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VetMed Year 4- Term 2 > Endocrinology week > Flashcards

Endocrinology week Flashcards

1
Q

Structure of campylobacter

A

Curved gram negative rod. Microaerophillic

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2
Q

Optimum temperature for Campylobacter

A

Thermophillic. Replicates best at 42 degrees.

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3
Q

2 types of Campylobacter

A

Poultry: C. jejuniPigs: C. coli

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4
Q

Incubation period for Camylobacter

A

2-5 days. Colonise small intestine causing an enteritis.

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5
Q

Structure of Listeria

A

<10 degrees. Faculative intracellular. Toxin- Lysterolysin to escape phagosome. Gram positive bacillus non spore forming

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6
Q

Which common food bourne pathogen causes haemorrganic colitis/ haemolytic uramic syndrome and renal failure?

A

STEC. Carriage by calves –> beef animals –> Low dose infects humansThrombi formation –> loss of limbs??!

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7
Q

General trend for a) Campylobacter b) Salmonella

A

Campylobacter = steady trendSalmonella = downwards trend. Infectious dose of salmonella is quite high.

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8
Q

Onset of diarrhoea/vomiting that completely resolves in 12 hours. Most likely to be…

A

Staph auerus. Common in nasal secretions. Must be incubated for 6-12 hours. HEAT STABLE TOXIN THEREFORE AUTOCLAVE WILL NOT KILL.

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9
Q

Type of virus; Classical swine fever

A

Pestivirus. Highly contagious, high morbidity and mortality. Last seen in 2000. Going to be seen in pet pigs fed food waste (e.g. palma ham)

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10
Q

Clinical signs of classical swine fever

A

Abnormal haemorrhaging anywhere think CSF. - Blue ears-Haemorrgaic LN (esp mesenteric LN)Haemorragic infacts in spleen

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11
Q

Blue ears in pigs is caused by

A
  • Septicaemia e.g. CSF- Ergot ingestion
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12
Q

Main clinically indisgtinguishable DDx for CSF?

A

African swine fever- spread by vectors; ticks of the Ornithodoros genus. Never been in UK

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13
Q

85% of hyperadrenocorticism is the result of ___

A

Pituatary adenoma.

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14
Q

Appetitite/Oestrous changes with cushings?

A 
Anoestrous in female entire dogs.
Good appetitite (therefore if present off food- unlikely to be cushings)
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15
Q

4 dermal changes seen with Cushings

A
  1. Hyperpigmentation
  2. Non-pruitic Symmetrical alopecia
  3. Comedones
  4. Calcinosis cutis
  5. Hyperkeratosis ‘flaking skin’
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16
Q

Why is Cushings under diagnosed in cats

A

80% of cats have concurrent Diabetes therefore only when cats don’t respond to insulin = further testing for Cushings

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17
Q

3 mechanisms by which Cushings causes PU/PD

A
  1. Reduce ADH production (primary DI)
  2. Reduced response to ADH (2nd Diabetes incipidus)
  3. Cytogenic polydipsea
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18
Q

Tests with High specificity are good for —

A

“S PIN”
ruling in diseases. (aren’t many false positives)
High sensitivity tests= good for ruling out

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19
Q

biochem changes in hyperadrenocorticism

A

Raised liver enzymes Esp ALP (steroid induced increase)

Urine Sp Gr not useful.

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20
Q

What cortisol measurement is better than blood?

A

Basal urinary corticoid excretion is brtter than basal plasma corticoid measurement

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21
Q

Post ACTH levels of

A

If post ACTH Cortisol levels are between 300-600 = normal

>1000 = highly positive (500-750 probably also positive)

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22
Q

How do you calculate specificity

A

“S PIN’

Specificity = True negative/ (True negative + false positive)

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23
Q

High ____ tests are good for ruling out diagnoses

A

High sensitivity tests are good for ruling OUT diseases.

Aren’t many false negatives.

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24
Q

Synthetic ACTH is known as

A

Tetracosactrin given IV

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25
Low dose dexamethasone suppression test measurements are taken at
4 hrs and 8 hrs. Both 4 and 8 hr samples should be suppressed.` Cortisol should be <20
26
Advantage of the low dose dextamethasone test over ACTH stim test
Low dose dextamethasone test can differentiate PTH (85% of dogs) from adrenal dependent
27
When is the low dose dexthamethasone test contraindicated?
DO NOT DO IN SYSTEMICALLY ILL ANIMALS! | FALSE RESULTS IF ALREADY STRESSED
28
If animal is hyper active in hospital, best way to diagnose cushings is
LDDST modified to be performed at home. | Urine samples over 3 day period.
29
ACTH has concerns regarding false _____ | LDDST has concerns regarding false _____
ACTH- false negatives | LDDST - false positives
30
Benefit of adrenal ultrasonography
Adrenal dependent hyperadrenocor will have one large adrenal and one small (has to be large to cause clinical signs) May see 'speckles' indicitive of mineralisation
31
Triolstane
Inhibits cortisol production for less than 24 hrs. Daily medicine for treatment of Cushings Concern that it causes haemorrage of adrenals, seen on ultrasound as 'fluid halo'
32
Mechanism by which Triolstane causes haemorrage of adrenals
Inhibits cortisol synthesis (for 24hrs) and increases ACTH priduction, increases adrenocortical blood flow; adrenocotical blood supply is very fragile--> haemorrage --> acute reduction in cortisol production --> addisonian crisis??
33
Adrenal haemorrage is far more profound in PDH or ADH?
Far more profound haemorrhage in PDH. as efficacy reduced in ADH Addisons concern if triostane given in PDH
34
Why is Triolstane used instead of Mitotane?
Triostane is mostly reversal./ Mitotane is cytotoxic and irreversible.
35
Mitotaine still a possible treatment for ___
PDH | not for ADH
36
Mitotane destroys which layers of the adrenal cortex?
``` Zona fasciulata (cortisol) Zono glomerulosa (aldosterone) INDUCTION DOSE THEN MAINTENANCE DOSE ```
37
Adverse effects of Mitotane
Variably reversible GIT digns Lack of sensitivity to mitotane Neuropathies- particularly cranial nerve Unpredictable onset of significant hypoadrenocorticism
38
Approach to Hypophysectomy
approach via soft palate.
39
Why does Thyroxine need to be given post Hypophysectomy
As removal of the pituatary gland removes TRH therefore need to supplement. Also need to give ADH. Hydrocortisone infusion during op.
40
Hyperadenocorticism in ferrets pathogenesis
``` Middle aged to older ferrets, normal pit gland. Marked adrenomegaly (85% unilat), hyperplasia, adenoma/ adenocarcinoma. NO INCREASED CORTISOL!! Associated with (early) neutering, neutering results in increased levels of GnRH and increased level of both LH/FSH-= secondary over expression in adrenal cortex of LH receptors. ```
41
Clinical presentation of Hyperadrenocorticism in ferrets
Symmetrical alopecia, usually starting in spring. Vulval enlargement in jills. return of sexual behaviour in hobs PRUITIS. Also associated with urethral obstruction in hobs and gynecomastia/mammary neoplasia
42
Diagnostic aids in Hyperadrenocorticism in ferrets
Serum hormone elevations. - androstenedione - dehydroepiandrosterone - 17-hydroxyprogesternoe - estrodiol
43
Treatment of Hyperadrenocorticism
PIT GLAND ALWAYS NORMAL Remove unilateral (85%0 adrenal gland. Or Mitotaine/ Trilostane
44
Prevention of Hyperadrenocorticism
Associated with early neutering in ferrets therefore use Desrolenin implants instead
45
Anterior lobe of the pit gland is divided into Posterior lobe of the pit gland is divided into IN HORSE
Anterior lobe: Pars intermedia/ pars distalis/pars tuberalis | Posterior lobe: Pars nervosa
46
What does the posterior lobe of the pituitary gland produce
= Pars nervosa that produces ADH and Oxytocin
47
How does the physiology differ in horses from dog hyperadrenocorticism
Horses: pars intermedia Dogs: Pars distalis (DD In dogs the Pars distalis is comprised of corticotropes that cleave POMC to produce ACTH/ B endorphine IN HORSES: LOSS OF DOPAMINERGIC INHIBITION OF PARS INTERMEDIA
48
Potential pathophysiology of Equine PPID
Pars Intermedia: Loss of dopaminergic inhibition possibly due to oxidative damage= over production of Pars Intermedia derived products i.e. Beta-endorphine, alpha-MSH, CLIP ONLY MODEST INCREASE IN ACTH. Compression of other areas of brain (blindness/seizures) GLUCOCORTICOID EFFECTS ARE RELATED TO MILD INCREASE IN ACTH but also INCREASED ACTIVITY of ACTH (6x) + NO NEGATIVE FEEDBACK.
49
Why might seizures and blindness be a sign of PPID in horses?
Compression of other areas of the brain by the pars intermedia (poss oxidative damage).
50
Average age of onset for PPID
v. rarely less than 10. Average age is 19. | Ponies more likely to be affected that horses.
51
Clinical signs of PPID
1. Hirsuitism (should be known as Hypertrichosis) 2. Laminitis (excess cortisol?) 3. Weight loss (88% of cases- NOT SEEN IN DOG!) 4. Hyperhidrosis 5. PU/PD 6. Bulging supraoribital fat 7. Susceptibility to infections
52
Why might a horse with PPID present with unilateral prulent nasal discharge
PPID = increased susceptibility to infections therefore commonly develop sinusitis = unilat discharge. Also bulging supraorbital fat in horse (19 year old) is unusual as normally depression.
53
Diagnosis of PPID
Can sometimes diagnosis on clinical signs alone but basal ACTH levels (difficult to handle sample) Do test in Autumn
54
Seasonal changes in ACTH concentrations in horses
Peak in autumn (do test in Autumn) | DO NOT DO DEXTAMATHASONE SUPPRESSION IN AUTUMN (no neg feedback so rubbish?)
55
How does a TRH stim test work in diagnosing PPID?
TRH is a physiological release factor for pituitary. Inject 1mg TRH iv and then measure ACTH (not CORTISOL!) MEASURE after 10 min and 30 min. Greater seasonal effect in July-Nov
56
How is insulin dysregulation related to PPID in horses?
Cortisol antagnosing insulin? Oral sugar test or Fasting. Loss of dopaminergic inhibition possibly due to oxidative damage= over production of Pars Intermedia derived products i.e. Beta-endorphine, alpha-MSH, CLIP ONLY MODEST INCREASE IN ACTH. CLIP =- stimulates insulin secretion.
57
How does Pergolide work ?
Dopamine agonist. Replace lost inhibition of pit gland. Licenced. Side effects: Diarrhoea/Depression/Anorexia/Colic
58
Apart from Pergolide other treatments for PPID in horses
Seratonin antagonists e.g. Cyproheptidine. Indirectly increasing dopamine. Less effective than dopamine agnosts e.g. pergolide
59
How do cortisol antagnosisrs work?
Triolstane. Only alters the clinical signs due to cortisol. 3- beta-HSD inhibitor.
60
Prodominant cell type in Pars Intermedia
Melanotropes. Process POMC to produce mainly Beta-endorphine, alpha-MESH and CLIP (stimulates insulin resistance). REGULATED by Dopamine and Seratonin (5-HT)
61
Categorise into Early and Advanced PPID signs 1. Laminitis 2. Recurrent infections 3. Hypertrichosis 4. Hyperglycemia
Laminitis is early PPID sign,. Recurrent infec, generalised Hypertrichosis and Hyperglycemia (due to CLIP stimulating insulin release) all ADVANCED PPID.
62
For Dexmethasone suppression test, have to inject the synthetic cortisol __-
IM then samples 18 to 24 hrs apart i.e.2 visits. | Not a good test in Autumn c.f. ACTH when DO in autumn
63
Abnormalities associated with EMS
1. Insulin dysregulation 2. Hyperleptinaemia 3. Increased adiposity 4. Hypertriglyceridaemia 5. Risk factors for Laminitis
64
How does Thyroxine work for treating EMS?
Increases metabolic rate resulting in weight loss. Side effects: Hyperphagia so restrict calaroies. Wean off once weight lost. IN UK EXPENSIVE AS CASCADE MEANS DOG TABS USED Short term while increasing exercise/management changes
65
How to test insulin dysregulation
Resting insulin concentration. Fast for 6 hrs (over night and test in morning) and hyperinsulinaemia. OR Oral Gluc test: 6 hr fast then feed glucose then test if blood gluc >85 =+ve
66
How does sodium help you determine type of polydipsia
PD is either due to pschygenic or dehydration. | If pschygenic would expect lower sodium if due to dehydration would expect normal sodium
67
ACTH has a lower change of false ____
ACTH has a lower change of false positive
68
Why would a urine culture normally be taken in animal with confirmed hyperadrenocorticism
Increased risk of bacterial infections i.e. cystitis esp if concurrent diabetes (cortisol antag)- 20% dogs/ 80% cats as increases risk. Cystocentesis and culture
69
What type of neutrophils are increased in stress leukogram
Mature neutrophillia /Lymphopenia BAND NEUTROPHILS UNCHANGED! Left shift: Bands> segemented = infec
70
When is ACTH stim and Dex suppression test contraindicated
Dex suppress if already on steroids? | NO IN SYSTEMICALLY ILL ANIMAL = FALSE POSITIVES

VetMed Year 4- Term 2 (14 decks)

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