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CAM III > Renal Part I > Flashcards

Renal Part I Flashcards

1
Q

What are the functions of the kidney?

A

Regulation of extracellular fluid volume and BP
-Renin synthesis (increases BP and blood volume)
Regulation of osmolarity and iron balance
Homeostatic regulation of pH
Erythropoietin synthesis
-Releases retics from bone marrow
Vit D synthesis (active form)
-Regulates mineral homeostasis
Gluconeogenesis in times of starvation
Waste removal

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2
Q

Acidosis

A

pH is <7.38
Life is threatened when <7.25
Death occurs if <7

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3
Q

Alkalosis

A

pH is >7.42
Very dangerous when pH is >7.55
Death occurs when pH is >7.6

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4
Q

Regulation of pH

A

The pH of urine may vary from as low as 4.5 to as high as 9.8 depending on what condition the kidney is trying to overcome
Kidneys can:
-Excrete H+ ions
-Reabsorb bicarb
-Excrete titratable acid (net acid excretion)
-Excrete NH4+ (ammonium)

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5
Q

Waste removal

A

Afferent arterioles bring blood from the renal artery (dirty blood) into the glomerulus of the nephron
Efferent arterioles carry filtered blood away from the glomerulus
Afferent arterioles are larger, causing a pressure buildup within the glomerulus which facilitates waste removal

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6
Q

Waste removal: glomerular capsule

A

The glomerular capillary wall determines what is filtered and how much is filtered
It has three layers:
-Endothelium: allows plasma proteins and fluid through, but not RBCs
-Basement membrane: prevents plasma proteins exiting the bloodstream
-Epithelium: filtration level of fluid within the glomerular space (podocytes)

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7
Q

Causes of vit D deficiency

A 
Sun:
-Sunscreen
-Melanin
-Latitude
-Winter
Meds and supplements
-Antiseizure meds
-Glucocorticoids
-Rifampin
-HAART
-St. John's wart
Hepatic failure
Renal failure
Nephrotic syndrome
Obesity
Malabsorption
-Crohn's 
-Whipple
-CF
-Celiac
-Liver dz
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8
Q

Vit D deficiency consequences

A 
Schizophrenia
Depression
Infections
-URI
-TB
Decreased FEV1
Asthma and wheezing diseases
HBP
CHD
AODM
Syndrome X
Autoimmune diseases
-Type 1 DM
-MS
-Crohn's
-RA
Cancer
-Breast
-Colon
-Prostate
-Pancreas
Muscle weakness
Muscle aches
Osteoarthritis
Osteomalacia
Rickets
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9
Q

Excretion

A

The nephron is the basic structural and functional unit of the kidney which allows for filtration
Fluid passes through the tubules and is modified either by reabsorption or secretion
Reabsorption removes substances from the filtrate back into the system
Secretion adds substances to the filtrate for excretion
Fluid enters Bowman’s space then into the loop of Henle. The bulk of the filtered solute and water are resorbed
The collecting tubules make the final urinary composition changes and allow solute and water excretion to vary with alteration in dietary intake

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10
Q

Renal corpuscle

A

Production of filtrate

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11
Q

Proximal convoluted tubule

A

Reabsorption of water, ions, and all organic nutrients

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12
Q

Loop of Henle

A

Further reabsorption of water (descending limb) and both sodium and chloride ions (ascending limb)

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13
Q

Distal convoluted tubule

A

Secretion of ions, acids, drugs, toxins

Variable reabsorption of water, sodium ions, and calcium ions (under hormonal control)

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14
Q

Collecting duct

A

Variable reabsorption of water and reabsorption or secretion of sodium, potassium, hydrogen, and bicarb ions

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15
Q

Papillary duct

A

Delivery of urine to minor calyx

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16
Q

BUN

A

Nl range 3-20 mg/dL
Urea is produced as a byproduct of metabolism in the liver which is then released into the blood to be removed in the urine
A measure of renal function (and liver function)
High BUN levels generally indicate poor renal function

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17
Q

Things that elevate BUN

A 
Urinary tract obstruction
CHF or recent MI
Severe GI bleeding
Dehydration/hypovolemia
High protein diet
Certain meds, esp abx
RENAL FAILURE
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18
Q

Things that may decrease BUN

A

Severe liver dz
Anabolic state (starvation)
SIADH

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19
Q

Creatinine

A

Chemical by-product of muscle function
Nl range: 0.6-1.2 mg/dL
Produced by creatine
About 2% of body’s creatine is converted to ccreatinine daily
Transported through the blood to the kidneys, whose job is to filter out and dispose most of it
Muscle mass doesn’t change daily, so creatinine shouldn’t either

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20
Q

Causes of elevation in creatinine

A 
Dehydration
Dietary supplements
Large meat intake
Meds
-Cimetidine
-Trimethoprim
-Ranitidine
-Ceaphalosporins
-Fenofibrate
Medical conditions
-DKA
-Pyelonephritis
-Urinary tract obstruction
-Rhabdomyolysis
KIDNEY FAILURE
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21
Q

Causes of decrease of creatinine

A

Generally less worrisome than increase
Decreased muscle mass (aging, dz)
Ultra low protein diet (not uncommon in vegans)
Pregnancy
Cachexia (severe malnutrition, cancer)
Severe liver dz (interferes with creatinine production)

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22
Q

Clearance

A

Rate at which a substance is removed from plasma

How much blood the kidneys can make creatinine free in one min

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23
Q

What is CrCl used to estimate?

A

GFR

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24
Q

GFR

A

Measures how well kidneys are filtering blood

Reduced GFR= retention of nitrogenous waste

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25
Q

There is a ______ relationship between clearance and serum creatinine

A

Inverse

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26
Q

FENA

A

Fractional excretion of Na

Used to help differentiate pre-renal vs extra-renal process

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27
Q

What does an FENA <1% indicate?

A

Prerenal cause, volume depletion
Kidney corrects for low fluid state by reabsorbing Na, indicates functional kidney
Hypovolemia, CHF, RAS, sepsis, contrast-induced nephropathy will often look pre-renal

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28
Q

What does an FENA > 1 % indicate?

A

ATN

Failing kidney, cannot compensate, leaks sodium, indicates kidney dx

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29
Q

Acute kidney injury

A

Refers to sudden loss or deterioration of kidney function resulting in an inability to maintain acid-based, fluid and electrolyte balance and to excrete nitrogenous wastes

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30
Q

RIFLE criteria

A 
The most commonly used criteria for determining the severity and extent of renal failure
Risk
Injury
Failure
Loss (of function)
End stage renal dz (ESRD)
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31
Q

Risk and GFR criteria

A

Increased creatinine x 1.5 or GFR decrease >25%

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32
Q

Risk and urine output criteria

A

UO < 0.5 mL kg-1h-1 x 6h

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33
Q

Injury and GFR criteria

A

Increased creatinine x2 or GFR decrease >50%

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34
Q

Injury and urine output criteria

A

UO <0.5 mL kg-1h-1 x 12h

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35
Q

Failure and GFR criteria

A

Increased creatinine x3 or GFR decrease >75% or creatinine >4 mg per 100 mL (acute rise of >0.5 mg per 100 mL)

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36
Q

Failure and urine output criteria

A

UO <0.3 mL kg-1h-1 x 24h or anuria x 12h

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37
Q

Loss criteria

A

Persistent ARF = complete loss of renal function >4 wks

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38
Q

AKI- components

A 
Sudden, hours or days, may be reversible
Often iatrogenic
Can be pre/intra/post renal cause
Identify the cause and treat
More common in pts with some CKD already present
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39
Q

S/sx of AKI

A 
Nausea and vomiting
Malaise
AMS
HTN
Asterixis
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40
Q

Anuria

A

No urine output OR
<100 cc/24 hrs OR
<0.5 cc/kg/hr

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41
Q

Oliguria

A

<500 cc/24 hrs OR
<20 cc/hr OR
<1cc/kg/hr

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42
Q

Polyuria

A

> 2.5L/24 hrs

43
Q

Prerenal AKI

A

Sudden and severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness

44
Q

Intrarenal AKI

A

Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply

45
Q

Postrenal AKI

A

Sudden obstruction of the urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury

46
Q

Causes of prerenal AKI

A 
MCC of acute kidney injury
Hypovolemia
-Hemorrhage
Dehydration
Increased GI losses
3rd space losses
Hypoxia
Sepsis
Cardiac failure
Hypotention
47
Q

Causes of postrenal AKI

A 
Obstruction
Stones
BPH
Tumor
Trauma
Spinal cord lesion
48
Q

Dx of postrenal AKI

A

US (hydronephrosis)

CT if you suspect stones

49
Q

Causes of intrarenal AKI

A 
Direct damage to the kidney
Acute tubular necrosis (MC)
Inflammation
-Acute interstitial nephritis
Toxins (heavy metals, solvents)
Drugs
Infection (glomerulonephritis, pyelonephritis)
Blood supply
50
Q

Drugs that can cause intrarenal AKI

A 
ACE inhibitors
ARBs
NSAIDs
Tramadol
Toradol
IV contrast dye
Amphotericin B
Aminoglycosides
IV acyclovir
51
Q

How to prevent ATN from contrast dye

A

N-acetylcysteine (Mucomyst)- used by RTs in nebs and given orally for acetaminophen overdose can also be used as a preventative medication before administering IV contrast dye to lower the likelihood of developing ATN
Dosed as 600 mg orally every 12 hrs, once before and once after a dye load (or occasionally 1200 mg IV once before emergent surgery or contrast administration)

52
Q

What are the three major classifications of intrarenal AKI

A

ATN
Acute glomerulonephritis
Acute interstitial nephritis

53
Q

Causes of ATN

A

85% of intrarenal dz
Typically results from necrosis secondary to extended hypovolemia (surgery, burns, hemorrhage)
OR nephrotoxic meds or both
Endogenous cause: myoglobin (rhabdo)

54
Q

Lab results in ATN

A 
BUN:Cr is >20:1
Hyperkalemia, hyperphosphatemia
Urine Na >40 mEq/L
Spec gravity <1.010
Fractional excretion of Na >1%
Urine osmolality typically around 350
UA will show granular (muddy brown) casts, renal tubular casts
55
Q

Phases of ATN

A

Initiating phase
Maintenance phase
Recovery phase

56
Q

Initiating phase of ATN

A

Lasts ~24-36 hrs from time of injury

Progressive azotemia, progressive oliguria

57
Q

Maintenance phase of ATN

A 
Oliguria (40-400 mL/24 hrs)
High azotemia
Metabolic acidosis
Hyperkalemia; may be highly transient and not evident clinically 50% of the time
Period of 1-2 weeks
Pts may require dialysis
58
Q

Recovery phase of ATN

A

Polyuria
Hypokalemia
Decreasing azotemia
Pts tend to need fluid resuscitation and close monitoring of electrolytes

59
Q

Tx of ATN

A

Primary goal: prevent further injury
If they are fluid deficient or hypotensive, address with IVF and inotropes
Treat any underlying sepsis
D/C all nephrotoxic drugs
-And adjust dosage on all renally excreted meds
If BP and cardiac stable may use loop diuretics to deal with oliguria
Good evidence supports dialysis before complications arise

60
Q

Generalized tx of ATN

A 
Refer to nephrologist
Avoid volume overload
Avoid hyperkalemia
Dietary protein restriction
Treat electrolyte imbalances carefully
Dialysis if needed
61
Q

Indications for dialysis

A 
Acid/base disorders
Electrolyte imbalances
Intoxication
Overload of volume
Uremia
62
Q

Acute interstitial nephritis

A

Immune-mediated cause of acute renal failure

Typically secondary to an allergic reaction, drug reaction, infection, or granulomatous dz

63
Q

Common presentation of acute interstitial nephritis

A

50-60s female with fever, arthralgia, rash, and hematuria

64
Q

Medication-induced acute interstitial nephritis

A

70% of AIN cases
Occurs around 2 wks after new med
Commonly abx: PCN, cephalosporin, bactrim
If induced by NSAIDs is associated with nephrotic syndrome

65
Q

What infections can AIN follow?

A 
Pyelonephritis
Staph
Strep
CMV
EBV
Hep C
Mycoplasma
Rocky Mountain Spotted Fever
66
Q

When can granulomatous interstitial nephritis be seen?

A

Sarcoidosis
SLE
Sjogrens
Renal tuberculosis

67
Q

PE of AIN

A 
General malaise
Nausea (from buildup of metabolites)
Polydypsia and polyuria (kidneys unable to concentrate urine appropriately)
Nl BP: NO edema (distinguishes from ATN)
-Unless from NSAIDs
If drug induced: maculopapular rash
68
Q

Lab results of AIN

A

Progressive increase in BUN and creatinine
UA will show WBCs, white cell casts
-Sterile pyuria (WBCs but no infection- eosinophils)
-90% also have hematuria
-Proteinuria if NSAID induced
CBC: eosinophilia in 80% of cases

69
Q

Dx of AIN

A

Gold standard is renal bx
Not needed in all pts (if you can be confident of dx without it)
Pts who do NOT improve after withdrawal of supposed offending agent WOULD benefit
Pts refusing bx can have renal u/s, but not as specific

70
Q

Tx of AIN

A

Recovery takes weeks to months
Supportive measures
Remove inciting agent
Short-term, high-dose prednisone IV with taper

71
Q

Nephritic syndrome

A 
Inflammation of the glomeruli
Oliguria
HTN
Cola-colored urine (hematuria)
Berger's dz (IgA nephropathy) is the most common cause of primary glomerulonephritis
72
Q

Nephrotic syndrome

A

Hypoalbuminemia
Hyperlipidemia
Peripheral edema
Massive proteinuria

73
Q

Urine casts in nephrotic syndrome

A

Fatty casts

74
Q

Urine casts in nephritic syndrome

A

RBC casts;

Cola/smoky urine

75
Q

Proteinuria in nephrotic syndrome

A

> 3.5 g/day

76
Q

Proteinuria in nephritic syndrome

A

< 3.5 g/day

77
Q

Nephrotic disease

A 
Bland urine sediment
Urine protein exceeds 3g per 24 hrs
Hypoalbuminemia (albumin <3 g/dL)
Peripheral edema
Hyperlipidemia
Elevated ESR
Hypercoagulability
Oval fat bodies in the urine
Renal bx may be helpful
78
Q

What do most patients with nephrotic syndrome also have?

A 
DM
Amyloidosis
SLE
Other causes:
Minimal change dz
Membranous nephropathy
Idiopathic
79
Q

Tx of nephrotic syndrome

A

Avoid negative nitrogen balance, replace protein last in urine
Low sodium diet, diuretics
Treat hyperlipidemia, hypercoagulable state
-Loss of protein C, protein S, antithrombin III
-Danger of renal vein thrombosis

80
Q

Minimal change dz

A

MCC of proteinuric renal dz in children, accounting for 80% of cases
S/sx of nephrotic syndrome: proteinuria, hypoalbuminemia, facial edema
In adults, there is a correlation with Hodgkin’s dz
Glomeruli show no changes on light microscopy. On electron microscopy, there is a characteristic effacement of the podocyte foot process

81
Q

Multiple myeloma/amyloid

A

Cancer of the plasma cells
Accumulation of protein in various organs
-Part of a series of protein-deposition diseases
Proteinuria, hypercalcemia
u/s- normal size kidneys
Dx- kidney or bone bx
Tx- oncology management with dialysis at end stage

82
Q

Glomerulonephritis

A

Antigen-antibody complex in glomeruli causing:

  • Inflammation
  • Decreased GFR
83
Q

S/sx of glomerulonephritis

A 
HA
Increased BP
Facial/periorbital edema
Lethargic
Low-grade fever
Weight gain (edema)
Proteinuria
Hematuria
Oliguria
Dysuria
84
Q

Demographics of glomerulonephritis

A

Usually children, ages 2-12 yrs
Status post group A strep infection= within 1-3 wks
-Can occur even after appropriate strep infection tx
RBC casts, hematuria, HTN

85
Q

Labs for glomerulonephritis

A 
\+ASO titer
\+ complement
anti-GBM
ANCA
ANA
Cryoglobin panel
Hep panel
U/A: hematuria, proteinuria, RBCs, WBCs, RBC casts = pathognomonic
86
Q

Diagnostics for glomerulonephritis

A

Renal u/s

Biopsy

87
Q

Tx for glomerulonephritis

A

Supportive
High-dose steroids
-60 mg/day x 12 wks

88
Q

Acute glomerulonephritis in adults

A 
Relatively uncommon
UA: RBC casts
Several types, including:
-Berger dz: MC in adults
-Peri-infection or post-infection glomerulonephritis
- Lupus nephritis
-Goodpasture syndrome (anti-GBM-associated acute glomerulonephritis)
-Pauci- immune glomerulonephritis
--Seen in vasculitis pts
89
Q

S/sx of acute glomerulonephritis

A

Hypertension
Edema most commonly in low tension tissue areas like the scrotum and periorbital area
Hematuria

90
Q

Lab results for acute glomerulonephritis

A 
BUN:Cr >20:1
Urine Na <20
FENA <1
Low serum albumin
May have hyperlipidemia
91
Q

Tx for acute glomerulonephritis

A

Depends on the cause, high-dose steroids are sometimes used

92
Q

Berger disease

A

Cause: IgA deposition in the glomerular mesangium
Can also occur as a secondary dz associated with hepatic cirrhosis, celiac dz, HIV, CMV, GABHS
M > F
Children > adults
Tends to present in individuals of Asian descent

93
Q

Presentation of Berger disease

A

Gross hematuria with upper respiratory tract infection

Occurs 1-2 days after initial URI sx or “synpharyngitic hematuria”

94
Q

Dx of Berger dz

A

Renal bx: IgA and C3 deposits

95
Q

Tx of Berger dz

A

Depends on the extent of the dz
HTN prevention
Renal transplant in some cases

96
Q

Post-infectious glomerulonephritis

A

Seen most commonly following a GABHS infection and occurring on average 7-10 days after initial infection

97
Q

Presentation of post-infectious glomerulonephritis

A

Appears most frequently in children and presents with abrupt onset of nephritic sx and acute kidney injury
Rising ASO titers and low complement levels can be seen

98
Q

Goodpasture syndrome

A

The clinical constellation of glomerulonephritis and pulmonary hemorrhage
Bimodal distribution in the second/third decades of life and again in the sixth/seventh decades

99
Q

Generalized sx of Goodpasture syndrome

A 
Anorexia
Fatigue
Fever
Arthralgia
Weakness
100
Q

Lung sx of Goodpasture syndrome

A

Hemoptysis
Dry cough
CP
SOB

101
Q

Renal sx of Goodpasture syndrome

A

Hematuria
RBC casts
Low level proteinuria

102
Q

CXR on Goodpasture syndrome

A

Fluffy infiltrates up to massive pulmonary hemorrhage

103
Q

Dx of Goodpasture syndrome

A

Confirmed by finding anti-GBM antibodies

CAM III (12 decks)

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