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166 Cards in this Set

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What fluid/non-fluid compartments can the total body weight be divided into (what percentages)?

- 40% non-water mass
- 60% total body water
- 40% non-water mass
- 60% total body water
What fluid compartments can the total body water be divided into? What percent of total body weight?
- 1/3 extracellular fluid (20% total body weight)
- 2/3 intracellular fluid (40% total body weight)
- 1/3 extracellular fluid (20% total body weight)
- 2/3 intracellular fluid (40% total body weight)
What fluid compartments can the extracellular fluid be divided into? What percent of total body weight?
- 1/4 plasma volume (5% total body weight)
- 3/4 interstitial volume (15% total body weight)
- 1/4 plasma volume (5% total body weight)
- 3/4 interstitial volume (15% total body weight)
What is the "rule" to remember the % of body weight of the different fluid compartments?
60:40:20 rule:
- 60% total body water
- 40% ICF
- 20% ECF
How do you measure the plasma volume?
Radio-labeled albumin
How do you measure the extracellular volume?
Inulin
What is the normal serum osmolarity?
290 mOsm/L
What is the glomerular filtration barrier composed of? What does each layer restrict?
- Fenestrated capillary endothelium (size barrier)
- Fused basement membrane with heparan sulfate (negative charge barrier)
- Epithelial layer consisting of podocyte foot processes
- Fenestrated capillary endothelium (size barrier)
- Fused basement membrane with heparan sulfate (negative charge barrier)
- Epithelial layer consisting of podocyte foot processes
What happens to the glomerular filtration barrier in nephrotic syndrome? Consequences?
Charge barrier (fused basement membrane with heparan sulfate) is lost in nephrotic syndrome, results in:
- Albuminuria
- Hypoproteinemia
- Generalized edema
- Hyperlipidemia
How do you calculate renal clearance?
Volume of plasma from which the substance is completely cleared per unit time

Cx = (Ux * V) / Px

Cx = Clearance of X (mL/min)
Ux = Urine concentration of X (mg/mL)
Px = Plasma concentration of X (mg/mL)
V = urine flow rate (mL/min)
What does it tell you if the clearance of a substance is less than the GFR?
Net tubular reabsorption of X
What does it tell you if the clearance of a substance is greater than the GFR?
Net tubular secretion of X
What does it tell you if the clearance of a substance is equal to the GFR?
No net secretion or reabsorption
What can be used to calculate the GFR? Why?
Inulin clearance because it is freely filtered and is neither reabsorbed nor secreted (C-inulin = GFR)

GFR = (U-inulin * V) / P-inulin

U-inulin = Urine concentration of inulin (mg/mL)
P-inulin = Plasma concentration of inulin (mg/mL)
V = urine flow rate (mL/min)
How can you calculate GFR based on the pressures in the glomerulus and Bowman's capsule?
GFR = Kf [ (P-gc - P-bs) - (π-gc - π-bs) ]

P = hydrostatic pressure
π = oncotic pressure
gc = glomerular capillary
bs = bowman's space

π-bs usually equals zero (protein shouldn't be in bowman's space)
What is a normal GFR?
~100 ml/min
Clearance of what can estimate GFR?
Creatinine clearance is an approximate measure of GFR; slightly overestimates GFR because creatinine is moderately secreted by the renal tubules
What is the staging of chronic kidney diseases based on?
Incremental reductions in GFR
How do you estimate the Effective Renal Plasma Flow (ERPF)?
Estimated using para-aminohippuric acid (PAH) clearance because it is both filtered and actively secreted in the proximal tubule; nearly all PAH entering the kidney is excreted

ERPF = (U-pah * V) / P-pah

Underestimates the true renal plasma flow (RPF) by ~10%
How do you determine the renal blood flow?
RBF = RPF / (1 - Hct)

RPF is estimated by ERPF = (U-pah * V) / P-pah
What are the characteristics of para-aminohippuric acid (PAH) in the kidney?
- Both filtered and actively secreted in proximal tubule
- Nearly all PAH entering the kidney is excreted
How do you calculate the filtration fraction? What is normal?
FF = GFR / RPF = normally 20%

- GFR is estimated by calculating clearance of inulin
- RPF is estimated by calculating clearance of PAH

Remember:
Cx = (Ux * V) / Px
How do you calculate the filtered load?
Filtered load (mg/min) = GFR (ml/min) * plasma concentration (mg/ml)
How do NSAIDs affect the filtration at the glomerulus?
NSAIDs inhibit prostaglandins, preventing dilation of the afferent arteriole 
- ↓ RPF, ↓ GFR, so Filtration Fraction remains constant

(remember FF = GFR/RPF)
NSAIDs inhibit prostaglandins, preventing dilation of the afferent arteriole
- ↓ RPF, ↓ GFR, so Filtration Fraction remains constant

(remember FF = GFR/RPF)
How do prostaglandins affect the filtration at the glomerulus?
Prostaglandins dilate the afferent arteriole 
- ↑ RPF, ↑ GFR, so Filtration Fraction remains constant

(remember FF = GFR/RPF)
Prostaglandins dilate the afferent arteriole
- ↑ RPF, ↑ GFR, so Filtration Fraction remains constant

(remember FF = GFR/RPF)
How do ACE-inhibitors affect the filtration at the glomerulus?
ACE-I inhibit AngII, preventing constriction of the efferent arteriole
- ↑ RPF, ↓ GFR, so FF decreases

(remember FF = GFR/RPF)
ACE-I inhibit AngII, preventing constriction of the efferent arteriole
- ↑ RPF, ↓ GFR, so FF decreases

(remember FF = GFR/RPF)
How does Angiotensin II affect the filtration at the glomerulus?
AngII preferentially constricts the efferent arteriole
- ↓ RPF, ↑ GFR, so FF increases

(remember FF = GFR/RPF)
How does afferent arteriole constriction affect RPF, GFR, and FF (GFR/RPF)?
- ↓ RPF
- ↓ GFR
- = FF
How does efferent arteriole constriction affect RPF, GFR, and FF (GFR/RPF)?
- ↓ RPF
- ↑ GFR
- ↑ FF
How does ↑ plasma protein concentration affect RPF, GFR, and FF (GFR/RPF)?
- = RPF
- ↓ GFR
- ↓ FF
How does ↓ plasma protein concentration affect RPF, GFR, and FF (GFR/RPF)?
- = RPF
- ↑ GFR
- ↑ FF
How does constriction of the ureter affect RPF, GFR, and FF (GFR/RPF)?
- = RPF
- ↓ GFR
- ↓ FF
How do you calculate the filtered load?
Filtered load = GFR * Px

Px = plasma concentration of X (mg/ml)
How do you calculate the excretion rate?
Excretion rate = V * Ux

V = urine flow rate (ml/min)
Ux = urine concentration of X (mg/ml)
How do you calculate the reabsorption rate?
Reabsorption = Filtered load - Excretion rate

Filtered load = GFR * Px
Excretion rate = V * Ux
How do you calculate the secretion rate?
Secretion = Excretion rate - Filtered load

Filtered load = GFR * Px
Excretion rate = V * Ux
What are the characteristics of glucose clearance in the kidney?
- Glucose at a normal plasma level is completely reabsorbed in the proximal tubule by Na+/glucose co-transport
- At plasma glucose of ~200 mg/dL, glucosuria begins (threshold)
- At plasma glucose of ~375 mg/dL, all transporters are fully saturated (Tm)
At what plasma glucose concentrations does all glucose get reabsorbed in the proximal tubule?
Up to ~200 mg/dL
- Above 200 mg/dL, glucosuria begins (threshold)
At what plasma glucose concentrations are all Na+/glucose co-transporters fully saturated (Tm)?
At ~375 mg/dL
What happens to glucose and amino acid reabsorption during pregnancy?
Normal pregnancy ↓ reabsorption of glucose and amino acids in proximal tubule → glucosuria and aminoaciduria
How are amino acids normally treated in the kidney?
Normally all amino acids are reabsorbed by Na+ dependent transporters in the proximal tubule
What disorder causes a deficiency of neutral amino acid (eg, tryptophan) transporters in the proximal renal tubular cells and on enterocytes? Implications?
Hartnup Disease:
- Leads to neutral aminoaciduria and ↓ absorption from gut
- Results in pellagra-like symptoms; treat with high-protein diet and nicotinic acid
What should you think of if you have a patient with a neutral aminoaciduria and decreased absorption from the gut with pellagra-like symptoms (dermatitis, diarrhea, and mental disturbance)? Cause?
Hartnup Disease
- Autosomal recessive deficiency of neutral amino acid (eg, tryptophan) transporters in the proximal renal tubular cells and on enterocytes
What are the characteristics of Hartnup Disease? Cause / Symptoms / Treatment?
- Autosomal recessive disorder, caused by deficiency of neutral amino acid (eg, tryptophan) transporters in the proximal renal tubular cells and on enterocytes
- Leads to neutral aminoaciduria and ↓ absorption from gut
- Results in pellagra-like symptoms (dermatitis, diarrhea, and mental disturbance)
- Treat with high-protein diet and nicotinic acid
What is reabsorbed and secreted in the proximal convoluted tubule?
Reabsorbed:
- All glucose and amino acids
- Most HCO3-, Na+, Cl-, PO4(3-), K+, H2O

Secreted:
- NH3 (buffers secreted H+)
Reabsorbed:
- All glucose and amino acids
- Most HCO3-, Na+, Cl-, PO4(3-), K+, H2O

Secreted:
- NH3 (buffers secreted H+)
Which hormones act on the early proximal convoluted tubule?
- PTH
- AngII
- PTH
- AngII
What is the action of PTH on the early proximal convoluted tubule?
Inhibits Na+ / PO4(3-) co-transport → PO4(3-) excretion
Inhibits Na+ / PO4(3-) co-transport → PO4(3-) excretion
What is the action of Angiotensin II on the early proximal convoluted tubule?
- Stimulates Na+/H+ exchange → ↑ Na+, H2O, and HCO3- reabsorption
- Permits contraction alkalosis
- Stimulates Na+/H+ exchange → ↑ Na+, H2O, and HCO3- reabsorption
- Permits contraction alkalosis
What percent of Na+ is reabsorbed in the early proximal convoluted tubule?
65-80% Na+ reabsorbed
65-80% Na+ reabsorbed
What is reabsorbed and secreted in the thin descending loop of Henle?
- Passive reabsorption of H2O via medullary hypertonicity 
- Impermeable to Na+
- Passive reabsorption of H2O via medullary hypertonicity
- Impermeable to Na+
What happens to urine in the thin descending loop of Henle?
- Concentrates urine
- Makes urine hypertonic
- Concentrates urine
- Makes urine hypertonic
What percent of Na+ is reabsorbed in the thin descending loop of Henle?
None - impermeable to Na+
None - impermeable to Na+
What is reabsorbed and secreted in the thick ascending loop of Henle?
Reabsorbs:
- Active reabsorption of Na+, K+, and Cl-
- Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ (through + lumen potential generated by K+ backleak)

Impermeable to H2O
Reabsorbs:
- Active reabsorption of Na+, K+, and Cl-
- Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ (through + lumen potential generated by K+ backleak)

Impermeable to H2O
What happens to urine in the thick ascending loop of Henle?
- Impermeable to H2O but reabsorbing Na+
- This makes urine less concentrated as it ascends
- Impermeable to H2O but reabsorbing Na+
- This makes urine less concentrated as it ascends
What percent of Na+ is reabsorbed in the thick ascending loop of Henle?
10-20% Na+ reabsorbed
10-20% Na+ reabsorbed
What is reabsorbed and secreted in the early distal convoluted tubule?
- Actively reabsorbs Na+ and Cl-
- PTH stimulates Ca2+/Na+ exchange → Ca2+ reabsorption
- Actively reabsorbs Na+ and Cl-
- PTH stimulates Ca2+/Na+ exchange → Ca2+ reabsorption
Which hormones act on the distal convoluted tubule? Action?
PTH - stimulates Ca2+/Na+ exchange → Ca2+ reabsorption
PTH - stimulates Ca2+/Na+ exchange → Ca2+ reabsorption
What percent of Na+ is reabsorbed in the distal convoluted tubule?
5-10% Na+ reabsorbed
5-10% Na+ reabsorbed
What is reabsorbed and secreted in the collecting tubule?
Reabsorbs Na+ in exchange for secreting K+ and H+
Reabsorbs Na+ in exchange for secreting K+ and H+
Which hormones act on the collecting tubule? Action?
- Aldosterone: acts on mineralocorticoid receptor → insertion of Na+ channel on luminal side
- ADH: acts at V2 receptor → insertion of aquaporin H2O channels on luminal side
- Aldosterone: acts on mineralocorticoid receptor → insertion of Na+ channel on luminal side
- ADH: acts at V2 receptor → insertion of aquaporin H2O channels on luminal side
What percent of Na+ is reabsorbed in the collecting tubule
3-5% Na+ reabsorbed
3-5% Na+ reabsorbed
In which segments of the nephron is sodium reabsorbed? What percentages?
- Proximal convoluted tubule: 65-80%
- Thin descending loop of Henle: none
- Thick ascending loop of Henle: 10-20%
- Distal convoluted tubule: 5-10%
- Collecting tubule: 3-5%
What are the types of renal tubular defects?
"The kidneys put out FABulous Glittering Liquid"
- Fanconi syndrome = 1st defect (PCT)
- Bartter syndrome = 2nd defect (thick ascending loop of Henle)
- Gitelman syndrome = 3rd defect (DCT)
- Liddle syndrome = 4th defect (collecting tubule)
Which renal tubular defect affects the Proximal Convoluted Tubule? What does it cause?
Fanconi Syndrome
- ↑ excretion of nearly all AAs, glucose, HCO3-, and PO4(3-)
- May cause metabolic acidosis (proximal renal tubular acidosis)
What causes Fanconi Syndrome? Where is the defect?
- Causes: hereditary defects (eg, Wilson disease), ischemia, and nephrotoxins/drugs
- Reabsorptive defect in the proximal convoluted tubule
Which renal tubular defect affects the Thick Ascending Loop of Henle? What does it cause?
Bartter Syndrome
- Affects Na+/K+/2Cl- co-transporter
- Causes hypokalemia, metabolic alkalosis and hypercalciuria
What causes Bartter Syndrome? Where is the defect?
- Causes: autosomal recessive defect of Na+/K+/2Cl- co-transporter
- Reabsorptive defect in thick ascending loop of Henle
Which renal tubular defect affects the Distal Convoluted Tubule? What does it cause?
Gitelman Syndrome
- Hypokalemia
- Metabolic alkalosis
- NO hypercalciuria
What causes Gitelman Syndrome? Where is the defect?
- Cause: autosomal recessive defect of NaCl reabsorption
- Reabsorptive defect in distal convoluted tubule
Which renal tubular defect affects the Distal and Collecting Tubules? What does it cause?
Liddle Syndrome
- Hypertension
- Hypokalemia
- Metabolic alkalosis
- ↓ Aldosterone
What causes Liddle Syndrome? Where is the defect?
- Cause: Autosomal Dominant defect leading to increased activity of epithelial Na+ channel
- Distal and collecting tubules
How do you treat Liddle Syndrome?
Amiloride
What syndrome causes ↑ excretion of nearly all AAs, glucose, HCO3-, and PO4(3-), which may lead to a metabolic acidosis? What causes this?
Fanconi Syndrome
- Reabsorptive defect in proximal convoluted tubule
- Causes: hereditary defects (eg, Wilson disease), ischemia, and nephrotoxins/drugs
What syndrome causes hypokalemia and metabolic alkalosis with hypercalciuria? What causes this?
Bartter Syndrome
- Reabsorptive defect in thick ascending loop of Henle
- Autosomal recessive, affects Na+/K+/2Cl- co-transporter
What syndrome causes hypokalemia and metabolic alkalosis without hypercalciuria? What causes this?
Gitelman Syndrome
- Reabsorptive defect of NaCl in distal convoluted tubule
- Autosomal recessive, less severe than Bartter syndrome
What syndrome causes hypertension, hypokalemia, metabolic alkalosis, and ↓ aldosterone? What causes this?
Liddle Syndrome
- ↑ Na+ reabsorption in distal and collecting tubules (↑ activity of epithelial Na+ channel)
- Autosomal dominant
- Treat with Amiloride
What is the meaning of the ratio of TF/P?
[Tubular Fluid] / [Plasma]
What does it mean if the [Tubular Fluid] / [Plasma] ratio is >1?
Solute is reabsorbed less quickly than water
What does it mean if the [Tubular Fluid] / [Plasma] ratio is =1?
Solute and water are reabsorbed at the same rate
What does it mean if the [Tubular Fluid] / [Plasma] ratio is <1?
Solute is reabsorbed more quickly than water
What happens to the tubular inulin concentration as it progresses along the nephron? How?
Inulin concentration increases in the tubule (but not in amount) along the proximal tubule as a result of water reabsorption
Which substance has net secretion in the proximal tubule?
PAH
Which substance has net reabsorption in the proximal tubule?
- Urea
- Na+, K+, Cl-
- Pi
- HCO3-
- Glucose and amino acids
Which substance has no net secretion or reabsorption in the proximal tubule?
Creatinine and Inulin
How does the reabsorption of Cl- compare to Na+ in the proximal tubule?
Cl- reabsorption occurs at a slower rate than Na+ in early proximal tubule and then matches the rate of Na+ reabsorption more distally; thus, its relative concentration increases before it plateaus
What is the action of Renin? Source?
Stimulates conversion of Angiotensinogen (from liver) to Angiotensin I
- Renin is from the kidney
What is the source of Renin? What stimulates it?
Renin is from the kidney, release stimulated by:
- ↓ BP (Juxtaglomerular cells)
- ↓ Na+ delivery to macula densa cells
- ↑ Sympathetic tone (β1-receptors)
What is the action of ACE? Source?
- ACE converts Ang I to Ang II
- ACE also stimulates Bradykinin breakdown
- ACE is from the lungs and the kidneys
What is the action of Angiotensin II?
- Vasoconstriction (via AT I receptors) → ↑ BP
- Constricts efferent arteriole of glomerulus → ↑ FF to preserve renal function (GFR) in low-volume states (when ↓ RBF)
- Stimulates Aldosterone (adrenal gland)
- Stimulates ADH (posterior pituitary)
- ↑ Proximal tubule Na+/H+ activity → ↑ Na+, HCO3-, and H2O reabsorption (can permit contraction alkalosis)
- Stimulates hypothalamus → thirst
How does AngII increase the BP?
Acts at AT I receptors on vascular smooth muscle → Vasoconstriction → ↑ BP
How does AngII affect the filtration fraction (FF)?
Constricts efferent arteriole of glomerulus → ↑ FF to preserve renal function (GFR) in low-volume states (ie, when RBF ↓)
What is the effect of Aldosterone release? Source?
- ↑ Na+ channel and Na+/K+ pump insertion in principal cells
- Enhances K+ and H+ excretion (upregulates principal cell K+ channels and intercalated cell H+ ATPases)
- Creates unfavorable Na+ gradient for Na+ and H2O reabsorption
- From adrenal gland
What is the effect of ADH release? Source?
- ↑ H2O channel insertion in principal cells, leading to H2O reabsorption
- From posterior pituitary
What is the effect of Angiotensin II on the proximal tubule?
- ↑ Proximal tubule Na+/H+ activity
- Leads to Na+, HCO3-, and H2O reabsorption (can permit contraction alkalosis)
Which hormone affects baroreceptor function, limiting the reflex bradycardia, which would normally accompany its pressor effects?
Angiotensin II
Which hormone is released from atria in response to increased volume, may act as a check on renin-angiotensin-aldosterone system, relaxing vascular smooth muscle via cGMP, causing ↑ GFR and ↓ renin?
ANP (Atrial Natriuretic Protein)
Which hormone is primarily responsible for regulating osmolarity and responds to low blood volume states?
ADH
Which hormone primarily regulates ECF Na+ content and volume, by responding to low blood volume states?
Aldosterone
What are the components of the juxtaglomerular apparatus?
- JG cells (modified smooth muscle of afferent arteriole)
- Macula Densa (NaCl sensor, part of the distal convoluted tubule)
What is the function of the Juxtaglomerular cells?
Secrete renin in response to:
- ↓ Renal blood pressure
- ↓ NaCl delivery to distal tubule
- ↑ Sympathetic tone (β1)
Which drugs can influence the juxtaglomerular apparatus?
β-blockers (specifically β1) can decrease BP by inhibiting β1 receptors of JGA, causing ↓ renin release
Which hormones are secreted by the kidney?
- Erythropoietin
- 1,25-(OH)2 Vitamin D
- Renin
- Prostaglandins
What is the source and function of Erythropoietin?
Released by interstitial cells in the peritubular capillary bed in response to hypoxia
What is the source and function of 1,25-(OH)2 Vitamin D?
- Proximal tubule cells convert 25-OH vitamin D to 1,25-(OH)2 Vitamin D (Active form)
- Enzyme: 1α-Hydroxylase (stimulated by PTH)
What is the source and function of Renin?
Secreted by JG cells in response to ↓ renal arterial pressure and ↑ renal sympathetic discharge (β1 effect)
What is the source and function of prostaglandins?
- Paracrine secretion vasodilates the afferent arterioles to ↑ RBF
- From kidney
What is the effect of NSAIDs on the kidney?
- NSAIDs block renal-protective prostaglandin synthesis → constriction of the afferent arteriole and ↓ GFR
- This may result in acute renal failure
Which hormones act on the kidney?
- Angiotensin II (ATII)
- Atrial Natriuretic Peptide (ANP)
- Parathyroid Hormone (PTH)
- Aldosterone
- ADH (Vasopressin)
What causes Angiotensin II (AT II) to be released and act on kidney? Function?
- Synthesized in response to ↓ BP
- Causes efferent arteriole constriction → ↑ GFR and ↑ FF
- Compensatory Na+ reabsorption in proximal and distal nephron

- Net effect: preservation of renal function in low-volume state (↑FF) with simultaneous Na+ reabsorption to maintain circulating volume
What causes Parathyroid Hormone (PTH) to be released and act on kidney? Function?
- Secreted in response to ↓ plasma [Ca2+], ↑ plasma [PO4(3-)], or ↓ plasma 1,25-(OH)2 vitamin D

- Causes ↑ [Ca2+] reabsorption from DCT, ↓ [PO4(3-)] reabsorption (PCT), and ↑ 1,25-(OH)2 vitamin D production
- Increases Ca2+ and PO4(3-) absorption from gut via vitamin D
Where are Ca2+ and PO4(3-) reabsorbed in nephron in response to PTH?
- Ca2+ reabsorbed in DCT
- PO4(3-) reabsorbed in PCT
What causes Atrial Natriuretic Peptide (ANP) to be released and act on kidney? Function?
- Secreted in response to ↑ atrial pressure
- Causes ↑ GFR and ↑ Na+ filtration with no compensatory Na+ reabsorption in distal nephron
- Net effect: Na+ loss and volume loss
What causes Aldosterone to be released and act on kidney? Function?
- Secreted in response to ↓ blood volume (via AT II) and ↑ plasma [K+]
- Causes ↑ Na+ reabsorption, ↑ K+ secretion, ↑ H+ secretion
What causes ADH (Vasopressin) to be released and act on kidney? Function?
- Secreted in response to ↑ plasma osmolarity and ↓ blood volume
- Binds to receptors on principal cells, causing ↑ number of water channels and ↑ H2O reabsorption
Which conditions/drugs cause K+ to shift out of cells (causing hyperkalemia)?
Patient with hyperkalemia? DO Insulin LAβ work
- Digitalis
- HyperOsmolarity
- INSULIN deficiency
- Lysis of cells
- Acidosis
- β-adrenergic antagonist
Patient with hyperkalemia? DO Insulin LAβ work
- Digitalis
- HyperOsmolarity
- INSULIN deficiency
- Lysis of cells
- Acidosis
- β-adrenergic antagonist
Which conditions/drugs cause K+ to shift into cells (causing hypokalemia)?
INsulin shifts K+ INto cells
- Hypoosmolarity
- Insulin (↑ Na+ / K+ ATPase)
- Alkalosis
- β-adrenergic agonist (↑ Na+ / K+ ATPase)
INsulin shifts K+ INto cells
- Hypoosmolarity
- Insulin (↑ Na+ / K+ ATPase)
- Alkalosis
- β-adrenergic agonist (↑ Na+ / K+ ATPase)
What electrolyte disturbance causes nausea, malaise, stupor, and coma?
Low serum Na+
What electrolyte disturbance causes irritability, stupor, or coma?
High serum Na+
What electrolyte disturbance causes U waves on ECG, flattened T waves, arrhythmias, and muscle weakness?
Low serum K+
What electrolyte disturbance causes wide QRS and peaked T waves on ECG, arrhythmias, and muscle weakness?
High serum K+
What electrolyte disturbance causes tetany, seizures, and QT prolongation?
Low serum Ca2+
What electrolyte disturbance causes stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria?
High serum Ca2+
What electrolyte disturbance causes tetany and Torsades de Pointes?
Low serum Mg2+
What electrolyte disturbance causes ↓ DTRs, lethargy, bradycardia, hypotension, cardiac arrest, and hypocalcemia?
High serum Mg2+
What electrolyte disturbance causes bone loss and osteomalacia?
Low serum PO4(3-)
What electrolyte disturbance causes renal stones, metastatic calcifications, and hypocalcemia?
High serum PO4(3-)
What is the effect of low vs high serum concentration of Na+?
- Low: nausea, malaise, stupor, coma
- High: irritability, stupor, coma
What is the effect of low vs high serum concentration of K+?
- Low: U waves on ECG, flattened T waves, arrhythmias, muscle weakness
- High: wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
What is the effect of low vs high serum concentration of Ca2+?
- Low: tetany, seizures, QT prolongation
- High: stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria
What is the effect of low vs high serum concentration of Mg2+?
- Low: tetany and torsades de pointes
- High: ↓ DTRs (reflexes), lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
What is the effect of low vs high serum concentration of PO4(3-)?
- Low: bone loss, osteomalacia
- High: renal stones, metastatic calcifications, hypocalcemia
What is the pH, PCO2, and [HCO3-] associated with metabolic acidosis? Compensatory response?
- ↓ pH
- ↓ PCO2
- ↓↓ [HCO3-]
- Immediate hyperventilation

↓↓ = 1° distrubance
↓ = compensatory response
What is the pH, PCO2, and [HCO3-] associated with metabolic alkalosis? Compensatory response?
- ↑ pH
- ↑ PCO2
- ↑↑ [HCO3-]
- Immediate hypoventilation

↑↑ = 1° distrubance
↑ = compensatory response
What is the pH, PCO2, and [HCO3-] associated with respiratory acidosis? Compensatory response?
- ↓ pH
- ↑↑ PCO2
- ↑ [HCO3-]
- ↑ Renal [HCO3-] reabsorption (delayed)

↑↑ = 1° distrubance
↑ = compensatory response
What is the pH, PCO2, and [HCO3-] associated with respiratory alkalosis? Compensatory response?
- ↑ pH
- ↓↓ PCO2
- ↓ [HCO3-]
- ↓ Renal [HCO3-] reabsorption (delayed)

↓↓ = 1° distrubance
↓ = compensatory response
What is the Henderson-Hasselbach equation in terms of [HCO3-] and PCO2?
pH = 6.1 + log [HCO3-] / 0.03 PCO2
How can you calculate the predicted respiratory compensation for a simple metabolic acidosis? What does it tell you?
Winters Formula
- If the measured PCO2 differs significantly from the predicted PCO2, then a mixed acid-base disorder is likely present

PCO2 = 1.5 [HCO3-] + 8 +/- 2
If you suspect an acidosis or alkalosis, what do you check first?
Check arterial pH
- pH <7.4 = Acidemia
- pH >7.4 = Alkalemia
What do you test after you establish a patient has an acidemia (arterial pH <7.4)?
Check PCO2
- PCO2 >40 mmHg = Respiratory Acidosis
- PCO2 <40 mmHg = Metabolic Acidosis with compensation (hyperventilation)
What do you test after you establish a patient has an alkalemia (arterial pH >7.4)?
Check PCO2
- PCO2 <40 mmHg = Respiratory Alkalosis
- PCO2 >40 mmHg = Metabolic Alkalosis with compensation (hypoventilation)
What is the diagnosis if a patient has pH <7.4 and PCO2 >40mmHg? What causes this?
Respiratory Acidosis, caused by hypoventilation, such as:
- Airway obstruction
- Acute lung disease
- Chronic lung disease
- Opioids, sedatives
- Weakening of respiratory muscles
What is the diagnosis if a patient has pH <7.4 and PCO2 <40mmHg? What should you check next?
Metabolic Acidosis with compensation (hyperventilation)
- Check for anion gap

Anion Gap = Na+ - (Cl- + HCO3-)
Normal: 8-12 mEq/L
What is the diagnosis if a patient has pH <7.4 and PCO2 <40mmHg and an ↑ anion gap? What are the potential causes?
Metabolic Acidosis with compensation (hyperventilation)

MUDPILES:
- Methanol (formic acid)
- Uremia
- Diabetic Ketoacidosis
- Propylene glycol
- Iron tablets or INH
- Lactic acidosis
- Ethylene glycol (oxalic acid)
- Salicylates (late)
What is the diagnosis if a patient has pH <7.4 and PCO2 <40mmHg and a normal anion gap (8-12 mEq/L)? What are the potential causes?
Metabolic Acidosis with compensation (hyperventilation)

HARD-ASS:
- Hyperalimentation
- Addison disease
- Renal tubular acidosis
- Diarrhea
- Acetazolamide
- Spironolactone
- Saline infusion
What is the diagnosis if a patient has pH >7.4 and PCO2 <40mmHg? What causes this?
Respiratory alkalosis, can be caused by:

Hyperventilation:
- Hysteria
- Hypoxemia (eg, high altitude)
- Salicylates (early)
- Tumor
- Pulmonary embolism
What is the diagnosis if a patient has pH >7.4 and PCO2 >40mmHg? What causes this?
Metabolic alkalosis with compensation (hypoventilation), caused by:
- Loop diuretics
- Vomiting
- Antacid use
- Hyperaldosteronism
What do these have in common? What would they cause?
- Airway obstruction
- Acute lung disease
- Chronic lung disease
- Opioids, sedatives
- Weakening of respiratory muscles
Causes of hypoventilation → Respiratory Acidosis
What do these have in common? What would they cause?
- Methanol (formic acid)
- Uremia
- Diabetic Ketoacidosis
- Propylene glycol
- Iron tablets or INH
- Lactic acidosis
- Ethylene glycol (oxalic acid)
- Salicylates (late)
Metabolic Acidosis with compensation (hyperventilation) with ↑ Anion Gap
What do these have in common? What would they cause?
- Hyperalimentation
- Addison disease
- Renal tubular acidosis
- Diarrhea
- Acetazolamide
- Spironolactone
- Saline infusion
Metabolic Acidosis with compensation (hyperventilation) with normal Anion Gap (8-12 mEq/L)
What do these have in common? What would they cause?
- Hysteria
- Hypoxemia (eg, high altitude)
- Salicylates (early)
- Tumor
- Pulmonary embolism
Causes of hyperventilation → Respiratory Alkalosis
What do these have in common? What would they cause?
- Loop diuretics
- Vomiting
- Antacid use
- Hyperaldosteronism
Metabolic Alkalosis with compensation (hypoventilation)
When should you calculate the anion gap? How? What is normal?
When you have a metabolic acidosis (pH < 7.4 and PCO2 < 40 mmHg)

Anion Gap = Na+ - (Cl- + HCO3-)
Normal = 8-12 mEq/L
What kind of disorder causes a non-anion gap hyperchloremic metabolic acidosis?
Renal Tubular Acidosis
What are the types of Renal Tubular Acidosis?
- Type 1: distal, pH >5.5
- Type 2: proximal, pH <5.5
- Type 4: hyperkalemic, pH <5.5
Which type of Renal Tubular Acidosis is caused by a defect in the ability of the α intercalated cells to secrete H+? Implications?
Type 1 (distal, pH >5.5)
- New HCO3- is not generated → metabolic acidosis
- Associated with hypokalemia, ↑ risk for calcium phosphate kidney stones (d/t ↑ urine pH and ↑ bone turnover)
What can cause Type 1 Renal Tubular Acidosis (distal, pH >5.5)?
Defects in ability of α intercalated cells to secrete H+
- Amphotericin B toxicity
- Analgesic nephropathy
- Congenital anomalies (obstruction) of urinary tract
Which type of Renal Tubular Acidosis is caused by a defect in the proximal tubule HCO3- reabsorption? Implications?
Type 2 (proximal, pH < 5.5)
- Leads to ↑ excretion of HCO3- in urine and subsequent metabolic acidosis
- Urine is acidified by α intercalated cells in collecting tubule
- Associated with hypokalemia and ↑ risk for hypophosphatemic rickets
What can cause Type 2 Renal Tubular Acidosis (proximal, pH <5.5)?
Defects in proximal tubule HCO3- reabsorption:
- Fanconi syndrome (eg, Wilson disease)
- Chemicals toxic to proximal tubule (eg, lead, aminoglycosides)
- Carbonic anhydrase inhibitors
- Multiple myeloma (light chains)
Which type of Renal Tubular Acidosis is caused by hypoaldosteronism, aldosterone resistance, or K+ sparing diuretics? Implications?
- Results in hyperkalemia
- Impairs ammoniagenesis in proximal tubule → ↓ buffering capacity and ↓ H+ excretion into urine
What can cause Type 4 Renal Tubular Acidosis (hyperkalemic, pH <5.5)?
- Hypoaldosteronism
- Aldosterone resistance
- K+ sparing diuretics
What are the characteristics of Type 1 Renal Tubular Acidosis?
Distal, pH>5.5
- Defect in ability of α intercalated cells to secrete H+
- New HCO3- is not generated → metabolic acidosis
- Associated with hypokalemia, ↑ risk for calcium phosphate kidney stones (d/t ↑ urine pH and ↑ bone turnover)

Causes:
- Amphotericin B toxicity
- Analgesic nephropathy
- Congenital anomalies (obstruction) of urinary tract
What are the characteristics of Type 2 Renal Tubular Acidosis?
Proximal, pH<5.5
- Defect in proximal tubule HCO3- reabsorption
- ↑ Excretion of HCO3- in urine and subsequent metabolic acidosis
- Urine acidified in α intercalated cells in collecting tubule
- Associated with hypokalemia and ↑ risk for hypophosphatemic rickets

Causes:
- Fanconi syndrome (eg, Wilson disease)
- Chemicals toxic to proximal tubule (eg, lead, aminoglycosides)
- Carbonic anhydrase inhibitors
- Multiple myeloma (light chains)
What are the characteristics of Type 4 Renal Tubular Acidosis?
Hyperkalemic, pH<5.5
- Results in hyperkalemia, which impairs ammoniagenesis in proximal tubule
- ↓ Buffering capacity and ↓ H+ excretion into urine

Causes:
- Hypoaldosteronism
- Aldosterone resistance
- K+ sparing diuretics
Which type of Renal Tubular Acidosis is associated with hypokalemia and and increased risk for calcium phosphate kidney stones?
Type 1 (distal, pH >5.5)
Which type of Renal Tubular Acidosis is associated with hypokalemia and increased risk for hypophosphatemic rickets?
Type 2 (proximal, pH <5.5)
Which type of Renal Tubular Acidosis is associated with hyperkalemia?
Type 4 (hyperkalemic, pH <5.5)