Endocrine System Flashcards
What are some classifications of endocrine diseases?
- Hormone excess
• Primary gland over-production
• Secondary to excess trophic substance
2.Hormone deficiency
• Primary gland failure
• Secondary to deficient trophic hormone
3.Hormone hypersensitivity
• Failure of inactivation of hormone
• Target organ over-activity/hypersensitivity
4.Hormone resistance
• Failure of activation of hormone • Target organ resistance
5.Non-functioning tumours
What are non-specific presentations of endocrine diseases?
Slide 13
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Diabetes Insipidus (DI) definition causes aetiology risk factors Hx Investigations Management? Complications? prognosis?
Definition
• Inability to concentrate the urine
• Production of large quantities of dilute (hypotonic) urine (5-30 L) • Clinically manifests as polyuria, nocturia, and polydipsia
• Causes
• Cranial (central) DI: Deficiency of vasopressin* (ADH)
• Nephrogenic DI: Unresponsive renal tubules (Resistance)
• Aetiology
• Cranial DI
• Pituitary surgery, head injury/trauma, idiopathic (autoimmune), CNS
infections, CVA • Nephrogenic DI
* aka Arginine vasopressin (AVP)
• Medications, genetic defects, chronic kidney disease
Risk factors
• Pituitary surgery, tumours of the area, lesions of pituitary,
trauma to brain, medication, other autoimmune diseases, FHx
• Hx/Ex
• Polyuria, nocturia, polydipsia, non-specific hypernatraemia,
muscle twitching, visual defects
Investigations
• Serum sodium
• Urine osmolality while normal or Serum osmolality • Normal serum glucose
• 24hr urine collection (<2 lit/d rules out DI)
• Water deprivation test
DI
Management
• Must be differentiated from primary polydipsia
• Fluid administration • Central
• DDAVP (desmopressin) – an analogue of AVP with a longer half-life
• Nephrogenic
• Fluid intake and treat underlying cause
• Low sodium diets
Complications
• Hypernatraemia
• Iatrogenic hyponatraemia
Prognosis
• DI is usually a lifelong condition
Diabetes Mellitus (DM
definition causes aetiology risk factors Hx Investigations Management? Complications? prognosis?
DM (Chronic hyperglycaemia) can affect every system in the body
• Type I
• AI – severe or absolute insulin deficiency
• Type II
• Insulin deficiency
• Insulin resistance • Both
In a diabetic patient, at every consultation check
• BP
• Eyes (visual acuity and Fundus) • Insulin injection sites
• Hands
• Feet
Common abnormalities in hands:
• Limited joint mobility which is a painless stiffness
• Dupuytren’s contracture
• Carpal tunnel syndrome
• Trigger finger (flexor tenosynovitis) • Muscle-wasting/sensory changes
Common abnormalities in feet
• Discoloration of the skin, localised infection and ulcers
• Charcot neuroarthropathy
• Fungal infection may affect skin between toes, and nails • Arterial insufficiency (diminished pulses)
• stocking & gloves distribution peripheral polyneuropathy
what is the criteria for the Dx of DM?
slide 20
What is the clinical presentation
and symotoms of hyperglycaemia?
Managament?
Clinical presentation
• Acute (within weeks)
• Subacute (months to years) • Asymptomatic
Symptoms of hyperglycaemia
• Polyuria, polydipsia, polyphagia, weight loss, fatigue, lethargy,
blurred vision, tingling and numbness in the feet, erectile dysfunction, arterial disease, nausea and vomiting, abdominal pain, tachypnoea, skin infections, mood changes, pruritus vulvae or balanitis
Management
• The goal is to
• Improve symptoms of hyperglycaemia
• Minimise the risks of long-term microvascular and macrovascular
complications
• Prevent development of hypoglycaemia
• Patient education is the cornerstone of the management • A multidisciplinary approach is usually needed
• In T1 DM an urgent treatment with insulin is required
• InT2DM
• Dietary / lifestyle modification
• Oral anti-diabetic drugs • Insulin
What are the complications of DM?
Macrovascular
• CVD
• CVA
• PVD
Microvascular • Retinopathy • Nephropathy • Neuropathy • Peripheral • Autonomic Diabetic foot • Infections • Cancers
Symptoms of hypoglycaemia
slide 27
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What is the function of Cortisol?
Cortisol is BBIIG!
• Maintains Blood pressure (Na+ retention, K+ loss)
• Bone formation
• Anti-Inflammatory
• Immune function
• Gluconeogenesis, lipolysis & proteolysis
Cushings syndrome
How would you confirm Cushing sysndrome or differentiate the casue?
slide 35
The clinical state of increased free circulating glucocorticoid. It can occur due to endogenous or exogenous causes:
slide 33
look at slide 34
Cushings Syndrome:
managment
Prognosis
Management
• Correct the causative factor
• Control complications such as diabetes, hypertension, and
dyslipidaemia
Prognosis
• Varies depend on the cause
• Most cases of Cushing’s syndrome can be cured • Some kinds of tumours may recur
Look at the renin-angiotensin system. slide 38 Hyperaldosteronism slide 39 Aetiology Hx/ex Invetigations
Excess production of aldosterone independent of renin- angiotensin-aldosterone system
Aetiology
• Renin & Aldosterone (secondary hyperaldosteronism)
• Inadequaterenalperfusion(diuretictherapy,cardiacfailure,liverfailure,
nephrotic syndrome, renal artery stenosis)
• Renin-secreting renal tumour (very rare)
• (dec) Renin & Aldosterone (primary hyperaldosteronism)
• Adrenal adenoma secreting aldosterone (Conn’s syndrome) • Idiopathic bilateral adrenal hyperplasia
Addisons disease: What is it? aetiology Clinical features? chronic Investigations management Prognosis
41-45
Cetecholamines
Synthesis and metabolism
Phaeochromocytoma
45
Phaeochromocytoma slide 47
Multiple Endocrine Neoplasia (MEN)
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