20 – Digestive System 2 Flashcards
1
Q
What are some examples of GI disease syndromes?
A
- Chronic maldigestion/malabsorption
- Protein losing enteropathy
- Intestinal hemorrhage
- Gastritis/gastroenteritis
2
Q
Maldigestion
A
- Food cannot be properly broken down with the intestinal lumen
- Common sequela with exocrine pancreatic insufficiency (EPI)
3
Q
Malabsorption
A
- Nutrients fail to pass from the intestinal lumen into the blood
- Can see it with: EPI, small intestinal lesions
- Chronic diarrhea*, weight loss, altered appetite (anorexia or polyphagia)
4
Q
What are the non-specific and inconsistent lab abnormalities with chronic malabsorption?
A
- Hypocholesterolemia
- Hypoglycemia
- Hypocalcaemia
- *often don’t see them though
5
Q
What are the ancillary tests for chronic malabsorption?
A
- Abnormal serum folate and cobalamin
- *not all malabsorptive disease are chronic/severe enough to decrease cobalamin/folate
- *misleading results may occur in animals with EPI and/or dysbiosis
6
Q
Where is folate absorbed?
A
- Proximal SI
7
Q
What might cause decreased folate?
A
- Malabsorptive disease of proximal SI
8
Q
What might cause increased folate?
A
- SI bacterial overgrowth: SIBO (produced by enteric bacteria)
o Lack folate carriers - Sometimes EPI: increased acidity from lack of bicarbonate-rich fluid=increased absorption of folate
9
Q
Where is cobalamin absorbed?
A
- Distal SI
10
Q
What might cause decreased cobalamin?
A
- Malabsorptive disease of distal SI: ileum
- SIBO: cobalamin used up +/- bound to bacteria
- EPI: decreased bicarbonate-rich fluid and decreased IF (carrier protein) in cats (only excreted by pancreas in cats)=decreased cobalamin absorption
11
Q
EPI may result in subnormal cobalamin: 100% of cats, 80% of dogs
A
- Recommended panel: TLI, cobalamin, folate in EPI suspects
- Cobalamin supplementation may be needed
12
Q
What might SIBO (SI dysbiosis) result in, in terms of cobalamin and folate?
A
- Decreased cobalamin/increase folate
- Poor sensitivity and specificity
13
Q
What are some causes of SIBO?
A
- Proton-pump inhibitors, broad-spectrum antibiotics
- BARF (bone and raw food) diet
- EPI, GI motility disorders, acute and chronic enteropathies
- Antibiotic responsive diarrhea (ARD) (formerly idiopathic SIBO)
14
Q
Antibiotic-responsive diarrhea
A
- Young, large-breed dogs (esp. German Shepherds)
- Pathogenesis not fully understood (may not reflect human idiopathic SIBO)
o Histo of intestinal biopsies often normal - Definitive diagnosis is challenging
15
Q
What is the tentative diagnosis of antibiotic-responsive diarrhea based on?
A
- Signalment
- Clinical signs
- Folate/cobalamin
- Rule out other conditions
- Positive response to antibiotic therapy (Ex. Tylosin)
- Fecal culture of limited use, molecular studies not reported
16
Q
Protein losing enteropathy (PLE)
A
- *syndrome NOT a disease
- Abnormal loss of albumin (and other proteins) through GI mucosa
- Hypoalbuminemia occurs when albumin synthesis (by the liver) CANNOT compensate
17
Q
What various disease conditions might protein losing enteropathy be associated with?
A
- Lymphangiectasia
- IBD
- Intestinal neoplasia (lymphoma in particular)
- Severe GI infection/parasites
18
Q
What are the supportive clin path/lab findings of protein losing enteropathy?
A
- Hypocholesterolemia: variable
- Panhypoproteinemia (non-selective protein loss)
o Globulins sometimes normal/increased if there is concurrent antigenic stimulation
o Serum albumin <~10g/L may lead to edema and ascites
o Loss of antithrombin can lead to thromboembolic disease
19
Q
How can you rule out other causes of hypoalbuminemia when trying to diagnosis PLE?
A
- PLE: urinalysis +/- UPC
- Hepatic dysfunction: bile acids
- Exudation from the skin: physical exam, etc)
20
Q
Fecal alpha-1 proteinase inhibitor (alpha 1-PI)
A
- Should only be present in serum (similar size as albumin), but resistant to GI hydrolysis (unlike albumin)
- Measure it on FRESHLY VOIDED FECES over 3 days (no intrarectal collection)
- Positive test confirms PLE and/or intestinal hemorrhage
o NEED to rule out intestinal hemorrhage by a FECAL OCCULT BLOOD TEST - Use it to screen dogs prone to PLE (ex. Lundehund) or dogs with poorly responsive IBD PRIOR to overt hypoalbuminemia
21
Q
What is some ancillary testing for PLE diagnosis?
A
- Coagulation panel: PT, PTT, AT III, d-dimers)
- Fecal parasite screening and systemic deworming
- Serum cobalamin/folate
- Imaging
o Abdominal ultrasound to select biopsy method, FNA any abnormal organs for cytology
o Thoracic radiographs to screen for pleural fluid - *biopsies are usually required to determine the etiology of PLE
22
Q
Intestinal hemorrhage
A
- Acute or chronic
- Occult (no visible blood) or overt
- Primary GI insult or secondary to systemic disease
23
Q
What are the 3 main pathological mechanisms of intestinal hemorrhage?
A
- **ulcerative disease
- Coagulopathies
- Vascular anomalies
24
Q
What are some common lab/clin path findings of intestinal hemorrhage?
A
- Anemia (may develop iron deficiency anemia if chronic)
- High BUN (normal creatinine)
- Other changes depending on underlying cause
25
What is the fecal occult blood test?
- Collect 3 different fecal samples as hemorrhage may be episodic
- Patient must have special diet 3 days prior to testing
26
Acute hemorrhagic diarrhea syndrome
- Young to middle-aged, small breed dogs
- Profuse bloody diarrhea (raspberry jam), often EXPLOSIVE
- Peracute fluid loss can lead to hypovolemic shock and death before clinically recognizable dehydration
- Unknown pathogenesis (maybe an abnormal response to a pathogen?)
27
What are some common lab/clin path abnormalities of acute hemorrhagic diarrhea syndrome?
- Elevated PCV (>60%)
- Total protein normal to decreased
- Hypoglycemia
- Electrolyte abnormalities (low K, Na, Cl)
28
What is the treatment for acute hemorrhagic diarrhea syndrome?
- Prompt IV fluid therapy +/- colloids +/- antibiotics
29
Gastritis/gastroenteritis
- Inflammation of stomach and intestinal tract
o Acute onset vomiting, anorexia, diarrhea
- Important to differentiate self-limiting vs. life-threatening problem
- Symptomatic therapy usually relieves clinical signs in 1-3 days
- If signs persist or intensify, further work up is recommended
30
What are the initial diagnostics for gastritis/gastroenteritis?
- Physical exam/history
- Fecal flotation
- +/- hematocrit, and plasma protein
31
What are the important clinical signs of severe, life-threatening or persistent problem? (ex. those that would prompt diagnostic work-up)
- Moderate to severe dehydration
- Abdominal pain
- Melena
- Presence of abdominal mass
- Frequent vomiting
- Signs of systemic illness
32
What are some additional work-up tests for gastritis/gastroenteritis?
- Minimum database (CBC/Chem/UA + T4 in cats)
- Baseline cortisol (to rule out hypoadrenocorticism)
- SNAP parvo test
- cPL or fPL
- radiographs or ultrasound (to rule out obstruction)
- fecal culture/testing for Clostridial enterotoxins
33
What is lymphangiectasia?
- Dilated intestinal lymphatics
o Primary: congenital due to abnormality of lymphatic drainage
o Secondary: obstructed lymphatics secondary to inflammation/fibrosis
34
What are some common clinical pathology abnormalities with lymphangiectasia?
- Panhypoproteinemia (may lead to edema and ascites)
- Lymphopenia (stress and loss in lymph fluid)
- Hypocholesterolemia
- Hypocalcemia
o Often due to decrease in protein-bound form (not clinically significant)
o Rarely see decrease in free calcium; likely Vit D malabsorption
35
Diagnosis of lymphangiectasia requires histo: what is seen?
- *endoscopic biopsy preferred given risk of impaired healing and infection
- Lacteal dilation
- Crypt lesions
- Villous stunting
- Variable inflammatory cell infiltrate in lamina propria
36
Lymphangiectasia in Yorkies
- More common to see severe PLE
o Marked panhypoproteinemia
o Hypocalcaemia, hypomagnesemia
- Treatment: low fat diet, immunosuppressive drugs, +/- calcitriol or IV Ca, +/- vitB12 injections
- Prognosis: 50% respond to therapy, no response=12 month survival time, 20% result in peracute death
37
Johne’s disease (paratuberculosis)
- MAP
- May affect all ruminants
- Less than 5% of those infected develop clinical signs
o Asymptomatic carriers act as source of contamination
o Severe PLE can lead to ventral edema (bottle jaw)
- Cannot reliably ID pre-clinical animals
o Test-and-cull approach can reduce (but NOT eliminate) it from herd
o Fecal PCR, blood ELISA
