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PATH MAGIC > RENAL PATHOLOGY 2 > Flashcards

RENAL PATHOLOGY 2 Flashcards

1
Q

acute renal failure

A

Oliguria/anuria, recent onset azotemia, HTN

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2
Q

Acute tubulointerstitial nephritis is often a drug hypersensitivity (1) are a common cause) in which numerous (2) are present in the urine as well as in the tissues.

A
  1. penicillins 2. eosinophils
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3
Q

Tophi- causes

A

Gout. tumor lysis syndrome

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4
Q

The maintenance phase of ATN:Urine output ____, ____ overload, rising BUN concentrations, ___kalemia, and metabolic acidosis

A

1) 400 mL/day (oliguria) OR low; salt and water;hyper

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5
Q

Acute tubular necrosis: The cells are then sloughed into the tubule, forming (1) which obstruct it, causing back pressure as well as tubuloglomerular feedback, which causes (2).

A
  1. casts 2. afferent arteriolar vasoconstriction and decreased filtration
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6
Q
  1. ___ is induced experimentally by mixture of aspirin and phenacetin,
  2. Analgesic nephropathy may lead to ___
A

Papillary necrosis;

transitional papillary carcinoma of the renal pelvis, tubulointerstitial nephritis, papillary carcinoma

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7
Q

AKI-ATN begins with an initiation phase over the first 36 hours with a decline in (1) and increased (2)

A
  1. urine output 2. BUN
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8
Q

(1) can cause what is termed post-renal azotemia which has (2) BUN/creatinine ratio.

A
  1. Obstruction to the urinary tract 2. HIGH
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9
Q

(1) can cause pre-renal azotemia, which is generally found with (2) BUN/creatinine ratio.

A
  1. Decreased renal blood flow 2. elevated
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10
Q

LOW GFR

A

increasing BUN

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11
Q

Acute renal failure can be a consequence of problems with ?

A

blood vessels, glomeruli, tubules, or the interstitium.

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12
Q

Patients with acute tubulointerstitial nephritis may also have (1)

A
  1. fever, peripheral eosinophila, hematuria, and proteinuria.
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13
Q

Acute Tubulointerstitial Nephritis

15 days after drug exposure–> fever, ___, maculopapular rash, hematuria, mild proteinuria, and leukocyturia (often including ___ in urine)

A

eosinophilia; eosinophils

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14
Q 
radiographic contrast agents
 heavy metals (mercury)
 organic solvents (carbon tetrachloride).
A

Nephrotoxic AKI

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15
Q

gentamicin and other antibiotics

A

Nephrotoxic AKI

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16
Q

Oliguria, azotemia, proteinuria, HTN, hematuria

A

Nephritic syndrome

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17
Q

In bilateral agenesis, the absence of urine prevents the development of (1) and the subsequent pressure needed for (2) development (this disorder is called (3): they have strange facial development as well, from the loss of amniotic fluid pressure).

A
  1. amniotic fluid 2. lung 3. Potter’s syndrome
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18
Q

Bilateral agenesis is a fairly common lethal congenital abnormality which leads to stillborn infants who are born with (1)

A
  1. hypoplastic lungs.
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19
Q

___ most frequently occurs with synthetic penicillins
(methicillin, ampicillin), other synthetic antibiotics (rifampin), diuretics (thiazides),
NSAIDs, and miscellaneous drugs (allopurinol, cimetidine).

A

Acute tubulointerstitial nephritis

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20
Q

Acute tubular necrosis: There can also be fluid leakage and inflammation within the interstitium between tubules if

A

BM is damaged

21
Q

what do these cause?

  1. gentamicin and other antibiotics
  2. radiographic contrast agents
  3. heavy metals (mercury)
  4. organic solvents (carbon tetrachloride).
  5. mismatched blood transfusions and other hemolysis causing hemoglobinuria
  6. skeletal muscle injuries causing myoglobinuria
    characteristic intratubular hemoglobin or myoglobin casts
    toxic iron content of these globin molecules contributes to the AKI
A

B. Nephrotoxic ATN

22
Q

GFR formula

A

(urine creatinine X urine volume)/ serum creatinine

23
Q

Recovery phase ATN/AKI

1) in urine volume that may reach up to 3 L/day;

Loss of 2) ;

Hypokalemia, rather than hyperkalemia; ALSO increased risk of 3)

A

1) Increase;
2) H20, Na, and K
3) INFECTION

24
Q

Most patients recover from ATN/AKI unless ___________

A

BM is damaged

25
Q

Ischemic acute tubular necrosis; type of necrosis? Inflammation present or absent?

A

Coagulative with LACK of inflammation

26
Q

If the cause of ATN is reversed or eliminated, then there is a (1) recovery phase, which can have (2)

A
  1. diuretic (high urine output) 2. ery high urine outputs.
27
Q

Ischemic changes

A. reversible injury–> signs?
B. lethal injury–> necrosis and apoptosis

A

cellular swelling, loss of brush border & polarity, blebbing, cell detachment

28
Q

Acute tubular necrosis: decreased (1) to the (2) produces necrosis of the (3)

A
  1. blood flow or oxygen delivery 2. proximal tubules 3. proximal tubule cells.
29
Q

Acute renal failure due to ethylene glycol (antifreeze) poisoning produces (1) histologically

A
  1. hydropic degeneration of the proximal convoluted tubules.
30
Q

The most common cause of AKI is a pathologic entity known as (1).

A
  1. acute tubular necrosis
31
Q

A maintenance phase follows the initiation phase of ATN/AKI with ?

A

oliguria, rising BUN, hyperkalemia, and metabolic acidosis (from inability to excrete urea, potassium and acid).

32
Q

Acute renal failure most commonly presents with ?

A

anuria (complete absence of urine) or oliguria (decreased urine flow), and azotemia (elevated BUN).

33
Q

Although pathologists enjoy looking at glomeruli, we must remind ourselves that (1) can be equally as, or potentially more, important in acute renal failure.

A
  1. tubular defects
34
Q

Because the flow rate is slow, most of the BUN can be reabsorbed, explaining the high ratio (more than 15 Fold) relative to the creatinine.

A

Pre-renal azotemia

35
Q

Ischemic ATN/AKI etiology:

Severe ___ and ____

Decreased blood flow accompanied by __ and ____

A

trauma; acute pancreatitis;

marked hypotension and shock

36
Q

Nephrotoxic AKI/ATN

Skeletal muscle injuries causing ___
characteristic ____ casts
toxic iron content of these globin molecules contributes to the ___

A

myoglobinuria; intratubular hemoglobin or myoglobin;

AKI

37
Q

Glomerular filtration rate can be calculated by determining the (1) clearance, which is equal to (2)

A
  1. creatinine 2. urine creatinine concentration x urine volume, divided by the serum creatinine concentration (UV/P)
38
Q

a decline in urine output with a rise in BUN

A

Initiation phase (36 hours) of ATN

39
Q

Biochemical changes in ischemia:

  1. depletion of ___
  2. accumulation of ___
  3. activation of proteases (calpain) which cause ____
  4. activation of phospholipases, which damage ___
  5. generation of reactive oxygen species
  6. activation of caspases, which induce apoptotic cell death
A

ATP;

2) intracellular calcium
3) cytoskeletal disruption
4) membranes

40
Q
  1. hyaline CAST is composed of
A
  1. Tamm-Horfstall urinary glycoprotein
41
Q

Osteomalacia/osteopenia/fracture

A

Uremia/renal failure

42
Q

PERIPHERAL NEUROPATHY- RENAL FAILURE IS DUE TO_____

A

ACCUMULATION OF AMYLOID

43
Q

ACUTE CHEST PAIN- RENAL FAILURE IS DUE TO_____

A

ACUTE FIBRINOUS PERICARDITIS

44
Q

GASTRIC PAIN AND HEMATEMESIS- RENAL FAILURE IS DUE TO_____

A

ACUTE GASTRITIS (RECALL EROSION)

45
Q

MANAGE THE UREMIA PATIENT WITH VITAMINE____

A

D

46
Q

PARATHORMONE IN RENAL FAILURE IS____

A

HIGH

47
Q

PROLONGED BLEEDING TIME IN RENAL FAILURE IS DUE TO_______

A

PLATELET DYSFUNCTION

48
Q

ANEMIA IN RENAL FAILURE IS DUE TO_______

A

DECREASED EPO

49
Q

METABOLIC ACIDOSIS IN UREMIA IS DUE TO_____________

A

LOSS OF BICARB

PATH MAGIC (21 decks)

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