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Y2S2 > Other Endocrine Conditions > Flashcards

Other Endocrine Conditions Flashcards

1
Q

What is the constant level conc that free calcium needs to be kept in and where?

A

1.25nm in the extracellular fluid and plasma

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2
Q

What are calcium levels controlled by?

A

*Parathyroid hormone (PTH)
-Calcitonin
-Vitamin D

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3
Q

What is calciums major role and give examples:

A

Ca2+ is important in controlling the permeability of the cell membrane to Na+
Low Ca2+, increase Na+ permeability so depolarisation
High Ca2+, decrease in Na+ permeability so hyperpolarization

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4
Q

What are the symptoms of hypocalcaemia and why?

A

Increase in muscle/ nerve excitability (as closer to threshold)
Muscle spasm (death via spasm of respiratory muscles)

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5
Q

What are the symptoms of hypercalcaemia?

A

Decrease in muscle/ nerve excitability
Causes cardiac arrhythmias

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6
Q

What are the main factors which controls extracellular calcium?

A

Ca2+ reservoir (bones and teeth) = 99% of all Ca2+ in body
Ca2+ kidney excretion
Dietary calcium

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7
Q

Describe the structure of the cortical (compact) bone:

A

Found on the outer part of bone
Have a central canal which has blood vessels
Made of osteocytes (network of these called lamella), which sit in microscopic channels called canaliculi- which contains the extracellular fluid of these cells (bone fluid)
Form a network with osteoblasts which forms connections called osteocytic-osteoblastic bone membrane
Osteoclasts sit on outside of bone and mulinucleate

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8
Q

Describe the mineralised bone:

A

Most of the bone
The majority of the bone compromises of hydroxyapatite crystals which precipitates around the collagen extracellular matrix (the osteoid) in the bone
The osteoblasts secrete the osteoid , causes the high levels of Ca2+ and PO43- in the fluid of the bone to precipitate out and form the hydroxyapatite crystals

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9
Q

Describe bone turnover:

A

Osteoclasts dissolve the bone, produces HCl (dissolves the mineralised bone)
Enzymes ‘cathepsin k’ breaks down collagen matrix
OCs die or migrates
OBs secrete extracellular matrix and fills the cavity

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10
Q

Describe cross talk for bone deposition and resorption:

A

Recruitment of OC precursors and differentiate and attach to surface of the bone
Within the bone as the OC breaks down the bone, it releases IGF and TGF-B from the bone to the bone fluid which causes more differentiation of OB from OB precursor cells and attach T-bone and increase bone deposition

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11
Q

Describe the regulation of OCs using RANKL and OPG:

A

Numbers of OC are controlled by factors from the OB
RANKL (RANK ligand (made by OB), RANK= Receptor Activator of NFkB) increases OC differentiation and decreases OC apoptosis, increasing the number and promoting bone resorption over the long-term
Osteoprotegerin (OPG) is a decoy receptor for the RANKL, decreases OC numbers and promotes bone deposition over long-term
The balance of these two factors is an important determinate of bone density

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12
Q

How is oestrogen involved in bone density?

A

Oestrogen stimulates production of OPG and promote apoptosis of OC and increases a number of OB

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13
Q

Describe the parathyroid hormone in Ca2+ homeostasis:

A

Peptide hormone (84 a.a)
Secreted from the parathyroid gland
Secretion increases with plasma Ca2+ conc falls
Acts to increase plasma Ca2+

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14
Q

How does the parathyroid cells monitor calcium concentration?

A

Monitor directly by the parathyroid cells via Ca-sensing receptors (GPCRs), negative feedback loop, as Ca2+ decrease causes signalling, therefore signalling of PTH
Acts on *bone, kidneys and GIT

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15
Q

What is the effect of PTH on the bone?

A

PTH leads to a release of Ca2+ from the bone to increase the plasma Ca2+ levels
This occurs in 2 phases:
-fast exchange
-slow exchange

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16
Q

Describe the fast exchange due to hypocalcaemia:

A

PTH induces a rapid efflux of Ca2+ within the canaliculi of the bone
There are PTH receptors on OBs and OCs
PTH receptors are GPCRs coupled to Gas, when stimulated there is an increase in cAMP and movement of Ca2+ into the cells from the bone fluid
Gap junctions allowing the movement of Ca2+ via the OCs out through the OBs and into the plasma to the BVs

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17
Q

Describe the slow exchange due to hypocalcaemia:

A

Activated under conditions of prolonged hypocalcaemia
PTH activates OBs to increase RANKL expression, so increases OCS
The OCs increase bone resorption which increases plasma Ca2+
OB building activity is inhibited
Plasma PO43- levels are also increases
Balance is restored when Ca2+ absorption in the GIT is increased

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18
Q

What is the effect of PTH on the kidneys?

A

PTH promotes Ca2+ retention (Ca2+ reabsorption occurs)
Promotes PO43- excretion (decreases PO43- reabsorption)
Causes an activation of Vitamin D (occurs in the kidney)
Activated Vitamin D causes an increase in the Ca2+ absorption of the GIT, so PTH indirectly causes an increase of uptake form the diet

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19
Q

Describe Calcitonin in Ca2+ homeostasis:

A

The antagonistic hormone to PTH
It is secreted by the cells of the thyroid hormone
Secretion is increased when there is an increase in plasma Ca2+
Peptide hormone (32 a.a)

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20
Q

How does Calcitonin monitor calcium concentration?

A

Receptors are GPCRs that increase cAMP
Acts to decrease levels of extracellular plasma Ca2+ by:
-decreasing Ca2+ movement from the canaliculi fluid into the plasma
-inhibiting OC activity
-inhibiting reabsorption of Ca2+ and PO43- in the kidney so increases excretion

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21
Q

Describe Vitamin D in Ca2+ homeostasis:

A

A pre-hormone, that following metabolism to active hormones, increases Ca2+ absorption in the GIT
It is a steroid like hormone

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22
Q

Where is Vitamin D obtained from?

A

Is synthesised in the skin in response to sunlight (precursor 7-dihydrocholesterol into Vitamin D3 in response to UV light)
It is also absorbed from the diet (especially dairy products)

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23
Q

Describe the process of activating vitamin D:

A

Activated in the liver and kidney
- 1 OH group added in the liver -> (25-OH-vitD3) Calcifediol, this is stored until required
- 2nd OH group added in the kidney -> (1,25-(OH)2-vitD3) Calcitrol, caused by PTH which is activated

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24
Q

How does vitamin D monitor calcium concentration?

A

Activated vitamin D acts at nuclear receptors- a transcription factor promoting gene expression
Genes expressed lead to increased absorption of Ca2+ and restoring Ca2+ balance
Also increases reabsorption of Ca2+ in the kidney and works with PTH to increase mobilisation of Ca2+ in the bone

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25
Q

What are the two main types of bone and describe them:

A

Cortical bone (80%)- compact bone that forms the dense outer supporting structure
Trabecular bone (20%)- spongy bone that forms the inner supporting structure, composed of a lattice or network of branching bone spicules or trabecular and spaces filled with bone marrow

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26
Q

When does skeletal maturing occur and what happens after that?

A

Happens at around 25-30 years and plateus for around 10 years
Faster deterioration in females at menopause

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27
Q

What is bone mass determined by?

A

Peak bone mass that was attained at around age 30
Rate of bone loss that commences at 40

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28
Q

What genetic factors can attribute to rate of bone loss?

A

Genetic factors (75%)
More likely to have osteoporosis if strong family history
Possible involvement of several genes:
-Vit D receptor gene
-Oestrogen receptor gene
-IL6 gene

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29
Q

What environmental factors can attribute to rate of bone loss?

A

Risk factors for osteoporosis:
- low Ca2+ intake and/ or absorption
- low vit D intake or lack of exposure to sunlight
-physical activity
-alochol
-smoking
-thin body type

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30
Q

What is osteoporosis?

A

Common metabolic bone disease characterised by a reduction in bone mass per unit volume that occurs with age
Increase in bone fragility and susceptibility to fracture

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31
Q

What does BMD stand for?

A

Bone Mineral Density

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32
Q

What is a T score in osteoporosis?

A

Number of standard deviations by which the individuals BMD differs from the mean peak for young adults of the same gender
Fracture risk doubles for every deviation below the mean

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33
Q

Describe the T scores and what do they mean for osteoporosis?

A

Normal = above -1
Osteopenia= between -1 and -2.5
Osteoporosis= -2.5 or less
Established osteoporosis= -2.5 or less and a fracture

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34
Q

Is an X-ray a good diagnostic factor to use in osteoporosis and why?

A

No, it is not capable of detecting bone loss until at least 30% of bone mass is lost

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35
Q

What is used to measure BMD?

A

Dual Energy Xray Absorptiometry (DEXA) scan is used
Enables accurate and reproducible measurements of BMD, but is expensive

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36
Q

Describe primary osteoporosis and give examples:

A

Diagnosed when pt has no other disorders known to cause osteoporosis
e.g post menopausal (women within 15-20 years after menopause)
e.g age related, or senile

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37
Q

Describe secondary osteoporosis and give examples:

A

Related to another medical condition:
-anorexia nervosa
-inflammatory bowel disease
-endocrine e.g T1D, Cushing’s, hyperthyroidism
Related to drug therapy
-most commonly steroid (glucocoritcoid) induced
-others, carbamazepine, phenytoin, heparin, furosemide , PPIS

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38
Q

How do corticosteroids cause secondary osteoporosis?

A

Decrease OB activity and active lifespan
Decrease Ca2+ absorption from the intestine and increase renal Ca2+ loss, causing abnormal PTH and vit D activity
Suppress sex hormone production

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39
Q

What is fragility fracture in osteoporosis?

A

Fracture that occurs as a result of mechanical forces that would not ordinarily cause fracture
WHO quantifies this as a force equivalent to a fall at standing height or less

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40
Q

What are the symptoms due to fractures of osteoporosis?

A

Can gradually cause the spine to collapse, resulting in height loss, pain and a deformed back
Forward curvature= kyphosis

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41
Q

What most common bones are fractured in osteoporosis?

A

Vertebra
Distal radius (wrist)
Neck of Femur (hip)

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42
Q

Which patients should receive osteoporosis prophylaxis when taking glucocorticoids?

A

Anyone with prior fragility fracture
Women 70 or above
Post menopausal women and men 50 or above prescribed high dose steroids i.e 7.5mg/day of prednisolone or equivalent over 3 months or more than 30mg day for 4 weeks
Post menopausal women and men aged 50 or above with a high risk FRAX score

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43
Q

What is a FRAX score?

A

Fracture Risk Assessment Tool
Online tool used to predict a persons 10 year risk in developing a major osteoporotic fracture

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44
Q

What is the treatment for low risk patients for osteoporosis?

A

Lifestyle + calcium/vitD

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45
Q

What is the treatment for intermediate risk patients of osteoporosis:

A

Assess BMD with DEXA scan + lifestyle+ calcium/vitD

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46
Q

What is the treatment for high risk patients?

A

Consider starting treatment without need for BMD assessment

47
Q

What are lifestyle changes made to reduce osteoporosis?

A

Regular exercise:
-low impact weight bearing exercise like walking
-high intensity strenth training to target muscles around hip/spine/wrist
Avoid smoking
Moderating of alcohol intake
Aim to take 3-4 portions of Ca rich food daily, min 700mg/day
-e.g 200ml milk, 4 slices of white bread, 30g hard cheese, 125g yogurt pot, 60g sardines
Vitamin D
- dietary intake 400IU daily and increase exposure to sunlight

48
Q

What should be given to all patients in a nursing home?

A

Vitamin D supplement
Including people who are house bound

49
Q

Describe calcium and vitamin D treatment for osteoporosis:

A

Calcium 1000mg per day
Vit D 800IU per day
e.g Calcichew D3 forte, Adcal D3
Dose depends on dietary intake
Higher doses required for frail and house bound pts

50
Q

What are risk factors for falls?

A

Drugs e.g antihypertensives, sedatives, diuretics
Other risk factors, balance, for vision, environmental factors such as loose carpets

51
Q

What is the first line drug treatment for osteoporosis and describe:

A

Bisphosphonates
Alendronic acid (daily or weekly)
Risedronate (daily or weekly)
Ibandronate (oral monthly, IV 3 monthly)
Zolendronate (annual IV)

52
Q

When should you review the BMD when taking bisphosphonates?

A

Oral treatment: after 5 years
IV treatment after 3 years

53
Q

What is the MoA of bisphosophonates?

A

Adsorbed into hydroxyapatite crystals in bone
Slow the rate of growth and dissolution
Decrease rate of bone turnover
Bind to Ca2+ in the bone and released as the bone is reabsorbed
Main action on OCs as BPs in the bone, as OC breaks down the bone, it causes BPs to be released, they inhibit the OC attachment to the bone, so can’t reabsorb the bone

54
Q

What is the patient counselling for bisphosphonates?

A

Take on an empty stomach (at least 30 mins (60 mins for ibandronate) before breakfast and any other oral medications including calcium supplements- wait 2 hours to take these)
Swallow whole with a full glass of PLAIN water
Take whilst sitting upright or standing
Remain upright for at least 30 mins (60 mins for ibandronate)
Dont lie down until after eating breakfast
Dont take at bedtime or before rising
Stop treatment and report any signs of oesophageal irritation
If pt can’t adhere to these then should be considered for IV therapy

55
Q

Why do pts have to sit upright when taking bisphosphonates?

A

If it gets stuck in oesophagus can cause oesophageal perforation

56
Q

What are rare but important side effects of bisphosphonates?

A

Osteonecrosis of the jaw (exposed nectroti bone)- maintain good oral hygiene, routine dental check ups, report any oral symptoms
Atypical femoral fractures- report any thigh/ hip/ groin pain
Osteonecrosis of the external auditory canal- report any ear pain or discharge

57
Q

What is the drug treatment for steroid induced osteoporosis?

A

1st line- alendronic acid or risedronate
2nd line- zolendronate, denosumab, teriparatide
Ca and Vit D supplements

58
Q

Describe the second line drug treatment in osteoporosis:

A

Denosumab
Raloxifene
Teriparatide
Strontium ranelate
Romosozumab
HRT
Adjunct with Ca/vit D supplements

59
Q

What level of vitamin D is someone at risk of having a vitamin D deficiency?

A

Serum 25-hydroxy vit D levels less than 25nmol/L

60
Q

What level of vitamin D does someone who is at hight risk have a vitamin D deficiency?

A

Serum 25-hydroxy vit D levels between 25-50 nmol/L

61
Q

What is an adequate level of vitamin D in a normal person?

A

Serum 25-hydroxy vit D levels higher than 50 mol/L

62
Q

What is the treatment for a vitamin D deficiency?

A

Colecalciferol 400IU= 10mcg
Loading dose:
-50,000 IU once weekly for 6 weeks
-40,000 IU once weekly for 7 weeks
-4000 IU daily for 10 weeks
Maintenance dose:
800-2000IU daily to start 1 month after LD completed
Max 4000IU per day if high risk

63
Q

Describe Raloxifene as a treatment for osteoporosis:

A

A selective oestrogen receptor modulator (SERM)
Mixed agonist/ antagonist at oestrogen receptors
Stimulates OB activity, inhibits OC activity
Blocks receptors on mammory and uterine tissue so no risk of breast/uterine cancer

64
Q

Describe Denosumab as a treatment for osteoporosis:

A

Moncolonial antibody to RANKL
Inhibits binding of RANKL to RANK

65
Q

Describe Calcitonin as a treatment for osteoporosis:

A

Has the same effect as the endogenous calcitonin
Stimulates OBs, inhibits OCs

66
Q

Describe Teriparatide as a treatment for osteoporosis:

A

Active fragment of PTH (a.a 1-34)
Acts at PTH receptors
Paradoxically has opposite effects to PTH

67
Q

Describe Strontium as a treatment for osteoporosis:

A

Increases the sensitivity of the Ca2+ sensing receptor in the parathyroid cells
Strontium round the same place as calcium in the periodic table
Decreases PTH secretion

68
Q

What is menopause and what is the average age of onset?

A

The permanent cessation of menstruation resulting from loss of the ovarian follicles
It can only be determined after 12 months of spontaneous amenorrhoea
Mean age is 51

69
Q

What occurs in the menopause in terms of hormones?

A

The number of eggs decrease until there are none left
The follicular activity falls
Oestrogen levels fall (this causes symptoms)
Negative feedback loop on pituitary starts to fail so levels of FSH and LH rise
Menopausal pattern=low oestrogen, high FSH and LH

70
Q

What is the perimenopause phase?

A

Gradual onset of endocrine changes as ovaries start to fail
Lasts approximately 4 years started at around 47.5 years
About 10% of women will not receive this transition

71
Q

In the early days of menopause, is it still possible to get pregnant and why?

A

Yes, as for some time the levels of FSH and LH can remain normal

72
Q

What is premature menopause?

A

Menopause occurs before the age of 40
Leads to an increase risk of developing osteoporosis and CVD

73
Q

What is post menopause?

A

Time after the menopause
Occurs after 12 months of spontaneous amenorrhoea
Difficult to recognise in women who have started HRT

74
Q

What are the short term symptoms of the menopause?

A

Menstrual cycle shortens or lengthens
Menstrual blood loss alters (increases)
Vasomotor symptoms; hot flushes, night sweats, palpitaitions
Psychological problems; mood changes, irritability, sleep disturbance, depression, decreased libido
Musculoskeletal symptoms; joint and muscle pain
Vaginal symptoms; dryness and dyspareunia
Urinary symptoms; UTIs, incontinence, eventually urethral symptoms e.g dysuria

75
Q

What are the long term symptoms of the menopause?

A

Loss of protective functions of oestrogen:
+ve effect on bone mass (forming OBs)
+ve effect on blood lipid profile (cholesterol)
-ve effect on coagulation and fibronolytic activity
Significant loss of Ca from bones giving an increased risk of fractures- osteoporosis
Change in blood lipid profile giving an increased risk of CVD

76
Q

What are the two types of HRT?

A

Oestrogen with progesterone
Oestrogen only

77
Q

When would oestrogen with progesterone be given as a HRT and why?

A

Women with an intact uterus
To stop over stimulation of the endometrium by unopposed oestrogen, as oestrogen can increase risk of endometrial cancer

78
Q

When would oestrogen only be given as a HRT and why?

A

Women without a uterus e.g who’s had a hysterectomy
If the uterus has been removed there is no endometrium to stimulate

79
Q

What are the aims of oestrogen therapy?

A

Aims to restore and maintain near normal oestrogen levels
Reinstalls the negative feedback loop so LH and FSH levels fall

80
Q

What type of oestrogen is used in HRT and why?

A

Naturally occurring oestrogen such as:
-estradiol -estrone- conjugated oestrogens
Natural oestrogen are better in this context then the synthetic oestrogen used in oral contraceptives as the synthetic are 200x more potent so the synthetic would increase the risk of serious side effects e.g adverse lipid profile, increases BP and increase risk of blood clotting

81
Q

Can HRT be used as a contraceptive and why?

A

No, HRT is less potent than oral contraceptives

82
Q

When is a woman considered potentially fertile while around the menopause age?

A

For 2 years after last period if under 50
For 1 year after the last period if over 50

83
Q

What should be given to women under 50 if they are also experiencing menopausal symptoms and potentially fertile?

A

Low dose COC

84
Q

What should be given to women over 50 if they are experiencing menopausal symptoms and potentially fertile?

A

Non-hormonal contraceptives and HRT

85
Q

How much progesterone is needed in HRT and give examples:

A

Is needed for a minimum of 10 days per 28 day cycle
Usually use less androgenic (synthetic) e.g dydrogesterone, medroxyprogesterone acetate
Rather than more androgenic such as norethisterone, levonorgestrel

86
Q

What are the different formulations of HRT?

A

Oral
Transdermal; patch, gel, spray
Vaginal; cream, ring
Implant (unlicensed- rarely used)

87
Q

Describe the combined oral HRT to mimic the menstrual cycle for perimenopausal women:

A

Oestrogen= 28 days
Progesterone= 12 or 14 days
No interval
Bleeding every 4 weeks
E.g Elleste-duet

88
Q

Describe the combined oral HRT for borderline post menopausal women:

A

Oestrogen= 70 days
Progesterone= 14 days
Then 7 day placebo
Bleed every 3 months
E.g Tridestra

89
Q

Describe the combined oral HRT for post menopausal women:

A

Oestrogen= 28 days
Progesterone= 28 days
Repeat without interval, no bleed
May be irregular bleeding for first 6 months
E.g Premique

90
Q

What are the benefits of the transdermal route of HRT compared to the oral route?

A

Gives a lower day to day variation in blood levels
Produces a more natural psychological oestradiol:oestrone ratio
Bypasses first pass metabolism and has less effect of clotting factors produced by the liver
Smaller dose needed

91
Q

When would the transdermal HRT be used first line?

A

There is a lower rate of VTE
So first line if increased risk of VTE, BMI is larger than 30, previous/ family history of VTE

92
Q

When would vaginal oestrogen be used as HRT?

A

Monotherapy when vaginal and/or bladder symptoms predominate
May also be required in addition to systemic HRT

93
Q

Name and describe examples of vaginal HRT:

A

Vaginal tablets e.g Vagifem
Ring e.g Estring
Creams or gel e.g Ovestin, Gynest
Pessaries

94
Q

Describe GINA as a vaginal HRT:

A

OTC
Estradiol 10mcg vaginal tablets
For vaginal atrophy due to oestrogen deficiency in POST menopausal women over the age of 50 who have not had a period for at least a year
One vaginal tablet daily for 2 weeks then one vaginal tablet twice weekly

95
Q

What is systemic HRT used for and give examples:

A

For vasomotor symptoms and other symptom control, prevention and treatment of osteoporosis
Tablets
Patches (Evorel)
Gel (Oestrogel, Sandrena)
Spray (Lenzetto)

96
Q

How long should HRT be used for and when should there be reviews?

A

For vasomotor symptoms, usually 2-3 years (initial review at 3 months to assess efficacy and tolerability)
Annual review recommended because of the increase risk of SEs

97
Q

What are the risk/benefits of using HRT and age together?

A

HRT prescribed before the age of 60 has a favourable risk/ benefit in healthy women
HRT can be used in women over 60 but lower dosages should be started, preferably with a transdermal route

98
Q

What are the side effects of oestrogen?

A

Nausea and vomiting
Abdominal cramps and bloating
Weight (gain)
Breast tenderness/ enlargement
Premenstrual like syndrome
Sodium and fluid retention
If can tolerate them, continue to use for 3 months as generally transient

99
Q

What are the side effects of progesterone?

A

More androgenic:
-causes greasy skin+ hair
-tend to off set some of the protective effect of oestrogen on lipid profile
Less androgenic:
-abdominal bloating
-mood changes
-breast tenderness

100
Q

What are the short term benefits of HRT?

A

Control of symptoms of peri/post menopause

101
Q

What are the long term benefits of HRT?

A

Decreased risk of osteoporosis
Possible some bone gain during the initial 18-24 months
Protection only lasts as long as HRT is taken

102
Q

What are the main side effects for HRT?

A

VTE- deep vein thrombosis, pulmonary embolism
Breast cancer
Endometrial cancer
Ovarian cancer
Stroke
Coronary heart disease
CVD

103
Q

Describe VTE as a side effect of HRT:

A

VTE increases in both types of HRT especially in the first year
Risk of VTE greater in oral vs transdermal

104
Q

Describe breast cancer as a side effect of HRT:

A

All systemic HRT increases risk after 1 year
Combined HRT particularly continuous increases risk rather than oestrogen only
No increased risk for vaginal oestrogen
Risk decreases after stopping but excess risk remains for over 10 years compared to those who have never used HRT

105
Q

Describe endometrial cancer as a side effect of HRT:

A

Associated with oestrogen only HRT if used in women with a uterus
Risk eliminated if progesterone used continuously

106
Q

Describe ovarian cancer as a side effect of HRT:

A

Small increased risk in both types of HRT
Excess risk disappears after stopping for a few years

107
Q

Describe stroke as a side effect of HRT:

A

Risk of stroke increases with age regardless of HRT or not
Both HRTs slightly increase risk

108
Q

Describe Coronary Heart Disease as a side effect of HRT:

A

Not conclusive
Before menopause, CHD increased in men
After menopause, CHD similar in both men and women
Oestrogen possibly no difference or reduced risk
O+P possible little or no increased risk

109
Q

Describe CVD as a side effect of HRT:

A

HRT doesn’t increase risk of CVD if started in women under 60

110
Q

Describe Tibilone as a second line treatment for menopausal symptoms:

A

2.5mg OD
Gonadomimetic- stimulates oestrogen receptors
Synthetic steroid derivative of norethisterone
Mixed oestrogenic and progestrogenic and androgenic activity
Licensed for short term treatment of symptoms and osteoporosis is prophylaxis

111
Q

Describe Clonidine as a second line treatment for menopausal symptoms:

A

50mcg BD
Increased if required to 75mcg BD after 2 weeks
For vasomotor symptoms especially if hot flushes
Centrally acting a-adrenergic agonist, possible reduces noradrenergic activity of BVs

112
Q

What are other (unlicensed) treatments for menopausal symptoms:

A

SSRIs
Gabapentin
Pregabablin

113
Q

What are natural remedies for menopause symptoms and give the disadvantages of these:

A

St John’s wort
Products containing phytoestrogens:
-Black cohosh
-Red clover
Little efficacy or safety data
Some risks:
-St Johns wort- interactions
-Liver impairment with black cohosh
-Red clover contains coumarins, interacts with warfarin
-Possible increased risk from oestrogen effects

114
Q

Name the formula of they hydroxyapatite crystals:

A

(Ca10(PO4)6(OH)2)

Y2S2 (14 decks)

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