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Bloc D - Renal > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What do kidneys do?

A

▪Filter your blood and clean it

▪Excrete waste

▪Regulate water and electrolytes: Na and K

▪Regulate acid base

▪Hormone secretion

▪Renin, angiotensin II

▪ Erythropoietin for RBC production

▪Activated vitamin D for bone metabolism

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2
Q

What’s the filtrate?

A

The liquid filtered by the glomerulus, before some of its content is reabsorbed and called urine

▪The filtrate (= ultrafiltrate) contains water, electrolytes, urea, Cr, sugar, amino acids

▪It does not contain cells, proteins, fats. Those stay in the glomerular capillary

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3
Q

What is the Glomerular Filtration Rate GFR?

A

▪GFR is the amount of plasma filtered through the glomeruli per unit time. It is expressed as ml/min.

▪It can refer to the function of a single nephron (SNGFR), but most often refers to the functions of all of the 2 million nephrons (i.e. both kidneys) collectively.

▪GFR assesses patient renal function.

▪Measurement of GFR relies on the concept of clearance

▪Clearance: how much of a substance is removed from the circulation by the kidney and put into the urine

▪The way we estimate GFR is by calculation of Creatinine clearance

▪CKD epi, MDRD, Cockroft Gault formulae are all acceptable (Schwartz formula in children)

▪Take into account patient’s age, ±weight, serum Cr (µmol/L) to estimate Cr clearance, and thus GFR

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4
Q

What are the Determinants of Glomerular filtration rate (GFR)?

A

Kf : ultrafiltration coefficient- total capillary area available for filtration

PGC : transcapillary hydraulic pressure- favors filtration

PT or PBS: hydraulic pressure in tubule opposes filtration

π : transcapillary oncotic pressure, which opposes filtration

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5
Q

What is creatinine clearance?

A

▪Creatinine Clearance (CrCl) is an estimate of GFR

▪Creatinine: produced at a constant rate from plasma creatine, which comes from skeletal muscle. Cr has stable plasma concentration, is freely filtered at the glomerulus and stays in the tubule to be excreted. Filtered amount = excreted amount

▪GFR x Plasma concentration Cr = Urine concentration Cr x urine Volume

▪GFR = UV/P

▪male: 0.18 to 0.22 mmol/kg/day

▪female: 0.13 to 0.18 mmol/kg/day

▪If plasma Cr concentration goes up, means GFR is down.

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6
Q

What are the stages of kidney failure?

A
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7
Q

When can’t we use the Cockroft Gault’s formula to calculare GFR?

A

If the GFR is not steady

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8
Q

What are the autoregulation mechanisms of the kidney?

A

For a sudden rise or fall in systemic blood pressure, autoregulation occurs so that GFR does not rise or fall just because blood pressure rises or falls

  • Myogenic reflex results in vasospasm of afferent arteriole; (50%of autoregulation)
  • Tubuloglomerular feedback

In situations of major drop in systemic blood pressure there is:

  1. activation of sympathetic nervous system, epinephrine, which causes vasoconstriction
  2. Activation of the renin-angiotensin-aldosterone system and angII causes vasoconstriction

▪BP too high? Myogenic mechanism constricts afferent arteriole

▪BP too low: AngII constricts efferent arteriole

▪Prostaglandins dilate glomerular afferent arteriole, to preserve GFR

▪TG feedback: if the distal tubule Cl is too low, means the GFR is low, so afferent arteriole opens up

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9
Q

What is the proximal tubule function?

A
  • The tubule cells have one side facing urine (apical side) and the other facing the blood (basolateral side) so they can reabsorb or secrete things (tubule cell polaity).
  • Proximal tubule reabsorbs ~60% of the filtered Na and water. It reabsorbs almost all of the filtered glucose, phosphate, amino acids by linking their transport to Na
  • Reabsorption of 90% of the filtered bicarbonate via the Na-H exchange
  • Removal of solutes creates an osmotic gradient promoting water reabsorption via aquaporins
  • Ca, K, Cl follow down their concentration gradients
  • Urinary glucose reabsorption threshold by the sodium glucose transport protein (SGLT; Tmax) may be exceeded in the PTC (ex. Diabetes)
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10
Q

What is the function of the Loop of Henle?

A

Two components to water regulation:

  1. The Loop of Henle sets up a high interstitial osmotic gradient (separation of Na and water) THE COUNTERCURRENT SYTEM**
  2. Site of ADH action and insertion of aquaporins-water channels so that the water can be resorbed

The thin descending limb of the loop is permeable to water and the thick ascending limb moves Na out via active Na transport by the Na-K-2Cl cotransporter in the apical (tubular) side and reabsorb Ca and Mg

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11
Q

What is the function of the distal collecting tubule?

A
  • Na is reabsorbed into the interstitium + circulation via the Na-Cl cotransporter
  • Calcium reabsorption
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12
Q

What is the function of the collecting tubule?

A
  • Principal cells important for Na and water reabsorption and K secretion
  • Selective Na channels under hormonal (aldosterone) control
  • Intercalated cells involved in regulation of acid base balance
  • Water transport- antidiuretic hormone
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13
Q

What is the major difference between water and sodium reabsorption?

A
  • Sodium reabsorption is an active process (uses ATP) occurring in all tubular segments (except the descending thin limb of Henle’s loop)
  • Water reabsorption is by osmosis and is dependent upon sodium reabsorption
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14
Q

What’s the Total Body Water (TBW) ?

A

= .6 of Body Weight

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15
Q

What’s the osmolarity equation?

A

Posm = [Na] x 2 + [urea] + [glucose] ≈ 275-290 mosm/kg

Not albumin because it’s a protein therefore contributes to oncotic pressure

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16
Q

What is the action of ADH / Vasopressin ?

A
  • Vasopressin is a peptide hormone, also called anti-diuretic hormone (ADH)
  • Produced by a group of hypothalamic neurons, and then released from the posterior lobe of the pituitary gland
  • Couples to V2, a vasopressin receptor in the collecting duct
  • Vasopressin stimulates the insertion of aquaporins in the luminal membrane (urine side) of the collecting duct cells to increase water permeability/reabsorption.

Stimulation:

  1. Hypertonicity sensed by osmoreceptors in the hypothalamus
  2. Hypovolemia felt at carotid sinus which signals hypothalamus
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17
Q

What are the determinants of the water regulation in the collecting duct?

A
  1. Permeability of collecting duct to water (regulated by ADH =vasopressin)
  2. High osmolarity of the medullary interstitium to draw the water out of the tubule into the interstitium and back to the blood stream
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18
Q

What does alcohol do on ADH?

A

It supresses it so you piss a lot

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19
Q

What is the Vasa Recta?

A
  • Medullary blood supply
  • Prevents the osmolarity from being dissipated
  • U-shape permits bulk flow of fluid and solutes into the blood via the usual colloid osmotic and hydrostatic pressure that favors resorption
  • Carries away only as much solute and water as the net absorbed from the medullary tubules, and the high concentration of solutes established by the countercurrent mechanism is maintained- steady state
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20
Q

What is the important channel in the Thick Ascending Limb- TAL that reabsorbs sodium?

A

The Na-K-2Cl channel

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21
Q

How is Na controled in the body?

A

Changes in intake and body Na content are sensed by pressure receptors in vascular wall (felt as volume), the renal afferent arteriole and the heart. Activation of these receptors leads to changes in renin angiotensin aldo axis, sympathetic system, vasopressin and Atrial Naturetic Peptide, ANP.

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22
Q

How is Na reabsorbed in the PCT?

A
  • Bicarbonate, Na, phosphate and glucose reabsorption while H is secreted into the urine
  • Na-K ATP-ase in the basolateral membrane actively pumps Na out of the cell (low cellular [Na])
  • Water Follows Osmotic Gradient: Lower tubular fluid osmolality creates an osmotic gradient that promotes water reabsorption
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23
Q

How is Na reabsorbed in the Thick Ascending Limb Loop of Henle?

A
  • 50% of Na reabsorption is transcellular. Passive entry into cell via: Na/2Cl/K symporter and Na-H antiporter
  • 50% of Na reabsorption is paracellular down electrochemical gradient together with K, Ca, Mg
  • Impermeable to H2O so tubular fluid becomes hypo-osmolar
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24
Q

How is Na reabsorbed in the DCT?

A
  • Vitamin D-dependant Ca binding protein
  • Exclusively transcellular: Na-Cl symporter and Basolateral Cl channel
  • Impermeable to water: tubular fluid becomes more hypo-osmolar
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25
Q

How is Na reabsorbed in the cortical collecting duct?

A

Regulated reabsorption: Na diffuses into cells via apical Epithelial Na Channels= E Na C, that creates lumen negative charge and then passive paracellular Cl reabsorption down electrochemical gradient and K diffusion from cell through a K channel, down electrochemical gradient

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26
Q

How does the renin-angiotensin-aldosterone system work ?

A

When a patient becomes volume depleted, the renin-angiotensin-aldosterone and sympathetic nervous systems are activated. Ang II and norepinephrine enhance proximal Na reabsorption by increasing the activity of the Na-H exchanger in the proximal tubule. Ang II stimulates aldosterone (secreted by the zona glomerulaos of surrenal gland), which then promotes maximal Na reabsorption in the CCD. Sodium’s presence is felt as volume. SNS can override renal autoregulation.

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27
Q

How does aldosterone work?

A
  • A steroid hormone secreted by the adrenal cortex, zona glomerulosa
  • Hypovolemia activates aldosterone
  • Ang II activates aldosterone
  • Stimulates sodium reabsorption in the cortical collecting ducts
  • No aldosterone: ~2 % of filtered load is excreted
  • High aldosterone: ~0 % of filtered load is excreted- the sodium is totally reabsorbed
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28
Q

What are the 4 main volume regulatory mechanisms of the body?

A
  1. Sympathetic nervous system
  2. Renin-angiotensin-aldosterone system (RAS)
  3. Atrial naturetic peptide (inhibits volume retention)
  4. Vasopressin (= antidiuretic hormone ADH)
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29
Q

What are the causes of hyponatremia?

A
  1. Appropriate/physiologic ADH release:
  • Intravascular volume contraction such as congestive heart failure, cirrhosis, nephrotic syndrome, reset of osmostat (pregnancy) where intravascular volume is low (even though the patient my have peripheral edema, the intravascular space is what dictates ADH release)
  • Diarrhea, vomiting, volume depletion with thiazides
  1. Pathologic: Syndrome of Inappropriate ADH (SIADH)
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30
Q

What are the 4 criterias of SIADH?

A
  1. Hyponatremia
  2. Euvolemic
  3. Urine osmolality inappropriately high (ADH secreted anyway)
  4. Urine Na above 40
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31
Q

What are the causes of SIADH?

A
  • Any CNS disorder (meningitis, abscess)
  • Tumors producing ADH like hormone- small cell lung cancer, duodenum, pancreas
  • Chest disorders- pneumonia, empyema
  • Drugs
  • Pain, nausea
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32
Q

What is the clinical presentation of hyponatremia?

A
  • Acute hyponatremia: cerebral edema and neurologic symptoms
  • Chronic: headache, nausea, vomiting, lethargy, restlessness, disorientation. May lead to seizures, coma, death.
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33
Q

How do we diagnose and treat hyponatremia?

A

Depend on the volume status

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34
Q

How do we treat peripherally edematous but hyponatremic?

A

Water restriction

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35
Q

How do we treat volume depleted hyponatremia due to GI losses?

A

Isotonic saline

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36
Q

How do we treat SIADH?

A

hypertonic saline (9%)

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37
Q

When do we give D5W?

A

hyperosmolar stress

38
Q

When do we use the Adrogue formula?

A

To calculate how many fluid and for how long

39
Q

What are the causes of hypernatremia?

A

Pure water deficit

  • Diabetes Insipidus DI
  • Central e.g. low ADH + hypothalamic e.g post pituitary surgery
  • Nephrogenic e.g. Kidney doesn’t sense ADH

Hypotonic fluid deficit

  • Renal losses
  • Diuretics, osmotic diuresis, postobstructive diuresis (urea)
  • GI losses (vomiting, NG drain, diarrhea)
  • Cutaneous losses- burn, sweat

Hypertonic Na Gain (rare + iatrogenic)

  • Hypertonic saline incorrectly administered
  • TPN incorrectly administered
  • Hypertonic NaHCO3 incorrectly administered

Secondary hypodipsia – very common

  • Dementia
  • Delerium
  • Mental status change
40
Q

Clinical manifestations of hypernatremia?

A
  • Consequence of altered brain water content
  • Brain shrinks
  • Traction on intracerebral veins which can rupture
  • Less profound hypernatremia: nausea, weakness, lethargy, coma
  • Seizures may develop after initiation of rehydration
41
Q

Treatment of hypernatremia?

A

Slow oral or IV replacement of water by .5 mEq/h using:

0.6x [Body Weight (kg)] x [(Na]/140) – 1] or C1V1=C2V2 à

42
Q

Too little water is?

A

Not enough ADH: hypernatremia

43
Q

Too much water is?

A

Too much ADH: hyponatremia

44
Q

Too much sodium is?

A

Edema

45
Q

Too little sodium is?

A

Volume depletion

46
Q

What is the pathophysiology of edema?

A
  1. Alteration in capillary hemodynamics favoring movement of Na and water from vascular space into interstitium
  2. Renal retention of dietary sodium and water with expansion of extracellular fluid volume
47
Q

What are the causes of edema?

A

Nephrotic syndrome

  • Impaired glomerular barrier function with protein loss in the urine (>3 g/day)
  • Low plasma albumin results, therefore low oncotic pressue, development of peripheral edema

CHF

  • ↓CO, release of hypovolemic hormones renin-ang-aldo, epinephrine, ADH cause renal Na and water retention, leading to edema formation
  • More proximal tubule Na resorption mediated by AngII and epinephrine
  • More collecting tubule Na and water absorption due to aldosterone and ADH
  • Right: peripheral / Left: pulmonary

Hepatic Cirrhosis and Ascites

  • Hepatic cirrhosis- fibrotic liver can not accept blood flow from intestine (splanchnic veins) – pressure in liver interstitum rises – fluid moves out of the liver into the peritoneal 3rd space= ascites
  • The intestinal (splanchnic) veins also vasodilate, which lowers SVR and systemic BP
  • Decreased effective circulating volume and reduced renal blood flow leads to activation of renin/ang/aldo system, as well as ADH release due to intravascular hypovolemia, Na and water retention, edema
  • Low GFR, very low urine sodium e.g. UNa <10
48
Q

What are the symptoms of edema?

A
  • Peripheral edema: swelling of the feet, hands, face esp. periorbital
  • Pulmonary edema: shortness of breath, orthopnea
  • Ascites: increased abdominal girth, may cause shortness of breath
49
Q

What’s the normal distribution of K in the ECF and ICF?

A
  • 98% of the body’s K is located in the cells
  • Normal Serum K: 3.5-5.0 mMol/L (< 3.5 = hypokalemia and > 5.0 = hyperkalemia)
  • The ratio of K in the cells to the K out of the cells (in the extracellular fluid) dictates the resting membrane potential Em = can cause major cardiac arrhythmias, muscle cramping, paralysis, rhabdomyolysis.
50
Q

Plasma [K] is regulated by ?

A
  1. By shifting K from extracellular to intracellular
  2. K excretion by the kidney (takes 6-8 hours)
51
Q

How is K shifted from extracellular to intracellular compartment?

A
  1. Plasma [K]
  2. Insulin stimulates Na-K ATPase for K uptake in skeletal muscles and liver
    This procress is dependant of glucose uptake: Insulin (given with glucose) is used to treat severe hyperkalemia
  3. Beta-adrenergic stimuli increases K uptake into cells: stimulate the Na-K-ATPase pump
    Can also be used as treatment
52
Q

How is K excreted by the kidney?

A
  1. Dependent on distal flow of Na and water (renal failure will lead to K retention - hyperkalemia)
  2. In PCT, K reabsorption is primarily passive and proportional to Na and water
  3. In TAL and CCD, excretion by ROMK= renal outer medullary K channel for K excretion
  4. Excretion in the CCD is regulated by aldosterone (binds to Aldo-R and acts as transcriptional regulator to synthesize more ENaC and eventually ROMK)
  • ­[K] causes adrenal release of aldosterone
  • K excretion is increased with alkalosis-elevated intracellular pH tends to increase activities of ENaC, ROMK
  • High salt diet will turn off renin-angiotensine-aldosterone
53
Q

Values for Hyperkalemia?

A

> 5.0 mMol/L

54
Q

Values for hypokalemia?

A

< 3.5 mMol/L

55
Q

How can you recognize hyperkalemia on an ECG?

A
  • The partial depolarization leads to faster repolarization of the T waves: peaked T
  • Above 7-8 mmol/L, depolarization delayed, widened QRS, eventual loss of P wave, followed by sine wave, followed by V fib and death
  • Arrhythmia not well correlated with level, ie V fib can happen at any level of hyperkalemia
56
Q

What are the causes of hyperkalemia?

A

1. Decreased GFR therefore ↓ K excretion +/- eating a high K diet

2. Hypoaldosteronism:

  • ACE inhibitors/ARBs which block AT2 which blocks aldo
    • NSAIDS inhibit the prostaglandins which stimulates renin
    • 1o adrenal insufficiency
    • hyporeninemic hypoaldosterionism- this sometimes happens to diabetic patients in middle age where adrenal gland doesn’t respond to renin
    • Hydronephrosis due to obstruction: aldosterone resistance in the collecting duct
    • Other Drugs: K sparing diuretics: Triamterine, Amiloride. Trimethoprim, an antibiotic acts the same way. Spironolactone- aldosterone blocker.

3. K shifts out of cells due to

  • Insulin deficiency.
  • Rhabdomyolysis, K comes out of damaged muscle, was patient found on floor after a fall?
57
Q

How do you recognize hypokalemia on an ECG?

A
  • Reduced ECF [K] impairs repolarization by decreasing K channel permeability
  • T wave flattens, U waves occur, bradycardia
58
Q

What are the causes of hypokalemia?

A
  • Electrolyte abnormality in hospital (most common)
  • Diet: may contribute, but not the sole cause
  • Urinary loss: often with hyperaldo and ­ distal Na flow.
    • Diuretics – loop and thiazide- plus renin/ang/aldo are turned on
    • Primary hyperaldosteronism: hypertension and low K
    • Renal artery stenosis
    • GI losses: vomiting, diarrhea, NG tube
  • ­Entry into cells: epinephrine
  • Alkalosis (explains why vomiting leads to hypokalemia, despite the fact that K content in vomit is low. HCl loss in vomit = adding HCO3 to blood. Stimulates K excretion in CCD)
59
Q

How do you treat hyperkalemia?

A
  1. Protect the Heart

Calcium gluconate IV

  1. Shift the K+

Ampule of IV 50% dextrose in water + insulin

Inhaled beta-2 agonists- salbutamol

  1. Get rid of the K+

Oral K+ exchange resin

Loop diuretics if volume-overloaded

Normal saline if volume-contracted

Dialysis if absent renal function

Stop other medication + diet review

60
Q

How do you treat hypokalemia?

A

Potassium replacement (for each 1 mmol/L serum level, 100-150 mmol/L deficit)

  • IV (no faser then 10 mmol/hour)
  • Oral (preferred, more efficient with large doses)
  • Replace Mg++ of low
61
Q

Non-carbonic or non-volatile acids are maintained by what?

A
  1. Buffering the acid

Major extracellular/blood buffer is the CO2/HCO3- system and major intracellular buffers are phosphates and proteins, and carbonate (C03-2) in bone. Then, the acid needs to be secreted in the urine. Kidneys also make bicarbonate to buffer the acid in the urine do not damage the urinary tract.

  1. Renal excretion of the acid
62
Q

How and where in the tubule H+ is secreted ?

A

Proximal tubule:

  • Reabsorption of filtered bicarbonate (reabsorbed by first combining with H ions to form H2CO3, which becomes CO2 and H2O, can be blocked by carbonic anhydrase inhibitor ex. MOUNTAIN SICKNESS)
  • Secretion of hydrogen ions:
  • Buffering by phosphate (1 molecule secreted = 1 molecule of bicarbonate absorbed)
  • Synthesis of ammonium (NH4+) that is excreted (1 molecule secreted = 1 molecule of bicarbonate absorbed)

Loop of Henle

  • Na-H exchanger that excretes H+ when the pH drops

Distal nephron (medullary and cortical collecting duct)

  • NH3 diffuses into tubular lumen and is trapped as NH4+ by H+ which is secreted by intercalated cells
63
Q

If patient arrives acutely ill in acidosis with renal inssuficiency in ER, what do you do?

A

give IV: D5W with 3 ampules of NaHCO3 each ampule of 7.5% sodium bicarbonate has 44.6 mEq HCO3 and 44.6 mEq of Na

64
Q

What other type of alkalosis can happen?

A

Contraction alkalosis

  • Occurs when in volume contraction, the fluid lost contains Cl but little or no HCO3.
  • Most commonly due to diuretics
  • Extracellular volume contracts around a relatively constant quantity of HCO3.
  • Patients have low serum Cl and thus low urinary Cl
  • The bicarb can’t leave b/c Na is conserved due to volume contraction
  • Na is reabsorbed in the prox tubule with bicarb perpetuating the alkalosis
  • Once NaCl is given, the plasma volume is restored, and HCO3 can again be excreted, as there is Na to spare, and the Cl- will allow also electroneutrality and promote bicarb secretion
65
Q

What are the Anion Gap metabolic acidosis (AGMA) causes of metabolic acidosis?

A

A B C

66
Q

What are the Non-anion gap metabolic acidosis (NAGMA) causes of metabolic acidosis?

A

C and ABC of “decreased acid excretion”

67
Q

When you have a patient with metabolic acidosis, what other things you have to calculate?

A

Anion Gap

With metabolic acidosis, we need to calculate the anion gap:

AG= [Na+] - ([Cl-] + [HCO3-])

Normal = 10 meq/L

You know if you measure the AG and it is larger than normal, you have an unmeasured anion that is causing this increase and it indicates a metabolic acidosis (ex. lactic acid, methanol, propylene glycol, oxoproline aka Tylenol OD)

Osmolal Gap for alcohol

Osmolality = 2 x [Na] + [glucose] + [urea] ex. 300

You request the osmolality to be measured by the lab with freezing point, and it is 344, = OG is 44

68
Q

What are the 3 types of Renal Tubular Acidosis?

A
69
Q

How do you interpret a blood gas value?

A
  1. Is there alkalemia or acidemia present?

pH < 7.35 acidemia

pH > 7.45 alkalemia

  1. Is the disturbance respiratory or metabolic? Look at the CO2

IF pH and CO2 change in the , the disturbance is

IF pH is ¯ and CO2 ­ (change in the opposite direction), the disturbance is respiratory

  1. Respiratory disturbance and expected compensation
70
Q

What are 3 other types of other types of metabolic acidosis?

A

Lactic acidosis: Anaerobic metabolism of glucose - increased endogenous acid production

Diabetic Ketoacidosis DKA: Due to insulin deficiency, can’t use glucose, so fatty acids burned but β-hydroxybutyric acid, acetoacetate are acids

71
Q

What is the only ion that is not reabsobed mainly in the PCT?

A

Magnesium! reabsorption in the TAL of the loop of Henle: passive paracellular absorption

72
Q

Calcium levels are dependant on what?

A
  1. Total amount of calcium in the body: determined by GI tract absorption vs. renal excretion
  2. The distribution of calcium between bone and the ECF compartments: mainly mediated by parathyroid hormone (PTH)
73
Q

What is the role of PTH?

A

The drop in calcium is sensed by a calcium-sensing receptor in the parathyroid glands that will secrete PTH. Then it stimulates bone resorption (resulting in the release of calcium and phosphate), increases intestinal calcium reabsorption and increases renal calcium reabsorption. Can be altered by hyperparathyroidism (primary-hypercalcelima, secondary-hypocalcemia and tertiary-hypercalcemia).

74
Q

What is the role of Calcitriol = active vitamin D =1,25-dihydroxy-cholecalciferol?

A

Stimulated by low calcium causing high PTH and low phosphate. Increases Ca and PO4 absorption from the intestine and works synergistically with PTH to stimulate bone resorption. 2 receptors in the parathyroid gland (calcium and calcitriol) will autoregulate via feedback of levels of thpse 2 hormones.

75
Q

What is the role of Calcitonin?

A

Do the opposite of PTH (stimulated by an increase in serum Ca)

76
Q

How is calcium reabsorbed?

A
  • PCT: passively and most of reabsorption is there
  • TAL: feedback loop with active reabsorption and calcium sensing receptor (CaSR)
  • DCT: regulated by PTH, only part of the nephron in which calcium and sodium are not coupled

Determined by :

  1. The filtered load of calcium (GFR x ionized calcium) and
  2. The pH (acidosis increases calcium excretion and alkalosis decreases calcium excretion)
77
Q

What are the causes of hypercalcemia?

A
  • Primary hyperparathyroidism
  • Excess production of 1,25D (e.g. sarcoidosis)
  • Excess ingestion of calcium or active vitamin D
  • Malignancy (usually due to calcium release from bones)
  • Prolonged immobilization
  • Thiazide diuretics (via ECF volume contraction leading to increased proximal reabsorption of Na+ and Ca++)
  • Familial hypocalciuric hypercalcemia
78
Q

What are the symptoms of hypercalcemia?

A
  • Bone pain
  • Kidney stones (increased urinary calcium causing crystal precipitation in urine)
  • Poor appetite, nausea, vomiting, abdominal pain
  • Confusion, lethargy
79
Q
A
80
Q

What is the normal response to hypercalcemia?

A
  • Decreased PTH
  • Decreased 1,25D (via decreased PTH
  • Less reabsorption in the thick ascending limb
  • Increased calcitonin
81
Q

What are the causes of hypocalcemia?

A
  • Hypoparathyroidism (congenital or after removal of parathyroid glands)
  • Vitamin D deficiency (has to be very low!)
  • Low magnesium
  • Chronic kidney disease (due to high phosphate, low calcitriol)
82
Q

What are the symptoms of hypocalcemia?

A
  • Neuromuscular irritability
  • Seizures
  • Arrhythmias
83
Q

What is the normal response to hypocalcemia?

A
  • Increased PTH
  • Increased 1,25D
  • Increased paracellular uptake in thick ascending limb
84
Q

Phosphate levels are dependant on what?

A
  1. Total amount of calcium in the body: determined by GI tract absorption vs. renal excretion
  2. The distribution of calcium between bone and the ECF compartments: mainly mediated by PTH and calcitonil
85
Q

The reabsorption of phosphate depends on what?

A
  1. Plasma phosphate: depends on your diet
  2. PTH: decreases activity of the Na-phosphate cotransporter in the PT
  3. FGF-23
86
Q

What are the causes of Hyperphosphatemia?

A
  • Renal failure (MOST COMMON)
  • Hypoparathyroidism (rare)
  • Release of phosphate from cells (muscle break down after injury and tumour)
87
Q

What is the normal response to hyperphosphatemia?

A
  • Decreased calcitriol (due to decreased 1-alpha hydroxylase) à less GI PO4 absorption
  • Increased PTH à increased renal excretion of PO4 in proximal tubules
  • Direct downregulation of Na-phos cotransporter in proximal tubule by high plasma PO4
88
Q

What are the causes of hypophosphatemia?

A
  • Shift from ECF into ICF
  • GI losses
  • Renal losses (primary hyperparathyroidism or Fanconi syndrome)
89
Q

What is the normal response to hypophosphatemia?

A

Increased calcitriol

90
Q

What is the most important determinant of renal Mg excretion?

A

Plasma magnesium concentration

Bloc D - Renal (7 decks)

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