Brainscape's Knowledge GenomeTM

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


See full index

Y4 - Small Animals > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

1
Q

What is the effect of hyperadrenocorticism on glucose?

A

*Insulin Resistance (reduced translocation of glucose
transporters)
* Gluconeogenesis

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

What is the effect of hyperadrenocorticism on Bone + collagen?

A
  • Reduces bone formation
  • Reduces calcium absorption in the intestine.
  • Down regulates the synthesis of collagen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the effect of hyperadrenocorticism on amino acids + protein?

A
  • Raises the free amino acids in the serum.
  • Inhibiting collagen formation
  • Decreasing amino acid uptake by muscle.
  • Inhibits protein synthesis.
  • Reduction of IgA, IgM but not IgE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the effect of hyperadrenocorticism on wound healing?

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

What is the effect of hyperadrenocorticism on electrolyte + water balance?

A
  • Increases water diuresis, glomerular filtration rate, and
    renal plasma flow from the kidneys.
  • Increases renal sodium retention and potassium excretion.
  • Increases intestinal sodium and water absorption and
    potassium excretion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What animals get hyperadrenocorticism?

A
  • Medium to older age dogs
  • V rare in cats
  • PDH = more common in small breeds (pituitary dependent hyperadrenocorticism)
  • ADH = more common in large breeds (adrenal dependent hyperadrenocorticism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are common signs of cushings?

A
  • Polydipsia
  • Polyuria
  • Polyphagia
  • Panting
  • Abdominal distention
  • Endocrine alopecia
  • Hepatomegaly
  • Muscle weakness
  • Systemic hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What would be seen on bloods + urine with cushings?

A
  • Haematology = Neutrophilic leukocytosis, Lymphopenia, Eosinopenia, Thrombocytosis, Mild erythrocytosis
  • Serum biochem = Increased ALKP + ALT, Hypercholesterolaemia, Hypertriglyceridaemia, Hyperglycaemia
  • Urinalysis = Specific gravity ≤1.018–1.020, Proteinuria, Urinary tract infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are other effects of cushings?

A
  • Reduced T4 + normal TSH
  • Increased cPLI + snap PLI w no evidence of pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What tests can be done to check for cushings?

A
  • Low dose dexamethasone suppression test - take bloods at 0, 3 + 8 hrs
  • ACTH stimulation test
  • Urine cortisol creatinine ratio
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can you differentiate between pituitary + adrenal mass?

A
  • Measure ACTH
    >45pg/ml in pituitary dependent hyperadrenocorticism
    <20pg/ml in Adrenal dependent hyperadrenocorticism
  • Normal = 20-100pg/ml
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How would you treat cushings?

A
  • Trilostane
  • Start dose = 2-5mg/Kg once daily or twice daily
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How would you monitor cushings treatment?

A
  • Clinical signs
  • ACTH stimulation - repeat q 3months for first year then q 6months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are side effects of trilostane?

A
  • Adrenal necrosis
  • Hypoadrenocorticism
  • Lack of efficacy
  • Vomiting + diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

If patient has hypertension, how would you treat?

A
  • Benazepril
  • If refractory = amlodipine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is tx of macroadenoma?

A
  • Hypophyesctomy
  • Radiotherapy
17
Q

Can you do surgical exicison of cushings masses?

A
  • Adrenal tumours = if not invading renal vein or vena cava
  • high morbidity but can cure
  • Pituitary tumours = survival improving
18
Q

What is the aetiology of addisons (hypoadrenocorticism)?

A
  • PRIMARY = destruction of >90% of adrenal cortices
  • Multiple autoimmune-associated genes may be involved
  • SECONDARY = deficient ACTH (trauma, tumour) leading to atrophy of the adrenal cortex
  • Primarily cortisol deficiency
19
Q

What animals are disposed to hypoadrenocorticism?

A
  • Middle aged female dogs
  • Nova scotia duck tolling retriever (x10 more common)
  • poodle, Gt dane, portugese waterdogs, rottie, WHWT
20
Q

What are clinical signs of addisons?

A
  • Vague malaise
  • Vomiting (haematemesis) and diarrhoea/Melaena
  • Lethargy, weakness
  • Pu, Pd
  • Abdominal pain
  • Hypovolaemic collapse
21
Q

What would you expect on physical exam of addisons?

A
  • Weak pulses
  • Increased CRT
  • Dehydration
  • Bradycardia
  • Abdominal pain
  • Collapse/syncope
22
Q

What would be seen on bloods with addisons?

A
  • Mild non-regenerative anaemia
  • Mild hypercalcaemia
  • Pre-renal azotaemia
  • Lymphocytosis +/- eosinophilia
  • Na:K ratio <27:1
  • Hyperkalaemia and hyponatraemia
  • Isosthenuric to hypesthenuric urine
  • Acidosis
23
Q

What are differentials for hyperkalaemia + hyponatraemia?

A
  • Gastrointestinal disease
  • Renal failure (acute or chronic)
  • Parasitic infection (whipworms)
  • Urinary obstruction
  • Chronic effusion with repeated drainage
  • Pregnancy
  • Congestive heart failure
  • Diabetes mellitus
  • Chronic blood loss
24
Q

What happens to ECGs with addisons?

A
  • Bradycardia
  • Tall, narrow T waves
  • Prolonged QRS interval
  • Decreased P wave amplitude
  • Prolonged P-R interval
  • Absent P wave
  • Complete heart block
  • Ventricular arrhythmias
25
Q

How can you test for addisons?

A
  • Single cortisol = if normal = rules out addisons
  • <55nmol/l will detect 100% of addisons (+37% fale positives)
26
Q

What is Tx of addisons?

A
  • Fluid therapy - v hypovolaemic (EMERGENCY)
  • tx hyperkalaemia = dextrose saline + insulin
  • dexamethasone sodium phosphate
  • prednisolone (if stress) - for life
  • DOCP - Desoxycorticosterone pivalate - for life
27
Q

What can go wrong with treatment of addisons?

A
  • Acute renal failure
  • Myelinosis
  • Depression, weakness, ataxia, tetraparesis, and decreased sensory perception
  • Signs occur days later and are often irreversible
  • Prevention =
  • Raise sodium no faster than 0.5 mEq/L/h
  • Dexamethasone may have protective effect
  • Avoid potent minerallocorticoid therapy during crisis
28
Q

What are signs of phaeochromocytoma?

A
  • anxiety
  • tachycardia
  • tachypnoea
  • vomiting
  • diarrhoea
  • weight loss
  • hypertension (retinal detachment)
29
Q

How are Phaeochromocytoma diagnosed + treated?

A
  • Dx = Radiography or Ultrasound
  • Tx = Radical excision (high risk), antihypertensive medication
30
Q

What are signs of hyperaldosteronism? Tx?

A
  • PUPD
  • weakness
  • neck ventroflexion (hypokalaemia)
  • hypertension (sodium retention)
  • Tx =
  • restrict sodium and supplement potassium
  • surgical excision
  • spironolactone (aldosterone antagonist)

Y4 - Small Animals (105 decks)

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