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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
Q

Low dose dexamethasone suppression test measurements are taken at

A

4 hrs and 8 hrs. Both 4 and 8 hr samples should be suppressed.`
Cortisol should be <20

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26
Q

Advantage of the low dose dextamethasone test over ACTH stim test

A

Low dose dextamethasone test can differentiate PTH (85% of dogs) from adrenal dependent

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27
Q

When is the low dose dexthamethasone test contraindicated?

A

DO NOT DO IN SYSTEMICALLY ILL ANIMALS!

FALSE RESULTS IF ALREADY STRESSED

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28
Q

If animal is hyper active in hospital, best way to diagnose cushings is

A

LDDST modified to be performed at home.

Urine samples over 3 day period.

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29
Q

ACTH has concerns regarding false _____

LDDST has concerns regarding false _____

A

ACTH- false negatives

LDDST - false positives

30
Q

Benefit of adrenal ultrasonography

A

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
Q

Triolstane

A

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
Q

Mechanism by which Triolstane causes haemorrage of adrenals

A

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
Q

Adrenal haemorrage is far more profound in PDH or ADH?

A

Far more profound haemorrhage in PDH.
as efficacy reduced in ADH
Addisons concern if triostane given in PDH

34
Q

Why is Triolstane used instead of Mitotane?

A

Triostane is mostly reversal./ Mitotane is cytotoxic and irreversible.

35
Q

Mitotaine still a possible treatment for ___

A

PDH

not for ADH

36
Q

Mitotane destroys which layers of the adrenal cortex?

A 
Zona fasciulata (cortisol)
Zono glomerulosa (aldosterone)
INDUCTION DOSE THEN MAINTENANCE DOSE
37
Q

Adverse effects of Mitotane

A

Variably reversible GIT digns
Lack of sensitivity to mitotane
Neuropathies- particularly cranial nerve
Unpredictable onset of significant hypoadrenocorticism

38
Q

Approach to Hypophysectomy

A

approach via soft palate.

39
Q

Why does Thyroxine need to be given post Hypophysectomy

A

As removal of the pituatary gland removes TRH therefore need to supplement.
Also need to give ADH.
Hydrocortisone infusion during op.

40
Q

Hyperadenocorticism in ferrets pathogenesis

A 
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
Q

Clinical presentation of Hyperadrenocorticism in ferrets

A

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
Q

Diagnostic aids in Hyperadrenocorticism in ferrets

A

Serum hormone elevations.

  • androstenedione
  • dehydroepiandrosterone
  • 17-hydroxyprogesternoe
  • estrodiol
43
Q

Treatment of Hyperadrenocorticism

A

PIT GLAND ALWAYS NORMAL
Remove unilateral (85%0 adrenal gland.
Or Mitotaine/ Trilostane

44
Q

Prevention of Hyperadrenocorticism

A

Associated with early neutering in ferrets therefore use Desrolenin implants instead

45
Q

Anterior lobe of the pit gland is divided into
Posterior lobe of the pit gland is divided into
IN HORSE

A

Anterior lobe: Pars intermedia/ pars distalis/pars tuberalis

Posterior lobe: Pars nervosa

46
Q

What does the posterior lobe of the pituitary gland produce

A

= Pars nervosa that produces ADH and Oxytocin

47
Q

How does the physiology differ in horses from dog hyperadrenocorticism

A

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
Q

Potential pathophysiology of Equine PPID

A

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
Q

Why might seizures and blindness be a sign of PPID in horses?

A

Compression of other areas of the brain by the pars intermedia (poss oxidative damage).

50
Q

Average age of onset for PPID

A

v. rarely less than 10. Average age is 19.

Ponies more likely to be affected that horses.

51
Q

Clinical signs of PPID

A
  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
Q

Why might a horse with PPID present with unilateral prulent nasal discharge

A

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
Q

Diagnosis of PPID

A

Can sometimes diagnosis on clinical signs alone but basal ACTH levels (difficult to handle sample) Do test in Autumn

54
Q

Seasonal changes in ACTH concentrations in horses

A

Peak in autumn (do test in Autumn)

DO NOT DO DEXTAMATHASONE SUPPRESSION IN AUTUMN (no neg feedback so rubbish?)

55
Q

How does a TRH stim test work in diagnosing PPID?

A

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
Q

How is insulin dysregulation related to PPID in horses?

A

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
Q

How does Pergolide work ?

A

Dopamine agonist. Replace lost inhibition of pit gland. Licenced. Side effects: Diarrhoea/Depression/Anorexia/Colic

58
Q

Apart from Pergolide other treatments for PPID in horses

A

Seratonin antagonists e.g. Cyproheptidine. Indirectly increasing dopamine. Less effective than dopamine agnosts e.g. pergolide

59
Q

How do cortisol antagnosisrs work?

A

Triolstane. Only alters the clinical signs due to cortisol. 3- beta-HSD inhibitor.

60
Q

Prodominant cell type in Pars Intermedia

A

Melanotropes.
Process POMC to produce mainly Beta-endorphine, alpha-MESH and CLIP (stimulates insulin resistance).
REGULATED by Dopamine and Seratonin (5-HT)

61
Q

Categorise into Early and Advanced PPID signs

  1. Laminitis
  2. Recurrent infections
  3. Hypertrichosis
  4. Hyperglycemia
A

Laminitis is early PPID sign,.
Recurrent infec, generalised Hypertrichosis and Hyperglycemia (due to CLIP stimulating insulin release) all ADVANCED PPID.

62
Q

For Dexmethasone suppression test, have to inject the synthetic cortisol __-

A

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
Q

Abnormalities associated with EMS

A
  1. Insulin dysregulation
  2. Hyperleptinaemia
  3. Increased adiposity
  4. Hypertriglyceridaemia
  5. Risk factors for Laminitis
64
Q

How does Thyroxine work for treating EMS?

A

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
Q

How to test insulin dysregulation

A

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
Q

How does sodium help you determine type of polydipsia

A

PD is either due to pschygenic or dehydration.

If pschygenic would expect lower sodium if due to dehydration would expect normal sodium

67
Q

ACTH has a lower change of false ____

A

ACTH has a lower change of false positive

68
Q

Why would a urine culture normally be taken in animal with confirmed hyperadrenocorticism

A

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
Q

What type of neutrophils are increased in stress leukogram

A

Mature neutrophillia /Lymphopenia
BAND NEUTROPHILS UNCHANGED!
Left shift: Bands> segemented = infec

70
Q

When is ACTH stim and Dex suppression test contraindicated

A

Dex suppress if already on steroids?

NO IN SYSTEMICALLY ILL ANIMAL = FALSE POSITIVES

VetMed Year 4- Term 2 (14 decks)

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