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DVM1 > Digestive System wks 3-6 > Flashcards

Digestive System wks 3-6 Flashcards

1
Q

What is the difference between intrinsic and extrinsic rumen contractions?

A

Extrinsic contractions depend on the vagus and splanchnic nerves being intact

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2
Q

What are the 6 different classes of anti-emetics?

A 
Dopamine receptor antagonists
NK1 receptor antagonists
5HT3 receptor anatagonists
Anti-histamines
Phenothiazines 
Anticholinergics
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3
Q

How do anti-histamine work relative to vomiting?

Do they have any side effects?

Give an example.

A

They act at the semi-circular canals and are used to stop vomiting caused by motion sickness.

Sedation

Promethazine

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4
Q

How do phenothiazines work?

Example.

A

They act as a dopamine antagonist at the CRTZ (chemoreceptor trigger zone) and as an ACh antagonist at the vomiting centre.

Prochlorperazine

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5
Q

Maropitant is what type of anti-emetic? Where does it act?

A

NK1 receptor anatagonist. Acts at the CRTZ and vomiting centre

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6
Q

Where does metaclopromide act?

A

CRTZ

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7
Q

What is pantoprazole?

A

A drug that reduces acid secretion in the stomach by inhibition of proton pumps

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8
Q

What is methadone?

A

An opioid analgesic drug

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9
Q

What is the difference between volvulus and torsion?

A 
Volvulus= twist in longitudinal direction
Torsion= twist along short axis
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10
Q

What is sucralfate?

A

Gastrointestinal cytoprotective agent

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11
Q

How do spasmolytics and prokinetics differ in their influence of gastric motility?

A

Prokinetics restore normal GI motility (dopamine antagonists, cisapride)

Spasmolytics reduce GI tone and motility and can be either parasympathetic blocking agents or direct smooth muscle relaxants

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12
Q

What is the oesophageal groove?

A

Region of reticulum formed by the reticular and omasal smooth muscle and the oesophageal muscles. It keeps contents out of the rumen by contracting reflexively in response to taste/ mechanoreceptors in buccal/ pharyngeal cavities (it is a vagal reflex).

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13
Q

What must happen for eructation to occur?

A

The reticulum must be emptied before the gas reaches the oesophageal area.
There needs to be clearance to the cardia.
Contraction of the ruminate walls.

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14
Q

Explain how gastrointestinal mobility is controlled (hierarchy of control).

A

GI mobility is controlled by 1). Autonomous activity, 2). Local intrinsic reflexes, and 3). Long extrinsic reflexes.
1). Calcium and sodium ions are continually changing the membrane potential of gut cells. Contraction of the gut muscle occurs when the membrane potential in these cells reaches a threshold. The threshold for contraction may be modulated by mechanical, hormonal and neural factors.

Imposed on this autonomous activity is a hierarchy of control that involves local (2) and long (3) reflexes.

2). The ENS:
chemo, osmo and mechano receptors on the mucosal surface
Intrinsic nerve plexuses with their cell body in the gut wall
3). Extrinsic nerves that have their cell bodies in the central nervous system or sympathetic chain.

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15
Q

What increases and decreases gastric emptying?

A

Increases: stomach distension, ⬆️ fluidity of chyme
Decreases: ⬆️ fat, ⬇ pH, hypertonicity, duodenal distension

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16
Q

The vomiting reflex is coordinated by the ___________. Vomiting is preceded by…?

A

Medulla

⬆️ salivation
⬆️HR
Pallor
Deep inspiration
Closure of glottis
Diaphragmatic and abdominal contractions
⬆️ increased intra-abdominal pressure
Stomach/ sphincter relaxation
Relaxation of the pharyngo-oesophageal sphincter
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17
Q

The lesser omentum houses the ________, __________, and the _____________. It also forms two ligaments including the…?

A

Portal vein, hepatic artery and bile/lymphatic ducts.

Hepatoduodenal and hepatogastric ligament.

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18
Q

The type of cells present in the following GLANDULAR regions of the stomach are…?
Cardiac
Fundic
Pyloric

A

Cardiac- mucous
Fundic- mucous neck, chief, parietal and endocrine
Pyloric- mucous

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19
Q

The greater curvature of the stomach gives attachment to….?

A

The greater omentum and the gastrosplenic ligament

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20
Q

The parietal and visceral layer of the greater omentum encloses a cavity called the __________. The opening of this cavity is the ____________.

A

Omental bursa

Epiploic foramen

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21
Q

The two parts of the lesser omentum are….?

A

The hepatogastric ligament

The hepatoduodenal ligament (contains the portal vein, hepatic artery, bile duct and lymphatic duct)

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22
Q

What cells are principally found in the cardiac region of the stomach?

A

Mucous cells

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23
Q

What cells are found in the fundic and pyloric regions of the stomach?

A

Fundic: mucous neck cells, chief cells, parietal cells, endocrine cells
Pyloric: mucous cells

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24
Q

In the cardiac and fundic zones, gastric pits are lined by _________. How do the glands in these two regions differ? How about the pyloric zone?

A

Simple columnar epithelium.
Glands in the cardiac region are short and coiled. In the fundic zone, the glands are tubular and branched and divided into neck, body and base regions.

Much deeper in pyloric zone

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25
Q

Cells in the fundic zone include….?

A 
Mucous neck cells (cuboidal/ low columnar; upper 1/3 of gland)
Chief cells (pepsinogen; body and base)
Parietal cells (HCl; body and base)
Endocrine cells (gastrin, secretin)
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26
Q

The supporting membranes of the duodenum are…? Those of the colon are…?

A

The mesoduodenum, hepatoduodenal ligament and the duodenocolic fold.

Mesocolon
Duodenocolic fold

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27
Q

What opens on the major duodenal papilla? How about the minor duodenal papilla?

A

Pancreatic duct and bile duct from gall bladder

Accessory pancreatic duct

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28
Q

The ileum ends where?

A

At the ileocaecocolic junction

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29
Q

The root of the mesentery occurs at the…?

A

Origin of the cranial mesenteric artery

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30
Q

The blood supply for the caudal rectum and anus is….?

A

Internal pudendal artery

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31
Q

The caudal mesenteric artery supplies the….?

A

Descending colon and cranial rectum

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32
Q

The small intestine, caecum and most of the colon are supplied (blood) by….?

A

The cranial mesenteric artery

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33
Q

What are the five factors contributing to the gastric mucosal barrier?

A 
High cell turnover
Mucous secretion
Bicarbonate secretion (buffer)
Good blood flow
Tight intercellular junctions
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34
Q

What enzymes are secreted by the acinar cells of the pancreas?

A 
Trypsinogen
Chymotrypsinogen
Procarboxypeptidase
Pancreatic lipase
Pancreatic amylase
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35
Q

How are pancreatic enzymes converted to their active form?

A

Trypsinogen is cleaved into trypsin by enterokinase upon entry to the duodenum. Chymotrypsinogen and procarboxypeptidase are activated by trypsin.

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36
Q

What stimulates pancreatic secretion?

A

Food in the stomach, stomach distension, increased protein, chyme in the duodenum

37
Q

What is the role of secretin in digestion?

A

It’s release is stimulated by acid in the duodenum. It is released by S cells in the duodenum.

It’s role is in stimulating duct cells (centroacinar cells) to secrete aqueous bicarbonate.

38
Q

What is the role of cholecystokinin in digestion?

A

CCK is released in response to increased fat or protein levels in the duodenum. It is released from EC cells and transported to the pancreas via the blood stream. Here, it stimulates acinar cells to secrete digestive enzymes.

39
Q

What species lack gall bladders?

A

Horses, elephants, rats and some deer 🦌🐘🐎🐁

40
Q

Tell me about bile salts.

A

They are derivatives of cholesterol. They’re synthesised by hepatoctes and then conjugated to taurine or glycine. Hydrophobic backbone and hydrophilic amino acid. They keep fats accessible to lipase by forming micelles.

41
Q

How are bile pigments formed?

A

Haeme&raquo_space; biliverdin&raquo_space; bilirubin

42
Q

The most common cause of rumenitis is….?

A

Lactic acidosis

43
Q

Explain how bloat occurs.

A

Consumption of succulent legumes&raquo_space; less saliva production&raquo_space; increased viscosity of the ruminate fluid&raquo_space; stable foam formation

Consumption of succulent legumes&raquo_space; soluble proteins from legume chloroplasts are degraded and float to surface of ruminate fluid&raquo_space; stable foam formation&raquo_space; no free gas cap/ inability to eructate.

44
Q

What is dyspnoea? Hypoxaemia?

A

Laboured breathing

Low O2 concentration in the blood

45
Q

What is the mechanism of lactic acidosis?

A

Carb fermentation&raquo_space; increased VFA&raquo_space; decreased pH&raquo_space; gram -ve bacteria die and streptococci proliferate and produce lactic acid» further decrease in pH&raquo_space; fluid moves into rumen&raquo_space; dehydration, hypovolaemic shock, death

46
Q

The following segments have how many haustra and taenia in the horse?

L/R ventral colon
L/R dorsal colon
Pelvic flexure 
Transverse colon
Descending colon
A 
L/R ventral colon: 4 of each
L/R dorsal colon: 3 of each
Pelvic flexure: 0 haustra, 1 taenia
Transverse colon: 2 of each
Descending colon: 2 of each
47
Q

Where is impaction common in impaction colic?

A

Base of the caecum
Pelvic flexure
Terminal end of the right dorsal colon

48
Q

Describe the attachments of the caecum in the horse

A

Base is attached dorsally by connective tissue and peritoneum on the ventral pancreas, right kidney and an area of abd. wall caudal to these.
Attached to transverse colon and great colon via cecocolic fold

Apex is freeeeee!

49
Q

What is the typical response of the gastric mucosa to injury?

A
  1. Restitution (rapid immigration of adjacent surface mucosa to cover the effect)
  2. Atrophy (of parietal cells. Can lead to maldigestion)
  3. Mucous metaplasia and hyperplasia (proliferation of mucous neck cells)
50
Q

How can you distinguish between post-mortem and ante-mortem ruptures?

A

Ante mortem ruptures have hyperaemic and haemorrhaging borders and there is distribution of stomach contents around the abdominal cavity

51
Q

What are some common causes of gastritis?

A 
Braxy
Chemical injury
Lymphoplasmacytic gastritis
Uraemia
NSAIDs
52
Q

What is the response of the gastric mucosa to injury?

A

Restitution (rapid immigration of adjacent surface mucosa to cover defect)
Atrophy of specialised cell types (chronic disease)
Mucous metaplasia and hyperplasia (proliferation of mucous neck cells)

53
Q

What are common causes of gastric impaction?

A 
Low quality roughage
Low water intake
Poor mastication
Pyloric obstruction
Vagaries nerve damage
54
Q

What are the sequelae of GDV?

A

Compression of VC and diaphragm&raquo_space; ⬇ venous return&raquo_space; ⬇ cardiac output and perfusion to abd viscera&raquo_space; shock&raquo_space; death

Vascular compression&raquo_space; decreased venous drainage to/from stomach&raquo_space; infarction of gastric mucosa

⬇ portal vein flow&raquo_space; pancreatic ischaemia&raquo_space; release of myocardial depressant factor&raquo_space; cardiac collapse

55
Q

How does the pancreas prevent auto-digestion?

A

🔹Synthesis of enzymes in inactive proenzymes
🔹Proenzymes and enzymes are sequestered in membrane-bound zymogen granules
🔹Muscular sphincters in pancreatic ducts prevent reflux of duodenal contents
🔹Acinar cells are resistant to enzyme action
🔹Trypsinogen inhibitors are present within acinar and duct all secretions and in serum
🔹Lysosomal hydrolysed within acinar cells are capable of degrading zymogen granules without activating proenzymes

56
Q

Congenital anomalies of the pancreas include…?

A

Ectopic pancreatic tissue
Anomalies of pancreatic ducts
Exocrine pancreatic hyperplasia (failed to reach normal size)

57
Q

What is EPI? What are some signs of the disease?

A

Exocrine pancreatic insufficiency. Weight loss, pale, voluminous faeces. Undigested lipid droplets (steatorrhea), muscle fragments (creatorrhea) and starch granules (amylorrhoea) may be present microscopically in faeces.

58
Q

The margo placates in the horse marks the boundary between….?

A

The non-glandular and glandular regions of the gastric mucosa.

59
Q

Some congenital malformations of the intestines include…..

Which is most common?

A

🔹Atresia ilei (especially in calves)
Atresia coli (most common segmental anomaly, especially in Holstein calves and foals)
🔹Atresia ani (especially pigs and calves. Can be caused by in utero vitamin A deficiency)
🔹Congenital colonic agangliosis

60
Q

Tell me about congenital colonic agangliosis.

A

It’s inherited as an autosomal recessive trait in white foals born to parents with multiple spots. It is analogous to Hirschsprung’s disease in humans.

It involves absence of ganglia of myenteric plexus of distal ileum, caecum and colon which means there are no peristaltic contractions. Colic and death usually result with 48 hours of death 😢

61
Q

In which animals in rectal prolapse most common? It may occur as a herd outbreak in which animals when exposed to what?

A

Pigs, sheep and cattle.

In pigs when exposed to zearalenone

(May also occur in sheep when exposed to oestrogenic pastures)

62
Q

What is an enterolith?

A

Magnesium ammonium phosphate deposited in concentric lamellae around a foreign body or feed particle (nidus)

63
Q

Describe the pancreatic ducts in horses, pigs, cows, sheep, cats and dogs.

A

🐎: 2 pancreatic ducts. Bile and pancreatic ducts open into major duodenal papilla. Accessory pancreatic duct opens onto minor duodenal papilla

🐷: common bile duct opens at major DP. pancreatic duct opens at minor DP.

🐮: 2 papillae. Bile duct opens onto major duodenal papilla. A single accessory pancreatic duct opens onto minor DP.

🐑: pancreatic duct and bile duct bathe open onto major duodenal papilla. There’s no minor.

🐶: same as horse

🐱: only one papilla and one duct

64
Q

What is congenital colonic agangliosis?

A

An autosomal recessive trait in white foals born to parents with multiple spots.
It involves absence of ganglia of the myenteric plexus of the distal ileum, caecum and colon which means that peristaltic contractions can’t occur. In the absence of peristaltic contractions, segmental stenosis occurs with the accumulation of meconium and gas proximal proximal to the stenosis.

Hence, colic and death usually result within 48 hours of birth.

65
Q

Rectal prolapse may occur as a herd outbreak in _________ that are exposed to ___________.

How does this occur?

A 
Pigs
Zearalenone (an oestrogenic mycotoxin produced by fusarium spp)

Congestion and oedema of vulval and vaginal mucosa leads to straining which can cause vaginal and/or rectal prolapse.

66
Q

Enteroliths are rare except in _________. What are they usually composed of?

A

🐴🐴🐴

Magnesium ammonium phosphate (struvite)

**they are associated with diets rich in magnesium and phosphate or with consumption of alkaline water.

67
Q

The colon is less/more sensitive to hypoxia than the small intestine in the dog and horse.

What are the relative time frames for necrosis of the crypt epithelium in the small and large intestines?

A

Less sensitive

Small intestine: 2-4 hours
Large intestine: 3-4 hours

68
Q

What conditions predispose to diffuse hepatic atrophy?

A

🔹starvation/ increased metabolic demand
🔹congenital or acquired PSS
🔹impaired mitotic division of hepatocytes

69
Q

What conditions predispose to localised atrophy of the liver?

A

🔹local compression atrophy -> pressure atrophy

🔹local obstruction of bile drainage

70
Q

What are causes of hydropic degeneration of hepatocytes?

A

🔹Sublethal hypoxia
🔹Sublethal toxic injury
🔹 Prolonged cholestasis

71
Q

What is meant by the term steroid hepatopathy? In which species does it occur and in what circumstances?

A

It is glycogen accumulation. Common in dogs with hyperadrenocorticism.

It can also occur in inherited glycogen storage disorders.

72
Q

Explain the pathogenesis of hepatic lipidosis?

A

Hepatic lipidosis is the excessive accumulation of triglycerides in the cytoplasm of hepatocytes.

Most FFA are esterified by hepatocytes to form triglycerides.
Triglycerides are packaged with apoproteins to form VLDL.
VLDLs are exported into sinusoids as a readily available energy source.

Hepatic lipidosis can result from:
🔹diminished ATP supply
🔹entry of excess fatty acids
🔹inadequate protein supply to permit synthesis of apoproteins
🔹damage to hepatocellular organelles in which lipoprotein synthesis and assembly occurs

73
Q

What gross features would make you suspect moderate to sever hepatic lipidosis?

A 
🔹greasy feel and appearance
🔹pallour
🔹enlarged with rounded edges
🔹soft and friable
🔹pieces may float in water
🔹if zonal, a zonal pattern may be obvious
74
Q

Provide examples of conditions that are typically associated with hepatic lipidosis. (15 were given)

A 
🔹physiological (i.e pregnancy, lactation etc)
🔹high energy/ high lipid diets
🔹fasting
🔹starvation
🔹sublethal toxic injury to hepatocytes
🔹sublethal hypoxia injury to hepatocytes
🔹pregnancy toxaemia
🔹bovine fatty liver syndrome
🔹ketosis
🔹feline hepatic lipidosis
🔹equine hyperlipaemia
🔹endocrine disorders
🔹deficiencies of cobalt or vit b12
🔹fatty liver haemorrhage syndrome
🔹fatty liver kidney syndrome
75
Q

What is amyloid? When does hepatic amyloidosis develop? What’s the prognosis?

A

Amyloid is an extracellular glycoproteins that forms b-pleated sheets of non-branching fibrils.

Amyloid deposition occurs when there is defective enzymatic degradation of serum amyloid A (SAA) by macrophages or when there is synthesis of an aberrant SAA protein that is resistant to degradation and prone to forming insoluble deposits.

Prognosis: amyloid is deposited in space of disse which impairs oxygen and nutrient supply. Affected livers are generally enlarged, pale, firm or soft and prone to rupture which may lead to fatal haemoperitoneum.

76
Q

What are the pigments that can grossly discover the liver? When do they accumulate?

A

🔹Bilirubin: bile duct obstruction. Green or orange-yellow
🔹melanin: blue-black. In calves and lambs
🔹iron: found in tissues in the form of ferritin or haemosiderin. Golden-brown. Develops after lysis or phagocytosis of erythrocytes, or if there is excessive absorption of iron from the GI tract
🔹lipofuscin: yellow-brown. Accumulates in lysosomes of old or atrophic cells. Oxidation of membrane phospholipids. Common in zone 3
🔹ceroid: similar to lipofuscin. Accumulates intra- or extracellularly and can be responsible for cellular dysfunction
🔹fluke: black iron-porphyrin pigments. Hepatic migratory tracks and cysts of liver flukes. Also accumulates in kupffer cells, bile and hepatic lymph nodes

77
Q

What are common causes of multifocal hepatic necrosis?

A

Viral, bacterial and protozoal infections. Enter liver via bloodstream.

78
Q

What is telangiectasis? In which species is it most common?

A

Multiple, randomly scattered red spots (pinpoint to a few mm) that ooze a tiny volume of blood when incised. They correspond to blood filled sinusoids.

Common in cattle livers

79
Q

What is zonal necrosis?

What is the most common type and why?

What are some causes?

A

Necrosis of hepatocytes restricted to distinct acinar zones.

Periacinar (centrilobular) necrosis. Hepatocytes in this region are most distant from the afferent blood supply and are therefore most susceptible to hypoxia.

Toxic insults, hypoxic injury, viral infections, equine serum sickness

80
Q

What is massive necrosis?

Causes?

Most likely cause in a young pig?

A

Necrosis of entire hepatic acini

Severe toxic injury, acute vascular accidents, severe damage by reactive oxygen species.

Hepatosis dietica in pigs- due to antioxidant deficiency caused by concurrent deficiencies of sulphur-containing aa, vit E and/or selenium (leads to peroxidation of hepatocellular membrane by ROS)

81
Q

In what circumstances does hepatic fibrosis occur? What is the major source of excess collagen?

A

Scarring of the liver.

New collagen mainly comes from stellate cells of the perisinusoidal space.

82
Q

What is bridging fibrosis and diffuse hepatic fibrosis?

Which of these are most likely to lead to progressive liver disease and why?

A

🔹bridging= fibrosis that links adjacent portal areas to central veins
🔹Diffuse hepatic fibrosis= fibrosis extending irregularly throughout the hepatic parenchyma, within and across acini

Both are commonly associated with progression to cirrhosis because they lead to I,paired perfusion of hepatocytes.

83
Q

What is cirrhosis? What are some gross features? What are the consequences?

A

End-stage liver disease.

Involves:
entire liver
Bridging or diffuse fibrosis
Regenerative hyperplastic parenchymal nodules
Permanent distortion of the architecture of the liver

Leads to portal hypertension, abnormal anastamoses between hepatic arterial and portal venous branches in areas of scarring.

84
Q

What causes acquired PSS?

A

Persistent portal hypertension, usually due to cirrhosis

85
Q

How can congenital and acquired PSS be distinguished?

A

Congenital: 1 anomalous vessel
Acquired: multiple venous channels (often between mesenteric veins and the CVC, right renal vein or gonadal vein).

86
Q

What would you expect to see at laparotomy in a dog with acquired PSS?

A

May be difficult to identify

87
Q

What clinical signs would you expect with acquired PSS?

A

Same as congenital- signs of hepatic encephalopathy, inability to metabolise drugs, stunted in growth etc.

88
Q

What are the three supporting membranes of the small intestine?

A

Hepatoduodenal ligament
Mesoduodenum
Duodenocolic fold

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