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ABIM 2015 > ABIM 2015 - Nephro > Flashcards

ABIM 2015 - Nephro Flashcards

1
Q

GFR is used to assess KIDNEY FUNCTION and SERUM Cr, to ESTIMATE the GFR. What happens to the Cr when the GFR is REDUCED by 50%?

A

It DOUBLES (so a GFR of 60 that drops to 30 will make a Cr that is 1.0 increase to 2.0)

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2
Q

What is the SERUM Cr expected to do in the setting of NEPHROTIC syndrome?

A

DECREASE ( due to tubular over secretion) and thus not well correlated with kidney function or GFR estimation

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3
Q

What effect do CIMETIDINE and TMP (TMP-SMX) have on SERUM Cr?

A

INCREASE it without any change in the GFR

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4
Q

Muscle wasting, Protein malnutrition, Cirrhosis, Poor kidney perfusion, GI BLEED, meds all AFFECT these COMMONLY-used renal laboratory markers WITHOUT any actual changes in KIDNEY FUNCTION?

A

BUN and Cr

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5
Q

In extremes of HEIGHT and WEIGHT, PREGNANCY, patients who have had AMPUTATIONS, or CIRRHOSIS should have their GFR measured how?

A

Based of 24 HOUR URINE collection

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6
Q

What test measures the GFR very precisely?

A

Radionuclide Kidney Clearance Scanning

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7
Q

What GFR estimation do MOST labs use and is the BEST estimation of GFR in CHRONIC KIDNEY DISEASE (CKD)?

A

MDRD equation and they report HIGH GFR levels as >60 mL/min

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8
Q

How is a PROPER urine sample obtained?

A

Clean Catch, Mid-stream or via Bladder Catheterization and EXAMINED within 1 HOUR of collection

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9
Q

This measurement of urine is a ratio of the weight of urine to an equal quantity of water and an indication of the kidney’s ability to maximally dilute or concentrate the urine?

A

SPECIFIC GRAVITY

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10
Q

A specific gravity of urine of 1.005 is? If 1.030?

A

SG - 1.005 is DILUTE (close to water)

SG - 1.030 is CONCENTRATED “dehydrated’

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11
Q

High protein diets result in consumption of a high “ACID-ash” content and the need for the kidneys to excrete the acid load making the urine more ACIDIC (pH 5.0 - 6.0), conversely, a STRICT VEGETARIAN diet results in a more alkaline urine with a pH of ≥7.0. What infections and condition causes an ALKALINE urine?

A

Distal RTA, PROTEUS and PSEUDOMONAS

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12
Q

High-alkaline urine (as in vegetarian diets) result in what false-positive component result on a urine DIP STICK?

A

False HIGH-PROTEIN (albumin) level

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13
Q

When the urine DIP STICK test is NEGATIVE for protein (albumin) but there is suspicion for MULTIPLE MYELOMA, what test can be done on the urine to evaluate for the presence of LIGHT-CHAINS?

A

SULFOSALICYLIC ACID (SSA)

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14
Q

What is the BEST estimate of GFR in PREGNANT WOMEN, EXTREMES of AGE/WEIGHT, AMPUTEES and CIRRHOSIS?

A

Cr Clearance

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15
Q

When does glucose spill into the urine and is therefore detected on urine DIP STICK?

A

When serum glucose >180 mg/dL OR in PROXIMAL RTA

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16
Q

ONE of these THREE (3) substances is detected on the urine DIP STICK when there is DKA, SALICYLATE TOXICITY, ISOPROPYL ALCOHOL POISONING, STARVATION, however, the OTHER TWO (2) are NOT detected (such as in ALCOHOLICS), why?

A

KETONES (acetoacetate)
Because alcoholics with ketoacidosis make β-hydroxybutyrate which is NOT detectable on urine DIP STICK, neither is acetone (the three ketoacids)

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17
Q

What TWO (2) commonly used drugs can result in FALSE-POSITIVE results for KETONES?

A

CAPTOPRIL and LEVODOPA

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18
Q

How many RBC’s/hpf are required to result in a POSITIVE urine DIP STICK for BLOOD?

A

1-3 (detects BOTH free Hb and RBC’s)

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19
Q

What can RIFAMPIN, CHLOROQUINE and MYOGLOBIN and INTRAVASCULAR HEMOLYSIS do to the urine DIP STICK?

A

Cause FALSE-POSITIVE BLOOD readings

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20
Q

What does Vitamin C (ascorbic acid) do to the urine DIP STICK?

A

It can cause FALSE-NEGATIVE results for RBC and BILIRUBIN detection

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21
Q

Can the urine DIP STICK be used to confirm MYOGLOBINURIA in patients with RHABDOMYOLYSIS?

A

NO! (have to use separate urine MYOGLOBIN test)

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22
Q

What cells contain the enzyme LEUKOCYTE ESTERASE and how many of them are needed to have the urine DIP STICK result POSITIVE for this?

A

LEUKOCYTES, 3/hpf

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23
Q

How are Gm NEG bacteria such as E.coli, Klebsiella, Proteus and Pseudomonas detected on urine DIP STICK?

A

By the presence of NITRITES (conversion of nitrates by the bacteria)

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24
Q

A UTI with what bacteria can result in FALSE NEGATIVE values on urine DIP STICK for NITRITES?

A

Gm POS bacteria like ENTEROCOCCUS

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25
Q

What is suggestive of the presence of BOTH urine NITRITES and LEUKOCYTE ESTERASE on urine DIP STICK? What about the ABSENCE of BOTH?

A

PRESENCE of BOTH - positive for UTI

ABSENCE of BOTH - negative for UTI

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26
Q

What does the presence of CONJUGATED (direct) BILIRUBIN in the urine suggest?

A

SEVERE LIVER disease or OBSTRUCTIVE JAUNDICE (colors the urine DARK like “coca cola” or “tea”)

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27
Q

Why is UNCONJUGATED bilirubin called “INDIRECT”?

A

Because it comes from the breakdown of RBC’s by the spleen and is BOUND to ALBUMIN for transport to the liver for conjugation, and note readily soluble in water without breaking the albumin-bilirubin bond, thus called “indirect.”

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28
Q

What drug causes FALSE POSITIVE results for the PRESENCE of BILIRUBIN on the urine DIP STICK?

A

CHLORPROMAZINE

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29
Q

What does a POSITIVE urine DIP STICK result for UROBILINOGEN mean?

A

Hemolytic Anemia or Hepatic Necrosis, NOT OBSTRUCTION

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30
Q

How many WBC’s in the urine are suggestive of PYURIA?

A

> 4 WBC’s/hpf

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31
Q

PYURIA in the urine (>4 WBC’s/hpf) usually suggests a UTI. When the PYURIA is STERILE (negative urine culture), what INFECTION can cause STERILE PYURIA?

A

TB

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32
Q

Acute Interstitial Nephritis (AIN) - typically caused by ANTIBIOTICS, NSAIDS and PPI’s, ACUTE kidney TRANSPLANT REJECTION and kidney STONES can all cause what type of PYURIA?

A

STERILE (not associated with UTI)

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33
Q

What drugs can typically cause Acute Interstitial Nephritis (AIN) which presents with some BLOOD and RBC CASTS?

A

Antibiotics, NSAIDS, PPI’s

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34
Q

The finding of these cells in the urine suggests an ALLERGIC reaction, ATHEROEMBOLIC disease, RPGN, SMALL-VESSEL VASCULITIS, PROSTATE disease or a PARASITIC INFECTION?

A

EOSINOPHILS

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35
Q

What can cause ISOMORPHIC (same size/shape) RBC’s in the urine?

A

GU tract TUMOR, STONE or INFECTION

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36
Q

What can cause DYSMORPHIC (varying sizes, shapes) RBC’s in the urine?

A

pH/Osmolality shifts

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37
Q

When ACANTHOCYTES (oddly/abnormally-shaped RBC’s) are found in the urine, this suggests?

A

glomeruloNEPHRITIS, SEVERE INTERSTITIAL NEPHRITIS and ACUTE TUBULAR NECROSIS (ATN) - acathocytes and RBC casts

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38
Q

What is the BASIC matrix of ALL urine CASTS (which are formed in the TUBULES and therefore cylindrical)?

A

Tamm-Horsfall mucoprotein also called HYALINE

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39
Q

What condition can cause HYALINE CASTS (made up of only the Tamm-Horsefall mucoprotein alone) in the urine?

A

HYPOVOLEMIA causing POOR KIDNEY PERFUSION

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40
Q

What are the TYPICAL CRYSTALS seen in the urine?

A

CA-OXALATE, CA-PHOSPHATE, URIC ACID, STRUVITE

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41
Q

A NORMAL urine SPECIFIC GRAVITY of 1.010 is related to a NORMAL (ISOSMOTIC) urine OSMOLALITY of?

A

300 (Same as Serum “isosmolar”)

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42
Q

A LOW urine SPECIFIC GRAVITY of 1.002 (close to water at 1.000) is related to a LOW (MAXIMALLY DILUTED) urine OSMOLALITY of?

A

50-100 (Maximally Diluted)

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43
Q

A HIGH urine SPECIFIC GRAVITY of 1.030 is related to a HIGH (MAXIMALLY CONCENTRATED) urine OSMOLALITY of?

A

1200 (Maximally Concentrated)

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44
Q

When there is kidney TUBULAR INJURY, this leads to the deposition of PIGMENTED tubular debris in the Tamm-Horsefall mucoprotein matrix or “HYALINE” forming pigmented-granular casts called what?

A

MUDDY-BROWN casts

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45
Q

Patients with glomeruloNEPHRITIS will have what type of TUBULAR CASTS?

A

ERYTHROCYTE (RBC) casts

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46
Q

In patients with tubulointerstitial inflammation of the kidney, including PYELONEPHRITIS, what types of TUBULAR CASTS are found?

A

LEUKOCYTE (WBC) casts

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47
Q

How is the daily amount of URINE PROTEIN (albumin) excreted measured?

A

By the urine PROTEIN-CREATININE ratio

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48
Q
  1. What is considered a NORMAL urine TOTAL protein excretion? 2. What is considered NEPHROTIC-RANGE proteinuria for TOTAL protein?
A
  1. NORMAL -
    SPOT-TEST: NONE to “TRACE” or “5-20 mg/dL” on DIP STICK (or 30 mg/dL on DIP STICK (or >0.2 mg/mg PROTEIN:Cr ratio)
    24-HOUR TEST: >300 mg/24h
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49
Q
  1. What is considered a NORMAL RANDOM urine PROTEIN:Cr RATIO? 2. NEPHROTIC RANGE?
A
  1. 3.5 mg/mg is nephrotic range (random urine PROTEIN:Cr ratio)
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50
Q

To make a DIAGNOSIS of PROTEINURIA, what is REQUIRED?

A

Collection of TWO (2) abnormal SAMPLES on TWO (2) DIFFERENT DAYS

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51
Q

How should urine be FURTHER tested if proteins found are IMMUNOGLOBULINS?

A

IMMUNOFIXATION (to determine which immunoglobulins)

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52
Q

What proteins BESIDES the DIP-STICK DETECTED ALBUMIN can be found in URINE and MUST be tested for by using SULFOSALICYLIC ACID (SSA) test?

A

Kidney-Derived Low Molecular Weight proteins, Immunoglobulins, Light-Chains, Myoglobin, Hb

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53
Q

If additional proteins in a urine SULFOSALICYLIC ACID (SSA) test are found to be Low-Molecular Weight proteins (kidney-derived), where is the associated disease anatomically?

A

Tubulointerstitial (within the TUBULES)

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54
Q

If the majority of the protein in PROTEINURIA is found to be ALBUMIN, where is the associated disease anatomically?

A

GLOMERULUS

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55
Q

When must the PROTEIN:Cr RATIO be measured for DM-I and DM-II patients in order to AVOID KIDNEY DISEASE?

A

DM-I: 5-YEARS after diagnosis

DM-II: AT TIME of DIAGNOSIS

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56
Q

A urine PROTEIN (alb):Cr RATIO of what is considered MICROALBUMINURIA when POSITIVE on 2 of 3 RANDOM samples obtained over 6 MONTHS which suggests HIGH-RISK for kidney and cardiovascular disease?

A

Urine Alb:Cr ratio of 30 - 300 mg/g (DM, HTN)

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57
Q

What MEDICATION DELAYS progression of KIDNEY DISEASE in patients with DM and MICROALBUMINURIA?

A

ACE-I and ARB’s

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58
Q

When PROTEINURIA is TRANSIENT (values not repeated on random tests), it is BENIGN and can be seen in what situations?

A

FEBRILE ILLNESS, RIGOROUS EXERCISE or in YOUNG patients

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59
Q

What is the BENIGN CONDITION called when YOUNG patients (

A

ORTHOSTATIC PROTEINURIA (BENIGN CONDITION) - obtain a “split urine collection”

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60
Q

What is the SHAPE of Ca-OXALATE crystals in the URINE?

A

ENVELOPE (but can also see dumbbell/needle and are associated with HYPERCALCIURIA, HYPEROXALURIA, Ca-OXALATE STONES and ETHYLENE-GLYCOL “antifreeze” poisoning)

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61
Q

What is the SHAPE of Ca-PHOSPHATE crystals in the URINE?

A

PRISM (can also see needle) and are associated with DISTAL RTA, ALKALINE pH >6.5 and TUMOR LYSIS SYNDROME

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62
Q

What is the SHAPE of URIC ACID crystals in the URINE?

A

RHOMBOID (can also see needle) and are associated with DM, OBESITY, GOUT, TUMOR LYSIS SYNDROME and an ACIDIC pH

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63
Q

What is the SHAPE of Mg-Ammonium-Phosphate “STRUVITE” crystals in the URINE?

A

COFFIN-LID and are associated with CHRONIC UTI’s with urease-producing bacteria

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64
Q

What is the SHAPE of CYSTINE crystals in the URINE?

A

HEXAGONAL and are associated with CYSTINURIA

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65
Q

A SPOT ALBUMIN-SPECIFIC DIP-STICK TEST(not 24h) for urine ALBUMIN of what is considered normal?

A

.

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66
Q

What is the most COMMON cause of HEMATURIA (>3 RBC’s/hpf on urine DIP STICK)?

A

UTI’s and Kidney STONES

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67
Q

For OLDER patients (>40) AND those with RISK factors, what should be done after a SINGLE episode of HEMATURIA?

A

FULL evaluation of the UPPER and LOWER GU tract (if

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68
Q

What is GROSS hematuria most COMMONLY associated with?

A

MALIGNANCY (if RED - urinary tract, if BROWN/TEA-colored - glomeruloNEPHRITIS)

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69
Q

What are the RISK factors for URINARY BLADDER CANCER?

A

SMOKING, MALE, AGE >40, GROSS HEMATURIA, PELVIC RADIATION, CYCLOPHOSPHAMIDE, Occupational Exposures (benzines, aromatic amines - Fuel Refineries, Rubber, Textile, Dyes)

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70
Q

A MALE SMOKER AGED >40 p/w ISOMORPHIC HEMATURIA (same size and shape RBC’s), what should be done next?

A

HIGH-RISK: do CYSTOSCOPY and UPPER GU tract IMAGING (CT-urography if GFR ≥60; MR-urography if GFR 30-60 mL/min) as well as CYTOLOGY

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71
Q

A MALE SMOKER AGED >40 p/w DYSMORPHIC HEMATURIA (different size and shape RBC’s) and ACANTHOCYTES, RBC CASTS, PROTEINURIA what should be done next?

A

Kidney US and Nephrology CONSULT for possible BIOPSY

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72
Q

What GU tract imaging is RECOMMENDED for young patients (

A

US (CT if very OBESE)

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73
Q

What is a NON-CONTRAST, HELICAL CT-abd/pelv scan used to diagnose when a patient presents with microscopic hematuria ± pain?

A

NEPHROLITHIASIS

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74
Q

AFTER a NEGATIVE UPPER GU tract evaluation by imaging in a patient with HEMATURIA, what is the PREFERRED method of evaluating the LOWER GU tract?

A

CYSTOSCOPY

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75
Q

Why is MR-urography for evaluation of the UPPER GU tract contraindicated in patients with a GFR

A

Because it uses GADOLINIUM contrast (NEPHROGENIC SYSTEMIC FIBROSIS)

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76
Q

What should be done if a patient is found to have HEMATURIA but also has an UNDERLYING bleeding condition or is on ANTICOAGULATION?

A

EVALUATE as if no underlying bleeding condition or anticoagulation

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77
Q

What is the FIRST imaging study that should be used to image the UPPER GU tract when looking for OBSTRUCTION, CYSTS, MASSES, Kidney Size and Cortical Thickness? Renal Artery Stenosis?

A 
US
Doppler US (for renal artery stenosis)
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78
Q

What GFR value is REQUIRED for patients to undergo CT-urography (for evaluation of the UPPER GU tract for hematuria, etc.)?

A

GFR ≥60 (normal)

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79
Q

When is RADIONUCLIDE Kidney Clearance Scanning done to EXTREMELY ACCURATELY determine the GFR keeping in mind that this test is VERY EXPENSIVE?

A

Evaluation of PERFUSION/FUNCTION of TRANSPLANTED KIDNEYS and PRIOR to NEPHRECTOMY, ASSESSMENT of functional significance of RENOVASCULAR disease and functional significance of HYDRONEPHROSIS in obstructed patient

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80
Q

What should be done in a patient in whom GLOMERULAR disease is suspected (nephRITIC, nephROTIC syndrome, acute kidney injury of unknown cause and kidney TRANSPLANT dysfunction)?

A

US or CT-guided BIOPSY!!

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81
Q

BLEEDING condition, ACTIVE GU infection, HYDRONEPHROSIS, ATROPHIC kidneys and UNCONTROLLED HTN are CONTRAINDICATIONS to what TEST for kidney disease?

A

BIOPSY

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82
Q

What complication, BESIDES PAIN, can COMMONLY be seen after KIDNEY BIOPSY?

A

HEMATURIA that can result in obstruction (clots) or requiring a transfussion

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83
Q

What is the OSMOLALITY (# of osmoles of substance - compounds, anions, cations, etc. per L of plasma) of PLAMA determined by?

A

Concentration of SODIUM (a cation “+”) and its ANIONS (-) “Cl, HCO3, etc.” GLUCOSE and BUN

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84
Q

The DIFFERENCE between the MEASURED and CALCULATED plasma osmolality is called what?

A

SERUM OSMOLAL GAP

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85
Q

What is considered an ELEVATED Serum (plasma) Osmolal GAP and what is it due to?

A

> 10 mosm/Kg H2O

Due to the presence of UNMEASURED solutes that were not accounted for when subtracted from the CALCULATED osmolality

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86
Q

What is considered NORMAL serum (plasma) osmolality, which is TIGHTLY regulated to maintain a CONSTANT INTRAcellular volume?

A

275-295 mosm/Kg H2O

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87
Q

What part of the BODY contains OSMORECEPTORS which SENSE changes in SERUM (plasma) osmolality?

A

HYPOTHALAMUS

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88
Q

What does the HYPOTHALAMUS do when it SENSES >1-2% INCREASE in SERUM (plasma) osmolality?

A

It triggers the release of ANTI-DIURETIC HORMONE (ADH) or “VASOPRESSIN” by the POSTERIOR PITUITARY, causing the renal COLLECTING DUCTS (last portion of the tubule system of the nephron) to REABSORB WATER and NOT EXCRETE it as it would otherwise)

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89
Q

When does PHYSIOLOGIC release of ANTI-DIURETIC HORMONE (ADH) or “VASOPRESSIN” occur by the POSTERIOR PITUITARY?

A

During HYPOVOLEMIA

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90
Q

When does does NON-PHYSIOLOGIC release of ANTI-DIURETIC HORMONE (ADH) or “VASOPRESSIN” occur by the POSTERIOR PITUITARY or BY TUMORS?

A

In the condition known as Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

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91
Q

What is it called when the SERUM SODIUM concentration is

A

HYPONATREMIA (can occur with increased, normal or decreased plasma osmolality)

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92
Q

In patients with HYPERGLOBULINEMIA or SEVERE HYPERLIPIDEMIA (usually visible in test tube), the SODIUM may be

A

PSEUDO-HYPOnatremia (not a true low sodium, but rather the presence of other solutes or “osmoles” in the serum causing an apparent “dilutional effect” on the amount of SODIUM which did not change, thus would have an INCREASED OSMOLAL GAP because these osmoles were not measured)

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93
Q

The relationship between the CONCENTRATION of SOLUTES (substances dissolved in EXTRAcellular fluid and INTRAcellular fluid) on EITHER SIDE of the CELL MEMBRANES is called what?

A

TONICITY

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94
Q

This is the most COMMON form of HYPOnatremia and can occur in patients with NORMAL, INCREASED or DECREASED EXTRAcellular FLUID?

A

HYPOtonic HYPOnatremia

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95
Q

What is the USUAL measured PLASMA OSMOLALITY in a patient with HYPOtonic HYPOnatremia?

A

LOW (however, it can be NORMAL or INCREASED if BUN, GLUCOSE or an exogenous solute like ALCOHOL is present)

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96
Q

What is HYPERtonic HYPOnatremia caused by?

A

SIGNIFICANT HYPERGLYCEMIA (elevated GLUCOSE) or exogenously administered solutes like MANNITOL or SUCROSE - because the presence of these EXTRA solutes in the plasma or “extracellular fluid” causes that fluid compartment to have a HIGHER concentration than the INTRAcellular fluid and therefore INTRAcellular fluid diffuses into the EXTRAcellular fluid compartment to equilibrate the concentration thus effectively DILUTING the SODIUM concentration there

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97
Q

HOW does the presence of HYPERGLYCEMIA affect WATER movement across CELL MEMBRANES?

A

It forces water OUT of the CELLS (lower solute concentration) in order to equilibrate the now higher concentration of solute in the EXTRAcellular fluid

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98
Q

What FLUID compartment is referred to when discussing TONICITY and hypo/hyper NATREMIA?

A

THE PLASMA or EXTRAcellular FLUID (anything that ends in “emia” is referring to the BLOOD (of which PLASMA is the greatest component)

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99
Q

When is ISOSMOTIC HYPOnatremia seen?

A

When ≥2 disorders are present simultaneously (ie, when a patient with HYPOnatremia due to SIADH develops HYPERglycemia having a NORMAL plasma osmolality as the INCREASE in osmolality resulting from the INCREASED GLUCOSE counterbalances the initial DECREASED osmolality caused by the SIADH - associated water retention

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100
Q

What is meant by ISOSMOTIC?

A

When two solutions (EXTRAcellular fluid and INTRAcellular fluid) have same number of solutes - therefore NO MOVEMENT of water (the solvent) exists

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101
Q

What is meant by ISOTONIC?

A

When a solution has the SAME CONCENTRATION as the blood (serum)

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102
Q

When the OSMOLALITY is increased, what does this MEAN?

A

It means that the CONCENTRATION of the solution (serum) has INCREASED due to the presence of increased OSMOLES

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103
Q

In the setting of elevated CHOLESTEROL, TRIGLYCERIDES or TOTAL SERUM PROTEIN with concomitant HYPOnatremia, what is the cause of HYPOnatremia?

A

PSEUDO-HYPOnatremia (caused by the presence of the unmeasured osmoles (lipids, protein) that cause a FLUID SHIFT from the INTRAcellular space to the EXTRAcellular space thus causing a DILUTIONAL effect. These osmoles are unaccounted for when the Plasma Osmolality lab value is measured which ONLY takes into account GLUCOSE, BUN and Na

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104
Q

How can the PLASMA SODIUM concentration be measured more accurately in cases of HYPO/HYPERnatremia?

A

By ABG

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105
Q

What patients have HYPOtonic HYPOnatremia with an APPROPRIATELY LOW Urine Osmolality (

A

Those with PRIMARY POLYDIPSIA “psychogenic” (because water EXCRETION by the kidney is partly SOLUTE-dependent, severely limiting solute intake also decrease water excretion thus causing HYPOnatremia with even SMALL increases in fluid intake - seen in patients with CHRONIC ALCOHOL ABUSE (mostly water) and LOW-SOLUTE intake (malnourished)

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106
Q

What patients have HYPOtonic HYPOnatremia with an INAPPROPRIATELY HIGH Urine Osmolality (>100 mosm/kg H2O in the setting of hypotonic hypernatremia)?

A

Those that have a NON-OSMOTIC ADH-secretion due to TRUE HYPOvolemia, DECREASED ARTERIAL BLOOD VOLUME or NON-PHYSIOLOGIC ADH release resulting in INCREASED total body water and EXTRAcellular FLUID volume (SIADH)

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107
Q

What is the typical Urine Na concentration in patients with SIADH (where the ADH secretion is not physiologic but abnormal)?

A

Urine Na >40 meq/L because there is increased EXTRAcellular FLUID volume and PHYSIOLOGICALLY, to decrease this volume, Na has to be EXCRETED

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108
Q

What is the typical Urine Na in patients with HYPOnatremia due to NON-OSMOTIC ADH secretion that IS PHYSIOLOGIC such as in TRUE HYPOvolemia (such as blood loss or HF, Nephrotic Syndrome or Cirrhosis)?

A

Urine Na

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109
Q

Condition in which the Urine Na (ie excreted Na) is >40 meq/L (high), FEna (fractional excretion of Na) “the % of Na that is filtered by the kidney and EXCRETED in the urine” >1% and BUN

A

SIADH

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110
Q

What is the FEna (fractional excretion of Na) - “the % of Na that is filtered by the kidney and EXCRETED in the urine” used for?

A
  1. If FEna is 2%, the problem is RENAL where either excess sodium is lost due to tubular damage, or the damaged glomeruli result in hypervolemia (they do not filter sufficient amounts of blood) resulting in the normal response of sodium wasting by the functioning glomeruli
  2. If the FEna is INTERMEDIATE (1-2%) the problem is POST-RENAL as in renal tract obstruction, where the value is lower in early disease, but with kidney damage from the obstruction, the value becomes higher
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111
Q

Condition in which Urine Na (ie excreted Na) is 15 mg/dL?

A

HYPOvolemia (kidney is HOLDING onto Na)

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112
Q

Hemorrhage, Cancers, 3,4-Methylenedioxymethamphetamine (ecstasy), COX-2 inhibitors, NSAIDS, Desmopressin (vasopressin), Opiates, SSRI’s/SNRI’s, endurance exercise, HIV, Rocky Mountain Spotted Fever, Anesthesia, Infections, Positive Pressure Mechanical Ventilation (NPPV - non-invasive positive pressure ventilation), SCLC (small cell lung CA) can all cause what renal syndrome?

A

SIADH

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113
Q

POST-OP administration of HYPOtonic fluids, THIAZIDE diuretics (chlorthalidone/hctz), use of ecstasy (3,4-Methylenedioxymethe..), OVERHYDRATION associated with extreme exercise and PRIMARY POLYDIPSIA “psychogenic” can result in ACUTE what with what consequences?

A

ACUTE HYPOnatremia - increased neuronal cell volume (BRAIN SWELLING) - “cerebral edema”

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114
Q

What occurs when the SERUM Na level DECREASES QUICKLY by more than 10 meq/L (ie 135 to 125 meq/L) over 1-3 days?

A

ACUTE HYPOnatremia with CEREBRAL EDEMA (high-mortality) with SEIZURES, OBTUNDATION, COMA, RESPIRATORY ARREST

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115
Q

What occurs when the SERUM Na level DECREASES by more than 10 meq/L (ie 135 to 125 meq/L) in a course of >3 days?

A

CHRONIC HYPOnatemia, no cerebral edema

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116
Q

What occurs when HYPOnatremia is OVERLY-RAPIDLY corrected?

A

OSMOTIC Demyelination Syndrome (high-mortality)

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117
Q

What type of symptoms do patients with CHRONIC HYPOnatremia (125-135 meq/L) present with?

A

SUBTLE - falls, hip fractures, osteoporosis

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118
Q

When patients have SYMPTOMATIC HYPOnatremia (cerebral edema, seizures, AMS, coma) or due to SIADH, what should be the treatment?

A

HYPERtonic SALINE (3%)

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119
Q

When patients have HYPOnatremia due to TRUE HYPOvolemia, what should be their treatment?

A

NORMAL SALINE (0.9%)

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120
Q

When SHOUD treatment with SALINE be stopped for HYPOnatremia?

A

When SYMPTPOMS resolve and serum Na correction should NOT EXCEED 10 meq/L in the FIRST 24 HOURS or 18 meq/L in the FIRST 48 HOURS while monitoring serum Na level every 2-4 hours

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121
Q

How is ACUTE HYPOtonic HYPOnatremia with SYMPTOMS of SEIZURES or COMA?

A

100 mL BOLUS of 3% SALINE (or 2 mL/kg) repeated up to TWO (2) times while monitoring serum Na level every 2-4 hours

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122
Q

Patients with SYMPTOMATIC SIADH and HIGHLY concentrated urine (

A

With 3% SALINE

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123
Q

While correcting HYPOnatremia in a patient with SYMPTOMATIC SIADH and HIGHLY concentrated urine (>750 mosm/kg H2O) with the appropriate 3% SALINE, the patient begins having WATER diuresis and begins correcting their HYPOnatremia too quickly, what can be done BESIDES STOPPING THE 3% SALINE infusion?

A

Give D5W (5% dextrose in water) or DESMOPRESSIN

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124
Q

Irreversible neurologic deficits such as PROGRESSIVE QUADRIPARESIS, SPEECH/SWALLOWING disorders, COMA, LOCKED-IN Syndrome while CORRECTING HYPOnatremia are associated with?

A

Osmotic Demyelination Syndrome caused by OVER-CORRECTION (or too rapid) of HYPOnatremia (>10 meq/L/24 HOURS or >18 meq/L/48 HOURS)

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125
Q

How are patients with ASYMPTOMATIC HYPOtonic HYPOnatremia (due to SIADH, HYPERvolemic HYPOnatremia or otherwise) treated?

A

WATER RESTRICTION (TOTAL INTAKE - both PO and IV, MUST be LESS than TOTAL OUTPUT), D/C offending drugs, Give DIURETICS (furosemide), Demeclocycline, Vasopressin Receptor Antagonists (-“vaptan”) and ensure adequate SOLUTE intake (nutrition)

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126
Q

HOW is HYPOtonic HYPOnatremia treated when the CAUSE is HYPERglycemia (called “pseudohyponatremia”)?

A

By the treatment of the HYPERglycemia with INSULIN, the SODIUM will correct by itself as water moves BACK into the INTRAcellular compartment following the GLUCOSE pushed there by insulin

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127
Q

HOW is HYPOtonic HYPOnatremia treated when the CAUSE is HYPERlipideia or HYPERproteinemia (called “pseudohyponatremia”)?

A

By the treatment of the UNDERLYING HYPERlipideia or HYPERproteinemia, the SODIUM will correct by itself as water moves BACK into the INTRAcellular compartment f

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128
Q

Although CORRECTING the SODIUM in a patient with SYMPTOMATIC HYPOnatremia (COMA, AMS, Cerebral Edema, Seizures) with 3% SALINE by NO MORE than 10 meq/L/24 HOURS or NO MORE than 18 meq/L/48 HOURS, RAPIDLY increasing the SODIUM concentration by WHAT range over the FIRST 24 HOURS is SUFFICIENT?

A

4-6 meq/L

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129
Q

Commonly seen in CRITICALLY-ILL patients, serum Na levels >145 meq/L are called what?

A

HYPERnatremia (high-morbidity and mortality)

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130
Q

How do you treat a patient with ASYMPTOMATIC HYPERvolemic HYPOnatremia (CHF, Cirrhosis, Nephrotic Syndrome)?

A

Treat UNDERLYING cause, RESTRICT BOTH Na and Fluids, Give DIURETICS (furosemide) and Vasopressin Receptor Antagonists (-“vaptan”)

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131
Q

What is the most COMMON cause of HYPERnatremia?

A

FAILURE to adequately replace water loss (elderly & infants, HYPOTHALAMIC lesions)

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132
Q

Urinary/GI fluid losses, Diuretic therapy and Osmotic diuresis WITHOUT adequate FLUID replacement can result in what condition?

A

HYPERnatremia

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133
Q

What is the cause of CENTRAL Diabetes Insipidus (DI) - Langerhans Cell Histiocytosis, Neurosurgery, Trauma, Sarcoidosis, Wegener Granulomatosis, Malignancy, Anorexia?

A

DECREASED release of ADH by the POSTERIOR PITUITARY

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134
Q

What is the cause of NEPHROGENIC Diabetes Insipidus (DI) - LITHIUM, foscarnet, amphotericin B, HYPERcalcemia?

A

Partial or Complete RESISTANCE of the KIDNEY to the effects of ADH

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135
Q

When PREGNANT women get Diabetes Insipidus (DI), during their pregnancy, it is most likely due to what condition?

A

GESTATIONAL DI, caused by circulating placental VASOPRESSINASE (enzyme that breaks down vasopressin causing water wasting)

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136
Q

What is ADIPSIC Diabetes Insipidus?

A

When a lesion affects BOTH the POSTERIOR PITUITARY gland and the HYPOTHALAMIC THIRST CENTER - sarcoidosis - thereby not only resulting in INADEQUATE ADH release, but also failing to trigger THIRST resulting in SEVERE HYPERnatremia

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137
Q

When a patient’s URINE VOLUME is >3 L/24 HOURS, what is that called? What does it cause?

A

POLYURIA, causing HYPERnatremia (except for in PRIMARY POLYDIPSIA “psychogenic” where HYPOnatremia is seen because pt just keeps drinking water) and OSMOTIC Diuresis

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138
Q

ABRUPT-ONSET Polyuria is most likely caused by?

A

CENTRAL Diabetes Insipidus (DI)

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139
Q

What is NORMAL urine OSMOLALITY?

A

300 mosm/kg H2O

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140
Q

OSMOTIC DIURESIS, occurs when substances that CANNOT be RE-ABSORBED by the KIDNEYS such as GLUCOSE (HYPERglecemia seen in DM) pass through the renal tubules and take water out with them. Urine OSMOLALITY during OSMOTIC diuresis is what?

A

NORMAL, 300 mosm/kg H2O

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141
Q

What is the URINE OSMOLALITY in patients with PRIMARY POLYDIPSIA and Diabetes Insipidus (DI)?

A

.

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142
Q

What is the TYPICAL SERUM Na concentration in PRIMARY POLYDIPSIA? What about in CENTRAL Diabetes Insipidus (DI)?

A

PRIMARY Polydipsia 142 meq/L - “HYPERnatremia”

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143
Q

Because PRIMARY POLYDIPSIA is a PSYCHIATRIC disorder and NOTHING is wrong with the POSTERIOR PITUITARY or KIDNEYS, what happens to the URINE OSMOLALITY during a WATER DEPRIVATION test?

A

Urine CONCENTRATES appropriately to >600 mosm/kg H2O

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144
Q

Because CENTRAL Diabetes Insipidus (DI) is a POSTERIOR PITUITARY disorder but NOTHING is wrong with the KIDNEYS, what happens to the URINE OSMOLALITY during a WATER DEPRIVATION test?

A

Urine FAILS to CONCENTRATE (inadequate or NO ADH release) and remains at 600 mosm/kg H2O (the same response to given desmopressin occurs with GESTATIONAL Diabetes Insipidus as well, which is caused by circulating placental vasopressinase enzymes that break down adequately-released vasopressin or “ADH” but cannot break down desmopressin)

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145
Q

Because NEPHROGENIC Diabetes Insipidus (DI) is an ADH-RECEPTOR DISORDER in the RENAL TUBULES of the KIDNEY, but NOTHING is wrong with the POSTERIOR PITUITARY, what happens to the URINE OSMOLALITY during a WATER DEPRIVATION test?

A

Urine FAILS to CONCENTRATE (NO respone by the KIDNEY to normally-released ADH by the POSTERIOR PITUITARY) and remains at

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146
Q

In the ABSENCE of HYPOVOLEMIC SHOCK, how should CIRCULATORY COLLAPSE be treated FIRST to restore organ HYPOperfusion prior to treating HYPERnatremia caused by the HYPOvolemia?

A

With ENOUGH ISOTONIC (normal, 0.9%) SALINE to CORRECT ORGAN HYPOperfusion (shock), then CHANGE to D5W (5% dextrose) to CORRECT the HYPERnatremia based on CALCULATED WATER DEFICIT, DO NOT GIVE NS BOLUSES (can cause cerebral edema) and DO NOT CORRECT HYPERnatremia any faster than 10 meq/L/24 HOURS carefully monitoring SERUM Na Concentration every 2-4 HOURS during correction

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147
Q

Because NEPHROGENIC Diabetes Insipidus (DI) does NOT respond to DEMOPRESSIN, how do you treat it?

A

THIAZIDE Diuretics - chlorthalidone/hctz - (increase PROXIMAL TUBULE Na and water RE-ABSORPTION), NSAIDS, LOW Na, and LOW PROTEIN diet, D/C LITHIUM if possible

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148
Q

How is the RISK of LITHIUM-ASSOCIATED NEPHROGENIC Diabetes Insipidus (DI) or its PROGRESSION due to collecting duct toxicity) DECREASED?

A

By adding AMILORIDE (a potassium-sparing diuretic) which BLOCKS LITHIUM uptake in the collecting duct limiting toxicity

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149
Q

What effect can DIURETICS have on LITHIUM?

A

INCREASE SERUM levels because the resulting diuretic-induced HYPOvolemia causes PROXIMAL TUBULE RE-ABSORPTION of LITHIUM

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150
Q

Besides 3% SALINE, what are THREE (3) other HYPERtonic IV solutions?

A

D10W (10% dextrose in water), D51/2NS (5% dextrose in 0.45% saline) and D5NS (5% dextrose in 0.9% or “normal” saline)

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151
Q

What is considered HYPOkalemia and HYPERkalemia?

A

HYPOkalemia - serum K 5.0 meq/L

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152
Q

Cellular REDISTRIBUTION (pushed out of cells), KIDNEY or GI LOSSES and DECREASED INTAKE of this ELECTROLYTE manifest as MUSCLE WEAKNESS, CRAMPS, RHABDOMYOLYSIS (

A

K (HYPOkalemia)

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153
Q

What is the most COMMON cause of HYPOkalemia?

A

The use of DIURETICS

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154
Q

What effect does MARKED LEUKOCYTOSIS (C.diff infection, myeloproliferative disorders like CML) have on SERUM POTASSIUM?

A

DECREASES it because it is DRIVEN inside of cells (pseudoHYPOkalemia)

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155
Q

An ASIAN or MEXICAN with personal SYMPTOMS of and FAMILY h/o ACUTE EPISODIC MUSCLE WEAKNESS following a HIGH-CARBOHYDRATE meal or STRENUOUS EXERCISE that has been treated in the past with INTERFERON therapy or had THYROTOXICOSIS has what SYNDROME?

A

HYPOkalemic Periodic Paralysis

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156
Q

ALDOSTERONE, INCREASED TUBULAR FLOW to the Collecting Duct of the nephron resulting in Na delivery to this area, can cause what ELECTROLYTE over excretion and thus deficiency?

A

K (HYPOkalemia)

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157
Q

What happens to Kidney POTASSIUM EXCRETION in a patient who has increased GI LOSSES (violent VOMITING episodes - emesis)?

A

It is reduced to

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158
Q

What does it mean, in a HYPOkalemic patient, when their Urine POTASSIUM EXCRETION is >30 meq/L?

A

ONGOING URINE-POTASSIUM LOSSES

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159
Q

Why do you commonly see HYPOkalemia in patients with HTN?

A

Because in states of HTN, usually caused by ELEVATED RENIN-ALDOSTERONE, the ALDOSTERONE causes increased POTASSIUM EXCRETION and H¯ ion EXCRETION (acidifying urine)

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160
Q

HYPOkalemia usually occurs together with which ACID-BASE disorder?

A

METABOLIC ALKALOSIS (diuretics, vomiting, NGT suction, Mg deficiency)

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161
Q

Bartter and Gitelman syndromes are CONGENITAL disorders with THICK-ASCENDING LIMB of the LOOP of HENLE (Bartter - LOOP diuretics) and DISTAL CONVOLUTED TUBULE (Gitelman - THIAZIDE diuretics) abnormalities that result in what ACID-BASE DISORDER?

A

HYPOkalemic METABOLIC ALKALOSIS

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162
Q

What CONGENITAL syndrome that results in HYPOkalemic METABOLIC ALKALOSIS when LOOP DIURETICS (furosemide) are used, due to abnormalities in the THICK-ASCENDING LIMB of the LOOP of HENLE is MIMICKED by the CHRONIC use of AMINOGLYCOSIDE ANTIBIOTICS (amikacin, tobramycin, gentamycin, streptomycin?)

A

BARTTER Syndrome

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163
Q

What does a Urine K:Cr ratio >20 meq/L suggest, what about when its

A

Urine K:Cr ratio >20 meq/L - Kidney Potassium Wasting

Urine K:Cr ratio

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164
Q

How do you replete K in a patient with a LARGE K deficit with symptoms of SKELETAL and CARDIAC muscle dysfunction?

A
  • IV 40 meq/L of KCl at 20 meq/h WTHOUT addition of sodium bicarb or glucose initially (drives K into cells)
  • If less serious, can be given PO
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165
Q

What formulation of POTASSIUM should be used in patients with concomitant metabolic acidosis due to RTA?

A

Potassium Citrate

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166
Q

What ELECTROLYTE DEFICIENCY contributes GREATLY to HYPOkalemia and its correction can help urine POTASSIUM loss?

A

MAGNESIUM (Mg)

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167
Q

Decreased RENIN-ANGIOTENSIN-ALDOSTERONE activity (acute/chronic kidney disease), ASCENDING muscle weakness, paralysis, ARRHYTHMIAS with ECG changes (TALL, PEAKED T-waves, short QT, increased PR and QRS, small P waves, Bradycardia) are seen in what electrolyte disturbance?

A

HYPERkalemia

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168
Q

When ECG changes are noted in the setting of serum K >5.0 what must be done?

A

EMERGENCY THERAPY

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169
Q

What can happen to SERUM POTASSIUM if SEVERE LEUKOCYTOSIS (>120,000) or SEVERE THROMBOCYTOSIS (>600,000) occurs?

A

INTRAcellular POTASSIUM is released into the INTERcellular space causing pseudoHYPERkalemia

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170
Q

What electrolyte disturbance can be caused by MECHANICAL TRAUMA and CRUSH injuries due to extravasation from the INTERcellular compartment?

A

pseudoHYPERkalemia

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171
Q

Why does the Kidney EXCRETE POTASSIUM (K) in response to ALDOSTERONE released by the ADRENAL glands?

A

Because ALDOSTERONE causes INCREASED Na and WATER RE-ABSORPTION and K and H EXCRETION (Na-K pumps)

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172
Q

What patients can develope HYPERkalemia simply from DIETARY POTASSIUM intake?

A

Those with a DECREASED GFR

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173
Q

If HYPERkalemia occurs in a patient with a GFR >20 mL/min and the RENIN-ANGIOTENSIN-ALDOSTERONE system is normal, what could be the cause?

A

Defect in the POTASSIUM (K) SECRETION in the COLLECTING DUCT

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174
Q

Drugs that INTERFERE with POTASSIUM SECRETION by the COLLECTING DUCT thus cause or worsen HYPERkalemia are interfering with the RENIN-ANGIOTENSIN-ALDOSTERONE system (this happens with chronic DM and HIV as well, in the condition of HYPOreinemic - HYPOaldosteronism) and are especially seen in drug COMBINATIONS such as?

A

ACE-I/ARB’s + SPIRONOLACTONE in the setting of Chronic Kidney Disease (CKD)

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175
Q

What can cause INJURY to the COLLECTING DUCT of the nephron resulting in HYPERkalemia as the COLLECTING DUCT cannot PROPERLY SECRETE K into the urine?

A

Sickle Cell Nephropathy, Chronic Glomerulopathy, Urinary Obstruction

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176
Q

When a disease/drug/congenital syndrome results in DECREASED ALDOSTERONE production (adrenal insufficiency), this results in what electrolyte disturbance?

A

HYPERkalemia

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177
Q

What electrolyte disturbance is seen in patients with a URETERO-JEJUNOSTOMY (high cancer rate) due to the ABSORPTION of this electrolyte by the JEJUNUM which is excreted in the urine?

A

HYPERkalemia

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178
Q

How is SYMPTOMATIC HYPERkalemia (muscle and cardiac manifestations) treated?

A
  1. Stabilize membranes: IV CaCl or Ca-gluconate every 5 min until ECG changes NORMALIZE, UNLESS pt is experiencing DIGOXIN TOXICITY in which IV Ca is CONTRAINDICATED and as such, you MUST use alternative treatment such as driving K into cells using IV INSULIN + GLUCOSE (when serum glucose
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179
Q

How do you treat HYPERkalemia when it occurs TOGETHER with METABOLIC ACIDOSIS?

A

SODIUM BICARBONATE (NaHCO3)

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180
Q

How is SEVERE HYPERkalemia treated in the setting of SEVERE KIDNEY FAILURE as conventional treatments that rely on KIDNEY FUNCTION cannot be used?

A

Dialysis

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181
Q

NSAIDS, COX-2 Inhibitors, ACE-I/ARB’s and Spironolactone all contribute to this electrolyte disturbance and MUST be D/C or MODIFIED in the setting of the disturbance?

A

HYPERkalemia

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182
Q

What MEDICATION can be used to DECREASE total body potassium (K) in patients with Chronic Kidney Disease (CKD) or CHF?

A

LOOP DIURETICS

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183
Q

How is MILD to MODERATE, ASYMPTOMATIC HYPERkalemia controlled?

A

DIETRARY POTASSIUM (K) restriction

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184
Q

What is considered HYPOphosphatemia and whom is it usually seen in?

A

Serum P

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185
Q

When SERUM PHOSPHATE (P) are

A

When P

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186
Q

How is HYPOphosphatemia treated?

A

By treating the UNDERLYING cause and ORAL SUPPLEMENTATION only if SYMPTOMATIC or chronic PHOSPHATE (P) WASTING

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187
Q

Why is IV PHOSPHATE not usually given (unless serum P

A

IV phosphate can cause ACUTE KIDNEY INJURY and HYPOcalcemia but when administered (when serum P

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188
Q

What ELECTROLYTE is DECREASED as PHOSPHATE (P) is INCREASED?

A

CALCIUM

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189
Q

Disturbances in serum POTASSIUM (K) and PHOSPHATE (P) both manifest with this COMMON SYMPTOM?

A

WEAKNESS

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190
Q

What is considered HYPERphosphatemia and whom is this usually seen in?

A

Serum P >4.5 mg/dL, seen in patients with ADVANCED Chronic Kidney Disease (CKD) or with INCREASED CELL TURNOVER (tumor lysis syndrome) or CELL INJURY or EXOGENOUS administration

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191
Q

How are patients with HYPERphosphatemia treated in the setting Chronic Kidney Disease (CKD)?

A

With PHOSPHATE (P) BINDERS to limit intestinal absorption of PHOSPHATE (P) - SEVELAMER (Ca-carbonate and Ca-acetate can also be used)

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192
Q

What is considered SEVERE HYPERphosphatemia that requires DIALYSIS?

A

Serum P >10 mg/dL

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193
Q

In the setting of TUMOR LYSIS SYNDROME with resultant SEVERE electrolyte disturbances such as HYPERkalemia, HYPERuricemia, HYPERphosphatemia (thus HYPOcalcemia) what MUST BE DONE to avoid DEATH?

A

EMERGENT DIALYSIS

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194
Q

What TWO (2) mechanisms are responsible for the TIGHT SYSTEMIC pH maintenance?

A

By BOTH the KIDNEYS (mainly via bicarb HCO3 regulation) and LUNGS (mainly via CO2 regulation)

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195
Q

The cause of MOST ACID-BASE disturbances is apparent by examining what TWO (2) factors on an ARTERIAL ABG?

A

pH and PCO2 as well as the VENOUS electrolyte measurement, primarily the bicarbonate (HCO3)

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196
Q

An arterial PCO2 >40 mmHg suggests? What if the arterial PCO2

A

PCO2 >40 mmHG - RESPIRATORY Acidosis (more CO2 dissolved in blood makes it more acidic)
PCO2

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197
Q

A SERUM bicarbonate HCO3 24 mmol/L?

A

HCO3 24 mmol/L - METABOLIC Alkalosis

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198
Q

What MUST be determined in an ACID-BASE disorder?

A
  1. What is the DOMINANT acid-base disorder (dictated by the pH)
  2. What is the SECONDARY (compensatory) RESPONSE (dictated by the PCO2 and HCO3)
    IF the MEASURED values (PCO2, HCO3) fall outside of the PREDICTED compensatory response, the acid-base disorder is MIXED (as in salicylate toxicity)
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199
Q

Loss of serum HCO3, Decreased excretion of acid, Imbalance between production/consumption of endogenous acids or Ingestion/IV administration of exogenous acids can cause what ACID-BASE disorder?

A

METABOLIC Acidosis

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200
Q

ACETAMINOPHEN poisoning, Vitamin D deficiency, HYPERparathyroidism (increased Ca), Osmotic diuresis, Osteomalacia, Kidney transplant Proximal TYPE-2 RTA (Fanconi Syndrome), Rickets and the HIV drug TENOFOVIR (used as art of the current “Ten-Em-Ef” ART single-pill combination therapy), CHRONIC Diarrhea and INTRAcellular uptake (re-feeding syndrome, treating DKA with insulin, parathyroidectomy causing HUNGRY-BONE SYNDROME and RESPIRATORY Alkalosis) are all causes of this ELECTROLYTE disturbance?

A

HYPOphosphatemia

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201
Q

What ELSE must be determined when the ACID-BASE disorder is METABOLIC Acidosis?

A

Whether or not there is an ANION GAP

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202
Q

A RAISED anion gap (just called “anion gap” or “increased anion gap”) in METABOLIC Acidosis (the only acid-base disturbance where an anion gap is analyzed) will tell you what about the METABOLIC Acidosis?

A

It tells you whether the DECREASED SERUM HCO3 (metabolic acidosis) is due to the presence of an ADDITIONAL, UNMEASURED ACID (lactate or ingested acid) that is raising the anion gap or whether the DECREASED SERUM HCO3 (metabolic acidosis) is due to a LOSS or LACK of PRODUCTION of SERUM HCO3 which CAUSES the SERUM Chloride (Cl¯) to INCREASE in order to maintain electroneutrality, in which case the anion gap would be NORMAL

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203
Q

What are the ONLY TWO (2) possible types of METABOLIC Acidosis scenarios in relation to anion gap?

A

IINCREASED anion gap (or just “anion gap”) or NORMAL anion gap METABOLIC Acidosis

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204
Q

What is the ANION GAP equation?

A

Anion Gap = SERUM Na - [SERUM Cl¯+SERUM HCO3¯]

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205
Q

What occurs with serum PHOSPHATE (P) in FANCONI Syndrome (Proximal RTA-II)

A

Serum PHOSPHATE (P) is DECREASED

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206
Q

What is the NORMAL range of the ANION GAP?

A

10 meq/L

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207
Q

What UNMEASURED anion(s) can affect the calculation of the ANION GAP and HOW is it affected?

A
  • ALBUMIN (and light-chains) - NORMAL is 4.0 g/dL

- For EVERY 1 g/dL DECREASE of serum albumin from NORMAL, the expected or “normal” anion gap also DECREASES by 2.3 meq/L

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208
Q

In METABOLIC Acidosis (serum HCO3 10 meq/L) and this has been CORRECTED for abnormal serum ALBUMIN “for EVERY 1 g/dL DECREASE of serum albumin from NORMAL (4.0), the expected or “normal” anion gap also DECREASES by 2.3 meq/L” what OTHER DETERMINATION must be made?

A
  • Whether the serum HCO3 was NORMAL BEFORE the development of the acidosis or if there was a PRE-EXISTING metabolic abnormality BEFORE the acidosis occurred that created the anion gap. This is done by calculating the CORRECTED HCO3 based on THE CHANGE in the anion gap (DELTA anion gap)
  • CORRECTED HCO3 = 24 meq/L - Δ anion gap meq/L
  • IF the MEASURED HCO3 > CORRECTED HCO3 it suggests that there is a concomitant METABOLIC Alkalosis in ADDITION to the INCREASED anion gap METABOLIC Acidosis
  • IF the MEASURED HCO3
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209
Q

How is the CORRECTED HCO3 calculated to determine the CHANGE in anion gap or “Δ anion gap”?

A

CORRECTED HCO3 = 24 meq/L - Δ anion gap meq/L

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210
Q

ACUTE/CHRONIC Kidney Disease, ALCOHOLIC Ketoacidosis, DKA, Lactic Acidosis, Poisoning with (Methanol, Ethylene/Diethylene/Propylene Glycol, CO, Acetaminophen), Metformin, Propofol, Salicylates, Liver Failure, Malignancy and G6PD ALL cause what ACID-BASE DISORDER?

A

INCREASED anion gap METABOLIC Acidosis

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211
Q

What is the most common form of INCREASED anion gap METABOLIC Acidosis?

A

LACTIC ACIDOSIS (serum lactate >4 md/dL), TYPES A & B
Type A - tissue HYPOperfusion
Type B - no hypoperfusion

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212
Q

When LACTIC ACIDOSIS (causing INCREASED anion gap METABOLIC Acidosis) is caused by ACETAMINOPHEN toxicity, what is the injury?

A

DIRECT Liver Injury by acetaminophen

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213
Q

In SEVERE ASTHMA, when HIGH-DOSES of β2-agonists and CORTICOSTEROIDS are used as well as the RESPIRATORY Alkalosis that develops (due to rapid breathing thus blowing off CO2, decreasing it), this type of ACIDOSIS develops?

A
  • LACTIC ACIDOSIS (causing INCREASED anion gap METABOLIC Acidosis)
  • So, in severe ASTHMA, treated with β2-agonists and CORTICOSTEROIDS, you would see BOTH a RESPIRATORY Alkalosis as well as an INCREASED anion gap METABOLIC Acidosis
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214
Q

How is Lactic Acidosis treated?

A

Treating the UNDERLYING cause as well as IVF if caused by HYPOperfusion such as in HYPOvolemic shock

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215
Q

When is the ONLY time, Sodium Bicarbonate (NaHCO3) should be used to treat LACTIC ACIDOSIS?

A

When pH ≤7.1 (and ONLY to raise it to 7.2) especially in those with CARDIOVASCULAR compromise

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216
Q

What ACID-BASE disorder do SEVERE ASTHMA, prolonged PROPOFOL administration (>48 HOURS usually in an ICU setting) and ACETAMINOPHEN toxicity cause?

A

ALL cause LACTIC ACIDOSIS (which is an INCREASED anion gap METABOLIC Acidosis), however SEVERE ASTHMA also causes a concomitant RESPIRATORY Alkalosis

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217
Q

A patient receiving prolonged sedation >48 HOURS in the ICU with this medication, develops LACTIC ACIDOSIS (which is an INCREASED anion gap METABOLIC Acidosis) with RHABDOMYOLYSIS, HYPERLIPIDEMIA and ECG shows J-point elevation, what’s the medication used?

A

PROPOFOL

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218
Q

How is PROPOFOL - caused LACTIC ACIDOSIS (which is an INCREASED anion gap METABOLIC Acidosis) with RHABDOMYOLYSIS, HYPERLIPIDEMIA and ECG showing J-point elevation TREATED?

A

D/C the PROPOFOL and treat supportively, unless SEVERE ACIDOSIS which may require DIALYSIS

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219
Q

What is the cause of this type of INCREASED anion gap METABOLIC Acidosis that p/w CONFUSION, SLURRED SPEACH and ATAXIA (loss of full control of body movements) in a patient with SHORT-BOWEL syndrome that has undergone recent SMALL BOWEL RESECTION or a JEJUNO-ILEAL bypass and has ingested a large CARBOHYDRATE meal and NORMAL serum LACTATE levels?

A

D-Lactic Acidosis (D-isomer of lactic acid), which is NOT DETECTED in SERUM LACTATE labs (different isomer)

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220
Q

How is D-Lactic Acidosis - an INCREASED anion gap METABOLIC Acidosis - (D-isomer of lactic acid seen in short bowel syndrome) TREATED?

A

With METRONIDAZOLE/Neomycin (against bowel flora which produce the isomer) as well as dietary CARBOHYDRATE RESTRICTION

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221
Q

What type of ACID-BASE disorder is seen in DKA?

A

INCREASED anion gap METABOLIC Acidosis (can be NORMAL anion gap as well if there is no hypovolemia, usually caused by excretion of the ketoacids “acetoacitate and β-hydroxybutyrate”)

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222
Q

In the presence of INSULIN DEFICIENCY, INCREASED CATECHOLAMINES and GLUCAGON an INCOMPLETE OXIDATION of FATTY-ACIDS occurs which leads to increased production of acetoacetate and β-hydroxybutyrate. What is this process called and what ACID-BASE disturbance does it cause?

A

DKA, causes an INCREASED anion gap METABOLIC Acidosis (but can cause “NORMAL anion gap” as well if there is no hypovolemia, usually caused by excretion of the ketoacids “acetoacitate and β-hydroxybutyrate”)

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223
Q

How is DKA and the resulting INCREASED anion gap METABOLIC Acidosis (can be NORMAL anion gap as well if there is no hypovolemia, usually caused by excretion of the ketoacids “acetoacitate and β-hydroxybutyrate”) TREATED?

A

INSULIN administration WITH GLUCOSE/POTASSIUM as needed (DKA patients tend to be HYPOkalemic)

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224
Q

When should DKA also be treated with SODIUM BICARBONATE (NaHCO3)?

A

ONLY when the pH

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225
Q

Does the HYPOphosphatemia require treatment when treating DKA?

A

NOT unless SEVERE symptoms specifically caused by this deficiency (corrects by itself)

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226
Q

In patients with CHRONIC ALCOHOL abuse, with POOR NUTRITION, with N/V and resulting HYPOvolemia, INCREASED CATECHOLAMINES resulting in mobilization of FATTY-ACIDS and increased production of specifically β-hydroxybutyrate. What is this process called and what ACID-BASE disturbance does it cause?

A

ALCOHOLIC Ketoacidosis (causing INCREASED anion gap METABOLIC Acidosis)

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227
Q

What does the NITROPRUSSIDE assay measure and why is it so limited in its use?

A

Measures KETOACIDOSIS, however it can ONLY detect ACETONE (isopropyl alcohol ingestion) and ACETOACETATE, but NOT β-hydroxybutyrate (which is seen in DKA and Alcoholic DKA)

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228
Q

How does KETOACIDOSIS happen?

A

Starvation (or fasting), DM, ALCOHOL w/malnutrition result in poor INTRAcellular GLUCOSE availability, causing increased circulating CATECHOLAMINES and the mobilization of LIVER GLUCAGON stores which INCOMPLETELY oxidize FATTY ACIDS into acetoacitate (an acid) which is subsequently made into acetone (not an acid) and β-hydroxybutyrate (another acid) resulting in KETOACIDOSIS

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229
Q

Why does the ingestion of ISOPROPYL ALCOHOL not result in KETOACIDOSIS?

A

Because ISOPROPYL ALCOHOL is metabolized into ACETONE, which is NOT an ACID nor is it further metabolized (unlike acetoacetate which IS an acid and IS further metabolized into β-hydroxybutyrate, another acid)

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230
Q

What is the predominant ACID causing the KETOACIDOSIS and hence the INCREASED anion gap METABOLIC Acidosis in ALCOHOLIC KETOACIDOSIS?

A

β-hydroxybutyrate (NOT detected by the nitroprusside assay which only detects acetone and acetoacetate)

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231
Q

How is ALCOHOLIC Ketoacidosis (causing INCREASED anion gap METABOLIC Acidosis) TREATED?

A

With NUTRITION or if SEVERE, same as with DKA treatment (THIAMINE - Vit B1, followed by INSULIN administration WITH GLUCOSE/POTASSIUM as needed)

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232
Q

Poisoning with these SUBSTANCES is HIGHLY LETHAL as they present with SEVERE, INCREASED anion gap METABOLIC Acidosis, with an OSMOLAL GAP >10 mosm/kg H2O (MEASURED osmolality - CALCULATED osmolality) and is caused by the breakdown (metabolism) of the PARENT COMPOUNDS into ACIDS as well as contributing LACTIC ACIDOSIS making this scenario into the MOST SEVERE type of INCREASED anion gap METABOLIC Acidosis there is. What are these SUBSTANCES?

A

METHANOL, Ethylene Glycol, DiEthylene Glycol, Methylene Glycol and Propylene Glycol (METHANOL and ALL of the GLYCOLS) - ANTIFREEZE-related compounds

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233
Q

What is the “INCREASED anion gap” due to in POISONING with Ethylene Glycol, DiEthylene Glycol, Methylene Glycol and Propylene Glycol and what can happen if a patient is NOT seen RIGHT AWAY after ingestion of the poisons?

A

The INCREASED anion gap is due to the PARENT COMPOUND (ie Ethylene Glycol, DiEthylene Glycol, Methylene Glycol and Propylene Glycol) however if the POISONED patient is NOT seen right away, the parent compound can be COMPLETELY METABOLIZED thus resulting in a NORMAL anion gap METABOLIC ACIDOSIS

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234
Q

How does a patient with Ethylene Glycol POISONING present?

A

Flank Pain or Oliguria due to the PRECIPITATION of CALCIUM OXALATE in the renal tubules causing ACUTE KIDNEY INJURY with HYPOcalcemia and NEPHROcalcinosis (deposition of calcium in the kidney parenchyma) with the presence of CALCIUM OXALATE crystals in the URINE sediment

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235
Q

CALCIUM OXALATE in urine sediment, as well as NEPHROcalcinosis (deposition of calcium in the kidney parenchyma) can be seen in a patient with what POISONING?

A

Ethylene Glycol (causes a SEVERE, INCREASED anion gap METABOLIC Acidosis)

236
Q

If a patient ingested BOTH Ethylene Glycol AND ETHANOL or METHANOL AND ETHANOL, what is seen and how do they present?

A

A DELAY in the formation of the expected INCREASED anion gap METABOLIC Acidosis occurs, because ETHANOL inhibits alcohol dehydrogenase therefore inhibiting the metabolism of both Ethylene Glycol and Methanol with INITAL inebriation (due to the effect of ETHANOL) FOLLOWED by OBTUNDATION, SEIZURES, COMA, CARDIOVASCULAR COLLAPSE, PULMONARY EDEMA seen with Methanol and Ethylene Glycol POISONING due to the EVENTUAL formation of the initially expected INCREASED anion gap METABOLIC Acidosis as the ETHANOL is metabolized and no longer protective

237
Q

What symptoms can up to 20% of patients who survive METHANOL POISONING have once treated for the SEVERE, INCREASED anion gap METABOLIC Acidosis?

A

BLINDNESS, PARKINSONISM (putamen injury) abd pain, pancreatitis

238
Q

What is seen on PHYSICAL EXAMINATION of a patient with METHANOL POISONING?

A

MYDRIASIS (WIDE pupils), AFFERENT pupillary defect caused by FORMIC ACID (toxic metabolite that causes the retinal injury and blindness seen in these patients)

239
Q

For this type of POISONING, because MOST LABORATORIES cannot provide appropriate test results QUICKLY enough, WHENEVER you see an INCREASED anion gap METABOLIC Acidosis with a SERUM HCO3 25 mosm/kg H2O (MEASURED osmolality - CALCULATED osmolality), YOU MUST ALWAYS SUSPECT this POISONING and TREAT IMMEDIATELY?

A

METHANOL or Ethylene Glycol POISONING

240
Q

How are METHANOL and Ethylene Glycol POISONING (SEVERE, INCREASED anion gap METABOLIC Acidosis) treated?

A

OPTIMIZE ventilation and ORGAN perfusion, give FOMEPIZOLE (prevents formation of toxic metabolites), THIAMINE, PYRIDOXINE, IV FOLIC ACID and DIALYSIS (if there is any evidence of end organ injury such as kidney failure, neurologic/visual symptoms)

241
Q

What is ONE of TWO EXCEPTIONS with the USE of SODIUM BICARBONATE (NaHCO3) when TREATING METHANOL and Ethylene Glycol POISONING (SEVERE, INCREASED anion gap METABOLIC Acidosis) and why is it used in this scenario?

A

The SEVERE ACIDOSIS seen in METHANOL and Ethylene Glycol POISONING facilitates INTRAcellular UPTAKE of TOXIC METABOLITES and as such, UNTIL DIALYSIS is available, SODIUM BICARBONATE (NaHCO3) MUST be given to maintain the pH >7.3 (the other exception is with salicylate toxicity)

242
Q

What can occur when a patient that is taking LORAZEPAM and has an INCREASED OSMOLAL GAP >12 mosm/kg H2O (MEASURED osmolality - CALCULATED osmolality) and what causes this?

A

INCREASED anion gap METABOLIC Acidosis due to Propylene Glycol toxicity (used as a solvent in certain IV meds) mainly due to L & D - Lactic Acid isomers (L & D - Lactic Acidosis) which are the ACID METABOLITES of Propylene Glycol

243
Q

How is the CONCOMITANT presence of INCREASED anion gap METABOLIC Acidosis and INCREASED OSMOLAL GAP >12 mosm/kg H2O that is seen with Propylene Glycol toxicity in patients receiving IV meds such as LORAZEPAM TREATED?

A

D/C the medication, if SEVERE, use DIALYSIS

244
Q

SALICYLATE TOXICITY (10-30 g of ASPIRIN, oil of wintergreen) affects the CENTRAL (medullary) RESPIRATORY CENTER DIRECTLY, initially causing this ACID-BASE DISORDER and if SEVERE enough, an additional ACID-BASE DISTURBANCE as well?

A
  1. Initially - RESPIRATORY Alkalosis (due to blowing off CO2 caused by hyperventilation)
  2. Secondarily - INCREASED anion gap METABOLIC Acidosis (due to the salicylate anion as well as the resulting lactic and ketoacidosis)
245
Q

A patient that presents with TACHYPNEA, TINNITUS, CONFUSION, LOW-GRADE FEVER, N/V as well as gastric mucosal toxicity (can cause a metabolic alkalosis as well due to the N/V) with AMS, progression to CEREBRAL EDEMA with FATAL brainstem HERNIATION with possible acute lung injury and non-cardiogenic pulmonary edema, has a likely TOXICITY with what SUBSTANCE?

A

SALICYLATE (ASPIRIN, oil of wintergreen)

246
Q

How is SALICYLATE TOXICITY (causing RESPIRATORY Alkalosis, INCREASED anion gap METABOLIC Acidosis and possibly METABOLIC Alkalosis due to N/V) TREATED?

A

IVF, SODIUM BICARBONATE (NaHCO3) to maintain pH between 7.45 - 7.6 which also serves to ALKALINIZE the URINE (to urine pH >7.5) which facilitates excretion of the salicylic acid as well as IV GLUCOSE (to treat neuroglycopenia) and if SEVERE enough, DIALYSIS

247
Q

Should patients with SALICYLATE TOXICITY be INTUBATED?

A

NOT if possible, because intubation induces a DECREASE in arterial pH which enhances INTRAcellular uptake and toxicity

248
Q

Patients who are VEGETARIANS or have LIVER DISEASE, CRITICAL ILLNESS, POOR NUTRITION or CHRONIC KIDNEY DISEASE (CKD) receiving THERAPEUTIC doses of ACETAMINOPHEN on a CHRONIC basis can develop an INCREASED anion gap METABOLIC Acidosis with AMS due to the accumulation of an ACID caused by the disruption of a liver process?

A

Pyroglutamic Acidosis

249
Q

How is PYROGLUTAMIC ACIDOSIS (an INCREASED anion gap METABOLIC Acidosis caused by chronic ingestion of therapeutic doses of ACETAMINOPHEN especially in the setting of LIVER DISEASE or as a VEGETARIAN, POOR NUTRITION, CHRONIC KIDNEY DISEASE (CKD) or CRITICAL ILLNESS) TREATED?

A

D/C ACETAMINOPHEN, give IVF’s and N-acetylcysteine

250
Q

What ACID-BASE DISTURBANCE is COMMONLY seen in patients with ACUTE or CHRONIC KIDNEY DISEASE (CKD) due to DECREASED AMMONIA BUFFER synthesis, especially when the GFR

A

GFR

251
Q

At what SERUM LACTATE level is it considered LACTIC Acidosis (an INCREASED anion gap METABOLIC Acidosis)?

A

Serum Lactic Acid >4 mg/dL

252
Q

When the KIDNEY fails to EXCRETE the FIXED DAILY ACID LOAD, when there is GI LOSS of BICARBONATE (HCO3) due to VOMITING or NGT suctioning, DIARRHEA or DIVERSION of URINE through the INTESTINE, what ACID-BASE DISTURBANCE exists?

A

NORMAL anion gap METABOLIC Acidosis (there is no “external acid” that would increase the anion gap)

253
Q

What is the KIDNEY’s NORMAL response to a state of ACIDOSIS where there is an increased amount of acid in the BLOOD (acidemia) provided that the GFR is NORMAL (>60 mL/min) and no concomitant HYPERkalemia?

A

INCREASED EXCRETION of URINE AMMONIUM (NH4) which is POSITIVELY charged and its EXCRETION results in the making of NEW BICARBONATE IONS (HCO3) which are NEGATIVELY charged which in turn results in H¯ ion excretion (acid) thus ACIDIFYING the URINE and making the BICARBONATE BUFFER needed to counteract the acidosis in the blood

254
Q

How can you tell, if in a state of NORMAL anion gap METABOLIC Acidosis, the KIDNEY is at fault or if there is another UNDERLYING process (such as GI LOSS of BICARBONATE (HCO3) due to VOMITING or NGT suctioning, DIARRHEA or DIVERSION of URINE through the INTESTINE)?

A

Since the KIDNEY’s NORMAL response to a state of ACIDOSIS where there is an increased amount of acid in the BLOOD (acidemia), in a patient with normal GFR (>60 mL/min) and no concomitant HYPERkalemia is to INCREASE EXCRETION of AMMONIUM (NH4), measuring the URINE NH4 quantity will provide the answer - if urine NH4 is elevated, there is an UNDERLYING process because the kidney is functioning properly with the expected response. If however the URINE NH4 is low, the kidney’s function is impaired

255
Q

SINCE it is NOT DIRECTLY measured, HOW is the URINE NH4 quantity estimated when trying to determine whether a patient’s NORMAL anion gap METABOLIC Acidosis is due to an UNDERLYING disease (normal HIGH kidney excretion of urinary NH4 in response to the acidemia) or due to KIDNEY dysfunction (abnormal LOW kidney excretion of NH4)?

A

Using the URINE anion gap and urine osmolal gap
URINE anion gap = Na + K - Cl
If URINE NH4 is INCREASED appropriately, the anion gap will be NEGATIVE, because NH4 is POSITIVE and not measured
If the URINE NH4 is LOW, the anion gap will be POSITIVE or “0” indicating inadequate kidney response to the metabolic acidosis

256
Q

This TYPE of METABOLIC Acidosis is caused by a REDUCTION in the REABSORPTION of BICARBONATE (HCO3) in the PROXIMAL TUBULE which initially leads to BICARBONATE WASTING in the URINE. Once a new steady state is established at a LOWER SERUM BICARBONATE (HCO3) LEVEL, with a DECREASED URINE pH

A
  • PROXIMAL (convoluted tubule) TYPE-2 RENAL TUBULAR ACIDOSIS (Proximal Type 2 RTA)
  • Associated with FANCONI SYNDROME which is Proximal Renal Tubule disease that is INHERITED or can be caused by DRUGS or HEAVY METALS and presents with mild HYPOkalemia and WASTING of PROTEIN (amino acids), PHOSPHATE, BICARBONATE and GLUCOSE in the urine which also leads to Vit D deficiency resulting in HYPOcalcemia and Osteomalacia
257
Q
  1. How is Proximal Type 2 RTA treated (FANCONI SYNDROME)? 2. What are other causes besides meds?
A
  1. D/C offending substance (Tenofovir “Ten-Em-Ef”, Didanosine, expired tetracyclines) and TREAT with THIAZIDE DIURETIC - chlorthalidone/hctz - (increases proximal tubule bicarbonate reabsorption)
  2. Amyloidosis, Multiple Myeloma, Kidney Transplant, Heavy Metals (LEAD, MERCURY, copper and cadmium) and Wilson Disease (copper metabolism)
258
Q

This TYPE of METABOLIC Acidosis is caused by a DEFECT in the ACIDIFICATION of URINE in DISTAL CONVOLUTED TUBULE either due to a PRIMARY disorder of the kidney or INJURY to the TUBULAR EPITHELIUM resulting in IMPAIRED EXCRETION of H¯ ions (acid), a URINE pH >6.0 Kidney POTASSIUM (K) wasting and resulting HYPOkalemia with the development of Ca-PHOSPHATE kidney stones and nephrocalcinosis?

A

HYPOkalemic, DISTAL (convoluted tubule) TYPE-1 RENAL TUBULAR ACIDOSIS (Hypokalemic Distal Type 1 RTA)

259
Q
  1. How is Hypokalemic Distal Type 1 RTA treated? What are the causes of this?
A
  1. FIRST, TREAT the HYPOkalemia!!! Then GIVE POTASSIUM (K) CITRATE
  2. A.I. disorders (Sjögren, SLE, RA); Cirrhosis; Meds (Amphotericin B, Lithium), Hyperglobulinemia and Hypercalciuria
260
Q

This TYPE of METABOLIC Acidosis is caused by 1. HYPOaldosteronism (ADDISON DISEASE) with resulting HYPERkalemia with resulting impaired ability to generate AMMONIUM and a URINE pH 6.0

A

HYPERkalemic, DISTAL (convoluted tubule) TYPE-4 RENAL TUBULAR ACIDOSIS (Hyperkalemic Distal Type 4 RTA)

261
Q
  1. How is Hyperkalemic Distal Type 4 RTA treated? 2. What are the causes of this?
A
  1. Fludrocortisone (when caused by ADDISON DISEASE - HYPOaldosteronism) or Relieve the Urinary OBSRUCTIOM, RESTRICT DIETARY POTASSIUM (K) and GIVE SODIUM BICARBONATE (NaHCO3) therapy
  2. ADDISON disease (HYPOaldosteronism), Sickle Cell Nephropathy and Urinary Obstruction
262
Q

Can you correct the ACIDOSIS in Hyperkalemic Distal Type 4 RTA with correction of the HYPERkalemia?

A

NO!! does not work, you MUST RESTRICT DIETARY POTASSIUM (K) and GIVE SODIUM BICARBONATE (NaHCO3) therapy

263
Q

What UNIQUE type of RTA can patients treated with TOPIRAMATE (anti-epileptic) develop?

A

BOTH PROXIMAL (convoluted tubule) and DISTAL (convoluted tubule) RTA with a Urine pH >6.0 due to INHIBITION of CARBONIC ANHYDRASE (at the proximal and distal convoluted tubules) resulting in formation of Ca-PHOSPHATE Stones and DECREASED CITRATE EXCRETION (HYPOcitraturia)

264
Q

The NET LOSS of ACID (H¯ ions) or RETENTION of SERUM BICARBONATE (HCO3) is called what?

A

METABOLIC Alkalosis

265
Q
  1. What cannot be used to treat METABOLIC Alkalosis when it occurs in the setting of HYPERvolemia and HTN? 2. When can it be used?
A
  1. SALINE (categorized as SALINE-RESISTANT - Ucl¯ >20 meq/L)

2. When METABOLIC Alkalosis occurs in the setting of true HYPOvolemia

266
Q

Why is METABOLIC Alkalosis associated with HYPERaldosteronism (Conn’s Syndrome) and resulting HYPOkalemia?

A

Because with INCREASED Aldosterone, Na and Water are REABSORBED at the distal COLLECTING DUCT in exchange for EXRETION of K¯ and H¯ ions, causing the HYPOkalemia and the ACID LOSS seen in Alkalosis

267
Q
  1. What generally causes SALINE-RESPONSIVE (Ucl¯
A
  1. Vomiting/NGT suctioning (loss of acid), Diuretics

2. Treated with NS and correction of electrolytes (KCl for HYPOkalemia)

268
Q

Two INHERITED syndromes that affect Na and Cl¯ handling by the kidney mimic the effects of LOOP and THIAZIDE diuretics and present with HYPOmagnesemia, MUSCLE CRAMPS, WEAKNESS and POSTURAL HYPOtension?

A 
BARTTER Syndrome (mimics LOOP diuretic effect) - affects the THICK-ASCENDING LIMB of the LOOP of HENLE
GITELMAN Syndrome (mimics THIAZIDE diuretic effect) - affects the DISTAL CONVOLUTED TUBULE
269
Q
  1. Because INHERITED syndromes Bartter and Gitelman affect Na and Cl¯ handling by the kidney, can the HYPOkalemic METABOLIC Alkalosis they cause be treated with Normal Saline? 2. How are they treated?
A
  1. NO! because the defect will continue to waste Na and Cl¯

2. DIET high in Na and K⁺ and AMILORIDE for symptomatic, persistent HYPOkalemia

270
Q

When METABOLIC Alkalosis is associated with HTN, there is an INCREASE in URINE Na and Cl¯ levels, why?

A

Because although increased ALDOSTERONE INITIALY results in INCREASED REABSORPTION of Na and Cl¯ and EXCRETION of K⁺ and H¯ (HYPOkalemia) and therefore increased VOLUME due to the INCREASED Na, within a few days this returns to NORMAL DUE TO THE INITIAL VOLUME EXPANSION, a process called “aldosterone escape” and no edema results

271
Q
  1. What is the most COMMON cause of SALINE-RESISTANT (Ucl¯ >20 meq/L) METABOLIC Alkalosis? 2. How is it treated?
A
  1. PRIMARY HYPERaldosteronism (Conn’s Syndrome) - presents with HYPOkalemia, LOW renin and HTN
  2. Treated with SPIRONOLACTONE (aldosterone antagonist)
272
Q

PRIMARY HYPERaldosteronism (Conn’s Syndrome) which causes HYPOkalemia and therefore METABOLIC Alkalosis and HTN (treated with SPIRONOLACTONE) is caused by ADRENAL HYPERsecretion of ALDOSTERONE. When BOTH adrenals are involved, the treatment is SPIRONOLACTONE, what is the treatment when ONLY one adrenal is involved?

A

SURGERY (ADRENALECTOMY)

273
Q

How is SALINE-RESPONSIVE (Ucl¯

A

Treat by correcting the volume as well as Na, Cl¯ and K⁺ DEFICITS with ISOTONIC SALINE (0.9% NS) and KCl

274
Q

Decreased VENTILATION leading to a buildup of CO2 in the BLOOD (HYPERcapnia) from normal metabolism (increased with HIGH consumption of CARBS and FATS) which when dissolved in the water matrix of the blood, forms CARBONIC ACID (H2CO3) and therefore the retention of H¯ ions (acid) leads to what ACID-BASE DISTURBANCE?

A

RESPIRATORY Acidosis

275
Q

What is the EXPECTED COMPENSATORY RESPONSE in a patient with RESPIRATORY Acidosis and how does this occur?

A

METABOLIC Alkalosis by INCREASING BICARBONATE REABSORPTION at the PROXIMAL CONVOLUTED TUBULE

276
Q

A patient with EXTREME EXERCISE, SEIZURES, MS/MG, PE, CHF and PULMONARY EDEMA, ASTHMA, COPD, DRUG OVERDOSE or VENTILATORY OBSTRUCTION presents with difficulty breathing and has symptoms of AMS, CEREBRAL EDEMA, ASTERIXIS, REDUCED CARDIAC OUTPUT with HYPOtension and CARDIAC ARRHYTHMIAS and an ELEVATED PaCO2, what is the ACID-BASE Disturbance that is causing this presentation?

A

RESPIRATORY Acidosis

277
Q

How is RESPIRATORY Acidosis treated?

A

FIRST, treat the HYPOXIA (supplemental oxygen!! Then NS with D/C of diuretics and starting ACETAZOLAMIDE for significant edema in the setting of post-hypercapnic metabolic alkalosis

278
Q

WHEN should you INTUBATE a patient with RESPIRATORY Acidosis?

A

WHEN BLOOD pH

279
Q

WHY must you SLOWLY decrease the PCO2 in an INTUBATED patient with RESPIRATORY Acidosis?

A

To MINIMIZE the effect of POST-HYPERcapnic METABOLIC Alkalosis which occurs in these patients

280
Q
  1. What do patients develop after being treated for RESPIRATORY Acidosis? 2. How is it treated?
A
  1. POST-HYPERcapnic METABOLIC Alkalosis

2. IVF’s with NS and D/C diuretics, starting ACETAZOLAMIDE for significant edema

281
Q

What is the most IMPORTANT (HIGH-MORTALITY) cause of RESPIRATORY Alkalosis?

A

SALICYLATE Toxicity!! (due to direct effect on CNS respiratory center causing HYPERventilation with BLOWING-OFF CO2 resulting in ALKALOSIS

282
Q

What should you suspect when a patient p/w MIXED RESPIRATORY Alkalosis (LOW PCO2) AND LACTIC Acidosis (an INCREASED anion gap METABOLIC Acidosis) but WITHOUT TACHYPNEA (hyperventilation)?

A

SEPSIS or SEVERE LIVER DISEASE

283
Q

What is the EXPECTED COMPENSATORY RESPONSE in a patient with RESPIRATORY Alkalosis and how does this occur?

A

METABOLIC Acidosis by DECREASING BICARBONATE REABSOPRTION at the PROXIMAL CONVOLUTED TUBULE resulting in hypobicarbonatemia

284
Q

Circumoral and Extremity paresthesias, Dizziness progressing to SPASM and TETANY are seen in this ACID-BASE DISORDER?

A

RESPIRATORY Alkalosis

285
Q

How is ANXIETY-RELATED RESPIRATORY Alkalosis treated?

A

By breathing into a bag to stop HYPERventilation and raise the PCO2 levels

286
Q

What is the GREATEST CONTRIBUTOR to CARDIOVASCULAR DISEASE and the GREATEST CARDIOVASCULAR DISEASE RISK FACTOR for STROKE?

A

HTN

287
Q

What is the most COMMON cause of KIDNEY DISEASE in the US, what is the SECOND?

A

Most common cause is DM, second is HTN (which also WORSENS primary kidney disorders (glomerulopathies)

288
Q

Lacunar infarction, white matter disease, retinal hemorrhage/exudate/cotton wool spots, S4 (atrial kick - suggests LV dysfunction), LVH, Polycystic Kidney Disease, ANKLE:BRACHIAL Ratio

A

HTN

289
Q

What do all of these substances have in common as an ADVERSE EFFECT? Ethanol, NSAIDS, Cyclosporine, SSRI’s, SNRI’s, Eryhtropoietins, ART, Amphetamines, Steroids, OCP, Cocaine and 3,4-methylenedioxymethamphetamine (ecstasy)

A

HTN

290
Q

HTN and HYPOkalemia suggest the presence of what?

A

HYPERaldosteronism and concomitant metabolic alkalosis

291
Q

What ECG changes are seen in a patient with HTN?

A

LVH (tall R waves in Lead I, V1-V6 tall S wave in V1-V3)

292
Q

Prior to obtaining a PROPER BP (the average of ≥2 measurements), the patients should be instructed to avoid what, ≥30 min before measurement?

A

Caffeine, Exercise and Smoking (then sit pt for 5 min in CHAIR with feet resting on the floor, pt’s arm at heart level, correct cuff size - cuff encircles at least 80% of arm - inflate cuff to 20-30 mmHg above SBP and deflate at 2 mmHg/second

293
Q

What time of day for BP measurements provides the most relevant information regarding cardiovascular risk?

A

NIGHT TIME

294
Q

What condition is Ambulatory Blood Pressure Monitoring (ABPM) - 24 HR BP monitoring every 15-30 min during the day and every 30-60 min at night - approved for?

A

WHITE COAT and MASKED HTN

295
Q

What constitutes proper HOME BP Measurements?

A

Taking TWO (2) measurements BOTH in the MORNING and in the EVENING (both between 7-10 am/pm) for 7 consecutive days

296
Q

What are the TYPICAL errors that ELECTRONIC BP monitors make in assessing SBP and DBP?

A

SBP is reported as SLIGHTLY LOWER and DBP is reported as SLIGHTLY HIGHER

297
Q

What is considered HTN?

A

A BP taken ≥2 times, ≥1 min apart at ≥2 visits that is >130/80 mmHg

298
Q
  1. What constitutes NORMAL BP? 2. What is HTN?
A
  1. NORMAL BP 140/90 mmHg
299
Q

For EVERY increase in SBP by 20 mmHg and for EVERY increase in DBP by 10 mmHg, what happens to CARDIOVASCULAR RISK?

A

It DOUBLES

300
Q

What should be RECOMMENDED to ALL patients that have a BP of 120-139/80-89 (pre-HTN)?

A

LIFESTYLE MODIFICATIONS

301
Q

In the ABSENCE of COMORBIDITIES (DM, CAD, CKD), what should be the BP GOAL for ALL patients 80 yo?

A

For those 80 yo - SBP

302
Q

What should be the BP GOAL for ALL patients with Diabetes Mellitus (DM), Coronary Artery Disease (CAD) or Chronic Kidney Disease (CKD)?

A

BP

303
Q

What are the most IMPORTANT and EFFECTIVE LIFESTYLE MODIFICATIONS recommended for those with PRE-HTN (BP 120-139/80-89 mmHg without comorbidities)?

A

WEIGHT LOSS, LOW-Na Diet, AEROBIC Exercise ≥30 min/day ≥3 days/wk, EtOH reduction

304
Q

What should be RECOMMENDED for patients 140/90 mmHg or those >80 yo with SBP >150 mmHg despite lifestyle modifications?

A

START anti-HTN medications

305
Q

The FULL effect of MONOTHERAPY for HTN is what reduction in SBP and in what time frame?

A

12-15 mmHg in 2-4 WEEKS

306
Q

When should COMBINATION anti-HTN therapy be recommended as INITIAL HTN therapy?

A

When the SBP goal must be reduced by ≥20 mmHg and/or DBP goal must be reduced by ≥10 mmHg

307
Q

What anti-HTN medication is associated with EDEMA and what anti-HTN medication (when used in COMBINATION) offsets this effect?

A

Ca-Channel Blockers cause EDEMA, ACE-I offset it when used in combination

308
Q

What COMBINATION drug therapy is preferred to treat HTN in patients with HIGH-CARDIOVASCULAR RISK, WITHOUT other CARDIAC COMORBIDITIES?

A

ACE-I + Ca-Channel Blocker (rather than ACE-I + Diuretic)

309
Q

What DIURETIC is CONTRAINDICATED in GOUT and can also cause IMPOTENCE?

A

Thiazide diuretics (chlorthalidone/hctz)

310
Q

What anti-HTN meds are BEST for use in HF and Post-MI?

A

ACE-I’s/ARB’s and β-blockers

311
Q

What anti-HTN med can WORSEN CHF, cause GINGIVAL HYPERPLASIA, HEART BLOCK as well as EDEMA and CONSTIPATION?

A

Ca-Channel Blockers

312
Q

A patient that is YOUNG, with NO FAMILY HISTORY of HTN, that develops HTN that is of RAPID ONSET or is RESISTANT to meds is likely caused by what?

A

Secondary HTN (KIDNEY) “renovascular HTN”

313
Q

What is the FIRST STEP in management of HTN in a patient with Chronic Kidney Disease (CKD)?

A

Determine whether or not there is PROTEINURIA

314
Q

What is the FIRST CHOICE MED for a patient with HTN AND PROTEINURIA in the setting of Chronic Kidney Disease (CKD), with what goal BP?

A

ACE-I or ARB (to reduce BP 500 mg/24 hours)

315
Q

When treating a patient for HTN in the setting of Chronic Kidney Disease (CKD), it is acceptable AT FIRST to notice a RISE in Cr to NO MORE THAN 25% of their BASELINE. If Cr RISES ABOVE 25%, what MUST be done?

A

D/C DIRURETICS, ACE-I’s or ARB’s if used and consider the possibility of B/L RENAL ARTERY DISEASE

316
Q

What type of RENOVASCULAR HTN can be found in patients with ATHEROSCLEROTIC vascular OCCLUSIVE disease?

A

HTN due to the NARROWING of ONE or BOTH of the RENAL ARTERIES (Renal Artery Stenosis)

317
Q

What does the KIDNEY do when blood flow to it is decreased, such as in cases of Renal Artery Disease (stenosis) - occurs at >75% stenosis (mid-epigastric bruits)?

A

It activates the RENIN-ANGIOTENSIN-ALDOSTERONE system

318
Q

What is the BEST imaging modality for patients with HTN in whom RENAL ARTERY DISEASE is suspected (provided GFR >30 mL/min)?

A

ANGIOGRAPHY > CT-angiography > MR-angiography > US w/Doppler (ok for GFR

319
Q

What is the TREATMENT of choice for a YOUNG WOMAN with RENAL ARTERY STENOSIS due to FIBROMUSCULAR DYSPLASIA?

A

Kidney ANGIOPLASTY (NOT RECOMMENDED for when the cause is due to ATHEROSCLEROSIS)

320
Q

What is the TREATMENT of choice for a patient with RENAL ARTERY STENOSIS due to ATHEROSCLEROSIS?

A

AGGRESSIVE RISK MANAGEMENT (treat HTN, HYPERlipidemia, SMOKING cessation)

321
Q

WHAT is the ONLY indication for Kidney ANGIOPLASTY/STENTING in the setting of RENAL ARTERY DISEASE caused by ATHEROSCLEROSIS?

A

When HTN is REFRACTORY to MEDICAL therapy with PROGRESSIVE WORSENING in Kidney Function

322
Q

When should a patient with HTN NEVER be treated with ACE-I’s or ARB’s in the setting of Kidney Disease?

A

In the setting of BILATERAL RENAL ARTERY DISEASE or in a SINGLE FUNCTIONING KIDNEY

323
Q

When a patient with ATHEROSCLEROTIC disease has a treatment regimen for HTN that includes either a DIURETIC, an ACE-I or an ARB and their Cr rises ABOVE 25% from BASELINE, what should be done and suspected?

A

STOP Diuretic, ACE-I and ARB

SUSPECT either BILATERAL RENAL ARTERY DISEASE or a SINGLE FUNCTIONING KIDNEY

324
Q

If suspecting HYPERaldosteronism in a patient with NEW-ONSET HTN but serum K⁺ and HCO3¯ are NORMAL, how can you test for the ALDOSTERONE level?

A

24-HOUR urine collection (can also do a plasma renin activity measurement)

325
Q
  1. How do PHEOCHROMOCYTOMAS increase BP? 2. How do you test for this? Treat?
A
  1. Through the release of CATECHOLAMINES (epinephrine and norepinephrine)
  2. 24-HOUR urine catecholamines & metanephrines
  3. SURGICAL resection
326
Q
  1. When blood pressure measured at HOME is LESS than when measured in the OFFICE and without evidence of end-organ damage, this is called? 2. What is it called when blood pressure at HOME is GREATER than when measured in the office? 3. What is the BEST diagnostic modality for these situations?
A
  1. WHITE COAT HTN
  2. MASKED HTN
  3. Ambulatory Blood Pressure Monitoring (ABPM)
327
Q

When HTN is UNSUCCESSFULLY treated when taking MAXIMAL anti-HTN therapy (THREE MEDS, one of which is a DIURETIC), what are the possible causes?

A

HIGH-SALT diet, use of NSAIDS (or other meds), OSA or ALDOSTERONE EXCESS (look for HYPOkalemia and metabolic alkalosis)

328
Q

What is considered MAXIMAL anti-HTN therapy?

A

THREE (3) anti-HTN meds, one of which is a DIURETIC

329
Q

Below WHAT DIASTOLIC BLOOD PRESSURE should HTN NOT be treated as it can result in INCREASED cardiovascular events?

A

Do NOT lower the DBP

330
Q

What is a common CBC LAB finding associated with CHRONIC Kidney Dysfunction (CKD)?

A

Anemia (due to damage to the erythropoietin-producing cells of the kidney)

331
Q

A slowly-progressive kidney disease (slowly declining GFR, wasting of GLUCOSE, PHOSPHATE, BICARBONATE and Amino Acids “protein”, decreased production of ammonium, POLYURIA and HYPERkalemia) with a urinalysis that shows a BLAND composition or one with STERILE PYURIA and MINIMAL HEMATURIA associated with low-molecular weight proteins

A

Chronic Kidney Disease (CKD)

332
Q

When should a BIOPSY of the KIDNEY be considered?

A

When the DIAGNOSIS is UNCLEAR and there is a POTENTIAL CHANGE in THERAPY based on results

333
Q
  1. This autoimmune syndrome causes Hypokalemic Distal Type 1 RTA (Sjögren, SLE, RA) and can cause MEMBRANOUS (MGN) or MEMBRANOPROLIFERATIVE Glomerulonephritis (MPGN)? 2. How is it treated?
A
  1. Sjögren Syndrome

2. Treated with CORTICOSTEROIDS

334
Q
  1. This autoimmune disease causes an INTERSTITIAL NEPHRITIS with NON-CASEATING GRANULOMAS and POLYURIA? 2. How is it treated?
A
  1. Sarcoidosis

2. Treated with CORTICOSTEROIDS

335
Q

This autoimmune disease causes Hypokalemic Distal Type 1 RTA (Sjögren, SLE, RA) with IMMUNE-COMPLEX DEPOSITS in the tubular BASEMENT MEMBRANE?

A

SLE

336
Q

What patients are typically SUSCEPTIBLE to KIDNEY involvement from INFECTIOUS DISEASES (TB, EBV, CMV, polyoma BK virus)?

A

Those with PRE-EXISTING KIDNEY DISEASE, TRANSPLANT recipients, IMMUNOCOMPROMISED

337
Q

What MALIGNANCIES are associated with INTERSTITIAL NEPHRITIS with Proximal Type 2 RTA?

A

Amyloidosis, Multiple Myeloma, Lymphoma, Leukemia, Plasmacytoma

338
Q

Casts formed in this disease are made up of PROTEIN, IMMUNOGLOBULINS and the Tamm-Horesfall Matrix, MULTINUCLEATED GIANT CELLS are found in the TUBULAR WALL and INTERSTITIUM of the KIDNEY lead to Proximal Type 2 RTA with tubular OBSTRUCTION and Acute Kidney Injury especially in the setting of VOLUME DEPLETION and HYPERcalcemia? How is it treated?

A
  1. Multiple Myeloma Cast Nephropathy

2. Treat the HYPERcalcemia and Restore Volume (IVF’s) and treating the UNDERLYING disease

339
Q

When LYMPHOMA or LEUKEMIA infiltrate the KIDNEY, what is seen in the URINALYSIS and IMAGING?

A

NON-Nephrotic Range Proteinuria, Sterile PYURIA and LARGE KIDNEYS on imaging

340
Q

What ANALGESIC AGENTS are associated with Chronic Kidney Disease (CKD) - p/w CKD with STERILE PYURIA, MILD PROTEINURIA?

A

Aspirin, Caffeine, Acetaminophen and NSAIDS (D/C)

341
Q

What is ANALGESIC-INDUCED NEPHROPATHY associated with that requires UPPER GU TRACT imaging, URINE CYTOLOGY and CYSTOSCOPY?

A

GU TRACT MALIGNANCY

342
Q

Chronic use of these anti-rejection drugs causes Hyperkalemic Distal Type 4 RTA and CHRONIC VASOCONSTRICTION with FIBROSIS and SCARRING of the KIDNEY?

A

CYCLOSPORINE, TACROLIMUS (calcineurin inhibitors)

343
Q

Chronic use of this medication results in CKD with Hypokalemic Distal Type 1 RTA as well as DIABETES INSIPIDUS which can be attenuated with AMILORIDE, a diuretic that BLOCKS the effect of the offending medication on the KIDNEY?

A

LITHIUM

344
Q

This and other HEAVY METALS can cause a Proximal TYPE-2 RTA (Fanconi Syndrome) as well as interstitial FIBROSIS and requires a SPECIAL 24-HOUR test (EDTA) to confirm etiology which is diagnosed when the levels of the heavy metal are >600 µg in 24 HOURS?

A

LEAD nephropathy (can also be seen with mercury, copper and cadmium)

345
Q

HYPERuricemia which is associated with CARDIOVASCULAR DISEASE and can lead to FIBROSIS and CKD due to the deposition of urate crystals in the medullary insterstitium of the KIDNEY and is associated with this HEREDITARY interstitial kidney disease?

A

Type II Medullary Cystic Disease

346
Q

Obstructive UROPATHY due to conditions such as BPH or MALIGNANCY can cause IRREVERSIBLE damage to the KIDNEY and CKD if untreated for how long?

A

> 6-12 weeks

347
Q

What is the clinical hallmark of GLOMERULAR (BOTH nephROTIC and nephRITIC syndromes) disease?

A

PROTEINURIA

348
Q

What is the predominant presentation of the nephROTIC syndrome?

A

SIGNIFICANT LEAKAGE of plasma PROTEINS into the urine

349
Q

What is the predominant presentation of the nephRITIC syndrome (glomeruloNEPHRITIS)?

A

Passage of BOTH plasma PROTEINS and CELLS (WBC’s, RBC’s)

350
Q

What is ESSENTIAL to obtaining the correct diagnosis and treatment in GLOMERULAR disease?

A

KIDNEY BIOPSY

351
Q

A nephRITIC syndrome that progresses over WEEKS to MONTHS with loss of kidney function is called?

A

RAPIDLY PPROGRESSIVE Glomerulonephritis (RPGN)

352
Q

Glomerular PODOCYTE damage resulting in a URINE PROTEIN:Cr ratio >3.5 g/24h with LOW SERUM ALBUMIN, HYPERlipidemia and EDEMA are findings in what type of GLOMERULAR disease?

A

nephROTIC Syndrome

353
Q

When there is INJURY or INFLAMMATION within the GLOMERULUS (tuft of capillaries within Bowman’s Capsule) with passage of PROTEIN, WBC’s and RBC’s into the renal TUBULE causing a decreased GFR, decreased kidney FUNCTION and abnormal BP regulation presenting as PROTEINURIA, HEMATURIA, PYURIA and HTN?

A

nephRITIC SYNDROME

354
Q

A nephrologic EMERGENCY in which there is a RAPID DECLINE in GFR and KIDNEY FUNCTION that can lead to CKD and ESKD in WEEKS to MONTHS if untreated with histology showing CRESCENTS (“the crescent-bearing muslim disease is rapidly advancing”)?

A

Rapidly Progressive Glomerulonephritis (RPGN)

355
Q

Glomerular capillary RUPTURE in Bowman’s Capsule with resulting extravasation of inflammatory cells, macrophages and fibrin taking on a CRESCENT shape is seen in?

A

Rapidly Progressive Glomerulonephritis (RPGN)

356
Q

Focal Segmental Glomerulosclerosis (FSGS), Membranous Glomerulopathy (MGN), Minimal Change Glomerulopathy, Membranoproliferative Glomerulonephritis (MPGN) and Fibrillary/Immunotactoid Glomerulopathy are all part of what type of GLOMERULAR disease?

A

nephROTIC SYNDROME (FSGS, MG, MPGN, M-C, FIG)

357
Q

This disease is the LEADING TYPE of GLOMERULAR nephROTIC SYNDROME and the most COMMON primary GLOMERULAR disease that leads to ESKD and is associated with [BLACKS, HIV, OBESITY, REFLUX NEPHROPATHY, PARVOVIRUS-B19, PAMIDRONATE and HEROIN] use (“Focus on the fat black osteoporotic heroin user with HIV and slapped cheeks”)?

A

FOCAL SEGMENTAL Glomerulosclerosis (FSGS)

358
Q

Although it is a nephROTIC SYNDROME, how does Focal Segmental Glomerulosclerosis (FSGS) present?

A

All of the common findings of GLOMERULAR disease (elevated serum Cr, low GFR, HTN, Kidney Failure, proteinuria and hematuria) HOWEVER, URINE PROTEIN >2 g/24h

359
Q

What is seen on KIDNEY BIOPSY in Focal Segmental Glomerulosclerosis (FSGS)?

A

FOCAL glomerular (not diffuse) SCARRING or SCLEROSIS only in a PORTION of the glomerular capillary bundle

360
Q

How do you treat Focal Segmental Glomerulosclerosis (FSGS)?

A

Control HTN with ACE-I’s/ARB’s and CORTICOSTEROIDS or immunosuppression with MYCOPHENOLATE MOFETIL, CYCLOPHOSPHAMIDE or RITUXIMAB (if URINE PROTEIN >3.5 g/24h)

361
Q
  1. This IMMUNE COMPLEX disease, a TYPE of GLOMERULAR nephROTIC SYNDROME occurs in [MEN >50 yo, SLE, Hep B & C, SYPHILIS, MALARIA, CANCER, NSAID’s, anti-TNF-α inhibitor, PENICILLAMINE use, MERCURY and GOLD exposure and THYROID disease] with BIOPSY showing BASEMENT MEMBRANE IgG IMMUNE COMPLEX DEPOSITION and DIFFUSE THICKENING of the GLOMERULAR CAPILLARY WALL and is USUALLY self-limited with SPONTANEOUS complete/partial remission HOWEVER RENAL VEIN THROMBOSIS can occur especially if PROTEINURIA >4g/24h lingers >6 MONTHS and GFR progressively declines, this suggests development of ESKD? 2. What Ab’s are found with this disease?
A
  1. MEMBRANOUS GLOMERULOPATHY (MGN) - treat HYPERlipidemia (STATINS) and if RENAL VEIN THROMBOSIS develops, treat with HEPARIN (unfractionated or LMWH and WARFARIN)
  2. Anti-Phospholipase A2 Receptor auto-Ab’s
362
Q

HOW should ALL patients with GLOMERULAR DISEASE be treated INITIALLY, REGARDLESS of whether the disorder is nephROTIC or nephRITIC?

A

Treat HTN with ACE-I’s/ARB’s, STATINS

363
Q

HOW should ALL patients with GLOMERULAR DISEASE be treated for REFRACTORY, PROGRESSIVE disease (PROTEINURIA >4g/24h), REGARDLESS of whether the disorder is nephROTIC or nephRITIC?

A

CORTICOSTEROIDS, Cyclophosphamide, Rituximab, Cyclosporine, Tacrolimus, Mycophenolate Mofetil

364
Q

This TYPE of GLOMERULAR nephROTIC SYNDROME is associated with ATOPIC (allergic - dermatitis, rhinitis, asthma) diseases and LYMPHOMA as it is a disease of LYMPHOCYTES which release immunoglobulins and inflammatory cytokines however this disease does NOT usually progress to CKD with NORMAL immunofluorescence and microscopy findings however electron microscopy shows FUSSION and EFFACEMENT of PODOCYTES (foot processes)?

A

MINIMAL-CHANGE Glomerulopathy

365
Q

How is MINIMAL-CHANGE disease treated?

A

CORTICOSTEROIDS

366
Q
  1. This VERY RARE TYPE of IMMUNE COMPLEX mediated GLOMERULAR nephROTIC SYNDROME is associated with FIBRIL/MICROTUBULAR structures that stain for COMPLEMENT and IgG and are associated with LYMPHOPROLIFERATIVE disorders (CLL, B-cell LYMPHOMA) and presents in patients >50 yo? 2. How are these treated?
A

FIBRILLARY/IMMUNOTACTOID Glomerulopathies

Treatment - treat UNDERLYING disorder and w/CORTICOSTEROIDS and IMMUNOSUPPRESSIVE agents

367
Q

What is NOT an expected finding in a patient with typical DIABETES-caused nephROTIC SYNDROME?

A

Urine HEMATURIA and PYURIA (features of nephRITIC SYNDROME) - must look for concomitant underlying glomeruloNEPHRITIS

368
Q

What is the BEST way to DETECT EARLY DIABETIC NEPHROPATHY?

A

Annual measurement of urine ALBUMIN:Cr ratio and MICROALBUMINURIA

369
Q

How is DIABETIC NEPHROPATHY treated with what end BP and glycemic GOALS?

A

TIGHT GLYCEMIC control and treatment of HTN with ACE-I’s/ARB’s (

370
Q

What is the most COMMON form of AMYLOIDOSIS?

A

AL-form (monoclonal light chain - λ “lambda” isotype) other forms are AH - heavy chains, AA (chronic inflammatory states - RA, TB, Osteomyelitis)

371
Q

20% of patients with AMYLOIDOSIS have a co-existing what ?

A

MULTIPLE MYELOMA or other LYMPHOPROLIFERATIVE disease (leukemia, lymphoma, Waldenstrom)

372
Q

Being SYSTEMIC, this disease affects the KIDNEY, besides heart, lungs and GI tract causing a nephROTIC syndrome that has a very POOR PROGNOSIS and PROGRESSES (5-34 months) to CKD and ESKD?

A

AMYLOIDOSIS (kidney BIOPSY when FAT-PAD/rectal biopsies are non-diagnostic demonstrating an AMORPHOUS material with GREEN BIREFRINGENCE w/CONGO RED stain or light/heavy or amyloid protein)

373
Q

If AMYLOIDOSIS (AL/AH/AA) is found to be the cause of nephROTIC SYNDROME, what should ALSO be checked for?

A

UNDERLYING disease (MULTIPLE MYELOMA, leukemia, lymphoma, Waldenstrom) by SPEP/UPEP (serum/urine) and ImmunoElectroPhoresis

374
Q

How is AMYLOIDOSIS treated?

A

Autologous HSCT if candidate, if not, COMBINATION of CORTICOSTEROIDS and MELPHALAN (alkylating agent also used in Multiple Myeloma)

375
Q

A PLASMA CELL (made by B-lymphocytes) DISEASE that results in PRODUCTION of a MONOCLONAL IMMUNOGLOBULIN causing nephROTIC SYNDROMES (amyloidosis and MPGN) due to DEPOSITION of IMMUNOGLOBULIN presenting with HYPERcalcemia, HYPERuricemia and HYPOvolemia?

A

MULTIPLE MYELOMA

376
Q

How is Multiple Myeloma-associated nephROTIC SYNDROME treated?

A

IVF’s and CHEMOTHERAPY (to treat the underlying disease)

377
Q
  1. A DISEASE that causes the nephROTIC SYNDROME FOCAL SEGMENTAL GlomeruloSclerosis (FSGS) especially in BLACKS (typical of FSGS), however is also associated with [IgA nephropathy, immune-complex mediated glomerulonephritis, MPGN, SLE-like glomerulonephritis, MG, thrombotic microangiopathy, M-C, and amyloidosis] and does NOT typically have the HTN and EDEMA seen with other nephROTIC SYNDROMES? 2. What is seen on BIOPSY?
A
  1. HIV-Associated Nephropathy

2. Biopsy shows - “COLLAPSING” FSGS (histology shows a COLLAPSED glomerulus, which is a BAD PROGNOSTIC sign)

378
Q

When HIV is the cause of the nephROTIC SYNDROME, what is seen histologically?

A

“COLLAPSING” FSGS

379
Q

How is HIV-Associated Nephropathy treated?

A

ART (“Ten-Em-Ef”)

380
Q

What nephROTIC SYNDROME is associated with Hep B > Hep C infection and is due to the DEPOSITION of Hep B Ag-Ab IMMUNE COMPLEX in the sub-epithelial membrane (basement membrane) resulting in LOW COMPLEMENT?

A

MEMBRANOUS Glomerulopathy “MGN” (also seen in MPGN) and Polyarteritis Nodosa (LE necrotizing vasculitis)

381
Q

What is the ONLY feature that differentiates nephROTIC SYNDROME from nephRITIC SYNDROME?

A

The AMOUNT of PROTEINURIA (usually >3.5 g/24h) causing EDEMA and associated with significant HYPERlipidemia

382
Q

IgA nephropathy, LUPUS nephritis, Pauci-Immune Crescentic Glomerulonephritis (PICG), MPGN, Thrombotic Microangiopathy, Post-Infectious Glomerulonephritis (PIGN), Anti-Glomerular Basement Membrane Antibody Disease (AGBMAD) and C3 Glomerulopathy are all part of what type of GLOMERULAR disease?

A

nephRITIC SYNDROME

383
Q

What is the ONLY GLOMERULAR disease that presents BOTH as nephRITIC (and less so, nephROTIC) SYNDROMES?

A

MEMBRANOPROLIFERATIVE Glomerulonephritis (MPGN)

384
Q

This GLOMERULAR nephRITIC SYNDROME that presents with GROSS HEMATURIA AT THE SAME TIME AS A URI or GI INFECTION, seen mostly in WHITE/ASIAN MEN, is the most COMMON type of PRIMARY Glomerulonephritis and is an IMMUNE COMPLEX disease in which IgA-Ag complexes are DEPOSITED in the mesangium (the material in the center of the tuft of capillaries and BETWEEN the capillaries of the GLOMERULUS) and is associated with [Henoch-Schönlein purpura, HIV, IBD, Celiac Disease and Chronic Liver Disease] and has crescents on biopsy and erythrocyte casts?

A

IgA nephropathy

385
Q

GLOMERULAR nephRITIC SYNDROME that presents with GROSS HEMATURIA AT THE SAME TIME AS A URI or GI INFECTION and erythrocyte casts?

A

IgA nephropathy

386
Q

Messangial Immune deposits are associated with this nephRITIC SYNDROME?

A

IgA nephropathy

387
Q

How are patients with MILD IgA nephropathy treated when not requiring STEROIDS or IMMUNOSUPPRESSIVE therapy?

A

omega-3 fatty acids

388
Q

Omega-3 Fatty Acids are used to treat this nephRITIC SYNDROME only when it is VERY mild?

A

IgA nephropathy

389
Q

This GLOMERULAR nephRITIC (and less so, nephROTIC) SYNDROME results from IMMUNE COMPLEX DEPOSITION (much like MG, IgA and FIGN) and is caused by [Hep C (cryoglobulinemia) > Hep B, ENDOCARDITIS, OSTEOMYELITIS, MASTOIDITIS, Syphilis, SLE, Sjögren and Cancers]?

A

MEMBRANOPROLIFERATIVE Glomerulonephritis (MPGN)

390
Q

What is the ONLY DIFFERENCE between MEMBRANOUS Glomerulopathy (MGN) and MEMBRANOPROLIFERATIVE Glomerulonephritis (MPGN)?

A

MGN involves ONLY the BASEMENT MEMBRANE whereas MPGN involves the BM and the MESANGIUM

391
Q

How is MPGN INITIALLY treated?

A

CORTICOSTEROIDS + IMMUNOSUPPRESSIVE agents (unlike MGN that is treated initially treated ONLY with corticosteroids)

392
Q

Hep C Glomerulonephritis with LOW COMPLEMENT (particularly low C4 and positive rheumatoid factor “RF”)?

A

MPGN + Cryoglobulinemia (IgG + IgM immune complexes)

393
Q

When Hep B with Polyarteritis Nodosa (LE necrotizing vasculitis) causes this GLOMERULAR nephRITIC (and less so, nephROTIC) SYNDROME with Ab-Ag IMMUNE COMPLEX DEPOSITION involving BOTH THE BASEMENT MEMBRANE (sub-endothelial space) AND MESANGIUM as well as FIBRINOID NECROSIS, THROMBOSIS, INFARCTION and ANEURYSMS, what’s the SYNDROME?

A

MEMBRANOPROLIFERATIVE Glomerulonephritis (MPGN)

394
Q

When a patient with Hep B infection develops MEMBRANOPROLIFERATIVE Glomerulonephritis (MPGN) with symptoms of FEVER, ABDOMINAL PAIN, ARTHRALGIA and WEIGHT LOSS with a LE NECROTISING VASCULAR RASH, what ELSE is involved that is associated with Hep B?

A

POLYARTERITIS NODOSA (can be checked with angiography, CT-angiography or MR-angiography, PROVIDED GFR >30 mL/min)

395
Q

How is MPGN treated?

A

Treat UNDERLYING disease (Hep B) + CORTICOSTEROIDS ± PLASMA EXCHANGE

396
Q

MPGN + Cryoglobulinemia?

A

Hep C

397
Q

MPGN + Polyarteritis Nodosa?

A

Hep B

398
Q

When [MORE THAN A WEEK AFTER!!!] an acute, self-limited infection such as a STREPTOCOCCAL URI, GI tract or STAPHYLOCOCCAL infection causes RAPID-ONSET EDEMA, OLIGURIA and ERYTHROCYTE CASTS that RESOLVE in WEEKS-MONTHS, diagnosed by anti-streptolysin O or anti-DNAse B Ab’s and LOW C3 (complement) what is the associated GLOMERULAR disease?

A

POST-INFECTIOUS Glomerulonephritis (PIGN)

399
Q

What is the DIFFERENCE in TIMING between the development of IgA nephropathy and Post-Infectious Glomerulonephropathy (PIGN) after a URI or GI tract infection?

A

IgA nephropathy occurs SIMULTANEOUSLY with the infection whereas PIGN occurs MORE THAN ONE WEEK AFTER the onset of the infection

400
Q

LOW C4 COMPLEMENT in this Glomerulonephritis?

A

Hep C MPGN

401
Q

LOW C3 COMPLEMENT in this Glomerulonephritis?

A

POST-INFECTIOUS Glomerulonephritis (PIGN)

402
Q

How is POST-INFECTIOUS Glomerulonephritis (PIGN) treated?

A

Treat UNDERLYING infection and if needed, Dialysis

403
Q

An IMMUNE-COMPLEX mediated GLOMERULAR disease with LOW COMPLEMENT and TYPICAL manifestations of the PRIMARY disease that caused it, with anti-ds-DNA Ab’s and has different degrees (CLASSES) of severity depending on the DEGREE of KIDNEY involvement ie SCLEROSING > MEMBRANOUS > DIFFUSE proliferative > FOCAL proliferative > MESANGIAL > MINIMAL MESANGIAL where the better prognostic classes affect WHITES and poorer prognostic classes affect BLACKS, HISPANICS and ASIANS?

A

LUPUS Nephritis

404
Q

What is ABSOLUTELY ESSENTIAL for the diagnosis but MORE SO, the HISTOLOGIC CLASS (subtype), DEGREE of DISEASE ACTIVITY which are of UTMOST IMPORTANCE in selecting the APPROPRIATE treatment for patients with LUPUS Nephritis?

A

Kidney BIOPSY

405
Q

In this GLOMERULAR disease, there is an Ab that forms DIRECTLY against the GLOMERULAR BASEMENT MEMBRANE and thus Ab-Ag COMPLEXES develop all along the BASEMENT MEMBRANE causing NECROTIZING CRESCENTIC Glomerulonephritis and can appear BOTH as KIDNEY-ONLY (Cr > 5 mg/dL - old patients) as well as KIDNEY-LUNG (pulmonary hemorrhage w/hemoptysis - young patients) and is found in those patients who develop RAPIDLY-PROGRESSIVE GLOMERULONEPHRITIS (RPGN) from whatever GLOMERULAR disease they had?

A

Anti-GLOMERULAR BASEMENT-MEMBRANE Antibody Disease (AGBMAD)
KIDNEY-ONLY - Linear STAINING of the glomerular BM (with fluorescein-tagged IgG Ab’s), RAPID (RPGN) and diffuse necrotizing glomerulonephritis
KIDNEY-LUNG - RAPID (RPGN), HEMOPTYSIS and RESPIRATORY FAILURE as well as Linear STAINING of the glomerular BM (with fluorescein-tagged IgG Ab’s) and diffuse necrotizing glomerulonephritis - GOODPASTURE syndrome

406
Q

How is Anti-GLOMERULAR BASEMENT-MEMBRANE Antibody Disease (AGBMAD) - BOTH KIDNEY-ONLY and KIDNEY-LUNG (Goodpasture Syndrome) treated?

A

PLASMAPHERESIS + ALBUMIN replacement + Cyclophosphamide w/Corticosteroids (3-6 MONTHS) followed by Azathioprine for 1-2 YEARS [alternative to cyclophosphamide is rituximab]

407
Q

When VASCULITIS (RAPIDLY PROGRESSING) affects the KIDNEY (Granulomatosis with Polyangiitis - WEGENER, Microscopic Polyangiitis and Churg-Strauss) they present WITHOUT immune complexes or anti-GBM Ab’s and when they are POSITIVE for ANCA and have GRANULOMAS in their respiratory tract, they are called Granulomatosis w/Polyangiitis (Wegener), if they DON’T have granulomas they are called (Microscopic Polyangiitis) and if they are associated with ASTHMA, they are called Churg-Strauss. What are these called collectively?

A

PAUCI-IMMUNE CRESCENTIC Glomerulonephritis (PICG)

408
Q

What is the indication that a patient with a GLOMERULONEPHRITIS has a RAPIDLY PROGRESSING disease (RPGN)?

A

Hematuria, Proteinuria, Pyuria, HTN, HYPERvolemia and Rapidly-Declining GFR

409
Q

How is PAUCI-IMMUNE CRESCENTIC Glomerulonephritis (PICG) treated?

A

PLASMAPHERESIS + ALBUMIN replacement + Cyclophosphamide w/Corticosteroids followed by corticosteroids w/azathioprine long term (depending on severity - if mild, can skip the plasmapheresis + albumin) [alternative to cyclophosphamide is rituximab]

410
Q

Glomerulonephritis that presents with CUTANEOUS VASCULITIS and RAYNAUD phenomenon with a MEMBRANOPROLIFERATIVE pattern on BIOPSY is likely associated with?

A

CRYOGLOBULINEMIA seen with Hep C (rarely HIV)

411
Q

How is the Glomerulonephritis treated that is caused by the vasculitis of CRYOGLOBULINEMIA seen with Hep C (rarely HIV) - MPGN?

A

Besides the treatment of the UNDERLYING Hep C, it is treated with PLASMAPHERESIS and IMMUNOSUPPRESSIVE agents

412
Q

A glomerulonephritis that occurs in the setting of THROMBOCYTOPENIA (TTP - associated with the decreased activity of the von Willebrand Factor-cleaving protease), MICROANGIOPATHIC HEMOLYTIC ANEMIA and HUS (caused by E.coli O157:H7 when the toxin is bound to the endothelium resulting in inflammation and platelet aggregation with thrombosis) as well as rarely with HIV and Strep PNA is caused by what condition?

A

THROMBOTIC MICROANGIOPATHY

413
Q

How is GLOMERULAR disease treated in the setting of TTP, HUS and SLE?

A
  • PLASMA EXCHANGE + IMMUNOSUPPRESSIVE therapy
  • If however this develops in the setting of TRANSPLANT or post Cancer CHEMOTHERAPY, NO plasma exchange
  • IVIG added if CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME is also present
414
Q

If a patient presents with a GLOMERULAR disease associated with FEVER, HEMOLYTIC ANEMIA, THROMBOCYTOPENIA and NEUROLOGIC FINDINGS, which TWO (2) conditions could be associated with this presentation?

A

TTP and HUS

415
Q

Mutations on CHROMOSOMES 16 and 4 cause the most COMMON INHERITED KIDNEY disorder?

A

Polycystic Kidney Disease (autosomal dominant)

416
Q

Large KIDNEYS and MULTIPLE CYSTS are seen on US in patients with this INHERITED autosomal dominant disease?

A

Polycystic Kidney Disease (PKD)

417
Q

At what AGE, in the absence of multiple B/L KIDNEY CYSTS regardless of INHERITABLE risk, is Polycystic Kidney Disease excluded?

A

> 30 yo (HOWEVER, a SINGLE KINDEY CYST in an at-risk patient

418
Q

Kidney ENLARGEMENT, Urinary Concentrating defects, decreased AMMONIUM production with progression to ESKD in older patients presenting with HTN, mild proteinuria, recurrent back/flank pain and occasional HEMATURIA (due to cyst rupture) with increased risk for INFECTIONS and PYELONEPHRITIS but NOT cancer is seen in this INHERITED autosomal dominant disease?

A

Polycystic Kidney Disease (PKD)

419
Q

How are GU tract INFECTIONS treated in Polycystic Kidney Disease (PKD) and why?

A

With FLUOROQUINOLONES or TMP-SMX because the infections typically involve the cysts that require penetration by the antibiotics used

420
Q

What are the STONES present in Polycystic Kidney Disease (PKD) made up of whereas in most patients without PKD, they are made up of calcium oxalate?

A

URIC ACID STONES

421
Q

What is the most COMMON cause of DEATH in patients with Polycystic Kidney Disease (PKD)?

A

Cardiovascular disease

422
Q

What screening is recommended in patients with Polycystic Kidney Disease (PKD)?

A

MR-angiography due to high-risk of CEREBRAL ANEURYSMS

423
Q

Cysts in the LIVER, PANCREAS, SPLEEN, THYROID, SEMINAL VESICLES and CEREBRAL ANEURYSMS are associated with this INHERITED autosomal dominant disease involving CHROMOSOMES 16 and 4?

A

Polycystic Kidney Disease (PKD)

424
Q

Another RARE type of Polycystic Kidney Disease (PKD) that presents usually in childhood, involves CHROMOSOME 6 (not 16 and 4) and is associated with HEPATIC FIBROSIS and PORTAL HTN as well as GROWTH RETARDATION and is treated with KIDNEY or KIDNEY + LIVER TRANSPLANTATION?

A

Autosomal Recessive Polycystic Kidney Disease

425
Q

A NEURO-CUTANEOUS disorder presenting with KIDNEY CYSTS, PAIN, HEMORRHAGE, BENIGN HAMARTOMAS of the KIDNEY, BRAIN, SKIN (facial, retinal, teeth, gums) and other organs with KIDNEY CYSTS and ANGIOMYOLIPOMAS detected by CT/MRI requiring US surveillance to monitor for MALIGNANT TRANSFORMATION?

A

Tuberous Sclerosis Complex (TSC)

426
Q

How are the ANGIOMYOLIPOMAS that HEMORRHAGE and cause PAIN in Tuberous Sclerosis Complex (TSC) kidney disease treated?

A

ARTERIAL EMBOLIZATION

427
Q

A RARE FAMILIAL KIDNEY disease seen usually during TEENAGE years caused by mutations in the gene for the Tamm-Horsefall mucoprotein resulting in impaired kidney function with benign urinary sediment with MEDULLARY CYSTS noted on US?

A

MEDULLARY CYSTIC KIDNEY DISEASE

428
Q

Mutations in TYPE IV COLLAGEN lead to this X-linked HEREDITARY KIDNEY disease p/w SENSORINEURAL HEARING LOSS, OCULAR abnormalities, MICROSCOPIC HEMATURIA and a FAMILY H/O KINDEY DISEASE and DEAFNESS and SKIN/KIDNEY BIOPSIES show ABSENCE of TYPE IV COLLAGEN, treatment is TRANSPLANT for ESKD?

A

ALPORT SYNDROME

429
Q

Family History of BENIGN HEMATURIA (microscopic and gross) that usually begins in CHILDHOOD and does not require treatment aside from HTN to limit proteinuria?

A

Thin Glomerular Basement Membrane Disease

430
Q

A RARE X-linked disorder of α-galactosidase A deficiency resulting in DEPOSITS of globotriaosylceramide (Gb3) in LYSOSOMES in young men that presents with PREMATURE CAD, SEVERE NEUROPATHIC PAIN, TELANGIECTASIAS and ANGIOKERATOMAS where the treatment is replacement of the deficient ENZYME α-galactosidase A?

A

FABRY Disease (“fails to FABRYcate enzyme”)

431
Q

Kidney INJURY with INCREASE in SERUM Cr or DECREASED URINE OUTPUT occurring

A

ACUTE KIDNEY INJURY (AKI)

432
Q

If ACUTE KIDNEY INJURY (AKI) is SEVERE, UREMIA (urine in the blood) and DECREASED URINE OUTPUT may occur with what SYMPTOMS?

A

Malaise, Anorexia, N/V, Edema, Dyspnea, Muscle Weakness, Palpitations, Arrhythmia

433
Q

What type of ELEVATION of Cr is seen when TMP-SMX or H2-blockers are used?

A

An elevation that is NOT associated with actual kidney INJURY

434
Q

What laboratory values are used to DISTINGUISH between PRERENAL and INTRINSIC Acute Kidney Injury (AKI)?

A

Urine Na, FEna (fractional excretion of Na) and Urine Osmolality

435
Q

What is considered OLIGURIA?

A

Urine OUTPUT

436
Q

When the Kidney is functioning NORMALLY but RETAINS Na (therefore also retaining water) due to HYPOvolemia and therefore LOW blood flow to the kidney, thus with a LOW FEna (500 mosm/kg) as the urine is more concentrated, with a BLAND sediment, the Acute Kidney Injury is associated with what?

A

A PRERENAL cause [in the absence of diuretic use which would alter these values so FE of urea (

437
Q

What are the THREE (3) MAIN INTRINSIC (RENAL) causes of ACUTE KIDNEY INJURY?

A
  1. Ischemic/Toxic Acute Tubular Necrosis (ATN)
  2. Acute Interstitial Nephritis (AIN)
  3. Acute Glomerulonephritis (AGN)
438
Q

URINE: Normal Urine Osmolality (~300 mosm/kg), HIGH Urine Na >40 meq/L with HIGH FEna >2% and DARK, PIGMENTED CASTS?

A

Ischemic/Toxin Acute Tubular Necrosis (ATN) - INTRINSIC (RENAL) cause of ACUTE KIDNEY INJURY

439
Q

URINE: Normal Urine Osmolality (~300 mosm/kg), HIGH Urine Na >40 meq/L with HIGH FEna >2% and WBC’s, RBC’s and WBC CASTS?

A

Acute Interstitial Nephritis (AIN) - INTRINSIC (RENAL) cause of ACUTE KIDNEY INJURY

440
Q

URINE: HIGH Urine Osmolality (>400 mosm/kg), LOW Urine Na 2% and HEMATURIA, PROTEINURIA, DYSMORPHIC RBC’s and RBC CASTS?

A

Acute Glomerulonephritis (AGN) - INTRINSIC (RENAL) cause of ACUTE KIDNEY INJURY

441
Q

What is the urine sediment like in PRERENAL and POSTRENAL (OBSTRUCTIVE) Acute Kidney Injury (AKI)?

A

BLAND (granular/waxy casts, no WBC’s, no RBC’s, etc.) urine sediment

442
Q

What do PIGMENTED GRANULAR CASTS indicate?

A

Acute Tubular Necrosis (INTRINSIC “RENAL” acute kidney injury) or RHABDOMYOLYSIS

443
Q

If the Acute Kidney Injury is determined to be POSTRENAL (OBSTRUCTIVE), what should be done NEXT?

A

Imaging (US) to evaluate for the obstruction because it does NOT involve RADIATION or CONTRAST

444
Q

When there is HYPOvolemia and thus LOW KIDNEY PERFUSION, the kidney activates the renin-angiotensin-aldosterone system resulting in reabsorption of Na and WATER, therefore LOW Urine Na and a Concentrated urine and DECREASED urine output resulting in INCREASED BUN & Cr with BUN&raquo_space; Cr due to slow flow and enhanced BUN reabsorption and Cr is secreted. this type of GENERAL Acute Kidney Injury results?

A

PRERENAL ACUTE KIDNEY INJURY (AKI)

445
Q

How is PRERENAL AZOTEMIA (Acute Kidney Injury - poor oral intake, volume loss due to diarrhea, vomiting, diuretics or low cardiac output as in HF or cirrhosis with symptoms of dizziness and light headedness) treated?

A

With HYDRATION (IVF - NS)

446
Q

What is the typical ACUTE KIDNEY INJURY seen after an ISCHEMIC event or use of a NEPHROTOXIC agent (medication, CONTRAST DYE)?

A

INTRINSIC (RENAL) ACUTE KIDNEY INJURY - Acute Tubular Necrosis (ATN) with high Urine Na (>40 meq/L), FEna (>2%) and normal Uosm (300 mosm/kg) and sediment with DARK PIGMENTED MUDDY BROWN CASTS following elevated Cr and decreased urine output

447
Q

How is INTRINSIC (RENAL) ACUTE KIDNEY INJURY - Acute Tubular Necrosis (ATN) treated?

A

D/C potentially offending agents and maintaining perfusion, HOLD ACE-I’s/ARB’s and DIURETICS (unless used to treat volume overload)

448
Q

An INCREASE of SERUM Cr of ≥0.5 mg/dL or ≥25% from BASELINE 48 HOURS after a CONTRAST study suggests what?

A

INTRINSIC (RENAL) ACUTE KIDNEY INJURY - CONTRAST INDUCED NEPHROPATHY (CIN)

449
Q

Initially INCREASED BASELINE SERUM Cr, H/O Kidney Disease, AGE >80 yo, CHF, DM, Intra-Aortic Balloon Pump (IABP) placement or Urgent/Emergent procedure are all RISK factors for developing INTRINSIC (RENAL) ACUTE KIDNEY INJURY - Acute Tubular Necrosis (ATN) due to what?

A

CONTRAST INDUCED NEPHROPATHY (CIN)

450
Q

What MEASURES can be taken to DECREASE the risk of developing CONTRAST INDUCED NEPHROPATHY?

A

HOLD NSAID’s, METFORMIN and DIURETICS, use NON-CONTRAST STUDY if possible (US, CT/MRI), OPTIMIZE hemodynamics (BP), IVF (NS or NaHCO3), use of LOW (600-800 mosm/kg) or ISO-OSMOLAR (300 mosm/kg) IODINATED CONTRAST and N-acetylcysteine prophylactically

451
Q

Aminoglycosides (amikacin, tobramycin, gentamicin, streptomycin), Amphotericin B, Pentamidine, Foscarnet, Tenofovir (“Ten-Em-Ef”), NSAID’s, Metformin, COX-2 inhibitors, IFOSFAMIDE, Platinic drugs, LEAD, Copper, Cadmium can all cause?

A

INTRINSIC (RENAL) ACUTE KIDNEY INJURY - Acute Tubular Necrosis (ATN)

452
Q

What preparation of Amphotericin B is not as NEPHROTOXIC?

A

LIPOSOMAL

453
Q

When a patient has HEMOLYSIS (anemia, INCRESED LDH and DECREASED HAPTOGLOBIN) or RHABDOMYOLYSIS (INCREASED CK and MYOGLOBIN), what type of KIDNEY INJURY can occur and how does it present?

A

Hb or Myoglobin - associated INTRINSIC (RENAL) ACUTE KIDNEY INJURY - PIGMENT NEPHROPATHY

454
Q

When the URINE DIP STICK is POSITIVE for BLOOD but the URINE SEDIMENT is NEGATIVE for RBC’s, whats going on?

A

HEMOGLOBINURIA due to HEMOLYSIS (check CBC, LDH and Haptoglobin) or MYOGLOBINURIA due to RHABDOMYOLYSIS (check CK)

455
Q

HYPOcalcemia, HYPERphosphatemia, HYPERuricemia, METABOLIC Acidosis, Muscle Compartment Syndrome and LIMB ISCHEMIA are all associated with?

A

Complications of RHABDOMYOLYSIS

456
Q

How is INTRINSIC (RENAL) ACUTE KIDNEY INJURY - Acute Tubular Necrosis (ATN) due to HEMOGLOBINURIA due to HEMOLYSIS or MYOGLOBINURIA due to RHABDOMYOLYSIS treated?

A

IVF’s to FLUSH kidneys (urine outpul of 200-300 mL/hr) and correction of ELECTROLYTES (Ca, P, K) and acid base balance

457
Q

If a patient with INTRINSIC (RENAL) ACUTE KIDNEY INJURY - Acute Tubular Necrosis (ATN) due to MYOGLOBINURIA due to RHABDOMYOLYSIS is suspected to have COMPARTMENT SYNDROME, what must be done?

A

URGENT SURGICAL Consultation (fasciotomy)

458
Q

What is the typical INTRINSIC (RENAL) ACUTE KIDNEY INJURY seen 7-10 DAYS AFTER a DRUG HYPERSENSITIVITY reaction (rarely due to multiple myeloma or autoimmune disease) with symptoms of FEVER, RASH, EOSINOPHILIA, ELEVATED Cr and SEDIMENT with WBC’s, RBC’s, WBC CASTS and negative urine cultures (STERILE PYURIA)?

A

INTRINSIC (RENAL) ACUTE KIDNEY INJURY - ACUTE INTERSTITIAL NEPHRITIS (AIN)

459
Q

How is INTRINSIC (RENAL) ACUTE KIDNEY INJURY - ACUTE INTERSTITIAL NEPHRITIS (AIN) treated?

A

D/C offending drug, and if VERY SEVERE, can use EARLY CORTICOSTEROIDS

460
Q

What is the typical INTRINSIC (RENAL) ACUTE KIDNEY INJURY seen when OBSTRUCTING THROMBI are seen from THROMBOTIC conditions like TTP/HUS with SEDIMENT showing RBC’s and PROTEIN (mimics glomerulonephritis)?

A

INTRINSIC (RENAL) ACUTE KIDNEY INJURY - THROMBOTIC MICROANGIOPATHY (TTP/HUS)

461
Q

How is INTRINSIC (RENAL) ACUTE KIDNEY INJURY - THROMBOTIC MICROANGIOPATHY (TTP/HUS) treated?

A

Supportive care (if shiga-like toxin w/HUS) or PLASMA EXCHANGE if TTP

462
Q

Patients with CKD who are DEHYDRATED are at RISK for a PERMANENT KIDNEY INJURY requiring DIALYSIS should AVOID BOWEL PREPARATIONS based on this compound?

A

PHOSPHORUS

463
Q

High-DOSE Vit C, ORLISTAT, Carambola Juice (star-fruit) and Gastric-Bypass Surgery can all cause this type of INTRINSIC (RENAL) ACUTE KIDNEY INJURY?

A

ACUTE OXALATE Nephropathy

464
Q

When does ACUTE KIDNEY INJURY occur due to OBSTRUCTION (POSTRENAL) as in secondary to bladder outlet obstruction, tumors, radiation, congenital, stones, infections, surgeries and BPH?

A

When it affects BOTH kidneys or one functioning kidney

465
Q

How is the possibility of ACUTE KIDNEY INJURY occur due to OBSTRUCTION (POSTRENAL) diagnosed after thorough history and physical exam?

A

BLADDER and GU tract US/NON-CONTRAST CT imaging

466
Q

What are LATE findings of KIDNEY INJURY due to OBSTRUCTION (POSTRENAL)?

A

RISING Urine Na and FEna with eventual HYPERkalemic METABOLIC Acidosis and HYPOnatremia due to IMPAIRED EXCRETION of K¯, H¯, Water

467
Q

If imaging FAILS to show obstruction but one is HIGHLY suspected (retroperitoneal fibrosis), what other test can be used?

A

DIURETIC RADIONUCLIDE KIDNEY CLEARANCE SCAN (also used to PRECISELY determine GFR)

468
Q

A patient who has had RECENT ABDOMINAL SURGERY, RECEIVED MASSIVE FLUID RESUSCITATION, SEVERE LIVER DISEASE w/ASCITES and presents with a TENSE ABDOMEN, INCREASED Cr, OLIGURIA and Intra-Abdominal Pressure measured via urinary bladder catheter is INCREASED (≥20 mmHg) should be suspected of having what etiology for the KIDNEY symptoms?

A

ABDOMINAL COMPARTMENT SYNDROME (ACS) - requires SURGICAL DECOMPRESSION (with or without medical therapy w/diuretics, dialysis, management of ascites)

469
Q

What can be used to treat CARDIO-RENAL SYNDROME where a DELICATE FLUID BALANCE exists between HEART FAILURE (HF/CHF) and ACUTE KIDNEY INJURY (AKI)/CHRONIC KIDNEY DISEASE (CKD) and cannot be achieved easily with DIURETICS ?

A

DIALYSIS

470
Q

Occurring SPONTANEOUSLY or during INSTRUMENTATION, ACUTE KIDNEY INJURY (AKI) with LIVEDO RETICULARIS RASH ± BLUE/ISCHEMIC TIPS of DIGITS (or a Hollenhorst plaque - plaque in the retinal artery) with INCREASED Cr and CRP, EOSINOPHILIA and LOW COMPLEMENT is seen in the setting of this disease?

A

ATHEROSCLEROSIS (dislodged cholesterol plaques) - treat by avoiding invasive intravascular procedures in HIGH-RISK patients and by secondary prevention (preventing worsening of existing disease) with STATINS, ASPIRIN and treating HTN

471
Q

When KIDNEY DYSFUNCTION with LOW Urine Na and ELEVATED Cr (>1.5 mg/dL) due to SPLANCHNIC VASODILATION and REDUCED KIDNEY PERFUSION occurs in the setting of CIRRHOSIS with ASCITES WITHOUT IMPROVING after FLUID CHALLENGE (hold diuretics, albumin 1 g/kg given x2 days max 100 g/day) and there is NO SHOCK, NEPHROTOXINS or PARENCHYMAL KIDNEY DISEASE, what is the cause of the KIDNEY DYSFUNCTION?

A

HEPATORENAL SYNDROME (type-1 is rapid, type-2 in chronic liver disease w/refractory ascites)

472
Q

How is HEPATORENAL SYNDROME treated?

A

By reversing the UNDERLYING cause (GI bleed, peritonitis, infection, SBP) and giving ALBUMIN in patients w/CIRRHOSIS and SBP (can sometimes use midodrine and octreotide) or LIVER TRANSPLANTATION for CURE

473
Q

ACUTE KIDNEY INJURY w/OLIGURIA and ARRHYTMIAS resulting from the release of K¯ (HYPERkalemia resulting in METABOLIC Alkalosis), P (HYPERphosphatemia resulting in Ca-Phos crystals), and Uric Acid during CHEMOTHERAPY p/w Uric Acid & Calcium Phosphate CRYSTALS in the RENAL TUBULES is due to what process?

A

TUMOR LYSIS SYNDROME

474
Q

IVF (to lower uric acid levels) + ALLOPURINOL + DIALYSIS (to control metabolic abnormalities - and if SEVERE, RASBURICASE) are used for treating what?

A

TUMOR LYSIS SYNDROME with ACUTE KIDNEY INJURY

475
Q

What should be done to PREVENT DIRECT KIDNEY INJURY caused by agents such as AMINOGLYCOSIDES, PLATINIC DRUGS, IFOSFAMIDE (alkylating agent) and Vascular Endothelial Growth Factor Inhibitors (VEGF-I’s)?

A

DOSE according to patient’s GFR

476
Q

What FACTORS in MULTIPLE MYELOMA are responsible for causing KIDNEY FAILURE (decreased GFR with increased serum Cr)?

A

HYPERcalcemia, LIGHT-CHAIN accumulation in tubules creating TUBULAR CASTS with obstruction (also seen in amyloidosis, cryoglobulinemia in Hep C/HIV and MPGN)

477
Q

Since a URINE DIP STICK will NOT show any other protein except for albumin, what MUST be added to the URINE in order for diseases like MULTIPLE MYELOMA, AMYLOIDOSIS to demonstrate etiology of TUBULAR CASTS and PARAPROTEINS?

A

SULFOSALICYLIC ACID

478
Q

What SERUM/URINE studies will IDENTIFY and QUANTIFY the MONOCLONAL IMMUNOGLOBULIN in diseases such as MULTIPLE MYELOMA and WEGENERS MACROGLOBULINEMIA?

A

Urine and Serum Protein ElectroPhoresis (Upep/Spep) with immunofixation

479
Q

How is KIDNEY FAILURE due to MULTIPLE MYELOMA treated?

A

Treating the UNDERLYING disorder (multiple myeloma) thereby REDUCING the PARAPROTEIN PRODUCTION with CHEMOTHERAPY or Autologous HSCT or KIDNEY TRANSPLANT

480
Q

ACUTE KIDNEY INJURY and PROXIMAL Type 2 RTA can be caused by this ART drug used to treat HIV?

A

Tenofovir (“Ten-Em-Ef”)

481
Q

What should be done for diagnosis of unexplained ACUTE KIDNEY INJURY in ALL patients with HIV?

A

Kidney BIOPSY

482
Q

MOST kidney STONES (80% of all stones) are made up of this Ca-CONTAINING compound and are INSOLUBLE in ACIDIC URINE (normal URINE pH range is 6.5-8.0)

A

CALCIUM OXALATE Stones

483
Q

Kidney STONES (10% of all stones) made up of this Ca-CONTAINING compound are INSOLUBLE in ALKALINE urine?

A

CALCIUM PHOSPHATE Stones (topiramate) - treated with Diet RESTRICTED in Na + THIAZIDE DIURETICS (chlorthalidone/hctz)

484
Q

HYPERcalciuria due to HYPERcalcemia (multiple myeloma, PRIMARY HYPERparathyroidism, Sarcoidosis, Vit D Excess, FAMILIAL) leads to kidney stone formation and is treated how?

A

Diet RESTRICTED in Na + THIAZIDE DIURETICS (chlorthalidone/hctz), DO NOT RESTRICT PO CALCIUM INTAKE (paradoxical increase in urine calcium)

485
Q
  1. Excessive intake of CHOCOLATE, SPINACH, GREEN/BLACK TEAS, states of MALABSORPTION such as seen with Roux-en-Y GASTRIC BYPASS and INHERITED FAMILIAL DISORDER, can all lead to INCREASED absorption of this compound in the COLON and formation of these stones? 2. How are these treated?
A
  1. OXALATE, Ca-OXALATE stones
  2. Treated with Ca-Carbonate to bind the oxalate in the GI tract. If FAMILIAL hyperoxaluria, use PYRIDOXINE (Vit B6) as well (prevents formation of oxalate)
486
Q

In the setting of METABOLIC Acidosis (Distal Type 1 RTA) or with HIGH-PROTEIN diets, INCREASED PROXIMAL TUBULAR CITRATE reabsorption occurs and IMPAIRING the usual CITRATE chelation of Ca in the urine thus allowing the formation of what kinds of stones?

A

Ca-PHOSPHATE and Ca-OXALATE

487
Q

INFECTIONS caused by UREASE-SPLITTING organisms such as PROTEUS and KLEBSIELLA hydrolyze the urea to ammonium which ALKALINIZES the URINE and results in the formation of STAGHORN-SHAPED MAGNESIUM AMMONIUM PHOSPHATE and CALCIUM CARBONATE APATITE stones in the KIDNEY PELVIS known as? 2. How are these treated?

A
  1. STRUVITE STONES (staghorn-shaped)

2. Treated with ANTIBIOTICS (for infections) and SURGICAL STONE REMOVAL

488
Q

Patients with LOW URINE VOLUME that eat a HIGH PROTEIN DIET, TUMOR LYSIS SYNDROME, GOUT, DM, METABOLIC SYNDROME or CHRONIC DIARRHEA p/w INCREASED EXCRETION of URIC ACID thus ACIDIFYING their urine and as such are at an INCREASED RISK for developing URIC ACID STONES which are INSOLUBLE in ACIDIC URINE. Increased FLUID INTAKE, ALLOPURINOL (if GOUT or when Urine URIC ACID >1 g/day) are required for treatment as well as URINE ALKALINIZATION with what agent?

A

CITRATE (potassium citrate) or Bicarbonate - alkalinizes the urine

489
Q

Ca-OXALATE stones, URIC ACID stones and CYSTINE stones all require WHAT modification of the urine for treatment?

A

ALKALINIZATION of the urine (with Potassium CITRATE or Bicarbonate)

490
Q

Ca-PHOSPHATE stones and STRUVITE stones require WHAT modification of the urine for treatment?

A

ACIDIFICATION of the urine (with Citric Acid, K-Phos, Na-Phos)

491
Q

Patients with an autosomal recessive disorder that results in the inability to process CYSTINE and therefore the formation of CYSTINE stones (HEXAGONAL CRYSTALS in the urine) as these are INSOLUBLE in ACIDIC URINE. How are these treated?

A

Treated by ALKALINIZATION of the urine (with Potassium CITRATE or Bicarbonate) and using chelating agents PENICILLAMINE or TIOPRONIN

492
Q

Colicky FLANK PAIN radiating to the GROIN, PENIS, TESTICLE or ABDOMINAL with eventual URINARY URGENCY and FREQUENCY are symptoms seen in what condition?

A

Kidney Stones (nephrolithiasis)

493
Q

Besides a URINALYSIS (hematuria, crystals, infection) and LAB studies in evaluating for KINDEY stones, what is the GOLD STANDARD IMAGING study?

A

NON-CONTRAST ABDOMINAL HELICAL CT

494
Q

What patients with KIDNEY STONES can be managed as outpatients and what should they be told to do?

A

Those that can maintain adequate oral hydration to produce AT LEAST 2L/day of URINE, take oral analgesic agents and STRAIN their urine for STONE ANALYSIS

495
Q

What is the role of α-blocker TAMSULOSIN or a Ca-Channel blocker (NIFEDIPINE) in management of KIDNEY STONES?

A

These agents ACCELERATE the PASSAGE of SMALL (

496
Q

WHEN should INVASIVE (PERCUTANEOUS NEPHROSTOMY or URETERAL STENTING) intervention be pursued in patients with KIDNEY STONES?

A

When the stones are LARGE (>7 mm) AND there are concerns for INFECTION, B/L OBSTRUCTION or OBSTRUCTION of a SOLITARY KIDNEY

497
Q
  1. When NOT URGENT, what method can be used to TREAT a SYMPTOMATIC KIDNEY STONE located EITHER in the PROXIMAL URETER or WITHIN THE KIDNEY? 2. What are the adverse effects of this procedure? 3. How are DISTAL URETER stones treated?
A
  1. EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY
  2. TISSUE INJURY and NEW-ONSET HTN
  3. Distal ureter stones are treated with URETEROSCOPY with lasers, US, etc.
498
Q

When should a patient with a KIDNEY STONE undergo a full work-up for etiology including ANALYSIS of PASSED STONES, 24-hour urine collection, labs and RADIOLOGIC (US) assessment of STONE BURDEN at ONSET, at ONE YEAR (if neg. every 2-4 years thereafter)?

A

WHENEVER the FIRST STONE is found

499
Q

What sized KIDNEY STONES tend to pass spontaneously? Which don’t?

A

Stones 7 mm usually do not

500
Q

Once a KIDNEY STONE passes, if WORK-UP is not done and patient is left UNTREATED, what is likely to happen?

A

40% will develop ANOTHER stone within 5 YEARS

501
Q

Changes during what time period including BLOOD PRESSURE lowering due to vasodilation AND DECREASE in vasoconstrictive RESPONSE to angiotensin II and vasopressin, with RETENTION of RENAL Na and WATER INCREASING the PLASMA VOLUME thus INCREASING the GFR with a DECREASE in Cr (to about 0.5 mg/dL) and MILD PROTEINURIA?

A

PREGNANCY (normal physiologic changes)

502
Q

WHY are PREGNANT WOMEN tested with a URINE CULTURE on their FIRST PRENATAL visit and TREATED for ASYMPTOMATIC BACTERURIA (>100,000 colony forming units)?

A

Because DURING PREGNANCY, the WOMAN is at HIGHER RISK for UTI and ASCENDING PYELONEPHRITIS due to HORMOMAL PHYSIOLOGIC DILATION of the RENAL PELVIS, CALICES and URETERS

503
Q

In a PREGNANT woman, findings of a relative HYPERVENTILATION with HYPOcapnia (PCO2 of 30 mmHg) and resulting INCREASED BICARBONATE EXCRETION (serum HCO3¯ 18-20 meq/L) with serum pH 7.4-7.45 with a MILD HYPOnatremia and DECREASE in PLASMA OSMOLALITY by 10 mosm/kg are considered what?

A

NORMAL PHYSIOLOGIC CHANGES of PREGNANCY

504
Q

What is DIAGNOSTIC of NEW HTN in a PREGNANT WOMAN?

A

HTN noted BEFORE the 20th week of gestation (because physiologically, pregnancy causes a DECREASE in BP)

505
Q

When should HTN be treated DURING PREGNANCY and BELOW what NUMBERS?

A

In those with SEVERE HTN, to LIMIT END-ORGAN DAMAGE, keeping it

506
Q

What are the SAFEST anti-HTN meds for use DURING PREGNANCY? Which are acceptable?

A

SAFEST: LABETALOL and METHYLDOPA (“LABor DOPA”)
Acceptable: Nifedipine, Hydralazine, Metoprolol, Thiazide diuretics - chlorthalidone/hctz

507
Q

What is the most COMMON cause of SECONDARY HTN?

A

CKD (also renovascular HTN in young women - fibromuscular dysplasia requiring antgioplasty)

508
Q

What is considered GESTATIONAL HTN?

A

HTN that develops AFTER the 20th week of gestation WITHOUT proteinuria or other END-ORGAN damage AND BP RETURNS to NORMAL WITHIN 6 WEEKS of DELIVERY (otherwise it’s likely chronic HTN)

509
Q

WHY is GESTATIONAL HTN a SERIOUS FINDING?

A

BECAUSE 45% of patients develop PREECLAMPSIA

510
Q

In a PREGNANT WOMAN, AFTER 20 WEEKS GESTATION, NEW-ONSET HTN AND PROTEINURIA (can have associated generalized edema) with symptoms of HA, Visual Changes and N/V suggests what DIAGNOSIS?

A

PREECLAMPSIA (severe disease is associated with HEAVY PROTEINURIA, THROMBOCYTOPENIA, INCREASING Cr and ELEVATED LFT’s

511
Q

Family History, NULLIPARITY, Multiple Gestations, OBESITY, CKD, Chronic HTN, DM and THROMBOPHILIA (antiphospholipid Ab’s) are all risk factors for this condition of PREGNANCY?

A

PREECLAMPSIA

512
Q

When is the ONLY time DURING PREGNANCY that there is PHYSIOLOGIC BP LOWERING?

A

BEFORE 20 WEEKS (returns to pre-pregnant state after that)

513
Q

What SYMPTOM transforms PREECLAMPSIA to ECLAMPSIA?

A

SEIZURE

514
Q

What is the treatment of PREECLAMPSIA?

A

DELIVERY (can give corticosteroids if delivery is anticipated BEFORE 34 weeks for fetal lung maturity)

515
Q

What is the ANTI-EPILEPTIC DRUG of CHOICE in PREGNANCY to PREVENT SEIZURES BOTH INTRAPARTUM and POSTPARTUM in patients with SEVERE PREECLAMPSIA?

A

MAGNESIUM

516
Q

What is the ONLY MEDICATION shown to REDUCE the RISK of PREECLAMPSIA (by 24% in women who are at HIGH-RISK)?

A

LOW-DOSE ASPIRIN (81 mg)

517
Q

Women with a Cr >1.4 mg/dL who are considering PREGNANCY are at HIGH-RISK for what complications?

A

Developing CKD, PREECLAMPSIA, Intra-Uterine GROWTH RESTRICTION and PRETERM DELIVERY

518
Q

In women with DM with HTN and Albuminuria, after D/C ACE-I’s and ARB’s BEFORE CONCEPTION and counseling on keeping a TIGHT GLYCEMIC CONTROL, what anti-HTN med has a KIDNEY-PROTECTIVE EFFECT?

A

Ca-Channel Blocker (NIFEDIPINE)

519
Q

What is considered SAFE SLE therapy during PREGNANCY?

A

CORTICOSTEROIDS + AZATHIOPRINE

520
Q

Because women who have SLE and their risk for HYPERTENSIVE DISORDERS, those with antiphospholipid Ab’s (miscarriages, HTN), or on Mycophenolate Mofetil or Cyclophosphamide for LUPUS NEPHRITIS should be recommended WHAT regarding PREGNANCY?

A

AVOID GETTING PREGNANT (also worsens SLE and can cause neonatal lupus)

521
Q

How should DIALYSIS be modified for women who become pregnant while on DIALYSIS?

A

INCREASED FREQUENCY and TIME (>20 hrs/week) undergoing DIALYSIS

522
Q

When should a woman consider PREGNANCY after a KIDNEY TRANSPLANTATION?

A

1-2 years after, once stable medication regimen is achieved

523
Q

Abnormal Kidney Function (decreased GFR for >3 MONTHS?

A

CKD

524
Q

Since CKD (Stages 1-4) can be ASYMPTOMATIC, what patients should be SCREENED (Cr, GFR, Urinalysis - blood, protein, casts and US) so as to AVOID ESKD and DIALYSIS?

A

Those with a FAMILY HISTORY of KIDNEY DISEASE, Acute Kidney Injury (AKI) and GU tract abnormalities (stones, cancer, obstruction, reflux)

525
Q

What are the GFR values for STAGE 4 CKD and ESKD?

A

Stage 4 CKD - GFR

526
Q

At what GFR level do KIDNEY FAILURE symptoms of PERICARDITIS, SEROSITIS (inflammation of mucus membranes such as lungs, peritoneum, etc.), GI Bleeding, Encephalopathy and Uremic Neuropathy appear?

A

At GFR

527
Q

In patients taking ACE-I’s or ARB’s for prevention of PROGRESSION of CKD, what should be done if HYPERkalemia develops (common when the renin-angiotensin-aldosterone pathway is blocked due to reduced K¯ and H¯ excretion) in order to PRESERVE the protective effects of these meds?

A

Dietary K⁺ Restriction, D/C NSAID’s and the ADDITION of LOOP or THIAZIDE DIURETICS (chlorthalidone or hctz)

528
Q

AFTER starting ACE-I’s/ARB’s, up to WHAT level of Cr ELEVATION is considered RENOPROTECTIVE and NOT PATHOLOGIC?

A

Cr elevation 30%, D/C ACE-I’s/ARB’s and look for possible B/L RAS or other Acute Kidney Injury) otherwise CONTINUE them even if Cr stays just below the

529
Q

In what cases should ACE-I’s/ARB’s be D/C’d besides in cases of B/L RAS?

A

If GFR approaches ESKD levels (

530
Q

In patients with CKD and on a diuretic (HCTZ) that has been increased but pt is still with EDEMA or volume overloaded, what should be the FIRST consideration?

A

ADDITION of LOOP DIURETICS (DO NOT DISCONTINUE THE HCTZ) and although these can lower SERUM K, agents such as ACE-I’s/ARB’s and SPIRONOLACTONE can balance the loss

531
Q

What combination is more KIDNEY-PROTECTIVE, ACE-I + Ca-NIFEDIPINE or ACE-I + THIAZIDE Diuretic?

A

ACE-I + NIFEDIPINE

532
Q

With WHAT GFR level is SPIRONOLACTONE safe to use?

A

GFR >45 mL/min

533
Q

If after the addition of ACE-I’s/ARB’s, Ca-Channel blocker and Diuretic, BP in the setting of CKD is still not well controlled, what agents can be used?

A

HYDRALAZINE or MINOXIDIL (vasodilators), CLONIDINE, α-blocker or SPIRONOLACTONE

534
Q

When should the VASODILATORS HYDRALAZINE or MINOXIDIL be started for HTN control in a patient with CKD?

A

ONLY as ADJUNCTIVE therapy and ONLY after a β-blocker and Diuretic have been started

535
Q

In patients with CKD, due to the LOSS of the ability of the KIDNEY to regenerate BICARBONATE via ammonium production, METABOLIC acidosis develops. How is this treated, which also helps in the delay of progression?

A

Oral Na-BICARBONATE to achieve a SERUM HCO3¯ of at least 23 meq/L

536
Q

Iodinated contrast in patients WITH KIDNEY DISEASE should be AVOIDED if the GFR is below what level?

A

GFR

537
Q

How is PROTEINURIA REDUCED in patients with CKD in order to preserve GFR?

A

By managing HTN with ACE-I’s/ARB’s and SPIRONOLACTONE when needed (MILD dietary reductions may also help)

538
Q

Decongestants, NSAID’s, Herbal Supplements, Salt Substitutes (K), Laxatives, Enemas, Na-Phos, Mg-hydroxide, Mg-citrate, Aluminum are examples of meds that should be AVOIDED in what patients?

A

Those with CKD (reduced GFR)

539
Q

What associated disease becomes of UTMOST importance with INCREASING CONSEQUENCES and MORTALITY at CKD stages >3A (GFR

A

CARDIOVASCULAR DISEASE (recommend smoking cessation, exercise and weight loss besides HTN control and use of STATINS for dyslipidemia)

540
Q

What is considered a NORMAL GFR?

A

GFR ≥90 mL/min

541
Q

CAD is HIGHER in CKD patients WITHOUT DM than it is in DM patients without CKD and MUST be treated aggressively with?

A

ACE-I’s/ARB’s, STATINS, ASPIRIN

542
Q

As the GFR DECREASES in patients with CKD, the kidney’s ability to convert Vitamin D into the form that absorbs intestinal Ca and P decreases as well resulting in LOW Ca and P in the blood and OSTEOPOROSIS due to activation of what?

A

Parathyroid Hormone (PTH) - (CKD - Mineral Bone Disorder)

543
Q

Vitamin D3 (cholecalciferol) is synthesized in the Skin by the effects of UV light and it is obtained from Dietary sources. It is converted in the liver then in the kidney into its FINAL form 1,25-dihydroxy vitamin D which is called CALCITRIOL, the form of Vitamin D that is responsible for INTESTINAL Ca and P absorption. The STORED form of Vitamin D (Calcidiol) or 25-hydrohy vitamin D should be measured as well as these other THREE (3) labs EARLY on in a patient with CKD for timely PREVENTION of CKD-Mineral Bone Disorder?

A

Serum Ca, P (low) and PTH (high)

544
Q

How does CKD directly cause HTN, LVH and resulting REDUCTION in END-ORGAN perfusion?

A

By VASCULAR CALCIFICATION (media layer of the arteries, unlike the intimal layer affected by atherosclerosis) leading to CALCIPHYLAXIS (ischemic and painful skin ulcerations seen especially in ESKD)

545
Q

Osteitis Fibrosis Cystica, Osteomalacia, Adynamic Bone Disease with BONE PAIN and FRACTURE RISK all have this ETIOLOGY in common?

A

CKD-caused BONE disease (Renal Osteodystrophy)

546
Q

A HIGH-TURNOVER BONE DISEAE associated with SECONDARY HYPERPARATHYROIDISM with Sub-periosteal bone reabsorption especially affecting the CLAVICLES and PHALANGES are seen in this RENAL OSTEODYSTROPHY and is treated how?

A
  • Osteitis Fibrosis Cystica
  • Treated by maintaining normal SERUM Ca (HYPOcalcemia) and P levels (HYPERphosphatemia) by using PHOSPHATE BINDERS as well as CALCITRIOL (1,25-dihydroxy vitamin D) or CINACALCET to maintain normal PTH levels
547
Q

When osteomalacia due to decreased bone mineralization occurs in patients with CKD, this is usually due to what toxicity?

A

Aluminum

548
Q

With AGGRESSIVE Vit D and Ca supplementation in patients with CKD and with those s/p parathyroidectomy, with PTH

A

Adynamic Bone Disease (low turnover of bone)

549
Q
  1. How should patients with CKD and GFR >30 mL/min and OSTEOPOROSIS with NORMAL PTH levels be treated?
  2. How should patients with CKD and GFR
A
  1. Same as NORMAL population with OSTEOPOROSIS

2. Correction of SECONDARY HYPERPARATHYROIDISM and STOPPING BISPHOSPHONATES because at a GFR

550
Q

What is the focus of treatment of CKD-MBD?

A

Treating the HYPERphosphatemia by BOTH dietary restriction and chelators (ALUMINUM salts, Ca-Carbonate and Ca-Acetate or SEVELAMER)

551
Q

How should patients with CKD and LOW Vit D be treated?

A

Supplement Vit D especially if PTH is elevated (D/C Vit D if there is HYPERcalcemia or HYPERphosphatemia)

552
Q

What medication is a calcium mimic and acts on the receptor of the PARATHYROID glands resulting in decreased PTH release and is used in DIALYSIS patients with elevated PTH and HYPERphosphatemia?

A

CINACALCET

553
Q

At what GFR level does ANEMIA due to KIDNEY underproduction of ERYTHROPOIETIN present in the absence of other causes and NORMAL IRON?

A

GFR

554
Q

What is the ONLY indication for use of Erythropoiesis Stimulating Agents (ESA’s)?

A

For use ONLY in patients WITHOUT CANCER, WITH SYMPTOMATIC ANEMIA attributable to ERYTHROPOIETIN DEFICIENCY when the Hb

555
Q

Is there ANY role for CHECKING or MONITORING ERYTHROPOIETIN levels in the setting of ANEMIA due to CKD?

A

NO

556
Q

When is it considered SAFE for a patient with CKD and a GFR

A

When they are on DIALYSIS

557
Q

When is it considered SAFE for a patient with CKD and a GFR

A

NEVER (regardless of being on DIALYSIS or not)

558
Q

Since CKD patients are considered IMMUNOCOMPROMISED, how and when should they be vaccinated?

A

Hep B vaccine, ANNUAL INFLUENZA vaccine and PNEUMOCOCCAL vaccine, AT time of DIAGNOSIS of CKD and EVERY 5 years thereafter. NO LIVE VACCINES AFTER TRANSPLANT, these should be done 3 MONTHS before TRANSPLANT

559
Q

What is the preferred CENTRAL LINE ACCESS in patients with CKD to avoid subclavian vein stenosis which will be needed for FUTURE DIALYSIS access?

A

Internal Jugular Vein (peripherally, the HAND veins are also preferred for routine blood draws and peripheral lines)

560
Q

When should a patient be referred to a KIDNEY TRANSPLANT CENTER?

A

When the GFR

561
Q

When is the prognosis of KIDNEY transplantation BEST?

A

When it is performed BEFORE initiation of DIALYSIS

562
Q

When should DIALYSIS be INITIATED in a patient with CKD?

A
  1. If VOLUME OVERLOADED or have ELECTROLYTE abnormalities that cannot be easily treated medically
  2. When SYMPTOMATIC from UREMIA and MALNUTRITION
  3. When GFR
563
Q

When should a patient be approached regarding the NEED for KIDNEY REPLACEMENT THERAPY such as DIALYSIS and TRANSPLANTATION?

A

Approximately ONE YEAR BEFORE it is needed

564
Q

When a patient requires DIALYSIS, why is an AUTOLOGOUS AV-FISTULA preferred to a tunneled INTERNAL JUGULAR CATHETER?

A

Because the AV fistula will not THROMBOSE or get INFECTED at the same rate as a catheter would

565
Q

What dietary requirements do DIALYSIS patients have?

A

LIMITED Na, K and Fluids

566
Q

Another DIALYSIS modality available that is a good option for ESKD patients with CARDIOVASCULAR disease from the point of view of smaller fluid shifts but NOT such a good option for DIABETICS due to the HIGH-DEXTROSE fluid that is used?

A

PERITONEAL DIALYSIS

567
Q

How long will a patient survive if they choose to STOP DIALYSIS?

A
568
Q

What is the LEADING cause of death in patients on DIALYSIS?

A

CARDIOVASCULAR DISEASE

569
Q

What is a COMMON finding in patients on DIALYSIS that may present with FLANK PAIN and occasional HEMATURIA and may PROGRESS to RENAL CELL CARCINOMA >3-5 years after INITIATING DIALYSIS?

A

Acquired Renal Cystic Disease (cysts that appear or enlarge after initiation of dialysis)

570
Q

What is the most COMMON infection risk of KIDNEY TRANSPLANTATION?

A

POLYOMA BK VIRUS and CMV

571
Q

What should be done to screen for infections POST KIDNEY TRANSPLANTATION?

A

URINE Cytology and PCR for Polyoma BK Virus and CMV in the FIRST YEAR AND with ANY DECLINE in DECLINE in KIDNEY FUNCTION post TRANSPLANT

572
Q

How would you DIAGNOSE Polyoma BK Virus infection in a transplanted kidney?

A

BIOPSY

573
Q

If POLYOMA BK VIRUS infection is definitively DIAGNOSED in a POST-TRANSPLANT patient, what MUST be done to AVOID REJECTION?

A

LOWER the anti-rejection drug DOSAGES to the LOWEST LEVEL POSSIBLE

574
Q

Associated with BOTH ACUTE and CHRONIC KIDNEY TRANSPLANT REJECTION, infection with this VIRUS can be avoided after proper screening and diagnosis by treatment with VALGANCYCLOVIR?

A

CMV infection (usually from donor’s kidney)

575
Q

A patient s/p KIDNEY TRANSPLANT presents with FEVER, DIARRHEA (enteritis), ELEVATED LFT’s (hepatitis), and CHEST PAIN WITH COUGH (pneumonitis/PNA), what’s going on?

A

Infection with CMV from DONOR’s KIDNEY

576
Q

As UTI’s are COMMON for the FIRST 6 MONTHS post KIDNEY TRANSPLANTATION, what should be given as PROPHYLAXIS for ALL transplanted patients?

A

TMP-SMX (also covers Pneumocystis jirovecii pneumonia in this population)

577
Q

This VIRAL-associated disease that ALL post KIDNEY TRANSPLANT (seen in all other solid organ transplants as well as HSCT) patients can get, presents with FEVER and LYMHADENOPATHY with enlarged TONSILS, SALIVARY GLANDS and SPLEEN is treated the SAME WAY as an infection with Polyoma BK Virus, ie with LOWERING the anti-rejection drug DOSAGES to the LOWEST LEVEL POSSIBLE?

A

EBV - caused Post Transplant Lymphoproliferative Disease (PTLD)

578
Q

What SKIN cancer is FREQUENTLY seen in POST KIDNEY (and all SOLID organ) TRANSPLANT patients especially those treated with AZATHIOPRINE?

A

SQUAMOUS-CELL CARCINOMA of the SKIN (ALL CKD AND post-transplant patients should LIMIT UV-light EXPOSURE)

579
Q
  1. Focal Segmental Glomerulosclerosis (FSGS), Thrombotic Microangiopathy (TTP/HUS) [Diabetic Nephropathy and IgA Nephropathy - are late complications] are all pre-existing diseases which can RECUR post-TRANSPLANT, the most SERIOUS of which is? 2. How is it treated?
A
  1. Focal Segmental Glomerulosclerosis (FSGS)

2. PLASMAPHERESIS

580
Q

This pre-existing disease which can RECUR post-TRANSPLANT especially if CALCINEURIN INHIBITORS (TACROLIMUS, CYCLOSPORINE) are used as part of the anti-rejection regimen?

A
  1. Thrombotic Microangiopathy (TTP/HUS)

2. D/C the calcineurin inhibitors and PLASMA EXCHANGE

581
Q
  1. Why is HYPERlipidemia in a POST-KIDNEY TRANSPLANT patient with CARDIOVASCULAR DISEASE DIFFICULT to manage when CALCINEURIN INHIBITORS (TACROLIMUS, CYCLOSPORINE) are used as part of the anti-rejection regimen? 2. How do you treat?
A
  1. Because STATINS + CALCINEURIN INHIBITORS (TACROLIMUS, CYCLOSPORINE) = RHABDOMYOLYSIS
  2. LIMITED to ATORVAstatin (also PRAVAstatin and FLUVAstatin)
582
Q

Why are these statins important: ATORVAstatin, PRAVAstatin and FLUVAstatin?

A

These are the ONLY THREE (3) statins that can be used to treat HYPERlipidemia in patients taking CALCINEURIN INHIBITORS (TACROLIMUS, CYCLOSPORINE), used as part of the anti-rejection regimen

583
Q

When PRE and POST - TRANSPLANT can ROUTINE VACCINES (annual INFLUENZA, PNEUMOCOCCAL, and LIVE VACCINES (MMR, Varicella, BCG, Oral POLIO, INTRANASAL INFLUENZA) be given?

A

PRE-TRANSPLANT: 3 MONTHS BEFORE, ALL vaccines (live and killed) can be given
POST-TRANSPLANT: 6 MONTHS AFTER, ONLY KILLED vaccines can be given (influenza, pneumococcal, tetanus) but NO LIVE VACCINATION EVER

584
Q

What type of IMMUNOSUPPRESSION is REQUIRED in KIDNEY (and most solid organs) TRANSPLANTATION?

A

INDUCTION and MAINTENANCE (to prevent rejection)

585
Q

Anti-Inflammatory (PREDNISONE), Calcineurin Inhibitors (TACROLIMUS, CYCLOSPORINE), Antimetabolites (MYCOPHENOLATE MOFETIL, AZATHIOPRINE) and Rapamycin Inhibitors (SIROLIMUS, EVEROLIMUS)?

A

Drugs used as anti-rejection regimen post-TRANSPLANTATION of KIDNEY and other SOLID ORGANS, HSCT

ABIM 2015 (11 decks)

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