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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
Q

postadrenalectomy care

A

1, consider adrenal testing: 30% genetic

  1. annual metanephrines (24 hr urine, plasma)
  2. Additional tx if malignant
26
Q

need for calcium in body

A 
1. exocytosis:
NT secretion
hormone secretion
2. physical properties of bone
3. biochemical processes
27
Q

hypocalcaemia

A

DESTABILISES NEURONES

  • therefore is someone has a fit check serum calcium conc.
  • hypocalcaemia can cause seizures
28
Q

physical signs of hypocalcaemia

A
  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
Q

consequences of hypercalcaemia

A
  • Acute: thirst, polyuria, abdopain

- Chronic: constipation, MSK aches/ weaknesses, neurobehavioural symptoms, renal calculi, osteoporosis

30
Q

measuring serum calcium

A
  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
Q

Ca2+ levels in blood controlled w/I tight range

A

2.15 - 2.55 mmoles/L

32
Q

chief cells

A

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
Q

Ca2+ behaves like a hormone for PTH release

A

less Ca2+ -> altered Ca2+ sensing rs formation -> modified chief cell process -> PTH secretion (provided there is sufficient Mg2+)

34
Q

PTH1 rs

A

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
Q

osteoclast activation (from PTH on bone PTH1 Rs)

A

PTH -> osteoblast PTH1 rs -> rank ligand cytokine -> RANK r

osteoclasts break down bone and release Ca2+ into blood stream

36
Q

Kidney actions of PTH

A
  1. ^ rapid Ca2+ reabsorption:
    - ^ Ca2+ reabsorption in LH, DT, CDs
  2. decreases PO4 reabsorption in PT (proximal tubule)
37
Q

renal synthesis of active Vit D

A

Vit D cholecalciferol:

  • Skin (sun UVIb)
  • diet: cod liver oil, mushrooms
  • > Liver: 25 OH Vit D (measure to determine deficiency)
38
Q

renal actions of PTH

A

25OHVitD ——> 1,25OH Vit D

converted via PTH (hydroxylates 25 OH Vit D)

39
Q

1, 25 OH Vit D causes:

A
  1. activation of Ca2+ trasporters and binding protein (calbindin) in gut cells
    Causes ^ Ca2+ absorption
40
Q

25 OH Vit D –> 1,25 OH Vit D

positive and negative feedback of conversion

A 
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
Q

The kidney and phosphate secretion

A

osteocyte –> FGF23 (fibroplastic growth factor) –> renal phosphate excretion

42
Q

FGF 23

A

fibroblastic growth factor

  • stops 1,25 OH vit D production
  • causes renal excretion of phosphate
43
Q

Ca2+ metabolism- clinical problems

A
  1. primary hyperparathyroidism
  2. hypercalcaemia
  3. hypoparathyroidism
  4. secondary hyperparathyroidism
  5. rickets
  6. osteomalacia
44
Q

primary hyperparathyroidism diagnosis

A
  • elevated serum PTH and Ca2+

- decreased levels of serum phosphate

45
Q

hypercalcaemia

A

renal calculi (kidney stones)

46
Q

Locating parathyroid adenoma

A
  1. isotope parathyroid scan (sesta Mibi)

2. neck ultrasound

47
Q

hypoparathyroidism

A

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
Q

secondary hyperparathyroidism

A

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
Q

rickets

A

reduced vit D

50
Q

osteomalacia

A

(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
Q

Low conc of Ca2+ in blood

A

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
Q

PTH

A

maintains blood ca2+ conc

-maintains bone mineral density

203 endocrinology and reproduction (6 decks)

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