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Veterinary Medicine > Alimentary > Flashcards

Alimentary Flashcards

1
Q

What is the dental formula and what is the dental formula for cats and horses?

A

Tells you how many teeth are on one side of the mouth on the upper and lower jaw, in the order of: Insicors-Canines-Premolars-Molars

Cats: 3-1-3-1

3-1-2-1

Horses: 3-1-4-3

3-1-4-3

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2
Q

Name the 3 main salivary glands in the head and where their located

A

Parotid - Base of the ear

Mandibular - origin of the mandible

Sublingual - very close to mandibular gland, slightly rostral.

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3
Q

What makes up the foregut and what is its blood supply?

A
  • Supplied by Coeliac artery
  • Stomach
  • Liver
  • Pancrease
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4
Q

What makes up the Midgut and what is its blood supply

A
  • Cranial mesenteric artery
  • Duodenum
  • Jejunum
  • Ileum
  • Ascending colon
  • Proximal 2 thirds of the transverse colon
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5
Q

What makes up the hingut and what is its blood supply

A
  • Caudal mesenteric artery
  • Later third of the transverse colon
  • Descending colon
  • Rectum
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6
Q

What is peristalsis?

A

Movement of a bolus/chyme in a antergrade direction. Contraction of circular muscle behind bolus ensures no retrograde movement, and longitudinal muscle contraction infront of bolus pushes it along

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7
Q

what occurs during interdigestive phase of peristalsis?

A

Peristaltic contractions over large segments of the intestine, known as the migrating motility complex. also used to transport bacteria

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8
Q

What prevents retrograde movement of food from colon back into ileum?

A

ileocecal sphincter

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9
Q

What are haustria & how are they formed?

A

Pouches in the colon giving it its segmented appearance. Cause by Teniae coli (smooth muscle).

The teniae coli are shorter than the colon so cause the formation of haustria

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10
Q

What is responsible for intrinsic control of GIT?

A

Basic Electrical Rhythm (BEM). Spontaneous slow wave activity of gut. When BEM reaches threshold, AP occurs.

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11
Q

what are the 2 subdivisions of ENS

A
  1. Submucosal plexus
  2. Mysenteric plexus
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12
Q

What are the 3 stages of gastric secretion ?

A
  1. Cephalic
  • Conditioned reflex to sight/smell/taste of food
  • via vagus nerve, release of histamine/gastrinStomach motility increased
  • Increased stomach motility
  1. Gastric
  • Stimulation of mechano/chemoreceptors leads to release of histmine and gastrin
  • negative feedback loop once gastric ph is <3
  1. Intestinal
    * Presence of chyme in duodenum inhibits acid secretions and motility. done by release of Secretin (release of bicarbonate), Gastric inhibitory protein/GIP (decrease hcl secretion and motility) & choleycytokinin/CCK (stimulates pancreatic juices and bile production)
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13
Q

What are the compostition of secretions?

A
  • Water
  • ions
  • mucous
  • enzymes
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14
Q

What are the secretions of the stomach ?

A
  • Gastrin - release when pylorus is distended. stimulates release of HCL from parietal cells
  • histamine - causes H+ release
  • chief cells secrete zymogen pepsinogen
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15
Q

What are the secretions of the small intestine ?

A
  • Gastric inhibitory protein (GIP) - secreted from mucosa of duodenum/jejunum. Decrease secretions of hcl & inhibit gastric motility
  • succus entericus
  • Secretin - stimulates release of bicarbonate. released in response to low ph in duodenum
  • Choleycytokinin (CCK) - synthesised in duodenum. inhibits gastirc emptying, stimulates release of pancreatic juices & increases bile production.
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16
Q

What are the secretions of the pancreas?

A
  • Pancreatic juice - contains pancreatic enzymes such as Trypsinogen, Chymotrypsinogen & Pro-elastase
  • Bicarbonate - neutralises chyme acting as a buffer
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17
Q

Explain the Entero-hepatic cirulation

A
  • Bile salts converted into lipid soluble bile acids
  • passively absorbed in hepatic portal circulation
  • venous blood from ileum goes into portal vein
  • bile acids then pass through the sinusoids of the liver where they are extracted
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18
Q

Describe the digestion and absorption of carbohydrates

A

Digestion

  • alpha-amylase (endogylcosidase) secreted by pancrease.
  • attacks the 1,4 glycosidic bond forming di, tri & most oligosaccharides

Absorption

  • Isomaltase breaks down products of digestion
  • glucose moves into cell by sodium glucose transporter (Na causes conformational changes)
  • Leaves cell and enters blood via GLUT-2
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19
Q

Describe the digestion and absorption of proteins

A

Digestion

  • Proteases attack peptide bonds and are secreted at zymogens to prevent autolysis
  • Pepsin only activates at low PH.
  • Main pancreatic endopeptidases are: trypsinogen, chymotripsinogen & pro-elastase
  • after being attacked by endopeptidases, attacked by exopeptidases carboxyopeptidase and aminopeptidase.

Absoption

  • 4 sodium dependant amino acid transporters. One for acidic, basic, neutral and amino acids. similiar to carbohydrate absorption
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20
Q

Describe the digestion on absorption of fats..

A

Digestion:

  • Bile acids break lipids into micelles
  • Lipase then digests thes TAG’s into free fatty acids, 2-monoacylglycerol, 1-monoacylglycerol and glycerol

Absorption:

  • Fatty acids and glycerol recombine and form tiacylglycerol in the lymphatic system
  • These TAG’s combine with cholesterol and phspholipds to for cholymicrons
  • These are secreted into thoracic ducts
  • lipoprotein lipase from capillary endothelium then break chylomicrons down, leaving remnants (metabolised into lipid particles eg HDL)
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21
Q

What are the muscles of facial epression and what nerve innervates them?

A

Innervated by cranial nerv VII

  • Obicularis oris
  • Levator labii superioris
  • Buccinator
  • Zygomaticus
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22
Q

Why must a horse be tube fed via intubation through the nasal cavity?

A

The horses soft palate and epiglottis come into contact, meaning if a tube was passed through the oral cavity the epiglottis would be pushed over the laryn/trachea. Making breathing difficult and causing respiratory problems

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23
Q

What are the 5 stages of tooth development?

A
  1. Thickening of oral epithelium causes formation of labiogingival lamina and dental lamina
  2. Underlying mesenchyme condenses, causing the formation of dental bud and labiogingival groove
  3. Dental bud epands and branches to form enamel organ. Surrounds Dental papilla (NC-derived)
  4. Small bud of cells called primordium buds off. This will form the perminant tooth.
  5. Primordium buds of completely. Inner layer of the enamel organ differentiates into ameloblasts (make enamel) & cells in dental papilla differentiate into odontoblasts (make dentine). This dentine will surround pulp to make root. Distal epithelial cells secrete cementum around tooth.
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24
Q

What are peridontal ligaments?

A

Suspend tooth in the alveolar pocket. Insert into alveolar bone and cementum.

25
Q

Whats a brachydont and hypsodont (two types) ?

A

Brachydont - 2 sets of teeth through lifetime

Hypsodont - continuouly erupting teeth

  • Radicular - Closed root, teeth continuously erupt but have finite size
  • Aradicular - no true root. Teeth continuously erupt and grow
26
Q

What is the temporomandibular joint?

A

Articulation occurs between the condylar process of the mandible and the mandibular process of the skull. Joint is compartmentalised by a fibrocarilagionous disk, allowing rotational and lateral movement

27
Q

What is the mandibular synthesis

A

Only found in dogs and ruminants. Fibrous joint at the most rostral end of the mandible, between the two halfes. Allows for compensation adjustments

28
Q

Describe the temparalis muscle and what innervates it ?

A

Origin: Lateral cranial surface

Insertion: Caronoid process

Use? Produce dorsal movement of mandible. Larger in carnivors

Innervation: Manibular branch of the trigeminal nerve

29
Q

Describe the masseter muscle and what innervates it

A

Origin - Zygomatic arch

Insertion - Lateral aspect of mandible

Use? Lateral medial movement, works with pterygoids

Innervation - Mandibular branch of the trigeminal nerve

30
Q

Describe lateral and medial pterygoids and what innervates them

A

Origin: Pterygopalatine region of skull

Insertion: Medial aspect of mandible

Use? Works contralaterally witth massete to bring about medial lateral movement

31
Q

Describe the Digastricus muscle and what nerves innervate it

A

Only muscle responsible for opening the jaw

Origin: Paracondylar process of occipital bone

Insertion: angle of the mandible

Two bellies to the muscle:

caudal 1/2 innervated by cranial nerve 7

cranial 1/2 innervated by mandibular arch of the trigeminal nerve

32
Q

What arethe extrinsic muscles of the tongue?

A
33
Q

What are the innervations of the tongue?

A
  • Rostral 2/3 of the tongues sensory innervation from lingual branch of mandibular nerve (V3)
  • Taste sensation for rostral 2/3 of tongue from chorda tympani
  • Caudal 1/3 sensory innervation by glossopharyngeal nerve
  • All muscles of the tongue innervated by hypoglossal nerve
34
Q

What are the 3 phases of deglutition?

A
  1. Buccal phase - voluntary. Tongue moves upwards and backwards pushing food onto hard palate pushing bolus backwards
  2. Pharyngeal phase - Involuntary. Bolus pushed into oesophagus. Soft palate blocks nasopharynx and epiglottis blocks trachea. upper oesophageal sphincter relaxes
  3. Oesophageal stage - Peristaltic contractions push bolus down oesphagus & into stomach
35
Q

What is the hyoid apparatus?

A

5 bones holding larynx in place and supporting pharynx and tongue.

  • basihyoid
  • stylohyoid
  • epihyoid
  • keratohyoid
  • thyrohyoid
36
Q

What are the muscles of the canine abdomen, in order from external to most internal?

A
  1. External oblique - Caudoventral fibres that compress abdomin and rotate trunk
  2. Internal obliques - Caudoventral fibres (oppose External obliques)
  3. Rectus abdominus - Fibres run longitudinal both sides of linea alba. Assist in breathing. Transverse band of fibrous tissue across muscle (6pack)
  4. Transverse abdominus - Attaches to linea alba and fibres run transversily. Help compress ribs and provide stability
37
Q

What are the ligaments of the canine abdoman?

A
  1. Falciform - Connects liver to body wall
  2. Nephrosplenic - Connects kidney to spleen
  3. Gastrosplenic - COnnect stomach to spleen (originates from, dorsal mesogastrium)
38
Q

Whats artery supplies the abdominal wall?

A

Epigastric arteries. these display anastomosis, the branching out and subsequent reconnection of blood vessels. Seperated into superficial and deep epigastric arteries

39
Q

How does blood drain from GIT?

A

Portal vein - Nutrient rich blood enters the liver to allow hepatocytes to bathe before leaving via the caudal vena cava

40
Q

What do yhr dorsal and ventral mesogatrium form in devolpment?

A
  • Dorsal mesogastrium forms gastrosplenic ligament. Spleen also develops here
  • Ventral mesogastrium forms omentum. Liver also develops here
41
Q

Describe the devolpment of the intestines

A
  1. Proximal end of tube becomes convoluted
  2. Bulge appears (caecum)
  3. tube take 90 degree turn
  4. Body cavity increases allowing return of proximal loop, which passes under distal loop and does another 90 degree turn
  5. Distal limb returns, making another 90 degree turn. 270 degrees in total.
42
Q

Describe the unique formation of colon in the horse and cow

A
  • Horse - Ascending colon grows at a faster rate, causing it to wrap around the mesentry
  • Cow - Ascending colon also grows at faster rate, wraps around its self, forming ansa spiralis (ansa proximalis & ansa distalis)
43
Q

What is uncoupling oxidation?

A

Inner mitochondrial matrix in brown fat contains many thermogenin. thermogenin transfers protons from cytosol to mitochondrial matrix, generating heat and disturbing electrochemical gradient

44
Q

Describe ketone body production, how they are used & accosiated disease

A
  • When fat breakdown predominantes, build up of Acetyl CoA. This is converted into acetoacetate, b-hydroxybutyrate and acetone.
  • Done in liver and kidney where HMG CoA synthase is present.
  • Acetoacetate & b-hydroxybutyrate can be converted back into Acetyl CoA to enter citric acid cycle
  • Important source of energy, preferentially used in cardiac muscle & used by brain in times of starvation and diabetes melitus
  • excess ketone bodies associated with neurological signs,wasting, metabolic acidosis. Production disease occurs when theres a negative energy imbalance. More energy consumed by production demands than is taken in
45
Q

Describe fatty acid synthesis

A
  • occurs in liver and adipose
  • Condensation of 2 carbon units to build up a even chain of FA. reverses b-oxidation
  • Controled by Acetyl CoA carboxylase
  • ACC activity increase by insulin
  • High cellular AMP/ATP ratios cause de activation of ACC by phosphorylation of AMPK
  • Once chain reaches 16C (palmitic acid) becomes too large for fatty acid synthase complex and iis released
46
Q

What are the 4 mechanisms of diarrhoea?

A
  1. Altered permeability - e.g Salmonella. Bacteria attach to brush border & secrete toxin blocking na pump, stopping apical surface absorption & promoting basolateral secretion. (self limiting)
  2. Altered permeability - a) bacterial infection of enterocytes. cytotoxins released, cause fluid leak from vilus into lumen e.g salmonella b) Cellular infiltrates e.g lymphoma. increase in cellularity. cause increase in width, epithelial cells stretch, loss of brush border and enzymes. c) viral infections - e.g parovirus & caronavirus. Destruction of vili or crypts
  3. Osmotic diarrhoea - lack of brush border enzymes = build up of solutes. draws water into lumen
  4. Altered motility - hyper or hypomotility. hypomotility leads to increased microbial load. can lead to secondary infection
47
Q

Describe the process of glycogenesis

A
  • Glucose converted into glucose-6-phosphate then glucose-1-phosphate.
  • Many glucose-1-phsophates joined together, by the action of glycogenin formin glycogen
  • Controled by insulin
  • phoshorylation
48
Q

Describe glycogenlysis

A
  • Glycogen phosphorylase removes a glucose-1-phosphate from the glycogen.
  • this glucose is then phosphorylated into glucose-6-phosphate where it can undergo glycolysis.
  • allosterically promoted by Calcium ions and AMP
49
Q

What is gluconeogenis?

A
  • The formation of glucose from non-carbohydrate substrate such as the breakdown of lipids and proteins or use of pyruvate & lactate
  • Oxaloacetate converted into PEP to be involved in glycolysis
  • Acetyl CoA allosterically promotes pyruvtate conversion to oxaloacetate VIA PYRUVATE CARBOXYLASE
50
Q

What is the cori cycle?

A
  • During anaerobic respiration in muscles, lactic acid accumulation causes the conversion of pyruvate into lactate (addition of 2 e- taken from NADH)
  • Lactate taken up into liver and converted back into pyruvate and then glucose-6-phosphate (gluconeogenesis)
  • Then transfered via blood back into muscle. If muscle is no longer active undergoes Glucogenesis.
51
Q

describe how we get from amino acid pool to urea cycle?

A
  • amino acidis deaminated
  • glutamate formed by transaminated to form glutamate
  • glutamate and alpha ketoglutarate are interchangable by glutamate dehydrogenase
  • Ammonia produced when glutamate is converted into glutamine
  • NH3 enters urea cycle
52
Q

How do we mobilise fats to create ATP (from triglyceride to ATP)

A
  • TAG hydrolises by hormone sensitive lipase forming Fatty acids
  • FA’s are metabolically activated by CoA producing Acyl CoA
  • Fatty acyl CoA converted into Acyl carnitine bye CPT1 so it can be transported across mitochondrial membrane into matrix, where it is converted back into Acyl CoA
  • B-oxidation occurs producing Acetyl CoA which enters CAC.
53
Q

What characterizes maldigestion, what are the causes, how can it be diagnosed and treated

A
  • Must be 90% loss of function for clinical signs
  • Insufficient amounts of pancreatic enzymes produced
  • insufficient bicarbonate

Exocrine Pancreatc insufficiency (EPI) (most common cause in cats) - due to pancreatic acinar atrophy and chronic pancreatitis.

Clinical signs - weight loss despite normal diet, increased feacal volume, yellow/greasy faeces, Flactulance and coprophagia

Diagnosis - Trpsin like immunoreactivity. detects digestive enymes in blood

Treatment - highly calorophic, low fat & fibre diet. pancreatic enyme replacement, antimicrobial therapy & suppliment fat soluble vitamins and Vit B12

54
Q

What are the exocrine pancreatic enymes and fat soluble vitamins?

A
  • Protein enzymes - trypsin, chymotrypsin ,carboxypolypeptidase
  • Carbs enzymes - Amylase
  • Fats enzymes - Pancreatic lipase, cholesterole estrase and phospholipase
  • Vitamin A - retina/eye sight
  • Vitamin D - Ca+2 metabolism
  • Vitamin E - Protection against toxins in the liver
  • Vitamin K - Activates clotting factors
55
Q

Describe 3 phases of malabsorption and primary and secondary causes

A
  1. Luminal - Dysmotility, pancreatuc enzyme deficieny, fat maldigestion
  2. Mucosal - Brush border enzyme deficiency & brush border protein transport deficieny
  3. Transport phase - lymphatic obstruction, vascular compramise
  • Primary GI - Infiltrative disease of gut wall. e.g inflammatory bowl disease, severe small intestinal bacterial growth & gastrointestinal lymphoma
  • Secondary GI - Hepatic disease, right sided cardiac disease and hyperthyroidism
56
Q

What are the glucose transporters/ where are they located, and explain the events post pradial

A
  • GLUT 1 & 3 - All cells at 1Mm
  • GLUT 5 - Small for small intestine absorption
  • GLUT 2 - Pacreatic Beta cells and hepatocytes at 15 Mm (hyperglycaemic)
  • GLUT 4 - Muscle and adipocytes at 5Mm

Post pradial uptake of glucose via GLUT 2, triggering insulin release. This causes Expression of GLUT 4 leading to rapid glucogenesis

57
Q

What is fatty liver, what gross changes are seen & what are the causes

A
  • Greesy, bulging looking liver
  • Many fat droplets can be seen histologically
  • Causes
  1. Starvation - Increased mobilisation of fats. Liver is unable to cope with the increase fat concentration. Stored in liver as neutral fats.
  2. Overeating - Dietary intake exceeds emergy expenditure
  3. Metabolic diseases - e.g diabetes mellitus & production diseases
58
Q

What are the 2 types of ruminal typany (BLOAT), what causes them and what are the treatments/prevention

A
  1. Free gas
  • anything preventing eructation of gas from cardia to oesophagus.
  • Recumbant cow must be sat up and encouraged to stand
  • Lack of movement in rumen/reticulum due to tetanus/ hypocalceamia & rumen acidosis
  • Can be released via stomach tube or cannula into rumen via lef sublumber fossa
  1. Frothy bloat
  • Gas forms stable foam, preventing eructation
  • Causes - Pasture too lush containing to many soluble proteins (clovers), Grain overload causing them to be fermented too quickly (especially if crushed up, increased surface area).
  • Prevented by buffer feeding and not feeding fine ground cereals and ensuring a diet of atleast 40% forage
  • Anti foaming agents used such as oil, liquid paraffin or cooking oil. redcues surface tension

Veterinary Medicine (11 decks)

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