Chapter 3 GI System Flashcards

1
Q

Why are VPCs common in GDVs?

A

VPCs and V-tach are common in GDV secondary to reperfusion injury, ischemia, and cardiac depressant released.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

GDV

A

Malposition of the stomach when it rapidly fills with air and rotates. Vena cava gets compressed, leading to a decrease in venous return to the heart through the vena cava.
A partial or complete blockage of the portal vein which can cause the liver or pancreas to become ischemic.
The spleen which is attached to the stomach on the upper left region of the abdomen can also be twisted and become ischemic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the signs of GDV?

A
Non-productive retching 
Abdominal distention
Pain 
Anorexia
Restlessness
Shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the treatment of GDV?

A

Treat shock with IV fluid therapy
Severe abdominal pain with pain medication
Oxygen for respiratory distress due to enlarged stomach pressing on diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does lactate response tell us about the GDV patient?

A

A decrease in 50% or greater from the starting lactate within 12 hours of presentation is a good indicator for survival.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the diagnosis for GDV?

A

Pre fluid bloods
Right lateral radiograph
Chest radiograph to rule out aspiration pneumonia and metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the treatment for GDV?

A

Gastric decompression - orogastric tube measured from nose to the last rib
Gastrocentesis (trocharization)but since prone to DIC - check coagulation factors first - 14-18 gauge needle, patient in left lateral recumbency
Surgery - always recommended as can’t confirm an atomic
Treat ventricular arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the complications of GDV post surgery?

A

Sepsis
DIC
Gastritis
Cardiac arrhythmias
Ischemia - reperfusion (I/R) injury
VPCs and ventricular tachycardia
- acid base and electrolyte abnormalities, myocardial depressant
factors and myocardial ischemia
- only treat if more than 160bpm or patient is clinical
-weak pulses, shock, perfusion decreased
- lidocaine or procainamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

I/R injury complications include

A

Systemic inflammatory response syndrome (SIRS)
Multiple organ failure (MODS)
Rhabdomyolysis (Damaged skeletal muscle breakdown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is hemorrhagic gastroenteritis (HGE)?

A

An intestinal disease characterized by:
-acute loss of blood, fluids and electrolytes from the GI tract

Symptoms:

  • acute vomiting (possible hematemesis - vomiting of coffee ground blood)
  • anorexia
  • hematochezia (fresh blood per anus)
  • rapid decline
  • moderate (7%) to severe (10-12%) dehydration
  • hypovolemic shock

Cause unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is melena?

A

Passage of black tarry stools

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is gastric or intestinal obstruction?

A

Inability of food to pass through part of the GIT

Symptoms:
Abdominal pain 
Vomiting 
Anorexia
Straining to defecate
Diarrhoea 
*Biggest concern = perforation= Septic peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is septic peritonitis?

A

Inflammation of the pertoineum (membrane that lines the abdominal cavity) due to bacteria in the abdominal cavity from perforation or rupture of a hollow viscus (tumour).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens systemically in septic peritonitis?

A

1) Bacteria in abdomen causes inflammatory cascade to become activated.
2) Neutrophils & macrophages attack affected tissues.
3) Inflammatory cytokines are released from activated neutrophils.
4) Cytokines signal to T-cells and macrophages to travel to injury site.
5) Bacteria can cause DIC, SIRS, hypertension & shock.
6) Cardiac functions are frequently compromised due to electrolytes and acid-base disturbances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the signs and symptoms of a patient in septic peritonitis?

A
Shock
Injected MM
Dull mentation 
Fever
Weak peripheral pulses 
Tachycardia 
Very painful abdomen in advanced stages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you diagnose septic peritonitis?

A
Increased white blood cell count.
Anemia
Thrombocytopenia 
Electrolyte imbalances 
Increased kidney or liver enzymes 
Coagulation factors to be monitored
Abdominal radiographs - loss of detail or free glass in abdominal cavity 
Ultrasound to find underlying cause 
Abdocentesis to obtain fluid sample for analysis, culture and susceptibility and view in house microscopically - presence of neutrophils & bacteria indicates septic peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you treat septic peritonitis?

A

IV fluids
Antibiotics
Analgesics to start immediately
If DIC - heparin & plasma to begin
Surgery once stable to eliminate contamination source - open or closed abdomen
Overall survival rate is 25% - guarded prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is protein losing enteropathy (PLE) and what are the causes?

A

Where protein leak into the gut lumen. Loss of albumin and globulin resulting in a decrease in intravascular oncotic pressure, development of abdominal and pleural effusion & peripheral edema.
Thromboembolisms may occur due to decrease in antithrombin.

Causes:
Lymphangiectasis
Parvovirus
Intussuception 
Lymphosarcoma
Lymphatic-plasmacytic enteritis 
Inflammatory bowel disease 
HGE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do you diagnose PLE?

A

Intestinal biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is acute abdomen/ abdominal pain?

A

When a patient presents with a sudden onset of severe abdominal discomfort or pain. Pain is due to the stretching and inflammation of nerve fibres located within the organs and GIT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is hypovolemic shock?

A

It is characterised by a significant decrease in intravascular volume resulting in a decrease in stroke volume and cardiac output.

*Stroke volume = vol. of blood pumped from the left ventricle per beat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What kind of medication should be avoided when a patient is suffering from acute abdomen?

A

Non-steroidal anti-inflammatories (NSAIDS) until GI ulceration can be ruled out and hypoperfusion is no longer a concern.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is DPL?

A

It stands for diagnostic peritoneal lavage used to rule out various diseases that causes acute abdomen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How much fluid must be present in the abdominal cavity to be able to perform a successful abdocentesis?

A

More than 6ml/kg.

Ultrasound guided abdocentesis will yield better results.
Using the 4 quadrant tap technique.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

At which point do you resort to a DPL?

A

When abdocentesis is unsuccessful.

26
Q

How is a DPL performed?

A

Patient in left lateral recumbency to avoid spleen
Scalpel blade to make 2-3 fenestrate side holes in a 14-18guage over the needle catheter with holes no larger than 50% of the circumference of the catheter to avoid it breaking off in the abdomen.
Insert catheter into the peritoneal cavity caudally and to the right of the umbilicus at the level of the nipples.
Remove stylet and look for any fluid at the hub of the catheter.
If no fluid present, insert 10-20ml/kg warm isotonic crystalloid into the abdominal cavity over 3-5 mins.
Remove catheter and rotate patient gently from side to side.
Collect sample via an abdominocentesis.

27
Q

What is Lymphangiectasia?

A

It is one of the many causes of PLE characterised by the dilation of lymph vessels in the mucosa and/or submucosa of the small intestine. It can be a primary (congenital) or secondary (acquired) disease.

28
Q

What is secondary Lymphagiectasia?

A

It is usually caused by intestinal lymphatic obstruction.
Pressure builds up in the lymph vessels causing the lacteals to rupture and leak lymph into the intestinal lumen.
Protein is lost by the leaking of the protein rich lymph into the intestinal lumen therefore causing hypoproteinemia to occur.
Due to hypoproteinemia, ascites or oedema may occur.

29
Q

A canine patient is diagnosed with lymphangiectasia. What laboratory finding would you expect to see and what clinical findings would you monitor for?
A. Hypercalcemia and bradycardia
B. Hyperkalemia and tachycardia
C. Hypoalbuminemia and third spacing of fluids (intravascular to intersitial space)
D. Lymphophilia and hypertension

A

C. Protein is lost by leaking of the protein rich lymph into the intestinal lumen thereby causing hypoproteinemia to occur. Due to hypoproteinemia, ascites or edema may occur. These patients may be hypocalcemic due to decrease in albumin, vitamin D or absorption of fat. Animals that are hyperkalemic will not be tachycardic, they will be bradycardic. These patients are also usually lymphopenic.

30
Q

What are the signs of Lymphangiectasia and how is it diagnosised?

A
Hypoproteinemia
Ascites or oedema 
*Hypoalbuminemia (most consistent lab finding)*
Anemia (due to chronic inflammation)
Lymphopenia
Neutrophila
Hypocalcemia (due to a decrease in albumin, vit D or absorption of fat)
Thromboembolism or DIC 

Diagnosis is through intestinal biopsies*

31
Q

Treatment for Lymphangiectasia

A
For secondary:
Managing the underlying cause 
Decreasing loss of enteric protein
Stopping intestinal or lymphatic inflammation 
Control edema 

For lympgangiectasia:
Dietary modification (bland, no fat diet)
Fat soluble vitamins
Glucocorticoid therapy (prednisolone)

32
Q

What is inflammatory bowel disease (IBD)?

A

A nondescript term used to characterise unknown causes of intestinal inflammation

33
Q

What are the causes of chronic intestinal inflammation?

A

Giardia
Toxoplasmosis
Lymphoma
Histoplasmosis

34
Q

What are the three main forms of idiopathic IBD?

A
Lymphocytic plasmacytic enteritis (LPE) - most common 
Eosinophilic enteritis (EE)
Granulomatous enteritis (GE)
35
Q

What is the treatment for idiopathic IBD?

A

Dietary modification
Antibacterials
Immunosuppressive drugs - glucocorticords (prednisolone, dexamethasome), cyclosporine & azathioprine
Anti-inflammatories - Sulfasalazine or mesalazine
Metronidazole (immunosuppressive and antimicrobial)

36
Q

What disease affect the GIT?

A

Heart

Liver diease

37
Q

What is the accepted cause of acute pancreatitis?

A

It is due to auto-digestion due to activated pancreatic enzymes within the small intestines leading to activation of the inflammatory process with the production of neutrophils, cytokines and free radicals.

38
Q

What are the risk factors for developing pancreatitis?

A
Nutritional factors (high fat diets)
Abdominal trauma
Inflammatory bowel disease
Hyperadrenocorticism (Cushing’s)
IBD
Biliary duct obstruction 
Hypothyroidism 
Diabetes mellitus
39
Q

What dog breeds are more susceptible to developing chronic pancreatitis?

A

Spaniels (Cockers and Cavaliers)
Collies
Boxes

40
Q

What are the signs of pancreatitis?

A

Vomiting
Anorexia
Severe abdominal pain (walking in a hunched appearance. Cats hide)

41
Q

How do you diagnose pancreatitis?

A

*Pancreatic lipase immunoreactivity (PLI) assay - most accurate

Trypsin-like immunoreactivity (TLI): detects serum trypsinogen which is only produced by the pancreas

Amylase and lipase are inaccurate as they can be elevated from GI disease or hepatic disease

CBC: leukocytosis and neutrophilia with a left shift

Hypocalcemia
Hypoalbuminemia (can cause decrease plasma = lower antithrombin= coagulopathy)
Hyperglycemia ( from increased glucocorticoids)
Elevated liver enzymes

Secondary biliary blockage causing icteric
IDEXX SNAP cPL test - canine pancreas-specific lipase
Radiographs (non-diagnostic) - can reveal a loss of detail in the right cranial quadrant=gas filled descending duodenum

Ultrasound * best choice as non-invasive and quick - false negatives found in cats

42
Q

Treatment for pancreatitis

A

Main = IV fluids
If DIC = plasma (for clotting factors and antithrombin)
Pain medication
Start nutrition ASAP:
-Dogs should not be fasted for more than 48-72 hours
-Cats should never be fasted
-helps decrease bacterial translocation and maintain enterocyte health and support immune function

43
Q

What type of feeding tube is thought to be effective for dogs with pancreatitis?

A

Intra-jejunal nutrition as it does not encourage enzyme-protein synthesis or pancreatic secretions.

44
Q

How fast should caloric intake be given in pancreatic dogs?

A

Slowly over 3-4 days towards maintenance of energy requirements of (30 x body weight (kg) ) + 70 = daily kcal needs

45
Q

Hepatic lipidosis

A

Intracellular accumulation of lipid within the liver.
Usually caused by anorexia.
Diets with excessive carbohydrates or protein can result in hepatic fat accumulation.
Any GI disturbances (especially in cats) can cause this.
Jaundiced and elevated liver enzymes.
X-ray: enlarged liver.
Liver biopsy or aspirate is the only way to diagnose hepatic lipidosis.
Concurrent diseases: IBD, pancreatitis and septic peritonitis.
Nutritional support must be started immediately.
Esophagostomy or PEG tube.
IV therapy, antiemetic therapy and VITAMIN K** due to prolonged coagulation times (Liver produces prothrombin (alpha globulin))**
Monitor for refeeding syndrome.
Hypokalemia, hypophosphatemia and hypomagnesemia can occur after prolonged catabolic state- which could result in a rapid rise in insulin and a shift of plasma potassium, magnesium and phosphate into the intracellular compartment.

46
Q

Liver

A

Globulin synthesis occurs here - alpha and beta globulins= transport lipids and fat-soluble vitamins.
Most important alpha globulins = prothrombin

47
Q

Why is nutritional therapy important in hospitalised patients?

A

Inadequate nutrition can cause:

  • Decreased tissue synthesis and repair.
  • Altered drug metabolism.
  • Decreased immunocompetence
48
Q

BCS = Body condition score

A
1 = cachexic
5 = obese      Or

1-10 with 10 being obese

49
Q

How long does a patient have to be anorexic before being considered high risk for nutritional intervention?

A

Anorexic for greater than 48 hours
Or
Consumes less than 50% of necessary food intake for more than 3 days

50
Q

Resting energy requirement (RER)

A

Cats: 40 X BW (kg)

Dogs: (70 x BW (kg)) x 0.75

Or

(30 x BW (kg)) + 70

51
Q

Illness factor

A

Where increased metabolic rates have been documented.
Conditions: burns, cancer, head trauma and sepsis
RER x 1.1 - 1.5

52
Q

What has hyperalimentation been associated with?

A

Refeeding syndrome:

  • Hepatic dysfunction
  • Increased CO2
  • Ammonia production
  • Hyperglycemia
  • Hypokalemia. - cardiac and skeletal muscle weakness
  • Hypophosphatemia - severe anaemia
  • Hypomagnesaemia - tetany or seizures
53
Q

How to avoid re-feeding syndrome?

A

Reintroduce nutrition:

  • First day: 1/4 to 1/3 RER and gradually increasing to full RER over 3 to 4 days
  • Monitor blood glucose, electrolytes and plasma lipids
  • Link between hyperglycaemia and morbidity in hospital
  • cats more susceptible due to less efficient conversion of glucose to glycogen
  • cats more than likely to have stress-related hyperglycaemia secondary to catecholamine release
54
Q

Nasogastric / nasoesophageal tube

A
  • Fairly easy to place
  • No general anesthesia
  • Ideal for short term feeding (3-14 days)
  • Topical anesthetic agent into the nostril
  • Small gauge tube is directed ventromedially through the nasal meatus and advanced to the second rib (nasoesophageal) or the last rib (nasogastric)
  • Saline can be infused to confirm placement
  • if cough = tracheal intubation should be suspected
  • Capnogrpahy or air can be used to determine placement unless carbonated beverages have been used to unblock a feeding tube
  • Can be used for gastric decompression and suctioning to assess gastric motility
  • Contraindicated in patients who are vomiting, have an unprotected airway, GI obstruction, airway or esophageal disease, or have facial or head trauma
  • Potential complications:
  • aspiration
  • inadvertent tracheal intubation
  • tube dislodgement
  • irritation
55
Q

Esophagostomy tube

A
  • Tolerate gastric feeding but for whom nasal tubes are contraindicated.
  • GA required
  • Larger tube size allows thicker feeds
  • Longer term placement and at-home feeding by owner
  • Great for head trauma or facial trauma patients
56
Q

Gastrostomy tube

A
  • Bypasses the oral cavity and esophagus
  • At-home feeds
  • Endoscpopy placed or laparotomy under GA
  • Must stay in place for a minimum of 14 days to allow for stoma adhesion
  • Larger tube allows for blended and more complete diets and some oral medications
57
Q

Jejunostomy tube

A
  • Where gastric tube is not tolerated
  • Does not stimulate pancreatic enzyme, therefore ideal for patients with pancreatitis
  • Placement via surgical laparotomy
  • Must be liquid and iso-osmolar to avoid translocation of fluid into the lumen of the intestine
  • CRI should be used
  • Elemental diet - contains small peptides or amino acids, mono- or di-saccharides, and medium chain triglycerides, requiring little to no digestion and permitting immediate absorption
58
Q

Glutamine

A
  • Amino acid
  • precursor for growth of enterocytes
  • Essential for the maintenance of GI mucosal structure and integrity
59
Q

Arginine

A
  • Essential amino acid
  • Wound healing
  • Immune function
  • Metabolism
60
Q

Omega-3 fatty acids

A
  • anti-inflammatory
  • Immune modulating effects
  • Useful in managing inflammatory states and sepsis
61
Q

Parenteral nutrition

A
  • IV administration of a combination of carbohydrates (dextrose), amino acids, lipids, vitamins, and trace minerals.
  • Can be partial (PPN) - 40-60% caloric needs or total (TPN) - 100%
  • PPN (Peripheral) or CPN (Central)
  • High osmolarity solutions (>700mOsmol/L)-centrally placed IV catheter to avoid damage to the vascular endothelium
  • Lower osmolarity solutions (<700) - peripheral catheters
62
Q

What is the most common reported metabolic complication of PN?

A

Hyperglycaemia which can be treated with insulin at 0.5U/kg/day