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Leah GIL > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Which striated muscle within the pharyngeal wall will dilate the pharynx?

A

stylopharyngeus caudalis

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2
Q

Which dental nerve would be appropriate to block when removing only an incisor on the mandible?

A

middle mental nerve

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3
Q

Roughly what is the capacity of food material in the caecum in horses?

A

25-35L

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4
Q

Which vessel provides venous drainage from the stomach?

A

hepatic portal vein

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5
Q

What is the normal rumen pH?

A

6.5

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6
Q

What is the outcome for 95% of bile salts?

A

they are recycled and reused

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7
Q

Why is digestion & transport of lipids difficult

A
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8
Q

How does bile acid reduce fat drop size

A

CCK (from stretched duodenum and low pH) stimulates bile acids to be secreted from gall bladder into SI

Bile acids start the emulsion process

Phospholipase A2 (from pancreas) transforms lecithin (in bile) into hysophospholipids which acts as strong detergents

Lingual lipase and pancreatic lipase catalyse the hydrolysis of triaglycerols (catalysed by colipase)

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9
Q

What happens to lipids in intestinal epithelium

A

Accumulate in endoplasmic reticulum and TAGs molecules are reformed via an intracellular fatty-acid binding protein

Cholesterol transformed into cholesterase

TAGs/lipids/cholesterol/cholesterase gather to form lipoproteins/chylomicrons

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10
Q

What is the major protein in chylomicrons

A

Major protein in chylomicrons is apolipoprotein B

This glycoprotein forms hydrophilic shell around lipid layer & allows it to form stable structure in blood

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11
Q

How do chylomicrons enter the blood

A

Chylomicrons leave cells via exocytosis

Too big to enter systemic circulation via capillaries, lipoproteins use lymphatic circulation then blood

Lymph drains into circulation via thoracic duct & thus bypasses hepatic metabolism

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12
Q

How do chylomicrons produce energy

A

Apoprotein on surface activates lipoprotein lipase

This catalyses hydrolytic cleavage of fatty acids from TAGs of chylomicrons

Released fatty acids and monoacylglycerols are picked up by body cells for use as energy sources

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13
Q

Describe the change in chylomicrons as they travel through the circulation

A

Become more dense as they travel through and TAGs are taken up by cells

  1. Chylomicron
  2. VLDL - very low density lipoprotein
  3. IDL - intermediate density lipoprotein
  4. LDL - low density lipoprotein
  5. HDL - high density lipoprotein
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14
Q

What are the 3 major classes of carbohydrates

A

Sugars (1-2 monosaccharide(s))
- Monosaccharides – 1 CHO molecule
- Disaccharides – 2 CHO molecules

Oligosaccharides (3-9* monosaccharides)

Polysaccharides (>9*)

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15
Q

What are the 4 monosaccharides

A

Glucose - ‘blood’ sugar

Fructose - ‘fruit’ sugar

Galactose - part of milk sugar

Lactose – ‘milk’ sugar
- (disaccharide of glucose+galactose)

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16
Q

What are the main classes of polysaccharides

A

Starch (plant)
- storage form of glucose for plants

Glycogen (animals)
- Storage form of glucose for animals

Non-starch polysaccharides (plant)
- Generally structural/functional roles in plants

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17
Q

Describe starch molecules

A

Glucose store in plants

Made up of two polysaccharides
- amylose (straight chains) alpha - 1-4 linkage
- amylopectin (branched chains, alpha 1-6 linkage)

Starch molecules are clustered in granules

Starch is insoluble in water

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18
Q

describe glycogen molecules

A

Glucose store in animals (incl. humans)

Made up of single highly branched polysaccharide

Stored as granules in liver & skeletal muscle

Glycogen is soluble in water

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19
Q

What are the 2 main non starch polysaccharides

A

Cellulose (ß1-4 linkage)
- Structural role - major component of plant cell wall
- Polysaccharide of glucose
- Chain linkage differs from that of starch - no branching
- Insoluble in water & indigestible in humans

Hemicellulose
- Composed of xylose, glucose, mannose & arabinose
- Component of plant cells

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20
Q

How are disaccharides formed + examples

A

Disaccharides are formed by condensation reaction between 2 monosaccharides:

Sucrose (table sugar) = glucose + fructose

Lactose (milk sugar) = glucose + galactose

Maltose (malt sugar) = glucose + glucose

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21
Q

How are monosaccharides formed

A

Monosaccharides are formed by hydrolysis of bond between linked polysaccharides

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22
Q

Describe carbohydrate digestion

A
  1. Digestion starts in mouth: salivary a-amylase initiates starch digestion
  2. Starch fragments formed: maltose, some glucose, dextrins
  3. a-amylase breakdown of starch completed in small intestine by pancreatic amylase
  4. Disaccharides broken down to monosaccharides by maltase, sucrase & lactase - ‘brush border’ enzymes
  5. Glucose & galactose transported across intestinal mucosa - ‘actively’
  6. Fructose transport is facilitated
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23
Q

Label the pancreatic ultrastructure

A
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24
Q

What pancreatic enzymes digest protein

A

Trypsin
chymotrypsin
elastase
pro-carboxypeptidase

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25
Q

What is a zymogen

A

Zymogen (or proenzyme) is inactive enzyme precursor

Are directly/indirectly activated in duodenum by enteropeptidase (secreted from small intestine)

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26
Q

What is protease

A

Protease is enzyme that conducts proteolysis i.e. begins protein catabolism by hydrolysis of peptide bonds between adjacent amino acids in polypeptide chain

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27
Q

What are exopeptidase and endopeptidase

A

Exopeptidase - detach terminal amino acids from polypeptide (e.g. aminopeptidases)

Endopeptidase - hydrolyse internal peptide bonds of protein (e.g. trypsin, chymotrypsin, pepsin, elastase)

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28
Q

Describe process of protein digestion

A
  1. Protein denatured by stomach acid
  2. Passes to SI
  3. Luminal phase
    - bond-specific proteases hydrolyse protein to short chain peptides
  4. Membranous phase
    - hydrolysed further to di/tripeptides and some free amino acids
  5. Specific membrane proteins transported across gut wall by secondary active transport
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29
Q

What are aminopeptidases

A

Aminopeptidases attack amino terminal (N-terminal) of peptides secreted from small intestine

Also considered as exopeptidases – detach terminal amino acids from polypeptide

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30
Q

Describe the routes of amino acid transport

A

2 routes

  1. peptide transporter
    - high affinity for di- & tri-peptides
    - prefers peptides with L-amino acids
    - driven by electrochemical gradient produced by Na+ pump.
    - majority of peptide transport
  2. Single amino acid transport
    - from intestinal lumen
    - active process that involves Na+ dependent, carrier-mediated co-transport system
    - Selective carrier systems are present for certain groups of amino acids:
    * neutral AAs
    * acidic (dicarboxylic) AAs
    * imino amino acids
    * basic amino acids
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31
Q

Describe active biological mechanisms involved in ion exchange across membrane of smooth muscle cells

A

Na+/K+ pump
- 3 Na out of cell & 2 K into cell against concentration gradient

calcium channels

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32
Q

How does smooth muscle cell contraction occur

A
  1. increase in intracellular Ca concentration
    - through voltage gated Ca channels
    - or released from sarcoplasmic reticulum
  2. Ca binds to calmodulin & undergoes conformational change
  3. activates myosin light chain kinase (MLCK)
  4. this phosphorylates myosin light chains which causes myosin to bind to actin
  5. cross-bridge forms which leads to contraction
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33
Q

Explain how a population of smooth muscle cells can synchronise contract mechanisms in a tissue

A

Gap junctions
- channels that directly link cytoplasm of adjacent cells enabling rapid exchange of ions
- allows action potentials to spread from one smooth muscle cell to another
- Known as electrical coupling

Chemical signalling
- hormones/neurotransmitters can act in multiple smooth muscle cells simultaneously

Pacemaker cells
- generate rhythmic electrical signals.

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34
Q

Describe the main difference between skeletal and smooth muscle cells with regard to the notion of neuromuscular junctions.

A

Neuromuscular junction is specialised synapse between motor neuron & muscle fibre

In skeletal muscle, each muscle fibre has its own neuromuscular junction leading to voluntary control

In smooth muscle, neuromuscular junctions aren’t as well defined & nerves influence multiple cells at once which leads to less precise innervation, allows for coordinated & involuntary contraction

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35
Q

What is secretory diarrhoea and give an example

A

Disease example: cholera

caused by bacteria (Vibrio cholerae) that releases enterotoxin that causes increased secretion of chloride ions into gut lumen
Excessive chloride results in osmotic movement of water into intestines causing watery diarrhoea

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36
Q

What is osmotic diarrhoea and give an example

A

Disease example: lactose intolerance

Impact: deficiency of lactase. Undigested lactose in intestines leads to osmotic effect, drawing water into bowel & causing diarrhoea

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37
Q

What is motility-related diarrhoea and give an example

A

Disease example: irritable bowel syndrome

Impact: characterised by altered motility. Hypermotility in intestines can result in rapid transit of food, reducing time available for water absorption.

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38
Q

What is inflammatory diarrhoea and give an example

A

Disease example: Crohn’s disease
Impact: chronic inflammation of intestinal mucosa which can lead to damage to mucosal lining, loss of brush border function & impairment of fluid & electrolyte absorption.

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39
Q

Describe the permeability of neonatal GIT

A

permeable to large molecules, including proteins and immunoglobulins
crucial for absorption of maternal antibodies present in colostrum

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40
Q

What is the zinc sulphate turbidity test

A

diagnostic test to assess passive transfer of immunoglobulins from mother to neonate
measures ability of serum to form turbid solution when mixed with zinc sulphate - turbidity indicates presence of immunoglobulins (successful passive transfer from colostrum)

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41
Q

What are the 3 parts of the large intestine

A
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42
Q

What are the functions of the large intestine

A
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43
Q

Describe the joining of the small intestine and large intestine

A

ileum joins at T-junction of caecum and colon

Horse: ileum goes into caecum which empties into colon

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44
Q

Fill in the histology table

A
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45
Q

Describe large intestine histology

A

goblet cell density:
rectum>colon>caecum

GALT present in mucosa & submucosa

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46
Q

label the large intestine histology

A
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47
Q

Label the large intestine histology

A
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48
Q

Describe blood supply to the large intestine

A

Cranial mesenteric artery - duodenum to descending colon

Caudal mesenteric artery - part of descending colon and most of rectum

Internal pudendal artery - caudal part of rectum

Veins run parallel to arteries and drain into hepatic portal vein (apart from veins of caudal rectum => caudal vena cava)

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49
Q

Describe innervation of the intestine

A

autonomic nervous system
submucosa: submucosal plexus
Muscular layer: myenteric plexus

controls motility and local hormone reflexes

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50
Q

Label the intestine innervation histology

A
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51
Q

what is caecum vs appendix and what are the species differences

A
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52
Q

What is the role of the caecum

A
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53
Q

Describe canine caecum

A

short & drawn into a spiral

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54
Q

describe felidae caecum

A

even shorter than dogs
comma shaped

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55
Q

Describe bovidae caecum

A

relatively small
no taenia or haustra
no clear junction between caecum & ascending colon

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56
Q

Describe suidae caecum

A

cylindrical blind sac laying on left half of abdomen
apex points caudoventrally
has 3 taeniae

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57
Q

Describe equidae caecum

A

enormous capacity
has base, body and blind-ending apex pointing cranioventrally
4 taeniae

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58
Q

What are taenia and haustra

A
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59
Q

What are equine caecal valves

A
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60
Q

label the divisions of the large colon in dogs and cats

A
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61
Q

Describe bovidae colon

A

long ascending colon with 2 sigmoid flexures and double spiralled area

short transverse colon followed by straight descending colon

(coil next to a coil)

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62
Q

Label bovidae colon

A
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63
Q

Describe suidae colon

A

cone-shaped and coiled ascending colon (base attached to left abdominal roof and apex points ventrally)

2 taenia and 2 rows of haustra

(Coil inside a coil)

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64
Q

Label the suidae colon

A
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65
Q

Describe the equine colon

A

large ascending colon arranged in 2 U-shaped loops laying on top of each other

Short transverse colon

long descending colon

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66
Q

label the equine colon

A
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67
Q

Label the equine colon

A
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68
Q

What is the main regulatory organ for appetite

A
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69
Q

Describe the lipostat hypothesis of appetite regulation

A

Adipose tissue produces leptin proportionally to amount of fat -> hypothalamus -> decreases food intake and increase energy output

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70
Q

Describe the gut peptide hypothesis of appetite regulation

A

gastrointestinal hormones released in response to food in GIT
- glucagon & CCK

act at hypothalamus to inhibit food intake

CCK also found in cells in brain - expansion of stomach after meal causes release of CCK

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71
Q

Describe ghrelin

A
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72
Q

Describe glucostat hypothesis of appetite regulation

A

High glucose e.g., after meal -> stimulates satiety (fullness) centre in hypothalamus

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73
Q

Describe thermostat hypothesis of appetite regulation

A
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74
Q

What are the phases of deglutition

A

Oral phase:
Bolus formed and voluntarily moved to pharynx (tongue thickens to push bolus)

Pharyngeal phase:
Pharynx is activated to propel food to oesophagus

Oesophageal phase:
Bolus moves to oesophagus via peristalsis -> stomach

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75
Q

describe the secretory role of the stomach

A

Exocrine:
- mucin producing cells (cardia, fundus, corpus)
- parietal cells - HCL (fundus and corpus)
- chief cells - pepsinogen + lipase (fundus and corpus)

Endocrine:
- histamine producing cells (pylorus)
- gastrin producing cells/G cells (fundus and corpus)

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76
Q

Label the stomach secretory cells

A
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77
Q

Describe the neural stimulation to the stomach

A

long reflex
1. stomach expansion & peptide stimulate sensory nerve ending
2. impulse to CNS
3. back to stomach via vagal nerve to stimulate secretion via acetylcholine

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78
Q

Describe hormonal stimulation of the stomach

A
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79
Q

What is the mechanism for stomach emptying (muscular)

A

Cajal cells between circular and longitudinal muscle layers stimulate contraction via gap junction to empty stomach
related to mesenteric nerve plexus

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80
Q

What inhibits gastric emptying

A
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81
Q

What happens when chyme enters duodenum

A

Chyme enters low pH environment in duodenum which, along with FAs and peptides triggers CKK and secretin release which increase pancreatic juice and bile flow into duodenum and also slows stomach emptying

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82
Q

How is small intestine motility managed

A
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83
Q

What are the 4 types of contraction in the large intestine

A

segmentation
peristalsis
antiperistalsis
mass movement

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84
Q

What stimulates large intestine contraction

A

Stomach and duodenum promote large intestine contraction via mesenteric NS (gastro-colic reflex)

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85
Q

Describe induction of vomiting

A

chemoreceptor zone of the emetic centre lies outside BBB so can be stimulated by toxins in the blood

GI inputs to the emetic centre:
- Cranial nerve X (Vagus) - activated when pharynx is irritated
- Vagal and enteric NS inputs that transmit information about GIT, irritation of the GI mucosa activates receptors of these inputs

86
Q

What is the approach for a horse with colic

A
87
Q

What are the problems of an equine grazing diet

A
88
Q

Describe equine dentition

A
  • lips & incisors to grasp & prehend food
  • large ridged molars to grind food
  • irregular surface for optimal grinding
  • rotational chewing movement
  • teeth erupt through life
  • concentrate diet leads to overgrowth due to chewing movement and slower rate of wear
89
Q

What can cause choke in a horse

A
90
Q

Describe the equine stomach

A

2 distinct regions of mucosa
- squamous and glandular

capacity is 5-15 litres
- more will rupture

2 powerful muscular sphincters
- cardiac and pyloric sphincter

secretes HCL, pepsinogen & mucus

main function is mixing of food with enzymes

Food held here for short period of time

91
Q

Describe equine small intestine

A

10-30m long

loosely coiled

long mesenteric attachment & no fixed position
- can tie itself into knots

digestion & absorption of carbohydrates, protein & fats

92
Q

Where are fructans digested in horse

A

by bacteria in large intestine

93
Q

What are the products of carbohydrate, protein and fat digestion

A
94
Q

What are some common equine small intestine diseases

A
95
Q

What is the capacity of the equine large colon

A

55-130 litres

96
Q

What is the function of the equine small colon

A
97
Q

What structures can be felt in the left hemisphere of horse via rectal palpation

A
98
Q

What structures can be felt in the right hemisphere of horse via rectal palpation

A
99
Q

What are the possible causes of abdominal disease in horse

A

diet
anatomical predisposition
motility disturbances
infection
parasites
ulceration
other organs/systems

100
Q

What diagnostic tests should be carried out in suspected abdominal disease in horses?

A

blood sample - hydration, infection, biochemistry, electrolytes
Nasogastric intubation
Faecal exam
Abdominal paracentesis
Ultrasound

101
Q

What is the purpose of nasogastric intubation in a horse with abdominal disease

A
102
Q

What is the purpose of a peritoneal tap in a horse with abdominal disease

A
103
Q

How do you calculate intracellular fluid, extracellular fluid and blood volume

A
104
Q

What does extracellular fluid include

A
105
Q

Complete the table

A
106
Q

Define anti-peristalsis

A
107
Q

define segmentation

A
108
Q

Define mass movements

A
109
Q

What effect does sympathetic stimulation have on motility

A
110
Q

What effect does parasympathetic stimulation have on motility

A
111
Q

Outline the process of rectum emptying

A
111
Q

What does a change in diet alter in the equine LI

A

number and type of bacteria
pH and conditions for VFA absorption
water balance

111
Q

what is the consequence of infrequent feeds in the equine LI?

A

decrease in pH and increase in lactate
massive influx of water

111
Q

What are the factors important in digestion of hind-gut fermenters

A
112
Q

What are the consequences of a change in bacterial flora in the horse

A

enteritis
colitis
laminitis

113
Q

What is the consequence of a change in water balance in the horse

A

impactions

114
Q

What is the function of the proximal colon in rabbits

A

separates ingesta based on particle size

115
Q

What are the 2 types of rabbit faecal pellets

A
116
Q

Where in the rabbit can you find lots of GALT

A
117
Q

What is the ampullae caecalis coli in rabbit

A

separates particles based on size

118
Q

Describe the anatomy of the rabbit proximal colon

A

Haustra/sacculations - increases SA
Warzen - protrusion on the mucosal surface
Taeniae
Fuses coli (base of proximal colon)

119
Q

What is the function of the fusus coli of the rabbit proximal colon?

A

innervated
muscular
goblet cells - produces mucous

120
Q

Label the rabbit GIT

A
121
Q

Describe the conditions in the rabbit caecum

A

Fine balance of bacteria, protozoa and yeasts

changes based on: time of day, age, diet, pH

Fermentation produces ammonia, VFAs, amino acids, water-soluble vitamins

Buffered by bicarbonate ions (from appendix) and dietary fibre

122
Q

Describe the hard faeces phase of hindgut motility in rabbits

A

During feeding

small particles -> haustra -> caecum

Water -> proximal colon

Caecal contractility greatest

Fuses coli squeezes out water

Distal colon reabsorbs water, K, Na, VFAs

Dry indigestible matter expelled - HARD FAECAL PELLETS

123
Q

Describe the soft faeces phase of hindgut motility in rabbits

A

Occurs at rest

Caecotrophs produced

decreased motility of caecum and proximal colon

increased motility of distal colon

Caecal material -> large colon

Fusus coli forms pellets, adds mucous (makes nicer to eat)

Rapid excretion of caecotrophs

124
Q

Describe the contents of rabbit caecotrophs

A

outer greenish mucus membrane

High protein
- from fermentation and bacteria

Low fibre

added essential nutrients

Vitamins B, K

Minerals

Lysozyme

125
Q

What is the function of lysozyme in rabbit caecotrophs

A

Digests bacterial cell walls allowing rabbit to access the protein in bacteria

126
Q

What is the function of the fusus coli in rabbits?

A

Pacemaker:
- initiates peristaltic waves in colon
- highly innervated
- hormonal influence (aldosterone and prostaglandins)

127
Q

What is the effect of fibre, fat, protein and carbs to motility and caecotrophy in rabbits

A

Fibre:
- good
- stimulates hindgut motility, buffer for VFAs
- increased caecotrophs

Fat:
- good
- increase motility
- energy source

Protein:
- bad
- decreased caecotrophs

Carbohydrate:
- bad
- glucose -> excess VFAs
- enterotoxaemia

128
Q

What is guinea pig and chinchilla dental formula

A
129
Q

Describe guinea pig GIT

A

long caecum

cannot make vitamin C - dietary source

essential - leafy greens, Vit C tablets/syrup

produce caecotrophs

130
Q

What is the palatal ostium in guinea pigs and chinchillas

A
131
Q

Describe chinchilla GIT

A

Long GIT
- Large coiled caecum
- colon highly sacculated

produce caecotrophs

132
Q

What is the dental formula of hamsters, gerbils, mice and rats

A
133
Q

Describe small rodent digestion

A

hindgut- fermenting monogastric herbivores

Produce caecotrophs

134
Q

Describe unique hamster stomach anatomy

A

Pre-gastric pouch for pre-gastric fermentation (high pH)

135
Q

Describe ferret GIT

A

simple stomach

short SI - poor nutrient absorption

no caecum or appendix

simple GI flora

rapid transmit time

136
Q

Describe ferret diet

A

obligate carnivores

high quality, highly digestible, well balanced, meat based diet

Main energy source = fat
NEVER CARBS - prone to insulinoma => hypoglycaemia

137
Q

What are the landmarks of the rectum

A
138
Q

Describe the anatomy of the rectum

A

Cranial rectum covered by visceral peritoneum = serosa
Caudal rectum surrounded by connective tissues (adventitia) = retroperitoneal

139
Q

What are rectum peritoneal pouches

A

where peritoneum ‘turns around’ within pelvic canal

140
Q

Label the male peritoneal pouches

A
141
Q

Label the female peritoneal pouches

A
142
Q

Describe the mesenteric support of the rectum

A

Mesorectum = extension of mesocolon

143
Q

Describe rectum histology

A

same as LI

Mucosa:
- no villi
- columnar epithelium
- long, tall intestinal glands
- goblet cells
- lymphoid nodules

Stratum longitudinale:
- forms rectococcygeus

144
Q

Describe rectum blood supply

A

Arteries:
- cranial rectal supply = caudal mesenteric artery
- middle + caudal supply = internal pudendal artery

Venous drainage:
- cranial rectal = hepatic portal vein
- middle + caudal = internal iliac (systemic)

145
Q

Define tenesmus & method

A

Tenesmus = straining

forced expiration against closed glottis, which raises intra-abdominal & intra-thoracic pressure

More force can be generated if limbs are fixed, i.e. stance for defaecation

146
Q

define dyschezia

A

painful straining

147
Q

Describe defaecation

A

Complex, synchronised event involving more than 1 reflex

Rectum is innervated by autonomic NS that initiates reflex contraction upon its distension

Smooth muscle contractions aided by conscious increases in intra-abdominal pressure (i.e. straining)

148
Q

Describe defaecation behaviour in large herbivores, small furries and carnivores

A

Large herbivores – tend to go anywhere
- Alpacas use faecal smell to define herd areas

Small furries – may have special toilet areas

Carnivores – use faeces as part of scent/territorial marking

149
Q

Describe the innervation of the internal anal sphincter

A

Autonomic
Excitatory supply from sympathetics via hypogastric nerves -> constricts

Inhibitory supply from parasympathetics via pelvic nerves -> relaxes

150
Q

Describe the innervation of the external anal sphincter

A

somatic (voluntary) by anal branches of pudendal nerves
Low tone normally

151
Q

What maintains continence at rest?

A

high tone in internal anal sphincter

152
Q

Describe the defaecation reflex

A

Process of defaecation is combination of both voluntary & involuntary processes

As faecal material enters rectum, it distends – if wall is sufficiently distended anorectal reflex produces concurrent contraction of rectal wall, relaxation of internal sphincter & (mostly) relaxation of external anal sphincter

Untrained animals, or those without behavioural constraints, will defaecate at this point

153
Q

How is defaecation controlled

A

conscious control increases tone of external anal sphincter, preventing defaecation

154
Q

What occurs if urge to defaecate is not acted upon

A

some species: reverse peristalsis => faeces returns to colon

If rectal pressure gets too high => anal sphincters relax => defaecation

155
Q

Why is there an urge to defaecate after eating

A

Related to distension of stomach, initiates gastrocolic reflex (gastrin release) causing onward passage (emptying) of faecal material from colon into rectum thus initiating anorectal reflex

156
Q

What is colitis and what is the main clinical sign

A

irritation of rectum

=> repeated attempts to defaecate even though rectum is empty

157
Q

Why do mothers lick the anus of pups/kittens

A

mother will lick anus to encourage defaecation. Can be mimicked by cotton bud if they need to be looked after due to illness in mother

158
Q

What is the pelvic diaphragm

A

Tent of mm (plus external & internal sphincters) supporting rectum within pelvic canal

Muscles:
- coccygeus
- levator ani

Sacrotuberous ligament

159
Q

Label the pelvic diaphragm

A
160
Q

Describe the coccygeus muscle of pelvic diaphragm

A

Origin – ischial tuber

Inserts - transverse processes of caudal vertebrae 2 to 4

Innervated by branches of sacral plexus & pudendal nerve

Function
- compresses rectum during defaecation
- pressing tail against anus

161
Q

Describe the levator ani muscle of pelvic diaphragm

A

Origin – medial ilium and pelvic symphysis

Inserts – caudal vertebra 3-7

Innervated by brs of sacral plexus and pudendal n.

Function:
- compresses rectum during defaecation
- pressing tail against anus

162
Q

Describe the anal sphincters

A

Present in domestic carnivores

Internal anal sphincter: smooth muscle

External anal sphincter: skeletal muscle
- Covers anal sacs in dogs & cats so compresses them during defaecation
- Under conscious control, hence lack of control leads to faecal incontinence
- Striated muscle

163
Q

What muscles form the internal anal sphincter

A

Fibres of rectal circular smooth muscles are organised caudally to form internal anal sphincter m.

164
Q

What are the 3 zones of the anus

A
165
Q

Describe the features of the intermediate zone of the anus

A

transition from columnar gut epithelium to stratified skin epithelium
stratified columnar cells

166
Q

Describe the features of the cutaneous zone of the anus

A

hairless skin
anal sac ducts open in this region
standard stratified squamous epithelium

167
Q

Describe the features of the columnar zone of the anus

A

Longitudinal ridges
folds create anal sinuses
columnar epithelium

168
Q

Describe the location and function of anal glands

A

dogs and cats

just cranial to anocutaneous line

fatty secretion

169
Q

Describe the location of the apocrine and sweat glands in the anus

A

cats and dogs

around anus in cutraneous zone

170
Q

Describe the location of circumanal glands

A

Dogs

all around anus in cutaneous zone:
- subcutaneous
- sebaceous

171
Q

Describe the location of the anal sacs

A
172
Q

How are anal sacs emptied

A

Embedded between internal & external anal sphincter muscles

Normally compressed during defaecation -> coats faeces with scent

173
Q

Describe the lining of the anal sacs

A

Cornified, stratified epithelium

Coiled, apocrine tubules contained within wall of sacs

Secrete foul smelling secretion!

174
Q

Describe the clinical relevance of anal sac ducts in dogs

A

prone to occlusion => sac engorgement with secretory material and dertritus

Cannulation of ducts for giving antibiotics e.g., treating anal sacculitis

175
Q

What are the consequences of anal sac impaction/abscesses

A

inflammation of anal sac ducts
impaction of anal sac secretion
secondary infection
abscess ruptures to skin surface

176
Q

What is anal furunculosis

A

Immune mediated fistulae

Can be seen in combination with anal sac abscessation

177
Q

What are Perianal (hepatoid or circumanal) gland adenomas

A

Commonest anal tumour of dog, with most in older intact male

Testosterone dependant benign masses

Found in external region of outer cutaneous zone

Single or multiple

Malignant form of tumour very rare

Rarely reported in cats

178
Q

describe Circumanal gland adenocarcinoma

A

Malignant lesion of perianal sebaceous glands – rare

Occur in same areas as adenomas

Can diffusely infiltrate anal areas

Often adherent to deeper tissues

Rapidly growing

Do not respond to castration

179
Q

Describe Anal sac (apocrine) adenocarcinoma

A

Predominantly affects older bitches (>90%)

Small discrete nodules in wall of either sac

Paraneoplastic syndrome often accompanies

Tumour secretes PTH-like substance

Hypercalcaemia causes pu/pd, depression, weakness, weight loss

Aggressive

180
Q

Describe rectal prolapse

A

Associated with endoparasites/enteritis in young animals & tumours or perineal hernias in middle aged/older animals

Incomplete prolapse - mucosa only

Complete prolapse - all layers of rectal wall in entire circumference

Everted tissue is oedematous, excoriated and can be bleeding

Recent straining; e.g. perineal surgery, constipation, urinary tract infection, dystocia, etc.

181
Q

What is perineal hernia

A

Degeneration of the pelvic diaphragm

Separation of:
- Anal sphincter & levator ani (usually)
- Levator ani & coccygeus (less common)

182
Q

What is a rectovaginal fistula

A

Communication of rectum with vagina

Vulva functions as common opening to GI tract as well as urogenital tract

May be accompanied by atresia (arrow) where rectum ends as blind pouch cranial to imperforated anus

183
Q

Define atresia

A

absence, closure or abnormal narrowing of passage/opening into body

184
Q

Define faecaloma

A
185
Q

Define fistula

A

abnormal passage between 2 organs or organ and body surface

186
Q

Define hernia

A

condition in which part of an organ is displaced and protrudes through the wall of the cavity containing it

187
Q

What is the inguinal canal

A

slit like flat space between the external oblique muscles and the pelvic tendon of the external oblique aponeurosis

188
Q

What is a cryptorchid

A

animal with retained testes

189
Q

What are the risks associated with cryptorchids?

A

reduced fertility
increased risk of testicular cancer
risk of torsion and trauma

190
Q
A
191
Q

What are the types of atresia ani

A
192
Q
A
193
Q
A
194
Q
A
195
Q
A
196
Q

What is a perineal hernia and what clinical signs would you expect to see

A
197
Q

What is diarrhoea

A

frequent discharge of the bowels in a liquid form

198
Q

complete the table

A
199
Q

Define borborygmi

A

rumbling, gurgling sounds of the GIT

199
Q

What can cause impacted anal glands

A

diarrhoea doesn’t exert enough pressure on anal glands to empty them

obesity => decreased muscle tone

diet

infections

allergies

199
Q

What structures can be examined on a rectal exam of small animals?

A

anal glands
rectal wall
repro tract
urethra
pelvis
lymph nodes

199
Q

Define pica

A

compulsive eating of material that may or may not be food

200
Q

What does small vs large intestine linked diarrhoea look like

A

Large intestine:
- smaller amounts more often
- fresh blood coming through
- straining
- fewer issues with absorption and weight loss

Small intestine:
- larger amounts less frequently
- weight loss
- no straining

201
Q

What is maldigestion vs malabsorption

A

Maldigestion – ingesta is not broken down enough to be absorbed

Malabsorption – the ingesta cannot be absorbed correctly

202
Q

What is trypsin-like immunoreactivity test

A

assesses pancreatic function
low TLI = points towards exocrine pancreatic insufficiency

203
Q

What method can be used to manage exocrine pancreatic insufficiency?

A

low-fat diet and pancreatic enzyme supplementation

can feed raw pancreases

204
Q

What is the risk of rectal exams

A

Tearing into peritoneal cavity => peritonitis

205
Q

What does this suggest in a horse

A

pelvic flexure impaction

Leah GIL (12 decks)

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