Wk 5: GIT Flashcards
Define acute pancreatitis
= acute inflammation of the pancreas
- presents with rapid onset of inflation and symptoms
- usually results wth resolution of function
What group is at risk of some risk factors for pancreatitis?
- middle age
- previous diagnosis of gall stones or gall bladder disease
- chronic alcohol consumers (this men)
*no gender disparity
What are the three levels of severity in pancreatitis? and what characterises each?
Mild
- no organ failure and there are only local and systemic complications
- low mortality rate and it resolves rapidly
- normally discharged home in a week
Moderately Severe
- transient organ failure and/or systemic complications but this is not persistent organ failure (> 48 hours)
Severe
aka. necrotising pancreatitis
- persistent organ failure
- with up to 50% of these patients having permanent impairment of their pancreatic function
- high risk of further complications such as pancreatic necrosis, organ failure and septic complications
- potential to result in a high mortality rate
What are the phases of acute pancreatitis? and what is the recovery time?
Early: lasts one week
Late: lasts weeks to months
Recovery time: 3-5 days when they have proper treatment
What are the three main causes of pancreatitis? (not necessarily acute)
- gall stones
- getting trapped at the ampulla of vater preventing the flow of bile and pancreatic juices into the duodenum thus resulting in a back up and inflammation of the gall bladder.
- more common in women and older pts - alcohol
- directly toxic to pancreatic cells resulting in inflammation
- more common in men - post- ERCP (type 0f endoscope to pancreas)
IGETSMASHED
I-idopathic
G- Gallstones
E- ethonol/alcohol
T- trauma
S- steroids
M- mumps
A- autoimmune
S- scorpion sting
H- hyperlipidemia
E- ERCP procedure
D- drugs (furosemide, thiazide diuretics, azathioprine)
What are the clinical manifestations of acute pancreatitis?
- sudden, sever epigastric pain, may rapiate to the back
- vomiting
- abdo tenderness
- systemically unwell (tachy, febrile)
What investigations should be carried out and how is acute pancreatitis diagnosed?
Investigations
- FBC (to see WBC)
- U + E (urea level)
- LFT (transaminases + albumin)
- calcium
- arterial blood gas (PaO2 and BGL)
- amylase (raised to x3 upper limit of normal in acute pancreatitis)
- CRP (used to monitor levels of inflammation in the body)
- u/s to assess fro gall stones if ?gall stone related
- CT abdomen to assess for complications e.f. necrosis, abscesses, fluid collections.
Diagnosis
- clinical presentations
- analyse levels
Explain the Glasgow score in the context of pancreatitis
= used to assess severity
- gives numerical score based on how many of the criteria are present
0-1= mild
2= moderate
3+= sever
P- PaO2 <8kPa
A- Age >55
N- Neutrophils (WBC >15)
C- calcium <2
R- urea >16
E- enzymes (LDH >600 or AST/ALT >200)
A- albumin <32
S- Sugar (BGL >10)
Explain the management of a pt with acute pancreatitis?
- ABCDE
- IV fluids
- NBM
- Analgesia
- Careful monitoring
- Treatment of gallstones (ERCP or colesystemicty)
- ABX
- treatment of complications (e.g. draining fluids)
What are some complications of acute pancreatitis?
- pancreatic necrosis
- infection secondary to necrosis
- abscess formation
- pancreatic pseudocyts= collects of fluid, pancreatic enzymes, debris and exudate
- usually resolve but can perforate, need drainage in OT - pancreatic abcess= collection of pus that can perforate into adjacent organs.
- need drainage in OT asap to prevent sepsis - pancreatic fluid collection
- chronic pancreatitis
Sever complications needing HDU care
- Systemic Inflammatory Response Syndrome (SIRS)
- Organ failure,
- Disseminated Intravascular Coagulation (DIC)
- Acute Respiratory Distress Syndrome (ARDS)
- due to the passage of exudate containing the enzymes form the peritoneal cavity. Also the enzyme induced inflammation of the diaphragm occurs causing atelectasis
Explain the assessment and typical findings of a pt with acute pancreatitis?
Danger
Response
Airway
- ?patent, laughing, talking
Breathing
- anticipate they are hypoxemic
- tachypnea
- can have pleural effusions
- alelectesis
Circulation
- IV access
- relevant bloods
- hypotensive
- tachycardia
- evidence of oliguria
- altered colouration or turners signs (bruising or bleeding look around umbli)
Disability
- GCS
- Pain assessment (massive amounts)
- low grade fever that can trend up
- BGL could be altered
Explain the management of a pt with acute pancretitis
Danger
Response
Airways
Breathing
- ?O2 administration, may be NP, non-rebreather, hudson
- may be ordered a CXR (PE or alelectesis)
Circulation
- O2 sat
- cardiac monitoring
- IV fluids thus 2x IV access (early hydration)
- ?CVC needed for extra fluid or inotroped
- ?ECG
- ?IDC for overall hydration status (particular if a renal pt)
- strict FBC (administration of fluid and vomiting indicates this)
- Pathology (FBE, U and E to see WBC, amalayse, lypase)
- ? TEDs
- ? cap refill and colour
Disability
- pain management
- narcotics (with antiemetics)
- ?PCA
- multimodal approach
- BGL (look for treands and may need insulin)
- look for temp treands
Other management
- antibiotics
- H2A
- PPI
- NGT
- CT of abdo
- ?surgery
- laparotomy
Define liver cirrhosis
= chronic progressive disease characterised by extensive degeneration and destruction of the liver.
- liver cells attempt to regenerate, however, their process is disorganised resulting in abnormal blood vessels and bile duct formation.
- liver lobes hen become disorganised and irregular in size and shape= impacting blood flow through liver = poor cellular nutrition and hypoxia which results in decreased function of the liver.
Explain the pathophysiology of cirrhosis
- liver cells are injured and damaged
e.g. continued alcohol, virus, long term of liver cell destruction.
-> bunch with other damaged cells and form regenerative nodules (classic sign of cirrhosis) with fibrotic tissue and collagen in between (the acts of fibrosis) - makes the liver not smooth and all bumpy
= cirrhosis
Closer look at fibrotic tissue formation
- stellate cells located in the perisinusoidal space, between sinusoid and hepatocytes.
- stellate cells main function is to store it A
- when hepatocytes get injured they lose Vit A and proliferate to produce TGF-Beta-> produce collagen which is the main component in extra cellular matrix.
-> fibrotic tissue builds up around stellate cells and compresses sinusoid veins= portal hypertension
-> fluid leaks form vessels and tissues into peritoneal cavity= acites
What are some complications of cirrhosis?
- ascites from portal hypertension where proteins from blood vessels shift into the lymph space and the lymphatic system is unable to remove the excess proteins and water.
- portosystemic shunt -> renal vasoconstriction-> low kidney BF -> low filtration-> hepatorenal failure
- congestive splenomegaly (enlarged spleen due to fluid backing up)
- hepatic encephalopathy due to liver not filtering blood.
- most prominent= amonia
- asterixis (shakey)
- coma - decreased estrogen metabolism, high in blood so causes
- gynecomastia
- spider angiomata
- palmar erythema - jaundice; increased unconjugated bilirubin due to the liver’s reduced ability to remove (excrete) bilirubin.
- low albumin production (hypoalbuminemia)
- liver stops being about to produce clotting factors so you can experience some bleeding issues.
- Oesophageal Varices: this results from portal hypertension where veins at the lower end of the oesophagus are enlarged and swollen
- Portal Hypertension: this develops from structural changes in the liver that cause compression and destruction of hepatic and portal veins
- Hepatic encephalopathy: this is a complex side effect that results from the neurotoxic effects of ammonia
What are the clinical manifestations of cirrhosis?
Early
(compensated cirrhosis w/ some fibrosis)
- fibrosis
- unrelated symptoms e.g. weight loss weakness, fatigue
Later
(decompensated w/ extensive fibrosis)
- jaundice
- pruritus
- ascites
- peripheral oedema
- skin lesions
- endocrine disturbances
- haematological disorders
- peripheral neuropathies
- hepatic encephalopathy
- easy bruising
- formation of collateral vessels so blood can bypass the high pressure liver-> that can break and bleed
* noted; related to lover failure and portal hypertension
How is cirrhosis diagnosed?
- liver biopsy (gold standard)
- blood work (elevated bilirubin, elevated enzymes including; AST, ALT, ALP, GGT)
- thrombocytopenia
What is the treatment for cirrhosis?
- prevent further damage
- identify underlying cause and rate e.g. alcohol
- liver transplant
What are some causes of cirrhosis?
- excessive alcohol consumption
- prolonged viral attack e/g. hep B or C
- jaundice
- ascites
- easy bruising
- hepatic encephalopathy
Explain the likely findings when assessing a pt with cirrhosis
Danger
Response
Airway
Breathing
- consider acities putting pressure on resp system
- assess pt position
Circulation
- colour and circulation (?jaundice)
- risk of bleeding
- distending collateral veins
- look for signs fo bleeding
- ? Iv access
- ?ECG
- do have coag concerns so be conscious of signs
- Blood tests: ammonia levels, haemoglobin levels
- cap refil
Disability
- skins checks for jaundice yellowing
- ?puritis
- GCS (risk of hepatic encolapathy)
- BGL
- Pain
Specific cirrhosis management
- daily weight
- daily abdo measurement
- rest
- manage risk of DVT cause they on bed rest
- manage risk of pneumonia by encouraging deep breathing and coughing
- promote oral hygiene, use of soft tooth brush
- no use of common rasor
- CT abdomen
- Low sodium diet when able to eat
- Paracentesis if indicated
Meds
- PPI: decrease gastric acidity
- Vit K: correct clotting abnormalities
- Propanolol: Reduces venous portal pressure and bleeding from varices
- Lactulose: traps ammonia in bowel for elimination
- Diuretics: to decrease reabsorption of sodium & water, & block aldosterone
- Vasopressin Octreotide: controls bleeding from oesophageal varices
List the four key complications of liver cirrhosis
- portal hypertension
- ascites
- Oesophageal Varices
- Hepatic Encephalopathy
