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203 endocrinology and reproduction > T1 L4&5 calcium & adrenal causes of hypertension > Flashcards

T1 L4&5 calcium & adrenal causes of hypertension Flashcards

1
Q

Cause of too much hormone

A
  1. nodule(s) (single or multiple

2. hyperplasia: generalised increase in tissue

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2
Q

endocrine problems caused by:

A
  1. too much hormone: nodule(s) or hyperplasia
  2. not enough hormone
  3. gland too big, squashes surrounding tissue
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3
Q

layers of the adrenal gland

A

GFR (outside to inside)
Salt, sugar, sex (the further in you go the sweeter it gets)
Glomerulosa: Aldosterone Na+ reabsorbed, K+ secreted)
Fasiculata: cortisol ^bgl
Retucularis: adrenal androgens
Medulla

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4
Q

adrenal causes of hypertension

A 
1. primary hyperaldosteronism
zona glomerulosa (adenoma, hyperplasia, rare genetic causes)
2. phaeochromocytoma
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5
Q

primary hyperaldosteronism (a.k.a Conn’s disease)

A

zona glomerulosa

  • adenoma
  • hyperplasia
  • rare genetic causes
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6
Q

aldosterone secretory pathway

A

angiotensinogen (from liver) + renin (from kidney)

  • > angiotensin I
  • > (converted by ACE) to angiotensin II
  • >
    1. at II receptor causes vasoilation, ADH secretion
    2. at I rs causes vasoconstriction and sympathetic action
    3. converted to aldosterone (works on kidneys)
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7
Q

hypertension

A
  • May be primary hyperaldosteronism (Conn’s disease)
  • screen patients:
    1. hypokalaemic
    2. resistant hypertension
    3. younger people
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8
Q

primary hyperaldosteronism (PA)

A

have more renal & vascular pathology than people with essential hypertension and similar blood pressure
caused by:
1. secreting adenoma
2. bilateral hyperplasia

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9
Q

to determine primary hyperaldosteronism

A
  1. initial screening tests e.g. suppressed renin or normal/ high aldosterone
  2. confirmatory tests: e.g. oral/ IV Na+ suppression tests
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10
Q

test for secreting adenoma or bilateral hyperplasia in primary hyperaldosteronism

A
  1. adrenal CT
  2. adrenal venous sampling
  3. metomidate PET CT
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11
Q

unilateral adenoma (causing primary hyperaldosteronism) treatment

A
  1. laparoscopic adrenalectomy

2. sometimes medical treatment

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12
Q

bilateral hyperplasia

A

1,. medication, aldosterone antagonists (spironolactone and eplerenone)

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13
Q

phaeochromocytoma

A

tumor of the adrenal medulla (neuroendocrine tissue)

- modified post-ganglionic nerve cells innervated by preganglionic nerves

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14
Q

products of the adrenal medulla

A

catecholamines: DA, NA, adrenaline

sympathetic neurons in spinal cord (ACh)-> (w/I adrenal medulla) tyrosine -> L-DOPA -> DA -> NA -> Adrenaline

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15
Q

biological effects of catecholamines

A
  1. noradrenalin (vasoconstriction (^ BP & pallor)

2. Adrenaline (alpha 1. Beta 1&2) (vasoconstriction, vasodilation in muscles, sweating, ^HR)

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16
Q

Phaeochromocytoma presentation

A
  1. spells
    - headache, sweating
    - pallor, palpitations
    - amxiety
  2. hypertension
    - permanent
    - intermittent
  3. family history
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17
Q

several genetic conditions associated w/ phaeochromocytoma

A
  1. Neurofibromatosis type 1
  2. Multiple endocrine neoplasia type 2
  3. Von Hippel-Lindau syndrome
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18
Q

NF1

A

axillary freckling

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19
Q

MEN2

A

medullary carcinoma of the thyroid

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20
Q

Von-hippel-Lindau

A
  • retinal hemangioglioblastoma

- cerebellar haemangioglioblastoma

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21
Q

biochemical diagnosis of phaeochromocytoma

A
  1. 24 hr urine
    - normetanephrines, metanephrines
    - 3 methoxytyromine
  2. plasma
    - NA & adrenaline
    - metanephrines
22
Q

Other things that elevate catecholamines

A
  1. obstructive sleep apnoea
  2. amphetamine like drugs
  3. L-DOPA
  4. Labetalol
23
Q

urine DA

A

comes from kidney + NA not adrenal medulla

24
Q

phaeochromocytoma management

A
  1. alpha blockers
    - phenoxybenzamine
    - doxazocin
  2. B blockers
    - propranolol
  3. laporoscopic adrenalectomy
25
postadrenalectomy care
1, consider adrenal testing: 30% genetic 2. annual metanephrines (24 hr urine, plasma) 3. Additional tx if malignant
26
need for calcium in body
``` 1. exocytosis: NT secretion hormone secretion 2. physical properties of bone 3. biochemical processes ```
27
hypocalcaemia
DESTABILISES NEURONES - therefore is someone has a fit check serum calcium conc. - hypocalcaemia can cause seizures
28
physical signs of hypocalcaemia
1. carpopedal spasm (trousseau's sign) when BP cuff inflated | 2. Chvostek's sign: low plasma calcium increases the neuronal membranes permeability to sodium causes twitching
29
consequences of hypercalcaemia
- Acute: thirst, polyuria, abdopain | - Chronic: constipation, MSK aches/ weaknesses, neurobehavioural symptoms, renal calculi, osteoporosis
30
measuring serum calcium
1. protein bound: 40% - 90% of this is albumin bound - 10% of this is globulin bound 2. bound to cations: 10% - phosphate & citrate 3. ionised (free) 50%
31
Ca2+ levels in blood controlled w/I tight range
2.15 - 2.55 mmoles/L
32
chief cells
in parathyroid gland, make parathyroid hormone - parathyroid hormone is determined by serum Ca2+ concentration - Ca2+ sensing receptors in parathyroid chief cells allow cells to know when to make PTH (low Ca2+ levels prompts biological effect) - Low Mg2+ prevents PTH release
33
Ca2+ behaves like a hormone for PTH release
less Ca2+ -> altered Ca2+ sensing rs formation -> modified chief cell process -> PTH secretion (provided there is sufficient Mg2+)
34
PTH1 rs
cause a biological effect at Bone: rapid action of PTH, osteocytic membrane pump releases Ca2+ into blood stream, calcium release from bone activates osteoclasts Kidney: (make sure Ca2+ isn't lost to kidney)
35
osteoclast activation (from PTH on bone PTH1 Rs)
PTH -> osteoblast PTH1 rs -> rank ligand cytokine -> RANK r | osteoclasts break down bone and release Ca2+ into blood stream
36
Kidney actions of PTH
1. ^ rapid Ca2+ reabsorption: - ^ Ca2+ reabsorption in LH, DT, CDs 2. decreases PO4 reabsorption in PT (proximal tubule)
37
renal synthesis of active Vit D
Vit D cholecalciferol: - Skin (sun UVIb) - diet: cod liver oil, mushrooms - > Liver: 25 OH Vit D (measure to determine deficiency)
38
renal actions of PTH
25OHVitD ------> 1,25OH Vit D | converted via PTH (hydroxylates 25 OH Vit D)
39
1, 25 OH Vit D causes:
1. activation of Ca2+ trasporters and binding protein (calbindin) in gut cells Causes ^ Ca2+ absorption
40
25 OH Vit D --> 1,25 OH Vit D | positive and negative feedback of conversion
``` PTH causes positive feedback of 1,25 )H Vit D production FGF 23(released from osteocytes) causes negative feedback of 1, 25 OH Vit D production ```
41
The kidney and phosphate secretion
osteocyte --> FGF23 (fibroplastic growth factor) --> renal phosphate excretion
42
FGF 23
fibroblastic growth factor - stops 1,25 OH vit D production - causes renal excretion of phosphate
43
Ca2+ metabolism- clinical problems
1. primary hyperparathyroidism 2. hypercalcaemia 3. hypoparathyroidism 4. secondary hyperparathyroidism 5. rickets 6. osteomalacia
44
primary hyperparathyroidism diagnosis
- elevated serum PTH and Ca2+ | - decreased levels of serum phosphate
45
hypercalcaemia
renal calculi (kidney stones)
46
Locating parathyroid adenoma
1. isotope parathyroid scan (sesta Mibi) | 2. neck ultrasound
47
hypoparathyroidism
serum Ca2+ low PTH low or normal Causes: Iatrogenic: thyroidectomy, radical neck surgery - Autoimmune: attack on parathyroid glands - hypomagnesaemia: chief cells need Mg2+ to release PTH - genetic mutations
48
secondary hyperparathyroidism
common causes: low/ low normal serum Ca2+ + high PTH - low serum 25 OH Vit D - lack of sun exposure - GI problems (malabsorption, extensive surgery) - renal failure
49
rickets
reduced vit D
50
osteomalacia
(aka Looser's zone) Vit D deficiency | - elderly people have reduced ability to make vit D in skin therefore levels decrease. Increased fall + fracture risk
51
Low conc of Ca2+ in blood
low conc Ca2+ in blood -> release of PTH -> - efflux of Ca2+ from bone - decrease Ca2+ loss in urine - 1, 25 Vit D causes enhanced Ca2+ absorption from kidneys
52
PTH
maintains blood ca2+ conc | -maintains bone mineral density

203 endocrinology and reproduction (6 decks)

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