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Quiz 1 Flashcards

1
Q

Define chronic kidey disease

A
  1. Kidney damaged for 3 months
    - w/ out w/out dec GFR
    - pathological abnormalities OR
    - markers of kidney damage
  2. GFR < 60mL/min/1.73m^2 for 3 months with or without kidney damage
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2
Q

Stage 5 kidney disease defined as

GFR for other stages?

A

Stage 5: Kidney failure <15

2: 60-89
3: (30-59)
4: (15-29)

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3
Q

Vast majority w/ CKD in which stages?

most die from?

A

1 - 3

CV disease - MCC cause of death

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4
Q

3 classes of kidney disease

A
  1. Tubulointerstitial
    - analgesic nephropathy
    - obstructive nephropathy
  2. Vascular
    - HTN nephrosclerosis
    - ischemic nephropathy
  3. Glomerular
    - primary -> idiopathic
    - 2ndary -> diabetes or lupus
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5
Q

Hallmark of glomerular disease?

A

proteinuria

>1g/day

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6
Q

Acute vs chronic disease

A

KIDNEY SIZE -> most important

  • small = chronic
  • normal = non committal
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7
Q

In which 4 disease do they kidneys not shrink with time?

A

Diabetes
HIV
infiltrative disease
PKD

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8
Q

List the non-discriminatory kidney disease

A 
Anemia
hypocalcemia
acidosis (low CO2)
hyperkalemia
hyperphosphatemia 
hyperPTH
pericarditis

OCCUR IN BOTH ACUTE AND CHRONIC dz

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9
Q

At what stage does uremia manifest?

Sx progression from earliest to latest

A

Stage 4 (GFR 15-29)

Nocturia -> GI -> CNS changes (LATE)

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10
Q

Positive dipstick for blood w/out RBCs indicates?

A

Heme pigment - hemoglobin or myoglobin

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11
Q

Gold standard method for quantifying urine protein?

protein/cr ratio measured using?

A

24 hr urine excretion = GS
-normal 100-200mg/day

Spot urine
-normal -> <0.2

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12
Q

BUN/Cr ratio

  • normal
  • disease states
A

Normal -> 10:1

parenchymal ARF or CKD -> normal

Pre-renal renal failure (Acute or chronic) - 20:1

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13
Q

Which lab values are high with renal failure

What other values can become abnormal and when?

A

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
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14
Q

Magic number for GFR?

Which abnormalities appear at this point?

A

GFR 25-30ml/min

Acidosis -> low CO2
hypocalcemia
hyperphosphatemia 
anemia
high PTH (levels at which tx is needed)
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15
Q

3 aspects of BUN

A

readily filtered
reabsorbed in tubule
urea clearance underestimates GFR

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16
Q

6 things that inc BUN disproportionately to Cr

A

 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

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17
Q

5 things that cause BUN to go into single digits? (hint one has 2 causes)

A

 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

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18
Q

Cr measurement of GFR?

how can truer measurement of GFR be established using Cr?

A
  • OVERESTIMATES b/c secreted by tubule
  • block secretion using Cimetidine

other blockers of Cr secretion:

  • trimethoprim
  • pyramethamine
  • dapsone
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19
Q

Serum Cr and clearance relationship

A

Clearance halves for each doubling of serum Cr - IMPORTANT

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20
Q

Cr depends on?

A

muscle mass, sex and age
M = 1.5g/day
F = 1g/day

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21
Q

Urea nitrogen depends on

A

Protein intake and tissue breakdown

6.25 g protein = 1 g nitrogen

22
Q 
List normal values:
Na
K
Cl
Bicarb
Plasma osmolality
A 
Na: 136 - 145 mEq/L
K: 3.5 - 5.0
Cl: 98 - 106
Bicarb: 23-28
Plasma osmolarity: 275-285 mOsm/kg
23
Q

MCC of ADH release NOT due to inc osmolality?

A

Volume contraction

  • ADH has a vascular receptor -> vasoconstriction
  • 5-8% dec in plasma volume triggers ADH release
24
Q

Uosm is a bioassay for?

A

ADH

No ADH: Uosm < 100
Some ADH: 200-300

25
Pseudohyponatremia - cause - labs
Cause - excess protein/lipids in blood Plasma osmolality is NORMAL w/ dec Na
26
Hypertonic hyponatremia | -cause
cause -> hyperglycemia -gluc diluting the Na concentration
27
Hypotonic hyponatremia | 4 classes broken down into causes
1. E.C.F. volume contraction - BUN and Cr will be HIGH 2. Excess ECF volume (edema) - liver disease - CHF - look at the patient! 3. Euvolemic - SIADH - BUN and Cr are LOW! - dx of exclusion 4. 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
28
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
29
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
30
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
31
Big 3 determinants for K secretion
1. Sodium delivery to the CD for Na + / K + exchange via ENaC (electrogenic sodium channel) 2. Cell K + concentration in the collecting duct 3. Aldosterone levels - hyperaldosteronism → hypokalemia - hypoaldosteronism → hyperkalemia
32
2 signs of K depletion (not the same as shift) What if you have HCO3- and K loss (e.g. RTA or diarrhea)
1. Polyuria -> nephrogenic DI 2. 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)
33
Major causes of hypokalemia - renal - GI
A. Renal 1. Loop and DCT Diuretics (Thiazides) 2. Aldosterone Excess 3. Osmotic Diuresis 4. Renal Tubular Acidosis B. Gut 1. Severe Diarrhea (and often Metabolic acidemia) 2. Vomiting and Metabolic Alkalemia
34
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)
35
Tx for hyperkalemia?
Calcium - to balance potential Glucose + insulin to get rid of the excess K HCO3- if acidotic
36
2 ways bicarb is reabsorbed
Na/H exchange in PCT Cl/HCO3 exchange in collecting duct - pendrin transporter - stimulated by low Cl -> metabolic alkalosis
37
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
38
Normal anion gap?
6-14
39
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
40
2 cause of maintenance of metabolic alkalemia
1. Cl Depletion -Vomiting – loss of HCl -Nasogastric aspiration -Diuretics inhibiting NaCl reabsorption (thiazides, loop diuretics-relative to plasma levels these cause more Cl depletion) 2. 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
41
How to calc arterial blood pH
pH = 6.1 + log [HCO3-]/(0.03PCO2)
42
Expected compensations 1. Metabolic acidemia 2. Metabolic alkalemia 3. Chronic resp acidosis 4. Chronic resp alk
1. HCO3 drop by 10 -> pCO2 drop by 12 2. HCO3 up by 10 -> pCO2 up by 6 3. pCO2 up by 10 -> HCO3 up by 4 4. pCO2 up by 10 -> HCO3 down by 4
43
If serum HCO3 is normal and if both pCO2 and pH are abnormal a (blank) disturbance is present
MIXED
44
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
45
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
46
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)
47
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
48
Equation of calculating proton nanoequivalents
H+ = (24 x pCO2/HCO3-) pH of 7.4 = 40 nanoEq
49
List clearances of major solutes
PAH, penicillin > creatinine > inulin > urea > K+ (diet dependent) > Cl-, Na+ > HCO3-, glucose, amino acids, proteins
50
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

Renal-Pulm (9 decks)

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