasilol
  10. Diuretics
  11. Cytostatics to stop secretion
  12. Hormones: glucocorticoids
  13. Antitoxic therapy – ringer
  14. correction of exocrine - krion, Mizhil
  15. Surgical treatment - in acute phase, present complication, organic duodenal stasis
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8
Q

complications

A
  • Jaundice
  • GIT (bleeding, enterocolitis, cholangitis, hepatitis, 2‘ peptic ulcer)
  • DM
  • Malignization
  • stenosis of diff levels of tract
  • local steato-necrosis in bones
  • Ascites
  • Abscess, cyst, stone
  • HR pleurisy, polyarthritis, relaxation of L dome of diaphragm, hypotonic state
  • Thrombosis of spleen veins
  • stone in duodenal
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