Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4th Year Medicine 2 > Endocrine (calcium and bones) > Flashcards

Endocrine (calcium and bones) Flashcards

1
Q

List 9 potential causes of hypercalcaemia?

A
  • Malignancy and metastatic bone destruction
  • Primary hyperparathyroidism
  • Tertiary hyperparathyroidism
  • PTHrp secretion from solid tumours
  • Excess vitamin D
  • Thiazides
  • Granulomatous disease
  • FHHC
  • Thyrotoxicosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Normal calcium range?

A

2.2 to 2.6 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presentation of hypercalcaemia?

A
  • Bones – pain, brown tumours can occurs in advanced disease
  • Stones – renal stones, also polyuria and polydipsia
  • Abdominal pain and constipation
  • Depression and in acute scenario confusion
  • Acutely hypercalcaemia will present with thirst, dehydration, confusion and polyuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations for hypercalcaemia?

A
  • Serum PTH – this will be raised or inappropriately normal in primary or tertiary hyperparathyroidism, this will be undetectable in malignancy
  • Check ALP – if elevated unlikely to be primary hyperparathyroidism
  • Measure 24 hour urinary calcium excretion
  • Sestamibi parathyroid uptake scan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Management of hypercalcaemia?

A
  • Acute management of hypercalcaemia is fluids and bisphosphonates
  • Then need to treat the underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe primary hyperparathyroidism?

A
  • Adenoma of the parathyroids producing uncontrolled parathyroid hormone
  • This leads to a raised blood calcium
  • PTH is high and calcium is high
  • This need removed surgically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe secondary hyperparathyroidism?

A
  • Occurs in chronic kidney disease as the kidneys cannot activate vitamin D anymore
  • There is hypocalcaemia
  • The parathyroids react by excreting increased parathyroid hormone
  • The serum calcium will be low but PTH will be high
  • Treatment involves giving activated vitamin D
  • Renal doctors tend to monitor PTH in clinic and they give activated vitamin D if PTH goes above a certain threshold to prevent development of tertiary hyperparathyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe tertiary hyperparathyroidism?

A
  • This occurs if secondary hyperparathyroidism has been left for an extended period
  • An autonomous area of parathyroid develops which excretes inappropriate amounts of PTH
  • Serum calcium is high and PTH is high
  • Glands need removed surgically
  • This tends to be rarer now because everyone with CKD has their PTH monitored and are given activated vitamin D when PTH gets above certain level to prevent this
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 things you need for calcium regulation?

A

PTH
magnesium
vitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe familial hypocalciuric hypercalcaemia? Does it need treatment?

A
  • This can be mistaken as primary hyperparathyroidism
  • It is a familial autosomal dominant condition that causes chronically elevated serum calcium and reduced calcium excretion
  • Usually due to defect in calcium sensors resulting in a new set point for PTH
  • Generally does not cause any symptoms and does not need treated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is vitamin D activated?

A

first step liver
second step kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List some causes of hypocalcaemia?

A
  • Chronic kidney disease
    • Hypoparathyroidism – this could be surgical, congenital absence in DiGeorge syndrome, idiopathic, or due to severe hypomagnaesia
  • Vitamin D deficiency
  • Resistance to PTH (pseudohypoparathyroidism)
  • Due to drugs – calcitonin or bisphosphonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Presentation of hypocalcaemia?

A
  • Neuromuscular irritability and neuropsychiatric manifestations
  • Paraesthesia (fingers, toes, perioral), muscle cramps, tetany, muscle weakness and fatigue
  • Bronchospasm or laryngospasm, convulsions can follow
  • Chvosteks sign – gentle tapping over the facial nerve causes twitching over the ipsilateral facial muscles
  • Trosseaus sign – inflation of BP cuff causes tetanic spasm of fingers and wrist
  • Can get prolonged QT on ECG and arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chvosteks sign?

A

sign of hypocalcaemia
gentle tapping over the facial nerve causes twitching over the ipsilateral facial muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Trosseaus sign?

A

sign of hypocalcaemia
inflation of BP cuff causes tetanic spasm of fingers and wrist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigations for hypocalcaemia?

A
  • Serum and urine creatinine for renal disease
  • PTH measurement – this will be absent or low in hypoparathyroidism but raised in other causes
  • Check 25 hydroxyvitamin D to confirm of vitamin D deficient
  • Check magnesium levels
  • X-rays of metacarpals for pseudohypoparathyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Management of hypocalcaemia?

A
  • Acutely should get IV calcium gluconate
  • May then require oral calcium and/ or vitamin D supplements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain pseudohypoparathyroidism?

A
  • Hypocalcaemia is caused by resistance to PTH due to mutations in the receptor
  • It is associated with short stature, short metacarpals, subcutaneous calcification and sometimes intellectual impairment
  • Decreased calcium but elevated PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain pseudopseudohypoparathyroidism?

A
  • This is very rare and describes someone having the phenotypic defects of pseudohypoparathyroidism but no abnormalities in calcium
  • May share gene defect and be in same family
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Paget’s disease of bone?

A
  • This is a disorder of bone turnover
  • Bone turnover is increased by uncontrolled
  • Increased bone resorption is followed by increased osteoblastic activity but it isn’t coordinated leading to patchy areas of sclerosis and lysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Who gets pagets disease of bone?

A
  • Unknown trigger – mixture of genetic/ environmental factors
  • Uncommon in under age 45
  • More common in males
  • More common if family history
22
Q

Presentation of pagets disease of bone?

A
  • Mostly affects the axial skeleton (skull and spine) and the long bones
  • There is bone pain, fractures and deformities
  • Can cause deafness if affects bones around the ear
  • Occasionally be asymptomatic and incidental finding on XR/ high ALP
23
Q

Investigations for pagets disease of bone?

A
  • Raised ALP but normal calcium and phosphate
  • XR – osteolysis and excessive bone formation seen
  • Radionuclide bone scans can be used to show distribution of disease
24
Q

Management of Pagets disease of bone?

A
  • NSAIDs for pain
  • Bisphosphonates
  • May need calcium and vitamin D supplements
  • Orthotics devices if problems with walking
  • Sometimes surgery is required, if fractures, deformities or nerve compression
25
Q

Complication of Pagets disease of bone?

A

osteosarcoma

26
Q

Raised ALP but normal calcium and phosphate?

A

pagets disease of bone

27
Q

What is osteomalacia?

A
  • This is a condition where there is defective bone mineralisation causing soft bones due to insufficient vitamin D
28
Q

Who gets osteomalacia?

A
  • More at risk if darker skin as need to spend longer in sunlight to generate same quantity of vitamin D
  • If spend lots of time inside e.g. those in care homes
  • If wear clothes that mean don’t have a lot of skin exposed to sun e.g. face coverings etc
  • Live in northern climates with less sunlight
29
Q

Presentation of osteomalacia?

A
  • May be asymptomatic
  • Fatigue
  • Bone pain
  • Muscle weakness
  • Muscle aches
  • Pathological or abnormal fractures
30
Q

Investigations for osteomalacia?

A
  • Check vitamin D level by measuring serum 25-hydroxyvitamin D
  • PTH may be high
  • Serum calcium may be low
  • Serum phosphate may be low
  • Serum ALP may be high
  • NICE also advice looking for other pathology: FBC and ferritin, inflammatory markers, UandEs, LFTS, TFTs, anti-TTG, autoimmune and rheumatoid tests
31
Q

Management of osteomalacia?

A
  • Oral vitamin D3
  • Assess need for calcium supplementation
  • Advise to maintain adequate vitamin D levels through safe sunlight exposure
  • Everyone in Scotland is advised to take a supplement between October to March
32
Q

What is rickets?

A
  • This is the equivalent of osteomalacia in children
  • Due to vitamin D or calcium deficiency
33
Q

Who gets rickets?

A
  • More at risk if darker skin as need to spend longer in sunlight to generate same quantity of vitamin D
  • Breastfed children at higher risk as bottle feeds are fortified with vitamin D
34
Q

Presentation of rickets?

A
  • Lethargy
  • Bone pain and deformities – bowing of legs, knock knees, rachitic rosary (lumps along chest), craniotabes (delayed closure of sutures and frontal bossing)
  • Poor growth
  • Dental problems – delayed teeth and underdevelopment of enamel
  • Muscle weakness
  • Pathological or abnormal fractures
35
Q

Investigations for rickets?

A
  • Check vitamin D level by measuring serum 25-hydroxyvitamin D
  • PTH may be high
  • Serum calcium may be low
  • Serum phosphate may be low
  • Serum ALP may be high
  • NICE also advice looking for other pathology: FBC and ferritin, inflammatory markers, UandEs, LFTS, TFTs, anti-TTG, autoimmune and rheumatoid tests
36
Q

Management of rickets?

A
  • Prevention in children – advise breastfeeding women and all children to be taking supplements
  • Treat those deficient with supplements
37
Q

Define osteoporosis and osteopenia?

A
  • Disease characterized by low bone mass and micro architectural deterioration of the bone tissue leading to enhanced bone fragility and an increase in fracture risk
  • Osteoporosis = bone mineral density > 2.5 standard deviations below the mean of normal young subjects
  • Osteopenia = 1-2.5 standard deviations below the adult mean
  • Most people reach their peak bone mass in there 20s and after this there is a slow decline (the higher your peak bone mass, the more you can lose before becoming osteoporotic)
38
Q

Risk factors/ who gets osteoporosis?

A
  • Age- risk increases with age
  • Gender- occurs more in women because oestrogen deficiency post menopause causes increased loss in bone mass
  • Ethnicity- Caucasians and Asians are more at risk
  • Those who have had a previous fracture
  • Family history (genetics affect your peak bone mass a lot)
  • Women who have had menopause before 45 are at increased risk because they are oestrogen deficient for longer
  • Also, women who are amenorrhoeic because of anorexia or intense exercising will be at increased risk as there will be an accelerated loss of bone mass
  • Long term steroid therapy increases risk
  • Weirdly this is a condition where being obese is actually protective because your bone mass will be higher because you put more weight through your bones
  • To an extent you can increase your peak bone mass/ slow down the loss by doing weight bearing exercises and strength work outs
  • Alcohol excess and smoking are associated with increased risk of osteoporosis
39
Q

Presentation of osteoporosis?

A
  • Osteoporosis causes no symptoms so will only present when there is a fracture
  • Generally, people are assessed for osteoporosis after their 1st low trauma fracture
  • Note: a low trauma fracture is usually defined as a fall from standing height or less or any incident that you wouldn’t usually expect someone to break a bone
  • Risk calculator is used and if the person has a greater than 10% risk they are referred for a DEXA scan
40
Q

Describe a DEXA scan and the scores it generates?

A
  • A DEXA scan generates a T score and a Z score
  • The T-score is a comparison of a person’s bone density with that of a healthy 30-year-old of the same sex
  • The Z-score is a comparison of a person’s bone density with that of an average person of the same age and sex
  • Z scores tend not to be used formally to diagnose osteoporosis
  • The T score is the one that if you score -2.5 or less then you have osteoporosis, score of -1 to -2.5 is osteopenia
41
Q

Management of osteoporosis?

A

Lifestyle changes:
- strength training and weight bearing exercise (weight bearing exercise is basically any exercise that involves using your feet to bear the rest of your body weight – so walking, running etc., swimming and cycling are not weight bearing)
- avoid excess alcohol
- smoking cessation
- fall prevention

Diet:
- ensure adequate calcium intake (calcium is mainly found in dairy products, but also fortified breads, fish with bones, nuts, green veg and beans)
- ensure adequate vitamin D, vitamin D can be found in some foods but we mainly get it from sunlight, should be noted that in Scotland from October to March it is actually recommended that everyone takes supplements
- supplements of calcium and vitamin D should be given in those at risk of deficiency

HRT:
- this is not recommended specifically for osteoporosis
- however, in women who have early menopause or significant perimenopausal symptoms HRT as well as relieve symptoms will reduce osteoporotic risk and women should be offered it

Steroids:
- for those on steroids, risk of osteoporosis should be considered
- courses should be as short as possible and if needed patients should be given bone sparing agents

Drug treatment
bisphosphonates are first linex

42
Q

How are bisphosphonates given?

A
  • Alendronate and risendronate are taken as once weekly preparations
  • Zoledronic acid is taken once yearly IV
  • Tend to take for 3-5 years then have a treatment holiday for 18 months to 3 years before repeating assessment
43
Q

Side effects of bisphosphonates?

A
  • Bisphosphonates can cause reflux and oesophageal erosions – need to take on an empty stomach sitting upright for 30 minutes before moving or eating
  • They can also cause osteonecrosis of the jaw and external auditory canal
  • Another side effect is atypical fractures
44
Q

What is hypothermia?

A
  • Temperature below 35C
  • Primary hypothermia – due to environmental exposure
  • Secondary hypothermia – low body temperature resulting from a medical illness lowering the temperature set point e.g. hypoadrenalism, hypothyroidism, drugs, impaired CNS thermoregulation e.g. stroke, parkinsons, tumours
45
Q

Presentation of hypothermia?

A
  • Usually occurs gradually
  • Shivering, slurred speech
  • Low RR
  • Cold and pale skin
  • Fatigue, lethargy and apathy
  • Depressed level of consciousness
46
Q

Investigations for hypothermia?

A
  • Temperature reading – low reading thermometers, preferably oesophageal are required
  • Blood gases and FBC
  • ECG – may show prolonged PR, QRS and QT intervals and atrial or ventricular arrhythmias
  • As body core temperature decreases, sinus bradycardia tends to give way to AF followed by VF and finally asystole – also get characteristic J waves
47
Q

Management of hypothermia?

A
  • Re-warming – aggressive management of temperature with faster rather than slower rewarming has been shown to improve the outcome
  • warmed, humidified oxygen, heated IV saline, warmed blankets and heat lamps
48
Q

What is hyperthermia?

A
  • Temperature above 40C
  • Usually as a result of high ambient temperature, humidity and physical exertion
  • Should also consider malignant hyperthermia if had an anaesthetic
49
Q

Who should be offered a DEXA scan?

A

everyone should have their fragility score calculated before receiving a DEXA using Frax or Q Fracture (preferred) except those who are 50 or older with a history of fragility fractures or those under 40 with a major risk factor for fragility fractures

50
Q

Bisphosphonates should be offered to

A

those with a t score of - 2.5 or less

51
Q

Initial management of hypercalcaemia involves?

A

initially involves rehydration
once rehydrated you can consider bisphosphonates

52
Q

What can respiratory alkalosis result in?

A

transient hypocalcaemia (with normal phosphate levels)

4th Year Medicine 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions