Week 9 - GIT Flashcards

1
Q

define pancreatitis

A
  • inflammation of the pancreas

- severity varies from mild oedema to severe haemorrhagic necrosis of pancreas

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2
Q

pancreatitis - causes

A
  • bilary disease (unable to break down bile)
  • alchohol consumption (increased production of enzymes which pancreas produces = leads to them being activated in the pancreas)
  • abdominal trauma
  • infections (of pancreatitis or systemic)
  • drugs (corticosteroids, NSAIDS)
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3
Q

Pathophysiology of pancreatitis

A

injury to pancreatic cells > activation of pancreatic enzymes

pancreatic enzymes leak into pancreatic tissue

pancreatic tissue & cell membrane breakdown (auto-digestion)

proteolytic enzymes activated

inflammation, oedema, vascular permability, heamorrhage, necrosis and fibrosis (due to hypoperfusion)

toxic enzymes and inflammatory mediators enter blood stream
^ injury to lungs, heart and kidneys

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4
Q

pancreatitis - 2 types

A

Oedematus:

  • mild
  • self limiting

Necrotising:

  • severe
  • necrosis of pancreatic tissue
  • degree of damage relates to severity of symptoms
  • can permanently affect function of pancreas (diabities)
  • results in necrosis of pancreas, organ failure and sepsis
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5
Q

pancreatitis - clinical manifestations

!!!!!!!!!!!!!!! choose 7 to remember

A
  • increased RR
  • hypoxaemia
  • decreased bp
  • increased HR
  • renal failure
  • cogulation abnormalities (bleed more)
  • low grade fever (due to inflammatory response)
  • hyperglycaemia (due to stress response and dysfunction of the pancreas)
  • nausea and vomiting
  • hypoactive or absent bowel sounds
  • jaundice (bilirubin not being broken down)
  • cullens sign
  • grey turner sign
  • abdominal pain/ distension
  • LUQ
  • sudden onset
  • severe, deep, piercing, continuous
  • worse with eating
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6
Q

pancreatitis - Management goals (2)

A
  • stop process of autodigestion (stop destroying pancreas)

- prevent systemic complications (prevent hypoperfusion, vasodilation and shock occurring)

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7
Q

pancreatitis - Management

DRSABCDE

A

Airway/ Breathing

  • CXR (looking for APO)
  • NGT (keep stomach empty)

Ciruclation:

  • IV access anticipating will go into shock state
  • IV naci and albium
  • correct electrolyte imbalance (will be decreased calcium levels need extra)
  • CVC, IDC (to monitor for renal failure)

Disability:

  • NBM
  • BGL (will be increased)
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8
Q

pancreatitis - Management (medications)

A
  • morphine
  • prophylactin IVAB
  • diamex to manage increased BGL
  • antacids
  • proton pump inhibitors
  • insulin (if BGL very high)
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9
Q

pancreatitis - Investigations

A

pathology:

  • amalyse and lipase
  • chest and abdo xray
  • abdo CT
  • ERCP
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10
Q

Cirrhosis of the liver - Define

A

irreversible inflammatory disease that distrupts liver function and structure

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11
Q

Cirrhosis of the liver - causes

A
  • alchohol
  • post necrotic cirrhosis (drugs (NSAIDS), viral infections)
  • biliary cirrhosis
  • metabolic cirrhosis
  • cardiac cirrhosis
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12
Q

Cirrhosis of the liver - patho

A
cell necrosis 
^ 
destroyed liver celss replaced by scar tissue (nodular irregular cells)
^
reduced blood flow (due to scar tissue)
^ 
poor nutrtion and hypoxia
^ 
cell death
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13
Q

Cirrhosis of the liver - clinical manifestations

A

EARLY:

  • GI disturbance;
  • anorexia, flactulence, nausea and vomiting, change in bowel habits
  • abdominal pain
  • fever
  • enlargement of liver

LATE:

  • jaundice (not breaking down bilirubin)
  • puritis (itchy skin)
  • skin lessions
  • spider angiomas (small blood vessels dilated and pop)
  • testicular atrophy (decreased testosterone)
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14
Q

Cirrhosis of the liver - management

A

liver transplant
- only definte treatment for end stage liver disease

management of complications is the key!

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15
Q

Cirrhosis of the liver - potential complications

A
  • portal hypertension
  • ascities
  • hepatic encephalopathy
  • oesophageal varices
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16
Q

portal hypertension

A

obstruction of portal system > high pressure in portal vien > results in development of collateral circulation > so blood bypasses portal vessel > means develop high pressure in the collateral system
- ultimately results in blockage in the venous system in liver and pressure backflows in portal vien
= portal hypertension!

17
Q

portal hypertension - clinical manifestations

A
  • maelena (blood in the stools)
  • haemoatemsia (vomiting blood0
  • ascites
  • infection
18
Q

portal hypertension - management

A
  • prevention of interal GIT bleeding

- prevention of complications

19
Q

Ascites

A
  • fluid in peritoneal cavity > reduces circulating volume
20
Q

Ascites - contributing factors

A
  • portal hypertension
  • liver failure
  • sodium retention
21
Q

Ascites - clinical manifestations

A
  • weight gain
  • increased girth
  • peripheral oedmea
22
Q

Ascites - managemtn

A
  • monitor WOB (will develop resp compromise)
  • analgesia (abdominal pain)
  • sodium restriction
  • diuretics
23
Q

GIT bleeding

A

can originate anywhere in GIT and occur at any age

- most common age 50 - 80years

24
Q

Upper GI bleed causes

A
  • varices
  • cirrohis
  • non variceal
  • peptic ulcer
  • drug induced erosions
  • retching & vomiting
25
Q

Lower GI Bleed - causes

A
  • diverticulitis
  • colon cancer
  • ulcers
  • gastritis
26
Q

Oesphageal Varices - define

A

enlarged sub mucosal vien in oesophagus which eventually ruptures, causing massive haemorrhage

27
Q

Oesphageal Varices - clinical manifestations

A
  • tachycardia
  • postural hypotension
  • syncope
  • pallor
  • diaphoresis
  • decreased cap refill
  • dizziness

specific:

  • jaundice
  • ascites
  • explosive diarrhea
  • malena
28
Q

Oesphageal Varices - management

A

Airway/ Breathing
- high flow 02

Circulation:

  • IV access x2
  • cardiac monitoring
  • IDC
  • NBM
  • ECG
29
Q

Oesphageal Varices

- what specific system focused assessment should you do?

A
  • focused abdominal assessment