Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology - 2nd year > Equine Endocrinopathies and Metabolic disorders > Flashcards

Equine Endocrinopathies and Metabolic disorders Flashcards

1
Q

PPID?

A

Pituitary Pars Intermedia Dysfunction
loss of dopaminergic inhibition of PI (due to neurodegeneration)
“Equine cushings”
High cortisol AND ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the most common equine endo dz?

A

PPID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PPID incidence?

A

> 15 years

ponies and morgans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pars intermedia is made up of ____ that produce ____ which is cleaved into _______.

A

melanotrope
POMC
alpha-MSh, beta-Endorphin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pars distalis is made up of _____ that produce ___ and are cleaved into _____.

A

Corticotrophs
POMC
ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Normal inhibitory control of melanotrophs?

A

Dopamine from hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Positive control of melanotrophs?

A

TRH –> MSH (seasonal regulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PPID path landmarks

A

hypertrophy –> hyperplasia –> adenoma formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PPID results in an abundance of ___.

A

ACTH, CLIP, beta-Endorphin, and alpha-MSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PPID signs?

A 
hirsutism - most common
PU/PD
Laminitis
muscle wasting/weight loss
bulging eyes
XS sweating
immunosuppresion 
infertility
increased appetite
lethargy/docile 
blindness, ataxia, seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Early signs of PPID?

A

delayed shedding
shift in metabolism
regional adiposity
+/- infertility problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PPID dx?

A

Endogenous ACTH - check in morning , quick baseline test, affected by seasons (higher in the fall)
TRH stim - give TRH, measure blood ACTH (increase in ACTH and cortisol)
can also measure MSH in response to TRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

TRH stim test

A

need early morning blood sample and in fall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dexamethasone suppression test

A

Give exogenous steroids, cortisol will not decrease, PI dx
antermortem gold standard
seasonal variations exist, need 2 farm visits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PPID treatment goals?

A

reduce clinical signs, avoid laminitis, dx and manage IR if present, may improve infertility
increase dopaminergic affect - dopamine agonists and serotonin antagonists
laminitis management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pergolide

A 
dopamine agonist (suppress PI activity)
primary side effects are depression and anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Permax/Prascend

A

PPID treatment $$$

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cyproheptadine

A

serotonin antagonist
block ACTH production from PI
variable efficacy

19
Q

Equine metabolic syndrome (EMS)

A

Insulin resistant
Obese/fat deposits
prior/current laminitis
“easy keeper” (low food requirement)

20
Q

EMS incidences?

A

Ponies, morgans, paso fino, fjords
5-20 years old
most are obese

21
Q

EMS clinical signs?

A 
laminitis 
obesity
easy keeper
abnormal repro cycling
cresty neck
22
Q

Prolonged _____ can induce laminitis

A

hyperinsulinemia (>100)

23
Q

EMS dx?

A

resting insulin/glucose concentration (>20-30)
oral sugar test if normal resting insulin - give light karo syrup, measure blood gluc in an hour, + if high glucose and insulin
combined glucose - insulin test

24
Q

EMS treatment

A 
improve insulin sensitivity by: 
reduce body fat
avoid high starch/sugar feeds 
exercise (increase weight loss and insulin sensitivity)
restrict pasture access
no sugar cubes/treats 
Levothyroxine- ONLY SHORT TERM because hypothyroid meds but they help weight loss and and insulin sensitivity
Metformin (PO pill)
25
Q

Thyroid dysfunction

A

NOT like adult acquired hypothyroidism

Euthyroid Sick Syndrome or non-thyroidal illness syndrome - during sepsis

26
Q

Primary site of Ca homeostasis?

A

GI

27
Q

HypoCa conditions?

A

Synchronous diaphragmatic flutter (SDF)
lactation tetany
seizures
colic-endotoxemia

28
Q

SDF

A 
depolarization of phrenic nerve
too fast, specific thumping sound 
horses anxious 
cln path: low Ca, metabolic alkalosis, Low K and Na
Mg may also be decreased
29
Q

Lactation tetany

A

pre-foaling to post-weaning
high sweat, anxious, tachycardia/arrhythnmia, colic
clin path: decreased Ionized Ca
treatment: IV Ca

30
Q

Sepsis/Endotoxemia/Colic

A

common cause in hospital patients
G- bacteria –> LPS —> blood
horses especially senstive to endotoxemia
insufficient PTH secretion and INC Ca sequestration

31
Q

Blister beetles

A 
found in Alfalfa
Cantharidin is toxic to all mucous membranes 
vesicant 
highly irritating
colitis
32
Q

Blister beetles toxicosis

A

fever, tachycardia/pnea, anorexia, colic, PD, dehydrated, hematuria

hypoCa leads to muscle fasciculations, sweating, arrhythmias and SDF

33
Q

HyperCa incidence?

A

HypoCa» Hyperca
primary/secondary (nutritional) hyperPTH
hyperVitD

34
Q

nutritional hyperPTH pathogenesis?

A

decreased Ca/XS P, oxalas
stimulates PTH
Ca and P mobilized from bone
bone —> fibrous connective tissue

35
Q

secondary (nutritional) hyperPTH history and clinical signs?

A

low Ca, high PO4 diet

“big head”
bones of maxilla widen, loose teeth, shifting leg lameness

36
Q

secondary (nutritional) hyperPTH dx?

A

nutritional history, clinical presentation

clin path: Ca low or normal, P normal or high, urinary fractional excretion (highP, lowCa)

37
Q

secondary (nutritional) hyperPTH treatment?

A

increase Ca, decrease P in diet
change Ca:P ratio to 4:1 temporarily
normally 1:1-2:1

38
Q

Anhidrosis

A

can’t sweat, commonly see splashing in water trough

39
Q

Anhidrosis incidence?

A

SE US

no breed or sex predilection

40
Q

Anhidrosis etiology?

A

Catecholamines –> sweat

etiology unknown! Acute –> chronic with irreversible gland unresponsiveness

41
Q

Anhidrosis clinical signs?

A

gradual or acute onset
tachypnea at rest
hyperthermia
limited/failure to sweat during exercise

42
Q

Anhidrosis chronic signs?

A 
poor performance
episodic fever spikes 
anorexia 
dry, flaky skin and/or alopecia 
decreased water consumption
43
Q

Anhidrosis diagnosis?

A

only in research setting

terbutaline sweat test - won’t sweat with injection of terbutaline if anhydrotic

44
Q

Anhidrosis treatment?

A

No evidence based treatment
remove from environment (AC) - can regain sweating ability
environmental management

Endocrinology - 2nd year (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions