Internal Medicine: Endocrine: Endocrine Disorders Flashcards

1
Q

What are the differential diganoses of PUPD?

A
  • Diabetes insipidus- central, primary, secondary
  • Iatrogenic- glucocorticoids, diuretics
  • Renal medullary washout
  • Primary polydipsia
  • Osmotic diuresis- diabetes, primary renal glucosuria, fanconi’s syndrome, post-obstructive diuresis
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2
Q

What are the different causes of diabetes insipidus?

A
  • Central diabetes insipidus
  • Primary nephrogenic diabetes
  • Secondary nephrogenic diabetes insipidus- pyometra, renal failure, hypercalcaemia, cushing’s, hyperthyroidism, addison’s, pyelonephritis, liver failure, acromegaly, hypokalaemia
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3
Q

What are the different causes of osmotic diuresis?

A
  • Diabetes mellitus
  • Primary renal glucosuria
  • Fanconi’s syndrome
  • Post-obstructive diuresis
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4
Q

What iatrogenic causes can cause PUPD?

A
  • Glucocorticoids
  • Diuretics
  • Phenobarbitone
  • High salt diet
  • Levothyroxine
  • Vitamin D toxicity
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5
Q
  1. What causes renal medullary washout?
  2. What causes primary polydipsia?
A
  1. Loss of hypertonicity of medulla because of long term PUPD
  2. Problem of thirst centre in brain ‘psychogenic’ or behavioural
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6
Q

What is the definition of polydipsia in terms of values?

A

over 100ml/kg/day

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7
Q

How should PUPD be initially worked up?

If after the initial work up what diseases must it be?

A
  • History- rule out iatrogenic
  • Physical examination- renal disease, pyo
  • Haematology- pyo/pyelonephritis
  • Biochemistry- hyperCa, hypo Na, renal disease, diabetes
  • Bile acids- liver disease
  • T4- hyperthyroidism
  • Urinalysis

If none of the above it must be:
* Hyperadrenocorticism
* Central diabetes insipidus
* Primary nephrogenic diabetes insipidus
* Primary polydipsia

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8
Q
  1. Following an initial work up to PUPD what needs to be excluded next?
  2. Following the above step what are the final tests done?
A
  1. Exclude Hyperadrenocorticism
  2. Water deprivation test, followed by response to exogenous DDAVP (synthetic vasopressin)

Vasopressin = ADH

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9
Q

What are the common pitfalls in workup of PUPD?

A
  • Failure to confirm true PU/PD
  • Disorganised approach
  • Water deprivation test performed too early

Remember CDI and primary NDI are rare, HAC is common

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10
Q

How is central diabetes insipidus treated?

A
  • DDAVP nasal drops applies into conjuntiva
  • 1-4 drops once or twice daily
  • Titrate to clinical signs
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11
Q

What are the different causes of poor growth?

A
  • Nutritional- underfed/poor diet
  • Physiological- mismate, breed variation
  • GI- paratism, megaoeosphagus, EPI, chronic obstruction
  • Cardiac- congenital, endocarditis
  • Renal- dysplasia, polycystic
  • Liver- shunts, hepatitis
  • Lysosomal storage disease
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12
Q

What are the different endocrine causes of poor growth?

A
  • GH deficiency
  • Hypothyroidism
  • Hypoadrenocorticsm
  • Diabetes mellitus

Rare pituitary endocrinopathies
* Pituitary dwarfism
* Acromegaly
* Diabetes insipidus

Parathyroid
* Hyperpatathyroidism
* Hypoparathyroidism

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13
Q

What is the function of ACTH?

A

ACTH is adrenocortitropic hormone

responsible for controlling the production of cortisol by the adrenal glands

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14
Q

What hormones does the pituirary gland produce?

A

FLAT PEG
* FSH
* LH
* ACTH
* TSH
* Prolactin
* Endorphins
* GH

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15
Q

What causes pituirary dwarfism?

What are the clinical features?

How is it diagnosed?

A
  • Rare congenital lesion
  • Almost exclusive GSDs
  • Failure of GH secretion
  • Isolated GH deficiency or combined (FSH, LH, TSH)

Clinical features
* Proportionate dwarfism
* Failure to develop adult coat
* Delayed dental eruption
* Delayed growth plate closure
* Thin, fragile, hyperpigmented skin
* Pyoderma
* Immature gonads

Diagnosis:
* Routine testing notmal
* Rule out other causes
* Definitive: dynamic test to assay GH, IGF-1

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16
Q

How is pituitary dwarfism treated?

A

Progestagens
* Induced GH secretion from mammary tissue
* Adverse effects

GH
* Results usually disapointing
* Skin signs may improve
* Adverve effects

Check thyroid status

Do Not Breed

16
Q

How is pituitary dwarfism treated?

A

Progestagens
* Induced GH secretion from mammary tissue
* Adverse effects

GH
* Results usually disapointing
* Skin signs may improve
* Adverve effects

Check thyroid status

Do Not Breed

17
Q
  1. What is acromegaly?
  2. What is the source in Dogs
  3. What is the source in Cats
  4. What is the signlament in dogs/cats
A
  1. Excess growth hormone
  2. Cats- pituitary tumour
  3. Mammary tissue in response to progesterone/prostagens
  4. Cats- older males, Dogs- intact females (luteal phase)
18
Q

What is the pathogenesis of acromegaly?

A
  • Chronic excess GH leads to insulin antagonism and anabolic effects (IGF-1)
  • Insulin antagnoism leads to diabetes mellitus
  • Anabolic effects on organs, cartilage and bone
19
Q

What are the clinical features of acromegaly?

A
  • Insulin resistant DM
  • Excessive growth of the extremities
  • Prognathism, wide interdental spaces
  • Soft tissue proliferation
20
Q

How is acromegaly diagnosed and treated?

A

Diagnosis
* Diabetes mellitus
* Liver enzyme elevation
* Elevated IGF-1
* MRI/CT

Treatment
* Bitch- OVH (spay) or stop progestagens (Bony changes irreversible)
* Cat- attempt to control DM, surgery, radiation of pituitary mass

21
Q
  1. What controls the secretion of parathyroid?
  2. What are the functions of parathyroid?
A
  1. Calcium controls the secretion
  2. Parathryoid increased Ca and PO4 by affecting osteoblasts, increases calcium reabsorption and decreases PO4, and causes calcitriol (active vitamin D) to increase absorption of Ca and PO4 from GI
22
Q
  1. What causes primary hyperparathyroidism?
  2. What symptoms does it cause?
A
  1. Functional tumour producing PTH
  2. Causes hypercalcaemia- PUPD, dehydration, dystrophic calcification, renal damage (acute renal failure)
23
Q

How can hyperparathyroidism be diagnosed?

A
  • High total calcium and iCA (ionised calcium)
  • Normal to low PO4
  • High PTH
  • Detect mass in thyroid/parathyroid area
24
Q

How is hyperparathroid treated?

A

Restore normal calcium
* Fluids (0.9% NaCl)
* Frusemide (after rehy)
* Prednisilone
* Calcitonin

Surgical removal of parathyroid tumour- monitor Ca post-op

25
Q

What can cause secondary hyperparathyroidism?

A
  • Renal secondary hyperparathyroidism
  • Nutritional secondary hyperparathyroidism- unbalanced diet
26
Q

What is pseudo-hyperparathyroidism

A

Caused a tumour secreting parathyroid hormone related protein

27
Q

What are the causes of primary and secondary hypoparathyroidism?

A

Primary- immune mediated
Secondary- surgery

28
Q

Other then hypoparathyroidism what can cause low Ca2+?

A
  • Hypoalbuminaemia
  • CKD
  • Puerperal tetany
  • AKI
  • Acute pancreatitis
29
Q

What are the clinical signs of low calcium from hypoparathyroidism?

How is it diagnosed?

A
  • Anxiety
  • Muscle twitching, spasm, tetany
  • Weakness, ataxia
  • Seizures
  • Tachycardia, weak pulses

Diagnosis- Low Ca, High PO4, low PTH

30
Q

How is hypoparathyroid treated?

A

Emergency
* IV fluids
* IV/SC calcium gluconate

Maintenance
* Oral calcium
* Oral Vitamin D