ENDO Flashcards

1
Q

What helps increase blood calcium

A

PTH and Vitamin D
Pulls Ca from bone and GIT

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2
Q

What protein can cause calcium to be low

A

Bound to albumin
low albumin = low calcium
(But there may still be some iCa so check) ionised

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3
Q

What high electrolyte can cause calcium to be low

A

Phosphate binds to calcium (complexed fraction)
High phosphate = more bound = low readings

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4
Q

Causes of hypercalcaemia in dogs and cats

A

commonly increased PTH, PTH-like, VD activity, or ostemolyitis
Dogs: malignancy, Hypoadrenocorticism common
cats: idiopathic, renal failure common

Categories:
Parathyroid dependent: neoplasia of the gland or hyperplasia
- see high PTH and high Ca

Parathyroid independent: Malignancy, vitamin D, feline idiopathic, renal failure, osteomyelitis, hypoAC
- see low PTH and high Ca

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5
Q

way to remember some hyperCa causes

A
  • H - Hyperparathyroidism
    • A - Addison’s
    • R – Renal (total Ca, horses)
    • D - Vitamin D
    • I - Idiopathic
    • O - Osteolysis
    • N - Neoplasia
    • S - Spurious
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6
Q

Categories of parathyroid independent causes of HyperCa

A

Malignancy: Lymphoma, anal sac adenocarcinoma, myeloma, bone caner, parathyroid adenoma

Vitamin D excess: poor diet or supplements, rodenticide

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7
Q

How to tell apart PTH mediated and vitamin D mediated hhypercalcamia on bloods

A

PTH: causes high calcium but low phosphorus (lost at kidneys)

Vitamin D: high calcium and phosphorus (causes both to be absorbed from GIT and bone)

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8
Q

What else can be measured in blood to investigate causes of hypercalcaemia (Other than calcium)

A

PTH and iCA

High iCa and low PTH = independent of parathyroid as gland is behaving as expected (Vit D and malignancy)

Originates from parathyroid gland:
- High iCa and high PTH = parathyroid not supressed appropriately so issue of parathyroid gland origin
- Low iCa and low PTH = Parathyroid not working as it should be secreting PTH to raise calcium, so issue originates from parathyroid gland

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9
Q

causes of hypocalcaemia in dogs

A

primary hypOparathyroidism (Low iCA and low PTH)
- Disease destroying cells or post thyroid surgery in cats

demands exceed supplies
- paripartuient (eclampsia), poor diet, renal issue
- this leads to secondary hyperparathyroidism, as iCa is low so PTH is high

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10
Q

types of Hyperadrenocorticism (Cushing’s)

A

Pituitary deponent = excess ACTH (and cortisol)
Adrenal dependent = excess cortisol
Iatrogenic = exogenous steroids

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11
Q

CS of HyperAC (Cushing’s)

A

PUPD (Cortisol antagonises ADH)
Hepatomegaly
Muscle wastage and weakness (Pot belly)
Polyphagia
DERM: Skin thinning, calcinosis cutis, symmetrical alpopecia

Bloods: high ALP, ALT, bile acids, glucose and low urea, stress leukogram (high N, low Ly)

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12
Q

Dx of Cushings (screening)

A

Screening:
Low dose dexamethasone test
- Normal = negative feedback leads to low cortisol (and low ACTH)
- Failure of cortisol suppression following dexamethasone administration. Pituitary may see slight decrease or flatline, adrenal will remain always high
- Long test (8 hours) and multiple samples (3)

ACTH stimulation test
- Normal = cortisol will rise with ACTH
- Adrenal dependent = exaggerated response as adrenals are larger (tumour or hyperplasia from steroids)

  • Urine cortisol:creatinine – high ratio means animal might have HAC
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13
Q

Diagnosis of Cushing’s (differentiation)

A

Differentiation
- Endogenous ACTH
Pituitary = high ACTH
Adrenal = low ACTH through negative feedback

  • High dose dexamethasone suppression test
    adrenal = cortisol stays high
  • Imaging (Brain and adrenals)
    Pituitary - both enlarged,
    adrenal = one atrophy and one hypertrophy
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14
Q

Tx for Cushing’s

A

Trilostane (synthetic steroid with no hormonal activity= competitive inhibition at adrenals)
lowers glucocorticoid levels
give SID

also Selegiline and Mitotane (not licensed)

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15
Q

what does a Phaeochromocytoma screte

A

catecholamine

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16
Q

3 roles of insulin

A

inhibits ketogenesis
stimulates cell glucose uptake
stimulates cell K+ uptake

17
Q

Two types of diabetes:

A

T1 Insulin deficiency diabetes: Most common in dogs, occurs when the pancreas is damaged or not functioning properly

T2 Insulin resistant diabetes: More common in older or obese dogs or temporarily in female dogs during heat (Mammary growth hormone drives insulin resistance)

T2 more common in cats but often not due to obesity

18
Q

Signs of diabetes

A

PUPD (Osmotic diuresis)
Polphagia
Weight loss/ex intolerance/ lethargy
Recurrent infections (especially UTI)
Ketotic breath
Cataracts (omstic effects of glucose => sorbital in lens)

19
Q

Dx for diabetes

A

Fasting hyperglycaemia
Glucosuria (has to be in combo with hyperglycaemia)

also:
high liver enzymes, cholesterol and TAG, fructosamine

20
Q

Tx for diabetes

A

Insulin injections
- Caninsulin has immediate action and is BID
- ProZin is BID as it has a longer action

If collapsed: IVFT, soluble insuline

diet and exercise:
- High quality protein with fibre and complex carbohydrates
- Consistent diet
- Regular, small and frequent exercise

Monitor: blood glucose checks to generate blood glucose curves

21
Q

Interpreting glucose curves

A

Want to see small fluctuations in glucose, remaining within normal values

Outside of normal = dose too low

Very low then very high = SID not enough, change to BID

22
Q

what is a nadir on a glucose curve

A

Lowest glucose concentration attained (nadir concentration)
Time of nadir represents time of peak effect

23
Q

Seeing a lack of response to what amount of insulin means resistance should be investigated

A

over 2iu/kg

24
Q

How is fructosamine useful

A

· Indicates the average BG during the preceding 1-3 weeks
· Often not affected by transient stress hyperglycaemia

25
Q

what is the somogyi effect

A

Somogyi effect = we induce hyperglycaemia by giving too much insulin

Hypoglycaemia develops initially so the body has an exaggerated response to induced hyper-glycaemia

26
Q

how do some feline diet lead to death of beta cells

A

inappropriate carbohydrates in diet = glucose toxicity = high BG = glycogen deposition in the pancreas = apoptosis of beta cells = less insulin so hyperglycaemia

27
Q

feline dietary treatment for DM

A

low carbs high protein (good quality)

28
Q

What leads to diabetic ketoacidosis

A

Reduced insulin → Reduced glucose uptake into cells → metabolic energy deficit
Ketones produced instead (from glucagon)

Ketones lead to:
- metabolic acidosis
- inappetence, nausea, reduced mentation, vomiting

29
Q

Signalment and presentation of DKA

A

Middle aged to older, newly diagnosed often
Since diagnosis – PUPD hasn’t resolved, weight loss has continued.
Progressive lethargy, anorexia and vomiting.

dehydrated, hypovolaemic

30
Q

Dx of DKA

A

BHB ketone in blood
metabolic acidosis on blood gas analysis

Also:
- Electrolytes: Low phosphorus, potassium, sodium, chloride, calcium
- Potassium can sometimes look high due to haemoconcentration (but really is slow due to anorexia, vomting, and PU)

31
Q

Tx of DKA

A

IVFT (Hartmann’s) to restore volume
Only give insulin once hydration stabilised to create normal glucose levels

32
Q

What is Hyperglycaemic Hyperosmolar Syndrome

A

Rare (<5%) but important.
Pathogenesis is similar to DKA BUT ketones not elevated
* Hyperglycaemia → glucosuria → osmotic diuresis → haemoconcentration → hyperglycaemia increases → osmotic diuresis ect ect

Get crazy high levels of glucose (over 33) and blood osmolality (measure this to differentiate)