Endocrine Flashcards
(57 cards)
1
Q
Cycle leading to clinical disease w/ insulin dysregulation
A
Feed abundance –> Increased adipose stores –> temporary adverse effects of adipose stores –> continued feed abundance –> temporary effects become permanent –> clinical disease
2
Q
Pathophys of EMS revolves around (2)
A
- increased adipose stores
2. Insulin dysregulation (ID)
3
Q
what is insulin dysregulation?
A
- excessive insulin response to NSC
- fasting hyperinsulinaemia
- insulin resistance - which is a normal response by cells to a normal level of insulin – to achieve a normal response by cells insulin levels increase
4
Q
how does obesity affect ID?
A
- inflammatory cytokines produced by fat
- adipokines produced by fat
- excessive metabolism of fat in cells = lipotoxicity
—> interferes w/ insulin signalling, causing insulin resistance/dysregulation
5
Q
how are obesity, insulin and laminitis linked?
A
- adipose - increases circulating inflammatory products
- increased insulin shown to cause laminitis + increased glucose may affect laminar vessels
6
Q
predisposing factors to laminitis?
A
- excessive pasture exposure
- carbohydrate overload
- endotoxaemia, systemic sepsis or toxaemia
- supporting limb laminitis-laminar failure
- equine metabolic syndrome/PPID
- previous episodes of laminitis
- corticosteroids w/ concurrent metabolic disease
7
Q
clinical signs of laminitis
A
- acute onset of lameness (bilateral)
- forelimbs > HLs
- reluctant to bear weight, land heel first - ‘heel-toe’ gait
- look uncomfortable behind
- increased digital pulses
- more sore on hard ground, worse on the turn
8
Q
laminitis hoof tester pain location
A
front of frog
9
Q
foot exam - laminitis findings
A
- palpable depression at the coronary band if there is sinking
- penetration of sole: discolouration, softening, draining pt w/ severe rotation
- hoof tester pain in front of frog
10
Q
laminitis blocks to
A
abaxial nerve block
11
Q
acute laminitis management
A
- tx primary disease and remove predisposing factors
- confinement
- sole support-palmar half of foot to point of frog: sand box, sole pack, dense foam, support shoes
- analgesia + NSAIDs: flunixin/bute
12
Q
post acute laminitis management
A
- farrier: rocker toe (bring break-over back), bar shoe w/ sole-pack/palmar support
- reg hoof care + analgesia
- rpt rads to monitor progression
- avoid predisposing factors
13
Q
EMS CS
A
- breeds (ponys), 6-20yo
- obese, regional adiposity
- laminitis
14
Q
EMS ddx
A
PPID, hypoT?
15
Q
EMS dx
A
- in feed glucose test/oral sugar test
- mod. insulin tolerance test
16
Q
fasting insulin levels consistent w/ ID
A
> 20-30uU/ml
17
Q
describe oral sugar test to dx EMS
A
- fast as baseline insulin
- 15ml/100kg corn syrup
- blood at 60 + 90 mins, normal insulin <45 and 60uU/ml
18
Q
describe in-feed glucose test to dx EMS
A
- overnight fast
- give 0.5-1g/kg BWT glucose powder in non-glycaemic feed
- measure serum insulin and plasma glucose after 2hrs
- normal:
0.5g/kg 2hrs <60uU/ml
1g/kg dose 2hr insulin <90uU/ml
19
Q
goal of EMS management
A
decrease ID and restore insulin sensitivity
–> weight reduction: exercise, decrease intake, decrease NSC
20
Q
EMS diet management
A
- consume 1.5-1% body weight
- limit grazing 1hr TID vs. muzzle (only late night/early morning graze)
- less than 10% NSC - remove grain/concentrates/treats
- no pasture access during growing season
- soak hay
21
Q
diets to maintain energy intake BUT w/ a low glucose and insulin response to manage non-obese EMS
A
- soaked beet pulp
- soaked soy hulls
- rice brain
- no fat supp
22
Q
drugs to use for EMS
A
- thyroxine
- metformin
23
Q
MOA metformin in EMS
A
- decreases glucose uptake, utilisation and systemic absorption
- cause a signif. decrease in plasma glucose and insulin
24
Q
PPID signalment
A
> 15 yo, fluffy (hypertrichiosis), cushings
25
pathophys of PPID
- primarily hypothal disease
- loss of dopaminergic inhibition of the pars intermedia
- leading to hyperplasia or adenoma formation of the pars intermedia
- oxidative stress and increased genetic risk
26
what causes clinical disease in PPID
CS dt increased circulation of POMCs and loss of neuroendocrine function of adjacent tissues
27
CS of PPID
- hypertrichiosis - late CS
- LAMINITIS (POMC --> ID)
- hyperhydrosis
- supraorbital fat pads/bags under eyes
- weight loss/wasted topline + pot belly
- PU/PD
- lethargy
- recurrent infections (dt suppression of IL-1, T-cells, APCs)
28
less common CS of PPID
- Neuro: blindness, collapse, seizures
| - infertility?? age related
29
Clinicopath abnormalities of PPID
- mild anaemia
- leukocytosis
- hyperglycaemia and glucosuria
- hyperinsulinaemia
- cortisol not indicative
+/- hepatic enzymes
30
dx of PPID
1. ACTH stims --> measure increased POMCs
2. TRH stim test --> testing hypothal pit axis
3. Dexamethasone suppression test --> tests hypothalmic pituitary adrenal axis
31
ACTH stim test as dx of PPID
- reference ranges vary depending on time of year and geographic location
- horses that exceed the reference interval do not necessarily have the disease - needs to be taken in light of CS
- 'grey zone' --> rest test during best time OR TRH stim
- best time to test: FEB- APRIL (peak of dynamic phase)
32
management of PPID horse
- reg. teeth care + worming
- aggressive tx of infections
- address laminitis/risk + hoof care
- pharmacological: pergolide
33
pergolide MOA in PPID horse
Dopamine agonist --> increases dopaminergic control of the pituitary gland using dopamine agonists
34
response to pergolide tx in PPID horses monitoring
7 days: ACTH levels improve
30 days: improved demeanour/attitude, ACTH/other hormones
6 months: hair coat improvement
Long-term: other CS improvements
35
recommended protocol for PPID/ID horses
1. Document findings:
- baseline feet
- plasma ACTH
- insulin concentration/in-feed glucose test
2. Encourage O to monitor appetite, hair coat, water intake, urination, BCS and general demeanour monthly
3. Pergolide low dose --> reassess in 1-2months
4. One or more CS should have improved + ACTH improved
* ** test at same time of day and under the same conditions
4b) if no improvement --> increased pergolide by 0.001mg/kg ---> until max dose 0.01mg/kg reached
5. Vet monitor 2x/yr ongoing
36
describe the progression of CS with hyperlipidaemia
1. Initial: assoc. w/ primary disease
- depression, failure to drink, lethargy, reduce GIT motility and faecal output
2. Mid: mild colic (stretching liver capsule), D+, icterus, SC oedema, CNS signs, HE
3. Late: recumbency, convulsions, death
Clinical course: days to 3 weeks
37
dx of hyperlipidaemia
TGL >85mg/dl up to 500mg/dl
38
dx of hyperlipaemia
TGL >500mg/dl and opalescent plasma
39
other clinicopath parameters of hyperlipaemia
- liver enzymes elevated
- azotaemia
- glucose
- metabolic acidosis
40
treatment goals of hyperlipaemia
1. Tx primary disease
2. Improve energy intake and balance: IV glucose
3. Decrease circulating TGL and improve uptake by peripheral tissue
4. Tx liver disease
41
hyperlipaemia prognosis and mortality
1. Primary: mortality 80%
| 2. Secondary mortality 25-50% (depends on underlying dz)
42
re. calcium homeostasis horses have ---
- high total and ionized calcium concentrations
- poorly regulated intestinal calcium absorption
- high urinary fractional excretion of calcium
- low serum concentration of Vit.D metabolites
43
acute CS of hypocalcaemia
- when calcium is low sodium channels become activated by smaller changes in the RMP causing CS of increased neuromuscular excitability
- decreased extracellular calcium leads to decreased smooth muscle contractility
- --> tremors
- --> SDF: synchronous diaphragmatic flutter (frenic nerve stim. of diaphragm)
44
CS of lactation tetany
- can occur from 2wks prior to foaling up to weaning dt large loss of calcium in milk
- varied CS: profuse sweating, termors, anxious expression, tachy +/- arrhythmia, ileus, may present w/ colic
45
tx of SDF
- self correct once alkalosis resolved + lytes replaced orally via feed/water
- or IV calcium
46
how do you give calcium borogluconate?
500mls Ca borogluconate in 5L until CS improve then slow to 50mls/hr
47
what conc. of calcigol is safe at 3x maintenance?
20ml/L
48
divisions of hypercalcaemia by cause
1. Dt parathyroid dysfunction--> primary vs. secondary
| 2. Independent of parathyroid dysfunction
49
what causes nutritional secondary hyperparathyroidism?
- diet rich in phosphorous and low in calcium
- high oxalate pastures
- -> increased PTH
50
CS of nutritional secondary hyperparathyroidism
- enlargement of the facial bones
- shifting lameness
- loose teeth
- pathologic fxs
51
dx of nutritional secondary hyperparathroidism
1. Bloods: serum calcium normal/low, P normal/high, serum PTH increased
2. Urinary fractional excretion of calcium is low + phosphorus high >4%
3. Faeces: Ca:P ratio elevated dt oxalates
52
tx of nutritional secondary hyperparathyroidism
1. Diet: Ca:P ration >4:1 (increase lucerne hay, reduce grain and supp. calcium)
Prevention diet: Ca:P ratio >1:1
53
influences of baseline thyroid levels
- age, daily rhythm, environment, exercise
- non-thyroidal illness syndrome
- decreased T3 and T4 dt corticosteroids, higher dietary iodine, PBZ
54
tx of hypothyroidism
- synthetic thyroxine
- iodinated casein
- bovine thyroid extract
55
what is anhidrosis?
- decreased ability to sweat in response to hyperthermia
56
dx of anhidrosis
intradermal sweat test w/ terbutaline dilutions
| - normal horse sweats at 1:1,000,000
57
tx of anhidrosis
- move to cooler/drier climate + aircon boxes
- supplement thyroxine
- feeding combination of KCl and NaCl for chloride replacement
