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Year 4 Small Animal Studies > Internal Medicine: Endocrinology: Adrenal Endocrinopathies > Flashcards

Internal Medicine: Endocrinology: Adrenal Endocrinopathies Flashcards

1
Q

What are the layers of the adrenal gland?

A
  • Capsule
  • Glomerulosa- cortex
  • Fasiculata- cortex
  • Reticularis- cortex
  • Medulla
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2
Q

What do the following layers of the adrenal gland show?
1. Glomerulosa
2. Fasiculata
3. Reticularis
4. Medulla

A
  1. Mineralocorticoids
  2. Glucocorticoids
  3. Androgens
  4. Adrenaline, nor-adrenaline
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3
Q

What are examples of mineralocorticoids

A

Aldosterone
* influence salt and water balance

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4
Q

What is an example of glucocorticoids?

A
  • Cortisol
  • Corticosterone
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5
Q

What are examples of androgens?

A
  • Testosterone
  • DHT
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6
Q

What is ACTH?

A

Adrenocorticotropic hormone

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7
Q

What is hyperadrenocorticism?

A

Over production of cortical (cortex) hormones

Cortisols the baddie

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8
Q

What are the different ways hyperadrenocorticism can be caused?

A
  • PDH- pituitary dependent HAC
  • ADH- adrenal dependent HAC
  • FAT- functioning adrenal tumour
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9
Q

What hormone is required for the production of cortisol and aldosterone?

A

Pregenalone

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10
Q

What are the effects of cortisol?

A
  • Breakdown of adipose to fatty acids
  • Affects hair follicles
  • Gluconeogenesis, insulin resistance
  • Reduced bone formation
  • Reduced calcium absorption in intestine
  • Down regulated the synthesis of collagen
  • Raises free amino acids in serum
  • Inhibits collagen formation
  • Decreasing amino acid uptake by muscle
  • Inhibits protein synthesis
  • Reduction of IgA, IgM IgE
  • Delayed wound healing
  • Increases water diuresis, GFR, renal plasma flow
  • Increases renal sodium retention of potassium excretion
  • Increases intestinal sodium and water absorption and potassium excretion
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11
Q

Who gets hyperadrenocorticism?

A
  • Medium to older age dogs
  • PDH: more common in small breeds
  • ADH: more common in large breeds
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12
Q

What are common clinical signs of cushings?

A
  • Polydipsia
  • Polyuria
  • Polyphagia
  • Panting
  • Abdominal distention
  • Endocrine alopecia
  • Hepatomegaly
  • Muscle weakness
  • Systemic hypertension
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13
Q

What would haematology, biochemistry and urinalysis show for cushings?

A

Haematology
* Neutrophilic leukocytosis
* Lymphopenia
* Eosinopenia
* Thrombocytosis
* Mild erythrocytosis

Serum biochemistry
* Increased ALKP
* Increased ALT
* Hypercholesteraemia
* Hypertriglceridaemia
* Hyperglycaemia

Urinalysis
* Specific gravity
* < 1.013- 1.02
* Proteinuria
* Urinary tract infection

Also- reduced T4, Normal TSH

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14
Q

How can cushings be definitively diagnosed?

A

Low dose dexamethasone supression test

  • 0.01mg/kg dexamethaons
  • Blood sample at 3 and 8 hours
  • Avoid feeding during test
  • High sensitivity
  • Lower but ok specificity

Best screening test

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15
Q

How is the ACTH stimulation test done?

A
  • 5 ug/kg ACTH
  • Blood sample at 0 and 1
  • Avoid feeding
  • Sensitivity higher for PDH
  • Specificity ok

Less effective

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16
Q

How can urine cortisol creatinine ratio be used for diagnosis of cushings?

A

Random sample- less sensitive/specific

Sampling 2 days after a clinical visit
Increases sensitivity/specificity

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17
Q

How can ACTH assay differentiate between PDH and FAT?

A

normal 20-100 pg/ml
* PDH >45 pg/ml in 90%
* FAT < 20pg/ml in 70%

Imaging

18
Q

What is used to treat cushings?
What is the MOA?

A

Trilostane

Competitively inhibits enzyme in adrenal cortex slowing production of cortisol production

19
Q

How is cushings treatment monitored?

A
  • Clinical signs
  • ACTH stimulation test- 3 months for first year then 6
20
Q

What are other effects of trilostane?

A
  • Adrenal necrosis
  • Hypoadrenocorticism
  • Lack of efficacy
  • Vomiting and Diarrhoea
21
Q

What is mitotaine used for in HAC?

A

Cancer of the adrenal gland

(FAC)

22
Q

What frequently occurs with treatment of HAC and how it is treated?

A

Hypertension

Benazepril

23
Q

When can surgery for HAC be used?

A

Adrenal tumuors- if not invading renal vein or vena cava

Pituitary tumours- survival improving

24
Q
  1. What is macroadenoma?
  2. How is it diagnosed?
  3. How is it treated?
A
  1. A benign tissue of the pituitary gland
  2. Patient gets duller when treated but ACTH stimulation and metabolic screens are good
  3. Hypophysectomy, radiotherapy
25
Q

What disease can scottish terriers have that presents as HAC?

A

Hepatopathy
Abnormal dynamic cortisol

Don’t need trilostane

26
Q

What is addison’s disease?

A

Hypoadrenocorticism

27
Q

What is the aetiology of hypoadrenocortism?

A

Primary
* Destruction of >90% of adrenal cortices
* Multiple autoimmune-associated genes may be involved

Secondary:
* Defecit ACTH leading to atrophy of adrenal cortex
* Primarily cortisol defiency

28
Q

What is the most common signalment of hypoadrenocorticism?

A
  • Uncommon
  • Middle aged female

Breeds
* Standard poodle
* Beardies
* Gt Dane
* Portugese water dog
* WHWT
* St B
* Wheaten
* Rottie

29
Q

What are the clinical signs of addisons?

A

Acute or chronic
* Vague malaise
* Vomiting and diarrhoea/Melaena
* Lethargy/weakness
* PUPD
* Abdominal pain
* Hypovolaemic collapse

30
Q

What may be identified on physical examination of addisons?

A
  • Weak pulses
  • Increased CRT
  • Dehydration
  • Bradycardia
  • Abdominal pain
  • Collapse/syncope
31
Q

What can show on haematology and biochemistry for addisons?

A
  • Mild non-regenerative anaemia
  • Mild hypercalcaemia
  • Pre-renal azotaemia
  • Lymphocytosis ± eosinophilia
  • Na:K ratio < 27:1
  • Hyperkalaemia
  • Hyponatraemia
  • Isothenuric to hypesthenuric urine
  • Acidosis
32
Q

What is atypical addisons?

A
  • Cortisol defiency
  • Normal mineralocorticoids
  • Usually progress to mineralocorticoid deficiency
33
Q

What are differentials for hyperkalaemia, hyponatraemia?

A
  • GI disease
  • Renal failure
  • Parasitic infection- whipworms
  • Urinary obstruction
  • Chronic effusion with repeated drainage
  • Pregnancy
  • CHF
  • Diabetes mellitus
  • Chronic blood loss
34
Q

How can hyperkalaemia present on ECG?

A

With increased hyperkalaemia
* Bradycardia
* Tall narrow T waves
* Prolonged QRS interval
* Decreased P wave
* Prolonged P-R interval
* Absent P wave
* Complete heart block ventricular arrythmias

35
Q

How can addisons be diagnosed and ruled out?

A

Endocrine testing
* Single cortisol- addisons ruled out
* < 55nmol will detect 100% addisons
* High false positive

36
Q

How does primary and atypical addisons differ?
* Electrolytes
* Pre/Post ACTH cortisol
* Endogenous ACTH
* Cortisol: ACTH
* Aldosterone: Renin

A

Both
* Pre ACTH cortisol- low
* Post ACTH low
* Endogenous ACTH- high
* Cortisol: ACTH- low
* Aldosterone: Renin- low

Primary- electrolytes abnormal
Atypical- electrolytes normal

37
Q

How does secondary addisons differ to primary:
* Electrolytes
* Pre/Post-ACTH cortisol
* Endogenous ACTH
* Cortisol:ACTH
* Aldosterone:Renin

A

Electrolytes
* P- abnormal
* S- normal

Pre/Post ACTH cortisol
* Both low

Endogenous ACTH
* P- high
* S- low

Cortisol:ACTH
* P- low
* S- high

Aldosterone:Renin
* P- Low
* S- high

38
Q

How is addisons disease treated?

A

Fluid therapy-
* shock rates initially

Hyperkalaemia-
* dextrose saline + insulin,
* calcium gluconate

Steroid
* Dexamethasone sodium phosphate
* Hydrocortisone
* Prednisolone sodium succinate
* Once eating- oral pred, fludrocorstisone

Maintenance therapy
* Oral pred- maybe only when stressed
* Fludrocortisone
* DOCP- desoxycorticosterone privilate

Life long therapy

39
Q

What are potential problems with addisons treatment?

A
  • Acute renal failure
  • Myelinosis

Prevention- raise sodium slowly

40
Q
  1. What is phaeochromocytoma?
  2. What are the clinical signs?
  3. How is it diagnosed?
  4. How is it treated?
A
  1. Tumour of adrenal medulla secreting catecholamines
  2. Episodic: Anxiety, tachycardia, tachypnoea, vomiting, diarrhoea, weight loss, hypertension
  3. Radiography/US
  4. Radical excision, antihypertensive
41
Q
  1. What causes hyperaldosteronism?
  2. What are the clinical signs?
  3. How is it treated?
A
  1. Adrenal tumour- produces aldosterone
  2. PUPD, weakness, hypokalaemia, hypotension
  3. Restrict sodium, supplement potassium, surgical excisoin, spironolactone

Year 4 Small Animal Studies (97 decks)

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