Kidney/Urinary: Congenital and Acute renal failure Flashcards

1
Q

What is the most common congenital renal anomaly

A

horseshoe kidney

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2
Q

What is horseshoe kidney

A

conjoined kidney usually at lower pole

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3
Q

where is horseshoe kidney abnormally located

A

lower abdomen

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4
Q

where do normal kidneys develop

A

pelvis

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5
Q

what problem occurs when horseshoe kidney ascends from pelvis to lower abdomen

A

get caught on inferior mesenteric artery

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6
Q

what is renal agenesis?

A

absent kidney formation

- may be unilateral or bilateral

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7
Q

renal agenesis unilateral leads to what consequence?

A

hypertrophy of existing kidney

- hyperfiltration increases risk of renal failure later in life

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8
Q

renal agenesis bilateral leads to what consequence?

A

oligohydramnios with lung hypoplasia

Potter’s sequence

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9
Q

What are the symptoms for Potter’s sequence? Is it compatible with life?

A

flat face
low set ears
developmental defects of extremities
- incompatible with life

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10
Q

what is dysplastic kidney disease

A
  • inherited, congenital malformation of renal parenchyma characterized by cysts and abnormal tissue (cartilage)
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11
Q

what is polycystic kidney disease

A
  • inherited defect leading to bilateral enlarged kidneys with cysts in renal cortex and medulla
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12
Q

what are two forms of polycystic kidney disease (PKD)

A

Autosomal recessive

Autosomal dominant

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13
Q

autosomal recessive polycystic kidney disease presents in who? How does it present

A

infants

  • worsening kidney failure and hypertension
  • newborns present with Potter sequence
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14
Q

autosomal recessive polycystic kidney disease is associated with what congenital abnormality

A

congenital hepatic fibrosis (leads to portal hypertension)

hepatic cysts

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15
Q

Autosomal dominant polycystic kidney disease presents in who and clinical features

A

young adults

  • hypertension ( due to increase renin)
  • hematuria
  • worsening renal failure
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16
Q

autosomal dominant polycystic kidney disease is due to what mutation which causes what

A

APKD1 and APKD2

cysts develop over time

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17
Q

autosomal dominant polycystic kidney disease is associated with what health problems

A
  • berry aneurysm
  • hepatic cysts
  • mitral valve prolapse
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18
Q

Which congenital kidney problem is not inherited

A

dysplastic kidney

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19
Q

What happens to the size of kidneys in polycystic kidney disease

A

enlarged

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20
Q

what is medullary cystic kidney disease inherited

A

autosomal dominant

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21
Q

what is medullary cystic kidney disease

A

cysts in medullary collecting ducts

- parenchymal fibrosis results in shrunken kidneys and worsening renal failure

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22
Q

oliguira

A

low production of urine

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23
Q

azotemia? what lab values are associated with it

A

increase nitrogen-containing waste products in blood

- increased BUN and creatinine [Cr]

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24
Q

what is a common cause of acute renal failure

A

prerenal azotemia

25
what causes prerenal azotemia
decreased blood flow to kidneys
26
how does prerenal azotemia impact the kidney, blood, and urine
decreases GF azotemia oliguria
27
what is the BUN: Cr ration in prerenal azotemia and why?
greater than 15 | - reabsorption of fluid and BUN back into system
28
what is the tubular function of prerenal azotemia? lab value?
remain intact | - fractional excretion of sodium [FENa] less than 1%
29
what is the urine osmolality in prerenal azotemia
[osm] greater than 500 mOsm/kg
30
what is postrenal azotemia
obstruction of urinary tract downstream from kidney
31
how does postrenal azotemia impact the kidney, blood, and urine
- decrease GFR - azotemia - oliguria
32
what happens during the early stages of postrenal azotemia? lab values?
1. increased tubular pressure 'forces' BUN into blood; BUN:Cr greater than 15 2. tubular function remains intact; FENa less than 1% 3. urine osmolality; osm greater than 500 mOsm/kg
33
what happens during the later stages of postrenal azotemia? lab values
1. tubular damage , decrease absorption of BUN; BUN: Cr less than 15 2. decreased reabsorption of sodium; FENa greater than 2% 3. inability to concentrate urine; less than 500
34
What is the MOST common cause of acute renal failure
acute tubular necrosis
35
What is acute tubular necrosis
injury and necrosis of tubular epithelial cells | - necrotic cells plug tubules
36
necrotic cells plug tubule in acute tubular necrosis, which causes what
- decrease GFR | - brown, granular casts seen in urine
37
dysfunctional tubular epithelial cells in acute tubular necrosis results in
1. decreased reabsorption of BUN (serum BUN:Cr greater than 15) 2. decreased reabsorption of sodium ( FENa less than 2%) 3. inability to concentrate urine ( urine osm less than 500 )
38
what are etiologies of acute tubular necrosis
ischemia and nephrotoxic
39
what is ischemia of acute tubular necrosis
- decreased blood supply results in necrosis of tubules
40
what usually precedes ischemia of acute tubular necrosis
prerenal azotemia
41
what parts of the kidney are susceptible in ischemia acute tubular necrosis
proximal tubule and medullary segment of thick ascending limb
42
what causes nephrotoxic acute tubular necrosis
toxic agents resulting in necrosis of tubules
43
what part of the kidney is susceptible to nephrotoxic acute tubular necrosis?
proxmial tubule
44
nephrotoxic acute tubular necrosis can be caused by
- aminoglycosides - heavy metals ( lead) - myoglobinuria ( from crush injury to muscle) - ethylene glycol ( associated with oxalate crystals in urine) - radiocontrast dye - urate ( tumor lysis syndrome)
45
what is ethylene glycol? characteristics
anti-freeze | blue and sweet
46
what is used prior to initiation of chemotherapy of acute tubular necrosis? this whole processes decreases what?
hydration and allopurinol decrease risk of urate-induced ATN
47
what are clinical features of acute tubular necrosis
- oliguria with brown, granular casts - elevated BUN and creatinine - hyperkalemia ( due to decreased renal excretion) with metabolic acidosis
48
Can you treat acute tubular necrosis
reversible, requires supportive dialysis, electrolyte imbalance can be fatal
49
what happens in oliguria and tubular cells during recovery of acute tubular necrosis
- oliguria persists for 2-3 weeks before recovery | - tubular cells ( stable cells) take time to reenter the cell cycle and regenerate
50
what is acute interstitial nephritis ? what causes it? what does it lead to?
- drug-induced hypersensitivity involving the interstitium and tubules - acute renal failure ( intrarenal azotemia)
51
what are some causes of acute interstitial nephritis
NSAIDS penicillin diuretics
52
clinically how does acute interstitial nephritis present
oliguria fever rash days to weeks after starting drug EOSINOPHILS may be present in urine
53
how do you treat acute interstitial nephritis
stop taking drug
54
what can acute interstitial nephritis progress to
renal papillary necrosis
55
what is renal papillary necrosis
necrosis of renal papillae
56
how does renal papillary necrosis present
gross hematuria and flank pain
57
what are 4 causes of renal papillary necrosis
1. chronic analgesic abuse 2. diabetes mellitus 3. sickle cell trait/disease 4. severe acute pyelonephritis
58
what can cause chronic analgesic abuse
long-term phenacetin or aspirin use