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x Pathoma > 12. Kidney and Urinary Tract Pathology > Flashcards

12. Kidney and Urinary Tract Pathology Flashcards

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1
Q

What are a few congenital disorders of the kidneys?

A

horseshoe kidney, renal agenesis, dysplastic kidney, polycystic kidney disease, medullary cystic kidney disease

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2
Q

describe a horseshoe kidney. how did it occur?

A

conjoined kidneys, connected at the lower pole. kidney unit got caught on the inferior mesenteric artery root during ascent from pelvis to abdomen

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3
Q

what is the most common congenital renal abnormality?

A

horseshoe kidney

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4
Q

what does agenesis mean?

A

“without production”

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5
Q

what is renal agenesis?

A

kidneys did not form. may be uni- or bi-lateral

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6
Q

what does unilateral renal agenesis lead to?

A

hypertrophy of the existing kidney

–> hyperfiltration which increases risk of renal failure later in life

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7
Q

what does bilateral renal agenesis lead to?

A

Potter sequence.

oligohydramnios with lung hypoplasia, flat face with low set ears, dev defects of the extremities. incompatible with life

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8
Q

what is Potter sequence?

A

lung hypoplasia, flat face with low set ears, dev defects of the extremities. due to oligohydramnios.

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9
Q

how should I think of the Potter sequence mechanistically?

A

think that due to oligohydramnios, there is not room in the uterus –> flat face and mis-formed extremities. the lung hypoplasia is because there is not room for the lungs to stretch and expand.

memory: Potter because the Pot was too small?

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10
Q

what is oligohydramnios? what causes it?

A

not enough amniotic fluid –> fetal abnormalities. many causes: bilateral renal agenesis is one.

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11
Q

how does bilateral renal agenesis cause oligohydramnios?

A

the amniotic fluid is formed from fetal filtrate (urine). if the fetus cannot make urine, there will be little amniotic fluid.

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12
Q

what is dysplastic kidney?

A

noninherited, congenital malformation of renal parenchyma characterized by cysts and abnl tissue. (one ex: cartilage growing where it should not be)

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13
Q

dysplastic kidney: inherited? uni or bilateral?

A

non-inherited. usually unilateral. if bilateral, must be distinguished from inherited polycystic kidney disease

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14
Q

what is polycystic kidney disease (PKD)?

A

inherited defect, leading to bilateral enlarged kidneys with cysts in the cortex and medulla.

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15
Q

what does polycystic kidney disease look like grossly?

A

kidney with lots of dark shiny bubbles on the surface

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16
Q

PKD: autosomal recessive form generally presents in what population? how does it present?

A

infants. presents as worsening renal failure, hypertension. may present as Potter sequence because so severe it’s as though they have oligohydramnios

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17
Q

PKD: auto dominant form generally presents in what population? how does it present?

A

young adults (ADults). presents as HTN (due to incr renin), hematuria, progressive renal failure

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18
Q

auto recessive form of PKD: associated with what?

A

congenital hepatic fibrosis and hepatic cysts.

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19
Q

auto dom form of PKD: why does it present as it does?

A

presents as HTN, hematuria, progressive renal failure: think about cysts in liver/brain/kidney.

Mutation of APKD1 or APKD2 gene. cysts develop over time.

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20
Q

what gene is responsible for the auto dom form of PKD?

A

mutation in the APKD1 or APKD2 genes (adult polycystic kidney disease genes). cysts develop over time.

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21
Q

auto dom PKD: what is it associated with?

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A

berry aneurysm, hepatic cysts, mitral valve prolapse.

22
Q

auto dom PKD: generally, what is the cause of death?

Study These Flashcards
A

berry aneurysm rupture

23
Q

what is medullary cystic kidney disease?

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A

inherited defect leading to cysts in the medullary collecting ducts.

24
Q

medullary cystic kidney disease: what type of inheritance?

25
medullary cystic kidney disease: presentation? Why?
presents as worsening renal failure, due to shrunken kidneys from parenchymal fibrosis
26
what is the most obvious difference between dysplastic kidney and polycystic kidney disease?
dysplastic kidney = usually unilateral (but might be BIL on USMLE) polycystic kidney disease = bilateral. presents with HTN, worsening renal failure.
27
# Define Acute Renal Failure. What are the hallmarks?
acute, severe decrease in renal function (occurs over days) Azotemia (incr BUN, incr Creatinine), often Oliguria Divided into Pre-renal, Post-renal, Intra-renal types.
28
Pre-renal Azotemia what is a common cause? Serum BUN:Cr ratio = ? FENa = ? Urine osm = ?
Decr blood flow to kidneys (cardiac failure is common cause) ## Footnote Serum BUN:Cr ratio \> 15 (high) FENa \< 1% (tubular function = intact) Urine osm \> 500 (tubules can concentrate urine)
29
NORMAL values are....? Serum BUN:Cr ratio FENa Urine osm
Normal Values: Serum BUN:Cr ratio = 15 FENa \< 1% (tubular function intact) Urine osm \> 500 (tubules can concentrate urine)
30
Pre-renal Azotemia why is Serum BUN:Cr ratio high?
low blood flow to kidney due to pre-renal obstruction or overall low volume. RAAS activated -\> aldosterone -\> **more Na, water, BUN resorbed. ** Cr is filtered and excreted as usual. Serum BUN:Cr ratio therefore increases.
31
Postrenal Azotemia, Early stage Serum BUN:Cr ratio = ? FENa = ? Urine Osm = ?
Serum BUN:Cr ratio \> 15 FENa \< 1% Urine Osm \> 500
32
Postrenal Azotemia, Later stage Serum BUN:Cr ratio = ? FENa = ? Urine Osm = ?
Serum BUN:Cr ratio \< 15 FENa \> 2% Urine Osm \< 500 All due to tubular damage
33
Acute Tubular Necrosis: clinical findings?
- Brown granular casts in urine - Elevated BUN and creatinine (decr GFR) - Hyperkalemia - Metabolic acidosis with anion gap
34
Acute Tubular Necrosis: 2 etiologies?
Ischemia Toxicity
35
Acute Tubular Necrosis due to toxicity: what are most common causes?
Aminoglycosides (gentamycin, tobramycin, amikacin) Heavy metals/lead Myoglobinuria (crush injury) Ethylene glycol ingestion (kid, accidental) Radiocontrast dye Urate due to tumor lysis syndrome
36
If a patient is on chemo for leukemia, what do we give to avoid Tumor Lysis Syndrome/Acute Tubular Necrosis?
- Hydration - Allopurinol to decr synthesis of urate. - Rasburicase (synthetic urate oxidase) to metabolize uric acid --\> Allantoin (more soluble)
37
Ethylene glycol ingestion: high-yield association?
kids (accidental ingestion) Oxalate crystals in urine
38
Acute Tubular Necrosis why does it take 2-3 weeks to recover from?
Tubular cells can regenerate, but they are Stable cells and need time to re-enter the cell cycle.
39
Acute Interstitial Nephritis: cause?
drug-induced hypersensitivity NSAIDs, penicillin, diuretics
40
Acute Interstitial Nephritis: presentation?
a few days/weeks after starting a new drug, oliguria, fever, rash ## Footnote **Eosinophils in urine**
41
Renal Papillary Necrosis Presentation? Cause?
(a form of intra-renal azotemia) Presents with gross hematuria, flank pain Causes: chronic analgesic abuse, diabetes, sickle cell, severe acute pyelonephritis
42
6 causes of nephrotic syndrome?
6 causes, grouped in pairs: minimal change and FSGS Membranous nephropathy and membranoproliferative glomerulonephritis diabetes mellitus and amyloidosis
43
Nephrotic syndrome: basic principles?
proteinuria hypoalbuminemia -\> pitting edema hypogammaglobilinemia -\> incr risk of infection hyperlipidemia and hyperchol (due to 'thin' blood; liver puts out lipids and chol) -\> fatty casts
44
minimal change disease: where is the damage? what cancer is it associated with?
effacement of foot processes associated with Hodgkin lymphoma (huge production of cytokines by Reed-Sternberg cells)
45
minimal change disease: what proteins are lost? treatment?
albumin but NOT immunoglobulin responds to steroids
46
Focal Segmental Glomerulosclerosis: associations? where is the damage? treatment?
associations: HIV, heroin use, sickle cell effacement of foot processes no response to steroids -\> progresses to renal failure
47
most common cause of death with SLE?
renal failure usually due to diffuse progressive glomerulo**nephritis** - or membranous **nephropathy**
48
membranous nephropathy where is the damage? associations? appearance on IF?
damage = subepithelial deposits of immune complexes associated with Hep B, Hep C, SLE, solid tumors, NSAIDs appearance = granular IF, spike and dome
49
membranoproliferative glomerulonephritis associations damage appearance
Tram-track appearance! granular IF associations: Type I: HBV and HCV Type II: autoantibody to C3 convertase -\> overactivation of complement cascade
50
Diabetes nephrosis damage? appearance? treatment?
high glucose -\> NEG of vascular basement membrane -\> hyaline arteriolosclerosis of efferent vessel high GFR, hyperfiltration, **albumin in urine** Kimmelstiel-Wilson nodules treatment: ACE inhibitors to counteract the efferent blockage effect
51
systemic amyloidosis damage? appearance?
amyloid deposits in mesangium apple-green birefringemce under polarized light w/ Congo red stain

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