Brainscape's Knowledge GenomeTM

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


See full index

Pathology by week > W1 - Calcium metabolism > Flashcards

W1 - Calcium metabolism Flashcards

1
Q

What are the roles of calcium in the body?

A
  1. skeleton maintenance
  2. Metabolic - APs and IC signalling (normal nerve and muscle function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is calcium stored in the body?

A

Skelton (99% of bone calcium)

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

What are the 3 forms of serum Ca2+?

A
  1. Free (ionised) - 50%, biologically active
  2. Protein-bound - 40%, albumin
  3. Complexed - 10%, citrate/phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the total serum Ca2+ range?

A

2.2 – 2.6 mmol/L

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

What is corrected Ca2+?

A

Corrected calcium takes into account the albumin. E.g., if albumin is really low, then a correction factor is applied.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the formula for calculating corrected Ca2+?

A

serum Ca2+ + 0.02 * (40 – serum albumin in g/L)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Calculate corrected Ca2+ if albumin = 30, calcium = 2.2 mmol/L

A

Corrected calcium = 2.2 + (0.02 x 10)
= 2.2 + 0.2 = 2.4 mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the physiological response to hypocalcaemia?

A

Detected by parathyroid gland –> release PTH –> PTH obtains Ca2+ from 3 sources:

  1. increased bone resorption
  2. increased intestinal absorption
  3. increased renal resorption and renal 1 alpha hydroxylase activation (which means increased 1,25-OH Vit D

all these lead to increased ECF Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the key 2 hormones involved in calcium homeostasis?

A 
PTH (84 aa peptide hormone) 
Vit D (Steroid hormone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the effects of PTH on the kidneys?

A
  1. Renal Ca2+ resorption
  2. Renal Pi wasting
  3. Stimulates 1,25 (OH)2 vit D synthesis (1α hydroxylation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does PTH stand for in terms of Amir Sam?

A

Phosphate Trashing Hormone

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

Explain the synthesis of Vitamin D3?

A

7-dehydrocholesterol (skin) –> sunlight –> cholecalciferol (D3) –> liver –> 25-OH-D3 –> kidney (1a-hydroxylase, with the presence of PTH) –> 1,25-(OH)2-D3 ACTIVE!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is mammalian and what is plant vitamin D?

A

mammalian - D3 (cholecalciferol)
plant - D2 (ergocalciferol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the stored and measured form of Vitamin D?

A

25-OH-D3 (inactive)

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

What is the rate-limiting step in vitamin D3 synthesis?

A

1 alpha hydroxylation (b/c it is under the control of PTH)

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

What happens to any absorbed vitamin d?

A

100% is hydroxylated at the 25 position in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where else is 1 alpha hydroxylase expressed?

A

Rarely, in the lung cells of sarcoid tissue - results in inappropriately raised calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the roles of 1,25(OH)2 vitamin D in the body?

A
  1. Intestinal Ca2+ absorption
  2. Intestinal Pi absorption
  3. Bone formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name 5 metabolic bone diseases

A

Osteoporosis
Osteomalacia
Paget’s disease

Parathyroid bone disease
Renal osteodystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Explain Vitamin D deficiency

A

Defective bone mineralisation

Childhood -> Rickets
Adulthood -> Osteomalacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the risk factors (6) for Vit D deficiency?

A
  • Lack of sunlight exposure
  • Dark skin
  • Dietary malabsorption
  • Anticonvulsants induce breakdown of vit D
  • Chappatis (phytic acid)
  • Renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the symptoms and imaging features of Osteomalacia?

A
  • Bone & muscle pain
  • Increased risk of fractures
  • Looser’s zones (pseudofractures)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the biochemical image of Osteomalacia?

A

low Ca2+ & Pi, raised ALP

24
Q

What are the clinical features of rickets?

A

Bowed legs
Costochondral swelling
Widened epiphyses at the wrists
Myopathy

25
Q

How does PTHrP act in body?

A

stimulates bone resorption and renal reabsorption, leading to increased [Ca2+]

26
Q

How is PTHrP implicated in certain cancers?

A

Causes hypercalcaemia, and also turns on osteoclasts and provides cancer with opportunity to invade bone

27
Q

Explain osteoporosis

A

Normal aging process of bone
- bone slowly lost after age 20

bone is NORMAL in structure, but there is a loss of BONE MASS - normal calcium!!

28
Q

In osteoporosis, there is a reduction in __________ _________.
In osteoporosis, the calcium is ____ and the phosphate is ________

A

bone density

normal, normal

29
Q

What is the first symptom of osteoporosis?

A

Fracture!!

30
Q

What are typical fractures in osteoporosis?

A

neck of femur (NOF), vertebral, wrist (Colle’s)

31
Q

How is osteoporosis diagnosed? Interpret the results

A

DEXA (Dual Energy X-ray Absorptiometry)
hip (femoral neck) + lumbar spine

Osteoporosis T Score < -2.5
Osteopenia T score between -1 & -2.5

32
Q

When does bone mass decline begin?

A

20-ish, if no childhood illness is present to cause failure to attain peak bone mass

33
Q

List 4 causes of rapid bone loss in adulthood (leading to osteoporosis) and give examples of each

A
  1. Lifestyle: sedentary, EtOH, smoking, low BMI/nutritional
  2. Endocrine: hyperprolactinaemia, thyrotoxicosis, Cushings
  3. Drugs: steroids
  4. Others eg genetic, prolonged intercurrent illness
34
Q

What are the treatments for osteoporosis?

A
  1. Lifestyle
    Weight-bearing exercise
    Stop smoking
    Reduce EtOH
  2. Drugs
    - Vitamin D/Ca
    - Bisphosphonates (eg alendronate) –↓ bone resorption
    - Teriparatide (PTH derivative) – anabolic
    - Strontium – anabolic + anti-resorptive
    - Oestrogens – HRT - reduce risk of osteoporosis and hot flushes, increase risk of cancer
    - SERMs eg raloxifene, tamoxifen
35
Q

Symptoms of hypercalcaemia

A
  1. Polyuria / polydipsia
  2. Constipation
  3. Neuro – confusion / seizures / coma

BONES (PTH bone disease) STONES (renal calculi) MOANS (constipation, pancreatitis), GROANS (confusion)

36
Q

What is the normal physiological response to hypercalcaemia?

A
  1. PTH release suppressed
  2. Vit D activation suppressed

trying to reduce ECF Ca2+

37
Q

What is the first thing to look for when Ca2+ is raised?

A

Is it a genuine result? repeat bloods.

Is the PTH suppressed?

38
Q

What is the likely cause (5) of hypercalcaemia if PTH is suppressed?

A

PTH suppressed = appropriate response

causes:

  1. MALIGNANCY (common)
  2. sarcoid
  3. vitamin D excess
  4. thyrotoxicosis
  5. Milk alkali syndrome
39
Q

What is the likely cause of hypercalcaemia if PTH is NOT suppressed?

A

PTH not suppressed = inappropriate response

causes:
1. Primary hyperparathyroidism (common)
2. familial hypocalciuric hypercalcemia (rare)

40
Q

What is the commonest cause of hypercalcaemia?

A

Primary hyperparathyroidism

41
Q

Primary hyperparathyroidism - what aetiology is most common?

A

Parathyroid adenoma > hyperplasia > carcinoma

42
Q

What is parathyroid hyperplasia associated with?

A

MEN1

43
Q

Which sex is Primary hyperparathyroidism more common in?

A

women

44
Q

What is the biochemistry of Primary hyperparathyroidism?

A

↑serum Ca
↑ or inappropriately normal PTH
↓serum Pi
↑ urine Ca (due to hypercalcaemia)

45
Q

What happens with a CaSR mutation? What is the disease called?

A

Higher setpoint for PTH release –> mild hypercalcaemia, reduced urine Ca2+

Familial hypocalciuric (/benign) hypercalcaemia (FHH / FBH)

46
Q

Describe the 3 types of hypercalcaemia in malignancy

A
  1. Humoral hypercalcaemia of malignancy (eg small cell lung Ca) –> PTHrP
  2. Bone metastases (eg breast Ca) –> Local bone osteolysis
  3. Haematological malignancy (eg myeloma) –> cytokines
47
Q

Describe how each of the following non-PTH driven hypercalcaemias happen:

  • sarcoidosis
  • thyrotoxicosis
  • hypoadrenalism
  • thiazide diuretics
  • excess vitamin D
A

Sarcoidosis (non-renal 1α hydroxylation)

Thyrotoxicosis (thyroxine -> bone resorption)

Hypoadrenalism (renal Ca2+ transport)

Thiazide diuretics (renal Ca2+ transport)

Excess vitamin D (excess absorption from gut, reabsorption from kidneys)

48
Q

Treatment of hypercalcaemia

A

Acute management

  • Fluids+++ (NORMAL SALINE)
  • Bisphosphonates (if cause known to be cancer) otherwise avoid.
  • bisphosphonates take days to work so you want to GIVE FLUIDS!

Treat underlying cause

49
Q

Clinical signs of hypocalcaemia

A

neuromuscular excitability:

  • Trousseau’s sign - pressure cuff
  • Hyperreflexia
  • Convulsions
  • Chvostek’s sign - cheek tap
  • laryngeal spasm (stridor)
  • choked optic disc
50
Q

Explain how trousseau’s sign happens and what it indicates

A

Trousseau’s sign – check BP. The albumin in the arm rises because it is squeezing so then the calcium sticks more to the albumin. If its low already and it falls a bit more, you will get the flexion.
- hypocalcaemia

51
Q

What is the first thing to look for when Ca2+ is low?

A
  1. Is it a genuine result? repeat bloods and adjust for albumin
  2. PTH levels
52
Q

What are the causes of hypocalcaemia?

A

PTH high (non-PTH driven):

  1. Vitamin D deficiency
  2. CKD (1a hydroxylation)
  3. PTH resistance (pseudohypoparathyroidism)

raised PTH - secondary hyperparathyroidism
–> can progress to tertiary hyperparathyroidism

PTH low (PTH driven):

  1. Surgical - post-thyroidectomy
  2. autoimmune hypoparathyroidism
  3. Congenital absence of parathyroid (DiGeorge Syndrome)
  4. Mg deficiency
53
Q

What is Paget’s disease? Which bones are commonly affected?

A

Focal disorder of bone remodelling

Pelvis, femur, skull and tibia

54
Q

What are the clinical features of Paget’s disease?

A

Focal PAIN, warmth, deformity, fracture, SC compression, malignancy, cardiac failure

55
Q

What is the biochemistry of Paget’s?

A

ELEVATED ALKALINE PHOSPHATASE

56
Q

How to test for Paget’s and how to treat it

A

Nuclear medicine scan or Xray

treatment - bisphosphonates for pain

57
Q

Which has the lowest calcium?
A) Primary hyperparathyroidism
B) Secondary hyperparathyroidism
C) Osteoporosis
D) Paget’s disease of the bone
E) Breast cancer

A

B

Pathology by week (70 decks)

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