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Nefrologi > Akutt nyresykdom - Amboss > Flashcards

Akutt nyresykdom - Amboss Flashcards

1
Q

Hvilken etiologi kan akutt nyreskade ha?

A

Prerenal akutt nyreskade

Intrarenal akutt nyreskade

Postrenal akutt nyreskade

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2
Q

Hva mener man med prerenal akutt nyreskade?

A

Prerenal causes include any condition that leads to decreased renal perfusion (∼ 60% of cases of AKI).

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3
Q

Hvilke tilstander kan føre prerenale akutte nyreskader?

A
Hypercalcemia often results in polyuria due to the suppression of aquaporin-2 in the collecting duct and the inhibition of sodium and chloride reabsorption in the loop of Henle, reducing the kidney's urinary concentrating ability, which leads to volume depletion. NSAIDs constrict the afferent arteriole, reducing intraglomerular hydrostatic pressure and thereby decreasing glomerular filtration rate (GFR). ACE-Is inhibit angiotensin II-mediated vasoconstriction of the efferent arterioles, reducing intraglomerular hydrostatic pressure and thereby decreasing GFR.
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4
Q

Hva mener man med intrarenale akutt nyreskade?

A

Intrinsic causes include any condition that leads to severe direct kidney damage (∼ 35% of cases of AKI).

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5
Q

Nevn noen tilstander som kan gi akutte intrarenale skader?

A

Akutt tubulær nekrose

Akutt interstitiell nefritt

Glomerulonefritter, f.eks. rask progressiv glomerulonefritt

Vaskulære sykdommer

Hemolytisk uremisk syndrom (HUS)

Trombotisk trombocytopenisk purpura

Hypertensive kriser

Vaskulitter; skleroderma renal krise

Renal venetrombose, renal atheroemboli og renalt infarkt.

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6
Q

Hva er akutt tubulær nekrose?

A
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7
Q

Hva kan gi akutt interstitiell nefritt?

A
Including penicillin, cephalosporins, sulfonamides, ciprofloxacin, acyclovir, and rifampin. Either systemic infections or those that directly affect the renal parenchyma.
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8
Q

Hva mener man med postrenal akutt nyreskade?

A

Postrenal causes include any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra (∼ 5% of cases of AKI).

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9
Q

Hva kan gi postrenal akutt nyreskade?

A
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10
Q

Fyll ut bildet som viser etiologien til akutt nyreskade?

A
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11
Q

Hvilke typer antimikrobielle midler er nyretoksisk?

A

Antibiotika

Antimykotika

Antivirale midler

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12
Q

Hvilke typer ab. er nyretoksisk?

A
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13
Q

Hvilke typer antivirale midler er nyretoksisk?

A
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14
Q

Nevn et eks. på et antimykotika som er nyretoksisk?

A

Amphotericin B

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15
Q

Nevn hhv. noen nyretoksiske medikamenter i gruppen:
- Antimetabolitter
- Kjemoterapeutiske midler
- Antiinflammatoriske og immundempende midler
- Andre

A
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16
Q

Hva er patofysiologien til prerenal akutt nyreskade?

A
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17
Q

Hvordan kan BUN gi oss svaret på hvilken årsak som er ansvarlig for nyreskade?

A
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18
Q

Fyll ut tabellen

A
Mechanism of action: renin-angiotensin-aldosterone system (RAAS) inhibitors: Renin is produced in response to changes in the glomerular filtration rate and solute content of the blood within the renal corpuscle. Renin catalyzes the conversion of angiotensinogen (produced by the liver) to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE; produced by the lungs). Angiotensin II acts to increase blood pressure by causing vasoconstriction, sodium retention, and ADH production. The specific targets of the different RAAS inhibitors are highlighted in red.
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19
Q

Hva er patofysiologien til intrarenal akutt nyreskade?

A
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20
Q

Hva er patofysiologien til prerenal akutt nyreskade?

A
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21
Q

Hvilke fire faser har den akutte nyreskaden?

A
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22
Q

Hva kjennetegner den første fasen ved akutt nyreskade?

A
Urine output may already be low.
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23
Q

Hva kjennetegner den andre fasen ved akutt nyreskade (ANS)?

A
In AKI, the glomerular filtration rate is initially reduced by hypoperfusion, urinary tract obstruction, or damage to the glomeruli, which results in accumulation of urinary waste products and reduced production of urine.
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24
Q

Hva kjennetegner den tredje fasen ved ANS?

A
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25
Q

Hva kjennetegner den fjerde fasen ved ANS?

A
In some cases, kidney function remains permanently compromised.
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26
Q

Hva kjennetegner klinikken ved ANS?

A

Kan være asymptomatisk

Oliguri eller anuri:
- Oliguri er lav diurese, som vil si liten urinmengde over et visst tidsrom. Oliguri defineres som mindre enn 500 milliliter urin per døgn (SNL).
- Anuri er manglende urinutskillelse. Det er definert som mindre enn 0,2 liter urin per døgn (SNL).

Tegn til væsketap (ved prerenal ANS skyldes volumtap).

Tegn til overvæsking (pga. Na+ og H20 retensjon).

Tegn til uremi

Tegn til renal obstruksjon (ved postrenal ANS).

Fatigue, forvirring og letargi:
- Letargi er en tilstand med endret bevissthetsnivå som ligner på en slags våken søvntilstand. Pasienten mangler energi, tiltak, viser ingen følelser og virker trøtt, utslitt, apatisk og tiltaksløs (SNL).

I alvorlige tilfeller kan det oppstå anfall eller koma

Individer som er rammet av ANS har en høyere risiko for sekundærinfeksjoner gjennom alle fasene. Er den vanligste grunnen til død:
- Fortsatt ukjent årsak til dette, men kan skyldes en forsinket/hemmet immunrespons og/eller eksogene infeksjoner (pga. urin kateter, suprapubisk kateter).

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27
Q

Hva er tegn på væsketap ved ANS?

A
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28
Q

Hva kan være tegn på overvæsking ved ANS?

A
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29
Q

Hva er tegn på uremi ved ANS?

A
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30
Q

Hva er tegn på renal obstruksjon ved postrenal ANS?

A
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31
Q

Hvordan er epidemiologien til akutt tubulær nekrose, og hvor sitter årsaken ved lidelsen?

A
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32
Q

Hvilken etiologi kan akutt tubulær nekrose?

A

Iskemisk

Toksisk

Sepsis

Infeksjoner

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33
Q

Hva er årsaken til iskemisk akutt tubulær nekrose?

A
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34
Q

Hva kan årsaken til toksisk vaskulær tubulær nekrose være?

A
E.g., in tumor lysis syndrome.
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35
Q

Hva er patofysiologien ved akutt tubulær nekrose?

A

Pathophysiology:

Necrotic proximal tubular cells fall into the tubular lumen → debris obstructs tubules → decreased GFR → sequence of pathophysiological events similar to prerenal failure (i.e., activation of RAAS).

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36
Q

Hvordan er klinikken ved akutt tubulær nekrose?

A

Samme som ved ANS

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37
Q

Hvordan kan man diagnostisere akutt tubulær nekrose?

A
In acute tubular necrosis (ATN), the epithelial cells of the renal tubules slough off and the tubular basement membrane is denuded.
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38
Q

Hvordan er prognosen ved akutt tubulær nekrose?

A
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39
Q

Fyll inn figuren

A
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40
Q

Hva viser bildet?

A
Renal infarction; Photomicrograph of a renal biopsy sample (H&E stain). The cells of the tubules and glomeruli show clumped and highly eosinophilic cytoplasm. The nuclei of these cells are either absent or palely staining. There is debris in some tubular lumens and thrombi are visible in the capillaries on the lower right. The main outlines of the tubules and glomeruli are still intact.
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41
Q

Hva viser bildet?

A
Urine casts in acute tubular necrosis. Photomicrograph of urine sediment (high magnification). Renal tubular epithelial cell casts (a) and muddy brown casts (b) were identified in this urine sample. Both findings indicate damage of the kidneys, likely due to acute tubular necrosis.
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42
Q

Hva viser bildet?

A
Coagulative necrosis in renal infarction; Photomicrograph of kidney tissue (H&E stain; 150x magnification). A large area of necrosis (green overlay) is visible. Necrotic glomeruli (green arrowheads) are also visible within a highly dense area of leukocytes (white overlay). This is in contrast to the appearance of a normal glomerulus (black arrowhead). These findings are consistent with coagulative necrosis caused by renal infarction.
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43
Q

Hva viser pilen til?

A
44
Q

Hva viser pilen til?

A
45
Q

Hva viser pilen til?

A
46
Q

Hva viser pilen til?

A
47
Q

Hva viser pilene til?

A
Arcuate vein: Corresponding to the artery to the left: an arcuate vein.
48
Q

Hva ser man i dette området?

A
49
Q

Hva viser pilene til?

A
Healthy tubule: Tubules in healthy renal tissue have cuboidal epithelial cells with round nuclei.
50
Q

Hva viser pilen til?

A
51
Q

Hva viser pilen til?

A
52
Q

Hva ser man i dette området?

A
53
Q

Hva ser man i dette området?

A
54
Q

Hva ser man i dette området?

A
55
Q

Hva er renal kortikal nekrose?

A

Definition:

Rare cause of AKI caused by acute generalized ischemic necrosis of the renal cortex in both kidneys

Etiology:

Septic shock, disseminated intravascular coagulation (DIC), hemolytic uremic syndrome (HUS), obstetric complications (e.g., abruptio placentae, septic abortion, postpartum hemorrhage)

Pathophysiology:

Vasospasms and microvascular injury with vascular thrombosis → prolonged severe renal ischemia → diffuse and/or patchy destruction of the renal cortex
- A shorter period of renal ischemia usually causes acute tubular necrosis, as renal tubular cells are most sensitive to a decrease in oxygen supply.

Clinical features:

Flank pain, CVA tenderness and signs of AKI

Management:

Dialysis can improve outcomes

Prognosis:

High mortality rates without treatment

56
Q

Hva er definisjonen for kontrastindusert nefropati, og hvilke risikofaktorer finnes?

A
57
Q

Hvordan utvikler kontrastindusert nefropati seg?

A
58
Q

Hvordan forhindrer man utviklingen av kontrastindusert nefropati?

A
Studies investigating acetylcysteine's effectiveness in preventing contrast-induced nephropathy have yielded conflicting findings.
59
Q

Hvordan diagnostiserer man ANS, og hvordan tilnærmer man seg evalueringen av diagnosen?

A
If no previous levels are available, evaluate the patient for other factors that indicate AKI such as a recent inciting event (e.g., diarrheal illness, medication or toxin exposure), evidence of urinary retention, signs of systemic illness, the recent onset of symptoms, oliguria or anuria, and/or a daily rise in creatinine levels. Identify potential inciting events and assess the patient's volume status. E.g., IV fluids, diuretics, relief of urinary tract obstruction.
60
Q

Hva er diagnostiske kriteriene for ANS?

A
These definitions are consistent with the 2012 Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury. Urine output may be normal or increased at disease onset due to impaired water reabsorption as a result of renal tubular dysfunction.
61
Q

Hvordan stager man ANS?

A
62
Q

Hvor mange stadier deler KDIGO ANS i?

A

AKI stage 1

AKI stage 2

AKI stage 3

63
Q

Hva kjennetegner stadie 1 i KDIGO sine kriterier for ANS?

A
64
Q

Hva kjennetegner stadie 2 av KDIGO sine kriterier for ANS?

A
65
Q

Hva kjennetegner stadium 3 av KDIGO sine kriterier for ANS?

A
66
Q

Fyll inn tabellen

A
67
Q

Hvordan kan man skille på hvor patologien ved ANS sitter ved bruk av ulike diagnostiske metoder?

A
68
Q

Hva viser prøveverdiene hvis patologien skyldes prerenal ANS?

A
69
Q

Hva viser prøveverdiene hvis patologien skyldes intrarenal ANS?

A
70
Q

Hva viser prøveverdiene hvis patologien skyldes postrenal ANS?

A
71
Q

Hva er den diagnostiske verdien av BUN:kreatinin ratio, FENa og FEUrea?

A
72
Q

Hva slags type prøve er:
- BUN:Kreatinin ratio
- FENa
- FEUrea

A

BUN/creatinine ratio

A ratio of the concentration of blood urea nitrogen to the serum creatinine concentration. Can be used to help identify the cause of acute kidney injury (AKI). A ratio ≥ 20:1 indicates renal hypoperfusion (e.g., hypovolemia, renal artery stenosis) which is referred to as prerenal AKI. A ratio < 15:1 indicates intrinsic renal damage (e.g., glomerulonephritis), which is referred to as intrarenal AKI. A ratio between 10:1 and 20:1 can also be seen in healthy individuals and patients with urinary tract obstruction that causes postrenal AKI.

FENa; Fractional excretion of sodium

The percentage of glomerular filtered sodium (Na) that is excreted in the urine in relation to filtered creatinine (Cr). FENa (%) = (serum Cr × urine Na)/(serum Na × urine Cr) × 100. Used to determine the mechanism of acute kidney injury and hyponatremia. FENa < 1% is consistent with prerenal causes, while FENa > 2–3% suggests intrinsic causes.

FEUrea; Fractional excretion of urea

The percentage of glomerular filtered urea (Ur) that is excreted in the urine in relation to filtered creatinine (Cr). FEUrea (%) = (serum Cr × urine Ur)/(serum Ur × urine Cr) × 100. Used to determine the mechanism of acute kidney injury and hyponatremia. FEUrea < 35% is consistent with prerenal causes, while FEUrea > 50% suggests intrinsic causes.

73
Q

Hvordan vil man i praksis kunne skille på lokalisasjonen til ANS?

A
74
Q

Hva viser bildet?

A
Urine casts in acute tubular necrosis; Photomicrograph of urine sediment (high magnification). Renal tubular epithelial cell casts (a) and muddy brown casts (b) were identified in this urine sample. Both findings indicate damage of the kidneys, likely due to acute tubular necrosis (intrarenal AKI).
75
Q

Hva viser bildet?

A
Red blood cell (RBC) casts in urine sediment; Photomicrograph of urine sediment (phase-contrast microscopy). A tubular cast (blue overlay) is visible in the center of the image. The cast is composed of numerous RBCs, identifiable by their characteristic biconvex shape (examples outlined in yellow), in a matrix of fibrin and plasma proteins. Several epithelial cells surrounding the RBC cast are also visible. RBC casts in urinary sediment are typically seen in glomerulonephritis.
76
Q

Hva viser bildet?

A
Maltese cross sign; Polarized light micrograph of lyotropic liquid crystals. These Lα liquid crystals have a characteristic Maltese cross appearance under polarized light. Fatty casts from urinary sediment have the same appearance under polarized light.
77
Q

Hva viser bildet?

A
White blood cell casts; Photomicrograph of urine sediment (phase-contrast microscopy; high magnification) White blood cell (WBC) casts (blue overlay) contain leukocytes (examples outlined in yellow) that are compressed in a matrix. Sharp margins are characteristic of WBC casts, differentiating them from randomly assembled leukocyte conglomerates.
78
Q

Hva finner man i blod- og urinprøver ved prerenal ANS? Hvilke kliniske tegn finner man?

A
Perfusion deficit to the kidneys → ↓ urinary filtration and ↓ urine flow within the renal tubules → prolonged urine passage → renal tubular cells reabsorb more urea than usual while creatinine is not reabsorbed. Other causes of elevated BUN:creatinine ratio include an increase in urea absorption in the gut, e.g., in patients with upper GI bleeding, and conditions that cause low creatinine, e.g., loss of muscle mass. This reflects an appropriate tubular response (i.e., avid reabsorption of sodium and urea) to a low-perfusion state. This is due to avid water reabsorption stimulated by antidiuretic hormone in the setting of low effective arterial volume and reflects a normal tubular response, as tubular function is still intact in prerenal AKI. E.g., IV fluids for hypovolemia or diuretics for hypervolemia in cardiorenal syndrome.
79
Q

Hva finner man ved blodprøver ved intrarenal ANS?

A
Tubular dysfunction leads to impaired reabsorption of urea.
80
Q

Hva finner man ved urinprøver ved intrarenal ANS?

A
Due to an impaired ability to reabsorb sodium and urea. Due to an inability to concentrate urine. A falsely low FENa may be seen in some patients with intrinsic AKI, e.g., due to glomerulonephritis, acute interstitial nephritis, rhabdomyolysis, or contrast-induced nephropathy.
81
Q

Når er det indikasjon for biopsi ved intrarenal ANS?

A

Ved. f.eks. mistanke om rask og progressiv glomerulonefritt.

82
Q

Hva er kliniske funn ved intrarenal ANS?

A

Clinical findings:

Lack of response to acute intervention

E.g., no decline in creatine level or increase in urine output following a trial of IV fluid therapy or after a trial of diuretics in patients with suspected cardiorenal syndrome with hypervolemia.

83
Q

Hva er blod- og urinprøvefunn ved postrenal ANS?

A
E.g., in obstructive nephropathy, urine osmolality is low (< 350 mOsm/kg) because of an impaired ability to concentrate urine.
84
Q

Hvilken bildemodalitet er akt. ved postrenal ANS?

A

Imaging (renal ultrasound or noncontrast CT scan) may show:

Bladder distention, high postvoid residual volume, bilateral hydronephrosis, and/or obstructing stones.

Distensjon; Utspenning.

85
Q

Hva er kliniske funn ved postrenal ANS?

A

Clinical findings:

Rapid improvement in renal function following resolution of the obstruction.

86
Q

Hva viser bildet?

A
Hydronephrosis, grade 4; Ultrasound right kidney (transverse plane). There is marked dilatation of the collecting system (green overlay) with calyceal clubbing. Renal atrophy is seen as cortical thinning (red overlay). The findings are consistent with grade 4 hydronephrosis (Society of Fetal Urology (SFU) grading system). Li: liver.
87
Q

Hvilke tilleggsus. bør man vurdere for å finne ut hvor patologien sitter ved ANS?

A
A urinary tract obstruction is unlikely to be detected on ultrasound in the absence of clinical suspicion. Ultrasound may provide additional useful information, e.g., it may detect signs of CKD and can assess for renal artery stenosis with doppler.
88
Q

Hva viser bildet?

A
Hydronephrosis; Ultrasound left kidney (longitudinal plane). The calyces (green overlay) are dilated and have lost their normal cup-shaped appearance. Flattening of papillae and blunting of fornices can be seen. Where visible, the renal cortical parenchyma is not thinned. RP: renal parenchyma; Arrowheads: hyperechoic renal sinus.
89
Q

Hva viser bildet?

A
Hydronephrosis Grade I; Sonogram of a kidney (left image - longitudinal section, right image - transverse section). The outline of the kidney is marked with a white dotted line. The renal pelvis is dilated (green overlay). This is the appearance of a grade I hydronephrosis.
90
Q

Hva viser bildet?

A
Hydronephrosis; Ultrasound of the left kidney (longitudinal view). The outline of the kidney is pictured (dashed line) in the center of the image. Multiple hypoechoic areas (green overlay), indicating pelvicalyceal dilatation (hydronephrosis), are visible in the central region of the kidney (white area: spreading central echo complex). This combination of findings indicates a grade II hydronephrosis. U: a section of the dilated ureter. Legend (bottom left): four grades of hydronephrosis as classified by the severity of pelvicalyceal dilation (grade I on left; grade IV on right; grade II has been highlighted).
91
Q

Hva viser bildet?

A
Chronic ureteral obstruction; CT abdomen and pelvis (without contrast; coronal plane) of a patient with a history of neurogenic bladder and recurrent urinary infections. The renal calyces, pelves, and ureters are dilated (green overlay), with normally concave (cup-shaped) renal calyces appearing convex (club-shaped; examples indicated by arrowheads). Thinning of the renal parenchyma (examples indicated by white dashed lines on the parenchymal edge) suggests that the dilatation is chronic rather than acute. Marked thickening of the bladder wall (red overlay) is likely responsible for chronic ureteral obstruction.
92
Q

Hva viser bildet?

A
Ureter calculus with hydronephrosis; CT abdomen (without contrast; axial plane). The rounded hyperdense structure (red arrow) medial to the left kidney is a ureteral calculus. Mild dilatation of the ureter (green overlay) is also visible. An additional, very small calculus (red overlay) is present in a dilated calyx. K: kidney.
93
Q

Hva viser bildet?

A
Uric acid crystals; Photomicrograph of a urine sample with a pH of 5 (phase contrast microscopy; high magnification). Multiple crystals of varying sizes and shapes can be seen (blue overlay). Their diamond-shaped (rhomboid) form is one of the characteristic appearances of uric acid crystals, which only form in urine samples with a pH < 5.5 and are typically seen in patients with gout or in healthy individuals on a high-purine diet. Uric acid crystals may also appear barrel-shaped and needle-shaped (not seen in this image).
94
Q

Når er det indikasjon for nyrebiopsi ved ANS?

A
95
Q

Hva er behandlingen avhengig av ved ANS?

A
96
Q

Hvordan bør man gå fram ved en ANS?

A
97
Q

Hvordan bør man behandle pas. med prerenal ANS som skyldes hhv.:
- Hypovolemi
- Sjokk
- Redusert, effektiv arterielt volum
- Medikamenter som affekterer glomeruli sin perfusjon

A
98
Q

Hvordan bør pas. med akutt tubulær nekrose og akutt interstitiell nefritt behandles?

Intrarenal ANS

A
There are no specific interventions for the treatment of established ATN. E.g., infectious or systemic diseases such as legionellosis, leptospirosis, CMV, or autoimmune diseases such as SLE, Sjögren syndrome, sarcoidosis.
99
Q

Hvordan bør man behandle intrarenal ANS med årsaker som:
- Kontrasindusert nefropati
- Glomerulonefritt
- Vaskulære årsaker

A
There are no specific interventions for the treatment of established contrast-induced AKI.
100
Q

Hvordan behandle postrenal ANS?

A
101
Q

Hvilke faktor gjelder for om en pas. utvikler KNS ved ANS?

A
102
Q

Når er det indikasjon for nyreerstatende behandling, og hvilke modaliteter kan man bruke?

A
The modality of choice varies depending on the circumstance, e.g., patient factors and the clinical setting. CRRT (Continuous renal replacement therapy) is preferred for hemodynamically unstable patients. PD are more commonly used in resource-limited settings.
103
Q

Hvordan er epidemiologien til neonatal akutt nyreskade (NANS), og hvilken etiologi har den?

A
104
Q

Hvilke risikofaktorer finnes for NANS?

A
Kidneys of preterm infants continue to mature after birth until week 35–36 of gestational age.
105
Q

Hvordan diagnostiserer man NANS?

A
Serum creatinine levels physiologically decrease after birth, making it impossible to determine a constant baseline value. Can be measured by urine bag collection, diaper weighing, or catheterization.
106
Q

Hvordan behandler man NANS?

A

Nefrologi (17 decks)

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