term 2 Flashcards

(414 cards)

1
Q

supra- omental recess in cattle

A

recess caudally abouve the two sections of omentum in whic the intestine is housed

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2
Q

name a general product of the rumen

A

volatile fatty acids

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3
Q

rumination

A

primary movment of rumen- Regurgitating food after a meal and then swallowing and digesting some of it. Cattle and other ruminant animals have a four-chambered stomach for the rumination of food and so can chew their cud

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4
Q

eruptation

A

secondary movemt of the rumen. burping, prevents bloat from gasses produced

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5
Q

how is the rumen inervated

A

Reticuloruminal movements are centrally regulated by the vagus.
Dorsal vagal nucleus of brainstem.
Afferents from the lumen of the ruminoreticulum monitor distension, ingesta consistency, pH, VFA concentration.

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6
Q

reticulum

A

sorts food particlales- regulates what moves to omasum

lies caudal to diaphram- when foreign object is injested strong contractions can cause it to pierce muscular wal and diaphram

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7
Q

omasum

A

same job a simple stomack

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8
Q

abomasum

A

glandular- protien digestion

proteoloitic enzymes- hca, pepsin

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9
Q

Gastric groove

A

In the unweaned animal the gastric groove forms a closed tube for milk to pass directly from the oesophagus to the abomasum.
Formation of the tube is a reflex action when the animal suckles.
The reflex is stimulated by ADH
The reflex may also be stimulated by chemicals such as copper sulphate

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10
Q

stomach of calf

A

rumen smaller

abomentum big

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11
Q

Motility of the omasum

A

Contractions are biphasic
Phase 1 squeezes ingesta into recesses between the laminae
Phase 2 is mass contraction of the omasum

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12
Q

Regulation of flow of ingesta from the reticulum to the omasum

A

The omasal orifice remains open.
Contraction of the reticulum causes substances to pass into the omasum. At this time the omasal orifice dilates further.
The omasal orifice then closes as it contracts to force the ingesta between the lamina
This requires innervation form the vagus nerve

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13
Q

Motility of the abomasum

A

General contraction of the abomasum with increased amount of peristalsis in the pyloric region.
Like simple stomach, regular flow of ingesta from abomasum to duodenum may be regulated by pylorus

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14
Q

Fibula of ruminentz

A

The shaft of the fibula regresses in ruminants. The proximal extremity persists as a tear-shaped process fused to the lateral condyle of the tibia. The distal extremity is isolated as a small compact malleolar bone that forms an interlocking joint with the tibia completing the articular surface of the talus.

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15
Q

describe the nerve origin, course, function and the consiquenses when damaged of the femoral nerve

A

L4-6
Short course within the thigh, finishing in the quadriceps (saphenous branch continues)
A saphenous branch arises from the femoral nerve close to its exit point from the iliopsoas and innervates the sartorius muscle. It then courses with the femoral artery distally
Femoral innervates:
the iliopsoas and quadriceps femoris muscles
The skin over the medial surface of the limb
Saphenous branch
providing general somatic afferents to the skin over the medial crus and, the dorsomedial metatarsus and fetlock joint
Newborn calves delivered by strong traction on hindlimbs may be unable to bear weight on the affected limb and have a loss of sensation on the medial aspect of the leg skin

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16
Q

describe the nerve origin, course, function and the consiquenses when damaged of the obturator nerve

A

L4-6
Crosses the ventral surface of the sacroiliac joint, runs medial to the shaft of the ilium, and penetrates the obturator foramen to reach the medial muscles of the thigh.
Innervates the adductor muscles
Loss of adduction:
Can be compressed during dystocia calvings-recumbency/dog sitting posture.
Fall-hind legs do the splits and may be unable to rise.

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17
Q

describe the nerve origin, course, function and the consiquenses when damaged of the sciatic nerve

A

L6-S2
On leaving the pelvis it passes around the dorsal and caudal aspects of the hip joint. Goes between the biceps and semi-membranosus. Divides into the tibial and common peroneal nerves before reaching the gastrocnemius.
Innervates the caudal thigh muscles.
Shared responsibility for innervating all structures distal to the stifle (except medial skin)
Goes between the biceps and semi-membranosus, a few centimeters caudal to the femur –at risk from damage by intramuscular injections.
Large/ill placed foetuses may damage the nerve during parturition. Affected limb hangs loose, stifle and hock extended, digits flexed, foot knuckled. No cutaneous sensation over the entire extremity except the area supplied by the saphenous.

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18
Q

describe the nerve origin, course, function and the consiquenses when tibial nerve

A

L6-S2
(branch of sciatic)
Passes between the heads of the gastrocnemius a short distance cranial to the popliteal lymph node. It branches to the caudal crural muscles. The main trunk (purely sensory) continues towards the hock. It divides opposite the point of the hock into the medial and lateral plantar nerves.
Innervates the caudal crural muscles.
Sensory: the lateral plantar nerve supplies the abaxial plantar portion of the lateral digit. The medial plantar nerve innervates the entire plantar medial digit and the axial surface of the lateral digit
Abnormal excessive innervation of the caudal crural muscles can cause spastic paresis.
Damage to the tibial nerve can cause over flexion of the hock, extension of the fetlock, producing a vertical pastern (innervation to the digital extensors remains intact so hoof placement is correct when the animal walks and weight is correctly carried)
No response to pain stimuli on plantar lower limb skin

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19
Q

describe the nerve origin, course, function and the consiquenses when damaged of the peroneal nerve

A

L6-S2
(branch of sciatic)
Crosses the lateral surface of the gastrocnemius under the cover of the biceps before becoming superficial and palpable as it passes caudal to the lateral collateral ligament of the stifle. Dives between the peroneus longus and lateral digital extensor muscles before dividing into superficial (3 divisions) and deep branches.
Generally:
Cranial crural muscles
Sensory nerves for the cranial aspect of the leg distal to the hock
Superficial:
medial branch that supplies digit III
middle branch that supplies the axial portions of digits III and IV
lateral branch that innervates the abaxial surface of digit IV
Deep:
sends branches that communicate with the middle branch of the superficial nerve to innervate the axial portions of the claws
Hyperextension of the hock, hyperflexion of the fetlock and digital joints. Unless passively placed in the correct position, the limb rests on the dorsal surface of the flexed digits.
The cow eventually learns to walk correctly by flicking the foot forwards and flat when taking a step.
No response to a pain stimuli on the cranial lower limb skin.

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20
Q

injection points on cattle

A

Pericardiocentesis - 5th intercostal space LHS abve costochondral junction
Blood sampling and IV injection– jugular groove, coccygeal vein

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21
Q

describe the dental formula of ruminents

A

Ruminants have a maxillary dental pad with no upper incisors or canines. This is followed by the diastema. They have 3 upper premolars and 3 upper molars.
On the mandible they have 3 incisors, 1 canine. Again, we have a matching diastema, then 3 lower premolars and 3 lower molars.
Ruminants have 20 deciduous teeth (no deciduous molars) and 32 permanent teeth
NB. It is customary to refer to the canine tooth as the fourth incisor in ruminants. The most rostral premolar is known as ‘PM2’ (there is no PM1). But molar 1 is still called M1.
Lack maxillary incisor - cornified dental pad

Mandibular brachydont incisors

Dental attrition is common

Hypsodont (long-crowned) premolar and molar teeth

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22
Q

describe the timeline of ruminent dentition

A

A: Deciduous incisors of a neonate.
The enamel still surrounds the crown

B: 2 years old, 1st incisor is permanent.
The distal border of I1 is slightly worn and dentine is exposed

C: 3.5yrs, I1+I2+I3 are permanent.
The occlusal surface of I2 is wider than I3.

D: 5yrs

E: 8yrs. The occlusal surface is at its greatest and the lingual surface of I1 and I2 is smooth, known as being ‘level’.

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23
Q

The facial muscles are supplied by the facial nerve (CNVII) which divides into its principle terminal branches underneath the parotid gland.
describe these branches

A
  1. The auriculopalpebral nerve supplies muscles of the external ear and eyelids. It reaches these by crossing the zygomatic arch directly in front of the temporomandibular joint where its superficial position makes it vulnerable. Damage to the nerve may be evident by drooping of the ear and sagging of the eyelids, and paralysis of the orbicularis muscle makes it impossible to close the eye-therefore blocking this nerve to eliminate the menace reflex (blink) is very handy for eye examinations. It is most easily palpated where it passes over the zygomatic arch.
  2. The dorsal buccal branch continues the parent trunk (facial), crossing the masseter muscle in an exposed and vulnerable position. Injury can cause loss of innervation to the muscles of the nose, upper lip and buccinator. The first loss leads to slight distortion of the face, which is pulled towards the unaffected side (as there are no counteracting muscles working), the second allow food to collect in a wad within the oral vestibule.
  3. The ventral buccal branch takes a more protected course caudomedial to the ramus of the mandible and reaches the face along with the facial artery and vein. It has limited distribution and so visible effects of injury are minimal.
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24
Q

Local anaesthetic points for disbudding, eye lid, nose/maxillary skin

A

The sensitive dermis of the horn is supplied mainly by the cornual nerve, which is a branch of the zygomaticotemporal division of the maxillary (lacrimal) nerve, plus a portion of the ophthalmic division of the trigeminal nerve.
The cornual nerve arises within the orbit and then passes backward through the temporal fossa where it is sheltered by the prominent ridge of the temporal line.
The nerve later divides into 2 or more branches that wind around this ridge and approach the horn separately under cover of the thin frontalis muscle.
The cornual nerve is blocked for disbudding and dehorning cattle. It can be found where it crosses the ridge-roughly midway between the postorbital bar and the horn (yellow dot).
Bovine specific Landmarks-Upper 3rd of the lateral temporal ridge of the frontal bone, 7-10mm deep, between the frontalis and temporal muscles. 2-3cm in front of the base of the horn
Infraorbital nerve which appears from the infraorbital foramen-anaesthesia of the nose and upper lip for placing a bull nose ring
Landmarks: Half way between the nasoincisive notch and the first upper premolar

Blue: Auriculopalpebral branch of the facial nerve-paralysis of the eyelids.
Landmarks: subcutaneously, where the supraorbital process of the frontal bone meets the zygomatic arch, point the needle posteriorly, inject for 3-5cm lateral to the zygomatic arch

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25
describe the thymus in young ruminents
The thymus produces and secretes thymosin, a hormone necessary for T cell development and production. The thymus is special in that, unlike most organs, it is at its largest in children. Once you reach puberty, the thymus starts to slowly shrink and become replaced by fat The thymus is large and lobulated. It extends from the larynx to the pericardium in young animals. The cervical part is connected to the thoracic by a narrow isthmus ventral to the trachea. The cervical part divides into 2 horns that taper over the lateral aspects of the trachea. It may reach the larynx, with the cranial tip sometimes detached, fragmented and more closely associated with The medial retropharyngeal lymph node and the mandibular and parathyroid glands. The thymus grows rapidly during the first 6-9monthds of life, although it reaches its greatest relative size much earlier. In some involution may begin as early as 8weeks old. But the tempo of regression varies and the thoracic part in particular may still be present in animals who are several years old. In general the isthmus and neck parts disappear completely. The thymus in young calves is bright pink/red but lightens with age and the consistency firms as the active tissue is replaced by fatty fibrous tissue.
26
describe horns in cattle
The size and conformation of horns depends on their age, sex and breed. Function remains for attack, defence, maintaining social hierarchy and foraging. The horns begin life as germinal epithelium which can be removed by disbudding, the surrounding epidermis which heals the wound, lacks the inductive capacity of the horn bud. If not disbudded, the softer outermost layer (episceras) is produced by an irregular epithelial strip at the base which is transitional to the ordinary epidermis. The cornual processes grow from the frontal bone at caudolateral angles to the head. It has a ridges and porous surface and is covered in papillated dermis that also serves as periosteum. The horn sheath/wall represents a modification of the cornified stratum of the epithelium and consists chiefly of tubules formed over the dermal papillae. The tubules run lengthways and are welded together by irregular, intertubular horn produced by the inter-papillary regions of the epithelium. Since the whole epithelial surface is productive, the older horn is thrust apically by the newer horn, so the horn thickness increases towards the tip where it is all horn. Horn growth is continuous but the rate may be slowed by periods of stress, similar to in the hooves, creating horn bands. Often produced at calving An extension from the frontal sinus invades the cornual process at around 6months old.
27
describe the horn in sheep and goats
The size and conformation of horns depends on their age, sex and breed. Function remains for attack, defence, maintaining social hierarchy and foraging. Small ruminants have a more domed head in comparison to cattle and the horns arrive closely behind the orbit in a parietal position unlike the temporal ones of cattle. HORN BUDS: Each horn is based upon a separate ossification centre that makes a secondary fusion to a projection of the skull quite close to its contralateral fellow. Due to this specialised ossification to the skull, disbudding can only take place before this process occurs, which is very young at under a week old.
28
describe the vascuar supply of the horns
The cornual nerve is accompanied by a considerable artery and vein that branch from the superficial temporal vessels within the temporal fossa. The artery ramifies before it reaches the horn. Its smaller branches run in the grooves and canals of the cornual process and retract when severed. Which is pretty impressive unless you are a very trying to tidily dehorn a cow and achieve good haemostasis without blood spurting everywhere. When they retract they cannot be easily grasped with haemostats to stop the bleeding, unless the cut is made close to the skull where the arteries are still embedded in soft tissue and easy to reach.
29
deascribe the interconnection between sinuses and horns
An extension from the frontal sinus invades the cornual process at around 6months old. Here we can see an opening into the caudal frontal sinus However in both sheep and goats, the frontal sinus later excavates the horn core at the base but does not reach as far inside as in cattle.
30
describe sinuses in cattle
The paranasal sinus system is very poorly developed in the young calf and it must be several years old before it gets to full size. Even in a mature animal , the maxillary compartment continues to adjust to extrusion of the cheek teeth. The complete set of sinuses is complicated: Frontal compartments within the bones of the cranial roof and side walls A palatomaxillary complex within the caudal part of the hard palate and the face, both before and below the orbit. A lacrimal sinus within the medial orbital wall Sphenoidal sinuses that extend past the orbit into the rostral part of the cranial floor Conchal sinuses within the nasal conchae. The maxillary sinus occupies much of the upper jaw above the alveoli of the cheek teeth. It communicates with the nasal cavity via a large nasomaxillary opening but natural drainage of pus or other fluid is hindered by the location of this opening high in the medial wall. The maxillary sinus is continuous with the palatine sinus over the plate of bone that carries the infraorbital nerve in its free margin. It also extends caudally (as the lacrimal sinus in front of the orbit) and within the fragile lacrimal bulla that intrudes into the ventral part of the orbit. The frontal sinus comprises of several compartments that communicate separately with ethmoidal meatuses. The 2 or occasionally 3, small rostral compartments are of little clinical interest. The caudal compartment is the largest and of most interest to us and spreads mainly within the frontal bone. It covers the dorsal part of the brain case and also extends into the lateral and nuchal walls and into the horn core as we saw earlier. It is separated from its fellow and from the smaller homolateral compartments by partitions which vary in position. The openings in these partitions are closed by mucosa. The major cavity, which continues to increase throughout life, is further subdivided by irregular and perforate septa. Inflammation of its mucosa is a common sequel to dehorning.
31
describe sinuses in small ruminents
The maxillary sinus is shallower and simpler. It does not communicate with the lacrimal sinus, which may open into the nasal cavity separately or via the lateral frontal sinus. The frontal sinus comprises separate medial and lateral compartments. They lie medial to the orbit (and extend slightly beyond this both rostrally and caudally) and are of irregular form. The lateral compartment corresponds to the caudal sinus of cattle and provides the extension to the horn core. The most common clinical involvement of the sinuses in sheep is that caused by the invasion of the frontal sinus by larvae of the nasal bot fly. Treatment involves surgical puncture to either the rostral to the horn or medial to the middle of the orbital rim where there is no risk to the frontal vein.
32
describe the reasons for ruminal acidosis
Often viewed as the most dramatic form of the forestomach fermentative disorders, clinical ruminal acidosis occurs when excessive levels of organic acids accumulate in the rumen, resulting in a rumen fluid pH of less than 5.2. Normal rumen pH=5.6-7 Subclinical rumen acidosis pH=5.2-5.6 Clinical acidosis pH= <5.2 Normally have a balance of fermentable carbohydrates and fibre, plus basic bicarbonate from saliva to help neutralise some of the acid. Good rumination and chewing the cud stimulate saliva production A common scenario for the development of clinical rumen acidosis is the excessive consumption of rapidly fermentable carbohydrates by ruminants that are unadapted to a high-concentrate diet. As a result, clinical rumen acidosis is often seen in the early feeding period when newly received growing beef cattle, accustomed to a primarily forage-based diet, are introduced to a primarily concentrate-based ration and the amount is increased too rapidly. Similar signs can also develop when concentrate-adapted ruminants are fed more concentrate than their ruminal microbial population can handle. This situation might occur following a feeding error, overprocessing of grain, changes in ration moisture, or when there is excessive competition for feed within an animal population. Excessive feeding of rapidly fermentable carbohydrates, commonly referred to as “grain overload,” is the classic scenario leading to clinical rumen acidosis. It is important to remember, however, that excess grain consumption is not essential to the development of the syndrome, because excess consumption of any rapidly fermentable carbohydrate (apples and other fruits, bakery waste products, incompletely fermented brewery products, and standing green corn) is capable of providing the necessary substrate for the development of clinical disease. Equally a sudden reduction I the amount of fibre fed, even when the carbohydrate amount stays the same can initiate a ruminal acidosis event due to the lack of buffering. In non-production systems, ruminal acidosis can be seen in pet goats following consumption of excessive amounts of animal crackers or bread given by the owners as treats.
33
describe the pathogenisis of ruminal acidosis
Ruminal bacteria that digest starches and sugars proliferate and increase their rate of carbohydrate fermentation. In the normal animal, or in animals with mild clinical disease, rumen buffering capacity and volatile fatty acid (VFA) absorption match the rate of carbohydrate fermentation. In this scenario, the pH within the rumen will stay in a normal range between 5.6 and 6.9, with the higher pH range being more common in New World camelids. However, when production of VFAs and lactate exceeds the rate of absorption, rumen pH will begin to drop. VFAs and lactate increase in concentration within the rumen fluid and are subsequently absorbed into the systemic circulation. Although numerous microorganisms have been implicated in the development of disease, the primary bacterium thought to be associated with the progression of clinical signs is Streptococcus bovis. S bovis, because of its rapid rate of division, ability to produce more ATP per unit time, and tolerance of a pH 4.5. As pH decreases, lactate production by S bovis decreases, and the growth of S bovis is slowed. At this point, the Lactobacilli become the dominant microbes present in the rumen and further serve to depress ruminal pH.
34
Describe the biochemical processes of acidosis
D- lactate is formed by fermentation and L-Lactate is formed during anaerobic glycolysis of hypoperfused tissues. Both isomers are powerful corrosive agents that can cause severe damage to the rumen epithelium. In addition, lactate and VFAs are osmotically active. Increased rumen osmolarity decreases absorption of lactate and VFAs, creating a cycle that perpetuates build up of these compounds and a continued drop in pH. With the continued accumulation of these compounds and further increases in rumen fluid osmolarity, the rumen epithelium is further disrupted. Yeast and fungi that are resistant to highly acidic environments readily colonize the denuded sites and contribute to the development of mycotic rumenitis and omasitis. In addition, organisms such as Fusobacterium necrophorum are able to invade the bloodstream and spread to the liver. In fact, rumen acidosis is thought to be one of the inciting causes for the development of liver abscesses in ruminants. In addition to their effects on the rumen, the osmotic pressure of these agents causes systemic dehydration and hypovolemia by pulling fluid from the circulation into the rumen, resulting in a reduction in tissue perfusion. The loss of circulating blood volume leads to cardiovascular collapse, reduced renal perfusion, and anuria. Reduced peripheral circulation also leads to anaerobic cellular metabolism and systemic acidosis Other compounds produced by rumen microbes include endotoxins and histamine. endotoxin concentrations will increase in the rumen of animals on a concentrate-based diet. If these animals become acutely acidotic, cause microbial death and release of endotoxin in large quantities all at once. histamine is also known to accumulate in the acidotic rumen. Allisonellla histaminiformans thrives at low pH, produces large quantities of histamine, histamine can be absorbed through the damaged rumen wall and into the systemic circulation. Histamine may further intensify the symptoms of acute acidosis, including vasodilation and arterioconstriction, and increase vascular permeability
35
describe the Sequelae of acidosis
blood pressure to increase in capillaries and edema, resulting in swelling, hemorrhage, and even rupture of the vessels. result in local ischemia and damage to the corium. Laminitis is commonly seen with acidosis in cattle and sheep, but less so in goats. Mild cases, animals can experience a transient lameness that seems to resolve following correction of the acidotic event. However, animals experiencing a severe acute case can have more serious lesions, and animals experiencing subacute acidosis can develop subclinical or chronic lesions because of long-term damage to the tissues of the hoof
36
describe ketosis in ruminents
Energy deficiency syndromes which focus around body fat metabolism, increased NEFAs and ketone bodies, and hepatic lipidosis. ``` Main syndromes are: Starvation ketosis (protein-energy malnutrition) Pregnancy toxaemia of beef cattle/sheep Fatty liver Fat cow syndrome Clinical ketosis (Type I or II) Chronic ketosis ``` It is exhibited in a range of ways depending on the species situation Post partum in cattle forms pre partum in sheep form Starvation form (either species)
37
describe the normal metabolic pathway in the cow
Ruminants are in a vulnerable position with respect to their carbohydrate metabolism when compared to species with simple stomachs. Their GIT provides little glucose for intestinal absorption (up to 10% of total glucose). Instead dietary carbohydrates are converted by the rumen microflora to the VFAs. Consequently the glucose requirements in cattle must be largely met by gluconeogenesis using primarily proprionate and amino acids. Acetate and butyrate are converted to acetyl-co-enzyme (Acetyl CoA) and can thereafter be used for the synthesis of factor be converted into energy via the tricarboxylic acid (TCA, Krebs) cycle. Entry to the TCA cycle requires that acetyl CoA combines with oxaloacetate to form citrate. Citrate passes through a series of intermediate steps to become oxaloacetate again, during which energy is released and 2 molecules of CO2 are produced. Propionate can be converted into glucose, whereas acetate is mainly used for fat synthesis and is stored as lipids or secreted as milk fat. Butyrate can be partially oxidized to ketone bodies. Thus acetate and butyrate are ketogenic, whereas propionate is glycogenic. Under normal conditions, these 2 groups of VFAs are produced in a ratio of 4:1.
38
describe clinical ketosis (type I, acetonaemia).
lactating dairy cows, first3-6weeks of lactation. Characterized by loss of bodyweight, reduced milk yield, Hypoglycaemia presence of ketone bodies in all body tissues and fluids. Occurrence: demands on their resources of glucose and glycogen cannot be met by their digestive and metabolic activity. Begin lactating-increase in energy demand but decrease in feed intake Negative Energy Balance (NEB). several metabolic adaptations to manage NEB, However, some animals will experience excessive NEB, who are associated with increased risk of disease development and a decrease in both milk production and reproductive performance
39
Physiology of energy metabolism-Ketosis
In early lactation, homeorhesis is the driving physiologic force breakdown of body stores of fat and protein insulin resistance, Milk production requires large amounts of glucose created by gluconeogenesis This process is generally diminished in animals affected by ketosis, leading to hypoglycemia. Providing glucose, stimulating gluconeogenesis, and decreasing fat breakdown form the foundation for rational ketosis treatment Adipose Tissue Glycerol and NEFA are released from adipose tissue in response to hormonal cues such as glucagon, corticosteroids, corticotropin, and catecholamines. Insulin is the only hormone that will act to inhibit lipolysis and therefore decrease the amount of NEFA released from adipose tissue. Early in the postpartum period, there is both a decrease in insulin production and a transient state of insulin resistance. These 2 mechanisms allow glucose sparing for lactogenesis by decreasing glucose use by insulin-sensitive tissues, and allowing continued lipolysis even when insulin concentrations increase. Fatty acid oxidation: fatty acids are derived from the diet or adipose mobilisation. Ruminants have little preformed fat int heir diet and microflora cause little fat to be absorbed intact from the gut. Fatty acids are taken up directly by the major energy requiring tissues of the body, where they can be oxidised completely to CO2 and energy. However in the absence of adequate gluose or precursors, fatty acids are more likely to be metabolised into ketone bodies The continual release of NEFA into circulation is not always detrimental: NEFA is a good source of energy for several tissues in the body, and can be used to synthesize milk fat. However, elevated levels of NEFA can result in ab=n inability to oxidise them so they are converted into ketones or re-esterified into triglycerides in the liver and kidney, resulting in hepatic lipidosis.
40
Homeorhesis
the orchestrated or coordinated changes in metabolism of body tissues necessary to support a physiologic state
41
Biochemistry of ketosis
Several factors determine the amount and proportion of the 3 major volatile fatty acids (VFA; acetic acid, propionic acid, and butyric acid) produced by microbes in the rumen. Acetic acid is used mainly in the liver as a major source of acetyl coenzyme A to generate adenosine triphosphate (ATP). Butyric acid is absorbed from the rumen as a ketone body, βHB. Propionic acid is taken up by the liver via portal circulation and serves as the major substrate for gluconeogenesis. Liver The liver receives approximately one-third of cardiac output and removes approximately 15% to 20% of the NEFA in circulation. Once inside the liver, fatty acids can follow 4 pathways: complete oxidation in the tricarboxylic acid cycle (TCA) pathway to produce ATP; transport out of the liver in very low-density lipoproteins; transformation to ketone bodies via the b-oxidation pathway or conversion to ketone bodies through peroxisomal oxidation; or storage in the liver as triglycerides. When levels of oxaloacetate are low and the cow is unable to oxidise all of the acetyl-CoA that she produces, excess acetyl-CoA is converted in the liver into the 3 major ketone bodies. The 3 major ketone bodies produced by the liver are 1. acetone, 2. acetoacetate (AcAc), AcAc can convert to acetone and CO2, or alternatively into βHB. 3. βHB. Acetone is excreted in urine or exhaled; it is responsible for the “pear drops/fruity” breath of ketotic cows. While βHB accounts for most of the total ketone body pool in bovines, in lactating animals with NEB the equilibrium between AcAc and βHB may be shifted even farther toward βHB Mammary Gland The mammary gland is not dependent on insulin for glucose use. During excessive NEB, circulating NEFA are regularly incorporated into milk fat. During NEB in the postpartum period, milk fat concentrations tend to increase and milk protein concentrations tend to decrease; thus, the ratio between fat and protein can be used as an indicator of excessive NEB and as a predictor of the risk of developing metabolic diseases. To use milk fat and protein information as a predictor of metabolic diseases that commonly occurs within 30 days in milk (DIM), samples should be evaluated within 9 days postpartum
42
Sequalae of ketosis
``` Following ketosis we may see: Hepatic lipidosis Poor immune function, An excessive amount of circulating fatty acids may promote inflammation, which is an important factor in common diseases such as metritis and mastitis. Left Displaced Abomasum Chronic Ketosis Poor reproduction May not hit expected peak milk yield ```
43
list parts of the male reproductive anatomy in ruminents
``` Paired testes – in scrotum Paired spermatic cord Two epididymis Two ductus deferens Two ampullae Two vesicular glands One prostate Paired bulbourethral gland (Cowper’s) Fibroelastic penis – with sigmoid flexure Spermatic cord (containing ductus deferens, vessels including pamp plexus, nerves, connect tissue and cremaster) ```
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what is the sigmoid flexure
At birth, the bull penis is short and slender and lacks a sigmoid flexure, and its apex is fused to the inner lining of the prepuce. With time (and under the influence of androgens), penile and preputial tissues separate, the penis elongates, and a sigmoid flexure develops
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Image result for luteolysis | Luteolysis
structural demise of the corpus luteum, which is preceded by loss of the capacity to synthesize and secrete progesterone.
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Changes that occur in the uterus with pregnancy
The progestational changes in the endometrium that are part of the normal reproductive cycle persist and intensify in the presence of an embryo. This response is evident from about 30days after fertilization. The blastocyst is first confined to one horn, and since ovulation is commoner from the right ovary (60%) the same preference for the side is present. The membranes soon spread into the other horn, but the embryo, and later the foetus, is almost always confined unilaterally; a pronounced asymmetry of the gravid uterus Is therefore the rule. Indeed the developing inequality in the size of the horns is one of the first clinically detectable signs of pregnancy in the cow. The distended amnion is palpable from 30days, and the foetus itself may be palpated around day 70. The 80-90 caruncles in the gravid horn increase in size and become converted from low, 15mm long, smooth-surfaced ‘bumps’ on the mucosa to large sessile swellings with a surface pitted for the reception of the chorionic villi making a Velcro-like reationship. Later, those in the non gravid horn enlarge but to a lesser degree. At term the largest caruncles are the size of a clenched fist. Broad ligament Hypertrophy After the 3rd month of gestation the ligament is fully stretched Uterus slips down over the abdominal floor
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placentome
Cotyledon + Caruncle | Cotyledon: the fetal side of the placenta. Caruncle: the maternal side of the placenta.
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describe the changes in blood flow during pregnancy
Blood flow: Increase Greatest growth of the uterine artery on the pregnant side Can be palpated per rectum as a mobile firm vessel passing forward across the shaft of the ilium ‘Fremitus’ of the uterine artery can be palpated Similar but smaller changes occur in the non gravid horn, vaginal and ovarian arteries
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Fremitus
Fremitus can be felt because of the hypertrophy of Middle Uterine Artery. There is a fluid turbulence that gives a 'buzz' feeling, or a kind of vibration to the artery. Middle Uterine Artery is located in the broad ligament
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Uterine topography as gestation progresses:
enters the supraomental recess between the right face of the rumen and the double layer of the greater omentum 2-3months gestation: Sinks towards the abdominal floor end of the fourth month: lies almost entirely within the abdomen, cervix carried across or beyond the pelvic brim passes cranially below the right costal arch, pressing on the rumen to the left and the intestines dorsally. The vagina becomes stretched, and as the cervix slides down the caudal part of the abdominal floor, the uterus passes out of reach of the hand within the colon 5th month of gestation: Difficult to palpate the uterus Further increase in size restores the uterus to reach, it extends forward to come into contact with the diaphragm and liver, pushing the diaphragm towards the thorax and reducing space available to the lungs. Near term the pregnant uterus occupies most of the ventral and right sections of the abdomen and has raised the rumen from the abdominal floor and crushed the intestines upwards Topography of the foetus: First months of gestation: calf moves freely within the surrounding fluid After 1st month: back is directed dorsally and to one side, toward the greater curvature of the uterus, and towards the mothers flank
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bovien placenta
Separate maternal (endometrium) and foetal components. Foetal placenta-chorioallantois, feotal membranes- amnion and chorioallantois Bovine placenta- synepitheliochorial. The three characteristics of a synepitheliochorial placenta are: presence of TGC in fetal tro-phectoderm, formation of fetomaternal syncytia, development of a placentomal chorioallantoic placental organization
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development of the placenta in large animals
uterine epithelium persists although initially modified trophoblastic binucleate/giant cells (TGCs) create fetomaternal hybrid syncytial plaques syncytial plaques replaced by Uterine Epithelial cells by Day 40, only transient trinucleate mini syncytia produced throughout the remainder of pregnancy. “cotyledonary” -localized areas of trophectodermal proliferation forming “cotyledons” in the placenta; each cotyledon is the fetal part of a placentome. The placentome is formed by the tuft of chorionic villi from the cotyledon enmeshed with corresponding maternal crypts of the caruncles. These crypts develop from the preformed flat endometrial caruncles. Placentome formation with a synepitheliochorial interhemal barrier provides the vast increase in surface area. The gross morphology and the pattern of fetomaternal interdigitation differ considerably among bovid species
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Pig placentas
non-invasive placenta classified as being epitheliaochorial and diffuse. Pig blastocysts elongate extensively beginning about day 11 and become evenly spaced throughout both uterine horns. The embryos become apposed to the uterine surface and begin to attach. After attachment the endometrial epithelial cells become rounded with bulbous protuberances around which chorionic epithelial cells become moulded. Processes from chorionic epithelial cells push between endometrial epithelial cells but do not penetrate the basement membrane. Attachment is strengthened by intertwining of microvilli from chorionic and endometrial epithelial cells and interlocking ridges that act like "tongue and groove" fasteners between the two epithelia. These attachments soon cover essentially the entire endometrial surface and the chorionic ridges become substantially larger as pregnancy progresses.
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Vaginal palpation
Wear PPE=gloves, apply lube to hand, no jewellery, short nails Approach cow safely, maintain contact Clean vulva of faeces Make hand into a beak shape and be gentle Palpate the structures with flat fingers and palms Scoop out vaginal discharge for examination Structures Vulva, external urethral opening, vaginal mucosa, caudal cervical ring Cranial cervical ring, uterus, (foetal membranes, calf)
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Rectal palpation
Wear PPE=gloves, apply lube to hand, no jewellery, short nails Approach cow safely, maintain contact Make hand into a beak shape and be gentle Advance arm up to just past the elbow Palpate the structures with flat fingers and palms Structures Rectum, cervix, uterus, uterine horns, ovaries, (Male: seminal vesicles, ampulla, prostate) Iliac artery, pelvis, rumen, caudal pole of the left kidney, abnormal intestines/caecum (RHS) uterine artery, foetus, placentomes, fluid filled amniotic vesicle,
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Definitive signs of pregnancy in large animals
Foetus Membrane slip (<45d) (feeling the chorioallantois in the uterine lumen) Placentomes (>8wk, felt appreciably >3m) Uterine artery fremitus (larger with gestation, don’t confuse with iliac artery which doesn’t move from bone)
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Sexing foetuses
60-80days gestation Male: hyperechoic umbilicus, penis (2 hyperechoic lines of the male genital tubercle), scrotum, followed by hindlimbs Female: hyperechoic umbilicus, hind limbs, vulva (2 hyperechoic lines of the female genital tubercle), tail
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camelid dental formula
1123/3123
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describe the basics of mammary glands
Modified cutaneous (sweat) glands Consists of body and papillae or opening (nipple/teat) – number varies across species Attached to, and suspended from the ventral body wall Typically paired structures Function: to nourish Each mammary gland is made of tubualveolar glands made of secretory units, grouped in lobules, separated by connective tissue septa Mammary gland development begins with the growth of the epithelial tissue from the embryonic mammary ridge. The gland continues its development until puberty, when the first hormonal stimulus occurs.
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Galactopoiesis
the phase during which the mammary glands maintain lactation
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describe the development of mammary gland
Epithelial buds grow from mammary ridges (ectodermal thickenings) Each bud raises a teat (papilla). In some species the draining point, at the teat is made of multiple duct systems. Cows are single whereas in the bitch there can many other ducts draining into it.
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Histological anatomy of the mammary gland
Each mammary complex comprises one of more mammary units. Mammary units are made of alveoli and ducts. The body of the mammary glands is made of epithelial tissue (alveoli) and connective tissue with nerves, blood and lymph vessels. Mammary units end in a system of ducts at the tip of the teat (papilla) The milk producing part of the gland is divided in lobules (for anatomy purposes!) which are made of alveoli-epithelial tissue. The milk drains into the intralobular duct and from there to a larger interlobular duct and from there to the lactiferous sinus which opens in the teat orifice. This sinus has a little constriction, which creates the part of the sinus close to the gland and the part of the sinus inside the teat itself. Glands separated by connective tissue Teat - smooth muscle and elastic fibres
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describe the streak canal of the mammary glands
Functions to keep milk in udder and bacteria out of udder
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describe the teat cistern of the mammary glands
Duct in teat with capacity of 30-45 millilitres. Separated from streak canal by folds of tissue called Furstenberg’s rosette
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describe the gland cistern of the mammary glands
Separated from teat cistern by the cricoid fold. Holds up to 400 millilitres of milk, collecting area for the mammary ducts
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isometric growth of mammary glands
Birth -> puberty
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allometric growth of mammary glands
Puberty -> pregnancy Oestrogen – duct development Progesterone (luteal phase) – alveoli formation Prolactin, Growth hormone contribute
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describe mammary growth in pregnancy
= final mammary development Terminal alveoli grow into lobules Prolactin, adrenal cortical hormones and placental lactogen for synthesis of milk
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describe the process of lactogenisis
During lactogenesis, the mammary epithelium becomes highly differentiated. This period is associated with an overall increase in the size and metabolic activity of each cell, closure of tight junctions between cells, an increase in mitochondrial size, and development of the endoplasmic reticulum In ruminants, PRL and glucocorticoids provide the primary stimulus for lactogenesis Rise in progesterone Tertiary branching of the ductal system Rise in prolactin in dogs Required for full development Initiates lactation ``` Some species (similar action) Placental lactogen (ruminants) Relaxin (sow, horse) ``` Lactogenesis initiated Alveoli accumulate colostrum Increased prolactin (PRL) just before parturition In other species it contributes to increase milk yield, but this has not been a consistent finding in ruminant Cortisol stimulates differentiation of the glandular epithelium GH – insulin growth factor signalling axis. At the start of lactation is a trigger, but mid-lactation GH increases milk yield Oxytocin – simply helps with the release of milk
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Milk ejection/let down
Milk ejection is active transfer of milk from alveoli and alveolar ducts into larger mammary ducts, cisterns and into the teat/nipples where it can be removed by the suckling neonate. Active neuroendocrine reflex Results in rapid transfer of milk from alveolus  teat of mammary gland Important to feed neonate and prevent pressure atrophy. More frequent removal = less pressure atrophy = greater quantity of milk can be secreted Majority of milk remains in alveoli Milk letdown is a neuroendocrine reflex Induces emptying of the mammary gland ``` Sensory activation Neural activation Oxytocin release: binds to myoepithelium in alveoli and ducts Causes smooth muscle in teat to relax ``` Tactile stimulation, sounds of neonate, visual triggers
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Involution
Return to non-secretory state Recovery time Less suckling by neonate  build up of pressure pressure atrophy Increase feedback inhibitor of lactation (FIL) – inhibits milk synthesis Secretory cells remain non functional until next pregnancy Next pregnancy  Alveolar cells restimulated Prolactin, adrenal cortical hormones, placental lactogen
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what muscles are involved in the pelvic diaphram
coccygeus | levator ani
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describe the origin, termination, inervation and function of the coccugeus
Spine of the ischichium and medial surface of the sacrosciatic ligament Transverse process of the first 3 caudal vertebrae Pudendal and caudorectal nerve from ventral branch of sacral nerve Unilateral contralateral draws tail laterally; bilateral contralateral draws tail ventrally
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describe the origin, termination, inervation and function of the levator ani
Spine of the ischichium and medial surface of the sacrosciatic ligament External anal sphincter, caudal fascia Pudendal and caudorectal nerve from ventral branch of sacral nerve Holds anus against the contraction of the rectum, aids coccygeus
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Innervation of and mechanisms involved in the erection of the cavernous tissue in males and females
Nerves: parasympathetic, from the pelvic nerves Erection of the penis is brought about by engorgement of the cavernous and spongy spaces 2 distinct phases of erection are recognised: Firstly : sexual excitement, blood flow into the penis increases as the walls of the supplying arteries relax. Secondly: at the same time the venous outflow is obstructed. Females: clitoris
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Erection in the fibroelastic penis
slight increase in diameter and length sigmoid flexure little additional engorgement is required and erection may be rapidly achieved. In the first phase of erection, there is parasympathetically mediated relaxation of the supplying arteries occurs. This raises the pressure within the corpus spongiosum and corpus cavernosum from the resting level (5 to 16mm Hg) to the arterial pressure (75 to 80mm Hg); the pressures within these bodies then fluctuate with the heart-beat. The apex of the penis protrudes at this stage, although the muscles of the penis (the ischiocavernosi and bulbospongiosus) are not yet active. Contractions of the ischiocavernosi now raise the pressure further and at the same time occlude both the arteries and the veins by compressing them against the ischial arch. These contractions impel blood forward through thick-walled dorsal and ventrolateral veins of the corpus cavernosum to discharge within the sigmoid flexure. The increase in pressure effaces the bends and straightens the penis, causing it to protrude about 25 to 40cm from the prepuce. After intromission, contact with the vaginal wall stimulates the receptors in the integument of the free part, reflexly stimulating completion of erection. During a short period pressure in the corpus cavernosum can rise remarkably, even to 60 to 100 times the arterial pressure
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MOET
Multiple Ovulation Embryo Transfer (embryo flush) Cause multiple ovulations from an ovary using hormonal therapy, inseminate the animal, retrieve the embryos and implant them into recipients/freeze Advantages: quickly multiply the genetics of the top females in the herd. produce calves with superior genetics. Females in the herd with less desirable genetics can serve as recipients Embryos can be produced and sold to other producers who transfer them into their own recipient females. Frozen embryos can be exported
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Heterotrophs
need to consume other organisms to live
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Chemoheterotrophs
use organic chemicals and compounds as carbon source
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saprotrophs
live off dead or decomposing organic matter
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heterotrophic fungi
Enzymes synthesised inside fungal hyphae Excreted via exocytosis Act on surrounding medium to break it down Digested organic compounds are then reabsorbed in solution through the cell wall Large surface area aids absorption
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Biotrophic
feed off living cells
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Necrotrophic:
invade living cells, kill them then digest
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Moulds grow by
hyphal tip extension Cell wall softened at tip Turgor pressure extends wall Increase in length as opposed to width Increases surface area for absorption
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cell wall of fungi
Cell wall is composed of β-glucan and chitin to provide strength and rigidity and resist osmotic stress Cell membrane is similar to other eukaryotes but has ergosterol instead of cholesterol
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mold
multicellular fungi
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yeast
unicellular fungi Unicellular, non-filamentous Facultative anaerobes: carry out aerobic respiration when O₂ is available and anaerobic (fermentation) when no O₂ available Reproduce by mitosis
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dimorphic fungi
display both yeastlike and moldlike growth
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mycelium
Made up of hyphae | Extensive tissue invasion
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septate Hyphae:
cross walls that form between cells but often have pores to allow movement of cytoplasm and organelles (oposite of coenocytic hyphae
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Ascomycetes produce
conidia on conidiophores
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Zygomycetes
produce sporangiospores on sporangiophores
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resting spores
Produced as a result of sexual reproduction Thicker cell walls protect from abiotic and biotic factors Harder to eradicat
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mycosis
Infection by a fungal agent is called mycosis Mycoses are generally chronic conditions because fungi grow slowly Classification is based on the type of tissue infected and the mode of entry into the body - Systemic (lungs, deep tissue/organs) - Subcutaneous (beneath the skin) - Cutaneous (skin, hair and nails) - Superficial (skin surface, hair shafts) - Opportunistic (immune suppression)
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Dermatophytoses:
the genera microsporum and trichophyton Microsporum canis; gallinae; gypseum; nanum Large, rough, thick-walled multiseptate macroconidia Fusiform to obovate Attack hair and skin Most commondermatophyte Trichophyton mentagrophytes; equinum; verrucosum Rarely produce macroconidia Single-cell microconidia are numerous Solitary or in clusters Attack hair, skin, nails, horns, claws
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Dermatophytes
Arthrospores/conidia are source of infection Entry via injured skin, scars and burns Colonisation of keratinised layers Invade and multiply within keratinised tissues Produce keratinase Induces inflammatory reactions Move away from infection site Need to overcome biotic and abiotic factors (primary defences) Adherence and penetration is slow (2-5 days) Carbohydrate-specific adhesins on surface of conidia Secreted proteases can facilitate adherence Fibrillar projections connect conidia to keratinocytes (skin surface Hyphae grow centrifugally from the initial lesion towards normal skin, producing typical ringworm lesions Alopecia, tissue repair and nonviable hyphae are found at the centres of lesions as they develop Growth of hyphae can result in epidermal hyperplasia (overgrowth of skin cells) and hyperkeratosis (thickening of outer layer of skin). Strategies: Adherence Invasion Colonisation and spread Immunosuppression
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Aspergillus
Primarily a respiratory infection Spores are very small Can pass through upper respiratory tract Carried to terminal part of bronchial tree Spore germination and invasion of tissue is controlled by many factors No true virulence factors Combination of factors leads to disease state
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fungal gleotoxin
assosiated with the hyphae induces cell apoptosis, eithelial cell damage inhibition of phagocitosis and t-cell response
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fungal restrictocin
assosiated with hyphae | inhibitd neutrophil mediated hyphal damage
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fungal verruculogen
assosiated with hyphae and condia | affects transepithelial resistance
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fungal fumagillin
assosiated with the hyphae | damages epithelial cells and slows ciliary beating. angiogenesis inhibitor
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fungal helvolic acid
assosiated with the hyphae | damages epithelial cells and slows ciliary beating.
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describe the invasion of aspergillus
Hyphal invasion of blood vessels Vasculitis and thrombus formation Formation of mycotic granulomas in the lungs Vascular dissemination Colonisation and invasion of other internal organs Additional mycotic granulomas
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Candida albicans
Commensal yeast that lives on mucosal membranes Pleomorphic switch from yeast to filamentous growth Phagocytic clearance eliminates most yeast cells Those that survive convert to hyphal forms ``` Enables tissue penetration and resistance to phagocytosis Adherence Avoidance Flexibility Integrin-like molecules on cell surface ``` Allows adhesion to matrix proteins on mucosal cells Secretion of toxins; proteinases; lipases and phospholipases to aid tissue invasion Msb2p counteracts complement system (antimicrobials) Pre-disposing factors e.g. defective cell-mediated immunity, concurrent disease, prolonged use of antimicrobials, damage from catheters Vascular invasion by hyphae Haematogenous spread Production of systemic lesions
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Principal features of mycotoxicoses
Outbreaks are often seasonal and sporadic * May be associated with particular batches of stored feed or certain types of pasture * No evidence of transmission to in-contact animals * Susceptibility can vary with the species, age and sex of the animals exposed * Clinical presentation may be ill-defined * Antimicrobial treatment is ineffective * Recovery depends on type and amount of mycotoxin ingested and the duration of exposure to contaminated food * Characteristic lesions in target organs of affected animals provide supporting diagnostic evidence * Confirmation requires demonstration of significant levels of a specific mycotoxin in suspect feed or in tissues of affected animals
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Aflatoxicosis
Aflatoxins are a group of approximately 20 related toxic compounds produced by some strains of Aspergillus flavus (Fig. 44.2), Aspergillus parasiticus and a number of other Aspergillus species during growth on natural substrates including growing crops and stored food. These fungi are ubiquitous, saprophytic moulds which grow on a variety of cereal grains and foodstuffs such as maize, cottonseed and groundnuts. About half of the strains of A. flavus and A. parasiticus are toxigenic under optimal environmental conditions. High humidity and high temperatures during preharvesting, harvesting, transportation and storage, as well as damage to field crops by insects, drought and mechanical injury during harvesting favour the growth of A. flavus and toxin production. effects all animals
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Aflatoxins
Aflatoxins are a group of related difuranocoumarin compounds with toxic, carcinogenic, teratogenic and mutagenic activity. The four major aflatoxins are B1, B2, G1 and G2. Aflatoxin B1 (AFB1) is the most commonly occurring and also the most toxic and carcinogenic member of the group Most of the other aflatoxins are metabolites formed endogenously in animals after ingestion or administration of aflatoxins. Aflatoxins are stable compounds in food and feed products and are relatively resistant to heat. They retain much of their activity after exposure to dry heat at 250°C and moist heat at 120°C but may be degraded by sunlight. They have a low molecular weight and are nonantigenic in their native state. The toxic effects of aflatoxins are dose-, time- and species-dependent. Mature ruminants are less susceptible to the effects of mycotoxins than young animals and monogastric animals. The toxins are absorbed from the stomach and metabolized in the liver to a range of toxic and nontoxic metabolites which are then excreted in urine and milk. The major biological effects of aflatoxins include inhibition of RNA and protein synthesis, impairment of hepatic function, carcinogenesis and immunosuppression. AFB1 is bioactivated in the liver to a highly reactive intermediate compound which reacts with various nucleophiles in the cell and binds covalently with DNA, RNA and protein. After deliberate administration of AFB1 there is marked interference with protein synthesis at the translational level which seems to correlate with disaggregation of polyribosomes in the endoplasmic reticulum. Many of the toxic responses observed in animals resulting from AFB1 activity can be attributed to alterations in carbohydrate and lipid metabolism and interference with mitochondrial respiration. Short-term effects include acute toxicity with clinical evidence of hepatic injury and nervous signs such as ataxia and convulsions. In acutely affected animals death may occur suddenly. Long-term consumption of low levels of aflatoxins probably constitutes a much more serious veterinary problem than acute, fulminating outbreaks of aflatoxicosis. With chronic aflatoxicosis there is reduction in efficiency of food conversion, depressed daily weight gain, decreased milk production in dairy cattle and enhanced susceptibility to intercurrent infections in most species due to immunosuppression. AFB1 is also an extremely potent hepatocarcinogen in many species of animals.
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Fumonisins
these substances are produced by several species of the genus Fusarium The presence of fumonisins in corn grains has been associated with cases of esophageal cancer in inhabitants of the region of Transkei in southern Africa, in China and in northeastern Italy (Peraica, Radic, Lucic, & Pavlovic, 1999). Fumonisins are also responsible for the leukoencephalomacia in equine species and rabbits (Bucci et al., 1996, Fandohan et al., 2003, Marasas et al., 1988); pulmonary edema and hydrothorax in pigs (Harrison, Colvin, Greene, Newman, & Cole, 1990); and hepatotoxic, carcinogenic and apoptosis (programmed cell death) effects in the liver of rats
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Trichothecenes
produced by fungi of the genera Fusarium, Myrothecium, Phomopsis, Stachybotrys, Trichoderma, Trichotecium, Verticimonosporium and possibly others strong capacity to inhibit eukaryotic protein synthesis, interfering in the initiation, the elongation and termination steps of protein synthesis.# DON is the mycotoxin most commonly found in grains. When ingested in high doses by animals it causes nausea, vomiting and diarrhea. When ingested by pigs and other animals in small doses it can cause weight loss and the refusal to eat. Due to these symptoms induced by deoxynivalenol it is known as vomitoxin or food refusal factor. Although less toxic than other trichothecenes, DON is more common in the seeds of safflower, barley, rye, and wheat and in feed mixtures
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Zearalenone
this is a secondary metabolite produced mainly by Fusarium graminearum The association between the consumption of moldy grains and hyperestrogenism in pigs has been observed since 1920. High concentrations of zearalenone in pig feed may cause disturbances related to conception, abortion and other problems In Brazil this toxin has been found on cereals and oak flakes
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Citrinin
Citrinin was first isolated from secondary metabolites of Penicillium citrinum, well before the Second World War (Hetherington & Raistrick, 1931). Subsequently, other species of Penicillium (Penicillium expansum and Penicillium viridicatum) and even of Aspergillus (Aspergillus niveus and Aspergillus terreus) also showed the capacity to produce these substances. It has also been considered responsible for nephropathy in pigs and other animals, although its acute toxicity varies depending on the animal species (Carlton & Tuite, 1977). Oat (moldy), rye, barley, corn and wheat grains are excellent substrates for the formation of citrinin
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Ergot alkaloids
cereal grains infected by Claviceps purpurea Also known as ergotism, this intoxication occurs after the ingestion of bread or other products prepared with rye bread grains infected by fungus. Ergotism has two classic forms: gangrenous and convulsive. The gangrenous form affects the supply of blood to the extremities of the body, while the convulsive form acts directly on the central nervous system With the modern techniques of grain cleaning the problem of ergotism has been practically eliminated from the human food chain. However, it remains a threat from the veterinary perspective. The animals which are susceptible to intoxication include cattle, ovine species, pigs and birds. The clinical symptoms of ergotism in these animals manifest in the form of gangrene, abortion, convulsions, suppression of lactation, hypersensitivity and ataxia (loss of coordination of voluntary muscular movements)
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Ochratoxin A
Ochratoxin A has been found in oats, barley, wheat, coffee grains and other products for human and animal consumption metabolite of Aspergillus ochraceus associated with nephropathy in all animals studied to date also shows hepatoxic, immunosuppressive, teratogenic and carcinogenic behavior
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name the four main categories of authorized veterinary medicines:
POM-V medicines that can only be prescribed by a veterinary surgeon (veterinarian) – POM-VPS medicines that can be prescribed by a veterinary surgeon, pharmacist or suitably qualified person (SQP) – NFA-VPS medicines that can be supplied by a veterinary surgeon, pharmacist or SQP – AVM-GSL medicines that can be sold by anyone
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The Veterinary Medicines Directorate (VMD)
an executive agency of the Department for Environment, Food and Rural Affairs (Defra), is the UK regulatory authority for veterinary medicines and has responsibility for the development of the Veterinary Medicines Regulations (VMR). The VMR regulate the authorization, manufacture, distribution and use of veterinary medicines in the UK. The VMR transpose EU legislation relating to veterinary medicinal products (VMP) and are explained in the Veterinary Medicines Guidance pages of the VMD website They are assessed for safety, efficacy and quality ■ All must have a Marketing Authorization (MA) ■ Authorized VMP must display a VM or EU code
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All POM-V medicines supplied by the practice must be legibly and indelibly labelled with:
Name and address of the animal owner ■ Name and address of the veterinary practice supplying the medicine ■ Date of supply ■ Name, strength and quantity of product ■ Dosage and directions for use ■ ‘For animal treatment only’ ■ For topical preparations: ‘For external use only’.
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Written prescriptions for Controlled Drugs
If a written prescription is issued for a Controlled Drug (CD) it can be typed, computer generated or handwritten, but it must be personally signed by the person issuing it. It is an offence to supply a Schedule 2 or 3 CD against a faxed or emailed prescription. In addition to the general prescription requirements above, a written prescription for a Schedule 2 or 3 CD should state an exact dose in words as well as in figures (e.g. not ‘as directed’), and it must include the RCVS number of the veterinary surgeon prescribing the drug. A written prescription for Schedule 2 or 3 CDs can only be dispensed once and only within 28 days. Single prescriptions with multiple dispenses (repeatable prescriptions) are not allowed for Schedule 2 and 3 CDs. It is good practice to mark the prescription ’no repeats’. It is a best practice recommendation to dispense only 28 days of CDs at a time. If it is considered necessary to dispense a CD for a longer period (e.g. in the case of an epileptic dog on long-term medication), the veterinary surgeon must make sure that the owner is competent to use and store it safely
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Cryptococcosis
C. neoformans and C. gatti are dimorphic basidiomycetous fungi Oval haploid budding yeast (vegetative growth) Transition to filamentous sexual stage (Filobasidiella neoformans) known as a teleomorph Important fungal infection of humans and animals Primarily infects immune-compromised patients Most common in cats Also seen in dogs, cattle, horses, sheep, goats, birds and wild animals Virulence factors: Polysaccharide capsule Melanin Mannitol Enzymes “Sugar coated killer” Phenotypic switching Development of pulmonary lesions Dissemination via hematogenous spread in macrophages Localisation in central nervous system Cross blood brain barrier (BBMB) via transcytosis or inside infected macrophages Formation of lesions in the brain Results in neurological signs Infection can spread to the eye along optic nerves or hematogenous dissemination Results in cryptococcal optic neuritis and retinitis Most common systemic mycosis Chronic infection causing listlessness and weight loss Cutaneous legions, some large and ulcerative Upper respiratory signs such as sneezing, chronic nasal discharge, polyp-like masses, subcutaneous swelling over the bridge of the nose Neurological symptoms include depression, changes in temperament, seizures, circling, paresis and blindness Optic signs include dilated, unresponsive pupils, blindness, inflammation of ocular structures Dogs present meningoencephalitis, optic neuritis and granulomatous chorioretinitis Disseminated disease with CNS or ocular involvement more common than respiratory Cytologic evaluation of: Nasal exudate Skin exudate Cerebrospinal fluid Paracentesis of aqueous or vitreous chambers of the eye Impression smears of nasal or cutaneous masses
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Phenotypic switching
Alterations in cell membrane and capsule structure Allows cells to persist in the host by minimising the inflammatory response
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Sporotrichosis
Seen in cats, dogs, horses, donkeys, pigs, fowl, goats and cattle Most common in cats and dogs Entry of spores (conidia) or mycelia through broken skin Directly through cut or puncture wound Indirectly through contamination of existing wound Also transmission in cat scratches Subcutaneous/lymphocutaneous: most common form Pulmonary: rare but possible via breathing in fungal spores Disseminated: spread of infection to other parts of the body (immunocompromised patient Conversion from mycelial to yeast form upon entry Production of extracellular enzymes and adhesins allow adhesion to and invasion of cutaneous and subcutaneous tissue Adhesion to extracellular protein fibronectin Proteinases I and II hydrolyse stratum corneum cells Definitive diagnosis relies on culture of both forms Prognosis is good Long treatment duration requires owner compliance Itraconazole is feline drug of choice
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expalne the mechanisms of common anti fungals
target the cell membrane- AMPHOTERICIN ECHINOCANDINS AZOLES MACROLIDES target mitosis/ replication- GRISEOFULVIN target by DNA synthesis- FLUCYTOSINE
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Amphotericin: Mechanism of Action
creates artificial ion channel Amphotericin binds fungal membrane ergosterol (fungal cholesterol) causing: Increased membrane permeability and Creation of transmembrane channels (pores) Resulting in: Leakage of monovalent ions (K+, Na+, H+, and Cl-), Leakage of macromolecules from fungal cell ``` Other mechanisms: Stimulates fungus to produce oxygen radicles Modulation of macrophage activity Stimulates pro-inflammatory cytokines Reactive oxygen intermediates Nitric oxide Eventually cell death ``` can enhance other antifungals good for disseminated aspergillus “Conventional” Amphotericin B deoxycholate (AmB-d) Newer (lipid-based) formulations Liposomal amphotericin B (L-AmB) Amphotericin B lipid complex (ABLC) Amphotericin B colloidal dispersion (ABCD) Many others- Fewer side effects: lipid vehicle acts as reservoirs, reducing binding to cells Improved tolerability Altered tissue penetration – more in liver, spleen and brain, less in lung and kidneys Reduced toxicity (esp. nephrotoxicity and anaemia) However, compared to AmB-D these formulations are less potent by mg dose Resistance: Dermatophytes- no ergosterol Pythium Candida- resistence ``` Antifungal Spectra: Candida spp  Rhodotorula spp  Cryptococcus neoformans Histoplasma capsulatum Blastomyces dermatitidis Coccidioides immitis Trichophyton Microsporum Epidermophyton spp ```
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Amphotericin: Pharmacokinetics
Absorption Poorly absorbed from the GI tract: Amphotericin B (IV, Topical, Local, Intrathecally, Intraocularly) Nystatin/Piramycin (Topically) Distribution Well distributed in most body compartments CNS penetration ~0%- unless there is inflamation, good for crytococcal meningitis Elimination Initial Phase (24 hours): 70% plasma reduction, 50% Urine reduction Second Elimination Phase: 15 day half life. Excreted unchanged in urine (21%) and faeces (43%)
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Imidazoles
``` enilconazole fluconazole itraconazole ketoconazole thiabendazole change permiability of membrane by inhibiting synthesis of ergosterol Resistance: No major Antifungal Spectra Blastomyces dermatitidis Paracoccidioides brasiliensis Histoplasma capsulatum Candida spp Coccidioides immitis Cryptococcus neoformans Aspergillus fumigatus used in mild to moderate disease or in combination in severe disease ``` ``` Inhibition of CYP450 results in reduction of: Progesterone Pregnenolone Corticosterone Aldosterone Cortisol Estrone Estradiol Estriol ``` toxicity more common in cats than dogs
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Imidazoles: Pharmacokinetics
Absorption Rapidly absorbed from the GI tract Distribution Well distributed in most body compartments CNS penetration poor (Fluconazole about 50-90% plasma conc) Highly protein bound (95%) ``` Elimination Initial Phase (1-2 hours): Rapid Second Elimination Phase (6-9 hours): Slower Roughly 5% unchanged in urine Roughly 80% bilary excretion ```
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Flucytosine
``` enhances other anti fungals Mechanism Converted to fluorouracil Inhibits RNA synthesis Inhibits protein synthesis Resistance Can develop over course of treatment Antifungal Spectra Cryptococcus neoformans Candida albicans, Candida spp Torulopsis glabrata Sporothrix schenckii Aspergillus spp ``` Adverse Effects and Toxicity: Vomiting Diarrhoea Reversible hepatic and hematologic effects (increased liver enzymes, anaemia, neutropenia, thrombocytopenia). Interactions: Synergistic antifungal activity between amphotericin B and ketoconazole. Renal effects of amphotericin B prolong elimination of flucytosine.
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Flucytosine: Pharmacokinetics
Absorption Rapidly absorbed from the GI tract Distribution Well distributed in most body compartments CNS Excellent Minimal protein bound Elimination Roughly 85% unchanged in urine
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Griseofulvin
Mitotic Inhibitor Inhibits formation of the mitotic spindle. ``` Fungistatic Prevents fungi growth rather than killing the fungi. Use Dermatophyte infections Resistance Can develop over course of treatment Antifungal Spectra Microsporum Epidermophyton Trichophyton spp. Actinomyces  Nocardia spp Adverse Effects and Toxicity: Rare Vomiting Diarrhoea Teratogenic (contraindicated in pregnant animals especially mares and queens) ``` Interactions Lipids increase GI absorption of griseofulvin.
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Griseofulvin: Pharmacokinetics
Absorption Rapidly absorbed from the GI tract, enhanced by high-fat diet. Distribution Well distributed in most body compartments Binds well to keratin Higher effect in growing nails/horn. Elimination Roughly 85% unchanged in urine
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Virion
is the infectious particle composed of nucleic acid, protein capsid, +/- envelope may be extracellular or intracellular Has viral surface proteins that attach to host cell surface proteins which allow entry into a cell.
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describe the four aspects of virus replication
Four aspects of virus replication Entry – binding to host cells and entering the cell Replication – Producing new copies of the genome Assesmbly – producing new virus particles Release – Exiting the cell to infect a new host or a new cell within the current host
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describe virus entry
Virus has to bind to cells Binding can occur via cellular proteins that act as receptors IMPORTANT to realize that receptors are normal cell proteins that viruses hijack they are not there just for the viruses – they have normal cellular functions Receptors tend to be virus-specific Multiple viruses can bind the same receptors Some receptors bind viruses but don’t facilitate infection – pseudo receptors Can also be cell type specific – if virus has specific host cell tropism Not all cell-surface molecules are able to bind virus, if the virus binds to a different molecule no entry is possible RSFV binds to lrp1 Found on all cell types a ubiquitous receptor allows the virus to enter lots of different cell types Rabies virus binds to Acetylcholine receptor Found on muscle cells and the synapses between the nerve and muscle cells – allows the virus to infect muscle and neurons Poxviruses thought to bind to glycosaminoglycans These are universal throughout the cells, but it is likely that the virus has specific tropisms to different cells, which is a result of downstream signalling within the cell, not binding
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describe Basics of virus replication
Viruses hijack the cells systems to replicate – they cannot do it without the cellular machinery Can occur in the cytoplasm or the nucleus – on membranes on in complexes Viral proteins also interact with the cellular systems to inhibit cellular transcription or activate other cellular pathways to facilitate infection Replication occurs in the nucleus for all but one group of DNA viruses One exception to the rule is Pox viruses (monkeypox) that replicate in Cytoplasm mRNA’s are then moved out to the cytoplasm for translation and assembly Viruses uncoat once they enter the cell – Genomic material released for replication Genomic material is either immediately transcribed (DNA/RNA viruses) or requires an extra step ( negative sense viruses, and retroviruses) Viruses hijack the host cell systems and produce proteins using the host cell resources, though RNA viruses use their own replication complex proteins
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Poxvirus Replication
complexes in the cytoplasm No use of the DNA so must carry their own polymerase Activation of various genes in early, intermediate and late phase to facilitate replication and assembly
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Positive strand RNA virus replication
Virus enters the cell Uncoats and the genomic RNA starts producing protein RNA then generates a replicative intermediate to generate a new genomic RNA Packaged and then exits the cell
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Negative strand RNA virus replication
Virus enters cell and uncoats mRNA is produced to produce protein Replication occurs by way of a dsRNA intermediate Virus assembly from proteins and the genomic RNA Cell exit
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Retrovirus replication
Virus enters the cell The RNA is reverse transcribed and then imported into the nucleus Integrated and then transcribed to produce mRNA Translated into proteins and then assembly of the virus and release from the cell
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describe Virus Assembly
Surface proteins, either envelope proteins and/or capsids packaged to produce new viruses
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describe Virus release
2 main ways: Budding from cell using host lipids and generating new enveloped viruses Lysis of the cell releasing virus into the environment
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list the aetiological agents that can contribute to the development of Kennel Cough in dogs in the UK (both bacterial and viral).
parainfluenza virus, canine adenovirus and Bordetella bronchiseptica, as well as mycoplasmas, Streptococcus equi subsp. zooepidemicus, canine herpesvirus and reovirus-1,-2 and -3.
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parainfluenza virus
Type of virus: 50- to 200-nm virion consisting of a nucleocapsid surrounded by a lipid envelope that is obtained as the nucelocapsid buds from the plasma membrane of an infected cell. 17 All PIVs, including CPIV, have a single-stranded, nonsegmented, negative-sense RNA genome Pathogenesis and relevant virulence factors: Incubation period: 3 to 10 days after infection, and viral shedding typically occurs 6 to 8 days after infection Clinical signs and potential outcome: Persistent cough Fever Nasal discharge Sneezing Eye inflammation Lethargy Loss of appetite CPIV suppresses the innate branch of the immune system and causes the loss of cilia and ciliated epithelium, it makes conditions more favorable for coinfections. In puppies or immunosuppressed adult dogs, the presence of CPIV in coinfections can lead to a more severe pneumonia and can be fatal. Diagnosis: based on the dog's medical history, clinical signs, vaccination history and physical exam. If a specific diagnosis of canine parainfluenza is needed, ocular and oral swabs can be submitted to the lab for PCR testing to confirm the presence of CPIV.
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CAV-2
``` Type of virus: Pathogenesis and relevant virulence factors: Incubation period: Clinical signs and potential outcome: Dry, hacking cough Conjunctivitis (causing redness and inflammation of the eye) Coughing up foamy discharge Retching Nasal discharge ``` Diagnosis: Your vet will want to hear some background history of your dog’s health, details of any symptoms and about any possible exposure to the virus through contact with other dogs. In addition to a thorough physical examination, blood and urine samples will be taken for testing and analysis as they will want to rule out any other more serious conditions such as canine adenovirus type-1, canine distemper and parvovirus which initially exhibit similar symptoms
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canine parainfluenza vaccine
non-core Administer at 6–8 weeks of age, then every 2–4 weeks until 16 weeks of age or older [EB4
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Rabbit haemorrhagic disease virus
Infection is easily transmitted between infected rabbits by the oral, nasal or conjunctival routes, with the digestive system and respiratory tract as the main portals. Only a few virions are required to produce infection. Food bowls and bedding can transmit infection. Carcases from wild rabbits that died from RHD can be a source of infection, by spreading the virus via the faeces of scavengers. RHD has a short incubation period of one to four days. The virus replicates in many tissues, including the lung, liver and spleen, with subsequent viraemia and haemorrhage. Viral tropism is for hepatocytes. The disease it causes is essentially a necrotising hepatitis, often associated with necrosis of the spleen. Disseminated intravascular coagulation produces fibrinous thrombi in small blood vessels in most organs, notably the lungs, heart and kidneys, resulting in haemorrhages. Death is due to disseminated intravascular coagulopathy or liver failure. Peracute, with animals found dead within hours of eating and behaving normally. This is a common presentation Acute, with affected rabbits showing lethargy, pyrexia (above 40°C) and increased respiratory rate. These animals usually die within 12 hours. Subacute, with rabbits showing mild or subclinical signs from which they recover and become immune to infection.
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Feline Enteric Coronavirus
Two forms of the disease Mild enteric disease in kittens – GI tract Feline Infectious Peritonitis – can be fatal Mutations in the virus lead to the difference in the virus resulting in FIPV – lethal version of the disease Mortality is high once symptoms occur FECVs show a pronounced tropism toward epithelial cells in the gut, but they are also able to infect monocytes, albeit inefficiently. It was suggested that in monocytes—rather than in intestinal epithelial cells
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FECV to FIPV
FIP develops in approximately 5% of cats that are persistently infected with FECV FECVs acquire mutations that can convert them into FIPVs (Pedersen et al., 2012). The resulting FIPVs display an altered cell tropism; they infect and replicate efficiently in monocytes and macrophages. This property is considered a key step in the development of FIP. One gene the 3c shows a full-length gene in FECV Essential for replication in the gut – pathogenesis of FECV In FIPV this 3c gene shows mutations and a truncated gene Hypothesise that this might result in increased tropisms for macrophages – FIPV Spike protein can also show 2 mutations in the protein consistent in FIPV sequences – results in increased disease outcome
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Bluetongue virus
Bluetongue is characterised by changes to the mucous membranes of the mouth and nose, and the coronary band of the foot. Clinical signs are generally more severe in sheep but cattle can show signs of disease.  A veterinary surgeon must be contacted by the farmer where large numbers of sheep or cattle present with lameness, high rectal temperatures, salivation, lacrimation and ocular and nasal discharges.  Bluetongue is a notifiable disease in the UK Midges – culicoides spp. are the vector Ruminants can be infected, primarily sheep Once the sheep is infected – enters the lymph nodes and then needs to get into the blood to continue transmission Symptoms are a result of the prolonged viremia Midge bite in the skin results in recruitment of APC’s at the bite site and virus migration to the lymphoid cells BTV replicates within mononuclear phagocytic and endothelial cells, lymphocytes and possibly other cell types in lymphoid tissues, the lungs, skin and other tissues. Followed by migration to the blood – circulates around the body Infected ruminants may exhibit a prolonged but not persistent viraemia and BTV is associated with erythrocytes during the late stages of this prolonged viraemia.  The prolonged viremia results in injury to small blood vessels in target tissues – show the characteristic blue tongue Shows haemorrhage and ulcers in the oral cavity and upper gastrointestinal tract; necrosis of skeletal and cardiac muscle; coronitis; subintimal haemorrhage in the pulmonary artery; oedema of the lungs, ventral subcutis, and fascia of the muscles of the neck and abdominal wall; and pericardial, pleural and abdominal effusions.
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Canine Herpesvirus
Clinical signs of canine herpesvirus if presented are: Lethargy Decreased suckling Diarrhea Nasal discharge Conjunctivitis Corneal edema Red rash, rarely oral or genital vesicles Soft, yellow-green feces Notable absence of fever CHV is primarily lethal in neonates (1-4 weeks old) If infected after 1-2 weeks they will generally survive Timing is therefore key to survival Infection is by oronasal secretions of other dogs/mother or otherwise Incubation period is 6-10 days Duration of illness is 1-3 days Herpesviruses only infect neonates due to the immature immune system Not just in dogs, but also in humans very similar disseminated herpes infection— the most dangerous type of herpes infection. The herpes virus is spread throughout the neonates body and can affect multiple organs, including the liver, brain, lungs, and kidney. Why do adults not get it? Functional immune system Can result in latency Latency is a hallmark of herpesvirus infections The viral genome exists as an episome (naked, circular DNA) in the host cell nucleus No virus is produced until reactivation Not the same as persistent infection (continuous viral production) E.g. VZV, which causes chickenpox in children, causes shingles when reactivated in the adult
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Rift Valley Fever virus
Most commonly seen in domesticated animals in sub-Saharan Africa, cattle, buffalo, sheep, goats, and camels. People can get RVF through contact with blood, body fluids, or tissues of infected animals, or through bites from infected mosquitoes. Mosquitoes are the main driver of transmission Take a blood meal from an infected animal Infected mosquitoes incubate for 7-14 days Then once it reaches the saliva it can transmit to the next animal perpetuating the cycle Cattle movement across boundaries Climate change expands range of mosquitoes – increases disease range Increased rains that allow increased mosquito numbers and therefore transmission rates Notifiable disease DEFRA
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High Pathogenic Avian Influenza H5N1
The flu virus is an RNA virus The genome codes for five viral proteins and is made of eight fragments. The virus has a lipid envelope with two glycoproteins present Haemagglutinin - this glycoprotein plays a part in infection and provides the “H” in the strain type. Haemagglutinin attaches the virus to cells and allows the viral envelope to fuse with the cell membrane and enter cells. Neuraminidase –its role is to allow the release of viruses to infect other cells Different combinations of H and N glycoproteins give rise to different strains Mutations which produce small changes in antigens are referred to as antigenic drift and these occur in the same strain Mutations which result in a major change and produce new strains are referred to as antigenic shifts The virus is spread by inhalation or by direct contact. Reservoirs of infection are primarily humans, but birds and pigs can act as reservoirs. The multiple host status makes for mixing of flu types Avian Influenza only transmits to humans in close contact Evidence of HPAI Avian Influenza – reportable disease
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African Swine Fever virus
Double stranded DNA virus Only DNA virus known to be transmitted by arthropods. Causes haemorrhagic fever- high mortality rate in domestic pigs Has an enzootic cycle in addition Warthogs and bushpigs with soft ticks as the vectors Eradicated outside of Africa in 1990’s with exception of epidemic in Portugal in 1999 Endemic in Africa Re-emerging in Europe Zoonotic disease Ticks bite wild animals – get infected with ASFV Once infected, they are infected for life – can transmit even as they moult from larvae – nymph – adult tick Bite domesticated animals – pigs get infected and can then transmit pig-pig. No horizontal transmission in wild animals If pigs are free-range – increased likelihood of contact with ticks Like other DNA viruses had early, intermediate and late gene expression Replicates in both nucleus and cytoplasm Changes in the host result in increased pathogenesis
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types of vaccine
whole innactivate virus- could cause outbreak recombinanat viral vector- DNA vaccine virus like particles- just envelope/ protiens recombinant bacterial vector vaccine recombinant sub unit protein live attenuated virus- very safe and good, basically non pathogenic virus vacciens are inactivate dor activated
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describe the benefits and draw backs of an innactivated vaccine
``` higher cost adjuvent needed good stability no reversion provided no mucosal immunity, antibody memory response the immunity is short lived ```
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describe the benefits and draw backs of an activated protien
``` lower cost adjuvent not needed poor stability reversion is possible provides mucosal immunity, antibody an dCTL imunity and long term immunity ```
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Issues with antivirals
Viruses use our own cells to replicate so anything that targets them also targets our cells Can have some issues with toxicity – even long-term HIV drug use can affect the body – have some long-term events Nucleoside analogues are commonly used in veterinary medicine
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Squamata
Lizards and snakes
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Chelonia
Tortoises and turtles
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How are reptiles different to mammals
Poikilothermic ectotherm- interanl temp vairies and outside temp influnces Jaw bones and auditory ossicles Quadrate bone, Articular bone & Columella- the singular ear bone Most reptiles are oviparous (some mammals are oviparous!)- egg laying Temperature dependent sex determination No mammary glands 3 chambered heart (Crocodilians - divided atrium, sometimes refered to as 4 chambered) Homodont dentition- uniform continually growing teeth except fanged snakes Scales instead of hair Shed No sweat glands No diaphragm- no division between abdomine and thorax so not refered to as such- refered to as coelom Nitrogenous waste product is uric acid, not urea
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Anatomy of the reptile integument
``` Epidermis Keratinised scales Largely overlapping in squamates Shell in chelonians Hard scales in the limbs and tail 2 forms of Keratin Alpha Keratin Flexible, between scales & in hinges Beta Keratin Harder, found in scutes and scales Dermis- Highly vascular Sensory tissue Osteoderms-mineralised bony structures in dermis Chromatophores- pigment cells ``` ``` Periodic sloughing and renewal Crocodilians and chelonians – continuous Lizards – cyclical - piecemeal Snakes – cyclical – single piece Resting phase & renewal phase Under thyroid control with multiple factors Vitamin D Activation Water uptake Desert species Anoxia tolerance Shells (Freshwater turtles) ```
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Nociceceptors in reptiles
More mu opioid receptors cf kappa
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Integument Overview - Snakes
``` Heavily keratinised epidermis Prevents water loss/waterproofs Protection Keratin formed into overlapping epidermal scales (non overlapping on head) Reptile skin is very inelastic Folds of skin between the scales to allow to expansion Single ventral scales – ‘gastropeges’ Thicker, larger scales for support Important for locomotion Scales caudal to cloaca – ‘subcaudal scales’ Usually paired Very few glands Cloacal glands Pits ``` Shedding Growth Replacement of worn out skin Parasite disposal Most snakes shed 2-4 times/year Growth Season (eg post hibernation) Reproduction (shed 8-10 days before oviposition/parturition) Shed more frequently when juvenile/rapid growth Shed ‘in toto’ in one single piece (incl. spectacles) Controlled by thyroid gland Environmental conditions key Lymph fluid builds up between old and new epidermal layers Bluish colouration to skin ‘blue’ Spectacle opacity ‘in milk’ (inhibits visibility) Reduced markings Spectacle clears before shed Skin circulation engorges to stretch and split old epidermal layer Colourless Pigment cells in the dermal layer Changes in feeding behaviour and activity Prior to shedding Irritable/Reduced activity/Seek shelter/humidity Post Shedding Defaecation/Thirst
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Ecdysis
shedding
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Dysecdysis- Snakes
``` Abnormal or impaired shedding Can affect entire integument Spectacles ofter retained- Inhibit vision and can cause inappetence retention around Cloaca Patchy shed Usually husbandry related -Humidity -Temperatures -Substrate & -Furniture Never remove retained shed Soak/lubricate Husbandry ```
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Integument Overview - Lizards
``` Heavily keratinised epidermis Prevents water loss/waterproofs Protection Keratin formed into epidermal scales similar to snakes Epidermal growth is cyclic Osteoderms in some species ‘Dermal Armour’ Modified scales Crests Spines Shields Dewlap Lamellae- allows geckops to cling- not lepord gecko ``` ``` Cloacal glands Scenting Temporal glands Chameleon Function unknown but likely defence/lure Pre cloacal pores Geckos Femoral pores Iguanas, Many agamids Gender determination Salt glands Marine iguanas ```
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Ecdysis - Lizards
``` Epidermal growth cyclic Regular patchy/piecemeal shed Some species eat shed skin Frequency varies: Species Size Growth – Juveniles may shed q. 2 weeks, Adults q. 3-4 times p.a. Temperature Humidity Nutrition Skin damage Endocrine function Controlled by thyroid gland ```
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Dysecdysis- Lizards
``` Abnormal or impaired shedding Fragmented ecdysis is normal Dysecdysis Constrictive bands of tissue Tail Digits- missing digits indicitive fo chronic shedding problem Usually husbandry related Humidity Temperatures Furniture Care removing retained shed Soak/lubricate Address Husbandry ```
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Integument Overview – Chelonians - Shell
``` Shell Dorsal convex carapace Carapace formed of 49 bony plates Dermal ossification Ventral flatter plastron Plastron formed of 9 bony plates Plastrocarapacial bridge Scutes Keratin shields Form from epithelial thickenings Reduced in soft shell turtles 38 carapacial scutes 16 plastral scutes Hinges Legs, head, tail, neck Soft, folded skin B Keratin containing scales Some areas scaleless Protected by shell Ecdysis Piecemeal continuous shedding Aquatic turtles shed their scutes Terrestrial tortoises retain scutes Glands Musk/Rathke’s glands Marine turtles Bridge/carapace junction Mental/chin glands ```
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Subcutaneous injections in reptiles
``` Not often used Limited subcutaneous space Poor absorption rates Delayed onset of action Protracted clinical effects Useful for fluid therapy Always inject between scales Snakes Lateral (dorsal) body wall Lizards Lateral thoracic area, inguinal space Chelonians Axillary and inguinal space Skin folds lateral to neck ```
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Common features of the reptile eye
``` Striated muscle in the iris & ciliary body Conscious pupillary control No consensual pupillary light response Miosis slower than in mammals drugs to dilate pupil do not workas it is not smooth muscle Spherical globe Pigmentary cells throughout sclera Ocular movement limited Poor development of rectus muscles Chameleons exceptional Well developed ocular muscles Normal intraocular pressure (IOP) low cf mammals Thin cornea Especially in squamates with spectacles Avascular retina ```
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Snake Eye anatomy
``` Very different to other reptiles Small Large cornea No scleral ossicles- connective muscle in its place Spherical eyeball Fibrous sclera No eyelids Highly mobile iris Spectacle or brille protects cornea No nictitating membrane Glands Harderian no Lacrimal Limited eye mobility Poor vision Reduced ciliary body Spherical lens Pupil shape species, habitat and life mode dependent Round Elliptical Horizontal Cones and rods present in retina Some diurnal snakes have lost rods Conus papillaris in very few species- provides back of eye with nutrient and oxogen ```
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Snake Pit organs
Eyes responsible for visible light Pit organs responsible for infrared radiation detection Pythons, Boas, Vipers Information from both merged Accurate prey detection Pit organ varies between species Boidae – shallow depression in labial scales Viperidae – concave membrane within maxillary bone Trigeminal nerve branch innervation
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Lizard Eye anatomy
``` Large orbits Thin interorbital septum Scleral ossicles Eyelids present Upper eyelid largely immobile Lower eyelid covers majority of cornea Most gecko spp. have brilles Descemet’s membrane present in most spp Nictitating membrane present Orbital Glands Harderian – opens medially Lacrimal- not in chamelions and some geckos Mucous gland Good vision Pupil Round in diurnal species Slit in nocturnal species Serrated pupil in some geckos Diurnal lizards have cones only Nocturnal lizards have rods and cones Conus papillaris ```
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Lizard Parietal Eye
Third eye, median eye, parietal accessory apparatus Most lizards Eyelike structure on dorsal head Situated in a depression below parietal bone Overlying scales show varying transparency Cornea like apparatus Primitive retina Neurological input Function Connected to pineal gland Role in hormone production and thermoregulation Timing of reproduction Navigational Largely absent in nocturnal lizards
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Chelonian Eye anatomy
``` Highly developed colour vision Scleral ossicles Scleral cartilage up to 1cm thick Scaled eyelids Nictitating membrane present Lacrimal gland Modified into a salt gland in marine spp. Nasolacrimal duct absent Tears lost by evaporation Thick cornea Descemet’s membrane Much more effective in air than water Two orbital lymphatic sinuses Drain into both eyelids Cornea more effective in air than water ```
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Reptile Olfactory Function
``` Olfactory epithelium Dorsal nasal cavity Jacobson’s/Vomeronasal organ Ventral nasal cavity Innervated by a branch of the olfactory nerve Reptile Vomeronasal Organ- Jacobson’s Organ Chemoreceptor organ Most developed in lizards and snakes Varies between species of reptile Innervated by a branch of the olfactory nerve Snakes Tongue flicking Tongue transfers particles to the Jacobson’s organ Pair of domed vomeronasal pits in roof of mouth Lizards Similar to snakes Chelonians Localised area of sensory epithelium in terrestrial spp Absent in some aquatic turtles ``` Olfactory function most developed sense in snakes Highly developed vomeronasal organ Paired function with forked tongue Flick tongue through lingual notch/fossa ``` lizards- Well developed olfactory function Nasal Cavity Jacobson’s/Vomeronasal organ Rostral to choana Tongue Organ of taste and smell Some species flick this like snakes Contain chemosensory receptors Buccal oscillation ``` ``` chelonian- Well developed olfactory function Large olfactory bulbs Esp in terrestrial spp. Nasal Cavity Jacobson’s/Vomeronasal organ Salt glands in some marine species Buccal oscillation ```
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Reptile Ears
``` Reptile ear is caudoventral to the eye Likely more important for balance than hearing Covered by cutaneous scale or semitransparent tympanum Outer ear External auditory meatus Absent in snakes, chelonians and some lizards Middle ear Tympanic membrane Columella Inner ear Semicircular canals Utricle Saccule Cochlear duct ``` snake ear- No external auditory opening, tympanic membrane or middle ear cavity Eustachian tube is absent Can pick up substrate vibrations Can also pick up low frequency airborne sound (150-600Hz) Quadrate bone connects mandible to columella Receives low frequency vibrations lizard ear- Visible tympanic membrane Varies between species Shallow depression or external ear Covered with a scale or scute Some burrowing lizards have no external or middle ear Transmit vibrations through bone similar to snakes Minimal differentiation between tympanic cavity and pharyngeal space Some chameleons have a thin membrane Eustachian tube present connecting middle ear to pharynx Chelonian Ear- Chelonians have excellent hearing No external ears Respond to low frequency tones (100-700Hz) Ground vibrations Predator approach Aquatic turtles most sensitive to underwater stimuli <1000Hz Large tympanic cavity extends caudally Blind pouch within squamosal bone Tympanic membrane Thin osseus columella Extracolumella cartilage Eustachian tube connects inner ear to oropharynx Aural abscesses common in aquatic turtles
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Acrodont
Teeth fused to the maxillary and mandibular ridges Worn down throughout life Agamids, Chameleons Acrodont teeth are seen in agamid lizards (e.g. water dragon, bearded dragon),uromastyx, chameleons, and tuataras (Table 1). Acrodont teeth are superficiallyankylosed to the rim of shallow, crater-like depressions on tooth-bearing bone (Fig1). This attachment is relatively weak and teeth are easily lost while feeding orcapturing prey (Klaphake 2015 O’Malley 2005, Mehler 2003, Cooper et al 1970,Edmund 1970).As the animal grows, new teeth can be added at the posterior end of the tooth row,however acrodont teeth are replaced “only very rarely” in the adult. Instead teethare worn down with age leaving only the dorsal crest of the mandible and theventral crest of the maxilla. The resultant cutting edge in older animals is similar tothe chelonian jaw, except the surface remains serrated. Glancing contact betweenthe occlusal surfaces when the jaws close, ensures wear maintains a sharp edge
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Pleurodont
Teeth sit in grooves on the medial aspect of mandible/maxilla Constantly shed & replaced Iguanas Pleurodont teeth are seen in snakes, many lizards, including iguanids, varanids(monitors), basilisks, chuckwallas, and anoles (Table 1) (Klaphake 2015, Edmund1970). With pleurodont dentition, a larger surface area is in contact with thejawbone, which creates a stronger attachment than acrodont dentition (Fig 1).Pleurodont teeth are constantly shed and replaced throughout life. The lifespan ofteeth varies along the jaws, with posterior teeth lasting longer than anterior teeth.Most teeth last only a few months before being shed and ingested with prey duringfeeding (Cooper et al 1970, Edmund 1970).As each tooth completes its life cycle, the bone of attachment is actively formedand resorbed. A new tooth sits in reserve in pits within the gum lingual to the oldtooth. Tooth replacement does not appear to occur in response to wear or injury ofindividual teeth. Instead each tooth is replaced as part of a regular wave-likepattern affecting the entire dental arcade (Klaphake 2015, O’Malley 2005, Edmund1970).Boids, pythonids, and colubrids (e.g. corn snake) display a back-to-frontprogression of alternating waves. Some venomous snakes, like viperids andcrotalids, tend to display simple alternate replacement, while in elapids, such as thecobra and coral snake, replacement waves progress from front to back. Thisreplacement rhythm may or may not be synchronous on both sides of the mouth. Ifsynchrony is present, it usually manifests only on the premaxilla
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Thecodont
The thecodont tooth has a relatively long cylindrical base set in a deep bony socket(Fig 1). All mammals exhibit thecodonty, however crocodilians are the only livingreptiles with thecodont dentition (Table 1). Thecodont teeth have deep attachments,allowing teeth to withstand strong forces. Lost teeth can be replaced by a limitednumber of replacement teeth in crocodilians, however the frequency and speed ofreplacement decreases as the animal ages (O’Malley 2005, Mehler 2003, Edmund1970).Traditionally, snake dentition has been described as pleurodont, however snaketeeth have more recently been described as modified thecodont because eachtooth is fused to the rim of a shallow socket
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What are the components of the cloaca
``` Coprodeum •Urodeum •Proctodeum- contains musk glands •Coprourodeal fold •Cloacal water intake •Some chelonian species •Cloacal respiration- Some diving turtles! Reliant on this form of respiration during diving. Underwater hibernation.Accessory air bladders ```
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Female reproductive tract - Squamates (snakes and lizards)
Paired ovaries in mid-caudal coelom •Snakes - located cranial to the kidneys (58-80% SVL) •Lizards – caudal ovarian pole attached to ventromedial kidney •Right ovary more craniad and usually larger •Left ovary may be reduce or absent (some snake spp) •Bilateral oviducts (some missing left) •Mesosalpinx •Seminal receptacles •Oviparous or viviparous •Shell laid down in isthmus •Calcification in oviduct •Cloaca •Tract terminates at urodeum •Hemiclitoris/Hemipenal homologue •Cloacal scent glands (snakes)
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Female reproductive tract - Chelonians
``` Paired ovaries located cranial to the kidneys •Symmetrical ovaries •Left ovary may be reduced or absent •Oviparous •Bilateral oviducts •Infundibulum •Isthmus – non glandular •Uterine tube/Albumin gland- Seminal receptacles. Can store semen for months- years •Shell gland/uterus •Muscular vagina •Mesosalpinx •Clitoris ```
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Describe Reptile ovarian follicles
Immature ovaries •Flat and granular •Mature ovaries •Variable with various stages of maturing follicles •Inactive follicles (previtellogenic)- Small and clear to white, Present for much of the season when ovary inactive •Active follicles (vitellogenic)- Larger, yellow/orange, Ovulate, regress or stasis
184
Describe the Hormonal control of reproduction in reptiles
Melatonin- GnRH •Vitellogenesis and gravidity- Vitellogenesis controlled by pituitary gonadotropins, FSH like hormone in squamates, FSH and LH like hormones in chelonians •Stimulate gonadal activity- Oestrogen from ovaries, Testosterone from testes, Oestrogen >hepatic conversion of stored lipid to vitellogenin •Progesterone- Produced by corpora luteum, Support egg and embryo development •Spermatogenesis- Under pituitary gonadotropin control, Release of steroid hormones as in mammals
185
Describe the Male Reproductive tract - Squamates
Paired asymmetrical Testes •Right testis usually cranial to left •Snakes – Dorsal, 65%-82% SVL •Lizards - Dorsal in mid to caudal coelom •Colour variable, elongated in snakes and legless lizards •Size varies seasonally •Mesorchium attaches to dorsal coelomic wall •Testicular Blood supply- Dorsal aorta>testicular arteries>ductus deferens •Testicular vein >renal vein >post cava •Epididymis-Absent in snakes •Seminiferous tubules Vas deferens- Runs along ventral kidney >urodeum at genital papillae * (Renal) sexual segment- Enlarged when reproductively active * Paired hemipenes- Ventral tail base! Retractor muscles! No urethra or direct connection with ductus deferens, Sulcus spermaticus * Cloaca, Tract terminates at urodeum, Paired Hemipenes, Cloacal scent glands
186
Male reproductive tract - Chelonians
``` •Paired testes Cranial to kidney Can retain sperm in the epididymis for months over winter •Symmetrical •No (renal) sexual segment •Large single phallus Dark, smooth expansile phallus Ventral urodeum and proctodeum No urethra •Tissue becomes engorged •Dorsal longitudinal ridges  seminal groove •Spade shaped glans- Three folds to direct sperm ```
187
Copulation & Fertilisation - Squamates
Brumation- boosts fertility, builds up energy reserves •Specific and elaborate courtship behaviour •Copulation may not coincide with vitellogenesis •Internal fertilisation- •only use Single Hemipene (Squamates)- Movement of sperm from vas deferens to female’s cloaca •Variable duration- Biting •Sperm storage- older sperm has less fertility •Second clutches don’t require second mating •Gestation times hard to estimate
188
Copulation & Fertilisation - Chelonians
•Specific and elaborate courtship behaviour •Aquatic turtles breed in the water •Box turtles and tortoises breed on land •Internal fertilisation •Single phallus Movement of sperm from vas deferens to female’s cloaca Increases dramatically in size to lock into cloaca Plastron concavity of male helps fit •Variable duration •Females can store sperm from several males Clutches may have multiple paternity
189
Reptile kidneys overview
``` Function •Excretion •Water & Salt balance •Acid Base regulation •Hormones •Vitamins •Nephrons-, shorter and fewer in number Glomeruli Bowman capsule Tubules Collecting ducts No loop of Henle Less complex nephrons due to preventing kidney damage in drought No renal pelvis •No medulla/cortex division •Renal portal system ```
190
Describe reptile Renal Physiology
``` Arginine vasotocin (AVT) •Pituitary hormone •Reduces GFR Prolactin •Increases GFR •Water absorption •30-50% filtered water absorbed in proximal tubule (60-80% in mammals) •Distal tubules, colon, cloaca, urinary bladder (if present) Control of K and Na poorly understood •AVT, Aldosterone •Temperature Vitamin C synthesis Vitamin D activation Erythropoietin Blood pressure regulation ```
191
Reptile Nitrogenous waste products
``` •Ammonia (Ammonotelic)- requires water for excrestion, more common inaquatic reptiles than terrestrial which are adapted to desert, Toxic! Soluble Urea (Ureotelic)- can be passed in semi solid state, requiering less water •Less toxic •Less soluble (requires less water) Uric Acid (uricotelic) •Insoluble •Conserves water •Reptiles primarily uricotelic •Post renal modification of urine ```
192
Renal Blood flow in reptiles
Supplied by arterial and portal venous blood •Aorta >Renal arteries •Caudal & Iliac veins >Renal portal vein Drained by renal veins >postcaval vein Low glomerular filtration rates (GFR) Renal portal system •Caudal blood can be diverted to or bypass kidneys •First pass effects Nephrotoxicicty when administering drugs Premature excretion when adminitering drugs
193
Urinary tract- snakes
``` Paired assymetrical kidneys •Right kidney cranial to left •Dorsocaudal coelom (75-96% STV) •Elongated, lobulated kidneys •Kidney length about 10-15% SVL Elongated ureters enter urodeum •Right longer than left •Distinct cloacal opening from genital ducts •Urogenital papilla No urinary bladder Sexually dimorphic kidneys •Sexual segment ```
194
Urinary tract - Lizards
``` Paired, retrocoelomic kidneys •Elongated, lobulated kidneys •Symmetrical •Within or cranial to the pelvis •Sexually dimorphic kidneys in some spp.- Sexual segment Ureters Urinary Bladder •Present in some species •Vestigial bladders •Absent bladder- Colonic urine storage ```
195
Urinary tract - Chelonians
``` Retrocoelomic kidneys •Large, flat lobulated kidneys •Deep to caudodorsal carapace •Adherent to inner carapace •Caudal to acetabulum •Symmetrical Short ureters open into urogenital sinus Urinary Bladder •Largest in terrestrial spp. •Retrograde passage of urine •Urodeum ``` Possible for eggs to passinto bladder Aquatic turtles have smaller thicker bladders
196
Reptile Ultimobranchial gland
``` Secretes calcitonin from C-cells •Embedded in the thyroid in mammals •Separate gland in reptiles •Left sided •Bilateral •Cranial to the heart •Calcium and phosphorus homeostasis •Skeletal remodelling •In tandem with PTH & Vitamin D3 •Elevated serum calcium levels  secretion of calcitonin •Inhibits calcium resorption from bone •Opposes PTH to reduce serum calcium levels ```
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Reptile parathyroid glands
Not closely associate with the thyroid gland •Position variable •May have one or two pairs of glands •Cranial pair near mandibular ramus associated with carotid •Caudal pair associated with aortic arch •Chief cells •Produce and release parathyroid hormone (PTH) •Major role in calcium homeostasis •Vitamin D3 & Calcitonin •Low levels of serum Ca stimualates PTH release •Sites of action •Bones, kidneys, intestines, lymph, dermal skeleton •Nutritional secondary hyperparathyroidism •Renal secondary hyperparathyroidism Tutle crainail parathyroid containded in thymus
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Reptile thyroid gland
``` Important multifunctional hormone •Snakes and chelonians •Single thyroid gland •Lizards •Single, bilobed or paired gland •Position varies with taxa •Ventral to trachea •Near heart base in lizards and chelonians •Cranial to heart base in snakes •Large blood supply •Anatomically distinct from Parathyroid glands •Thyroid physiology similar to other vertebrates •T4, T3 •Iodine required ```
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Reptile pancreas
* Variable location and anatomical relationships * Lizards * Trilobed * Large islets confined to dorsal lobe * Snakes * Simple * Some species have a splenopancreas * Chelonians * Variable splenic ad duodenal association * Smaller islets, diffusely distributed * No segregation of alpha and beta cells in squamates * Glucose regulation * Alpha cells – glucagon Alpha cells •Glucagon  increases blood glucose Beta Cells •Insulin  promotes absorption of glucose lowers blood glucose Delta cells •Somatostatin (GH inhibiting hormone)  regulates insulin & glucagon
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Reptile adrenal glands
``` Chelonians •Retrocoelomic •Symmetrical •Dorsally flattened glands lie against kidney Squamates •Closely adhered to gonads •Asymmetrical •Right gland cranial to left •Incorporated into mesovarium/mesorchium Yellow/red in colour Central ‘cortex’ Peripheral ‘medulla’ Secretions- Catecholamines, Glucocorticoids ```
201
Hibernation and brumation
``` Not true hibernation as thegut must be empty before entering it Hibernation/Brumation normal physiology •Temperate reptiles •Precedes reproduction •Cold temperatures •Thryoid levels drop •Anorexia •Hibernaculi •Areas/nests to provide some protection •Bladder is water source •Intestines should be empty •Emergence triggered by rising temperatures ```
202
Locomotion - Snakes
``` Relatively low in energy expenditure Function of scales Weight distribution Various modes of locomotion Lateral undulation Rectilinear Locomotion Concertina Locomotion Sidewinding (Flying) ```
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Skull - Lizards
``` Head typically narrower than body Kinetic skull Wide gape Fused mandibular symphysis No temporal arch  Braincase Thin vertical interorbital septum  Variation in skulls Bony protruberences Dentition Pleurodont Attached to the sides of the mandible Shed & Replaced throughout life Acrodont Attached to the biting edges of the jaws Not replaced ```
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Skull- Snakes
``` Most kinetic skull of all reptiles No temporal arch No interorbital septum No middle ear cavity No mandibular symphysis All tooth bearing bones can move independently Heavily ossified braincase Loose articulation of quadrate bone ```
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lizrd tail autonomy
``` Many lizard species Predatory escape and/or distraction Vertical fracture plane throughout body Cartilagenous plate Tail is regenerated Cartilagenous rod Rplaces lost vertebrae New tail Small, dark scales, irregulat pattern Shorter, blunter Care with handling, injections & blood sampling ``` in some species its only seen in juviniles before fracture plate ossifies
206
Dentition- Snakes
``` Swallow prey whole Modified pleurodont Six dental arcades Two maxillary Two mandibular Two palatal Fangs Front Fanged- Large, venom gland, Single duct , Rostral, hollow fangs, Modified fangs in vipers, Fold back into sheath Elapids, Vipers ``` Rear fanged- Duvernoy’s Gland Colubrids Grooved caudal fang Fixed Venom-Not all bites evenomate
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Dentition - Lizards
``` Acrodont or pleurodont dentition No sockets Acrodont Teeth fused to the maxillary and mandibular ridges Worn down throughout life Agamids, Chameleons Some agamids have a few rostral pleurodont teeth Pleurodont Teeth sit in grooves on the medial aspect of mandible/maxilla Constantly shed & replaced Iguanas Egg tooth ```
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Oral cavity - Chelonians
``` Keratinised beak Broad, fleshy mobile tongue Unable to extend from mouth Some specialised lingual features Salivary glands Mucus No digestive enzymes Tubular glottis ```
209
what is in the first quarent of the snake
treachea esophagus thyroid heart
210
what is in the second quarent of the snake
right lung left lung liver left air sack
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what is in the third quarent of the snake
``` right air sack stomach gall bladder pancreas gonads ```
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what is in the fourth quarent of the snake
intestines and kidneys
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Upper gastrointestinal tract - Snakes
``` Simple relatively short GIT Oesophagus- Long & thin walled Distensible Can assist in food storage Stomach- Difficult to differentiate from oesophagus & duodenum More glandular mucosa No well defined cardiac sphincter Storage and early digestion Capable of rapid drops in pH ```
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traid- snakes
``` Pancreas Ovoid- Caudal to bladder on duodenal mesenteric border Some species have a splenopancreas Gallbladder- Multiple bile ducts Spleen ```
215
how many lobes does the snak liver have
2-3
216
Lower gastrointestinal tract - Snakes
Intestines straight & relatively uncoiled Small intestine Empties into colon- Colon - Small caecum present at proximal colon- Only in boas and pythons Empties into Coprodeum (cloaca) Colon and cloaca important for water conservation Fat bodies- Present within the coelom Larger with increasing body condition
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Gastrointestinal Tract - Lizards
``` Oesophagus- Short, thin walled Enters stomach on left of coelom Stomach - Simple tubular/C shaped Fundic region Parspylorica region Rugae- seen in some Carnivores & Insectivores ``` ``` Herbivores- Hindgut fermenters Rely on high ambient temperatures Very slow gut transit time Short small intestine Large intestine – long/large Caecum- Right caudal coelom Colon- Sacculations,Microbial flora, Some lizards have increasing sacculations with age ``` ``` Pancreas- Trilobed Elongated structure Lies along mesenteric duodenal border Liver- Encapsulated, bilobed organ Right lobe larger Gall bladder- Usually associated with right hepatic lobe Bile storage Fat digestion Coelomic fat pads- Can be very large ```
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Upper gastrointestinal tract - Chelonians
``` Oesophagus- Ciliated/papilla Stomach- Ventral left side Caudal to liver Gastroesophageal sphincter – Left Pyloric Sphincter – Central Digestive enzymes- Stomach, small intestine pancreas Bile- Produced in liver Stored in gall bladder ```
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Lower gastrointestinal tract - Chelonians
Liver bilobed- Gall bladder in right lobe Intestines in caudal coelomic cavity Small intestine- Short No clear divide between duodenum, jejunum, ileum Joins large intestine at ileocolic valve Large intestine- Primary site of microbial fermentation in herbivores Caecum- Right caudal coelom ,not well developed, no mesenteric attachments, Ascending, transverse & descending colon, Mesenteric attachments, Coprodeum (cloaca), Colon termination Pancreas- Empties into pylorus via short duct Alkaline buffer to neutralise stomach acid in duodenum High levels of tissue amylase and lipase ``` Liver- Large ventral dark red/brown liver Pale yellow/tan colour Hepatic lipidosis or vitellogenesis in females 2 major lobes Gallbladder sits on the right Indentations for heart and stomach GI Transit time variable Temperature key ```
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General cardiovascular anatomy of non crocidillians
Pericardium 3 chambered heart (2 atria + 1 ventricle) Muscle ridges inside ventricle and AV valves prevent blood mixing Sinus venosus – large chamber dorsal to RA; receives venous blood; Right atrium Left atrium – receives arterial blood Ventricle – 3 subdivisions: Cavum pulmonale → Pulmonary Artery Cavum venosum ← R Atrium Cavum arteriosum ← L Atrium
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Renal Portal system | of reptiles
Blood from caudal 1/3 body can be directed to kidneys OR general circulation Can affect drug metabolization, excretion or allow nephrotoxic effects Not very clinical significant
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Hepatic portal system of reptiles
Blood from caudal ½ body AND gut always go through the liver before general circulation Can affect drug metabolization, excretion or allow hepatotoxic effects Clinically significant Reduces bioavailability of oral drugs
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Temperature and cardiovascular function in reptiles
``` HR depends on Temperature, species, size, metabolic rate, RR Increase of Environmental Temp: Cutaneous vasodilation BP reduces + HR increases L to R heart shunt Warmed blood returns and increases core body temperature Reduction of Environmental Temp: Cutaneous vasoconstriction Blood pooled in muscles keeps body heat HR reduces ```
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Locating reptiles heart
Most species: cranial coelomic cavity Monitor lizards: more caudal Snakes: 1/3 cranial part of coelom, location depends on species Heart auscultation is unrewarding HR can be determined with a doppler probe: Different heart position Affected by temperature
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Vascular access in reptiles
``` Blood collection: Done routinely in clinical practice Vessels not usually visible (landmarks) Collection site depend on species Plan to collect 0.5 – 1% patient’s b.w. (g) ``` IV administration: Occasionally performed (e.g. anaesthesia induction) Challenging to place IV catheters (except in some Chelonians) IO route preferred over IV Lizards- ventral tail vein- preffered Ventral abdominal vein External jugular Snakes- Ventral tail vein – medium to large species Intra-cardiac – ideally US guided Palatinal veins – large species ``` Chelonia- External jugular (Right) Sub-carapacial venous sinus Occipital venous sinus –terrapins Dorsal tail vein – large species, risk of hemodilution Cephalic vein – large species ```
226
describe the resperatory system of chelonians
Glottis – base of the tongue Short trachea with complete rings Gular movements (olfactory) – not RR! ``` Lungs: Dorsal sac-like structures Lack alveoli (have flaveoli) ``` ``` Breathing: Insp/exp are active processes No intercostal muscles Ribs fused with shell 2 paired antagonistic abdominal muscles Horizontal septum ``` Additional respiratory exchanges: Skin – some aquatic turtles Oropharyngeal mucosa
227
describe the resperitory system of lizards
Glottis at the base of tongue Trachea with incomplete rings Caudal part of lungs function as air sacs Ventilation: Active ins/exp Mainly intercostal muscles Smooth muscle on lungs (some sps.) Monitor lizards have a non-functional diaphragm Some Chameleons with accessory ventral lung
228
describe the resperatory system of snakes
Glottis rostral Trachea with incomplete tracheal rings Tracheal lung (dorsal): Some species Allows gas exchange while swallowing large prey Left lung small (Boids) or absent (all other species) Caudal part of lungs function as air sacs
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Assessing respiratory function in reptiles
``` Upper respiratory tract: Check for nasal discharge Lower respiratory tract: Assess breathing pattern (e.g. open mouth breathing) RR – direct visualization Check for tracheal discharge Auscultation is unrewarding Consider ancillary tests (e.g. radiography) ```
230
describe the skeletal system of ferrets
``` similar to dogs and cats 15 ribs c7, t15, l5, s3, cd18 posses a clavcal non retractible claws plantigrades ```
231
describe the musculature of ferrets
similar to dogs sub cut: scruff IM: biceps femoris ( be careful of ishiatic nerve), epaxial lumbar musculature im done in smakk volumes
232
describe the skeletal system of hedghogs
similar to dogs and cats- same no. of vertebrae 5 digits in front 4 in back plantigrade c7, t13, s3, cd variable
233
describe the musculature of hedghogs
orbicularis muscle sits atop IM injection sites subcut in spiny or furres areas IM in tricepts, quadrecepts, gluteals or obicularis
234
describe the skeletal system of rats
C7, T13, l5, s3, cd vairable but higher than cats and dogs bone ossifies later in life have a clavicle- musch more present than cats and ferrets 5 toes on front limb but one is vestigal 5 digits in back limb no gall bladder like horses
235
describe the musculature of rats
large masseter sub cut between shoulder blades IM: epiaxial musculature, high risk of ishiatic nerve in quads- nerve damage may cuse rats to self mutilate no sweat glands
236
describe the skeletal structure of marsupials
ossa marsupiala- extr bone, extention of pubic bone, not sure of function- sugar gliders have none or is very small bi pedal hopping long HL
237
describe the digits of a sugar gliner
membrane goea from 5th digit of forelimb to metatarsals of hind limb syndactylous- hl second and thirddigit fused
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describe the injection sites of sugar gliders
sub cut: intrascapular area | IM: triceps
239
ferret eye anatomy
large cornea, spherical lens, and a tapetum lucidum that is highly receptive to dim light, all of which make the ferret well-adapted to nocturnal living. Dorsal and ventral nasolacrimal puncta are present, although the dorsal punctum is smaller. There is a well-developed nictitating membrane which can be used for ulcer treatment as a third eyelid flap. The cornea is relatively large in relation to the eye structure and the lens is nearly spherical and placed back in the posterior eye chamber The pupil is a horizontal elliptical slit The tapetum is well defined with a 7-10 cell layer, the structure being the same in both pigmented and albino ferrets The myelinated optic disk is relatively small. The retina is similar in form and vascular pattern (holangiotic) to that found in the dog. The ferret retina has a high proportion of rods in the photoreceptor layer that are particularly sensitive to low-intensity light, and predominate the cones in the ratio 50-60:1. Ferrets have a retrobulbar venous plexus that is similar to that of rodents which has been suggested as a site for blood collection.
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ferret ear anatomy
physiologically similar to that of the cat, but it is thought auditory response in the ferret is more primitive. The external ear consists of a pinna and an external ear canal, which differs markedly in shape from that in the dog and cat. The ferret pinna is set close to the head and half-moon shaped, some 2 cm wide in adult hobs and pointing forward, as is compatible with a hunting animal. There is no distinct tubular ear canal as in the dog and cat. The whole ear canal is protected by a screen of fine hairs around the anterior margin. The relatively large tympanic bullae indicate excellent hearing. The lateral margin of the ear canal has a more pronounced recession, intertragal notch, which is more tube-shaped than seen in the cat and some 5 mm long. Almost opposite, medial to the base of the intertragic incisure, is the opening of the horizontal canal, which passes anteriomedially to the tympanic membrane. The structure of the middle and inner ear is similar to that in the dog. The inner ear may show idiopathic otitis internal (IOI) with head tilting, and loss of balance due to extensive middle ear infections or blood-borne pathogens.
241
ferret olfactory system
The ferret's sense of smell ranks in importance with its sense of hearing and scenting another animal’s presence and following the scent of prey is important to all mustelids. The pointed, short face of the ferret has a tapering nasal organ. The nasal cavity is formed by the maxilla and nasal bones dorsally and laterally, with the maxillary and palatine bones supplying the cavity floor, similar in shape to the long-nosed dog. The bony nasal aperture is composed of two symmetrical halves. Ferrets have an elaborate nasal turbinate system like other carnivores and may assist in providing increased surface area for olfactory receptors. The ethmoid plate in the ferret does not completely pass ventrally to the cartilage of the nasal septum to divide the nasal fossa as it does in the dog, thus it is more difficult to pass a nasal tube in the ferret, but it is not impossible. The closeness of the cribriform plate to the brain meninges can be an entry to such pathogenic fungi as Cryptococcus neoformans, leading to acute meningitis in the ferret. The vomeronasal organ is well developed.
242
rat eye anatomy
The eyes are black (except in albinos), are placed laterally, are spherical in shape and there is frequent blinking. Although it can see through 360 degrees the rat has a blind spot in front of its nose. The cornea is large, and the large lens is round, with little power of accommodation. Although the rat does not move its eye, the ocular muscles are quite well developed. The third eyelid is poorly formed, giving the eyes a bulging appearance. The uveal tissues of albino rodents, like other parts of their bodies, have no pigment which gives a bright red semi-transparent appearance when illuminated by ophthalmic instruments. Mice and rats have a rod-dominated holangiotic retina with arterioles and venules that radiate from the optic disc like spokes on a bicycle wheel. The optic nerve head of mice and rats often appears small and cupped because optic nerve fibres do not become myelinated until after leaving the eye. Rats have an orbital plexus formed by deep orbital veins - in contrast, mice have a large dilated channel, a venous sinus.
243
glands assosiated with the eye in rats
Mice and rats have three lacrimal structures, the intraorbital gland, the extraorbital gland and the Harderian gland. The intraorbital gland is located deep in the retrobulbar space. The extraorbital gland is located near the base of the masseter muscle and commonly has been misinterpreted as a neoplasm because of its unusual location. The two lacrimal ducts open at the puncta located at the medial canthus of the eye and these join to form nasolacrimal duct, which opens just caudal to the nostril in the vestibule. harderian gland- This gland secretes lipids and a porphyrin red pigment which fluoresces under ultraviolet light. These secretions play a role in ocular lubrication and pheromone behavior and are spread over the skin during grooming. The most common abnormality associated with the lacrimal structure of mice and rats is dacryoadenitis or inflammation of the Harderian gland. The gland hypersecretes when the animal is stressed, creating a red-brown deposit around the eyes and nose known as chromodacryorrhoea which can be mistaken for blood. A useful way to tell blood from porphyrin is the fact that porphyrin glows pink under UV light, whereas blood does not. Porphyrins are irritant, which can result in rubbing of the face, self-trauma and secondary infection. The underlying cause should be investigated and treated appropriately.
244
ear anatomy in rats
Rats are less sensitive than humans to noises below 1000Hz so will be less affected by noises like air conditioning. Ears - the pinna is covered by thin, short hairs. The tympanic cavity is large, as in most rodents. A gland called the zymbal gland lies at the ear base (see integument notes).
245
olfactory system in rats
The olfactory lobes of the brain are large and over 50% of the nasal cavity is lined by olfactory epithelium, giving rats their acute sense of smell. Rats, like all rodents, use their scent glands, faeces, urine, and vaginal secretions for olfactory communication. Rats, are obligate nose breathers and rely on healthy nares not only for respiration but also for olfaction and feeding, hence, the rapid debilitating effects of respiratory disease.
246
eye anaotmy in hamsters
Being nocturnal, vision is less important than hearing, olfaction, and sensation, however the hamster has a panoramic field of vision, long streak-shaped specialization areas in the retina, an obvious area centralis or fovea and a large binocular visual field. A large orbital venous sinus is present, and this has been used for blood sampling in laboratory animals. Marked sexual dimorphism of the Harderian gland has been described in Syrian hamsters but not other species of hamsters. The dimorphism is androgen-dependent, with female hamsters secreting 100–1000 times more porphyrin than males and containing a different lipid profile. Ocular prolapse – when restraining a hamster by scruffing, it is important to ensure that excessive pressure is not applied around the eyes, which may potentially result in ocular prolapse.
247
ear anatomy in hamsters
hamsters have large tympanic bullae giving them a keen sense of hearing. Sensitive vibrissae are the main channel for somatic sensory input and are important for spatial orientation and communication as they are in many species. The hamster is unique in that it moves its cranial vibrissae in various complex patterns keyed to particular exploratory situations. This movement repertoire suggests that a precisely operating motor system controls the vibrissae
248
olfactory system in hamsters
The hamster has several nasal serous glands which open into the internal ostium of the external nares, nasal glands with mucus components and the vomeronasal (Jacobson's) gland. The vomeronasal organ is a sensory organ that is found in most terrestrial vertebrates and that is principally implicated in the detection of pheromones. The vomeronasal organ is a 7 mm long tubular structure that is located bilaterally in the rostroventral nasal septum and completely enclosed in a bony capsule. The cranial end communicates with the nasal cavity through a rostral orifice. The organ plays a role in pheromone behaviour as well as olfaction – it has been shown in the hamster that removal of the main and accessory olfactory bulbs completely removes sexual behaviour
249
integrument of ferrets
Normal ferret skin has a compound hair follicle arrangement composed of one primary hair and a collection of secondary hairs with a primary to secondary ratio of 1/5 - 1/15 - the secondary hairs increasing in number with the ferret’s age until maturity. All hairs emerge through the same follicle outlet of the skin surface and associated with each primary follicle is an arrector pili muscle, a multilobular sebaceous gland, and a coiled tubular sweat gland (secondary hairs lack these features). Moulting, which usually occurs twice a year, appears to be controlled by hormones responsive to changes in the photoperiod thus oestrogens cause hair and weight loss in ferrets. This moult may result in bilaterally symmetric alopecia of the tail, perineum and inguinal area, or the ferret may lose most of the guard hairs and appear “fluffy.” As the hair thins, red-brown waxy deposits, often sebaceous secretions, may be visible on the skin. Hair that is shaved, for example for surgery, during seasonal hair loss may not regrow for several weeks or months and hair regrowth sometimes imparts a bluish appearance to the skin, which may be mistaken for bruising or cyanosis The thick skin and muscle found on the neck and shoulders of a ferret protect it from trauma during fighting and mating, however the thick skin can make venepuncture and subcutaneous injections difficult. The skin contains numerous sebaceous glands which are under androgenic control with secretions increasing during the breeding season. Sebaceous secretions can cause the hair coat to have a greasy feel and produce the characteristic musky odour. Secretions may be so profuse that intact male albino ferrets can appear yellow and dirty. Owners will sometimes bathe ferrets to remove this “dirty appearance” and to reduce odour, but frequent bathing can remove essential oils from the skin and result in pruritus and keratinopathies. Ferrets are fastidious groomers, and so frequent bathing is not necessary. Ferrets originate from dry, temperate climates and can suffer from warm temperatures and damp. They have epitrichial (apocrine) sweat glands on the body and atrichial (eccrine) sweat glands on the footpads. However, their thick fur prevents significant body cooling by evaporation, making them susceptible to hyperthermia, heatstroke and dehydration. Ferrets possess a pair of well-developed anal glands, as do all mustelids. These glands produce a serous yellow liquid with a strong odour. Ferrets that are frightened or threatened can express their anal glands but, unlike skunks, are unable to project the fluid over long distances. These glands rarely become impacted, but if it occurs the treatment is the same as for other species. neutering decreses odour
250
hedghog integrument
The crown and dorsum (collectively called the mantel) are covered in a dense coat of several thousand smooth spines. Each spine has a round basal bulb that firmly attaches it within the follicle, while a more narrowed portion at the skin surface allows each spine to bend when force is applied. Healthy spines are difficult to pull from the follicle without breaking at this narrowed portion. Hedgehog spines are composed of keratin and have a complex internal structure that confers lightness, strength, and elasticity. Hair and sebaceous glands are absent in the spiny skin. The epidermis in this area is thin, and there is a thick fibrous dermal layer that contains significant layer of fat and few blood vessels. Hedgehog spines are naturally impact resistant - in the wild, hedgehogs will climb trees and plants in search of food and will often fall from significant heights. A falling hedgehog rolls into a ball and uses its dorsal muscles to erect its spines before impacting the ground which allows the animal to survive the impact unharmed due to the shock-absorbing capabilities of its spines, which buckle under load. Spines are absent from the midline of the crown, and hair on the feet and muzzle is sparse to absent. The haired skin and the soles of the feet are rich in sweat and sebaceous glands. The toenails are round in cross section and are highly curved.
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integrument of rats
Rat hair is divided into guard hairs and undercoat. Aged male rats develop brown, granular sebaceous secretions at the base of their hair shafts, which some owners may mistake for ectoparasitism. The tail becomes more dry and scaly with age. Vibrissae - the rat has tactile vibrissae which are essential for the animal's orientation - they have sensory bulbs at their base, and an extensive nerve and blood supply. There are 50 to 60 vibrissae located on each side of the upper lip and nose in 8 to 10 rows and they are innervated by the infraorbital nerve. Smaller tactile hairs are also found on the lower lip, chin, and upper eyelid Sebaceous glands - found around the hair follicles with modified sebaceous glands found in the region of the oral commisure, the anus and prepuce, and around the teats. Sweat glands - only found around the footpad which function not for evaporative cooling but for maintaining adhesive friction between the foot and surfaces. Having few sweat glands and, being unable to pant, rats have poor heat tolerance. They do not increase their water intake at high ambient temperatures but instead try to cool down by increasing salivation and seeking shade. Death occurs at temperatures over 37° C. The tail and ear are very important for heat dispersion, with blood vessels vasoconstricting and dilating according to ambient temperatures. Adult brown rats have good tolerance to cold and can adapt extremely well to cold climates by laying down brown fat within 3 or 4 weeks. The preferred ambient temperature range for captive rats is 18-26° C and with a relative humidity of 40-70%. Scent glands - rats have no specialized scent glands but produce pheromones through urine, faeces, milk, and skin - these affect reproductive behaviour, dominance, and territorial behaviour. Zymbal's gland - large modified sebaceous glands that surround the base of the ear.
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hamster integrument
Hamster fur is soft and smooth, and the ears are bald and grey. Around the neck region the skin is very loosely attached and capable of extensive stretching. There is soft underfur and this is covered by longer and thicker guard hairs. The hair is sparse on the feet and tail and there are fine hairs on the pinnae. Cranial sensitive vibrissae are essential for orientation, particularly in nocturnal mammals. Hamsters have large, potentially reversible cheek pouches that are paired muscular sacs extending as far back as the scapula. The pouches are evaginations of the oral mucosa and are used for transporting food, bedding material, and occasionally young. Cheek pouches can develop abscesses and tumours and also can be subject to eversion and impaction. Golden hamsters have distinctive hip or flank glands that have short sparse hairs, often darkly coloured. Found bilaterally along the lumbar area, the glands are androgen dependent they are poorly developed in the female, but in the mature male they are prominent and become wet and matted during sexual excitement. May play a role in lipogenesis, hair and flank gland growth. Occasionally these glands can become inflamed, swollen and crusted.
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Rodent –Myomorph–Dental Formula
1003/1003 | Cheeks drawn in across diastema•Can gnaw for long periods without wearing molars or swallowing debris
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describe the myomorph rodent stomach
Monogastric•Divided into two parts–Non-glandular forestomach•pH is higher than in the glandular stomach•Small amount of fermentation occurs here –Glandular •Similar to other monogastricstomachs•Chief and parietal cells–Separated by a ‘limiting ridge’•Food does not mix between compartments•Spleen attached over the greater curvature
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describe the myomorph rodent intestines
Small intestine –Makes up the largest component of intestines–Long mesentery attachment–Jejunum usually 2-2.5 X the length of the duodenum–Varying length overall depending on species Large intestine –Caecum •Comma shaped•Base, body and apex (appendix)•Body thin walled•Base and apex –lymphoid rich•Sacculatedin most rodent species (not in rats)–Colon•Ascending, transverse and descending•Similar terminology as in dogs and cats•Formed faecalpellets–Rectum•Distally sebaceous glands (“anal glands”) help to scent the faeces
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describe the myomorph rodent liver
Standard is 4 liver lobes•Left lateral lobe•Left medial lobe•Middle lobe•Right lobe Gallbladder–As with dog and cat–Exception -Rats = no gallbladder
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describet tthe myomorph rodent pancreas
Well defined–Varying colours(species variations) e.g. rat –white/grey, hamsters white/yellow
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Ferret –Dentition
ypical Carnivore Dentition–Deciduous teeth•Erupt at 3-4 weeks•30 teeth•Very sharp–Adult/permanent teeth•Start erupting at 50-55 days •All present by 11-12 weeks•34 teeth 3131/3132
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descriebe the ferret esophagus and stomach
Oesophagus–Similar to cats and dogs–Ferrets are able to vomit, therefore fasting prior to an anaestheticprocedure is required to reduce the risks of aspiration pneumonia, secondary to regurgitation/vomiting •Stomach–Simple, monogastricstomach–Prone to gastric ulcerations –Helicobacterinfections–Ferrets can engorge when eating and the stomach is able to accommodate this with good ‘stretching’ properties
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describe the ferret intestines
Short’ start and end–Duodenum -10cm length approximately–Ill-defined junction between jejunum and ileum •150-160cm length approximately–Large intestine -10cm length approximately•No caecum•Small intestine (ileum) enters into colon –No ileocolonicvalve–Anatomically appear the same (grossly)–At surgery differentiate by blood supply•Jejunalartery anastomoses with the iliac artery•Paired scent glands at the external sphincter of the anus–‘Musky’ odour–Descentingperformed in the US not the UK
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describe the ferret liver
Sits in the curvature of the diaphragm–5 Lobes:•Right lateral•Right medial •Quadrate central lobe–‘Hides’ the gallbladder•Left lateral •Left medial
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descriebt eh ferret pancreas
Lies parallel to the duodenum–Well defined–Lobulated, irregular appearance–Pale pink/red colour – prone to Insulinomas
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African Pygmy Hedgehog –Dentition
36 teeth | 3133/2123
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Sugar Glider -Dentition
3134/1-2,034 Diprotodont•Meaning ‘two front teeth’•Marsupial•Pair of large procumbent incisors on the lower jaw•Ability to retract the gums to expose more of the teeth Closed rooted teeth•Do NOT constantly grow•Do NOT chew for behaviour enrichment•Unlike rodents•Teeth function:•‘scoop out’ fruit •pry open bark
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descrieb the intestines of a sugar glider
Small Intestines–Approximately 3X the length of the large intestine–Brunner’s glands are located distal to the pylorus in the submucosa of the duodenum and drain directly into the duodenal lumen•Secrete alkaline fluid and mucus•Large Intestines–They are hindgut fermenters and possess a well-developed caecum –Utilize bacterial fermentation to break down dietary products e.g. gum from the acacia tree–The mesenteric attachments to the colon are loose
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descrieb the intestines of a sugar glider
Small Intestines–Approximately 3X the length of the large intestine–Brunner’s glands are located distal to the pylorus in the submucosa of the duodenum and drain directly into the duodenal lumen•Secrete alkaline fluid and mucus•Large Intestines–They are hindgut fermenters and possess a well-developed caecum –Utilize bacterial fermentation to break down dietary products e.g. gum from the acacia tree–The mesenteric attachments to the colon are loose
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apterylae
one of the spaces between the feather tracts of birds abouve the jugular
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tomial tooth
Falcon beaks are equipped with a tomial tooth, a sharp triangular-shaped ridge on the outer edges of the upper mandible. They use this to kill prey quickly by biting their necks and severing the vertebrae. Other raptors need a bit more than just their beaks and feet to help them get the food they need.
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fox dental formula
3142/3143= 42
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badger dental formula
3141/3142 =38
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hedgehog dental formula
3133/2123 =36
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rabbit/hare dental formula
1033/1023 =28
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squirrel dental formula
1023/1013 =22
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otter dental formula
3141/3132 =36
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deer dental formula
0033/3133 =32
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ferret reproductive anatomy
induced ovulators- fertilisation 12 hours after ovulation, 42-52 hours after mating long day seasonally polyoestrus breeders remain in oestrus if not mated suseptible to oestrogen assosiated anemia if not mated
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myomorph rodents reproduction
bicornate uterus- seperate urinary and vaginal openings 5-6 pairs of mamary glands males do not have nipples
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sugar gliders reproduction
4 teats cloaca seasonally polyoestrus pouch for young
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Sub-metacentric
Centromere is just off center in Chromosome
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Acrocentric
Most chromosomes in Dogs are acrocentric | Centromere are very off center
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Metacentric
Centromere is in the center of chromososme
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aneuploidy
Ank abnormal number of chromosomes associates with physical or mental abnormalities
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Euploidy
an exact multiple of the haploid (n) chromosome number As oposed to triploidy or tetraploidy Assosiated with spontaneous abortion
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Aneuploidy
Any other abnomal number of chromosomes thats not an exact multiple eg downs syndrome in humans
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Monosomy
Monosomy for an entire chromosome is almost always lethal; an important exception is monosomy for the X chromosome, as seen in Turner syndrome- only one X chromosome Known as a mosaque karyotype Effects fertility as gametes with no genetic info are produced
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Deletion
A break in a chromosome results in deleted genetic material
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Duplication
A duplication on genetic material
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Inversion
A break in the chromosome causes reinserted and reordered genetic material
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Translocation
Genetic material from one chromosome attaches to another
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Robertsonian translocation
Most common form of translocation Breakage and rejoining in acrocentric chromosomes results in a long chromosome and a fragmet which is lost, reducing the number of chromosomes. Does not always result in health conditions
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Breifly describe the cell cycle checkpoints
G1 Checkpoint: Rest or divide? S Checkpoint: DNA OK? G2 Checkpoint: Fully equipped? M Checkpoint: Is everyone lined up?
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Lysosomal storage diseases
``` Build up of substrate will interfere with cellular function Clinical signs include: • failure to thrive • incoordination and balance issues • exercise intolerance • abnormal vision • fainting • seizures ``` Ceroid lipofuscinosis: Missing enzyme that breaks down lipofuscin • Accumulates in nerve cells, liver, kidneys and spleen • Progressive permanent loss of motor function • Decreased vision, dementia, seizures, balance problems • Affects border collies, Border Collies, Chihuahuas, Cocker Spaniels, Dachshunds, English Setters, & Salukis
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Autosomal recessive
Individual must receive two copies of the abnormal (recessive) gene • Asymptomatic carrier parents • 25% probability of offspring being affected • Breeding to remove from gene pool Myoclonic epilepsy in Rhodesian ridgebacks due to defective DIRAS1 gene One trait, 2 alleles A = dominant normal allele a = recessive abnormal allele There are five hallmarks of autosomal recessive inheritance: • Males and females are equally likely to be affected. • On average, the recurrence risk to the unborn sibling of an affected individual is 1/4. • It misses generations • Parents of affected offspring may be related. The rarer the trait in the general population, the more likely a consanguineous mating is involved. • The trait may appear as an isolated (sporadic) event in small sibships.
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Autosomal dominant
One trait, 2 alleles A = dominant abnormal allele a = recessive normal allele Hallmarks of autosomal dominant inheritance 1. Every affected individual has an affected biological parent. There is no skipping of generations. 2. Males and females equally likely to inherit the mutant allele and be affected. The recurrence risk of each offspring of an affected parent is 0.5 3. Normal siblings of affected individuals do not transmit the trait to their offspring 4. The defective product of the gene is usually a structural protein, not an enzyme. • structural proteins are usually defective when one of the allelic products is non-functional; • enzymes usually require both allelic products to be non-functional to produce a mutant phenotype. Polycystic kidney disease (PKD) in Persian cats
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hemizygous
Males are always hemizygous for X linked traits, that is, they can never be heterozygotes or homozygotes. They are never carriers. A single dose of a mutant allele will produce a mutant phenotype in the male, whether the mutation is dominant or recessive
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Sex linkage
When the locus for a gene for a particular trait or disease lies on the X chromosome, the disease is said to be X-linked • The inheritance pattern for X-linked inheritance differs from autosomal inheritance only because the X chromosome has no homologous chromosome in the male, the male has an X and a Y chromosome • Very few genes have been discovered on the Y chromosome. • The inheritance pattern follows the pattern of segregation of the X and Y chromosomes in meiosis and fertilization • A male child always gets his X from one of his mother's two X's and his Y chromosome from his father. X-linked genes are never passed from father to son • A female child always gets the father's X chromosome and one of the two X's of the mother. An affected female must have an affected father Males are always hemizygous for X linked traits, that is, they can never be heterozygotes or homozygotes. They are never carriers. A single dose of a mutant allele will produce a mutant phenotype in the male, whether the mutation is dominant or recessive • On the other hand, females must be either homozygous for the normal allele, heterozygous, or homozygous for the mutant allele, just as they are for autosomal loci. Males get their X from their mother • Fathers pass their X to daughters only • Females express it only if they get a copy from both parents. • Expressed in males if present • Recessive in females
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X-linked dominant (XD)
Mothers pass their X’s to both sons and daughters • Fathers pass their X to daughters only. • Normal outsider rule for dominant pedigrees for females, but for sex-linked traits remember that males are hemizygous and express whichever gene is on their X. • X D = dominant mutant allele • X d = recessive normal allele
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Genetic mosaicism
One individual has two or more populations of cells with different genotypes The sooner the mutation happens in developmet the bigger potentail fpr more cells to posses the trait in question
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mutation
A mutation is a permanent and heritable change or disruption in the base sequence of the genome Nucleotides are added one by one during DNA replication Mistakes made every 1 in 10⁵ pairings Proofreading increases accuracy to 1 in 10⁷ pairings
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mismatch repair
Post-replication mismatch repair further improves accuracy of dna replication it occurs when a mismathc is deteted in newly synthesised DNA the new DNA is cut and the mispaired nucleatide and its neighbours are removed and then replaced with the correct nuclueotide by DNA polymerase DNA ligase seals the gap
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Sequence mutations
substitution, insertion or deletion | Alters sequence of bases within gene
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Open reading frames
section of DNA or RNA that runs from START codon to STOP codon ORF is read in triplets of bases (codons) from START codon onwards
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DNA mutation - substitution
One base in the DNA sequence changed to another base - Transcript affected too Missense mutation = mutated codon calls for incorrect amino acid. Nonsense mutation = mutated codon is now a stop codon. Silent mutation = amino acid sequence not affected Due to redundancy of code
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Missense mutation
= mutated codon calls for incorrect amino acid.
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Nonsense mutation
mutated codon is now a stop codon.
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Silent mutation
amino acid sequence not affected | Due to redundancy of code
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DNA mutation – insertion/deletion
Inappropriate number of bases in a DNA sequence following mutation Affects entire reading frame of 3-letter codons after the point of change Frameshift mutation Potential catastrophic change in functionality of protein
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describe the mutation involved in Canine haemophilia B
Substitution of A for G at nucleotide 1477 Results in glycine instead of glutamic acid at position 379 Found in over 25 breeds of dog Milder than haemophilia A Sex-linked recessive trait Dogs should not be used for breeding
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give some conditions caused by missense DNA mutation
Bovine leukocyte adhesion deficiency (BLAD)- marked neutrophilia leucocytes cannot migrate into blood also seen in irish setters single point missesnse mutation anmals tend to die young Hyperkalaemic periodic paralysis (HYPP) results in paralysis due to disruption of sodium ion channel adenine to gaunine substitution increses potassium in blood porcine stress syndrome- death, inability to walk, blanched apearence of carcus Missense mutation in ryanodine receptor gene X-linked tremours- shaking puppy syndrome Missense mutation in ryanodine receptor gene progressive fatal condition
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give examples of conditions caused by nonsense mutation
Hereditary goitre in Afrikander cattle- Nonsense mutation in thyroglobulin gene effects some goats Bovine citrullinemia in Holstein-Friesian cattle- Nonsense mutation in argininosuccinate synthetase gene effects urea cycle- build up of amonia in blood lethal early in post natal period Deficiency of uridine monophosphate synthase (DUMPS Hypotrophic axonopathy in quail Maple syrup urine disease- in cattle Nanomelia- chickens connective tissue disorder
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Mutagens
A substance or agent that causes DNA impairment that results in the alteration of the DNA sequence ``` Radiation: UV light, x-rays etc. Directly damage DNA or nucleotides Induce cross-linking Break chromosomes Break DNA strands Delete bases Nucleotide dimers ``` Chemical agents: Base analogs – structurally similar to nucleotides so get incorporated into DNA Base altering agents – induce methylation, alkylation, deamination of DNA bases Intercalating agents – similar structure to base pair heterocyclic ring Biological agents: Transposons and insertion sequences Viruses Bacteria Physical, chemical and biological mutagens increase incidence above spontaneous level Not all damage/impairments are mutations DNA repair (polymerase) will fix the majority
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Somatic mutations:
Occur in the non-reproductive cells (somatic cells) May not be manifested to affect an individual due to the reparative and compensative processes of the body. Somatic mutation that alters the cell division patterns of the cell can eventually result in the formation of cancerous cells or tissue
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Germ-line mutations
Occur in gametes or in the reproductive cells that produce gametes Mutations are inheritable Transferred to the next progeny in all their cells
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teratogen
agents that can induce an effect on a fetus in eutero withot effect to the mother
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Inborn errors of metabolism
Cellular metabolism comprises hundreds of enzymatic pathways with many steps Each step requires an enzyme or other protein with a particular function Each step is part of a cascade, inhibition etc. Non-functional protein stops the pathway Often results in accumulation of a product Product can have toxic effects
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mendelian disorder
a type of genetic disorder primarily resulting due to alterations in one gene or as a result of abnormalities in the genome.
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Citrullinemia
Clinical signs begin at 1 to 4 days ``` Apparent blindness Depression Head pressing Convulsions Terminal coma Death by 1 week ``` Meningitis, hypoglycaemia and sodium ion toxicity should be ruled out Urea cycle converts toxic ammonia to urea Each step carried out by specific enzyme Occurs primarily in the liver Urea excreted via kidneys Argininosuccinate synthetase (ASS) converts citrulline to argininosuccinate Comparison of ASS gene in affected and normal animals shows single base substitution Substitution of T for C in the first position of the 86th triplet codon CGA (arginine) becomes TGA (STOP) Polypeptide terminated at the 85th amino acid Biochemical detection of carrier status All heterozygotes have 50% ASS activity compared to normal animals Affected individuals have 0 ASS activity
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Ehlers-Danlos syndrome
Born with easily extendible or very fragile skin Ehlers-Danlos / dermatosparaxis / cutaneous asthenia Slight scratch can cause severe lacerations Collagen fibres formed from triple-helix pro-collagen Pro-collagen requires enzymatic modification to form mature functioning collagen More than one type of collagen Collagen one contains α-1 chains (x2) and α-2 chains (x1) Both are coded for by separate genes Type-1 procollagen becomes type-1 collagen through removal of terminal amino acids Mutations can occur in any of these genes: α-1 procollagen chain α-2 procollagen chain Procollagen I mutations in these genes are dominant disorders carboxy-proteinase (PCP-C-I) endopeptidase Procollagen I aminoproteinase (PCP-N-I) endopeptidase- THIS IS THE ONE THAT MUTATES IN CATLE AND SHEEP- recesive inherited disorder heterozygous effected animals still have enough enzyme Mutation in any of these will lead to the clinical symptoms of stretchy and fragile skin Genetically heterogeneiic ``` Dominant form in: Horses Cats Dogs Rabbit Recessive form in: Sheep Cattle ```
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Genetic heterogeneity
If a specific set of clinical signs arises from more than one mutation, there is genetic heterogeneity for that disorder If genetic heterogeneity is undetected it can be difficult to establish the form of inheritance if clinical signs have a genetic basis
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Progressive retinal atrophy
``` Late-onset, autosomal recessive photoreceptor degeneration Starts with night blindness Progresses to total blindness Age of onset varies between breeds Puppies are born normal ``` PRCD (progressive rod cone atrophy) is one of several inherited diseases grouped under the progressive retinal atrophy (PRA) rubric Autosomal recessive disorder due to mutation in the Progressive Rod-Cone Degeneration (PRCD) gene Mapped to canine chromosome 9 Substitution of guanine with adenine Changes cysteine to tyrosine (C2Y) Genetic tests are available PRA causes retinal cells to degenerate and die Initially loss of rods then cone Ophthalmic evaluation may only take place after first clinical signs Electroretinography (ERG) is a very sensitive indicator of PRA Genetic tests are available Early diagnosis aids lifestyle adjustments recessive disorder
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Penetrance
: Proportion of individuals with genetic variant (mutation) who exhibit signs and symptoms of genetic disorder
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Liability
the combined effect of all factors (environmental and genetic), that render an animal more or less likely to develop that disorder Liability is continuous Classification is ‘normal’ or ‘affected’ Threshold allows classification Example of a multifactorial trait
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Heritability
proportion of total variation in a trait that can be attributed to variation in genetic factors Relative importance of genetic and environmental factors Contribution of each to disease aetiology
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SNPs
Single nucleotide polymorphisms | a difference in a single DNA building block, called a nucleotide
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Epistasis – coat colour
The action of one gene depends on the action of another gene Coat colour: Different combinations of alleles from different loci Agouti (ASIP) gene causes hair pigment cells to switch from black/brown to yellow/white Expression of ASIP is driven by gene promoters Different promoter alleles drive different colour patterns- promoter region is part where polymerase enzyme binds to start expression controls when its expressed, where and for how long
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Complex inherited disorders
Caused by multiple genes and influenced by environmental factors Inheritance is not always straightforward Lots of gene contribute to risk ``` Bell-shaped curve: Few individuals with all pre-disposing factors (genetic & environmental) Many with some factors (either, or both) Few with no pre-disposing factors Example of a multifactorial trait ```
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Heritability of liability
Proportion of liability that can be attributed to genetics or Proportion of differences in liability that are a result of genetic differences among animals Most familial disorders have intermediate heritability Heritability for liability is usually greater than zero Selection for decreased liability can reduce incidence Non-genetic means can also alleviate inherited disorders
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canine type 1 diabetes
Common endocrine disorder Influenced by genetic factors Similar genes and/or genetic pathways in humans Destruction of pancreatic beta-cells No insulin produced Sugar cannot be absorbed into cells Blood sugar levels remain high Genetic basis Altered immune response- body attacks pancreas in autoimune response posibly on respone to pancrratitis or viral infection Environmental factors - things that cause pancrreatitis, high fat diet ect no type 2 diabetes found in dogs but is found in cats genetic factors assosiated with brain, thymus, pancreaus lymphocyte activation ect
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feline type 2 diabtetes
Type II is most common form Between 0.2 and 1% of cats will develop diabetes Risk factors include: - Obesity - Increasing age - Physical inactivity - Male gender - Use of steroids- from feline asthma ect- prolonged use
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neoplasia
the abnomal growth of cells It is an abnormal growth of cells that leads to a neoplasm (tumour) Neoplasia can occur in any tissue type in the body and in any body system Neoplasms can either be described as benign or malignant. The term ‘cancer’ is sometimes used to describe malignant neoplasms Neoplasia is the result of uncontrolled cell proliferation. DNA damage is very common and repair sometimes fails. Genetic mutations lead to increased cell growth (via mitosis) and decreased cell death (via apoptosis) Neoplastic cells are able to stimulate angiogenesis. New vascular tissue grows into the mass to nourish the ever growing mass of cells. Further mutations allow invasion and metastasis in malignant neoplasms
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summarise the cell cycle
G1 – Growth in cell size and preparation for DNA replication S – Replication of DNA G2 – Continuation of growth and preparation of other cell components for division M – Growth stops and division takes place
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cell cycle regulators
each checkpoint is controlled by protiens that control the progression of a cell through the cycle: Stimulating proteins (encoded by proto-oncogenes)- enhance cell division and inhibit cell death- CDK-cyclins Inhibitory proteins (encoded by tumour suppressor genes)- control cell division and simulate cell death- P53 tumour suppressor
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P53 tumour suppressor
Stops progression through G1 to s phase if DNA is damaged stalls cell cycle Allows cell time to repair DNA If irreparable, triggers apoptosis mutation can lead to cancer
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CDK-cyclins
cytokine dependent kinases Enzymes that activate or inhibit other proteins via phosphorylation Can activate proteins that stimulate cell cycle progression once cyclin concentration reaches threshold mitosis is triggered mutation can lead to cancer
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DNA repair protiens
prevent mutations that can lead to cancer
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Oncogene
mutated proto-oncogene that stimulates cell division and proliferation
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Angiogenesis
creation of new blood vessels to support growth and spread of cancer normal process outside the process of cancer Angiogenesis is regulated by competing pro and anti‐angiogenic signalling The transition to a pro‐angiogenic status occurs when anti‐angiogenic signalling is overwhelmed Tumour cells secrete growth factors to stimulate blood vessels
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Dysplasia
presence of abnormal cells within tissue or organ- eg structure of nucleus, structure of DNA
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Carcinoma
Malignant tumours of epithelial origin
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Sarcoma
: Malignant tumours of mesodermal origin
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describe the formation of a carcinoma
normal mucosa> hyperplasia> dysplasia > carsinoma in situ> invasive carcinoma
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Hyperplasia
increase in tissue or organ size due to cell proliferation- possible mutation in cell cycle
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Benign tumours
``` Tend to grow slowly Expansive, but well circumscribed Often encapsulated Cells are well differentiated i.e. closely resemble the tissue of origin Few mitotic figures (slower growth rate) Do not metastasise ```
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Lipoma
Benign tumour of adipose cells | Common in subcutaneous tissues of older, obese animals
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Adenoma
Benign tumour of glandular epithelial tissue | Perianal adenoma commonly seen in older entire male dogs
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Histiocytoma
Rapidly growing benign tumour of round cells Commonly seen in young dogs on the face and limbs Can spontaneously regress with T cell invasion
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Papilloma
Benign wart-like tumour of epithelial cells Often seen in oral cavity and on lip margins, eyelids, ears Papilloma virus: develop warts 1-2 months post infection
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Fibroma
Benign tumour of fibrous connective tissue Biopsy required to distinguish from malignant form Often caused by poxvirus or papillomavirus infections
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Malignant tumours
``` More rapid growth Invasive and infiltrative Non encapsulated Cells are anaplastic – do not resemble tissue of origin Many mitotic figures (rapid division) Metastasise ```
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Carcinomas
malignat tumours: Squamous cell carcinoma Transitional cell carcinoma Adenocarcinoma
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Squamous cell carcinoma
Commonly found on ear tips or in oral cavity | On skin: associated with exposure to UV light
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Transitional cell carcinoma
Found in the urinary tract, commonly bladder
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Adenocarcinoma
``` Malignant tumour of glandular tissue e.g. mammary glands Mammary tumours in dogs The most common neoplasia of the bitch Caudal glands most commonly affected Highly malignant, metastasise readily ```
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Sarcomas
``` Fibrosarcoma Osteosarcoma Feline injection site sarcoma Lymphosarcoma Hemangiosarcoma ```
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Fibrosarcoma
Malignant tumour of fibrous tissue | Often invasive
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Osteosarcoma
Malignant tumour of osteoblasts Common in large breed dogs Away from the elbow/towards the knee
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Feline injection site sarcoma
Mainly associated with inactivated rabies and FeLV vaccines | Exact aetiology unknown by likely stimulation of inflammation from repeat injections
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Lymphosarcoma
Malignant tumour of lymphoid tissues | Some cases in cats associated with FeLV infection
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Hemangiosarcoma
``` Malignant tumour of endothelial cells Can affect Skin Spleen Liver Heart Bone Kidneys, bladder, lungs… ```
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Mast cell tumours
Malignant tumour in dogs arising from mast cells, usually affects the skin Contain histamine, highly reactive when irritated by handling/FNA/biopsy Some can be cured by surgical excision (low grade)
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Leukemias
Neoplastic hematopoietic cells in peripheral blood or bone marrow Leukemia represents less than 10% of hematopoietic neoplasias in dogs and around 15-35% in cats. Besides FeLV infection in cats, there is not any other proven etiology for leukemia in small animals Cell lineage identification is an important step in the classification of leukemia
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Myelomas
Type of plasma cell neoplasm originating from terminally differentiated B lymphocytes that have undergone malignant transformation Most important plasma cell neoplasm which results in diffuse disease Accounting for less than 8% of all hematopoietic tumours in dogs No breed or sex predilections exist, and older dogs are most commonly affected, with a mean age of 8 to 9 years
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Metastasis
When malignant cells of the original tumour transfer to another part of the body an invasive phenotype is aquired cells invade the surounding stroma and then enter the hematogenous circulation they travel to a distant organ and invade they then adapt and proliferate to form metastases
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Heterogeneity
Evolution of tumour to form different clonal stem cell lines Additional mutations Selection pressures treatment of a cancer can be a heterogenis selection pressure
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metastasis via circulation
Most commonly spreads to organs with large blood supply | Liver and lungs, also skin/bone
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metastasis via lymphatic system
Spread through the lymphatic drainage system and seed in lymph nodes remove lymphnodes to treat and prevent
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metastasis through extention
Spread to neighbouring organ by direct contact e.g. liver and spleen
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metastatis via transplantation
Exfoliation of tumour cells into a cavity or another site e.g. incision site can occur becuase of surgery via instruments
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halmarks of cancer
``` sustained proliferative signalling activating invasion and metastasis evading growth supression inducing angiogenisis enabling replicative imortality resisting cell death ``` underlying hallmarks (driving factors)- genome instability and mutation tumor promoting inflamation deregulating cellular genetics- reprograming energy metabolism avoiding imune distruction all targets for cancer treatment
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Diagnosing cancer
Imaging techniques can be a useful aids to locate abnormal growths however they give no information about the type of growth The most helpful aid to diagnosis is to take a biopsy. Histopathological examination will enable definitive diagnosis and allow grading of the tumour to determine its degree of malignancy. ``` Collection of the sample Fine needle aspiration Impression smear Biopsy: Needle core biopsy Bone marrow biopsy Punch biopsy Wedge biopsy Excisional biopsy Processing of the sample: Cytology Histopathology (formalin) ```
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Complications of cancer
Paraneoplastic syndromes Hypercalcaemia – adenocarcinoma, lymphoma, multiple myeloma Hypoglycaemia – insulinoma, hepatic tumours Coagulopathy – hemangiosarcoma, MCTs, thyroid tumours Changes in blood pressure Hyperviscosity – multiple myeloma, lymphoma ``` Other complications Anaemia - through myelosuppression or haemorrhage Ulceration and infection Weight loss and cachexia Obstruction Histamine release - MCTs ```
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cancer treatment options
``` Surgery Radiotherapy Chemotherapy Cryotherapy Hyperthermia Photodynamic therapy Adjunctive therapies ``` more often palliative
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species used for studying aging
yeast- can rapidly provide information about aspects of cellular ageing roundworms- live only 2-3 weeks, allows mutations relating to lifespan to be identified Fruit flies-commonly used. extremely effective tool for studying evolutionarily conserved aspects of ageing. additional interactions at play within and between tissues of a multicellular, differentiated, organism (such as insulin signalling pathway) can be modelled in worms and flies. When combined for their individual experimental strengths, flies can function as an effective pipeline of discovery of evolutionarily conserved interventions to enhance lifespan, which can be targeted for experiments in the longer-lived vertebrate systems, such as mice (approx. 3y) and rats (approx. 3y). Drosophila- convinient,easy husbandry, distinct tissues with human equivilents that can be genetically manipulated rodents- more closly related to humans. cost effective, convinient, Mice are better models than flies or worms for studying complex biological systems found in humans, such as the immune, endocrine, nervous, cardiovascular and skeletal systems - like humans, mice naturally develop diseases that affect these systems, including cancer and diabetes. non-human primates- allows the integrated system of genes to be studied. rhesus monkey, common marmoset. similar aging process to humans birds- high metabolic rates body temperatures and blood sugar levels, and yet some species are among the most long-lived of all animal species. birds have mechanisms to protect them from oxidative damage and that they can regenerate certain neurones in the brain
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Genes and ageing.
Ageing in both human and yeast cells is not only the result of passive wear and tear, it is also caused by an active process orchestrated by a distinct set of genes, some of which slow down ageing while others speed it up. For example, by exposing yeast to lithocholic acid (an ageing-delaying natural molecule) scientists created long-lived yeast mutants that they dubbed “yeast centenarians.” These yeast mutants lived five times longer than their normal counterparts because their mitochondria consumed more oxygen and produced more energy than in normal yeast. The centenarians were also much more resistant to oxidative damage – a key process that causes ageing.
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Clock genes
investigators have looked at a mechanism controlled by a group of genes called clock genes that regulate metabolism in the roundworm and affect lifespan. The roundworm genes that seem to confer increased longevity do so by supporting resistance to external stresses, such as – Bacterial infections, High temperatures, Radiation, Oxidative damage (oxidative damage results when the toxic by-products of oxygen metabolism damage the components of cells).
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Co-enzyme Q7 (COQ7)
There has been significant research in roundworms has focused on the gene that regulates the activity of a particular type of protein, co-enzyme Q7, hydroxylase (COQ7) that plays a crucial role in electron transport within mitochondria that produce energy. Investigators have discovered that mutations that diminish COQ7 lead to a modest increase in life span. These mutations have a bigger effect when combined with other mutations, such as those in the insulin pathway and affect resistance to oxidative damage.
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DAF-16
other research has studied a variant of roundworms that possess a mutant gene labelled DAF-16. These mutant worms carry large amounts of DAF-16 in their nuclei, which cause the worms to live longer than worms without an excess of DAF-16. Although the explanation for this phenomenon is still not fully known, it does offer an opportunity to screen drugs to see if they increase nuclear levels of DAF-16. If certain drugs can increase the amount of DAF-16, then they might be beneficial in increasing life span.
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Insulin pathway and TOR.
Past research on the Insulin Signalling (ISS) and TOR pathways shows that altering certain genes, usually yields a 100% and 30% lifespan increase, respectively. The assumption was then, that altering them together would boost lifespan by 130%, however when scientists tested this they found that the effect was much greater than the sum of its parts. The study, published in 2020, showed that altering the IIS and TOR pathways together yields a lifespan extension of about 500 percent. These findings demonstrate well that nothing in nature exists in a vacuum, i.e. in order to develop the most effective anti-ageing treatments it can be most effective to look at longevity networks rather than individual pathways. The findings suggest that future anti-ageing therapies might involve a combination of treatments, similar to how combination treatments are sometimes used for cancer and HIV.
379
what are the five majour symptom clusters for assesing cognative decline
``` Disorientation Social Interactions Sleep-wake cycles House-training Activity ``` Codes for presence over severity. Quick and easy.
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Canine Dementia Scale (CADES)
``` Four symptom clusters: Spatial orientation Social interaction Sleep–waking cycle House soiling ``` each section cored from 0 to 5 points based on frequency and then added to form an acumulative score allows dog to be graded on cognative disfunction
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mechanisms of cognative decline
Atrophy (shrinkage) of tissue in some regions Increased ventricular volume Loss of neurons and synapses and reduced formation of new neurons Accumulation of abnormal proteins decline in glucose metabolic rates in the brain chemical loss- degeneration of neurons that provide neurottansmitters, eg dopamine,acetylecholine
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Mechanisms Cognitive Decline: Dopamine
Dopamine cells located in the Ventral tegmental area (VTA) and Substantia nigra (SN). Three main projections: Mesocortical Mesolimbic- reward Mesostriatal regulates behahviour, emotion learning Dopamine cells are limited in supply. Less than 50,000 Degenerate easily during ageing. Degeneration linked to mechanisms to compensate for failed function. Balance of degeneration vs chemical compensation.
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Mechanisms Cognitive Decline: Acetylcholine
Acetylcholine cells located in the Medial septal nucleus (MSN), Nucleus basalis (NB), and Tegmental nucleus (TN). Three main projections: Frontal Septal Basal plays role in memory loss degenerate easily but more prone to enviromental factors than other neurones
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Treatment of Cognitive Decline: Selgian
Active ingredient is Selegiline Hydrochloride. Inhibits monoamine oxidase B. ensures higher levels of dopamine ``` Low dose (sub 20mg per Kg) Increased dopamine levels ``` ``` High dose (20mg per Kg) Increased dopamine, serotonin and noradrenaline. ``` Selegiline is a selective MAO-B inhibitor at low doses. Prevents breakdown of dopamine therefore increasing levels in the brain. At high doses inhibits MAO-A. Prevents breakdown of noradrenaline and serotonin increasing levels in the brain. Counter indicated with selective serotonin reuptake inhibitors (SSRI’s).
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Treatment of Cognitive Decline: Vivitonin
Active ingredient is Propentofylline. Inhibits phosphodiesterase (PDE) and adenosine reuptake transporters. Low dose (6mg per Kg) High dose (10mg per Kg) Propentofylline inhibits phosphodiesterase (PDE) and adenosine reuptake transporters. Increases adenosine signalling and nitric oxide production. Significant vasodilation affect, resulting in increased cerebral blood flow.
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dietery suplimentation for congnative deterioration
vitamine B, D and E Flavonoids-improve blood vessel function and communication between nerve cells Fish Oils
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golden retriever Muscular dystrophy
Muscular dystrophy (MD) is a progressive fatal disease characterized by degeneration of skeletal and cardiac muscle Most common form is Golden Retriever MD (GRMD) Also seen in rottweiler; pointer; beagle and others phenotypic variability due to differencec in muscle metabolism Characterised by degeneration of skeletal and cardiac muscle Affected individuals exhibit atrophied muscles Seen early in life (1 month) – often ineffectual sucklers effects dystrophin gene ``` clinicla signs: Stiff gait Decreased agility Decreased exercise tolerance Muscle atrophy Prominent bones along spine, ribs and skull Megaoesophagus Large tongue Excessive drooling ``` diagnosis: Elevated creatine kinase in bloodwork Muscle biopsy Histopathological examination of muscle tissue Degenerating muscle fibres Changes in diaphragm and heart observed during necropsies genetic test
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GRMD – molecular pathology
Defect in a gene on the X chromosome X-linked recessive disorder Higher prevalence in males as they only have one X chromosome Males are always hemizygous for X linked traits Females must receive two copies to display GRMD phenotype Gene is responsible for production of dystrophin Very long gene product Very large protein mutation is on splicing site substitution results in exon not being recognised as exon and is removed results in frame shift and new stop codon created protien loses regions that interact with sarcolema
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Dystrophin in the context of GRMD
Dystrophin acts as a shock absorber Connects the actin cytoskeleton to the extracellular matrix Each end of the molecule is tailored to interact with cytoskeleton or glycoproteins Mitigates any damage in muscle when muscle cells contract transferes force of muscle contracts from insidd to outside sarcolema becomes weaker with every muscle contration without it reaulting in leaky muslce cells and subsiquently degeneration Reduced membrane integrity allows enzymes such as creatine kinase (CK) to leak out Calcium influx leads to protease activity Results in muscle abnormalities and necrosis Stimulates inflammation and further muscle damage Muscles deteriorate with loss of myofiber membrane integrity muscle is repalced with connective tissue and fat eventualy effecting cardiac and respiritory muscle
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Equine sarcoids
Most common cutaneous tumour in horses. Prevalence 04-15.8% Non life threatening but big effect on welfare and material value of the horse (Gerber, 1989; Marti et al., 1993): Pre-purchase examination! Exclusion from insurance coverage Infection of the site Diffulties defecating, urinating, mastication, locomotion Tack issues Prevalence is higher in younger horses (as early as 6 months and the average is 3.5-4 y.o) Genetic predisposition: equine major histocompatibility complex (MHC) is encoded in the equine leucocyte antigens (ELA) in chromosome 20 ELA haplotypes A3 and B1 higher susceptibility But… not all B1 horses suffer sarcoids! Markers in chromosomes 20, 22, 23 and 25 identified Breed: Standardbred and Warmblood at least risk. Quarter horse, arabs, appaloosa and TB higher risk. Donkeys the highest risk! Anatomical region: any! First described papillomavirus cross-species non-productive infection . In horses non-permissive for virus production and non regressing There is great variability in the histopathological signs and to date there are no pathognomonic features in equine sarcoids diagnosis: Clinical presentation Histology – expert clinical pathologist! As easily confused with fibroma and fibrosarcoma (Roberts, 1970; Martens et al., 2001c) (Weiss, 1974; Taylor & Haldorson, 2013) Detection of BPV-1 (equine sarcoid variants) and -2 (Nasir & Reid, 1999; Carr et al., 2001a; Nasir & Campo, 2008). Modern technologies: microRNA detection
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cinical types of equine sarcomas
Occult, verrucose, nodular (types A1, A2, B1 and B2), fibroblastic (types 1a, 1b and 2), mixed and malignant
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Occult equine sarcoids
most benign form of ES and are thought to represent an early stage of the disease. Occult sarcoids are often circular alopecic lesions with a grey colour, that lack hair and their appearance is of a hyperkeratotic dry lesion. On palpation, skin feels thickened, dry and has small nodules underneath. This form is easily misdiagnosed as ‘ring-worm’ (dermatophytosis) or skin rubs from tack or other equipment (see Figure 1.2, Image 1). Verrucose sarcoids are prominent from the skin and they are similar to warts in appearance. The skin on these lesions is dry, alopecic and scaly. The margins are not well defined. Due to the ‘wart-like’ appearance these can be mistaken for equine papillomas.
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Nodular equine sarcoids
are circumscribed firm subcutaneous masses that can appear as single or multiple lesions. Type A are characterised by no skin involvement (the skin can be freely moved over the nodules). If the underlying tissues are not involved it is classified as nodular type A1 and if there is deep tissue involvement it is named A2 (Knottenbelt, 2005a). Nodular type B sarcoids are nodular sarcoids with visible and palpable skin involvement. When they have defined margins they are classified as B1 and if they have ill-defined margins they are named B2.
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fibrielastic equine sarcoma
Fibroblastic tumours have a ‘fleshy’ appearance (see Figure 1.2, Image 5). They are an aggressive form of sarcoids and have a tendency to ulcerate and become infected. Fibroblastic pedunculated sarcoids have a clear margin and a ‘neck’ that separates the lesion from healthy skin. Depending on deep tissue involvement, fibroblastic pedunculated sarcoids are classified as type 1a with no deep tissue involvement, and type 1b with deep tissue involvement. Fibroblastic sessile sarcoids on the other hand have ill-define margins, a broader base and there is always involvement of underlying tissue. It can become difficult to macroscopically differentiate any of the fibroblastic sarcoids from fibrosarcoma and squamous cell carcinoma in which case biopsy will be recommended. Other skin diseases that fibroblastic sarcoids may be mistaken with are exuberant granulation tissue (‘proud flesh’), a common complication in horses in wound healing. Mixed sarcoids are very variable in appearance and they can combine two or more of the forms described above.
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Malevolent equine sarcoids
Malevolent equine sarcoids sometimes called malignant, are rarely described in the literature. The tumour infiltrates the lymphatic system and the progression is fast. It affects extensive areas and it may comprise different clinical types of ES.
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melenoma
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Nutritional deficiencies
longterm, steady-state conditions | corrected through dietary supplementation.
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Metabolic diseases
acute states dramatically respond to systemic administration of the deficient nutrient or metabolite accurate and rapid diagnosis is important Ideally, diagnostic tests can be used to predict the occurrence of disease. Pathogenesis of each disease is primarily related to alterations in metabolism. In most cases, the basis of disease is from an increased demand for a specific nutrient that has become deficient under certain conditions. Diseases are augmented by management practices directed toward improving and increasing production. considered production diseases. also metabolic diseases because management of the animal is directed at production, hypocalcemia hypomagnesimia hypoglycemia milk fever of cows occurs when the mass of calcium in the mammary secretion is greater than the cow’s diet or its skeletal reserves can supply.
399
what are macroelemens and what 7 minerals come under this catagory
``` concentrations in the body higher than 50 mg kg-1 BW calcium, phosphorus, potassium, sodium, chloride, Magnesium sulphur, ``` The structural function involves elements that build organ and tissue structures calcium, magnesium, phosphorus, silicon in bones and teeth, phosphorus and sulphur in muscle proteins. The physiological function is responsible for the supply of electrolytes to body fluids and tissues in order to regulate osmotic pressure, maintain the acid-base balance, regulate membrane permeability and nerve impulse transmissions sodium, potassium, chloride, calcium, magnesium. The catalytic role of minerals is probably the most important function. Macronutrients and micronutrients act as catalysts in enzyme and endocrine systems; coenzymes to initiate enzyme and endocrine functions, constitute integral and specific structural elements of metalloenzymes and hormones. mineral elements are also responsible for cell replication and differentiation. Zinc influences transcription, iodine is a component of thyroxine (a hormone responsible for thyroid function and energy processes)
400
what are microelemens and what 15 minerals come under this catagory
concentrations in the body below 50 mg kg-1 BW. ``` iron, iodine, zinc, copper, manganese, cobalt, molybdenum, selenium, chromium, tin, vanadium, fluoride, silicon, nickel arsenic ``` The structural function involves elements that build organ and tissue structures calcium, magnesium, phosphorus, silicon in bones and teeth, phosphorus and sulphur in muscle proteins. The physiological function is responsible for the supply of electrolytes to body fluids and tissues in order to regulate osmotic pressure, maintain the acid-base balance, regulate membrane permeability and nerve impulse transmissions sodium, potassium, chloride, calcium, magnesium. The catalytic role of minerals is probably the most important function. Macronutrients and micronutrients act as catalysts in enzyme and endocrine systems; coenzymes to initiate enzyme and endocrine functions, constitute integral and specific structural elements of metalloenzymes and hormones. mineral elements are also responsible for cell replication and differentiation. Zinc influences transcription, iodine is a component of thyroxine (a hormone responsible for thyroid function and energy processes)
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mineral deficiencies
Mineral deficiency can impair or inhibit metabolic pathways required for normal body function Severe macroelement or microelement deficiencies symptoms corresponding to the function of the deficient element in the body accurate diagnosis Minor deficiency, the symptoms are non-specific, often transient difficult to diagnose. Frequently occur ``` Mineral deficiency generally leads to impaired immunity, inhibited growth, reproductive disorders lower productivity ``` Mineral deficiencies can result from low quality feed, impaired absorption or assimilation increased demand for minerals
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Milk fever
disruption of Calcium homeostasis What is calcium involved with normally? ossification, blood coagulation, milk, cardiac rhythm control, cell membrane permeability and linkage between cells, nerve and muscle excitation, activation and secretion of hormones through exocytosis and activation of enzymes. Structural integrity of teeth and bones…………… Where does it come from-food! (Stored and released from bones). The major absorption site of Ca in the gastrointestinal (GI) tract of ruminants is the small intestine Major increase in requirement-start of lactation, have to meet that demand. The severity and duration of a hypocalcaemic event depends on the integrity of the cows Ca homeostasis mechanisms. Plasma calcium is distributed in 3 major fractions: About 50% of total plasma Ca is bound to negatively charged sites on proteins, such as albumin. parasites can decrese albumin levels and have knock on effect Free calcium. Between 42-48% of total plasma Ca is present as free ions in plasma. This is the portion of total Ca that is hormonally regulated and which contributes to certain Ca-associated pathological states. About 5-8% of total plasma Ca is bound to non protein anions What happens physiologically 99% is in the bone in the form of hydroxyapatite crystals. The next largest pool of calcium is intracellular calcium. In the inactive cell state, calcium concentrations are relatively low in the cytosol; calcium is bound to proteins or contained within the mitochondria or granules of the endoplasmic reticulum. Calcium concentrations are indicative of cell activity. How much? Blood Ca in the adult cow is maintained around 2.1-2.5mmol/L 3g Ca in the plasma pool 8-9g in all compartments outside of the bone in a 600kg cow. The smallest pool of calcium, which resides in the Extra Cellular Fluid (ECF), is the most important pool for physiological control of calcium concentrations in the blood. This component comprises interstitial calcium, blood calcium and a small (0.5%) but important part of the bone calcium pool, which exists as amorphous crystals or in solution. The soluble bone calcium pool allows access to the large reserve of calcium that resides in bone. The regulation of calcium levels involves control of the movement of calcium between the ECF and three body organs: bone, GI tract and kidneys (less so in ruminants due to the contributon of the salivary glands). The exchange of calcium ions Fluid within the canaliculi of the bone may contain another 6-15g Ca; dependant on the acid base status of the animal Around 50% of the total plasma calcium is bound to proteins (primarily albumin), with another 5% bound to organic compounds in the blood, such as citrate. From 42-48% of the total plasma Ca exists in the ionised, soluble form (Ca2+), the amount being closer to 48% at low blood pH and closer to 42% at elevated pH. As the pH of blood becomes acidic, the calcium ions (Ca2+)will increase due to the competition of hydrogen ions (H+) for binding to the negatively charged site on serum proteins. During the dry period, Ca requirements are minimal 10-12g/day. At parturition -sudden increase in cows Ca requirements. A dairy cow producing colostrum or milk needs to withdraw 20-40g Ca from her pools each day. not available in the plasma pool withdrawer calcium from bone or increase the rate of absorption of dietary Ca. these processes may take 2-3days to become fully active and if they fail, hypocalcaemia results. In common with their other homeostatic controls, all ruminants are able to regulate with strict precision the concentration of Ca in plasma, under the influence of three hormones: parathyroid hormone (PTH), calcitonin (CT) 1,25-dihydroxyvitamin D 3 (l,25(OH) 2D3 ). (1,25-DHD) In principle PTH and 1,25-DHD increase blood calcium, where as calcitonin decreases it. Calcium metabolism from bone is less rapid: in older cows in cows fed pre-partum diets high in Ca. So a sudden and large increase in loss of Ca from the extracellular pool can result in hypocalcaemia before the Ca homeostatic mechanisms can act. Calcitonin is secreted by cells in the thyroid gland, principally in response to Ca concentrations in blood and extracellular fluids. Calcitonin and PTH act in together to provide a negative feedback mechanism to maintain the concentration of Ca in extracellular fluids within narrow limits. The major inhibitors to PTH synthesis and secretion (stimulated by elevated Ca in blood) are calcitonin and 1,25-DHD.
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Calcium homeostasis
In common with their other homeostatic controls, all ruminants are able to regulate with strict precision the concentration of Ca in plasma, under the influence of three hormones: parathyroid hormone (PTH), calcitonin (CT) 1,25-dihydroxyvitamin D 3 (l,25(OH) 2D3 ). (1,25-DHD) In principle PTH and 1,25-DHD increase blood calcium, where as calcitonin decreases it. Concentrations of Ca in the carotid artery blood are monitored by Ca-sensing receptor molecules located on the surface of parathyroid cells. The parathyroid gland secretes PTH when Ca concentrations are too low. The primary target cells for PTH are bone osteoblasts and osteocyte, as well as renal tubular epithelial cells. Under normal conditions PTH is the major factor concerned with the minute-by-minute regulation of blood Ca concentrations that protect the animal against hypocalcaemia. The short term effects of PTH are: Increased renal absorption of Ca from the glomerular filtrate Stimulation of intestinal Ca absorption If the disturbance in plasma Ca is small or short term, plasma concentrations return to normal and PTH secretion drops back to baseline level. Where the drain of Ca from the extracellular pool is continuous there is also continued PTH secretion, whose main effect is to stimulate resorption of bone Ca stores. Calcium is initially derived from the extracellular fluid of bone canaliculi, ….but thereafter it must come from the osteoclastic resorption of the inorganic bone matrix. The main mechanism of action of PTH in ruminants is through increasing 1,25-DHD production. There are 1,25-DHD receptors in many tissues, main effects on Ca metabolism are mediated via absorption from the gut (small intestine) and resorption from the bone. Most Ca is absorbed from the gut by active transport mechanisms regulated by 1,25-DHD, ….although when concentrations in the digesta are very high (eg oral drenches of Ca as a preventative) -then passive transfer can occur. PTH triggers the production of 1,25-DHD by the kidney by stimulating the enzyme 1α-hydroxylase, which converts vitamin d3 into the physiologically active form 1,25-DHD
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Absorption of Ca from the GIT can be reduced by high concentrations of....
dietary potassium, high rumen nitrogen low dietary phosphorus.
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metabolic alkalosis predisposes cows to
hypocalcaemia by reducing the sensitivity of tissues to PTH. a lack of osteoclastic bone resorption failure to upregulate renal 1α-hydroxylase activity. Metabolic alkalosis commonly occurs as a result of a diet that supplies more strong basic cations (K+, Na+, Ca2+, Mg+) than strong acidic anions (Cl-, SO42-, phosphate).
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High concentrations of K+ in the diet of a cow
reduce the absorption of Ca from the gut and reduce the mobilisation of Ca from bone. High rumen ammonia concentrations also reduce Ca absorption.
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Milk fever clinical signs
Where is there low calcium-blood What do we see clinically: blood coagulation (enzymes) cardiac rhythm control-tachycardia cell membrane permeability and linkage between cells, nerve and muscle excitation-lack of smooth and skeletal muscle contraction Recumbent/paresis of limbs&neck, no uterine involution, RFM cannot swallow, cannot urinate, cannot ruminate/eructate (become bloated), teat sphincter cannot close Reduced activation and secretion of hormones
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describe calciums relationship with magnesium
What happens physiologically-relationship with magnesium Mg absorption from the rumen-variable, mostly due to intakes, Surplus is rapidly compensated for -excretion by the kidneys. Small reductions in blood Mg may impair the capacity to mobilise Ca in response to hypocalcaemia. Low magnesium status (hypomagnesaemia) affects Ca metabolism by Reducing PTH secretion in response to hypocalcaemia Reducing the ability of PTH to act on its target tissues Interfering with the hydroxylation process of vitamin D3 in the liver. Magnesium absorption from the rumen is dependent on the concentration of Mg in solution in the rumen fluid the integrity of the Mg transport mechanism (Na+ linked active transport process). High dietary K+ reduces Mg absorption from the rumen.
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Magnesium homeostasis
Bones and muscles are the main magnesium pools in the body. Magnesium has major roles in physiological processes and cellular metabolic pathways The ability of magnesium to stabilize cell membranes is one of its most important functions . Magnesium and calcium remain in a dynamic equilibrium Mg plays a significant role in the secretion of the hormone for calcium homeostasis and the responsiveness of tissues to hormones. It is estimated that more than 75% of hypocalcaemia cases seen in mid-lactation are due to inadequate dietary Mg supply Magnesium (Mg) is the second most abundant intracellular cation in mammals after potassium. Bones and muscles are the main magnesium pools in the body. Magnesium plays vital roles in nearly all physiological processes and participates in many cellular metabolic pathways. -It activates nearly 30 enzymes and participates in the metabolism of carbohydrates, nucleic acids and proteins. -Magnesium stabilizes DNA structure and influences RNA transcription as well as the formation of ribosomal subunits. -The presence of Mg2+ ions is required in all processes involving ATP. -The ability of magnesium to stabilize cell membranes is one of its most important functions (Soetan et al. 2010). Magnesium and calcium remain in a dynamic equilibrium, Mg plays a significant role in the secretion of the hormone that controls blood calcium and the responsiveness of tissues to that hormone. It is estimated that more than 75% of hypocalcaemia cases seen in mid-lactation are due to inadequate dietary Mg supply and a higher intake of magnesium than calcium can stilt the bone growth (Zimmermann et al. 2000). Magnesium improves potassium absorption and protects cardiac muscle cells and neurons against free radicals and toxic substances. It activates classical and alternative complement pathways (McCoy, Kenney 1992).
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Grass staggers: disruption of Magnesium homeostasis
In adult ruminants, particularly in animals fed fast growing grass with low Mg content High levels of potassium (application of potash fertilisers) disrupt the absorption of magnesium. High levels of ammonia (from nitrogenous fertilisers) inhibit magnesium absorption. low in fibre and increase the rate of passage of food material through the rumen reducing time for Mg absorption. Reduced food intake e.g. due to bad weather or transportation. Hypomagnesaemia doesn’t correlate well with clinical signs, even a minor magnesium deficiency can lead to reduced dry matter intake, nervousness, a reluctance to be milked or herded, reduced milk fat and yield nerve and muscle excitation (aggressive!!), incoordinated movements, hyperexcitability, muscle spasms and seizures (chomping of jaws and frothy salivation) further drop in Mg concentrations increases the risk of hypomagnesemic tetany and death
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absorbtion sites for magnesium in ruminents
Adult cows Rumen mainly absorbs Mg Sheep reticulorumen is a main absorption site of Mg Mg uptake from the site is achieved by an active transport process Calves the omasum is the main absorption site for Mg
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Disruption of Magnesium homeostasis in young ruminents
milk replacers deficient in magnesium. Other factors that increase the demand for magnesium or lower its availability, such as exercise, low temperature, decreased appetite/fasting and diarrhoea affects mostly rapidly growing animals at the age of 1.5 to 4 months, . The first symptoms of nerve and muscle excitation are observed after several days or weeks of hypomagnesemia. anxiety, twitching of the ears, bulging eyes, jerking movements of the head, kicking at the abdomen, stiff and unsteady gait it is followed by contraction episodes lasting 5 to 20 minutes After each episode, the animal remains weak, may exhibit tremor and signs of allotriophagy. Contractions may reappear 1-2 days later, and they can lead to death
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Osteoarthritis
``` Progressive degeneration of the joint Inflamitory disorder Pain and stiffness in joints Degeneration of carilage Hypertorphy of bone at margins Changes in synovila membrane Formation of bony outgrowths at joint Age relataed changes in skeletal system combined with injury ``` Stiff gaiute Joint pain Sensitive legs Loss of joint space Osteophytes Subchondral cysts Subchondral sclerosis Risk factors: Genetics * Joint alignment * Injury * Activity level * Obesity Treatment: Lifestyle advice (weight loss, activity level, diet etc.) * Pain relief (NSAIDs; corticosteroids; fluid modifiers) * Surgery (joint fusion; replacement; amputation) Outlook: OA is a non-curable, progressive, degenerative condition * Pain relief is key outcome * Major cause of euthanasia due to quality of life
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Parhogenisis of osteoarthritis
Carilage lost-Exposure of underlying bone Formation of oseophys and subcondral bone cysts Joint space lost and bones rub toghter Articular cartilage degradation and synthesis destabelises- chondrochtes maintainds EXM Chondrocytes however have limited potential for replication do when damaged it is hard to recover Link to aging- osteoarthritis is linked to aging due to decreased cellular synethesnse, this esspecially effects condrocytes due to the low potentail for replication Senescent manifest dramatic changes in what they secret, proinflamitory secretions contribute to ectracellular matrix decline Stem cell decrease Altered intracellular communication- pro inflammatory tissue damage Summary, Arrest of cell cycle * Necrosis of chondrocytes * Release of degradative enzymes * Breakdown of ECM * Release of proinflammatory cytokines- from break down of ecm, bones rubbing and senesence secrerory changes