Brainscape's Knowledge GenomeTM

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


See full index

Y2 Endocrine Block > Disorders of calcium and sodium regulation > Flashcards

Disorders of calcium and sodium regulation Flashcards

1
Q

what are the main mechanism that regulate water status

A
  • Thirst

- Anti-diuretic hormone (ADH) from posterior pituitary gland

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

_____ and _____ regulation is closely linked

A

sodium

water

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

plasma osmolality is tightly regulated through _____

A

sodium

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

ADH is released by the posterior pituitary in response to what things?

A
  • Decreased plasma volume (sensed by baroceptors in atria/veins/carotids)
  • Increased plasma osmolality (sensed by osmoreceptors in hypothalamus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ADH acts mainly via which receptor

A

AVPR2

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

Where is AVPR2 found and what are its action

A
  • Basolateral membrane of kidney collecting ducts

- Inserts aquaporin channels to increase renal water reabsorption

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

what is the effect of aldosterone on the kidneys

A

increases sodium reabsorption through ENaC- so water reabsorption happens too because water follows sodium and potassium excretion in the distal nephron

This increase in sodium status also increases plasma volume and raises blood pressure

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

what is hyponatraemia defined as

A

Serum sodium < 135 mmol/l

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

what is the cause of hyponatraemia

A

Almost always due to disorder of water balance
- Inability to suppress ADH release so inappropriate retention of water (opposite of Diabetes insipidus)
Renal impairment
- Diuretic effect (especially thiazides)

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

what are the 3 main reasons for hyponatraemia

A
  • Na and water deficit (hypovalaemia)
  • Water excess (euvolemia)
  • Na and water excess (hypervalaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the causes of hypovalaemia (Na and water deficit)

A 
1) Renal Losses:
Diuretic excess
Mineralcorticoid deficiency
Salt-losing nephritis
Ketonuria 
Osmotic diuresis

2) Extra renal losses:
Vomiting
Diarrhoea
Pancreatitis

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

what are the causes of euvolemia (Water excess)

A 
Glucocortioid deficiency
Hypothyroidism
Pain 
Psychiatric disorders 
Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the causes of hypervalaemia (Na and water excess)

A

Nephrotic syndrome
cardiac failure
Acute and chronic renal failure
cirrhosis

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

What is ‘Syndrome of inappropriate anti-diuretic hormone (SIADH)’

A

Excess ADH or inappropriate ADH for plasma osmolality

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

Why is SIADH the commonest cause of low plasma sodium

A

due to increased body water- dilutes plasma osmolality

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

what are the causes of SIADH

A

Cancer: lung/lymphoma/leukaemia
Chest disease: pneumonia
CNS disorders: infections, injury
Drugs: opiates, thiazides, anti-convulsants, proton pump inhibitors, anti-depressants

17
Q

How to diagnose SIADH

A

Presence of these:

  • Hyponatraemia with inappropriate low plasma osmolality
  • Urine osmolality> plasma osmolality
  • Urine sodium> 30 mmol/l
  • pivotal for DIAGNOSIS (both would be high)
  • no recent use of diuretic agents

Absence of adrenal, thyroid, pituitary or renal insufficiency

18
Q

why is it important that intracellular and extracellular osmolality must be equal

A

When the serum [Na] is low, water moves into cells to increase plasma osmolality causing cell swelling

19
Q

what happens to the brain when there is a sudden decrease in Na

A

Cerebral Oedema (swelling)

20
Q

what happens to the brain when there is a sudden increase in Na

A

Osmotic demyelination syndrome (water moves out of brain to bring down plasma osmolality)

21
Q

What are the neurological clinical features of Hyponatraemia

A 
Begins as being asymptomatic but as plasma Na falls
brain swelling occurs leading:
- Mild confusion
- Gait instability
- Marked confusion
- Drowsiness
- Seizures
22
Q

what is the management of hyponatraemia

A

1) Severe and acute
Unconscious or seizures- symptoms
Give infusion of hypertonic (3%) saline
Can increase sodium quickly

2)Less severe +/- chronic (common)
Establish causes- e.g. diuretics
Fluid Restriction- increase in fluid will cause further hyponatraemia
Increase Na slowly- if sodium increased too quickly then risk of osmotic demyelination

2nd line Treatment:
AVPR2 antagonists (‘vaptans’)- antagonise effect of ADH
Very expensive

23
Q

What are the cuases of hypernatraemia

A

Most usually due to water loss (‘dehydration’) and inability to access water
Main causes:
Insensible/sweat losses (severe burns/sepsis)
GI losses- severe diarrhoea or vomiting
Diabetes Insipidus
Osmotic diuresis due to hyperglycaemia

24
Q

what is the management of hypernatraemia

A 
Treat Cause
Estimate total body water deficit if possible and correct loss
Avoid overly rapid correction
- Aim for ↓ 10 mmol/l in 24 hours
- Concern is cerebral oedema
Use IV 5% dextrose
25
Q

What are the sources of Calcium

A

GI tract
Bones
Kidney

26
Q

How does the GI tract contribute to Calcium homeostasis

A

Absorbed throughout small intestine from dietary sources (only approx 10% absorbed)
Vitamin D dependent

27
Q

How does bone contribute to Calcium Homeostasis

A

Body Calcium reservoir

Regulates plasma Ca via action of osteoblasts and osteoclasts

28
Q

How does Kidney contribute to Calcium Homeostasis

A

Free Ca filtered by glomerulus

97-99% is reabsorbed

29
Q

What role does Vitamin D play in calcium homeostasis

A

Increases GI absorption
Increases bone resorption
Increased renal reabsorption

30
Q

WHat role does PTH play in calcium regulation

A

When decreased Plasma calcium Levels:
Parathyroid glands release PTH, which acts on:

1) Bones
Resorption
Release of Calcium and Phosphate

2) Kidneys
Increased Phosphate excretion
Increased Calcium Reabsoprtion
Increased Calcitriol Formation–> Increased CaHPO4 absorption

31
Q

what is hypercalcaemia

A

High calcium levels in blood

32
Q

what are the clinical features of hypercalcaemia

A

Neurological:

  • Confusion
  • Fatigue
  • Stupor, coma
  • Decreased concentration

o MSK:

  • Muscle weakness
  • Bone pain
  • Osteopenia/osteoporosis

o GI:

  • Anorexia, Nausea and vomiting
  • Bowel hypomotility and constipation
  • Pancreatitis
  • Peptic ulcer disease

o Renal:

  • Polyuria
  • Polydipsia
  • Nephrolithiasis and nephrocalcinosis
  • Nephrogenic DI
  • Acute and chronic renal insufficiency
  • Distal renal tubular acidosis
33
Q

What are the ECG changes in hypercalcaemia

A

Shortened QTc interval
Bradycardia- slow heartbeat
–> becomes a life threatening problem

34
Q

what are the causes of hypercalcaemia

A

Primary Hyperpararhyroidism:
- Due to single parathyroid adenoma with raised PTH and Ca

Malignancy:
secretion of PTH-related peptide (produced by cancers)
Breast, lung and multiple myeloma are commonest tumours
Also, seen in bone metastases due to direct osteolysis

35
Q

what is the diagnosis of hypercalcaemia

A

Measure PTH
If ↓ then malignancy likely
If ‘normal’ or ↑ then primary hyperparathyroidism

36
Q

what is the management of hypercalcaemia

rehydration, biphosphonates, other agents

A

Treat underlying cause

1) Rehydration
- Patients often hypovolaemic
- Hypovolaemia impairs renal clearance of calcium
- Isotonic (0.9%) saline infusion corrects hypovolaemia
- Be careful of fluid overload
- Hourly bags of saline to bring Ca down to normal

2) Biphosphonate Therapy
- Inhibit bone resorption by inhibiting osteoclasts activity
- Agent of choice for treating hypercalcaemia of malignancy or acute hypercalcaemia
- Zolendronic acid is most commonly used
- Delayed effect, maximal at 2-4 days after treatment

3) Other agents
Calcitonin 
- Increases renal calcium excretion 
- Decreases bone resorption of calcium
- Only effective for 48 hours- so can be used while waiting for bisphosphonate to work

Glucocorticoids
- Inhibit vitamin D production

Parathyroidectomy

  • Only if resistant to treatment
  • Rarely indicated urgently and Carried out further down the line
37
Q

what are the complications of acute hypocalcaemia

A

Tetany

  • Increased neuromuscular excitability
  • Peri-oral numbness, muscle cramps, tingling of hands/feet
  • If severe: carpopedal spasm, laryngospasm, seizures

Cardiac complications

  • Dysrhythmia
  • hypotension
  • Prolonged QT on ECG
38
Q

what are the causes of hypocalcaemia

A

Low PTH

  • After parathyroid/ thyroid surgery
  • Autoimmune hypoparathyroidism

High PTH

  • Vitamin D deficiency
  • Chronic renal failure
  • Loss of Calcium

Drugs

Hypomagnesaemia
Leads to PTH resistance

39
Q

what is the management of hypocalcaemia

A 
Intravenous calcium replacement if tetany or cardiac manifestations
May also need magnesium infusion
Chronic management:
Vitamin D replacement (D2 or D3)
Oral calcium salts
Treat underlying cause

Y2 Endocrine Block (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions