Exam 1 (Lectures 2-12) Flashcards
How can you calculate nutrition body weight (NBW) and maintenance IV fluid (MIVF) requirements?
First, calculate ideal body weight (IBW):
- male = 50kg + (2.3 x inches over 60”)
- female = 45.5kg + (2.3 x inches over 60”)
Then, if the actual body weight is over 130% of IBW, then use NBW:
- NBW = IBW + 0.25(wt - IBW)
We want fluid intake = fluid losses; we take in consideration the sensible and insensible fluid losses.
- MIVF = 30-40 mL/kg/day
- usually use multiples of 25
What is osmolality and how can you calculate osmolality given a patient’s lab data?
Osmolality - # of particles per liter of water
Osm = (2 x Na) + (BUN/2.8) + (Glucose/18)
- Need to know sodium, BUN, and glucose)
What is osmolarity and how can you calculate osmolarity given the components of an IV solution?
Osmolarity - How much solute is in that volume of fluid (mOsm/L); dependent on pH and temp
- Isotonic: 275-290 mOsm/L
Total osmolarity = osmolarity of IV solution + osmolarity of added electrolytes.
How can you give recommendation for the type of IVF and rate of IVF given a patient’s clinical scenario/labs?
Type: Crystalloids & Colloids
- Crystalloids: Can be iso, hypo, or hypertonic; provide water and/or sodium; Resuscitation: NS, Lactated ringers, Normosol-R, Plasma-lyte; Maintenance: 1/2 NS, D5W (not alone)
- Colloids: Only hypertonic; will never be a maintenance fluid; Used to increase plasma oncotic pressure (increase BP); Albumin 5% when volume needed, Albumin 25% when protein needed, blood (1 unit increases Hb by 1g/dL); synthetics aren’t good
Rate for maintenance: 30/40 mL/kg/day; then find what the rate would be per hour
D5W + 1/2NS + 20mEq KCl / L is the most common MIVF has similar composition to urine, used to increase plasma oncotic pressure
What are the factors affecting fluid balance and the 3 specific monitoring parameters to assess a patient’s fluid balance?
Factors affecting fluid balance - ??
Monitoring parameters -
- Daily weight
- Daily ins/outs
- Volume status (volume overload, euvolemic, dehydration)
- Urine output (UOP; mL/kg/hr)
- Vitals (HR/BP, central venous pressure, Invasive hemodynamic parameters)
What is the normal range, types & causes (& symptoms) of deficiency for: sodium
Normal range: 135 - 145 mEq/L
Isotonic “pseudo” hyponatremia: 275-290 mOsm; extreme elevations of lipids and proteins increase the total plasma volume, which makes the sodium appear to be low. Here we will see a low calculated Osm, but the measured serum Osm will be normal, leading to an osmolality gap.
Hypertonic hyponatremia: >290 mOsm; Most frequently seen with high BG. We want to use the Corrected Na equation in this case.
Hypotonic hyponatremia: <275 mOsm
- Hypovolemic: Volume is low, but sodium is extra low; If due to renal cause (diuretics, adrenal insufficiency, kidney/brain salt wasting), we will see urine Na+ go up > 20mEq/L. If non-renal (blood/skin/GI loss), urine Na+ < 20mEq/L; Will see dehydration symptoms
- Isovolemic: Volume is good, sodium is low; Caused by adrenal insufficiency, hypothyroidism, psychogenic polydipsia, and SIADH; May see malaise, psychosis, seizures, coma.
- Hypervolemic: Holding on to so much fluid, that now it appears sodium is low; Seen with organ failure; Will see edema/weight gain
What is the normal range, causes(7)/symptoms(5) of deficiency, and treatment options for: potassium
Normal range: 3.5 - 5 mEq/L
K+ is important in cardiac/non-cardiac resting potential across cell membranes; can lead to arrhythmias if out of range
Causes: Diuretic loss, b-agonists (albuterol), insulin, NG drainage, metabolic alkalosis, diarrhea, magnesium depletion (Mg is a co-factor for NA/K ATPase)
Symptoms: Highly variable; Weakness, N/V, arrhythmias, cramping, muscle weakness
Treatment: Goal is to prevent serious cardiac arrhythmias, normalize serum K+ conc., identify/correct underlying causes, & prevent overcorrection.
- if 3.5-4 mEq/L: no therapy recommended
- if 3-3.4 mEq/L: treatment debatable; PO potassium if pt has cardiac conditions
- if <3 mEq/L: always treat; PO preferred if asymptomatic; IV for symptomatic pts or NPO patients (*arrhythmia or cardiac arrest can happen if given too quickly)
*always correct Mg deficiency if needed
**no faster than 10mEq/hr infusion rate if no cardiac monitoring; no faster than 20mEq/hr if cardiac monitoring!!!
What is the normal range, causes/symptoms of deficiency, and treatment options for: phosphorous
Normal range: 2.5 - 4.5 mg/dL
Causes: decreased intake, impaired absorption, intracellular shifts
Symptoms: Muscle, neuro, heme, bone, pulm, cardial, renal problems
Treatment:
- Mild to moderate hypophosphatemia: 1-2 mg/dL -> correct with oral phos (Phos-NaK or Fleets Phospho-Soda) BID-TID for absorption
- Severe hypophosphatemia: <1 mg/dL -> correct with IV; If K+ <4mEq/L, use KPhos; If K+ ≥4mEq/L, use NaPhos
What is the normal range, causes/symptoms of deficiency, and treatment options for: calcium
Normal range: 8.5 - 10.5 mg/dL; ionized Ca2+ range is 4.6-5.1 mg/dL
must use corrected Ca2+ equation to ensure that albumin isn’t skewing results; ionized Ca2+ is more accurate indicator
Causes: Mg deficiency, pt recieved large volume of blood products, hypoalbuminemia, medications, Vit D deficiency, etc.
Symptoms: Neuromuscular (muscle cramps, numbness), CNS (depression, anxiety, memory loss, confusion), dermatologic (hair loss, eczema, brittle grooved nails), cardiac (prolonged QT, hypotension, bradycardia, arrhythmias, decreased myocardial contractility)
Treatment:
- Acute: 100-300 mg elemental Ca2+ IV over 5-10 mins; Administer 1gm/hr if not coding & correct hypomagnesemia
**1g Ca Chloride = 3g Ca Gluconate (270mg elemental Ca2+)
- Chronic: 1-3g/day of elemental Ca2+ (CaCO3 650mg PO QID = 1g elemental Ca2+ daily)
What is the normal range, causes/symptoms of deficiency, and treatment options for: magnesium
Normal range: 1.5 - 2.5 mg/dL
Causes: Disorders of GI tract or kidneys, diarrhea, severe malnutrition, drugs (diuretics, aminoglycosides, etc.), alcohol
Symptoms: Often associated with other abnormalities (hypocalcemia or hypokalemia), cardiovascular (tetany, convulsions, ventricular arrhythmias), neuromuscular (ataxia, seizures), or CNS symptoms (lethargy, confusion)
Therapy: Goal is to restore NL Mg2+ conc., resolve symptoms, correct concomitant electrolytes, identify underlying cause.
- PO: Asymptomatic pts with Mg > 1mg/dL; Milk of Mag OR Mag-Ox
- IV: Symptomatic or NPO pts; If Mg 1-2mg/dL -> 0.5 mEq/kg; If Mg < 1mg/dL -> 1 mEq/kg
- 8mEq = 1 gram; dose in mEq, order in grams; infuse 1g per hour!!
What are the appropriate rate of administration of IV and oral potassium treatment options for hypokalemia?
rate: no faster than 10mEq/hr infusion rate if no cardiac monitoring; no faster than 20mEq/hr if cardiac monitoring!!!
- if 3.5-4 mEq/L: no therapy recommended
- if 3-3.4 mEq/L: treatment debatable; PO potassium if pt has cardiac conditions
- if <3 mEq/L: always treat; PO preferred if asymptomatic; IV for symptomatic pts or NPO patients
*always correct Mg deficiency if needed
- lots of PO options, such as liquid, powder, effervescent tabs, etc.
How do you calculate a patient’s serum calcium?
Be sure to use corrected Ca2+ equation or get ionized Ca2+ measurement.
Corrected Ca2+ = Measured Ca2+ + [(4 - measured albumin) x 0.8]
Range of serum Ca2+: 8.5 - 10.5 mg/dL
Range of ionized Ca2+: 4.6 - 5.1 mg/dL
What are the advantages and disadvantages of calcium replacement with calcium chloride vs. calcium gluconate?
1g Ca chloride = 3g Ca gluconate
Chloride is good if the patient is coding (IV push)
- More predictable increase in Ca2+ concentration
Gluconate is preferred for peripheral IV (PIV) administration: (safer)
- Lower % of elemental Ca2+
- Less risk for extravasation (necrosis)
What role does magnesium play in the management of the other electrolyte deficiencies and what are the treatment options for hypomagnesemia?
- Related to Ca2+ and K+ metabolism; Be sure to correct magnesium if pt has hypokalemia or hypocalcemia
Treatment:
- PO: Asymptomatic pts with Mg > 1mg/dL; Milk of Mag OR Mag-Ox
- IV: Symptomatic or NPO pts; If Mg 1-2mg/dL -> 0.5 mEq/kg; If Mg < 1mg/dL -> 1 mEq/kg
- 8mEq = 1 gram; dose in mEq, order in grams; infuse 1g per hour!!
How would you recommend a NaPhos or KPhos treatment dose for a pt with hypophosphatemia based on the patient’s labs and clinical scenario?
If the pt also had a K+ < 4 mEq/L, give KPhos: no faster than 7mMol/hr
If pt had K+ ≥4 mEq/K, give NaPhos
Treatment guidlines:
Phos conc. 2.3-2.9mg/dL -> 0.32 mMol/kg
Phos conc. 1.6-2.2mg/dL -> 0.64 mMol/kg
Phos conc. <1.6mg/dL -> 1mMol/kg
always infusion, never push
1mMol KPhos = 1.47 mEq K+
10mEq of K+ increases pt serum K+ by 0.1, so we may need to spit dose with KPhos and NaPhos to avoid hyperkalemia.
What are some possible signs of dehydration? (5)
- Upon physical exam: decreased skin turgor, dry mucous membranes, delayed capillary refill
- Tachycardia + hypotension
- Weak peripheral pulse
- Decreased urine output (less than 0.5 mL/kg/hr), dark urine
- BUN/SCr ratio is above 20
What is SIADH and what does it commonly cause? What causes SIADH? How do we treat it?
SIADH - Syndrome of Inappropriate AntiDiuretic Hormone release; Water intake greatly exceeds the capacity of the kidneys to excrete water.
Most common cause of isovolemic hypotonic hyponatremia.
Caused by: tumors, CNS disorders, and DRUGS (antipsychotics, carbamazepime, SSRIs, etc.)
Treatment: Remove the underlying cause (ex. medication) if possible.
1. Restrict free H2O.
2. If 24-48 hours of H2O restriction doesn’t work, can use Vaptans (Conivaptan, Tolvaptan)
What are the treatment options for hypo-, iso-, and hyper- volemic hyponatremia? What rate of sodium increase can we not go over?
- Hypovolemic: Symptomatic -> Hypertonic NaCl (3% NaCl); Asymptomatic -> Isotonic NaCl (0.9% NaCl)
- Isovolemic: Symptomatic -> Furosemide + 3% NaCl; Asymptomatic -> Isotonic NaCl (0.9% NaCl) + water restriction
- Hypervolemic: Symptomatic -> Furosemide + lots of 3% NaCl; Asymptomatic -> Furosemide
Goal is to avoid rise in serum sodium greater than 0.5 mEq/L/hr OR no more than 8-12 mEq/L/day!!
What are some differences between acute and chronic hyponatremia? How can you treat acute symptomatic hyponatremia?
Chronic (>48 hours): The brain cells extrude solutes, there’s minimal brain swelling, mild neurologic symptoms, and brain bleeding/death is rare. The body kind of adjusts.
Acute (<48 hours): The brain quickly swells with water, leading to severe neurologic symptoms, brain bleeds, and eventually death.
Treatment: increase serum Na+ by 1-2 mEq/L/hr until symptoms resolve.
- Use 3% NaCl to replace 1/2 of sodium deficit in first 24 hours, then the other half within 24-72 hours.
- Increase of 4-6 mEq/L is usually sufficient (remember don’t go over 8-12 mEq/L in the first 24 hours)
- Complete correction is unnecessary, and demyelination can occur if corrected too rapidly.
- These pts should be monitored regularly (q2-4h) until asymptomatic.
What do these important structures in the kidney do: Kidney as a whole, glomerulus, PCT, thin & thick limb of loop of henle, DCT, collecting tubule, medullary collecting duct
Functions of kidneys - Endocrine, control of solutes and fluids, blood pressure control, acid/base balance, drug metabolism and excretion, metabolic waste.
Glomerulus: Filtration
PCT: Active and passive reabsorption happens here, and drugs/H+/etc. can be secreted into PCT from efferent arteriole.
Thin limb of Loop of Henle: Passive reabsorption of water
Thick limb of Loop of Henle: Acitve reabsorption of filtered Na+/K+/Cl- and secondary reabsorption of Ca2+ and Mg2+.
DCT: Active reabsorption of small amount of filtered Na+ & Cl- and Ca2+ reabsorption under parathyroid hormone control. Active secretion.
Collecting tubule: Na+ reabsorption coupled to K+ and H+ secretion
Medullary collecting duct: water reabsorption under vasopressin control.
What is the pathophysiology of acute renal injury (3 types) and chronic renal injury?
Acute - Criteria includes an increase in SCr ≥ 0.3mg/dL in 48 hours, OR more than 50% increase in SCr within 7 days, OR reduction in urine output.
- Prerenal: This occurs when the pressure going into the glomerulus is messed up. Seen commonly with blood loss. Also, the body has a mechanism with prostaglandins and angiotensin II to regulate the pressure going into the glomerulus, but drugs can interfere with this.
- Intrinsic: Primary causes include sepsis, ischemia, and nephrotoxins.
- Postrenal: Seen when blockages block the flow of the urine. Caused by kidney stones, blood clots, cancers, etc.
Chronic - When the kidney issues last longer than 3 months.
- Common pathway: The initial injury causes reduced filtration area, leading to increased glomerular capillary pressure, leading to more cell injury and then protein in the urine, glomerulosclerosis, and then the disease keeps progressing.
- Causes lots of issues with electrolyte balance and mechanical weakening of bone due to impaired phosphate excretion causing unusual calcifications and decreased production of 1,25-dihydroxyvitamin D3, meaning Ca2+ isn’t able to be absorbed well enough.
What are the physical principles of diuretic action (osmosis, ion gradients, charge gradients)?
Diuretics are agents that induce sodium excretion (natriuresis) and water excretion (diuresis).
Osmosis - Water follows sodium. If a diuretic blocks the reabsorption of sodium, then water will flow out of the blood and towards the sodium, and will then be excreted through the urine.
What’s the mechanism of action, drug target, and toxicities of: Carbonic Anhydrase inhibitors
MOA: Blocks CA channels so that NaHCO3 reasborption is blocked. This leads to no H+ in the cell, so the osmotic gradient is altered. Water will follow the Na+ and H+ to the lumen.
Site: PCT
Toxicities:
- Hyperchloremic metabolic acidosis: We no longer have the bicarb buffer, so the blood is getting acidic.
- Renal stones
- Renal potassium wasting: The K+ channels are no longer working due to the Na+ staying in the lumen, so K+ never gets into the interstitial space.
- Drowsiness
Ex. Acetazolamide, dichlorphenamide, methazolamide
What’s the mechanism of action, drug target, and toxicities of: Osmotics
MOA: Add lots of non-reabsorbable solute to the luminal fluid so that H20 will follow the solutes to the lumen for excretion.
Site: Loop of Henle + PCT (anwhere with high water permeability)
Toxicities:
- Hypernatremia: The total volume of the blood would be going down due to the water leaving the blood for the lumen, but the Na+ would be staying the same. So relatively, there would be more Na+.
Ex. Mannitol, Urea, Glucose, Isosorbide, Glycerine
What’s the mechanism of action, drug target, and toxicities of: Na+-K+-2Ck- symport inhibitors
loop diuretics, high-ceiling diuretics
MOA: Block the Na+-K+-2Cl- symport, thus blocking Na+, K+, and Cl- from getting through the cell to be reabsorbed.
Site: Ascending limb of loop of henle
Toxicities:
- Hyperuricemia
- Hypomagnesemia: Blocking Na+ and K+ also messes with Ca2+ and Mg2+ being able to cross into the interstitial space, thus leading to hypomagnesemia.
- Hypokalemic metabolic alkalosis: Due to the K+ not leaving the lumen, the blood gets more basic.
- Ototoxicity
- Dehydration
Ex. Furosemide, Bumetanide, Ethacrynic acid, Torsemide
What’s the mechanism of action, drug target, and toxicities of: Na+-Cl- symport inhibitors
thiazides
MOA: Block the Na+-Cl- symport, thus making NA+ unable to get reabsorbed.
Site: Distal convoluted tubule
Toxicities:
- Hypokalemia metabolic alkalosis: Blocking Na+ from getting into cell also stops K+ from getting out of the cell, so more K+ gets excreted, leading to hypokalemia and causing the cell to be more basic.
- Hyponatremia
- Hyperlipidemia
- Hyperuricemia
- Impaired carbohydrate tolerance
Ex. Thiazides, Chlorthalidone, Indapamide, Metolazone
What’s the mechanism of action, drug target, and toxicities of: Renal epithelial Na+ channel inhibitors
K+ sparing
MOA: blocks Na+ channels so that Na+ cannot get into the interstitial space for reabsorption.
Site: Late distal tubule & collecting duct
Toxicities:
- Hyperkalemia: Due to Na+ not leaving the lumen, K+ isn’t transported to the lumen, leaving more K+ to be reabsorbed??
- Hyperchloremic metabolic acidosis: Bicarbonate is affected, leading to less of the buffer in the blood, leading to acidosis.
Ex. Amloride, Triamterene
What’s the mechanism of action, drug target, and toxicities of: Mineralocorticoid receptor antagonists
aldosterone antagonists, K+-sparing diuretics
MOA: Block the mineralocorticoid receptor, which blocks aldosterone induced protein production, meaning Na+ channels don’t get made.
Site: In the cell in late DCT and collecting duct.
Toxicities:
- Hyperkalemia: Na+ not being pumped out, so K+ not being pumped in??
- Hyperchloremic metabolic acidosis
- Gynecomastia
- Impotence
- Benign prostatic hyperplasia
Ex. Spironolactone, Eplerenone, Canrenone, Potassium canrenoate
What’s the mechanism of action and drug target of: Non-specific cation channel inhibitors
MOA: Block the channels that let ions in, thus reducing the amount of Na+ that is able to be reabsorbed
Site: Lumen anywhere with CNGCs
Ex. Nesiritide (Natrecor)
What’s the mechanism of action and drug target: Vasopressin antagonists
MOA: Block vasopressin from binding to V2 receptors, thus blocking the phosphorylation of aquaporins, which inhibits their ability to relocate to the collecting duct to allow water to pass. (Keeps water in the lumen)
Site: Collecting duct
Ex. Conivaptam, Tolvaptam
Which diuretics are secreted and why? Is increased doses a good or bad idea? What happens due to the braking phenomenon? How do CHF and CRF impact our response to diuretics?
- Site of action is in the lumen (except MRAs)
- CA inhibitors, furosemide, and thiazides are highly bound to plasma protein, so they are secreted, not filtered.
- Secretion is saturable, so increased doses won’t increase the effect, it’s most likely better to increase frequency of dose instead
- Braking phenomenon: More drug is needed to have the same effect.
- CHF decreases efficacy, CRF decreases potency
What can these tell us about the function of a patient’s kidneys?
Serum Creatinine - Mainly removed by filtration in glomerulus, so if there’s an increase in SCr, it means the kidneys are messed up.
BUN (Blood Urea Nitrogen) - This is a measure of waster from the liver’s breakdown of amino acids, so if there’s an increase, it means we aren’t excreting enough waster from the kidneys.
Creatine Clearance - Used to predict secretion and drug clearance (used for dosing).
GFR (Glomerular Filtration Rate) - Measures how quickly filtrate is being made in the glomerulus.
What happens to the nephrons as humans get older?
We lose nephrons as we get older, so our single-nephron GFR gradually goes up to compensate that, but the total GFR still goes down. Eventually, around age 70-75, there will be a compensatory effect in which the nephrons increase in capacity and filter things really fast, but that can’t last for very long. This hypertrophy leads to sclerosis and more loss of nephrons, leading to death.
What is uremia, glomerulonephritis, pyelonephritis, interstitial nephritis, nephrolithiasis, and contrast-induced nephropathy?
Uremia - The accumulation of organic waste products that are normally cleared by the kidneys. There are lots of signs and symptoms of uremia; ex. proteins and nucleosides in the urine.
Glomerulonephritis - Inflammation of glomerulus. Can be acute or chronic. Primary cause is due to Alport syndrome, but it can also be caused by drugs.
Pyelonephritis - Inflammation of kidney tissues due to bacteria in the blood or urinary tract. This may lead to sepsis if untreated.
Interstitial Nephritis - Autoimmune response that reduces the kidney’s ability to filter. A primary injury to the renal tubules results in edema in the interstitium. Mostly caused by drugs (antibiotics, esp. penicillins).
Nephrolithiasis - Kidney stones formed due to supersaturation of solutes like calcium. When the solute doesn’t get reabsorbed, they start to crystallize. We usually want these patients to drink lots of fluid and we will treat their pain.
Contrast-induced nephropathy - Seen when SCr increases after patient uses contract media. This causes 1/3 of hospital-acquired AKI. We try to hydrate the patient to avoid this and we try to avoid concurrrent nephrotoxins.
What is the difference between nephritic and nephrotic syndromes?
Both involves issues with filtration in the glomerulus by compromising the membrane.
Nephritic - Inflammation disruption glomerular basement membrane, leading to blood cells in the urine.
Nephrotic - Spillage of protein into the urine, generally caused by compromising the podocyte layer.
- We will see a decrease in the serum albumin, which keeps the appropriate osmotic gradient in the body, so water spills out of blood, causing edema.
What is the pathogenesis of glomerular diseases?
- Antibody-associated injury - Antibodies circulate in body, they engage the glomerulus, the membrane rejects these large antibodies, which results in the activation of the immune system (T cells), leading to a cascade that eventually causes inflammation of the glomerulus.
- Cell-mediated immune - Damage to the membrane causes a change of shape and function of the podocytes. Now we have lost the ability to filter across the membrane.
- Other - Involves toxic agents that cause damage to cells in the nephron, leading to cell death. Necrosis in particular leads to a lot of inflammation (cascade). DAMPs and PRRs recruit immune cells that release toxic factors. (Because of this, we may treat it with immunosuppressants to try to stop this pathway).
What’s the difference between autosomal dominant and autosomal recessive cystic kidney diseases?
Autosomal dominant - Intially have resonably good renal function, but cysts grow as person gets older, which leads to HTN due to lack of filtering. When the person is in 40-50s, we will start seeing lack of renal function. Transplantation is necessary.
Autosomal recessive - The cysts form very quickly. These patients usually make it past 2-3 years old.
What are the 3 major causes of CKD and why do they cause kidney disease?
Diabetes mellitus - Glucose is big and sticky, which makes the blood very viscous. The kidney has a lot of intricate vasculature, so the blood with glucose messes with the filtering.
Hypertension - Messes with the pressure that is going into the glomerulus.
Glomerulonephritis - Inflammation messes with the intricate vasculature of the kidney.
What can creatine clearance tell us about kidney function? What else is significant about CrCL and kidney disease?
- It’s a good predictor of GRF and it’s easy to use
- It’s only accurate in pts with stable kidney function (includes CKD because the decline is steady)
- With declining kidney function, the CrCL will appear to be higher than it actually is due to secretion
- CrCL is used for dosing stuff, whereas GRF is used for staging
What are the 5 main function of the kidneys are what are the complications that are associated with each function?
- Excrete waste products of metabolism from the blood (ex. urea, ammonia, bilirubin, uric acid, etc.)
- Complication: Uremia - Build up of waste products in the blood (presents like the flu) - Regulate body’s conc. of water and salt
- Complication: Fluid retention - Edema, fluid overload, CV complications due to HTN - Maintain acid balance of plasma (secretes H+ ions)
- Electrolyte balances: Metabolic acidosis, hyperkalemia, etc. - Synthesize calcitriol (active from of Vit D)
- Complication: Mineral and bone disorder - Due to decreased absorption of Ca2+ - Secrete hormones (erythropoietin, renin, PGAs)
- Anemia: Hemoglobin decreases, supplemental iron and ESAs needed
What is uremia and what effects does it have on the body? What can we do about it
Uremia - Associated with ESRD. Symptoms are due to the accumulation of waste molecules in the blood that are usually removed by the kidneys.
Effects - Breath smells like urine, skin gets really itchy to do the acid concentration getting so high, anemia due to EPO deficiency, GI symptoms like anorexia, N/V, constipation, metallic taste, mineral and bone disorder, etc.
These patients need dialysis. (SCr ~10 and BUN~100)
What do we do when a pt has fluid retention?
- Don’t really need to fluid restrict, as long as their Na intake is controlled.
Diuretics won’t work unless the pt has working kidneys, but they can be used to treat volume overload and HTN in pts with renal insufficiency
- If loop diuretic doesn’t work, they all won’t work
- Thiazides won’t work with a CrCL under 30mL/min, but loops will
- Don’t use K+ sparing (MRAs and Na+ channel inhibitors)
- Thiazide can be added if loop by itself doesn’t work
What do we do when a patient has electrolyte imbalances (K+ and Na+)?
Sodium - Don’t have to severely restrict sodium besides a “no salt added diet” unless there’s HTN or edema. Make pts away of high sodium content foods, be careful when using saline containing IV solutions.
- <2g Na/day or <5g NaCl/day
Potassium - Restrict to 3g/day (4.5-5.5 mEq/L for ESRD pt before dialysis. Avoid high potassium foods, treat hyperkalemia if needed.
How does mineral and bone disorder happen and what can we do about it?
Mechanisms:
1. Kidney disease causes impaired phosphate excretion, and that retained phos causes an increase in PTH production, which ends up causing Ca2+ to be taken from bone because it thinks it needs for calcium.
2. Kidney disease causes decreased amount of activated Vit D (1,25-dihydroxyvitamin D3), which leads to increased PTH production.
3. Hypocalcemia causes increased PTH production.
Treatment:
1. Treat hyperphosphatemia - Phosphate binders to bind phos from diet before it gets to blood
- Dietary restrictions - 800-1000mg Phos daily if phos > 4.6 in CKD 3-4 or phos > 5.5 in CKD 5, or if PTH is > range for states 3-5
2. Treat Vit D insufficiency
3. Treat calcium homeostasis and secondary hyperparathyroidism (cinacalcet (Sensipar) to lower PTH, but contraindicated in hypocalcemia (Ca <7.5mg/dL))
What are our options for phosphate binders? (7)
**all must be given with meals or else they do nothing (never give IV…)
- Calcium carbonate (40% elemental calcium): cheap; don’t exceed 1500mg elemental Ca2+
- Calcium acetate (PhosLo; 25% elemental calcium); may bind phos better than tums, but it’s more expensive; don’t exceed 1500mg elemental Ca2+
- Sevelamer carbonate: wonder drug, but expensive; Not absorbed, so low risk of toxicity, decreases uric acid concentrations (good for gout), no ADRs, decreases LDLs
- Lanthanum carbonate: Has a greater range of activity over spectrum of pHs.
- Sucroferric oxyhydroxide (Velphoro): Has iron, but it binds so tightly to phos that there is no change seen in iron concentrations.
- Auryxia (ferric citrate): Has iron, and it does get absorbed
- Aluminum hydroxide: Bad because it can cause aluminum toxicity. Don’t use this.
What are our options to treat the Vit D sufficiency in CKD patients with mineral and bone disease? (5)
Vitamin D that still requires kidney function to activate:
- Ergocalciferol (D2)
- Cholecalciferol (D3)
Already activated Vitamin D:
- Calcitriol: has greater risk of hypercalcemia and hyperphosphatemia, but it’s cheap
- Paricalcitol: Most favorable in terms of AEs
- Doxercalciferol: Prohormone that becomes activated in the liver (don’t give if pt has liver problmes)
What are the 4 ways ESRD patients can develop anemia?
- Decreased production of erythropoietin
- Uremia causes a decreased life span of RBCs
- Vitamin losses during dialysis (folate, B12, B6)
- Dialysis (loss of blood through dialyzer)
What is MCV and how is low, normal, and high MCV anemia caused? What does RDW tell us?
MCV - Mean corpuscular volume, average size of RBCs
Low - Iron deficiency, aluminum toxicity
Normal - Anemia of chronic disease, GI bleed, erythropoietin deficiency
High - Folate deficiency, B12 deficiency
RDW - Red cell distribution width. If it’s over 14.5%, then we know the distribution of points is not normal. Ex. when pts have folate AND iron deficiency.
