1
Q
3 stages of vomiting
A
- Nausea
- Retching - forceful gastric contents enter the esophagus
- Vomiting - expulsion of gastric contents by contraction of abdominal muscles and diaphragm
Intrathoracic pressure is negative during retching and positive during vomiting.
2
Q
Vomiting is controlled by 2 centers
A
- Emetic center
- Medulla oblangata (CRTZ) - floor of the 4th ventricle
3
Q
How is the emetic center stimulated?
A
- Humoral pathway - blood borne substances
- Neural pathways
- afferent vagal pathway
- sympathetic pathway
- vestibular pathway
- cerebrocortical pathway
- Direct extension from brain disease
- inflammatory
- space occupying lesion
4
Q
How is the neural pathway activated?
A
Via peripheral receptors throughout the body
- especially those of duodenum ~ “organ of nausea”
5
Q
How does the humoral pathway stimulate vomiting?
A
Limited blood brain barrier in the medulla allows the CRTZ to be exposed to blood-borne chemicals (drugs, uremia, etc)
6
Q
What are the three phases of swallowing and what CN are involved in each?
A
Oral phase
- Tongue makes bolus and moves bolus on midline and back (CN 12, sensory for this CN 5). This is voluntary until the bolus reaches pharynx.
- Dysphagia from oral phase disorders due to reduction in tongue function for the most part.
Clinical signs:
- Inability to hold food in mouth or transport it back
- Poor bolus formation
- Inability to initiate pharyngeal phase
- Weak tongue-action during pharyngeal phase.
- Rarely aspirate
_Pharyngeal phas_e
- Soft palate is elevated, palatopharyngeal folds move inward, vocal folds pull together, larynx elevated against epiglottis, Cripcopharyngeal muscles relax, UES opens, bolus enters esophagus, UES closes, pharyngeal muscles relax (CN 5, 7, 9, 10, 12 all involved)
- Geniohyoideus and mylohyoideus pull larynx forward letting the epiglottis close over the glottis. Concurrently the adductor muscles close the glottis
- Tongue stops forward and backward movements and prevents food going back into oral cavity.
- Dorsal pharyngeal constrictors stops food egress from pharynx, palatopharyngeal arch contracting stops food going back into nasopharynx5
- There’s a bunch of nuclei in the reticular formation termed the swallowing center. Vagus sends visceral info to medulla oblongata from tongue, pharynx and esophagus
Nerves involved:
CN 5 - Trigeminal:
- Sensory nerves from oral cavity
- Motor fibers for mucles of mastication, mylohyoideus and soft palate muscles
CN 7 - Facial:
- Sensory nerves from visceral receptors in the soft palate and nasopharynx
- Motor fibers to stylohyoideus and jugulohyoideus
CN 9 - Glossopharyngeal
- Sensory nerves to pharynx and part of tongue, with vagus
- Motor fibers to constrictors and dilators of pharynx
CN 10 - Vagus
- Motor with glossopharyngeal nerve (CN 9) to constrictors and dilators of pharynx.
- Also carries visceral efferent and afferent fibers to pharynx so intimately involved with all stages of swallowing
- Pharyngoesophageal nerve - from vagus and glossopharyngeal
- Motor nerves to caudal pharyngeal muscles (cricopharyngeus and thyropharyngeus), laryngeal muscles and cervical esophagus
CN 12 - Hypoglossal
- Motor fibers to tongue
Dysphagia of the pharyngeal phase usually with poor contractility and transport function of cranial and caudal pharyngeal constrictors.
Clincial signs:
- See deficiencies in the contractions delivering bolus from the oropharynx to the esophagus and contrast/food stuck in the valleculae, pharynx opening and piriform recesses but ability to form bolus and push it back, so incoordination of the cricopharynx, normal esophagus4
- Predominantly aspiration (also seen with cricopharyngeal dysphagia).
- Food can be stuck in pharyngeal recesses for hours, and pharyngral recesses enlarge so can regurg food from there hours later.
Esophageal phase:
- Transports bolus through esophagus, through gastroesophageal sphincter, to stomach (esophagus innervations vagus).
- A bolus should always stay a bolus…if it breaks up in the esophagus it indicates a motor deficiency, has been seen with myasthenia gravis.
Primary peristalsis = esophageal motility triggered by pharyngeal contraction.
- May need sufficient tactile or stretch stimulus for this to occur
Secondary peristalsis = esophageal motility triggered by esophageal luminal distension and tactile stimuli.
- Esophageal peristalsis can follow a couple of different sequences (normal)
- Swallow is followed by immediate peristalsis of esophagus (primary peristalsis)
- After a swallow the bolus sits in the cranial esophagus until another 1 or 2 swallows occurs, then all boluses are sent down together (still primary peristalsis)
- After a swallow the bolus sits in the cranial esophagus for a short period of time, then stimulates a peristaltic wave (secondary peristalisis)
- A few boluses accumulating in the cranial esophagus finally trigger a peristaltic wave (secondary peristalsis)
- Boluses can occasionally stall in the esophagus until a secondary peristaltic wave comes along
- Some separate esophageal from gastroesophageal phases where the gastroesophageal phase is the passage of food through the LES
- There is sometimes a small amount of reflux through the open LES, without contraction of the stomach and with almost immediate secondary peristaltic wave to push it back. That can be normal (relaxation can last 8-12 sec).
The LES is functional, not anatomic. It is the association between a bunch of things:
- Gastric rugal folds interdigitate near the cardia
- Focal thickening of inner smooth muscle of distal esophagus
- The oblique insertion of the esophagus into the stomach
- Flap-like cardiac incisura pushed up against the esophageal opening
- The deep oblique smooth muscle of the lesser gastric curvature forms a sling around the left side of the cardia
- Compression of the intra-abdominal esophagus by the intra-abdominal positive pressure
- The muscular sling of the diaphragm as the esophagus goes through it helps with closure.
Some add in the cricopharyngeal phase- relaxation of the cricopharyngeal sphincter, passage of bolus into UES, closure of the sphincter, relaxation of the pharyngeal muscles4
Dysphagia of this phase from inability to open or close UES, or incoordination between UES opening and pharyngeal contraction4
7
Q
How does GDV lead to hypoxia?
A
Thoracic and diaphragmatic impingement results in decreased tidal volume, which causes ventilation/perfusion mismatch and results in hypoxia.
8
Q
How does GDV result in arrhythmias, hemorrhagic enteritis?
A
Due to decreased tissue perfusion
9
Q
How does a GDV result in anemia and hemoabdomen?
A
Avulsion of short gastric and right gastroepiploic vessels
10
Q
Liver usually has ___ blood flow and ___ vascular resistance.
A
Liver usually has high blood flow and low vascular resistance.
- Portal vein pressure is 9mmHg
- Pressure of hepatic vein leading to CVC is 0mmHg
11
Q
Functions of liver
A
- Blood reservoir
- Fat/protein metabolism - has high lymph flow: pores in hepatic sinusoids are very permeable and allow passage of fluids/proteins into the space of Disse
- Carbohydrate metabolism
- Blood cleansing - the louder cells (tissue macrophages) will clear GI origin bacteria and endotoxins from the portal vein via phagocytosis
- Immunoregulatory function
- Detoxifying
- Biliary excretion
12
Q
How does PSS result in microhepatica?
A
Decreased blood flow and lack of insulin, glucagon and nutrients in the liver results in hepatic atrophy.
13
Q
How does liver disease result in hepatic encephalopathy?
A
It’s related to decreased clearance of GI toxins such as ammonia, mercaptans, short fatty amino acids, GABA and endogenous benzodiazepines.
14
Q
How does PSS result in urate stones?
A
Inadequate clearance of ammonia by the liver (because blood is getting shunted and bypasses the liver) results in increased urinary excretion of ammonia and uric acid - renal, cystic or urate urethral calculi may form.
15
Q
Causes of acquired PSS
A
Portal hypertension:
- Liver disease
- Cirrhosis
- Idiopathic fibrosis
- Chronic hepatitis
- Portal vein thrombosis
- Post surgical occlusion of PSS
- Neoplasia
- Extra luminal compression of portal vein
16
Q
Causes of acute hepatitis
A
Toxin/Drug:
- Acetaminophen
- Carprofen
- Tetracycline
- Sulfonamides
- Diazepam
- Methimazole
Hepatic lipidosis (cats):
- During starvation more fatty acids are mobilized and less lipoproteins are produced, which causes lipid accumulation
Vascular compromise:
- Liver love torsion
- Portal vein thrombosis
Infectious causes:
- Adenovirus type 1
- Helicobacter canis (rare)
- FIP: usually dry form which results in immune complex vasculitis and pyogranulomatous inflammation
- Hepatic abscess: can occur for many reasons
- immunosuppressed animals
- diabetes mellitus
- umbilical infection in young animals
- penetrating abdominal wound
- direct extension from local infection
- primary septic focus with seeding of liver through bloodstream (pyelonephritis, pyometra, endocarditis, other cause of sepsis)
17
Q
How does liver disease result in decreased copper excretion?
A
Copper is usually excreted in bile. Liver disease with cholestasis and decreased bile flow could cause copper accumulation.
18
Q
What breeds are predisposed to copper storage disease?
A
Belington terriers
- Bellington terriers accumulate copper throughout their life due to mutation that results in mellathionein that has strong affinity to copper.
West Highland White Terrier
- West Highland White Terriers do not accumulate copper throughout their life. They usually peak copper levels at around 6-12 months of age. Mechanism unknown.
Doberman
Cocker Spaniel
19
Q
What is cholangiohepatitis?
A
Inflammation of bile ducts and adjacent hepatocytes. Usually seen in cats. Persians are predisposed. Thought to be due to ascending infection from GI (E. Coli).
20
Q
What’s is cholecystitis?
A
Inflammation of gall bladder and associated bile ducts. Emphysematous cholecystitis commonly seen in pets with DM
21
Q
Causes of biliary obstruction
A
Extra hepatic:
- Pancreatitis
- Pancreatic abscess/cyst
- Pancreatic neoplasia
- Bile duct neoplasia
- Intestinal neoplasia
- LN neoplasia
- Scar formation around the bile duct
- Cholelith
Intra hepatic:
- Cholestasis
- Periportal inflammation (cholangiohepatitis)
- Hepatic lipidosis
22
Q
Causes of mucocele formation?
A
- Cholestasis resulting in biliary stasis
- Mucinous hyperplasia +/- chronic inflammation
Bacterial infection may occur secondarily
23
Q
Describe the course of the esophagus.
A
Cervical - midline or left of midline
Heart base - aorta is now on the left with the esophagus on the right
24
Q
Cat esophagus differ in 3 ways:
A
Cat esophagus:
- The proximal 70% of the esophagus is striated muscle, while the distal 30% is smooth muscle (whereas in dogs the entire esophagus is striated muscle).
- Herring bone I in cats the terminal esophagus is arranged in transverse ripples, which create this herringbone appearance
- “Cone” shaped at terminal portion
25
**What nerve** and what part of the brain controls **peristalsis**?
**Vagus nerve (CN 10)** Medulla - nucleus ambiguous
26
What is **achlasia? Chalasia?**
**Achlasia** = failure of the cricopharyngeal muscle to **relax**
**Chalasia** = failure of the lower esophageal sphincter to **contract**
* Causes GE reflux
27
Dogs with **v- shaped esophagus** will most likely have what disease?
**Chalasia**
28
What do you think when the **aorta is to the right**?
Vascular ring anomaly
29
What enzymes does the stomach produce?
**Gastrin** - stimulates
* **HCl** and **pepsin** secretion
* Growth of the mucosa
**Rennin**
**Pepsinogen**
30
What does **cholecystokinin** do and **where is it secreted** from?
Secreted from the **duodenum and jejunum**.
* Promotes **gall bladder contractions**
* **Inhibits gastric emptying**
* Increases **pylorus contractions**
* Induces p**ancreatic secretions**
31
What does **secretin** do and where is it secreted from?
Secreted from **duodenum** -
* Stops gastric emptying
* Increases pyloric contraction
* Increases bicarbonate secretion
* Promotes pacreatic enzyme secretion
32
What enzymes does the duodenum secrete?
1. Cholecystokinin
2. Secretin
33
What does a **coil spring** demonstrate?
Intususseption?
34
Describe the **oropharyngeal phase of swallowing**?
* Once in the oral cavity the food is pushed against the palate by tongue and forced into the oropharynx by muscular contractions.
* Pharyngeal pressure receptors activate the swallowing center in the medulla.
* Once here, the **soft palate is elevated** to **block the nasopharynx**.
* At the same time the **laryngeal muscles contract** which **close the glottis** and then the epiglottis lays on top of the glottis and covers the trachea.
* The **cricopharyngeous muscle** (upper esophageal sphincter) **relaxes** when the **pharyngeal muscles contracts** and push the bonus forward to enter the esophagus.
35
Describe the **esophageal swallowing**?
**Primary peristalsis** - initiated by the pharynx, usual transit time 8-10 sec to reach to the stomach
**Secondary peristaltic** waves - if primary peristaltic waves fails, the secondary peristaltic waves will move the bolus because of distention of the esophagus. These continue until the bolus reaches the stomach.
36
Which part of swallowing is **voluntary** and what part of the Brian mediates it?
**Oropharyngeal**
Cerebral cortex
37
The remainder of swallowing is mediated by what? Activated by what? And what coordinates it?
_Mediated by_ - the **swallowing center** in the **medulla**
_Activated by_ - **oral and pharyngeal pressure receptors** via the
* Trigeminal nerve (CN 5)
* Glossopharyngeal nerve (CN 9)
* Vagus nerve (CN 10)
_Coordinated by_ - Vagus nerve (CN 10)
38
What is necessary for secondary contractions to occur?
The bolus size has to be big enough to meet the "threshold"
39
What are tertiary contractions? When do they occur?
Titanic contractions which can be lack, diffuse, stationary, or slowly advancing. Commonly seen with **abnormal function or foreign body**.
40
As the bolus approached the stomach, what normally happens just before?
**Momentarily delayed** at the gastroesophageal junction
41
Describe the **physiology** of the **lower esophageal sphincter**?
The **esophageal hiatus** (esophagus and vagus nerve pass) is in the **right crus** of the diaphragm. The cardiac valve is formed by the bunching of the mucosa to help form a seal, intaabdominal press oil also very helpful in maintaining competency.
42
In what 3 ways does the anatomy of the **feline gastroesophageal region** differ?
1. The hiatus is more of a **slit**
2. More prominent folds - **rosette**
3. Esophagus is more free to **slide back and forth**
43
What controls the activity of the hiatus?
* **Vagus Nerve** (CN 10)
* **Splanchic nerve** (sympathetic system of abdominal organs)
44
What is segmentation?
The **rhythmic movement** of **chyme**
45
What is peristalsis?
**Ring like stripping contractions** that propel chyme
46
What does the mucosa of the **stomach secrete**?
**Gastric glands secrete:**
* **HCl** - parietal cells
* Pepsinogen - chief cells
* intrinsic factor
* Mucus - mucus secreting cells
**Pyloric glands secrete:**
* Pepsinogen - chief cells
* Mucus - mucus secreting cells
* **Gastrin** - G cells
47
What 3 things **stimulate** activity of the **gastric glands**?
1. Acetylcholine from the Vagus nerve (CN 10)
2. Gastrin
3. Histamine
48
What **regulates pepsinogen** secretion from the **chief cell**?
* **Acid secretion** in the stomach
* **Acetylcholine** from the Vagus nerve (CN 10)
49
What occurs when food enters the duodenum?
* Inhibits further secretion of gastric recreations
* Bicarbonate secretion
* Pancreatic enzyme secretion
50
What are the **pancreatic enzymes**?
1. Protease:
1. Trypsin
2. Chymotrypsin
3. Carboxypolypetide
2. Amylase
3. Lipase
51
What 3 things **stimulate** secretion of **pancreatic enzymes**?
Once food enters the duodenum :
* Secretin (S cells)
* Cholecystokinin (I cells)
Cephalic phase and gastric phase stimuli:
* Acetylcholine from the Vagus nerve (CN 10)
52
What does the **LI secrete**?
Mucus
53
How does the lining of the LI differ from the SI?
* No villi
* No digestion
54
Which **cranial nerves** are involved in **vomiting**?
* Trigeminal nerve (CN 5)
* Facial nerve (CN 7)
* Vestibulocochlear nerve (CN 8)
* Glossopharyngeal nerve (CN 9)
* Vagus nerve (CN 10)
* Hypoglossal nerve (CN 12)
55
Describe 6 events of vomiting?
1. Deep breath
2. Hyoid raises to open the UES
3. Glottis closes
4. Soft palate lifts to cover the internal nostrils
5. Strong downward contraction of the diaphragm and stimulus squeeze of the abdomen
6. Expulsion
56
What is the basic electrical process underlying motility of the bowel?
The basic electrical rhythm with **spike complexes** causing contractions
57
Describe **gastric emptying**
The fundus acts as a reservoir for food and liquid, and maintains a pressure gradient to the duodenum. Liquids empty fastest but depends on caloric density. The antrum and pylorus control solid emptying at a constant rate. There is feedback from the content in the duodenum to control rate and maximal particle size is 1-2 mm. When the stomach is emptied the MMC clears out large remaining particles.
58
Name **3 hormone**s that are produced in the **duodenum** that **affect GI motility**?
1. Cholecystokinin
2. Secretin
3. Gastrin inhibitor peptide
59
What are the **different types of cells in the stomach** and what do they produce?
* Chief cells = pepsinogen
* Parietal cells = HCl
* Mucus neck cells = mucous
* Mucus surface cells = mucous
* G cell = gastrin
60
What are the **different parts of the gastric mucosa** and how to they differ?
1. **Cardia** - is **glandular** and secretes alkaline mucus, parietal secreting acid and pepsinogen
2. **Pyloric antrum** - secretes **gastrin** and pepsinogen
\*Horse has a non-glandular part
61
How is secretion regulated in the stomach?
**Anticipation** of eating causes parasympathetic stimulation of the **G cells,** which produce gastrin.
**Presence of food in the stomach** triggers **stretch receptors** which cause stimulation of G cells directly.
* Food in the stomach lowers the pH which removes inhibition of **gastrin** secretion.
* Gastrin is absorbed in blood and **stimulates chief and parietal cells** to produce **pepsinogen and HCl**, respectively.
When **food** moves into the **duodenum** **secretin and gastrin inhibitory peptides** cause decrease in acid secretion. **Histamines** accelerate acid secretion by **unknown mechanism.**
62
List enteric reflexes that help control motility?
1. **Cephalogastric** = relaxation
2. **Gastrogastric** = motility
3. **Gastroenteric** = inhibition of gastric secretion
4. **Gastroilial** = ileum empties
5. **Gastrocolic** = rectum empties
63
What are general mechanism of **causing diarrhea**?
1. **Increased secretion** = secretory diarrhea usually caused by toxins of bacteria toxins (E. coli)
2. **Increased permeability** = intestinal inflammation or portal hypertension
3. **Reduced absorption/Hyperosmolar contents** = loss of GI epithelium such as with viral, bacterial or protozoal infections (parvovirus)
4. **Maldigestion** = EPI results in decreased trypsinogen, lipase, amylase, etc
5. **Dysmotility** = hypothyroidism, ileum, etc
6. **Hypo-segmentation**
64
How is **gastrin eliminated**?
**Renal excretion**
Has implications in renal failure --\> uremic gastritis?
65
What are the **endocrine cells of the pancreas** and what do they produce?
1. **Alpha** = glucagon
2. **Beta = insulin**
3. **Delta** = somatostatin
4. **f cells** = pancreatic polypeptide
66
Which pancreatic cell type **regulates other endocrine functions**?
**Delta cells** = somatostatin
* inhibits the production of glucagon (alpha cell), insulin (beta cell) and pancreatic polypeptide (delta cell)
67
What hormones **stimulate release of pancreatic enzymes**?
1. Secretin
2. Cholecystokinin
68
Which **enzyme inhibits release of pancreatic enzymes**?
**Pancreatic polypeptide**
69
What factors **stimulate exocrine pancreas** release?
1. **Cephalic phase** = anticipatory and neurogenic
2. **Gastric** = neurogenic
3. **Inestinal** = neurogenic and hormonal
70
What are 2 main **exocrine products** of the **pancreas**?
1. **Digestive enzymes**
1. Amilase
2. Lipase
3. Trypsinogen
2. **Bicarbonate**
71
How are **carbohydrates** digested?
**Disaccharides** in saliva
* Continues to digest in the fundus
* Stop with low pH
**Amylase** secreted by the **pancreas** completes the digestion
72
How are **proteins** digested?
**Pepsin** produced by the **stomach** needs low pH to digest the protein and breakdown occurs in the fundus, then stops with low pH, then finally can become completely digested to disaccharides by **petidasese** (trypsin, chymotrpsinogen, procarboxypeptidase) secreted by **pancreas**.
73
How are **fats digested**?
Minimal digestion by lingual lipase in mouth/saliva
74
What cranial nerve innervates the muscles of the tongue?
CN 12 - Hypoglossal
75
What are some causes of acquired megaesophagus?
* Myasthenia Gravis most common (25% of cases)
* Dysautonomia (megaesophagus and hypomotility)
* Foreign body
* Stricture
* Vascular ring anomalies
* Esophagitis
* Neuromuscular disease
* Lead or OP toxicity
* Addison's disease
* Polymyositis
* DDV
* Hiatal hernia
* Distemper
* Tetanus
76
Describe the pathogenis of a vascular rin anamoly?
Any malformation of the main vessels that trap the esophagus.
Most common PRAA occurs when the right rather than the left arch becomes the functional aorta. Esophagus is **trapped by aorta on the right, ligamentum arteriosum dorsolaterally on the left, pulmonary trunk on the left and heart base ventrally**
**German Shepherds** and **Irish Setters** are predisposed
Other anomalies:
* Persistent right or left subclavian
* Double aortic arch
* Persistent right dorsal aorta
* Left aortic arch with right ligamentum arteriosum
* Aberrent intercostals
Tx with sx, 90% do better but often still have problems
77
What should be a differential for esophageal diverticula? What breeds are predisposed to this?
_Esophageal diverticula_
**Congenital** due to developmental abnormalities allowing herniation of the mucosa through the muscularis
**Acquired:** pulsion diverticula is from increased pressure secondary to obstruction or altered motility. Traction diverticula is from periesophageal inflammation with fibrosis leading to eversion of the esophageal wall
Food stuck in the diverticula leads to esophagitis, mechanical obstruction and altered motility.
C/S= regurg, odynophagia, retching. If perf see mediastinitis, resp distress
\*\*\* **Don’t confuse** with **normal esophageal redundancy** in young **brachycephalic breeds, Shar-peis, and Bulldogs**!!
78
Sliding hital hernias vs. paraesophageal hernia
**Sliding hiatal hernia:**
* Cranial displacement of the distal esophagus and stomach into **the mediastinum through the esophageal hiatus**
**Periesophageal:**
* Cranial displacement of a **part of the stomach** into the mediastinum through a defect **adjacent to the esophageal hiatus**
Casues:
* Most prob congenital and due to a big hiatus or phrenicoesophageal ligament
* Occasionally due to trauma or respiratory distress
* Shar-peis, male dogs predisposed
Always leads to decreased LES pressure, reflux, esophagitis, hypomotility
79
What GI disease are Soft Coated Wheaton Terriers predisposed to?
Familial Protein-losing Enteropathy and Protein-Losing Nephropathy of Soft Coated Wheaten Terriers. **Immune mediated PLE which progresses to PLN** as well.
80
What sonographic feature is highly indicative of malignancy in the SI?
US loss of wall layering highy predictive- **50 fold increase in chanc**e of neoplasia
81
What is a paraneoplastic syndrome of leiyomyosarcoma?
* Nodular, on the **antimesenteric** border
* GI Stromal Cell Tumor similar but arises from Interstitial **Cells of Cajal**
* Paraneoplastic things like **hypoglycemia, diabetes insipidus, erythrocytosis.**
82
What is short bowel syndrome?
Short bowel syndrome:
* **\>2/3 of SI absent** because of rare congenital cause or resection.
* Problems with **malabsorption** because less surface area, changes in GI hormones. Can be transient before hypertrophy increases surface area again. Worse if ileocolic valve removed b/c ascending bacterial infections occur
83
What is a common colonic disease seen in Bowers?
**Histiocytic Ulcerative Colitis of Boxers** (usually young dogs)
* Also seen less commonly in other breeds:
* Mastiff
* Malamute
* Frenchie
* Bulldog
* One cat case
* **Unknown cause,** infectious organism is suspected but not confirmed (tx w/ **Baytril** helpful). Genetics have to be involved- initial cases all traced back to one Boxer sire
* Can see severely thickened colon wall on US but can be normal
84
What is the normal transit time of the stomach and SI in dogs?
Gastric Transit
* 30min-2h but in some studies it has taken un to 4h
Small intestinal transit
* 30m-2h and small intestinal emptying time 3-5h
85
What are some parasitic causes of gastritis?
_Ollulanus Tricuspis_
* Worm in **cat** stomach
* Transmission cat to cat in vomit, **autoinfection** common
* See no change to rugal hyperplasia and nodular gastritis
* Diagnosis:
* Gastric content/vomit or histopathology
* Not in feces
_Physalloptera:_
* Rare species most common in **coyotes**
* Worms sporadically in stomach of dog and cat
* Transmission via ingestion of **intermediate hosts**, cockroaches and beetles, and **paratenic hosts**- lizards, hedgehogs
* Diagnosis:
* Difficult to diagnose - burden usu low and eggs are transparent
_Gnathostoma:_
* In **cats**
* Rare
* Associated with **gastric nodules** needing resection
_Spirocerca:_
* In **dogs**
* Rare
* Associated with **gastric nodules** needing resection
_Aonchotheca:_
* In **cats**
* Rare
* **Associated with** gastric nodules needing resection
86
Pathogenesis of pithiosis
**Pythiosis:**
Causes chronic **GI disease or cutaneous disease**
_Pythium insidiosum:_
* Aquatic pathogen of class oomycete- more algae than **fungus** (no ergosterol in wall).
* Motile zoospore in water ingested, encyst and adhere to gut wall
* In **tropical** climates, in US is mostly gulf coast states
* Usually in **young, large,** immunocompetent, healthy dogs, usually **exposed to water**
* Can be seen in cats
Ultrasound findings:
* In the gut see **severe transmural thickening** of stomach, small intestine, colon, rectum, rarely esophagus or pharynx.
* Most common gastric outflow, ileocolic, duodenum
* Mesenteric **lymphadenopathy** accompanies
* Can necrose vessels resulting in **GI rupture** and **hemoabdomen**
_Clinical signs:_
* Weight loss
* Vomiting
* Diarrhea
* Hematochezia
* Palpable abdominal mass
_Diagnosis:_
* Abdominal mass or thickening of GI segment w/ loss of wall layering w/ GI lymphadenopathy on Rad or U/S.
* Looks just like neoplasia.
* Histology = eosinophilic pyogranulomatous inflammation in submucosal and mucosal layers (need full biopsies to see with GMS stain).
* Easy enough to grow.
* ELISA sensitive and specific
Treatment:
* Surgical resection of masses if cutaneous and 1 limb, amputate.
* Don’t respond to azoles.
* Medical management usually doesn’t work.
* Usually die regardless.
* In skin causes non-healing wounds and invasive masses
Veterinary Physiology
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