Quiz 1 Flashcards
Define chronic kidey disease
- Kidney damaged for 3 months
- w/ out w/out dec GFR
- pathological abnormalities OR
- markers of kidney damage - GFR < 60mL/min/1.73m^2 for 3 months with or without kidney damage
Stage 5 kidney disease defined as
GFR for other stages?
Stage 5: Kidney failure <15
2: 60-89
3: (30-59)
4: (15-29)
Vast majority w/ CKD in which stages?
most die from?
1 - 3
CV disease - MCC cause of death
3 classes of kidney disease
- Tubulointerstitial
- analgesic nephropathy
- obstructive nephropathy - Vascular
- HTN nephrosclerosis
- ischemic nephropathy - Glomerular
- primary -> idiopathic
- 2ndary -> diabetes or lupus
Hallmark of glomerular disease?
proteinuria
>1g/day
Acute vs chronic disease
KIDNEY SIZE -> most important
- small = chronic
- normal = non committal
In which 4 disease do they kidneys not shrink with time?
Diabetes
HIV
infiltrative disease
PKD
List the non-discriminatory kidney disease
Anemia hypocalcemia acidosis (low CO2) hyperkalemia hyperphosphatemia hyperPTH pericarditis
OCCUR IN BOTH ACUTE AND CHRONIC dz
At what stage does uremia manifest?
Sx progression from earliest to latest
Stage 4 (GFR 15-29)
Nocturia -> GI -> CNS changes (LATE)
Positive dipstick for blood w/out RBCs indicates?
Heme pigment - hemoglobin or myoglobin
Gold standard method for quantifying urine protein?
protein/cr ratio measured using?
24 hr urine excretion = GS
-normal 100-200mg/day
Spot urine
-normal -> <0.2
BUN/Cr ratio
- normal
- disease states
Normal -> 10:1
parenchymal ARF or CKD -> normal
Pre-renal renal failure (Acute or chronic) - 20:1
Which lab values are high with renal failure
What other values can become abnormal and when?
BUN
Cr
PO4
- Electrolyte probs occur late when patient is unable to excrete all the water
- Hyperkalemia is not seen often (until late)
- Albumin effects are due to nutrition
Magic number for GFR?
Which abnormalities appear at this point?
GFR 25-30ml/min
Acidosis -> low CO2 hypocalcemia hyperphosphatemia anemia high PTH (levels at which tx is needed)
3 aspects of BUN
readily filtered
reabsorbed in tubule
urea clearance underestimates GFR
6 things that inc BUN disproportionately to Cr
Protein Intake – high with high intake, low with low
Tissue Destruction (Protein Breakdown)
GI Bleed
Tetracyclines (Tagycycline) – catabolic
Cortico-steroids – catabolic
Hypoperfusion – BUN rises disproportionately
5 things that cause BUN to go into single digits? (hint one has 2 causes)
Advanced liver disease – acute or chronic
Alcoholism (w or w/o clinical liver disease)
Severe wasting illness/malnutrition
-Malignancy
-HIV/AIDS
Syndrome of Inappropriate ADH (SIADH) release Pregnancy
Cr measurement of GFR?
how can truer measurement of GFR be established using Cr?
- OVERESTIMATES b/c secreted by tubule
- block secretion using Cimetidine
other blockers of Cr secretion:
- trimethoprim
- pyramethamine
- dapsone
Serum Cr and clearance relationship
Clearance halves for each doubling of serum Cr - IMPORTANT
Cr depends on?
muscle mass, sex and age
M = 1.5g/day
F = 1g/day
Urea nitrogen depends on
Protein intake and tissue breakdown
6.25 g protein = 1 g nitrogen
List normal values: Na K Cl Bicarb Plasma osmolality
Na: 136 - 145 mEq/L K: 3.5 - 5.0 Cl: 98 - 106 Bicarb: 23-28 Plasma osmolarity: 275-285 mOsm/kg
MCC of ADH release NOT due to inc osmolality?
Volume contraction
- ADH has a vascular receptor -> vasoconstriction
- 5-8% dec in plasma volume triggers ADH release
Uosm is a bioassay for?
ADH
No ADH: Uosm < 100
Some ADH: 200-300
Pseudohyponatremia
- cause
- labs
Cause - excess protein/lipids in blood
Plasma osmolality is NORMAL w/ dec Na
Hypertonic hyponatremia
-cause
cause -> hyperglycemia
-gluc diluting the Na concentration
Hypotonic hyponatremia
4 classes broken down into causes
- E.C.F. volume contraction
- BUN and Cr will be HIGH - Excess ECF volume (edema)
- liver disease
- CHF
- look at the patient! - Euvolemic
- SIADH
- BUN and Cr are LOW!
- dx of exclusion - Thiazides (1+3)
- Thiazides work in the diluting segment
- Free water clearance diminished if on thiazide
- This can be become problematic for people who take in large amounts of fluid
- Can lead to the hyponatremia
- This is the most common cause of hypotonic hyponatremia over the age of 60
- Importance of checking electrolytes if pt started on thiazide
- May cause a little bit of volume contraction due to salt loss
NaCl vs H20
- distribution
- determines
- clinical presentation (Excess vs deficiency)
- [PNa] in dx
NaCl -ECF only -determines ECF volume -high -> edema -low -> shock P[Na] useless
H2O
- total body water
- determines osmolality of ECF and Cell
- CNS presentations
- P[Na] x 2 = serum osmolality
K internal balance regulated by?
Beta-2 catecholamine’s; insulin
-beta blockers -> hyperkalemia
Acid-Base changes; osmolar changes
- acidemia -> proton goes into cell -> K comes out -> hyperkalemia
- alkalemia -> proton comes out of cell -> K goes in -> hypokalemia
- proton and K move in opposite directions
Complete sentence:
Patient w/ acidemia and hypokalemia is likely to have a (low/high) total body K
Patient w/ alkalemia and hyperkalemia is likely to have a (low/high) TBK
Patient w/ acidemia and hypokalemia is likely to have a LOW total body K
Patient w/ alkalemia and hyperkalemia is likely to have a HIGH TBK
Big 3 determinants for K secretion
- Sodium delivery to the CD for Na + / K + exchange via ENaC (electrogenic sodium channel)
- Cell K + concentration in the collecting duct
- Aldosterone levels
- hyperaldosteronism → hypokalemia
- hypoaldosteronism → hyperkalemia
2 signs of K depletion (not the same as shift)
What if you have HCO3- and K loss (e.g. RTA or diarrhea)
- Polyuria -> nephrogenic DI
- Metabolic alkalosis
- impaired fx of ascending limb of loop
- protons go into cells to balance the low K -> inc HCO3- reabsorption -> metabolic alkalosis
EXAMPLE - hyperaldosteronism
IMPORTANT
w/ HCO3- and K loss -> metabolic ACIDOSIS
-loss at urine pH -> will be 6-7 or greater w/ RTA but normal w/ diarrhea (5.4 or less)
Major causes of hypokalemia
- renal
- GI
A. Renal
- Loop and DCT Diuretics (Thiazides)
- Aldosterone Excess
- Osmotic Diuresis
- Renal Tubular Acidosis
B. Gut
1. Severe Diarrhea (and often Metabolic acidemia) 2. Vomiting and Metabolic Alkalemia
Major causes of hyperkalemia
A. Renal (most causes are much more common in patients with Acute and Chronic Renal Failure)
1. Diuretics acting on collecting duct (Examples: Amiloride and spironolactone)
2. Distal hyperkalemic R.T.A.
(Example obstructive uropathy)
3. Aldosterone deficiency ( Example: Addison’s Disease)
4. Excess intake (rare with normal renal function)
B. Acidemia
C. Cell necrosis or hemolysis
(Examples: rhabdomyolysis or falciparum / malaria)
Tx for hyperkalemia?
Calcium - to balance potential
Glucose + insulin to get rid of the excess K
HCO3- if acidotic
2 ways bicarb is reabsorbed
Na/H exchange in PCT
Cl/HCO3 exchange in collecting duct
- pendrin transporter
- stimulated by low Cl -> metabolic alkalosis
Which buffer is inc in production in response to acidemia?
-what regulates production
NH3
- deamination of Gln
- intracellular pH in PCT regulates enzyme activity
- example DKA
Normal anion gap?
6-14
Anion gap correction factor for low albumin
2.5mEq/1g reduction from normal (4g/100ml)
Example
If albumin is 2g/ml -> subtract 5 from patient anion gap to get normal for the PATIENT. Use this value to determine if patient has elevated anion gap
2 cause of maintenance of metabolic alkalemia
- Cl Depletion
-Vomiting – loss of HCl
-Nasogastric aspiration
-Diuretics inhibiting NaCl reabsorption
(thiazides, loop diuretics-relative to plasma levels these cause more Cl depletion) - K depletion
- With sodium retention; an example is hypertension due to primary hyperaldosteronism -
- With sodium loss -> normotension or hypotension due to Gitelman’s Syndrome (“Congenital Thiazidemia”)
- Severe chronic renal failure with bicarbonate loading
How to calc arterial blood pH
pH = 6.1 + log [HCO3-]/(0.03PCO2)
Expected compensations
- Metabolic acidemia
- Metabolic alkalemia
- Chronic resp acidosis
- Chronic resp alk
- HCO3 drop by 10 -> pCO2 drop by 12
- HCO3 up by 10 -> pCO2 up by 6
- pCO2 up by 10 -> HCO3 up by 4
- pCO2 up by 10 -> HCO3 down by 4
If serum HCO3 is normal and if both pCO2 and pH are abnormal a (blank) disturbance is present
MIXED
If pH is normal, and if pCO2 and HCO3 are both abnormal a (blank) disturbance is present
MIXED -> b.c physiological response is NEVER fully protective
In metabolic acidemia, if the 2 decimal points of arterial pH are close to the value for the value of pCO2 a (blank) compensated (blank) disturbance is present
- can move on to the anion gap
- example 7.20 and 20mmHg
normally compensated single disturbance
example - metabolic acidemia
How to measure accuracy of data and eliminate lab error?
serum HCO3 (measured chemically) will be within +/- 2 or 3 of arterial bicarb (calculated from measured ApH and pCO2)
pH and proton nanoequivalents:
Acidemia
Normal
Alkalemia
Acidemia
pH 7 - 7.38 = 100-44 nanoEq
Normal
7.38 - 7.44 = 44-36 nanoEq
Alkalemia
7.44-7.80 = 36-16 nanoEq
Equation of calculating proton nanoequivalents
H+ = (24 x pCO2/HCO3-)
pH of 7.4 = 40 nanoEq
List clearances of major solutes
PAH, penicillin > creatinine > inulin > urea > K+ (diet dependent) > Cl-, Na+ > HCO3-, glucose, amino acids, proteins
Arrange major solutes in order of decreasing TF/P
PAH > Cr > Inulin > Urea > Cl- > K > Na > Pi > HCO3- > amino acids = glucose
TF/P > 1: water being reabsorbed more quickly than solute
TF/P < 1: water being reabsorbed less quickly than solute
