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203: Theme 1 - 304 - Endocrinology > Adrenal gland Physiology + Calcium > Flashcards

Adrenal gland Physiology + Calcium Flashcards

+ clinical biochemistry of Calcium/ bone

1
Q

What are the layers of the Adrenal Gland

(GFR)

A
  • Glomerulosa
  • Fasciulata
  • Reticularis
  • Medulla
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2
Q

What are the adrenal causes of hypertension?

A
  • Primary Hyperaldosteronism (Conn’s syndrome)
    • Zona glomerulosa
      • adenoma
      • hyperplasia
      • rare genetic causes
  • Phaeochromocytoma (Phaeo)
    • tumour of the adrenal medulla
  • some forms of congenital adrenal hyperplasia
    • enzyme defect (uncommon)
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3
Q

Who should be screened for Primary Hyperaldosteronism (Conn’s syndrome)?

A

those with

  • hypokalaemia
  • resistant hypertension (resistant to 3 drugs)
  • younger people
  • they have more vascular and renal pathology than people with essential hypertension &similar blood pressure
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4
Q

What investigations/ assessments would indicate Primary Hyperaldosteronism?

A
  • during initial screening tests
    • suppressed renin
    • normal/ high aldosterone
  • a confirmatory oral or IV Na+ suppression test would be done
  • to get the specific aetiology the following would be done
    • an adrenal CT scan
    • an adrenal venous sampling
      • is also secretion unilateral?
    • Meeomidate PET scan
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5
Q

What is the treatment for Primary Hyperaldosteronism?

  • unilateral vs bilateral adenoma treatment
A
  • Unilateral Adenoma
    • Laparoscopic Adrenalectomy
    • Medical Treatment ( sometimes )
  • Bilateral Hyperplasia
    • Medical Treatment ( Aldosterone Antagonists)
      • Spironolactone
      • Eplerenone
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6
Q

What are the products of the adrenal medulla?

  • how is it stimulated?
A
  • Catecholamines
    • Dopamine
    • Noraepinpherine (Noraadrenalin)
    • Epinephrine (adrenalin)
      • requires cortisol for the conversion from NE
  • sympathetic neurons in the spinal cord stimulate the adrenal medulla
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7
Q

What are the biological effects of Catecholamines?

A
  • Noradrenalin (Alpha 1 & 2 )
    • Vasoconstriction
      • Increased BP
      • Pallor
    • Glycogenolysis (increased blood sugar)
  • Adrenalin ( Alpha 1, Beta 1 & 2 )
    • Vasoconstriction
    • Vasodilatation in Muscle
    • Increased heart rate
    • Sweating
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8
Q

What is the presentation of Phaeochromocytoma?

A
  • “Spells” of
    • Headache, Sweating
    • Pallor, Palpitation
    • Anxiety
  • Hypertension
    • Permanent
    • Intermittent
  • Family history
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9
Q

What genetic conditions are associated with Phaeo?

A
  • Neurofibromatosis Type 1 (NF1)
    • tumours under the skin that grow on nerves
  • Multiple Endocrine Neoplasia type 2 (MEN 2)
    • a familial disorder where one or more of the endocrine glands are overactive or form a tumour.
  • Von Hippel-Lindau Syndrome
    • visceral cysts and benign tumours with potential for subsequent malignant transformation
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10
Q

What is Neurofibromatosis Type 1 (NF1)?

A
  • genetic condition where tumours grow under the skin or deeper
  • appear at any age but predominantly during adolescence
  • these tumours grow on nerves are made up of cell surrounding the nerve and other cell types called - neurofibromas
  • varying number of tumours
  • may or may not be painful
  • Axillary freckling may be present
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11
Q

What is this an image of?

  • in which condition does it occur?
A
  • Cerebellar Haemangioglioblastoma in Von Hippel - Lindau
  • CT + contrast. Right Enhancing cystic Mass
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12
Q

What biochemical investigation/ result would suggest Phaeochromocytoma?

A
  • 24 hour urine
    • Normetanephrines & Metanephrines
    • 3 Methoxytyromine
  • Plasma
    • Noradrenalin & Adrenalin
    • Metanephrines
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13
Q

What factors should be considered when carrying out diagnostic tests for Phaeo?

A
  • Other things can elevate catecholamines
    • obstructive sleep apnoea
    • amphetamine-like drugs
    • L-DOPA
    • Labetalol
  • Urine DA comes from the kidney 7 Nervous system, not the adrenal medulla
    • so the urine methoxytyramine should be measured
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14
Q

What pathology is seen in this image?

A

Phaeochromocytoma of the adrenal medulla

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15
Q

What is the management of Phaeo?

A
  • Alpha-blockers
    • Phenoxybenzamine
    • Doxazocin
  • Beta-blockers
    • Propranolol
  • Laparoscopic adrenalectomy
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16
Q

Go over Post Adrenalectomy care

A
  • Consider Genetic testing
    • 30% are genetic ( 13 mutations so far)
  • Annual Metanephrines (a metabolite of epinpherine)
    • 24 hour urine
    • Plasma
  • Additional treatment if Malignant
    • 10%
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17
Q

What should you do if someone has a fit/seizure for the first time?

  • why?
A
  • check the serum calcium levels
  • hypocalcaemia can cause seizures
    • decrease in extracellular Ca2+ conc. increases the neurons permeability for Na+
    • allows sodium to easily depolarize the neuron’s membrane and cause an action potential
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18
Q

What are physical signs of hypoglycaemia?

( the same for hypoparathyroidism)

A
  • Neuromuscular inability
    • Chvostek’s sign
      • when the facial nerve is tapped at the angle of the jaw, facial muscles on the same side of the face contract momentarily
    • Trousseau’s sign of latent tetany
      • carpal spasm when the brachial artery is occluded for 3 minutes
      • less sensitive than Chvostek’s sign
  • Neurological sign and symptoms
    • Personality disturbance
    • Parkinsonism
    • Irritability
  • Mental status disturbed
    • confusion/ disorientation
    • psychosis/ psychoneurosis
  • Ectodermal changes
    • Dry skin
    • coarse hair
    • brittle nails
    • Psoriasis
    • alopecia
  • Cardiac changes
  • Ophthalmologic manifestations
  • smooth muscle involvement
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19
Q

What are the acute and chronic consequences of hypercalcaemia

A
  • Acute
    • Thirst & Polyuria
    • Abdominal Pain
  • Chronic
    • Constipation
    • Musculoskeletal aches / weakness
    • Neurobehavioral symptoms
    • Renal calculi
    • Osteoporosis
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20
Q

What state would serum calcium be found in?

A
  • Protein Bound: 40%
    • Albumin bound: 90%
    • Globulin Bound: 10%
  • Bound to Cations: 10%
    • Phosphate & Citrate
  • Ionised ( free ): 50%
    • this should be measured directly not through the corrected total serum Ca++
    • 1.1-1.35mmol/L
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21
Q

What is the serum Calcium level range?

A

2.15-2.55mmols/L

22
Q

How are blood calcium levels controlled within their range?

A
  • Parathyroid chief cells in the parathyroid glands produce parathyroid hormones
    • increased secretion of PTH –> increase in serum calcium
  • Calcium-sensing receptor (CaSR) in the chief cells, sense an increase in serum Ca++ and stimulate the uptake of Ca++ by the parathyroid chief cells
23
Q

How does the Calcium sensing receptor CaSR function?

A
  • this is a type of G protein-coupled receptor that is activated by two major signal-transducing effects
    1. Activation of phospholipase C
      • leads to the generation of the second messenger diacylglycerol and inositol triphosphate
    2. Inhibition of adenylate cyclase
      • _​​_suppresses intracellular conc. of cyclic AMP
  • the presence of this receptor in various areas in the body suggests that Calcium behaves like a hormone
24
Q

How does Calcium effect PTH secretion

25
Q

What are the receptors for Parathyroid Hormone

and PTHrP?

A
  • Type 1 parathyroid hormone receptor: Binds both parathyroid hormone and amino-terminal peptides of PTHrP
    • binding activates adenylyl cyclase and phospholipase C systems
    • mRNA coding for type 1 receptor is most abundant in bone and the kidneys,
    • also expressed at lower levels in may other tissues
    • Mutations lead to Jansen’s metaphyseal chondrosplasia ad BLomstrans chondroplasia
  • Type 2 parathyroid hormone receptor: Binds parathyroid hormone, but shows very low affinity for PTHrP
    • expressed in a few tissues also coupled to adenylyl cyclase
    • ligand binding induces a rise in intracellular conc. of cyclic AMP
26
Q

What is the action of PTH in the bone?

A
  • increases renal calcium reabsorption and posphate excretion
    • PTH blocks reabsorption of phosphate in the proximal tubule while promoting calcium reabsorption in the ascending loop of Henle, distal tubule, and collecting tubule
  • promotes the absorption of calcium from the bone
    • In the rapid phase when PTH binds to receptors on these cells, the osteocytic membrane pumps calcium ions from the bone fluid into the extracellular fluid
    • In the slow phase which happens over several days osteoclasts are activated to digest formed bone, and second, proliferation of osteoclasts occurs - stimulates cytokines released by by differentiation of immature osteoclast precursors that possess PTH and it. D receptors
27
Q

What is Rank Ligand?

A

Receptor activator of nuclear factor kappa B ligand

  • RANKL, produced by osteoblasts and other cells, causes osteoclast precursors to form and differentiate into active (mature) osteoclasts
  • implicated in altering the adherence of osteoclasts to the bone surface and suppresses apoptosis of mature osteoclasts
  • body naturally produces a protein called osteoprotegerin (OPG) that neutralizes the effects of RANKL, keeping the bone loss process in check
  • RANKL has direct catabolic effects on cortical and trabecular bone including reductions in bone density, volume and strength
28
Q

Renal Synthesis of Active Vitamin D

29
Q

How is vitamin D production regulated in the kidney?

A
  • PTH stimulates and
  • FGF23 inhibits 1,25(OH)2D
    • leads to renal phosphate excretion
  • In turn 1,25(OH)2D inhibits PTH production and secretion from the parathyroid glands and stimulates FGF23 production from bone
30
Q

What is Primary Hyperparathyroidism?

  • what are its causes
A
  • excess production/ secretion of Parathyroid hormone (PTH) –> increased calcium levels

Causes

  • enlargement of one or more parathyroid gland
  • most common in over 60’s
  • women are more likely to be affected than men
  • radiation to the head and neck increases risk
  • rarely caused by parathyroid cancer
31
Q

What are the symptoms of Primary Hyperparathyroidism?

A
  • Fatigue
  • Fractures
  • Decreased height
  • Upper abdominal pain
  • Loss of appetite/ Nausea
  • Muscular weakness/ Muscle pain
  • Depression/ Personality changes
  • Stupor and possibly coma
  • Kidney stones/ Increased urination

Complications: Osteoporosis, bone cysts in severe cases

32
Q

What investigations can be done to confirm Primary Hyperparathyroidism?

A
  • A test called radioimmunoassay shows an increased level of PTH.
  • Serum calcium is increased.
  • Serum phosphorus may be decreased.
  • Serum alkaline phosphatase may be increased.
  • Bone x-ray may show bone reabsorption (the body breaks down the bone), or fractures.
  • Imaging of the kidneys or ureters may show calcification or blockage.
  • ECG may show abnormalities.
  • This disease may cause changes in the results of the following tests:
    • Calcium - urine
    • Calcium (ionized)
    • Bone density
    • Markers of bone resorption (N-telopeptide, pyridinoline, and deoxypyridinoline)
33
Q

What is the treatment for Primary Hyperparathyroidism?

A
  • treatment depends on the severity of the disease
  • If calcium levels are minimally raised, they may simply be monitored,
    • unless renal dysfunction, renal calculi or osteoporosis are present.
  • Treatment may include:
    • Drinking more fluids to prevent the formation of kidney stones
    • Avoiding immobilization
    • Avoiding thiazide-type diuretics
    • Using Bone protective treatment if osteoporosis is present
    • Treating with a calcium-receptor sensitizer (cinacalcet) to decrease levels of PTH
  • Surgery: if indicated by
    • osteoporosis, renal calculi, <50yrs, serum Ca++ >2.8mmol/l
    • dependent on patient
34
Q

What type of scan is this?

  • what does it show?
A

Sesta Mibi Parathyroid scan

Ectopic Parathyroid adenoma

35
Q

What is this a scan of?

  • type of scan?
A

Parathyroid adenoma

4D CT scan

36
Q

What are the causes of Hypoparathyroidism?

A
  • Iatrogenic
    • thyroidectomy
    • radical neck surgery
  • Autoimmune
  • Hypomagnesaemia
  • Genetic mutations
37
Q

What are the common causes of secondary Hyperparathyroidism?

A
  • Low / low normal serum Calcium + HIGH PTH
    • Low serum 25 OH vitamin D
      • Lack of sun exposure
      • Gastrointestinal problems
        • Malabsorption
        • Extensive surgery ( small bowel )
    • Renal Failure
38
Q

What is rickets?

A
  • A softening of the bones in children potentially leading to fractures and deformity predominantly due to vitamin D deficiency
    • lack of adequate calcium may also lead to rickets
  • majority of cases occur in children suffering malnutrition- famine/ starvation
  • Osteomalacia is used to describe a similar condition occurring in adults
39
Q

What is the overall physiological effect of Parathyroid Hormone?

A
  • Mobilisation of calcium from bone
  • Enhancing absorption of calcium from the SI
    • works indirectly by stimulating the production of the active form of vitamin D in the kidney.
    • Vitamin D induces synthesis of a calcium-binding protein in intestinal epithelial cells that facilitates efficient absorption of calcium into the blood
  • Suppression of calcium loss in urine
    • loss of phosphate ions in urine in exchange for calcium
40
Q

What can cause a disruption to calcium homeostasis?

A
  • Disorders of the gut, kidney, skeleton
  • Disorders of the parathyroid glands
  • Abnormal vit D metabolism
    • intake
    • synthesis
    • metabolism to 1,25-dihydroxycholecalciferol
41
Q

Give an overview of Parathyroid Hormone

A
  • it’s secreted as Intact-PTH (1-84 AA)
    • this is metabolised in the periphery mainly the liver and kidney and stored in the gland and some goes into circulation
    • the active form is PTH 1- 30 AA
  • release stimulated in
    • low plasma ionised calcium (acute stimuli)
    • rise in plasma phosphate (chronic hypocalcemia)
42
Q

What are the key actions of PTH?

A
  • Increase in calcium via
    • renal tubular reabsorption
    • bone resorption (action of osteoclasts)
    • GI tract absorption
      • increased renal generation of active vit D
  • acts as a Hypophosphataemic agent
    • reduces proximal tubular reabsorption of phosphate by decreasing activity of type II sodium-phosphate co-transporter
43
Q

How is intestinal absorption of calcium facilitated?

  • biological reaction
A
  • 1alpha-hydroxylation of 25 hydroxyvitamin D in the kidney forms calcitriol which
  • 1,25 vitD (calcitriol) increases calcium and phosphate uptake,
    • it also stimulates bone resorption, intestinal absorption and renal reabsorption
44
Q

What is the calculation to give the corrected plasma calcium?

A

corrected calcium = calcium + 0.02(40-albumin)

  • disturbances in albumin (the bound fraction of calcium) can cause misinterpreted values
    • abnormally high albumin levels may indicate hypocalcaemia
    • abnormally low albumin levels may indicate hypercalcaemia
45
Q

What are the causes of Hypercalcaemia?

A
  • Malignancy - 65%
    • may be due to local bone resorption due to metastases, or the production of PTH-related protein which activates osteoclasts
  • Hyperparathyroidism - most common in ambulatory patients
  • Hypervitaminosis D
  • Familial hypoclaciuric hypercalcaemia
    • autosomal dominant - inactivation of calcium genes coding for calcium-sensing receptors on the parathyroid cells and the kidney
46
Q

what does plasma PTH levels in hypercalcaemia indicated about the cause of the pathology?

A
  • If there is suppressed PTH
    • non-parathyroid cause: malignant, it D excess, sarcoidosis
  • if there is Raised or detectable PTH
    • PTH mediated cause: 1y or 3y hyperparathyroidism + calcium receptor defects
47
Q

What are the different Hyperparathyoid states?

A
  • Primary
    • adenoma, hyperplasia
    • plasma calcium is high
  • Secondary
    • ​a normal response to chronic hypocalcaemia: CRF malabsorption
    • plasma calcium is low/normal
  • Tertiary
    • ​developed from prolonged secondary state
    • PTH secretion becomes autonomous
    • plasma calcium is high
48
Q

What does the plasma PTH levels in hypocalcemia indicate about the cause of the pathology?

A
  • increased PTH
    • non-parathyroid cause: vit D deficiency, renal failure
  • low/normal PTH
    • parathyroid cause: hyperparathyroidism, Mg deficiency
49
Q

What are the markers of bone formation?

A
  • increase osteoblast activity
  • alkaline phosphatase
  • bone alkaline phosphatase
  • collagen peptides
50
Q

What are the markers of bone resorption?

A
  • Osteoclast activity
  • collagen peptides
  • pyridinolines (x-links)
  • urine hydroxyproline

203: Theme 1 - 304 - Endocrinology (15 decks)

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