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Disease of Major Organs > phosphate > Flashcards

phosphate Flashcards

1
Q

What forms of phosphate exist in the body?

A

Organic
- ATP, DNA, RBC and mostly as PO43
Inorganic (Pi)

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2
Q

Match the following (extrapoints for structures)

  1. 85%
  2. 1%
  3. 14%

A. ICF
B. Bones
C. ECF

A

1B
- formed as hydroxyapatite crystals

2C
- Mostly inorganic:inorganic form of HPO42- and H2PO42- with a ratio of 4:1

3A
- inorganic or organic forms (ATP, DNA, RBC and mostly as PO43-)

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3
Q

What forms does phosphate have in ECF?

A

The inorganic phosphate in the ECF can be protein bound (10%), complexed with Ca2+/Mg2+ (35%), or free (55%)

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4
Q

Function of phosphate

A

functions including ATP formation, phospholipids, intracellular metabolic pathways, tissue oxygenation, acid excretion, bone mineralisation and nucleic acid synthesis.

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5
Q

What factors affect phosphate homeostasis?

A

Vit D, FGF-23 and PTH are the main ones.

- Others: acid-base status, corticosteroids, GH, thyroxine, insulin, calcitonin, dopamine, serotonin

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6
Q

What does Vit D, FGF23 and PTH do in terms of phosphate?

A

PTH
- act to release phosphate using bone storage
VitD
- act to increase intestine reabsorption

Both PTH and FGF23 have negative effect on kidney reabsorption of phosphate and increases its excretion.

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7
Q

Where does renal reabsorption take place?

A

80-95 is reabsorbed in the PCT using Na/PO3 co transporters

- acid-base status, corticosteroids, GH, thyroxine, insulin, calcitonin, dopamine, serotonin

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8
Q

What effect does PTH has?

A

Stimulates the conversion of 25-OH to 1,25diOH vitamin D - to release phosphate from bone
- act on the kidney by reducing NPT2a/c expression to increase phosphate excretion

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9
Q

What effect does FGF23 has?

A

FGF23 is released by osteocytes and osteoblasts. Acts to inhibit the conversion of 25-OH to 1,25diOH vitD to decrease absorption of phosphate.
- FGF23 act on the kidney to reduce NPT2a expression cauisn increased phosphate excretion

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10
Q

What symptoms will patients with mild, severe and chronic hypophosphataemia have?

A

Mild - no signs
Chronic - rickets/osteomalacia
Severe - hematopoietic, muscular, nervous and GI systems

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11
Q

Describe the severe (hypophosphataemia) symptoms in detail

A

Haemopoietic system - decreased2,3-BPG in RBC (reduced oxygen release - hypoxia), increased red cell fragility (haemolysis), abnormal platelet function

  • Muscular system: decrease in contractility of the diaphragm, heart, skeletal muscle (can lead to respiratory failure), and/or rhabdomyolysis
  • Nervous system: decreased energy available to the brain, in the form on lethargy, confusion, seizure and possibly comas
  • GI problems: smooth muscle breakdown
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12
Q

What causes hypophosphataemia?

A

Inadequate absorption from the intestine, redistribution into cells or bones, or increased urinary phosphate loss

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13
Q

Describe how inadequate intake causes hypophosphataemia

A

Malnutrition, alcoholism, malabsorption, Vit D deficiency, or use of antiacids

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14
Q

Describe how redistribution into the bone causes hypophosphataemia

A

Seen in hungry bones syndrome where rate of bone formation is greater than breakdown.

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15
Q

Describe how redistribution into cells causes hypophosphataemia

A

Seen in refeeding syndrome, DKA recovery, alkalosis, increased muscle uptake

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16
Q

Describe how increased loss causes hypophosphataemia

A

Either GI or renal
GI- diarrhoea
Renal - alcohol, hyperparathyroidism, fanconi, post kidney transplant

17
Q

What is refeeding syndrome?

A

Redistribution of K

  • Periods of malnutrition, followed by intake of carbohydrates
  • Intracellular ions (Mg2+, PO3-, K+) have leaked from cells and been lost in the urine during malnutrition but following intake they are rapidly taken up by cells due to insulin release
18
Q

What is respiratory alkalosis?

A

Redistribution of K
- (hyperventilation and H+ ICF decrease)This activates a phosphofructokinase which increases the phosphorylation of glucose to allow phosphate to be rapidly taken up

19
Q

What are some FGF-23 related conditions?

A

In renal failure FGF23 increases causing hyperphosphataemia and hypophosphataemic rickets.
Range of genetic disorders associated with elevated FGF23
- X-linked hypophosphataemic rickets (XLH)
- AD hypophosphataemic rickets (ADHR)
- AR hypophosphataemic rickets (ARHR)
- Tumour induce osteomalacia

20
Q

Briefly explain what X-linked hypophosphataemic rickets (XLH) is?

A

Mutation to PHEX gene causing renal phosphate wasting due to the actions of FGF23

21
Q

Briefly explain what AD hypophosphataemic rickets (ADHR) is?

A

Mutation in FGF-23 at is cleavage site that prevents proteolysis

22
Q

Briefly explain what AR hypophosphataemic rickets (ARHR) is?

A

Mutation to DMP1 gene encoding a restraining FGF23 protein

23
Q

Describe the investigations for hypophosphateamia

A

Review clinical details: IV treatment, history of alcoholism/eating disorders, drugs, any renal impairment/transplant.

Repeat phosphate according to glucose/insulin throughout the day.

Further assessment includes:

  • U&E: renal function
  • bone profile
  • Mg measurement
  • pH
  • Urine phosphate
  • urine amino acids
  • Urine AA and glucose
  • PTH/FGF23/vitD
24
Q

How is the reabsorption of phosphate assessed?

A

A paired fasting 2nd void urine & blood for calculations of TmP/GFR. This tells us renal tubular maximum reabsorption of phosphate per litre of GFR
- TRP<0.86 phosphate reabsorption is maximal and relationship is linear

25
Q

What are signs and symptoms of hyperphosphataemia?

A

No complications however, once Ca and phosphate exceed a certain conc soft tissue calcification of blood vessels, skin, lungs, hearts, kidneys and joints can occur.

  • Calcification of the kidney reduces renal capacity to excrete phosphate even further
26
Q

State the mechanisms of hyperphosphataemia

A
  • pseudohyperphosphataemia
  • Increased input/intake
  • Redistribution from ICF
  • Decreased phosphate excretion
27
Q

What is pseudohyperphosphataemia?

A

The redistribution from cells.

  • Occurs in haemolysis (results should be knocked out and not reported)
  • Delayed seperation: check date. Especially if there is no obvious cause of increase phosphate except an increase in K+
28
Q

When does redistribution from ICF (into the plasma) causing hyperphosphataemia occur?

A

Tumour lysis syndrome
Rhabdomyolysis
Heat stroke/hyperpyrexia

29
Q

What effect does CKD and AKI have on TmP/GFR?

A

Will cause it to increase

30
Q

What investigation is necessary in hyperphosphataemia?

A
  • Clinical history: IV, rhabdomyolyisis, tumour lysis syndrome
  • UE profile (renal function)
  • urine phosphate for TmP/GFR
  • Calcium

Further testing includes

  • Mg
  • PTH
  • 25 OH vit D

Disease of Major Organs (14 decks)

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