Exam 1 Flashcards
What are the functions of the kidney?
Excretory (urine)
Regulates BP
Hormones- erythropoietin, calcitriol, renin
Metabolism
Typical GFR
125mL/min
Needs to be relatively constant
Net filtration pressure
Has to be positive for the kidney to filter
NFP= GBHP-CHP-BCOP
How does the kidney increase perfusion pressure?
RAAS system
What systems decrease NFP
Myogenic stretch
Tubuloglomerular feedback
ANP
Myogenic stretch
Allows blood flow to remain the same even with risking BP.
When arterial BP rises, the afferent arteriole is stretched, which increases blood flow.
Vascular smooth muscle responds by contracting and increasing resistance and decreasing GFR. This increases vascular tone and returns the flow to normal.
Tubuloglomerular Feedback
Activated with disturbance in homeostasis (Increased BP)
Cells on the JGA detect increased delivery of Na, Cl, and water. This causes the JGA to decrease secretion of nitric oxide (a natural vasodilator). This causes the afferent arteriole to constrict and decrease blood flow to the glomerulus.
This in turn decreases GFR and BP
ANP
Released with increased NaCl, ECF volume, and BP
Decreases the sympathetic NS causing a decrease in BP
ATII Stimulus, MOA, and effect
Stimulus- decreased renal perfusion
Mechanism of action- Enhances Na and H2O reabsorption in PCT
Effect- Increases blood volume
Aldosterone stimulus, MOA, and effect
Stimulus- Increased ATII and K
MOA- Enhances Na (exchanges K) and H2O reabsorption in the late distal and collecting duct
Effect- Increases blood volume, lowers K
ADH stimulus, MOA, and effect
Stimulus- increased osmolarity of ECF or decreased blood volume
MOA- Inserts aquaporin channels in the DCT and collecting duct.
Effect- Increases BV
ANP stimulus, MOA, and effect
Stimulus- Atrial stretch due to increased blood volume
MOA- Suppresses Na and H2O reabsorption, decreases ATII and aldosterone
Effect- Increases Na (and H2O) excretion to decrease BV
PTH stimulus, MOA, and effect
Stimulus- low serum Ca
MOA- enhances Ca reabsorption in the DCT
Effect- Increases serum Ca
Kidney and calcium
PTH controls calcium
PTH stimulates reabsorption of calcium from urine and activation of vitamin D in the kidney
Kidney and erythropoietin
When there is a decreased oxygenation to the kidneys the kidneys secrete EPO into the blood, which stimulates erythropoiesis and increase the RBCs in the blood stream
When do you use adjusted BW?
In obesity BMI >25
Adj BW= IBW + 0.4(ABW-IBW)
Why is CrCl not an accurate representation of GFR?
CrCl OVERestimates GFR due to the fact that creatinine is secreted by the proximal tubule as well as filtered by the glomerulus. Insulin would be the ideal substance.
MDRD vs CG
Use MDRD for detection, evaluation, and monitoring of CKD. More accurate when GFR <60mL/min, equation in labs
Use CG for drug dosing decisions
Why is SCr lower in elderly patients?
Because they have less muscle mass
For AKI or critically ill patients, what do you use to measure?
No formula is accurate
Osmolality
The concentration of solutes in a fluid
Osmolar gap
A difference in plasma osmolality >10
Typically worried about alcohols (ethanol)
Normal plasma osmolality
280-295mosmol/kg
Osmotic receptors vs pressure receptors
Osmotic receptors- Respond to osmolality
Pressure receptors- Respond to plasma volume
Thirst receptors and ADH and aldosterone
What is the role of ADH?
ADH is secreted in response to increased osmolality or decreased ECF volume
ADH binds to vasopressin 2 receptors resulting in the insertion of aquaporins into the collecting duct.
Net effect:
Reabsorption of FREE water (free of Na)
Increase plasma volume
Decrease plasma osmolality
What is the role of aldosterone?
Activated as a result of hypovolemia causing decreased perfusion to the kidneys
Aldosterone stimulates the reabsorption of sodium from the distal tubules and collecting ducts (water follows sodium)
Net effect:
Re-absorption of water and Na
Increase in plasma volume
Edema
Clinically detectable increase in interstitial fluid volume
Movement of fluids from the intravascular to interstitial space is influenced by BP and oncotic pressure. The alterations in these pressures leads to edema (third spacing)
Tx with Na restriction and/or diuretics
Changes in fluid physiology with aging
Decreased total body water Decreased GFR Decreased urination Decreased thirst mechanism Decreased aldosterone Increased ADH levels but a decreased response to ADH
BUN:SCr ratio
Normally 20:1
Any higher and worry about patients being dry
Increased BUN and SCr= Dryer
Hct in relation to fluid status
Increased Hct concentration may mean decreased fluid
FENa
UNa(SCr)/ SNa(Ucr) x100
Tells us if the patient is dry
Less than 1% indicates hypovolemia
Osmolality vs tonicity
Osmolality is the number of osmoles of solute per liter of solution. This includes both ineffective and effective osmoles
Tonicity is the total concentration of solutes which exert an osmotic force across a membrane (effective osmoles)
Dextrose is an INEFFECTIVE osmole
Hypotonic IVF
D5W
Low Na
Cells swell, can burst if given too much
Hypertonic IVF
3% saline
Cells shrink and can be damaged. Pulls water out of cells and into intravascular space
Max osmolality
Peripheral veins- 900mOsm/L
Central- any
Where is D5W primarily found?
In the intracellular space
Where is LR and NS primarily found?
Interstitial space
Where is 3% NaCl primarily found?
Plasma space
Pulls fluid from interstitial
What is the free water in 1L NS?
0
What is the free water in 1L D5W?
1000mL
Causes of volume deficit
Decreased intake Abnormal losses GI- vomiting, diarrhea, fistula Renal- diuretics, hyperglycemia, adrenal insufficiency 3rd spacing
Presentation of volume deficit
Decreased BP, UOP, skin turgor, mental status, strength, temp (maybe)
Increased HR, BUN:Cr (prerenal azotemia), urine specific gravity or osmolality
Volume deficit treatment
Goal is to rapidly restore intravascular volume
NS or LR
Volume overload causes
Chronic diseases- CHF, liver disease, cancer, starvation
Mobilization of interstitial fluid
Psychogenic polydipsia
Volume overload presentation
Edema JVT Rales CHF Increased BP
Volume overload treatment
Fluid restriction, diuretics, dialysis
Hyponatremia/ Hypernatremia
Imbalance of sodium relative to the amount of water
Hyponatremia
Serum sodium <135mEq/L
Assess measured serum osmolality
Isotonic hyponatremia
pseudohyponatremia
Hypertonic hyponatremia
Suggests the presence of excess, non-sodium osmoles in the ECF
Most commonly caused by hyperglycemia
Estimated decrease in Na: 1.6x(glucose-100)/100
Hypotonic hyponatremia
Need to assess patients extracellular fluid and determine if it is decreased, increased, or normal
Hypovolemic hyponatremia
Decreased water, very decreased Na
Need to check UNa
If >20, caused by renal losses (diuretics, adrenal insufficiency, cerebral salt wasting)
If <20, caused by extrarenal losses (third spacing)
Often caused by chronic hyperglycemia
Euvolemic hyponatremia
Normal sodium, increased water
Causes- SIADH, primary polydipsia, hypothyroidism
Tx- fluid restriction, 3% NS with furosemide
Primary polydipsia
Compulsive water consumption
Could be caused by phenpthiazines or beer potomania
SIADH
Euvolemic hyponatremia
Urine osmolality >100mosm/L and UNa >20mEq/L
Caused by SSRIs, carbamazepine, TCAs, antipsychotics, NSAIDs, opioids, theophylline, ectasy
Fluid restriction is primary treatment
Hypervolemic hyponatremia
Increased sodium, very increased water Most common Occurs with chronic diseases (CHF, cirrhosis, renal dysfunction) Volume overload/ascites present Tx- water restriction Diuretics ADH antagonists
Treatment goals of hyponatremia
Asymptomatic or chronic patients- Increase plasma Na by no more than 0.5-1 mEq/L per hour and by <8mEq/L over 24 h
Severe (Na <115)
Increase Na by 1mEq/L per hour but no more than 8mEq/24 hours
What happens when you correct hyponatremia too rapidly?
Central pontine myelinolysis
Osmotic demyelination
Hypernatremia
> 145
Results from a deficit of water relative to ECF sodium volume
Most commonly observed in patients without access to water
Hypovolemic hypernatremia
Decreased Na, very decreased water
Most common
Occurs with hypotonic fluid loss
Tx with volume expansion and isotonic fluids
Then need a low Na fluid to replace free water deficit (D5W)
Free water deficit
Typically replace 1/2 of water deficit in the first 24 hours via feeding tube or IV D5W
Euvolemic hypernatremia
Normal sodium, decreased water
Causes- diabetes insipidus
Tx- hypotonic fluid, vasopressin, HCTZ
Diabetes insipidus
Central DI- impaired ADH secretion
Nephrogenic DI- renal resistance to the actions of AVP
Can be caused by lithium, hypercalcemia, and hypokalemia
What is the effect of ADH (vasopressin)?
Decreased urinary volume, increased urine Osm
Hypervolemic hypernatremia
Very increased Na, increased water
Causes- Na administration, hyperaldosteronism
Tx- hypotonic fluid, diuretics
Treatment goals of hypernatremia
Rate of correction depends on neurological dysfunction, rapidity of onset, and magnitude of Na rise
General- Decrease plasma Na conc. by no more than 0.5-1mEq/L and no more than 8mEq/day
What happens if you correct hypernatremia too rapidly?
Cerebral edema/seizures
Acidemia
pH less than 7.35
Alkalemia
pH greater than 7.45
Lungs (respiratory) acid/base
Pulls O2 to alveoli (inhalation) and takes pCO2 away from alveoli (exhalation)
ACID- pCO2
Kidneys (metabolic) acid/base
Maintain water, sodium, and acid-base balance
Maintain ionic balance through retention or excretion of cations and anions
Primary: base (HCO3)
Secondary: Acid (chloride)
If there is an increase in pCO2 what type of acidosis is it?
Respiratory acidosis
If there is a decrease in HCO3 what type of alkalosis is is?
Metabolic alkalosis
Respiratory vs metabolic compensation
Respiratory compensation occurs quickly and metabolic compensation is delayed
Causes of respiratory acidosis
Decreased respiratory drive (opioids, sedation)
Apnea: Cardiac arrest
Airway disorders: bronchospasm, edema, ARDS, etc.
Chronic causes- COPD
Compensation of respiratory acidosis
Increased pCO2 and HCO3
Respiratory alkalosis causes
Increased expiration (tachypnea) Causes- anxiety, pain, CHF, sepsis, pneumonia, stroke, theophylline, salicylates
Respiratory alkalosis primary compensation
Decreased pCO2
Decreased HCO3
Anion Gap metabolic acidosis causes
Anion gap >12mEq/L Presence of accumulation of nonvolatile acids Methanol toxicity Uremia DKA Paraldehyde toxicity Infection (sepsis) Lactic acidosis Ethylene glycol toxicity Salicylate toxicity
Anion gap metabolic acidosis compensation
Decreased HCO3
Decreased pCO2
Nonanion gap metabolic acidosis causes
HCO3 loss leading to hyperchloremia (diarrhea, pancreatic fistula, renal tubular acidosis)
Hyperchloremia (iatrogenic)
Nonanion gap metabolic acidosis compensation
Decreased HCO3, increase Cl
Decreased pCO2
Metabolic alkalosis causes
Loss of chloride (vomiting, diuretics)
Excessive bicarbonate administration
Metabolic alkalosis compensation
Increased HCO3
Decreased Cl
Increased pCO2
Rules of thumb for acidosis/alkalosis
Systems do not over compensate
There can only be one respiratory disorder at a time
Calcium
Normal 8.6-10.2mg/dL
You have to correct calcium for albumin and the ionized fraction will change
Corrected total calcium=
Measured Ca + [0.8x (4-measured albumin)]
If albumin is normal, calcium is likely low
Do formula in all ICU patients
Hypercalcemia
Total calcium >10.2
Severe >13 requires treatment even when asymptomatic
Commonly caused by cancer and hyperparathyroidism
Medication causes of hypercalcemia
Thiazides Lithium Vit D Vit A calcium Aluminum/magnesium antacids Theophyllines Tamoxifen Ganciclovir
Hypercalcemia presentation
Fatigue, weakness, anorexia, depression, anxiety, cognitive dysfunction, abdominal pain, constipation, kidney stones
Shortened QT interval
Coving of the ST wave
Treatment of hypercalcemia
May not treat if patient is asymptomatic
Nonpharm- hemodialysis, surgery if hyperthryoidism
Pharmacologic:
1st line- IV NS + loop
1st line for hemodialysis- Calcitonin
1st line for cancer- bisphosphonate
Other treatments- cinacalcet, denosumab, corticosteroids
Hypocalcemia
<8.5
Tetany, parathesia, muscle cramps, laryngeal spasms, dry puffy and coarse skin, hypotension
Prolonged QT interval
Arrhythmias
Bradycardia
Causes of hypocalcemia
Vit D deficiency Post op hyperparathyroidism Mag deficiency Blood transfusions Medications- furosemide, cinacaclet, biphophonates, calcitonin, fluoride, ketoconazole, phenytoin, phenobarbitol
Treatment of hypocalcemia
Give calcium in symptomatic patients 100-300 elemental calcium IV Max rate of 60mg of calcium/minute 1g CaCl= 27% elemental 1g calcium gluconate= 9% elemental Oral- give 1-3 g calcium/day +/- Vit D
Phosphorous
Normal 2.7-4.5mg/dL
Hypophosphatemia
<2.5mg/dL
Rarely signs/symptoms unless severe
Can have irritability, weakness, numbness, paresthesia, confusion
Seizures or coma in very severe cases
Hypophosphatemia causes
Decreased GI absorption- corticosteroids, Vit D deficiency
Increased excretion- diuretics, glucocorticoids, sodium bicarb
Internal redistribution- Refeeding syndrome, insulin, catecholamines, calcitonin, TPN, alcoholism, chronic antacid use
Treatment of hypophosphatemia
Mild to moderate (asymptomatic)- use oral therapy 50-60mmol/day. Be cautious of K in KPhos unless pt has low K levels
Severe- IV phosphorous
<2mg/dL- 0.32mmol/kg
<1.5mg/dL- give 0.64mmol/kg
Potassium
Most abundant cation in the body
Normal- 3.5-5mEq/L
Insulin is the most important regulator of K! Hypokalemia inhibits insulin secretion
Metabolic acidosis associated with hypokalemia
Hypokalemia
<3.5mEq/L
Cramping, weakness, myalgia, malaise, impaired muscle contractions
ST segment depression
T wave inversions
Causes of hypokalemia
V/D Hypomagnesemia Ephedrine Catecholamines Beta 2 agonists Caffeine Loop and thiazide diuretics
Tx of Hypokalemia
Correct magnesium first!
Oral- potassium chloride, phosphate, bicarbonate
20mEq/day prevention
40-100mEq/day treatment
Divide into 3-4 doses due to stomach upset
IV- 10mEq/hr peripheral, 20mEq/hr central
Too rapid administration can lead to death!
Hyperkalemia
> 5mEq/L
Usually asymptomatic
Can cause heart palpitations or skipped beats
Peaked T wave
Causes of hyperkalemia
Decreased intake (fruits, veggies)
Decreased excretion- K sparing diuretics, Trimethoprim
Aldosterone resistance- ACEis, ARBs, NSAIDs, heparin
Redistribution- Beta blockers (blocks catecholamine receptors), digoxin (inhibits pump)
Treatment of hyperkalemia
1.) Stabilize cardiac membrane with calcium
2.) Hide K extracellularly with dextrose + insulin
OR
Eliminate K with furosemide, Na Bicarb, or albuterol
3.) Can give SPS to bind K and excrete in gut
4.) New drugs- patiromer, sodium zirconium cyclosulfite are great in chronic cases but not in acute patients due to long onset
Magnesium
Normal 1.4-1.8mEq/L
OR
1.7-2.3mg/dL
Hypomagnesemia
<1.4mEq/L
Usually asymptomatic
Can cause tetany, heart palpitations, widened QRS interval, prolonged PR interval, peaked T wave
Causes of hypomagnesemia
Low serum potassium and calcium
Decreased GI absorption, increased excretion, alcoholism
Thiazide and loop diuretics, cyclosporine, tacrolimus
Treatment of hypomagnesemia
Oral-magnesium containing laxatives or antacids, mg containing tabs
400-800mg 3-4 doses/day
IV- 8-12mg Mg in 1st 24 hours. May take 3-5 days to replete body stores because 50% is excreted in urine
Hypermagnesemia
Rare
>2mEq/L
Loss of tendon refluxes, lethargy, confusion, arrhythmias, muscle weakness
Hypermagnesemia Causes
acute renal failure, CKD, excessive intake, lithium, hypothyroidism, addisons disease, acute DKA
Tx of hypermagnesemia
Reduce intake, enhance elimination, antagonize physiologic effects
100-200mg IV elemental calcium if cardiac events present
Hemodialysis
Diuretics
