Fa: Renal - Physiology

Front 1

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

Back 1

- 40% non-water mass
- 60% total body water

Front 2

What fluid compartments can the total body water be divided into? What percent of total body weight?

Back 2

- 1/3 extracellular fluid (20% total body weight)
- 2/3 intracellular fluid (40% total body weight)

Front 3

What fluid compartments can the extracellular fluid be divided into? What percent of total body weight?

Back 3

- 1/4 plasma volume (5% total body weight)
- 3/4 interstitial volume (15% total body weight)

Front 4

What is the "rule" to remember the % of body weight of the different fluid compartments?

Back 4

60:40:20 rule:
- 60% total body water
- 40% ICF
- 20% ECF

Front 5

How do you measure the plasma volume?

Back 5

Radio-labeled albumin

Front 6

How do you measure the extracellular volume?

Back 6

Inulin

Front 7

What is the normal serum osmolarity?

Back 7

290 mOsm/L

Front 8

What is the glomerular filtration barrier composed of? What does each layer restrict?

Back 8

- Fenestrated capillary endothelium (size barrier)
- Fused basement membrane with heparan sulfate (negative charge barrier)
- Epithelial layer consisting of podocyte foot processes

Front 9

What happens to the glomerular filtration barrier in nephrotic syndrome? Consequences?

Back 9

Charge barrier (fused basement membrane with heparan sulfate) is lost in nephrotic syndrome, results in:
- Albuminuria
- Hypoproteinemia
- Generalized edema
- Hyperlipidemia

Front 10

How do you calculate renal clearance?

Back 10

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)

Front 11

What does it tell you if the clearance of a substance is less than the GFR?

Back 11

Net tubular reabsorption of X

Front 12

What does it tell you if the clearance of a substance is greater than the GFR?

Back 12

Net tubular secretion of X

Front 13

What does it tell you if the clearance of a substance is equal to the GFR?

Back 13

No net secretion or reabsorption

Front 14

What can be used to calculate the GFR? Why?

Back 14

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)

Front 15

How can you calculate GFR based on the pressures in the glomerulus and Bowman's capsule?

Back 15

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)

Front 16

What is a normal GFR?

Back 16

~100 ml/min

Front 17

Clearance of what can estimate GFR?

Back 17

Creatinine clearance is an approximate measure of GFR; slightly overestimates GFR because creatinine is moderately secreted by the renal tubules

Front 18

What is the staging of chronic kidney diseases based on?

Back 18

Incremental reductions in GFR

Front 19

How do you estimate the Effective Renal Plasma Flow (ERPF)?

Back 19

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%

Front 20

How do you determine the renal blood flow?

Back 20

RBF = RPF / (1 - Hct)

RPF is estimated by ERPF = (U-pah * V) / P-pah

Front 21

What are the characteristics of para-aminohippuric acid (PAH) in the kidney?

Back 21

- Both filtered and actively secreted in proximal tubule
- Nearly all PAH entering the kidney is excreted

Front 22

How do you calculate the filtration fraction? What is normal?

Back 22

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

Front 23

How do you calculate the filtered load?

Back 23

Filtered load (mg/min) = GFR (ml/min) * plasma concentration (mg/ml)

Front 24

How do NSAIDs affect the filtration at the glomerulus?

Back 24

NSAIDs inhibit prostaglandins, preventing dilation of the afferent arteriole
- ↓ RPF, ↓ GFR, so Filtration Fraction remains constant

(remember FF = GFR/RPF)

Front 25

How do prostaglandins affect the filtration at the glomerulus?

Back 25

Prostaglandins dilate the afferent arteriole
- ↑ RPF, ↑ GFR, so Filtration Fraction remains constant

(remember FF = GFR/RPF)

Front 26

How do ACE-inhibitors affect the filtration at the glomerulus?

Back 26

ACE-I inhibit AngII, preventing constriction of the efferent arteriole
- ↑ RPF, ↓ GFR, so FF decreases

(remember FF = GFR/RPF)

Front 27

How does Angiotensin II affect the filtration at the glomerulus?

Back 27

AngII preferentially constricts the efferent arteriole
- ↓ RPF, ↑ GFR, so FF increases

(remember FF = GFR/RPF)

Front 28

How does afferent arteriole constriction affect RPF, GFR, and FF (GFR/RPF)?

Back 28

- ↓ RPF
- ↓ GFR
- = FF

Front 29

How does efferent arteriole constriction affect RPF, GFR, and FF (GFR/RPF)?

Back 29

- ↓ RPF
- ↑ GFR
- ↑ FF

Front 30

How does ↑ plasma protein concentration affect RPF, GFR, and FF (GFR/RPF)?

Back 30

- = RPF
- ↓ GFR
- ↓ FF

Front 31

How does ↓ plasma protein concentration affect RPF, GFR, and FF (GFR/RPF)?

Back 31

- = RPF
- ↑ GFR
- ↑ FF

Front 32

How does constriction of the ureter affect RPF, GFR, and FF (GFR/RPF)?

Back 32

- = RPF
- ↓ GFR
- ↓ FF

Front 33

How do you calculate the filtered load?

Back 33

Filtered load = GFR * Px

Px = plasma concentration of X (mg/ml)

Front 34

How do you calculate the excretion rate?

Back 34

Excretion rate = V * Ux

V = urine flow rate (ml/min)
Ux = urine concentration of X (mg/ml)

Front 35

How do you calculate the reabsorption rate?

Back 35

Reabsorption = Filtered load - Excretion rate

Filtered load = GFR * Px
Excretion rate = V * Ux

Front 36

How do you calculate the secretion rate?

Back 36

Secretion = Excretion rate - Filtered load

Filtered load = GFR * Px
Excretion rate = V * Ux

Front 37

What are the characteristics of glucose clearance in the kidney?

Back 37

- 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)

Front 38

At what plasma glucose concentrations does all glucose get reabsorbed in the proximal tubule?

Back 38

Up to ~200 mg/dL
- Above 200 mg/dL, glucosuria begins (threshold)

Front 39

At what plasma glucose concentrations are all Na+/glucose co-transporters fully saturated (Tm)?

Back 39

At ~375 mg/dL

Front 40

What happens to glucose and amino acid reabsorption during pregnancy?

Back 40

Normal pregnancy ↓ reabsorption of glucose and amino acids in proximal tubule → glucosuria and aminoaciduria

Front 41

How are amino acids normally treated in the kidney?

Back 41

Normally all amino acids are reabsorbed by Na+ dependent transporters in the proximal tubule

Front 42

What disorder causes a deficiency of neutral amino acid (eg, tryptophan) transporters in the proximal renal tubular cells and on enterocytes? Implications?

Back 42

Hartnup Disease:
- Leads to neutral aminoaciduria and ↓ absorption from gut
- Results in pellagra-like symptoms; treat with high-protein diet and nicotinic acid

Front 43

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?

Back 43

Hartnup Disease
- Autosomal recessive deficiency of neutral amino acid (eg, tryptophan) transporters in the proximal renal tubular cells and on enterocytes

Front 44

What are the characteristics of Hartnup Disease? Cause / Symptoms / Treatment?

Back 44

- 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

Front 45

What is reabsorbed and secreted in the proximal convoluted tubule?

Back 45

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

Secreted:
- NH3 (buffers secreted H+)

Front 46

Which hormones act on the early proximal convoluted tubule?

Back 46

- PTH
- AngII

Front 47

What is the action of PTH on the early proximal convoluted tubule?

Back 47

Inhibits Na+ / PO4(3-) co-transport → PO4(3-) excretion

Front 48

What is the action of Angiotensin II on the early proximal convoluted tubule?

Back 48

- Stimulates Na+/H+ exchange → ↑ Na+, H2O, and HCO3- reabsorption
- Permits contraction alkalosis

Front 49

What percent of Na+ is reabsorbed in the early proximal convoluted tubule?

Back 49

65-80% Na+ reabsorbed

Front 50

What is reabsorbed and secreted in the thin descending loop of Henle?

Back 50

- Passive reabsorption of H2O via medullary hypertonicity
- Impermeable to Na+

Front 51

What happens to urine in the thin descending loop of Henle?

Back 51

- Concentrates urine
- Makes urine hypertonic

Front 52

What percent of Na+ is reabsorbed in the thin descending loop of Henle?

Back 52

None - impermeable to Na+

Front 53

What is reabsorbed and secreted in the thick ascending loop of Henle?

Back 53

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

Front 54

What happens to urine in the thick ascending loop of Henle?

Back 54

- Impermeable to H2O but reabsorbing Na+
- This makes urine less concentrated as it ascends

Front 55

What percent of Na+ is reabsorbed in the thick ascending loop of Henle?

Back 55

10-20% Na+ reabsorbed

Front 56

What is reabsorbed and secreted in the early distal convoluted tubule?

Back 56

- Actively reabsorbs Na+ and Cl-
- PTH stimulates Ca2+/Na+ exchange → Ca2+ reabsorption

Front 57

Which hormones act on the distal convoluted tubule? Action?

Back 57

PTH - stimulates Ca2+/Na+ exchange → Ca2+ reabsorption

Front 58

What percent of Na+ is reabsorbed in the distal convoluted tubule?

Back 58

5-10% Na+ reabsorbed

Front 59

What is reabsorbed and secreted in the collecting tubule?

Back 59

Reabsorbs Na+ in exchange for secreting K+ and H+

Front 60

Which hormones act on the collecting tubule? Action?

Back 60

- 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

Front 61

What percent of Na+ is reabsorbed in the collecting tubule

Back 61

3-5% Na+ reabsorbed

Front 62

In which segments of the nephron is sodium reabsorbed? What percentages?

Back 62

- 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%

Front 63

What are the types of renal tubular defects?

Back 63

"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)

Front 64

Which renal tubular defect affects the Proximal Convoluted Tubule? What does it cause?

Back 64

Fanconi Syndrome
- ↑ excretion of nearly all AAs, glucose, HCO3-, and PO4(3-)
- May cause metabolic acidosis (proximal renal tubular acidosis)

Front 65

What causes Fanconi Syndrome? Where is the defect?

Back 65

- Causes: hereditary defects (eg, Wilson disease), ischemia, and nephrotoxins/drugs
- Reabsorptive defect in the proximal convoluted tubule

Front 66

Which renal tubular defect affects the Thick Ascending Loop of Henle? What does it cause?

Back 66

Bartter Syndrome
- Affects Na+/K+/2Cl- co-transporter
- Causes hypokalemia, metabolic alkalosis and hypercalciuria

Front 67

What causes Bartter Syndrome? Where is the defect?

Back 67

- Causes: autosomal recessive defect of Na+/K+/2Cl- co-transporter
- Reabsorptive defect in thick ascending loop of Henle

Front 68

Which renal tubular defect affects the Distal Convoluted Tubule? What does it cause?

Back 68

Gitelman Syndrome
- Hypokalemia
- Metabolic alkalosis
- NO hypercalciuria

Front 69

What causes Gitelman Syndrome? Where is the defect?

Back 69

- Cause: autosomal recessive defect of NaCl reabsorption
- Reabsorptive defect in distal convoluted tubule

Front 70

Which renal tubular defect affects the Distal and Collecting Tubules? What does it cause?

Back 70

Liddle Syndrome
- Hypertension
- Hypokalemia
- Metabolic alkalosis
- ↓ Aldosterone

Front 71

What causes Liddle Syndrome? Where is the defect?

Back 71

- Cause: Autosomal Dominant defect leading to increased activity of epithelial Na+ channel
- Distal and collecting tubules

Front 72

How do you treat Liddle Syndrome?

Back 72

Amiloride

Front 73

What syndrome causes ↑ excretion of nearly all AAs, glucose, HCO3-, and PO4(3-), which may lead to a metabolic acidosis? What causes this?

Back 73

Fanconi Syndrome
- Reabsorptive defect in proximal convoluted tubule
- Causes: hereditary defects (eg, Wilson disease), ischemia, and nephrotoxins/drugs

Front 74

What syndrome causes hypokalemia and metabolic alkalosis with hypercalciuria? What causes this?

Back 74

Bartter Syndrome
- Reabsorptive defect in thick ascending loop of Henle
- Autosomal recessive, affects Na+/K+/2Cl- co-transporter

Front 75

What syndrome causes hypokalemia and metabolic alkalosis without hypercalciuria? What causes this?

Back 75

Gitelman Syndrome
- Reabsorptive defect of NaCl in distal convoluted tubule
- Autosomal recessive, less severe than Bartter syndrome

Front 76

What syndrome causes hypertension, hypokalemia, metabolic alkalosis, and ↓ aldosterone? What causes this?

Back 76

Liddle Syndrome
- ↑ Na+ reabsorption in distal and collecting tubules (↑ activity of epithelial Na+ channel)
- Autosomal dominant
- Treat with Amiloride

Front 77

What is the meaning of the ratio of TF/P?

Back 77

[Tubular Fluid] / [Plasma]

Front 78

What does it mean if the [Tubular Fluid] / [Plasma] ratio is >1?

Back 78

Solute is reabsorbed less quickly than water

Front 79

What does it mean if the [Tubular Fluid] / [Plasma] ratio is =1?

Back 79

Solute and water are reabsorbed at the same rate

Front 80

What does it mean if the [Tubular Fluid] / [Plasma] ratio is <1?

Back 80

Solute is reabsorbed more quickly than water

Front 81

What happens to the tubular inulin concentration as it progresses along the nephron? How?

Back 81

Inulin concentration increases in the tubule (but not in amount) along the proximal tubule as a result of water reabsorption

Front 82

Which substance has net secretion in the proximal tubule?

Back 82

PAH

Front 83

Which substance has net reabsorption in the proximal tubule?

Back 83

- Urea
- Na+, K+, Cl-
- Pi
- HCO3-
- Glucose and amino acids

Front 84

Which substance has no net secretion or reabsorption in the proximal tubule?

Back 84

Creatinine and Inulin

Front 85

How does the reabsorption of Cl- compare to Na+ in the proximal tubule?

Back 85

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

Front 86

What is the action of Renin? Source?

Back 86

Stimulates conversion of Angiotensinogen (from liver) to Angiotensin I
- Renin is from the kidney

Front 87

What is the source of Renin? What stimulates it?

Back 87

Renin is from the kidney, release stimulated by:
- ↓ BP (Juxtaglomerular cells)
- ↓ Na+ delivery to macula densa cells
- ↑ Sympathetic tone (β1-receptors)

Front 88

What is the action of ACE? Source?

Back 88

- ACE converts Ang I to Ang II
- ACE also stimulates Bradykinin breakdown
- ACE is from the lungs and the kidneys

Front 89

What is the action of Angiotensin II?

Back 89

- 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

Front 90

How does AngII increase the BP?

Back 90

Acts at AT I receptors on vascular smooth muscle → Vasoconstriction → ↑ BP

Front 91

How does AngII affect the filtration fraction (FF)?

Back 91

Constricts efferent arteriole of glomerulus → ↑ FF to preserve renal function (GFR) in low-volume states (ie, when RBF ↓)

Front 92

What is the effect of Aldosterone release? Source?

Back 92

- ↑ 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

Front 93

What is the effect of ADH release? Source?

Back 93

- ↑ H2O channel insertion in principal cells, leading to H2O reabsorption
- From posterior pituitary

Front 94

What is the effect of Angiotensin II on the proximal tubule?

Back 94

- ↑ Proximal tubule Na+/H+ activity
- Leads to Na+, HCO3-, and H2O reabsorption (can permit contraction alkalosis)

Front 95

Which hormone affects baroreceptor function, limiting the reflex bradycardia, which would normally accompany its pressor effects?

Back 95

Angiotensin II

Front 96

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?

Back 96

ANP (Atrial Natriuretic Protein)

Front 97

Which hormone is primarily responsible for regulating osmolarity and responds to low blood volume states?

Back 97

ADH

Front 98

Which hormone primarily regulates ECF Na+ content and volume, by responding to low blood volume states?

Back 98

Aldosterone

Front 99

What are the components of the juxtaglomerular apparatus?

Back 99

- JG cells (modified smooth muscle of afferent arteriole)
- Macula Densa (NaCl sensor, part of the distal convoluted tubule)

Front 100

What is the function of the Juxtaglomerular cells?

Back 100

Secrete renin in response to:
- ↓ Renal blood pressure
- ↓ NaCl delivery to distal tubule
- ↑ Sympathetic tone (β1)

Front 101

Which drugs can influence the juxtaglomerular apparatus?

Back 101

β-blockers (specifically β1) can decrease BP by inhibiting β1 receptors of JGA, causing ↓ renin release

Front 102

Which hormones are secreted by the kidney?

Back 102

- Erythropoietin
- 1,25-(OH)2 Vitamin D
- Renin
- Prostaglandins

Front 103

What is the source and function of Erythropoietin?

Back 103

Released by interstitial cells in the peritubular capillary bed in response to hypoxia

Front 104

What is the source and function of 1,25-(OH)2 Vitamin D?

Back 104

- Proximal tubule cells convert 25-OH vitamin D to 1,25-(OH)2 Vitamin D (Active form)
- Enzyme: 1α-Hydroxylase (stimulated by PTH)

Front 105

What is the source and function of Renin?

Back 105

Secreted by JG cells in response to ↓ renal arterial pressure and ↑ renal sympathetic discharge (β1 effect)

Front 106

What is the source and function of prostaglandins?

Back 106

- Paracrine secretion vasodilates the afferent arterioles to ↑ RBF
- From kidney

Front 107

What is the effect of NSAIDs on the kidney?

Back 107

- NSAIDs block renal-protective prostaglandin synthesis → constriction of the afferent arteriole and ↓ GFR
- This may result in acute renal failure

Front 108

Which hormones act on the kidney?

Back 108

- Angiotensin II (ATII)
- Atrial Natriuretic Peptide (ANP)
- Parathyroid Hormone (PTH)
- Aldosterone
- ADH (Vasopressin)

Front 109

What causes Angiotensin II (AT II) to be released and act on kidney? Function?

Back 109

- 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

Front 110

What causes Parathyroid Hormone (PTH) to be released and act on kidney? Function?

Back 110

- 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

Front 111

Where are Ca2+ and PO4(3-) reabsorbed in nephron in response to PTH?

Back 111

- Ca2+ reabsorbed in DCT
- PO4(3-) reabsorbed in PCT

Front 112

What causes Atrial Natriuretic Peptide (ANP) to be released and act on kidney? Function?

Back 112

- 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

Front 113

What causes Aldosterone to be released and act on kidney? Function?

Back 113

- Secreted in response to ↓ blood volume (via AT II) and ↑ plasma [K+]
- Causes ↑ Na+ reabsorption, ↑ K+ secretion, ↑ H+ secretion

Front 114

What causes ADH (Vasopressin) to be released and act on kidney? Function?

Back 114

- Secreted in response to ↑ plasma osmolarity and ↓ blood volume
- Binds to receptors on principal cells, causing ↑ number of water channels and ↑ H2O reabsorption

Front 115

Which conditions/drugs cause K+ to shift out of cells (causing hyperkalemia)?

Back 115

Patient with hyperkalemia? DO Insulin LAβ work
- Digitalis
- HyperOsmolarity
- INSULIN deficiency
- Lysis of cells
- Acidosis
- β-adrenergic antagonist

Front 116

Which conditions/drugs cause K+ to shift into cells (causing hypokalemia)?

Back 116

INsulin shifts K+ INto cells
- Hypoosmolarity
- Insulin (↑ Na+ / K+ ATPase)
- Alkalosis
- β-adrenergic agonist (↑ Na+ / K+ ATPase)

Front 117

What electrolyte disturbance causes nausea, malaise, stupor, and coma?

Back 117

Low serum Na+

Front 118

What electrolyte disturbance causes irritability, stupor, or coma?

Back 118

High serum Na+

Front 119

What electrolyte disturbance causes U waves on ECG, flattened T waves, arrhythmias, and muscle weakness?

Back 119

Low serum K+

Front 120

What electrolyte disturbance causes wide QRS and peaked T waves on ECG, arrhythmias, and muscle weakness?

Back 120

High serum K+

Front 121

What electrolyte disturbance causes tetany, seizures, and QT prolongation?

Back 121

Low serum Ca2+

Front 122

What electrolyte disturbance causes stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria?

Back 122

High serum Ca2+

Front 123

What electrolyte disturbance causes tetany and Torsades de Pointes?

Back 123

Low serum Mg2+

Front 124

What electrolyte disturbance causes ↓ DTRs, lethargy, bradycardia, hypotension, cardiac arrest, and hypocalcemia?

Back 124

High serum Mg2+

Front 125

What electrolyte disturbance causes bone loss and osteomalacia?

Back 125

Low serum PO4(3-)

Front 126

What electrolyte disturbance causes renal stones, metastatic calcifications, and hypocalcemia?

Back 126

High serum PO4(3-)

Front 127

What is the effect of low vs high serum concentration of Na+?

Back 127

- Low: nausea, malaise, stupor, coma
- High: irritability, stupor, coma

Front 128

What is the effect of low vs high serum concentration of K+?

Back 128

- Low: U waves on ECG, flattened T waves, arrhythmias, muscle weakness
- High: wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness

Front 129

What is the effect of low vs high serum concentration of Ca2+?

Back 129

- Low: tetany, seizures, QT prolongation
- High: stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria

Front 130

What is the effect of low vs high serum concentration of Mg2+?

Back 130

- Low: tetany and torsades de pointes
- High: ↓ DTRs (reflexes), lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

Front 131

What is the effect of low vs high serum concentration of PO4(3-)?

Back 131

- Low: bone loss, osteomalacia
- High: renal stones, metastatic calcifications, hypocalcemia

Front 132

What is the pH, PCO2, and [HCO3-] associated with metabolic acidosis? Compensatory response?

Back 132

- ↓ pH
- ↓ PCO2
- ↓↓ [HCO3-]
- Immediate hyperventilation

↓↓ = 1° distrubance
↓ = compensatory response

Front 133

What is the pH, PCO2, and [HCO3-] associated with metabolic alkalosis? Compensatory response?

Back 133

- ↑ pH
- ↑ PCO2
- ↑↑ [HCO3-]
- Immediate hypoventilation

↑↑ = 1° distrubance
↑ = compensatory response

Front 134

What is the pH, PCO2, and [HCO3-] associated with respiratory acidosis? Compensatory response?

Back 134

- ↓ pH
- ↑↑ PCO2
- ↑ [HCO3-]
- ↑ Renal [HCO3-] reabsorption (delayed)

↑↑ = 1° distrubance
↑ = compensatory response

Front 135

What is the pH, PCO2, and [HCO3-] associated with respiratory alkalosis? Compensatory response?

Back 135

- ↑ pH
- ↓↓ PCO2
- ↓ [HCO3-]
- ↓ Renal [HCO3-] reabsorption (delayed)

↓↓ = 1° distrubance
↓ = compensatory response

Front 136

What is the Henderson-Hasselbach equation in terms of [HCO3-] and PCO2?

Back 136

pH = 6.1 + log [HCO3-] / 0.03 PCO2

Front 137

How can you calculate the predicted respiratory compensation for a simple metabolic acidosis? What does it tell you?

Back 137

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

Front 138

If you suspect an acidosis or alkalosis, what do you check first?

Back 138

Check arterial pH
- pH <7.4 = Acidemia
- pH >7.4 = Alkalemia

Front 139

What do you test after you establish a patient has an acidemia (arterial pH <7.4)?

Back 139

Check PCO2
- PCO2 >40 mmHg = Respiratory Acidosis
- PCO2 <40 mmHg = Metabolic Acidosis with compensation (hyperventilation)

Front 140

What do you test after you establish a patient has an alkalemia (arterial pH >7.4)?

Back 140

Check PCO2
- PCO2 <40 mmHg = Respiratory Alkalosis
- PCO2 >40 mmHg = Metabolic Alkalosis with compensation (hypoventilation)

Front 141

What is the diagnosis if a patient has pH <7.4 and PCO2 >40mmHg? What causes this?

Back 141

Respiratory Acidosis, caused by hypoventilation, such as:
- Airway obstruction
- Acute lung disease
- Chronic lung disease
- Opioids, sedatives
- Weakening of respiratory muscles

Front 142

What is the diagnosis if a patient has pH <7.4 and PCO2 <40mmHg? What should you check next?

Back 142

Metabolic Acidosis with compensation (hyperventilation)
- Check for anion gap

Anion Gap = Na+ - (Cl- + HCO3-)
Normal: 8-12 mEq/L

Front 143

What is the diagnosis if a patient has pH <7.4 and PCO2 <40mmHg and an ↑ anion gap? What are the potential causes?

Back 143

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)

Front 144

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?

Back 144

Metabolic Acidosis with compensation (hyperventilation)

HARD-ASS:
- Hyperalimentation
- Addison disease
- Renal tubular acidosis
- Diarrhea
- Acetazolamide
- Spironolactone
- Saline infusion

Front 145

What is the diagnosis if a patient has pH >7.4 and PCO2 <40mmHg? What causes this?

Back 145

Respiratory alkalosis, can be caused by:

Hyperventilation:
- Hysteria
- Hypoxemia (eg, high altitude)
- Salicylates (early)
- Tumor
- Pulmonary embolism

Front 146

What is the diagnosis if a patient has pH >7.4 and PCO2 >40mmHg? What causes this?

Back 146

Metabolic alkalosis with compensation (hypoventilation), caused by:
- Loop diuretics
- Vomiting
- Antacid use
- Hyperaldosteronism

Front 147

What do these have in common? What would they cause?
- Airway obstruction
- Acute lung disease
- Chronic lung disease
- Opioids, sedatives
- Weakening of respiratory muscles

Back 147

Causes of hypoventilation → Respiratory Acidosis

Front 148

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)

Back 148

Metabolic Acidosis with compensation (hyperventilation) with ↑ Anion Gap

Front 149

What do these have in common? What would they cause?
- Hyperalimentation
- Addison disease
- Renal tubular acidosis
- Diarrhea
- Acetazolamide
- Spironolactone
- Saline infusion

Back 149

Metabolic Acidosis with compensation (hyperventilation) with normal Anion Gap (8-12 mEq/L)

Front 150

What do these have in common? What would they cause?
- Hysteria
- Hypoxemia (eg, high altitude)
- Salicylates (early)
- Tumor
- Pulmonary embolism

Back 150

Causes of hyperventilation → Respiratory Alkalosis

Front 151

What do these have in common? What would they cause?
- Loop diuretics
- Vomiting
- Antacid use
- Hyperaldosteronism

Back 151

Metabolic Alkalosis with compensation (hypoventilation)

Front 152

When should you calculate the anion gap? How? What is normal?

Back 152

When you have a metabolic acidosis (pH < 7.4 and PCO2 < 40 mmHg)

Anion Gap = Na+ - (Cl- + HCO3-)
Normal = 8-12 mEq/L

Front 153

What kind of disorder causes a non-anion gap hyperchloremic metabolic acidosis?

Back 153

Renal Tubular Acidosis

Front 154

What are the types of Renal Tubular Acidosis?

Back 154

- Type 1: distal, pH >5.5
- Type 2: proximal, pH <5.5
- Type 4: hyperkalemic, pH <5.5

Front 155

Which type of Renal Tubular Acidosis is caused by a defect in the ability of the α intercalated cells to secrete H+? Implications?

Back 155

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)

Front 156

What can cause Type 1 Renal Tubular Acidosis (distal, pH >5.5)?

Back 156

Defects in ability of α intercalated cells to secrete H+
- Amphotericin B toxicity
- Analgesic nephropathy
- Congenital anomalies (obstruction) of urinary tract

Front 157

Which type of Renal Tubular Acidosis is caused by a defect in the proximal tubule HCO3- reabsorption? Implications?

Back 157

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

Front 158

What can cause Type 2 Renal Tubular Acidosis (proximal, pH <5.5)?

Back 158

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)

Front 159

Which type of Renal Tubular Acidosis is caused by hypoaldosteronism, aldosterone resistance, or K+ sparing diuretics? Implications?

Back 159

- Results in hyperkalemia
- Impairs ammoniagenesis in proximal tubule → ↓ buffering capacity and ↓ H+ excretion into urine

Front 160

What can cause Type 4 Renal Tubular Acidosis (hyperkalemic, pH <5.5)?

Back 160

- Hypoaldosteronism
- Aldosterone resistance
- K+ sparing diuretics

Front 161

What are the characteristics of Type 1 Renal Tubular Acidosis?

Back 161

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

Front 162

What are the characteristics of Type 2 Renal Tubular Acidosis?

Back 162

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)

Front 163

What are the characteristics of Type 4 Renal Tubular Acidosis?

Back 163

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

Front 164

Which type of Renal Tubular Acidosis is associated with hypokalemia and and increased risk for calcium phosphate kidney stones?

Back 164

Type 1 (distal, pH >5.5)

Front 165

Which type of Renal Tubular Acidosis is associated with hypokalemia and increased risk for hypophosphatemic rickets?

Back 165

Type 2 (proximal, pH <5.5)

Front 166

Which type of Renal Tubular Acidosis is associated with hyperkalemia?

Back 166

Type 4 (hyperkalemic, pH <5.5)