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MBBS IV - Junior Clerkship WCS > JC59 (Medicine) - Peptic ulcer, Gallstones, Pancreatitis > Flashcards

JC59 (Medicine) - Peptic ulcer, Gallstones, Pancreatitis Flashcards

1
Q

Ddx GI causes of epigastric pain

A

Gastroduodenal

  • Peptic ulcer
  • Atypical GERD
  • Gastric cancer

Hepatobiliary:

  • Pancreatitis
  • Gallstones
  • Pancreatic cancer

Functional dyspepsia (*60%)

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2
Q

Ddx non-GI causes of epigastric pain

A

Cardiac: MI, myocarditis, ACS…etc

Chest: Pneumothorax, PE…etc

Haematological: Acute leukaemia, hemolytic anaemia..etc

Metabolic: Uremia, DM, porphyria, Addision’s

Toxin: lead poisoning, hypersensitivity

Infections: Herpes zoster (shingles)

Neurological: radiculitis, tabes dorsalis

Misc: muscular contusion, narcotic withdrawal, psychiatric disorders..etc

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3
Q

Differentiate the likely organs involved in constant vs Colicky vs episodic/ plateau epigastric pain

A

Constant moderate pain - likely ulcers

Colicky - likely intestinal or renal colic

Episodic/ plateau - likely biliary colic/ pancreatic pain

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4
Q

Ddx acute epigastric pain radiating to back

A

Biliary pain
Acute pancreatitis
Dissecting aortic aneurysm
Posteriorly penetrating PU

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5
Q

Ddx epigastric pain with repeated vomiting

A

Food poisoning/ gastroenteritis
Acute pancreatitis
Gastric outlet obstruction

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6
Q

Ddx agonizing, generalized abdominal pain

A

Mesenteric thrombosis
Ischemic colitis
Peritonitis
Perforated acute pancreatitis

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7
Q

Alarming features of acute epigastric pain

A

Age: >45 years old

Constitutional symptoms: Anaemia/ bleeding, Unintentional weight loss, Anorexia, lymphadenopathy

Alarming S/S

  • Early satiety
  • Abdominal mass
  • Jaundice
  • Dysphagia or odynophagia
  • Persistent vomiting

PMH:

  • Upper GI cancer
  • Ulcers

Family history: upper GI cancer

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8
Q

Peptic ulcers

  • Specify possible locations of ulceration
A

Gastric ulcer (20%) - usu. at lesser curvature and corpus-antrum junction

Duodenal ulcer (75%) - usu. solitary D1 if no NSAID use

Esophageal ulcer

Merkel’s diverticulum (ectopic epithelium)

Anastomotic ulcer/ Stoma opening (gastroenterostomy)

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9
Q

Peptic ulcer complications and S/S

A

Ulcer complications: ‘bleed’, ‘burst’, ‘block’ and ‘burrow’ (fistulization to other organs)

→ Bleeding: symptomatic UGIB, anaemia

→ Perforation: abrupt severe epigastric pain secondarily generalized, fever, shock

→ Gastric outlet obstruciton: nausea, vomiting (of old food >1h), epigastric distension

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10
Q

Peptic ulcer

- Aetiologies

A

H. pylori infection: 92% DU, 70% GU

NSAIDs: 5% DU, 25% GU

Stress, ICU setting esp if mechanical ventilation or coagulopathy

Zollinger-Ellison syndrome (gastrinoma, G cell hyperplasia)
→ Features: hypergastrinaemia + ulcers at atypical location

Smoking

Drugs: alcohol, antiplatelets, steroids

Crohn’s Disease

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11
Q

Pathogenesis of stress peptic ulcers

A

Stress ulcers are due to biliary reflux, uraemic toxins and impaired perfusion to stomach, leading to impairment of mucosal protection of stomach

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12
Q

H. pylori

  • Pathophysiology of gastric mucosa inflammation
A

Pathology: Expresses certain cytotoxins to provoke gastritis in underlying epithelium

Antral gastritis (majority) → ↓somatostatin, ↑gastrin release → ↑acid production → DU ± GU

Pangastritis (minority, 1%) → chronic atrophic gastritis ± GU → hypochlorhydria → proliferation of other bacteria → mutagenic nitrites → ↑risk of CA stomach

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13
Q

H.pylori

  • Gram stain, morphology
  • Survival mechanism in stomach
  • Transmission
  • Risk factors of infection
A

Bacteriology: G- bacilli, spiral w/ unipolar flagella
→ Resides in mucus layer overlying mucosa where pH is~7
→ Expresses urease to convert urea into ammonia + bicarbonate → counteract stomach acidity

Transmission: unknown, likely person-to-person contact via oro-oral or feco-oral route

RFs: unclean water supply, poor sanitary conditions, crowded environment, ↓socio-economic status

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14
Q

H. pylori-associated diseases

A 
Dyspepsia, 
chronic gastritis, 
PUD (GU/DU)
Gastric adenocarcinoma, MALT lymphoma
Extra-GI: anaemia (due to B12 or Fe def)
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15
Q

Diagnostic tests for H. pylori infection

Which tests used for post-treatment monitoring

A

Invasive endoscopic tests: 3 biopsies at antrum/ proximal stomach

  • Rapid urease test (CLO test)
  • Biopsy for histology
  • Culture for S/T
Non-invasive: 
Whole blood/ serum test for antibodies (Specific IgG)
Urine antibody 
Stool antigen 
Urea breath test with C-13 isotope

Stool antigen and urea breath test are used for post-treatment monitoring

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16
Q

Mechanism of rapid urease test/ CLO test

A

Rapid urease test (CLO test): sens 90%, spec 95%

→ Bx sample added to a solution of urea + phenol red
→ urease-positive H. pylori will hydrolyze urea into NH3 + CO2
→ ↑pH turns phenol red from yellow to pink
→ usually read at 1h and 4h (85% will change colour ≤1h)

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17
Q

Treatment regimens of H. pylori infection

A

Triple therapy: PPI + amoxicillin + clarithromycin bi-daily ×7d

Bismuth quadruple therapy: PPI + bismuth + tetracycline + metronidazole

Non-bismuth quadruple therapy: PPI + amoxicillin + clarithromycin + Metronidazole

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18
Q

Indication for Bismuth-containing quadruple therapy

A

Dual clarithromycin and metronidazole resistance (>15%)

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19
Q

Post H pylori treatment monitoring

A

NON-invasive tests, eg. stool antigen tests, urea breath tests

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20
Q

Pathogenesis of NSAID-related peptic ulcer

A

Pathology:

Impair gastric mucosa defense:

  • Block prostaglandin production
  • Block bi-carbonate and mucus production

> > Impair mucus layer, lowers pH and increase susceptibility of gastric acid and pepsin attack
pH dependent gastric mucosal damage

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21
Q

NSAID-related peptic ulcer

Risk factors: patient factors and drug factors

A

Patient factors:

  • Age >60y
  • Hx of PUD or UGI complications

Drug-related factors:

  • ↑COX-1 selectivity
  • High dose or concurrent use
  • Concurrent anticoagulants or steroids
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22
Q

Which NSAIDs cause most peptic ulcer

Which cause the least

A

Most PU:
Aspirin, Ketoprofen, Etodolac, Piroxicam

Least PU:
Fenoprofen, Diclofenac, Naproxen

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23
Q

Prevention of NSAID-related peptic ulcer

A

Prevention:
→ Review meds: review indications for NSAIDs, consider switching to less ulcerogenic NSAIDs or COX-2 inhibitor

→ Prior H. pylori testing ± eradication

→ Co-therapy by PPI, H2 receptor antagonist, misoprostol (Prostaglandin analogue)

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24
Q

Prevention of aspirin related GI complications

A

H. pylori eradication

H2 receptor antagonist, PPI, Misoprostol use

Substitute aspirin with Clopidogrel

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25
Q

Clinical features of peptic ulcer

Differentiating S/S between gastric ulcer and duodenal ulcers

A

Dyspepsia (80%): variable discomfort at epigastrium ± radiation
- ulcer-like (burning/gnawing pain) or
- dysmotility-like (bloating, early satiety, anorexia, nausea)
Pain localizes to epigastrium, related to food and episodic

GU vs DU:

  • GU is exacerbated by eating vs DU relieved by eating → corresponding weight changes
  • DU a/w pain at night and 2-3 hours after eating vs GU pain during eating
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26
Q

Diagnostic investigations of peptic ulcer disease

Management plan of uncomplicated PUD

A

OGD with biopsy:

  • Diagnotic: Biopsy to confirm PUD, r/o malignancy, H. pylori testing
  • Therapeutic: stop ulcer bleeding

Mx of underlying cause:
→ H. pylori eradication therapy as above
→ Avoid NSAIDs, stop smoking and limit alcohol intake

Antisecretory therapy: PPI

Re-scope at 6mo for GU to detect non-healing ulcers

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27
Q

Management plan of refractory/ complicated PUD

A

Surgical therapy for refractory or complicated ulcers: lower risk of malignancy

→ GU: ulcer excision, eg. partial gastrectomy + Bilroth I (or II) reconstruction

→ DU: acid-reducing procedures, eg. truncal vagotomy + pyloroplasty

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28
Q

Management of urgent peptic ulcer bleeding

A

IV PPI: bolus + maintenance → mandatory for any UGIB

Endoscopic Treatments: e.g. hemoclip, heater probe…etc

Angiography for transcatheter arterial embolization (TAE)

Surgical Mx:

  • DU: duodenotomy with 3-point ligation of gastroduodenal a.
  • GU: plication + Bx vs partial gastrectomy + B1/2 reconstruction
29
Q

Presentation of perforated PU

A

S/S: triad of
→ Sudden abdominal pain:
- Epigastric onset, secondarily generalized
- ± radiation to shoulder tip (diaphragm irritation) and RLQ (spillage into paracolic gutter)

→ ‘Board-like’ rigidity due to generalized peritonitis

  • Absent bowel sounds
  • ↓liver dullness due to free gas under diaphragm

→ Systemic upset: tachycardia, fever, tachypnoea, septic/hypovolemic shock

30
Q

Investigations to confirm perforated PU

A

Pneumoperitoneum on imaging:
- Erect CXR: free gas under peritoneum (≥50%) ± continuous diaphragm sign

  • AXR: ↑clarity of organ outlines,
    eg. double wall sign (Rigler sign) eg. falciform ligament sign eg. urachus sign eg. hepatic edge sign
  • USG for peritoneal stripe sign
  • CT for free gas or fluid in peritoneal cavity
31
Q

Ddx perforated PU

A

→ SB: perforated diverticulum, SB ulcer (eg. CMV), tumours (lymphoma (most common), CA lung and breast)
→ LB: closed loop obstruction, diverticulum
→ Acute appendicitis: NO GAS because of obstruction
→ Others: colonoscopy-related, FB-related

31
Q

Management of perforated PU

A

→ Prompt resuscitation + NPO + NGT suction

→ IV broad spectrum Abx, PPI and analgesics

→ Urgent OT:

  • GU: direct repair in young (↓risk of CA), partial gastrectomy + reconstruction in old
  • DU: omental patch repair60 ± acid-reducing procedure

→ Post-op eradication of cause, eg. PPI, HP eradication, NSAID avoidance

32
Q

Ulcer-related gastric outlet obstruction

Pathogenesis
S/S
Dx

A

Pathogenesis:
spasm, oedema, pyloric dysmotility due to acute inflammation + fibrosis due to chronic inf’n
» gastric atony after prolonged GOO

S/S:
→ Early satiety, bloating, indigestion, anorexia, weight loss
→ Nausea, vomiting (large quantities, characteristically of content 8-12h after eating)
→ Epigastric distension w/ succussion splash or visible peristalsis after eating
→ Electrolyte disturbance: dehydration (↑urea), hypoK, hypoCl metabolic alkalosis

Approach:
→ Resuscitation + correction of electrolytes + NGT suction
→ OGD: Bx for underlying pathology (esp to exclude malignancy)

33
Q

Gallstones

  • Define terms for stone in gallbladder, CBD, intrahepatic ducts
  • Define complicated vs uncomplicated gallstones disease
A

→ Cholecystolithiasis: stone in gallbladder
→ Choledocholithiasis: stone in the common bile duct
→ Hepatolithiasis: stones in intrahepatic bile ducts (i.e. RPC)

→ Uncomplicated gallstone disease: biliary colic w/o gallstone-related complications
→ Complicated gallstone ds: a/w gallstone-related complications, eg. acute cholecystitis, cholangitis, gallstone pancreatitis, gallstone ileus, Mirizzi syndrome

34
Q

List 4 major types of gallstones, appearance and respective composition

A
  1. Cholesterol - cholesterol monohydrate crystals; Yellow, fine granular, hard, faceted
  2. Black Pigmented - calcium bilirubinate; Jet-black, hard, speculated and brittle
  3. Brown Pigmented - calcium bilirubinate, palmitate, sterate with dead bacteria; Brown, softer, clay-like
  4. Mixed (majority) - both cholesterol and calcium salts; ‘egg-shell’ appearance on plain XR films
35
Q

Pathogenesis of cholesterol gallstones

A

Liver secretes cholesterol in vesicular form with phospholipids
→ dissolved in GB by bile salts into micelles
→ GB concentration of bile results in overwhelming of dissolving capacity of bile salts
→ supersaturation and crystallization

36
Q

Risk factors of cholesterol gallstones

A

“Fat + Female + Fertile + Forty”

  1. Excessive cholesterol secretion
    - Hormonal: multiparity, OCP
    - Metabolic: obesity, DM, ↑lipids
  2. Gallbladder stasis
    - ↓enteric intake: aggressive weight reduction, NPO on TPN
    - Neurogenic: SCI, truncal vagotomy
    - Hormonal: pregnancy, OCP, HRT
37
Q

Pathogenesis of black pigmented gallstones

Risk factors

A

Stone formation requires unconjugated bilirubin which can come from

(1) spillage from ↑haeme turnover [cause of black stones]
(2) bile acid malabsorption

Risk factors:
1. ↑haeme turnover
Haemolysis: G6PD (commonest), cirrhosis-related hypersplenism, thalassaemia
Gilbert syndrome

  1. Bile acid malabsorption
    Ileal disease: resection, Crohn’s disease
  2. GB stasis
38
Q

Pathogenesis of brown pigmented gallstones

Risk factors

A

Unconjugated bilirubin is formed within an infected biliary tree where there is bacterial β-glucuronidase

Bacteria also hydrolyze phospoholipids to release FAs from fat vesicles → form calcium salts → accounts for softer texture

Risk factors:

  1. Bacterial infection of biliary tree
  2. Strictures: parasitic-induced (RPC), prior ERCP strictures, malignancy
  3. Other causes, eg. stents
39
Q

Pathogenesis of mixed gallstone

A

Prior cholesterol stone causes stasis and bacterial colonization

→ deconjugation of bilirubin forming calcium bilirubinate component on top of cholesterol stone

40
Q

Four stages of gallstone disease

A
41
Q

Gallstone disease

  • Typical presentation
  • Complications
A

Typical presentation

  • Mostly asymptomatic, incidental finding
  • Biliary colic, nausea, vomiting, dyspepsia, fat intolerance

Complications:
GB: cholecystitis (± gangrene, empyema, perforation), CA GB, Mirizzi syndrome
CBD: CBD stone, cholangitis
Others: gallstone pancreatitis, gallstone ileus, pancreatitis

42
Q

Gallstone disease

  • Pathophysiology of biliary colic
  • S/S (OPQRST)
A

Pathogenesis: impaction of gallstones or sludge in cystic duct during GB contraction → pain due to GB distension

stereotypical attacks of upper abd pain after ingestion of fatty meal

  • Onset: begins quite suddenly and increases steadily over 10-20min
  • Precipitation: usually begins post-prandially, or at night
  • Quality: intense, dull pain
  • Region/radiation: occurs in epigastric region initially and may migrate to RUQ; may radiate to right scapular tip (Collin’s sign)
  • Severity: intense, waxing-and-waning
  • Timing: usually lasts 1-5h
43
Q

First-line investigations for gallstones

A

P/E + blood tests: should be normal

AXR: for pigmented stones (cannot see cholesterol stones)

Trans-abdominal US**

  • Stones: echogenic foci that casts an acoustic shadow
  • Sludge: heterogenous enhancement w/o shadow

ERCP/PTBD: usually for therapeutic purposes

Additional:
EUS ± bile collection: identify small stones missed on TAUS esp CBD ones
MRCP: usually as 2nd line if TAUS -ve

44
Q

Indications for cholecystectomy

A

Asymptomatic gallstones
Symptomatic or complicated gallstones
risk of CA gallbladder, eg. GB polyp >0.5cm, porcelain gallbladder

45
Q

Causes of acute pancreatitis

A

Idiopathic (15-25%)

Gallstones (55%)
Ethanol (35%): acute exacerbation of chronic alcoholism
Trauma

Steroids: ↑viscosity of pancreatic juice
Mumps and other infections:
→ Viruses: mumps, coxsackievirus, hepatitis B, CMV, VZV, HSV, HIV
→ Bacterial: Mycoplasma, Legionella, Leptospira, Salmonella
→ Fungal: Aspergillus
→ Parasitic: Toxoplasma, Cryptosporidium, Ascaris
Autoimmune: SLE, Sjogren’s syndrome, vasculitis (eg. PAN)
Scorpion/ toxins, eg. organophosphate poisoning (cholinergic stimulation)
Hypercalcaemia (3rd commonest) and Hypertriglyceridaemia (4th)
ERCP-related (2-5%)
Drugs (1-2%), eg. Sulphamethoxazole-trimethoprim, Azathioprine, NSAIDs, Diuretic, valproate

46
Q

Neoplastic, congenital and genetic causes of acute pancreatitis

A

→ Neoplasm: pancreatic or ampullary tumour
→ Congenital: pancreas divisum, choledochocele type V
→ Genetics, eg. cystic fibrosis, PRSS1, SPINK1 and other mutations

47
Q

Pathogenesis of acute pancreatitis

A

Inciting event = acinar cell injury leading to premature trypsinogen activation within acina + inflammation

→ Ductal obstruction (eg. gallstones) → interstitial oedema → impaired blood flow → acinar cell injury
→ Acinar cell injury (eg. alcohol, drugs, hyperCa) → ↑inappropriate intracellular release + activation of enzymes
→ Defective intracellular transport

48
Q

Acute Pancreatitis:

Local histological changes

Systemic responses

Progression

A

Early local changes:
→ Autodigestion of pancreatic tissues, fat necrosis
→ Microcirculatory injury: interstitial oedema and ischaemia-reperfusion injury
→ Inflammatory changes (esp NFκB activation) with cytokine release and leukocyte activation

Systemic responses:
SIRS due to systemic spillage of cytokines and activated pancreatic enzymes
Bacterial translocation: systemic hypovolemia + gut A-V shunting, systemic sepsis with endotoxaemia

Progression:
Necrotizing pancreatitis: persistent ampullary obstruction + hypoperfusion

49
Q

Acute pancreatitis

Clinical presentation (OPQRST) + associated S/S

A

Severe epigastric pain that radiates to the back

→ Acute onset, of increasing intensity over 15-60min, lasts for several hours to days
→ Severe, constant, boring sensation that radiates to the back (50%)
→ Usually localized to upper abdomen, occ. in RUQ or rarely LUQ
→ Usually ↑ by movement and ↓by sitting up and leading forward
→ Initially a/w very little peritoneal signs

Associated S/S
□ Nausea and vomiting (90%)
□ Fever
□ Features of retroperitoneal haemorrhage

50
Q

List Features of retroperitoneal haemorrhage in haemorrhagic pancreatitis

A

→ Cullen’s sign: bruises of periumbilical region
→ Grey Turner’s sign: bruises of flank region
→ Fox’s sign: bruises over inguinal ligament

51
Q

Complications and S/S of acute pancreatitis

A

Diffuse peritonitis

Hypovolaemia ± shock

Dyspnoea: due to pleural effusion or ARDS

Palpable pseudocyst

Pancreatic ascites when fluid leaks from disrupted pancreatic duct into peritoneal cavity

Splanchnic venous thrombosis

Abdominal compartment syndrome due to tissue oedema, ascites, ileus

52
Q

Diagnostic criteria of acute pancreatitis

A

≥2 out of 3 of (Revised Atlanta classification, 2013)

□ Epigastric pain: acute onset of persistent, severe epigastric pain often radiating to the back

□ ↑serum lipase/amylase to ≥3× ULN

□ Characteristic imaging finding of acute pancreatitis on contrast CT, MRI or trans-abdominal USG

53
Q

First-line investigations of acute pancreatitis

A

LFT: high ALT for gallstone pancreatitis, high bilirubin for gallstone at ampulla

Abdominal ultrasound: Swollen pancreas, Peripancreatic fluid anechoic collection
Endoscopic US: occult biliary stones
ERCP for gallstone clearance

Serum amylase
Serum Ca, lipids → hyperCa, hyperlipidaemia

CXR: mainly to r/o PPU, complications like pleural effusions or ARDS
AXR: focal ileus with sentinel loop sign, or calcification of chronic pancreatitis

Contrast CT to confirm diagnosis and find cause later

54
Q

Indications for additional Contrast CT for acute pancreatitis

A

TAUS shows:
→ Focal or diffuse enlargement with homogeneous enhancement
→ Peripancreatic fat stranding
→ ± complications: necrosis, abscesses…etc

55
Q

D/dx acute pancreatitis

A

Peptic ulcer disease

Perforated Peptic ulcer

Cholangitis, CBD gallstones

Cholecystitis

Intestinal obstruction

Mesenteric ischemia

56
Q

Severity score for acute pancreatitis

A 
Glasgow’s criteria: ≥3 within first 48h indicates a severe attack
□ PaO2: <8kPa = 60mmHg
□ Age: >55 years
□ Neutrophils: >15× 109/L
□ Calcium: <2mmol/L
□ Renal: urea >16mmol/L
□ Enzymes: LDH >600IU/L or AST/ALT >200IU/L
□ Albumin: <32g/L
□ Sugar: glucose >10mmol/L
57
Q

Outline the Atlanta classification for severity/ complications of acute pancreatitis

A
58
Q

Severity/ Mortality score for acute pancreatitis

A

Mortality: 0-2% (0-2), 15% (3-4), 50% (5-6), 70-90% (≥7)

59
Q

Supportive treatment for mild acute pancreatitis

A
  1. IV fluid resuscitation
  2. NPO + NGT aspiration if persistent vomiting, significant gastroparesis or ileus
  3. Enteral feeding/ Parenteral feeding
  4. Analgesics: Opioids: preferred, usually fentanyl, hydromorphone, tramadol, NOT MORPHINE (tighten sphincter of Oddi)
  5. Antibiotics: therapeutic (NOT prophylactic) for infected necrosis
  6. Serial contrast CT
60
Q

Definitive treatment for severe acute pancreatitis

A
  1. Infected necrosis: empirical antibiotics and percutaneous drainage/ endoscopic debridement
  2. Bowel ischemia, acute necrotizing cholecystitis, ongoing bleed: surgical debridement/ necrosectomy
  3. ERCP for biliary stone removal
  4. Manage complications or organ failures
61
Q

Chronic pancreatitis

Pathogenesis
Causes

A

Chronic pancreatitis: prolonged inflammation of pancreas a/w irreversible destruction of exocrine parenchyma, fibrosis and, in late stages, destruction of endocrine parenchyma

Aetiology: NOT gallstones
- Alcohol
- Toxic-metabolic: tobacco smoking, hyperCa, chronic renal failure
- Severe, recurrent acute pancreatitis 
- Autoimmune: IgG4-related disease
- Ductal obstruction
(genetics and congenital...etc)
62
Q

Chronic pancreatitis

Clinical presentation

A

Abdominal pain

  • Epigastric with radiation to back
  • Worse post-prandial
  • Improve by sitting forward, drink alcohol

Pancreatic exocrine insufficiency (90% exocrine mass loss)

  • Fat malabsorption: steatorrhoea ± vitamin A, D, E, K, B12 malabsorption
  • Protein malabsorption

Pancreatic endocrine insufficiency, i.e. secondary diabetes mellitus

Loss of weight: 2o to combination of anorexia, avoidance of food (post-prandial discomfort) and DM

63
Q

Chronic pancreatitis

Physical findings

A

Weight loss: thin, malnourished

Epigastric tenderness

Enlarged pancreas: occ. palpable, esp in thin pt (d/dx pseudocyst)

Erythema ab igne: skin pigmentation over abdomen/back

64
Q

First-line investigations for chronic pancreatitis

A

Radiological diagnosis: usually 1st line:

Plain AXR: calcifications in pancreatic duct
USG: ductal dilatation, parenchymal changes with ↑echogenicity and irregular gland contour
CT: ductal dilatation, calcification, pseudocysts
EUS
ERCP: current gold-standard: Characteristic chain-of-lakes appearance of ductal anatomy

Biochemical: 
Faecal pancreatic elastase
Secretin stimulation test
72h fecal fat collection
OGTT for endocrine insufficiency
65
Q

Major ddx of chronic pancreatitis

A

CA pancreas
□ Clinical features: older age, absence of Hx of alcohol use, weight loss, protracted flare of Sx, significant constitutional symptoms

66
Q

Treatment plan of chronic pancreatitis

A
  1. Lifestyle modifications:
    Abstinence from alcohol
    Small low-fat meals with hydration/ fat-restricitons
    Cessation of smoking
  2. Pain relief:
    Analgesics: opioids, low-dose amitriptyline + NSAIDs
  3. Oral pancreatic enzyme supplements, eg. pancreatin
  4. Endoscopic dilatation of ductal strictures/ Surgical drainage/ resection e.g. Whipple’s procedure
  5. Medium-chain triglycerides (MCTs) + Vitamin supplementation: vitamin D, calcium
  6. Insulin for secondary DM
67
Q

Complications of chronic pancreatitis

A

Pseudocyst formation (10%)

CBD/duodenal obstruction (5-10%): inflammation and fibrosis of HOP or pseudocyst

Pancreatic ascites and pleural effusion/ fistulation into peritoneal/pleural cavity

Splenic vein thrombosis (11%)

CA pancreas

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