Renal - Pathology (Renal Failure, Osteodystrophy, and Cysts) Flashcards

Pg. 544-545 in First Aid 2014 Pg. 496-498 in First Aid 2013 Sections include: -Acute renal failure -Consequences of renal failure -Renal osteodystrophy -Renal cyst disorders (42 cards)

1
Q

In a normal nephron, is BUN reabsorbed? Is creatinine reabsorbed?

A

In normal nephron, BUN is reabsorbed (for countercurrent multiplication), but creatinine is not.

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2
Q

What is the definition of acute renal failure?

A

Acute renal failure is defined as abrupt decline in renal function with increased creatinine and increased BUN over a period of several days

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3
Q

What causes prerenal azotemia?

A

As a result of decrease RBF (e.g., hypotenstion) –> decreased GFR

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4
Q

In response to pre-renal azotemia, what does the kidney do, and why? What clinical significance does this have?

A

Na+/H2O and urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ratio increased.

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5
Q

What is generally the cause of intrinsic renal failure? What is a less common cause of intrinsic renal failure?

A

Generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis (e.g., RPGN).

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6
Q

What effect does intrinsic renal failure have on GFR, and how?

A

Patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule –> decreased GFR.

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7
Q

What is seen in the urine of intrinsic renal failure patients?

A

Urine has epithelial/granular casts

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8
Q

What happens to the BUN/creatinine ratio is intrinsic renal failure, and why?

A

BUN reabsorption is impaired –> decreased BUN/creatinine ratio

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9
Q

In general, what causes postrenal azotemia? Give 4 reasons this cause might happen. What is required for development of postrenal azotemia?

A

Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies); Develops only with bilateral obstruction

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10
Q

What is the expected urine osmolality (mOsm/kg) in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal?

A

(1) > 500 (2) < 350 (3) < 350

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11
Q

What is the expected urine Na (mEq/L) in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal?

A

(1) < 20 (2) > 40 (3) > 40

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12
Q

What is the expected FE Na in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal (mild versus severe)?

A

(1) < 1% (2) > 2 % (3) > 1% (mild), > 2 % (severe)

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13
Q

What is the expected serum BUN/Cr in each of the following conditions: (1) Prerenal (2) Intrinsic Renal (3) Postrenal?

A

(1) > 20 (2) < 15 (3) > 15

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14
Q

What are the 2 forms of renal failure? Give at least one example of each.

A

2 forms of renal failure - acute (e.g., ATN) and chronic (e.g., hypertension, diabetes, congenital anomalies)

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15
Q

What 2 main things are the kidneys of a patient in renal failure unable to do?

A

Inability to (1) make urine and (2) excrete nitrogenous wastes.

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16
Q

What are 8 consequences of renal failure?

A

Consequences: (1) Metabolic Acidosis (2) Dyslipidemia (especially increased triglycerides) (3) Hyperkalemia (4) Uremia (clinical syndrome marked by high BUN and high creatinine) (5) Na+/H2O retention (CHF, pulmonary edema, hypertension) (6) Growth retardation and developmental delay (in children) (7) Renal osteodystrophy; Think: “MAD HUNGER”

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17
Q

What are 3 conditions that may result from Na+/H2O retention due to renal failure?

A

(1) CHF (2) Pulmonary edema (3) Hypertension

18
Q

What defines uremia? What are 5 of its signs/symptoms?

A

Clinical syndrome marked by increased BUN and increased creatinine; (1) Nausea and anorexia (2) Pericarditis (3) Asterixis (4) Encepalopathy (5) Platelet dysfunction

19
Q

What causes anemia in renal failure patients?

A

Failure of erythropoietin production

20
Q

As a consequence of renal failure, dyslipidemia especially pertains to what change?

A

Dyslipidemia (especially increased triglycerides)

21
Q

What consequence can renal failure have especially on children?

A

Growth retardation and developmental delay (in children)

22
Q

What is the definition of renal osteodystrophy? In other words, what factors cause it & what results?

A

Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia –> secondary hyperparathyroidism

23
Q

Besides leading to secondary hyperparathyroidism, like all factors involved in renal osteodystrophy, what additional independent effect does hyperphosphatemia have?

A

Hyperphosphatemia also independently decreases serum Ca2+ by causing tissue calcifications, whereas decreased 1,25-(OH)2 vitamin D –> decreased intestinal Ca2+ absorption

24
Q

What symptom/sign does renal osteodystrophy cause?

A

Causes subperiosteal thinning of bones

25
What are 3 different diseases involving renal cysts?
(1) ADPKD (Autosomal-Dominant Polycystic Kidney Disease) (2) ARPKD (Autosomal-Recessive Polycystic Kidney Disease) (3) Medullary cystic disease
26
What does ADPKD stand for? What was it formerly known as?
Autosomal-Dominant Polycystic Kidney Disease; Formerly adult polycystic kidney disease.
27
What gross features are found in ADPK, and what effect do they have?
Innumberable cysts causing bilateral enlarged kidneys that ultimately destroy the kidney parenchyma
28
How does ADPK present?
Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure
29
What are the 2 mutations associated with ADPK? What percentage of cases does each cause, and on what chromosome is each found?
Autosomal-Dominant mutation in PKD1 (85% of cases, chromosome 16) or PKD2 (15% of cases, chromosome 4)
30
What causes death in ADPK patients?
Death from complications of chronic kidney disease or hypertension (caused by increased renin production).
31
What are 3 conditions with which ADPK is associated?
Associated with (1) berry aneurysms, (2) mitral valve prolapse, (3) benign hepatic cysts
32
What does ARPKD stand for? What was it formerly known as?
Autosomal Recessive Polycystic Kidney Disease; Formerly infantile polycystic kidney disease
33
Describe the presentation of ARPKD.
Infantile presentation in parenchyma.
34
With what disorder is ARPKD associated? What can ARPKD lead to if there is significant real failure in utero?
Associated with congenital hepatic fibrosis; Signifiant renal failure in utero can lead to Potter's syndrome
35
What are 3 ARPKD concerns beyond the neonatal period?
Concerns beyond neonatal period include hypertension, portal hypertension, and progressive renal insufficiency
36
What is Medullary cystic disease? In other words, what causes it & what does it cause?
Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine.
37
What defines Medullary cystic disease on imaging? What is not visualized?
Shrunken kidneys on ultrasound; Medullary cysts usually not visualized
38
What is the prognosis like for Medullary cystic disease?
Poor prognosis
39
Where are simple renal cysts usually found, and with what are they filled?
Simple cysts usually found in outer cortex, filled with ultrafiltrate
40
In general, how common are simple renal cysts?
Very common, and account for majority of all renal masses
41
How are simple renal cysts found, and how do they typically present?
Found incidentally and typically asymptomatic.
42
What kind of cysts are included in the term complex renal cyst? How are they managed, and why?
Complex cysts, including those that are septated, enhanced, or have solid components as seen on CT, require follow-up or removal due to risk of renal cell carcinoma