Endocrine system Lecture Flashcards

1
Q

Endocrine regulation

A

An endocrine gland can be regulated via direct regulation, neuronal control or feedback regulation (slide 3)

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2
Q

What are the anterior pituitary hormones and what are their target organs and actions?

A
  1. GH- liver- stimulates IGF-1 production which promotes tissue growth and differention
    - inhibits action of insulin on carbs and lipids
    - stimulates lipolysis
2. LH and FSH- Repro organs 
M: 
-LH- causes leydig cells to make testosterone 
-FSH- spermatogenesis 
F:
-LH- ovulation 
-FSH- follicle development 
3. ACTH
MSH (melanocyte stimulating hormone)
Adrenal cortex and melanocytes
-stimulates synthesis of glucocorticoids and androgens by adrenal cortex 
-MSH-melanin synthesis 
  1. Prolactin- mammary glands and repro organs
    - promotes secretion of milk
    - initiates lactation
  2. TSH
    - thyroid gland
    - stimulates production of thyroid hormones
    - maintains size of follicular cells.
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3
Q

What is the posterior pituitary hormones
target organ
effect

A
  1. ADH or vasopressin
    - kidney
    - promotes insertion of aquaporins into DCT + CD
    - decreases H20 excretion
    - vasoconstriction
2. Oxytocin 
Uterus and mammary glands 
-smooth muscle ocntractions
-uterus - labour 
-lactation- milk ejection.
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4
Q

What are the different types of endocrine disease you can get?

A
  1. Hormone excess
  2. Hormone deficiency
  3. Hormone hypersensitivity
    - failure of inactivation of hormone
    - target organ over-active/ hypersensitive
  4. Hormone resistance
    - failure of activation hormone
    - target organ resistance
  5. Non-functioning tumors
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5
Q

What are the pertinent investigations?

A
  1. Adrenal tests
    - plasma cortisol
    - ACTH stimulation
  2. Thyroid tests:
    - TSH
    - T3/T4
  3. Parathyroid tests;
    - PTH
    - serum calcium
    - serum phosphate
  4. Pancreatic tests
    - glucose tolerance
    - fasting
    - postpranial
    - HbA1C
  5. Other:
    - serum electrolytes
    - urinary ketons
    - urinary creatinine
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6
Q

List some of the common condition:

A
  1. Pituitary
    - diabetes Inspidus
  2. Pancreatic dysfunction
    - Diabetes Mellitus (t1 and t2)
  3. Adrenal
    - cushings syndrome
    - hyperaldosteronism (conn’s syndome)
    - Addisons
    - pheochromocytoma
  4. Thyroid disease
    - hypothyroidism (hashimotos)
    - hyperthyroidism (graves diseas)
    - Thyroid neoplasia
  5. Parathyroid dysfunction
    - hyperparathyroidism
    - hypoparathyroidism
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7
Q

What are non specific presentations of endocrine disease?

A

lethargy and depression

  • weight gain
  • weight loss
  • polyuria
  • polydipsia (excessive thirst)
  • heat intolerance
  • palpitations
  • headache
  • muscle weakness (usually proximally)
  • coarsening of features
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8
Q
Diabetes Inspidus (DI
definition 
causes 
aetiology 
risk factors 
Hx/ Ex
Investigations 
managament 
complications 
prognosis
A

Def: inability to concentrate urine so produce large amounts of dilute urine.

causes: Cranial (central)- ADH deficiency
- nephrogenic: unresponsive renal tubules

Atiology:
cranial: headtrauma, surgery, autoimmune, CNS infection, CVA
nephrogenic- medications, genetic defects, chronic kidney disease

risk factors:
Pituitary surgery, tumors in area, lesions of pituitary, trauma to brain, medication, autoimmune disease,

Hx/Ex: polyuria, nocturia, polydipsia (thirst), hypernatraemia (elevated sodium levels in blood), muscle twtiching, visual defects

Investigations:

  • increase serum sodium
  • decrease urine osmolarity while normal or increase serum osmolarity
  • 24hr urine collection (<2lt rules out DI)
  • water deprivation test

management:
-must be differentiated from primary poldipsia
-fluid administration
-central (desmopressin)- an analogue of AVP with longer half-life
nephrogenic- fluid intake and treat underlying cause
-low sodium diets.

Complications:

  • hypernatraemia
  • iatrogenic hypoatraemia

prognosis:
DI is usually a lifelong condition

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9
Q
Diabetes Mellitus 
What are the abnormalities you see in hands and feet?
clinical presentation
symptoms 
management 
Complications
A
Chronic hyperglycaemia- can affect every system in the body 
Type1- insulin deficiency 
Type 2- insulin deficiency 
-insulin resistance 
-both 

In a diabetic patient, at every consultation check:

  • BP
  • eyes
  • insulin injection sites
  • hands
  • feet

Common abnormalities in hand:

  • limited joint mobility which is painless, stiffness
  • Dupuytrens contracture
  • carpal tunnel syndrome
  • trigger finger
  • muscle wasting/ sensory changes

Common abnormalities in feet:

  • discolouration of skin, localised infection, ulcers
  • charcot neuroarthropathy
  • fungal infection may affect skin between toes, and nails
  • arterial insufficiency (diminished pulses)
  • stocking and gloves ditribution peripheral polyneuropathy
Clinical presentation:
-acute (within weeks)
-subacute (months to years)
-asymptomatic 
Symptoms of hyperglycaemia:
-polyuria, polydipsiam polyphagia, weight loss, fatigue, lethargy, blurred vision, tingling and numbess in feet, erectile dysfunction, arterial disease, nausea and vomiting, abdominal pain, tachypnoea, skin infections, mood changes

management:

  • patient education
  • multidisiplinary apprach needed
  • In type 1 DM urgent treatment with insulin required
  • oral anti-diabtetic drugs
  • insulin

complications of DM:

  • macrovascular:
    • CVD
    • CVA
    • PVD
  • microvascular:
  • retinopathy
  • neuropathy (peripheral, autonomic)
  • nephropathy
  • diabetic foot
  • infections
  • cancers
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10
Q

Difference between type 1 and 2 DM

slide 19

A

h

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11
Q

What is teh criteria for the Dx of DM

A
  • fasting plasma glucose >7mmol/L
  • random plasma glucose >11.1mmol
  • glucose tolerance test is only required for boarderline cases and diagnosis of gestational diabetes
  • HbA1C >6.5
  • urine glucose (glycosuria) -not reliable in early stages
  • urine ketons (ketonuria)-
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12
Q

Look at the acute effects of Insulin deficiency

A

22

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13
Q

what are the targets for glucose control?

A

25

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14
Q

What are the effects of cortisol?

A
  • maintains BP (Na retention and K+ loss)
  • decrease bone formation
  • anti-inflammatory
  • decrease immune function
  • inc. gluconeogenesis, lipolysis and proteolysis
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15
Q
Cushings syndrmome 
Cushings disease vs cushings syndrome?
Causes:
ACTH dpendant and ACTH dependant 
Clinical signs and symptoms:
A

symptoms are a aresult of chronic exposure to excess glucocorticoid. There is large spectrum of symptoms depending on duration and intensity of excess steroid production.

Cushings disease: pituitary dependant cause of Cushings syndorme. A adenoma in the pituitary gland produces ACTH, causing elevated levels of cortisol
Cushing syndrome: ACTH decrease= Cushings syndrome: due to increased -ve feedback of cortisol

Causes:

m. c iatrogenic administration of glucocorticoids
- seconly: adenoma produces ACTH. or ACTH tumor and tumors from other areas.

ACTH depenent (ianotropic)

  • normal or elevated levels of ACTH
  • bilateral adrenocortucal hyperplasia
  • increased cortisol
  • inhibited hypothalmic (corticotropic releasing hormone)

ACTH dependant tumor

  • increased cortisol secretion (due to adenoma, carcinoma or any primary issues inside the adrenal gland.
  • suppressed CRH and ACTH.
clinical signs and symptoms: 
Progressive centripetal obesity (moon face, neck, trunk and abdomen), buffalo hump. 
-waisted extremities
Dermatologic manifestations:
-skin atrophy
-easily bruised 
-fragile skin stretch (purple)
-fungal infections 
-hyperpigmentation 
Menstural irregularities
Signs of adrenal androgen excess
-hirsutism
--oily facial skin (Acne)
-increased libido
-virilisation (balding, deep voice etc)

Bone changes:

  • bone loss
  • vertebral compression
  • rib and long bone fractures
  • LBP

Other:

  • glucose intolerance(gluconeogenesis)
  • HTN, CV and thromboembolic events
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16
Q

What tests would you do for Cushings?

What are life threatening consequences if cushings isnt treated?

A
  • 24hr urinary cortisol excretion
  • low dose dexamethasone suppression tests
  • late evening salivary cortisol

Life threatening consequences:

  • depression
  • fractures of bones
  • increased infections.
17
Q

What is the managament, complications and prognosis of Cushings?

A
  1. Management:
    - remove the causative factor and normalise cortisol levels whilst preserving pituitary function
    - care should be taken to control complications like diabetes, hypertension etc. Patients should be advised that following medical care of this condition can improve quality of life and life expectancy.
  2. Complications:
    - adrenal insufficiency
    - CV disease
    - hypertension
    - diabetes
    - osteoporosis
    - treatment related GH insufficiency
  3. Prognosis:
    - without treatment, symotoms persits and pt worsens.
    - untreated 50% die within 5 yrs
    - depending on cause will depend on prognosis.