Metabolic Diseases Flashcards
1
Q
what is a congenital disease
A
- metabolic disorders can be congenital (an animal born with a disorder) or acquired at birth
- can be hereditary or acquired in utero
- in most cases the hereditary component of metabolic disorders is a genetic predisposition to the disease and responds to environmental conditions
2
Q
examples of congenital hereditary
A
- LFS = lavender foal syndrome
- HYPP = hyperkalemic periodic paralysis
3
Q
examples of congenital aquires
A
- congenital hyperthyroidism
4
Q
examples of aquired
A
- laminitis
5
Q
examples of hereditary predisposition triggered by the environment
A
PSSM =equine polysaccharide storage myopathy
RER = recurrent exertional rhabdomyolysis
EMS = equine metabolic syndrome
6
Q
examples of endocrine metabolic diseases
A
- cushings
- equine metabolic syndrome
7
Q
examples of organ disfunction
A
- liver, kidney, lungs
8
Q
examples of orthopedic disease
A
- developmental orthopedic disease
- arthritis
- fragile bone syndrome
9
Q
what is ECD
A
- equine cushings dieases
- chronic, progressive neuroendocrine
- no cure
- treatment focused on managing conditions associated with the disease
- average afe of confirmed diagnosis of ECD is 20 years ( considered to be a disease mostly middle aged geriatric horses)
10
Q
what happens when hypothalamic control of dopamine is disrupted
A
- dopamine normally inhibits hormone production and release from the pituitary pars intermedia and absense of controls results in excessive production and release of pituitary pars intermedia hormones
- pituitary pars intermedia produces and releases pro-opiomelanocortin (POMC)
- POMC - is converted into ACTH by PC1
- stimulates cortisol release from the adrenal cortex
- hypertrophy, hyperplasia, and adenoma formation within pituitary pars intermedia disfunction
- enlarge causes compresses pituitary lobes and interfear with function
11
Q
what are the metabolic effects of cortisol
A
- elivated effects of cortisol = increased cortisol and clearance
- stress response
- blood pressure and heart function
- muscle tone
- immune reponse to infection
- inflammation
- nerve function
- connective tissue repair
- balance insuling effects
- regulation of carbs, fat and protein metabolism
12
Q
clinical signs of cushings disease
A
- hypertricosis
- hyperhydrosis
- chronic reoccuring laminitis
- epaxial muscle wastage
- polydipsia and polyuria
- infertility
- weight loss
- pot belly
- immunosuppresion
- delayed wound healing
- abnormal mammary gland development
- lethargy and poor athletic performance
13
Q
management of cushings disease
A
- nutrition - low WSC (functions)
- dental and hoof care
- thermoregulatory assistance
14
Q
pharmacologic treatment of cushings
A
- dopamine receptor agonist - perolide
15
Q
what is EMS
A
- equine metabolic syndrome
- occurs in animals with excessive adipose tissue (not all)
- metabolically and hormonally active abdominal, hepatic and muscle adipose tissue trigger a cascade events that lead to insulin dysregulation and persistent hyperglycemia
- characterized as a collection of risk factors that predispose the horse to endocrinopathic laminitis
- insulin dysregulation manifests as basal hyperinsulemia and elevated prolonged hyperglycemia
16
Q
what is the development pathway for metabolic syndrome
A
it has not been clearly elucidated
- number of proposed mechanisms linking obesity, insulin resistance and other features of metabolic syndrome exist
- EMS may develop through more than one pathway
- suspected genetic component
- susceptible horses in the triggering environment develp EMS
17
Q
what is the diagnosis of EMS
A
- obesity = abnormal fat distribution (eye fat pads, neck, shoulder, loin and tailhead)
- age of onset (8-18 years )
- specific breeds
- high body condition score, founder rings and reginal adoposity
- high neck crest score
- low adiponectin
- high c petide
18
Q
management of EMS
A
- exercise
- 40% NSC DIET
19
Q
treatment of EMS
A
- levothyroxine (not long term) - induce weight loss, increase insulin insensitivity
- metformin hydrochloride - decreases hyperglycemia and increases insulin sensitivity
prevention is key
20
Q
what is EAS
A
- equine asthma syndrome, respiratory conditions ranging from mild (inflammatory airway disease) to severe (recurrent airway obstruction)
21
Q
what is IAD
A
- inflammatory airway disease
- condition usually observed in young to middle aged horses that present with coughing and poor performance
-condition persists for a minimum of 4 weeks and resolves either spontaneously or with treatment - recurrence is uncommon
- some horses are at risk for ROA but not always
- do not present with increased respiratory effort at rest and airflow limitation is minimal
- hyperresponsiveness ( heightened sensitivity to particular matter
- race horses in training suffer a form of IAD characterized by coughing, mucous in the trachea and high bacterial counts in the trachea
22
Q
what is ROA
A
- recurrent airway obstruction
- chronic, non infectious, inflammatory lower airway disease
- occurs mostly in hay fed, stabled horses that are exposed to dusts or organic matter (aerosols) particularily molds and actinomycetes (Aspergillus)
23
Q
what is stage 1 of ROA
A
- chronic coughing
24
Q
what is stage 2 of ROA
A
- audible breathing sounds
- exercise intollerance
- tracheolbrochial secretions increase
- neutrophils may increase
25
Q
what is stage 3 or ROA
A
- noticeable wheezing
- abdominal effort required for expiration (heaves)
- heave line ( physical force of side squeezing abdomin )
- high nuetrophil content of respiratory secretions
26
Q
what is genetic susceptibility of ROA
A
- develop hypersensitivity to antigens in th emoulds
- display immediate bronchiospasmatic response (contraction of smooth muscle lining airways) producing an airway obstruction reversible with bronchodilators and inflammatory response ROA
27
Q
what happens during inflammatory response of ROA
A
- mucous accumulates in the lumen of airways and alveoli
- the thickness of small airway walls increases (negatively affecting oxygen exchange
- peribronchial accumulation of lymphocytes
- intralumenal accumulation of neutrophils in response to cytokines produced by resident macrophages and lymphocytes
- results in airway obstruction as well as nonspecific airways hyperresponsiveness
28
Q
what are clinical signs of ROA
A
- coughing
- exercise intollerance
- increased breathing efforts
- abdominal effects
- dilated notrils
- mucopurelent nasal discharge
- airway inflammation
- airway obstrution
- altered gas exchange
29
Q
management of horses affected with RAO
A
- no hay
- allergies to something on pasture
- keep out of barn to avoid dust
- hay steamer to remove NS carbs
30
Q
parmacologic management of horses with RAO
A
- systemic and inhalation of glucocorticoids = alliviate clinical signs, airway obstruction, inflammation
- systemic and inhalation of bronchodialtors = alliviate airway obstuction and bronchospasms
- phospohodiesteraie inhibators = alliviate airway obstruction
- nanoparticulate CpG immunotherapy = removes allergic and inflammatory induced variables (currently not available )
31
Q
what is EIPH
A
- exercise induced pulmonary hemorrhage
- bleeding from lungs during exercise
- confirmed by the presence of blood on tracheobronchoscopic examination and or red blood cells present in bronchoalveolar lavage (BAL) fluid
- conditions affect the majority of racehorses as well as horses in strenuous disciplines
- approximately 5% of horses with EIPH will display epistaxis
- ## might influence performance in race horses - poor finishes
32
Q
diagnosis of EIPH
A
- if horse displayes epistaxis
- most widley accepted diagnostic technique for detection of EIPH is via tracheobronchoscopy performed between 30-120 minutes post race ( ranked on a scale from 0-4 0 being mild and 4 being severe )
- bronchoalveolar lavage (BAL) - also used for diagnostic purposes with the presence of free red blood cells
33
Q
what is the treatment for EIPH
A
- administer furosemide (lasix or salix) to affected horses pryer to racing
- diuretic that controls bleeding in the lungs by reducing pulmonary capillary pressure and promoting bronchial dilation
- contriversial and not permitted in some racinf districts
- external nasal stripes have also been used to reduce the severity of bleeding in affected horses although their efficacy has been question and they are also not permitted in all jurisdictions
34
Q
what is the prevention method for EIPH
A
- avoid racing horses with level 3-4 tracheobronchoscopy scores on cold days
- increase intervals between races
- alter racing strategy : avoid early speed
35
Q
what is extertional rhabdomyolysis
A
- disorder of fast twitch muscle fibres
- occurs in genetically susceptible horses in the presence of environmental triggers or can be idiopathic (without known cause) and sporadic
36
Q
symptoms of ER
A
- stilted movement of the hind limbs and frequent reluctant to move
- large freshly muscles over the rump, back and thighs may exhibit spasms and the muscels are excessively firm to the touch
- cramped muscles are painful to the horse and the horse demonstrates a pain response to palpation of the muscles
- horse may have myoglobinuria which occurs when myoglobim is present in the urine; urine is dark and coffee coloured
- distress signs = sweating, elevated pulse, respiratory rate and temperature
- lay down and be reluctant to rise
- increase muscle enzymes and blood urea nitrogen - elevated levels of lactate in blood
37
Q
what does treatment look like for horses with ER
A
- purpose is to limit further damage to muscle tissue, reduce pain, prevent or limit kidney damage, balance electrolytes and replenish fluids
- restrict movement of the horse
- provide hay and water but no grain
- muscel relaxants dantrolene sodium
- fluids and electrolytes can be provided intravenously or nasogastric intubation
- nonsteroidal anti-inflammatories may be administered to alleviate pain
38
Q
how can you prevent ER in predisposed horses
A
- high fat low carb diet
- minimize stress
- keep horse on regular exercise schedule with moderate workouts
- dietary suppliments ( vitamin E selenium, milk of magnesium and sodium bicarbonate)
39
Q
what is the two pathways for EMS
A
- lipotoxicity
- adipokines Lipton resistance
40
Q
what is lipotoxicity
A
- adipose tissue at fatty acid storage capacity
- increased fatty acid uptake by other tissues
- increased fatty acid uptake by other tissues
- fatty acids compete with glucose for oxidation within muscle
- intracellular lipid metabolites accumulate
- phosphorylation of serine/threonine on insulin receptor substrates
- disrupts signalling pathway
41
Q
A
