Renal Flashcards
Is the vast majority of potassium in the intracellular or extracellular space?
HIKIN’: HIgh K+ INtracellularly
The 60–40–20 rule refers to ——— for average person):
- 60% of body mass is ——— (while 40% of body mass is ———)
- % of body weight
- total body water (TBW)
- non water mass (NWM)
The 60–40–20 rule refers to ——— for average person):
- 40% ———, mainly composed of what 3 things: ———
- % of body weight
- ICF (I.e., ICF 2/3 of total body water)
- K+, Mg2+, organic phosphates (eg, ATP)
The 60–40–20 rule refers to ——— for average person):
- 20% ———, mainly composed of what 4 things:
- % of body weight
- ECF (I.e., ECF 1/3 of total body water)
- Na+, Cl–, HCO3 –, albumin
ECF is made up of ———% plasma and ———% interstitial fluid
- 25
- 75
Plasma volume can be measured by:
radiolabeling albumin
Extracellular volume can be measured by:
inulin or mannitol
In Fanconi syndrome there is a ———defect in the ———, leading to decreased excretion of:
- generalized reabsorption
- PCT
- amino acids, glucose, HCO3 –, and PO4 3–, and all substances reabsorbed by the PCT
List 3 key findings in Fanconi syndrome:
- metabolic acidosis (proximal RTA)
- hypophosphatemia
- hypokalemia (most K+ reabsorbed at PCT)
List 4 causes of Fanconi syndrome:
- Hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease)
- ischemia
- multiple myeloma
- drugs (eg, ifosfamide, cisplatin, tenofovir, lead poisoning)
List 2 common associated findings in Franconia syndrome:
- Growth retardation and rickets/osteopenia common due to hypophosphatemia
- Volume depletion also common
Bartter syndrome is a reabsorption defect in ——— (affects ———transporter)
- thick ascending loop of Henle
- Na+/K+/2Cl– cotransporter
List 3 key findings in Bartter syndrome:
- Metabolic alkalosis
- hypokalemia
- hypercalciuria
Mode of inheritance for Bartter syndrome:
Autosomal recessive
Bartter syndrome presents similarly to chronic ——— use
loop diuretic
Gitelman syndrome is a reabsorption defect of ——— in ———
- NaCl
- DCT
List 4 key findings in Gitelman syndrome:
- Metabolic alkalosis
- hypomagnesemia
- hypokalemia
- hypocalciuria
Mode of inheritance in Gitelman syndrome:
Autosomal recessive
Gitelman syndrome presents similarly to chronic ——— use
thiazide diuretic
Which is more severe Gitelman syndrome or Bartter syndrome?
Gitelman syndrome less severe than Bartter syndrome
Liddle syndrome refers to a ——— mutation leading to decreased ——— and increased ——— in ———
- gain of function
- Na+ channel degradation
- Na+ reabsorption
- collecting tubules
List 4 key findings in Liddle syndrome:
- Metabolic alkalosis
- hypokalemia
- hypertension
- decreased aldosterone
Mode of inheritance in Liddle syndrome:
Autosomal dominant
Liddle syndrome presents similarly to ———, but ——— is nearly undetectable
- hyperaldosteronism
- aldosterone
List 1 treatment for Liddle syndrome:
amiloride
Normally, cortisol activates mineralocorticoid receptors, and enzyme ——— converts cortisol to ——— (inactive on these receptors); Hereditary deficiency of this enzyme (resulting in: ——— disease) leads to increased ———, and thus increased ——— activity
- 11β-HSD (11β-hydroxysteroid dehydrogenase)
- cortisone
- SAME (Syndrome of Apparent Mineralocorticoid Excess)
- cortisol
- mineralocorticoid receptor
List 4 key effect of SAME (Syndrome of Apparent Mineralocorticoid Excess):
- Metabolic alkalosis
- hypokalemia
- hypertension
- decreased serum aldosterone level
(cortisol tries to be the SAME as aldosterone)
Mode of inheritance for SAME is ———; also, can acquire SAME from ——— (present in ———), which blocks activity of ———
- Autosomal recessive
- glycyrrhetinic acid
- licorice
- 11β-hydroxysteroid dehydrogenase
Treatment of SAME include:
- ——— diuretics (decrease ——— effects)
- ——— (exogenous ——— will decrease endogenous ———, and thus decrease ——— activation)
- K+-sparing
- mineralocorticoid
- corticosteroids
- corticosteroid
- cortisol production
- mineralocorticoid receptor
Metabolic acid-base disorders cause ——— alterations; Respiratory acid-base disorders cause ——— alterations
- HCO3 –
- PCO2
Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in metabolic acidosis:
pH: decreased
pCO2: decreased (compensatory)
HCO3–: decreased
Compensatory response: hypERventilation (immediate)
Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in metabolic alkalosis:
pH: increased
pCO2: increased (compensatory)
HCO3–: increased
Compensatory response: hypOventilation (immediate)
Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in repiratory acidosis:
pH: decreased
pCO2: increased
HCO3–: increased (compensatory)
Compensatory response: increased renal [HCO3 –] reabsorption (delayed)
Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in respiratory alkalosis:
pH: increased
pCO2: decreased
HCO3–: decreased (compensatory)
Compensatory response: decreased renal [HCO3 –] reabsorption (delayed)
Winters formula calculates the ——-; If measured Pco2 > predicted Pco2, there is ———; if measured Pco2 < predicted Pco2, there is ———
- Predicted respiratory compensation for a simple metabolic acidosis
- concomitant respiratory acidosis
- concomitant respiratory alkalosis
Acidemia is defined as pH of ———, and Alkalemia is defined as pH of ———
pH < 7.35
pH > 7.45
Respiratory acidosis is caused by ———; list 5 specific causes:
- Hypoventilation
- Airway obstruction
Acute lung disease
Chronic lung disease
Opioids, sedatives
Weakening of respiratory muscles
In order to asses the cause of metabolic acidosis, check the ———, which is:
Anion gap
= Na + – ((CI–) + (HCO3-))
List 7 causes of metabolic acidosis with normal anion gap (which is ———): by
8-12 mEq/L
HARDASS:
Hyperchloremia/hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
List 8 causes of metabolic acidosis with increased anion gap (which is ———):
> 12 mEq/L
GOLDMARK:
Glycols (ethylene glycol, propylene glycol)
Oxoproline (chronic acetaminophen use)
L-lactate (lactic acidosis)
D-lactate (exogenous lactic acid) Methanol (and other alcohols)
Aspirin (late effect)
Renal failure
Ketones (diabetic, alcoholic, starvation)
Respiratory alkalosis is caused by ———; list 6 specific causes:
- hyperventilation
- Anxiety/panic attack
Hypoxemia (eg, high altitude) Salicylates (early)
Tumor
Pulmonary embolism
Pregnancy
In order to asses the cause of metabolic alkalosis , check the ——— in order to asses if ———
Check urine Cl–
Saline-resistant or Saline-responsive
List 4 causes of Saline-resistant metabolic alkalosis:
Hyperaldosteronism
Bartter syndrome
Gitelman syndrome
Current loop/thiazide diuretics
List 3 causes of Saline-responsive metabolic alkalosis:
Vomiting
Recent loop/thiazide diuretics
Antacids
Presence of casts in the urine indicates that hematuria/pyuria is of ——— origin
glomerular or renal tubular
In terms of nomenclature of glomerular disorders, define and give an example of Focal:
< 50% of glomeruli are involved
Focal segmental glomerulosclerosis
In terms of nomenclature of glomerular disorders, define and give an example of Diffuse:
> 50% of glomeruli are involved
Diffuse proliferative glomerulonephritis
In terms of nomenclature of glomerular disorders, define and give an example of Proliferative:
Hypercellular glomeruli
Membranoproliferative glomerulonephritis
In terms of nomenclature of glomerular disorders, define and give an example of Membranous:
Thickening of glomerular basement membrane (GBM)
Membranous nephropathy
In terms of nomenclature of glomerular disorders, define and give an example of Primary glomerular disease:
1° disease of the kidney specifically impacting the glomeruli
Minimal change disease
In terms of nomenclature of glomerular disorders, define and give an example of Secondary glomerular disease:
Systemic disease or disease of another organ system that also impacts the glomeruli
SLE, diabetic nephropathy
List the 4 key processes underlying Nephritic syndrome:
Glomerular inflammation, leading to
GBM damage, leading to
loss of RBCs into urine, leading to
dysmorphic RBCs and hematuria
List the 5 key clinical presentations of Nephritic syndrome:
Hematuria
RBC casts in urine
Decreased GFR with oliguria and azotemia
Increased renin release leading to HTN
Proteinuria often in the subnephrotic range (< 3.5 g/day) but in severe cases may be in nephrotic range
List the 5 key examples of Nephritic syndrome:
Infection-associated glomerulonephritis
Goodpasture syndrome
IgA nephropathy (Berger disease)
Alport syndrome
Membranoproliferative glomerulonephritis
List the 3 key processes underlying Nephrotic syndrome:
Podocyte damage, leading to
impaired charge barrier, leading to
proteinuria
List 4 key clinical presentations of Nephrotic syndrome:
Massive proteinuria (> 3.5 g/day) with edema, hypoalbuminemia leading to hepatic lipogenesis leading to hypercholesterolemia
Frothy urine with fatty casts
Associated with hypercoagulable state due to antithrombin III loss in urine
Increased risk of infection (loss of IgGs in urine and soft tissue compromise by edema)
List the 5 key examples of Nephrotic syndrome; and list if 1° (eg, direct podocyte damage) or 2° (podocyte damage from systemic process):
Focal segmental glomerulosclerosis (1° or 2°)
Minimal change disease (1° or 2°)
Membranous nephropathy (1° or 2°)
Amyloidosis (2°)
Diabetic glomerulonephropathy (2°)
List the 3 key processes underlying Nephritic-nephrotic syndrome:
Severe GBM damage, leading to
loss of RBCs into urine + impaired charge barrier, leading to
hematuria + proteinuria
List 2 key clinical presentations of Nephritic-nephrotic syndrome:
Nephrotic-range proteinuria (> 3.5 g/day) and concomitant features of nephritic syndrome
Nephritic-nephrotic syndrome can occur with any form of ——— syndrome, but is most common with: (list 2)
nephritic
Diffuse proliferative glomerulonephritis
Membranoproliferative glomerulonephritis
