GIT conditions Flashcards

1
Q

Define Pancreatitis

A

acute inflammation of the pancreas. most commonly caused by gall stones or gall bladder disease. The other common reason for the cause of pancreatitis is by chronic alcohol consumption

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2
Q

How many levels of severity does pancreatitis have?

A

three
mild, moderately severe, and severe

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3
Q

Define mild pancreatitis

A

There is no organ failure and there are only local and systemic complications
There is a low mortality rate and it resolves rapidly
The patient is normally discharged home in a week

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4
Q

Define moderately severe pancreatitis

A

There is transient organ failure and or systemic complications but this is not persistent organ failure (> 48 hours)

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5
Q

Define severe pancreatitis

A

Also referred to as necrotising pancreatitis
There is persistent organ failure, with up to 50% of these patients having permanent impairment of their pancreatic function
There is also a high risk of further complications such as pancreatic necrosis, organ failure and septic complications
These complications have the potential to result in a high mortality rate

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6
Q

What are the phases of acute pancreatitis?

A

Early: lasts one week

Late: lasts weeks to months

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7
Q

What is the main management goal of pancreatitis?

A

stop autodigestion and prevent systemic complications

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8
Q

What are some potential Breathing findings for pancreatitis?

A

tachypnoea, hypoxia, increased WOB, SOB
may have pulmonary effusions/infiltrates
distended abdomen may impede breathing

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9
Q

What are some potential circulatory findings for pancreatitis?

A

weak & fast radial pulses, tachycardia, hypotension, oliguria. elevated lipase, amylase and WCC
manage fluid losses (antimietucs for vomiting), IDC and FBC

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10
Q

What are some potential disability findings for pancreatitis?

A

Acute coronary syndrome from cerebral hypoperfusion (severe), abdominal pain from oedema and inflammation and obstructed biliary tract, nausea and vomiting, hyperglycaemia as glucagon released from damaged pancreas
NBM initially, insluin, analgesia

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11
Q

What pharmacological methods can be used to manage pancreatitis?

A

multimodal analgesia, PCA, antacids/proton pump
inhibitors, antispasmodics

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12
Q

What are some potential exposure findings for pancreatitis?

A

fever from infection, cullens (bruising of the abdo)/grey turner sign (bruising of the flanks), abdominal distention
treat with ABs, CT for the abdo, NGT if indicated

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13
Q

What are the clinical signs of pancreatitis?

A

pain and tenderness in abdo, nausea and vomiting, fever, tachycardia, SOB, jaundice

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14
Q

What are the potential complications of pancreatitis?

A

Pancreatic fluid collection
Abscess formation
Pseudocysts
Necrosis

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15
Q

What are the potential systemic complications that can occur in severe pancreatitis?

A

Systemic Inflammatory Response Syndrome (SIRS)
Organ failure,
Disseminated Intravascular Coagulation (DIC)
Acute Respiratory Distress Syndrome (ARDS)

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16
Q

Outline Liver cirrhosis

A

a chronic progressive disease characterised by extensive degeneration and destruction of the liver. The liver cells attempt to regenerate but their regeneration process is disorganised, resulting in abnormal blood vessel and bile duct formation. The liver lobules become disorganised and irregular in size and shape. This results in impeded blood flow throughout the liver, resulting in poor cellular nutrition and hypoxia, which results in decreased function

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17
Q

What is the function of the liver

A

removing toxins, processing food nutrients and regulating body metabolism

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18
Q

What is the function of the pancreas

A

The exocrine pancreas produces enzymes that help to digest food, particularly protein. The endocrine pancreas makes the hormone insulin, which helps to control blood sugar

19
Q

What are early symptoms of liver cirrhosis?

A

can include fatigue, but most patients may not be aware of their liver condition. often not detected until more significant signs occur

20
Q

What are later symptoms of liver cirrhosis?

A

Can be related to both liver failure and portal hypertension (elevated BP in the portal vein (carries blood from GIT organs to liver))
The patient can be jaundiced, have ascites (swollen abdo) and peripheral oedema
Skin lesions, endocrine disturbances, haematological disorders and peripheral neuropathies (loss of feeling in peripheries)

21
Q

What are the potential breathing findings that can occur in liver cirrhosis?

A

tachypnoea, hypoxia, increased WOB, SOB, may have distended abdomen from ascites impeding breathing and causing pulmonary effusions

22
Q

What are potential circulatory findings in liver cirrhosis?

A

warm, jaundiced, weak & rapid pulse. signs of bruising, oesophageal varices (enlarged veins in throat), distended veins and oedema, hypotension
manage fluid loss (antimietics), FWT to assess for haematuria (blood in urine)

23
Q

What are potential disability findings in liver cirrhosis?

A

ACS (severe cases), abdo pain, nausea and vomiting, hyperglycaemia
analgesia, anti-mietics, insulin, NMB

24
Q

What are potential exposure findings in liver cirrhosis?

A

fever if infection is present, abdo distention, jaundice and pruritis
ABs if needed

25
Q

What are some common management considerations of liver cirrhosis?

A

CT of the abdo, low sodium diet if not NBM, paracentesis (drainage of fluid in abdo) if needed

26
Q

What are some pharmacology of liver cirrhosis?

A

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

27
Q

What complications can occur from liver cirrhosis?

A

jaundice, Ascites, Oesophageal varices, portal HTN, hepatic encephalopathy

28
Q

Define jaundice

A

develops due to the liver’s reduced ability to remove (excrete) bilirubin. turns the skin and eyes a yellow colour

29
Q

Define ascites

A

Causes swelling in the abdominal space via fluid
Results 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

30
Q

Define oesophageal varices

A

results from portal hypertension, where veins at the lower end of the oesophagus are enlarged and swollen

31
Q

Define portal hypertension

A

this develops from structural changes in the liver that cause compression and destruction of hepatic and portal veins: GIT and liver blood vessels
causes elevated blood pressure in these veins

32
Q

Define hepatic encephalopathy

A

a complex side effect that results from the neurotoxic effects of ammonia
due to liver damage, ammonia and other toxins can build up in your brain, causing you to lose brain function

33
Q

what are complications of ascites?

A

weight gain, abdominal distension and respiratory compromise due to the diaphragm being displaced. The patient is also at risk of developing bacterial peritonitis (an infection of abdominal fluid)

34
Q

Outline a paracentesis procedure

A

For the management of ascites
when the abdomen is drained (fluid is removed) by a needle puncture. Often 5L MAX at one time. It is only a temporary measure as fluid tends to re- accumulate. the pt will require special vitals monitoring during the procedure and strict FBC
Post procedure the patient may require fluid replacement such as albumin

35
Q

What are some pharmacological options for hepatic encephalopathy?

A

NBM initially
- Analgesia: multimodal analgesia
- Anti-emetics and lactulose
- Neomycin (antibiotic) to eradicate bacteria in the bowel & reduce
production of ammonia
- Insulin to manage hyperglycaemia

36
Q

What are some managements for precipitating causes of hepatic encephalopathy?

A

Renal failure: nitrogenous metabolites are retained
- Infection: the brain becomes more sensitive to toxins
- Hypovolaemia: increase in ammonia due to hepatic hypoxia &
impaired functioning of kidneys, brain & liver from hypoperfusion
- Constipation: increases ammonia level
- Hypokalaemia: the brain needs potassium to metabolise ammonia
- Metabolic alkalosis: this increases production of ammonia (by
kidneys) and facilitates transport of ammonia across the blood
brain barrier
- Dehydration: can cause ammonia toxicity

37
Q

Outline Gastrointestinal bleeding

A

A serious complication of various GIT disease states Patients can have an upper GI bleed or a lower GI bleed
patients with ascites, varices or coagulation issues significantly at risk

38
Q

What are some clinical manifestations of GI bleeding

A

paleness, cramps, fatigue, blood in stool

39
Q

What is the difference between bright red stools and black tarry stools?

A

bright red stools indicate lower GI bleed, while black tarry stools indicate older, upper GI bleeds

40
Q

What are some potential breathing findings for a GI bleed?

A

tachypnoea, hypoxia, increased WOB, SOB, may have hypoxaemia from blood loss, may have distended abdo from ascites casing pulmonary effusions

41
Q

What are some potential circulatory findings for a GI bleed?

A

clammy skin, assess amount of blood loss (haematemesis & malena), hypotension, tachycardia, arrhythmias
consider blood tranfusion or NGT insertion

42
Q

What are some potential disability findings for a GI bleed?

A

confusion, pain, vomiting/nausea, hyperglycaemia
NMB initially, analgesia, insulin, PPI stat dose and infusion (lower stomach acid), antacids

43
Q

What are some potential exposure findings for a GI bleed?

A

fever, abdo distention, jaundice and pruritis, external signs of bleeding

44
Q

What are some surgical considerations for a GI bleed?

A

Surgery or endoscopic therapies
Interventional radiology to stop bleeding
Balloon tamponade (Sengstaken-Blakemore tube)