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Pathoma Bina > Kidney/Urinary: Congenital and Acute renal failure > Flashcards

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
Q

what causes prerenal azotemia

A

decreased blood flow to kidneys

26
Q

how does prerenal azotemia impact the kidney, blood, and urine

A

decreases GF
azotemia
oliguria

27
Q

what is the BUN: Cr ration in prerenal azotemia and why?

A

greater than 15

- reabsorption of fluid and BUN back into system

28
Q

what is the tubular function of prerenal azotemia? lab value?

A

remain intact

- fractional excretion of sodium [FENa] less than 1%

29
Q

what is the urine osmolality in prerenal azotemia

A

[osm] greater than 500 mOsm/kg

30
Q

what is postrenal azotemia

A

obstruction of urinary tract downstream from kidney

31
Q

how does postrenal azotemia impact the kidney, blood, and urine

A
  • decrease GFR
  • azotemia
  • oliguria
32
Q

what happens during the early stages of postrenal azotemia? lab values?

A
  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
Q

what happens during the later stages of postrenal azotemia? lab values

A
  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
Q

What is the MOST common cause of acute renal failure

A

acute tubular necrosis

35
Q

What is acute tubular necrosis

A

injury and necrosis of tubular epithelial cells

- necrotic cells plug tubules

36
Q

necrotic cells plug tubule in acute tubular necrosis, which causes what

A
  • decrease GFR

- brown, granular casts seen in urine

37
Q

dysfunctional tubular epithelial cells in acute tubular necrosis results in

A
  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
Q

what are etiologies of acute tubular necrosis

A

ischemia and nephrotoxic

39
Q

what is ischemia of acute tubular necrosis

A
  • decreased blood supply results in necrosis of tubules
40
Q

what usually precedes ischemia of acute tubular necrosis

A

prerenal azotemia

41
Q

what parts of the kidney are susceptible in ischemia acute tubular necrosis

A

proximal tubule and medullary segment of thick ascending limb

42
Q

what causes nephrotoxic acute tubular necrosis

A

toxic agents resulting in necrosis of tubules

43
Q

what part of the kidney is susceptible to nephrotoxic acute tubular necrosis?

A

proxmial tubule

44
Q

nephrotoxic acute tubular necrosis can be caused by

A
  • 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
Q

what is ethylene glycol? characteristics

A

anti-freeze

blue and sweet

46
Q

what is used prior to initiation of chemotherapy of acute tubular necrosis?

this whole processes decreases what?

A

hydration and allopurinol

decrease risk of urate-induced ATN

47
Q

what are clinical features of acute tubular necrosis

A
  • oliguria with brown, granular casts
  • elevated BUN and creatinine
  • hyperkalemia ( due to decreased renal excretion) with metabolic acidosis
48
Q

Can you treat acute tubular necrosis

A

reversible, requires supportive dialysis, electrolyte imbalance can be fatal

49
Q

what happens in oliguria and tubular cells during recovery of acute tubular necrosis

A
  • oliguria persists for 2-3 weeks before recovery

- tubular cells ( stable cells) take time to reenter the cell cycle and regenerate

50
Q

what is acute interstitial nephritis ? what causes it? what does it lead to?

A
  • drug-induced hypersensitivity involving the interstitium and tubules
  • acute renal failure ( intrarenal azotemia)
51
Q

what are some causes of acute interstitial nephritis

A

NSAIDS
penicillin
diuretics

52
Q

clinically how does acute interstitial nephritis present

A

oliguria
fever
rash days to weeks after starting drug
EOSINOPHILS may be present in urine

53
Q

how do you treat acute interstitial nephritis

A

stop taking drug

54
Q

what can acute interstitial nephritis progress to

A

renal papillary necrosis

55
Q

what is renal papillary necrosis

A

necrosis of renal papillae

56
Q

how does renal papillary necrosis present

A

gross hematuria and flank pain

57
Q

what are 4 causes of renal papillary necrosis

A
  1. chronic analgesic abuse
  2. diabetes mellitus
  3. sickle cell trait/disease
  4. severe acute pyelonephritis
58
Q

what can cause chronic analgesic abuse

A

long-term phenacetin or aspirin use

Pathoma Bina (38 decks)

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