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USMLE Step I Pathology > Renal Pathology (Pathoma) > Flashcards

Renal Pathology (Pathoma) Flashcards

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USMLE® Step 1 flashcards
1
Q

Horsehoe Kidney

A

Conjoined kidney usually (90%) at lower pole.

Most common congenital renal anomaly

Kidney is located in lower abdomen –> horseshoe kidney gets caught on the IMA root during ascension.

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2
Q

Bilateral Renal Agenesis

A

Uncompatible w/ life.

Leads to oligohyraminos w/ lung hypoplasia, flat face w/ low set ears, and developmental defects of the extremeties (potter sequence)

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3
Q

Unilateral Renal Agenesis

A

Leads to hypertrophy of the existing kidney; hyperfiltration increasing risk of renal failure later in life.

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4
Q

Dysplastic Kidney

A

Noninherited

Congenital malformation of the renal parenchyma characterized by cysts and abnormal tissue.

Usuallly unilateral (in life); when bilateral (often on tests) must be differentiated from PCKD

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5
Q

Autosomal Dominant Polycystic Kidney Disease

A

Inherited defect leading to BILATERAL enlarged kidneys w/ cysts in the renal cortex AND medulla

Autosomal Dominant (ADult) mutation in APKD1 (more common and worse prognosis) or APKD2 gene

Presents in young adults as HTN, hematuria, and worsening renal failure.

Associated w/ berry aneurysm, hepatic cysts, mitral valve prolapse, and cysts in the colon.

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6
Q

Autosomal Recessive Polycystic Kidney Disease

A

Inherited defect leading to BILATERAL enlarged kidneys w/ cysts in the renal cortex AND medulla

Presents in INFANTS with worsening renal failure and HTN; newborns may present w/ Potter sequence.

Associated w/ congenital hepatic fibrosis (leads to portal HTN) and hepatic cysts.

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7
Q

Medullary Cystic Kidney Disease

A

Autosomal Dominant inherited defect leading to cysts in the MEDULLARY collecting ducts.

Parenchymal fibrosis results in SHRUNKEN kidneys and worsening renal failure.

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8
Q

Acute Renal Failure

A

Acute severe decrease in renal function.

Hallmark is azotemia often w/ oliguria

Divided into prerenal, postrenal, and intrarenal azotemia.

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9
Q

Prerenal Azotemia

A

Due to decreased blood flow to the kidneys (CHF); common cause of ARF.

Decreased blood flow results in decreased GFR, azotemia, and oliguria.

Reabsorbtion of fluid and BUN ensues (serum BUN:Cr ratio >15); tubular function remains intact (FENA

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10
Q

Post Renal Azotemia

A

Due to urinary obstruction (stone; BPH; cancer)

Decreased outflow results in decreased GFR, azotemia, and oliguria.

Early stage –> increased tubular pressure “forces” BUN into the blood (serum BUN/CR >15); tubular function remains intact (FENA 500 mOsm/kg

Late stage –> tubular damage ensues, resulting in decreased BUN reabsorbtion (serum BUN/Cr

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11
Q

Ischemic Acute Tubular Necrosis

A

Decreased blood supply results in necrosis of tubules (often preceded by prerenal azotemia) –> proximal tubule and medullary segment of thick ascending limb are particularly susceptible to ischemic damage (move most solute –> most dependent on ATP)

Most common cause of ARF (intrarenal azotemia)

Injury and necrosis of tubular epithelial cells –> necrotic cells plug tubules (brown, granular casts); obstruction decreases GFR.

Decreased reabosrbtion of BUN (serum BUN/Cr patients usually recover

Oliguria can persist for 2-3 weeks before recovery; tubular cells (stable cells in G0) take time to reenter cell cycle and regenerate

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12
Q

Nephrotoxic Acute Tubular Necrosis

A

Toxic agents result in necrosis of tubules (esp. proximal tubule)

Causes: Aminoglycosides (most common), heavy metals (lead), myoglobinuria (crush injury), ethylene glycol (oxalate crystals in the urine), radiocontrast dye, and urate (tumor lysis syndrome)

Most common cause of ARF (intrarenal azotemia)

Injury and necrosis of tubular epithelial cells –> necrotic cells plug tubules (brown, granular casts); obstruction decreases GFR.

Decreased reabosrbtion of BUN (serum BUN/Cr patients usually recover

Oliguria can persist for 2-3 weeks before recovery; tubular cells (stable cells in G0) take time to reenter cell cycle and regenerate

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13
Q

Acute interstitial nephritis

A

Drug induced hypersensitivity involving the interstitium and tubules results in acute renal failure.

Causes include NSAIDS, penicillin, and diuretics

Presents w/ oliguria, fever, and rash days to weeks after starting a drug; eosinophils may be in the urine

Resolves with cessation of drug

May progress to renal papillary necrosis

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14
Q

Renal papillary necrosis

A

Necrosis of the papillae

Presents w/ gross hematuria and flank pain

Causes include:

  1. ) Chronic analgesic abuse
  2. ) DM
  3. ) Sickle cell trait or disease
  4. ) Severe acute pyelonephritis
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15
Q

Neprhotic Syndrome

A

Glomerular disorders characterized by proteinuria (>3.5 g/day) resulting in:

  1. ) Hypoalbuminemia - pitting edema
  2. ) Hypogammaglobulinemia - increased risk of infection
  3. ) Hypercoaguable (loss of ATIII)
  4. ) Hyperlipidemia and hypercholesterolemia (fatty casts in the urine)
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16
Q

Minimal Change Disease

A

Most common cause of nephrotic syndrome in children

Usually idiopathic; may be associated w/ Hodgkin lymphoma

Lose foot processes –> cytokine mediated

Selective proteinuria (albumin only)

Excellent response to steroids

Microscopy- Normal glomeruli on H&E; lipid may be seen in proximal tubule cells.
IF- Negative
EM- Effacement of foot processes

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17
Q

Focal Segmental GlomeruloSclerosis (FSGS)

A

Most common cause of nephrotic syndrome in Hispanics and Africans Americans.

Usually idiopathic

Associated w/: HIV, heroin use, sickle cell disease and obesity.

Microscopy: Focal (some glomeruli) and segmental (involving only part of the glomerulus) on H&E.
IF: Negative
EM- Effacement of foot processes

Poor response to steroids; progresses to CRF

HIV - especially poor prognosis

18
Q

Membranous Nephropathy

A

Most common cause of nephrotic syndrome in caucasians

Usually idiopathic

Associated w/: Hep B; Hep C; solid tumors. SLE, or drugs (NSAIDS or penicillamines)

Microscopy: Thick basement membrane on H&E
IF: Granular
EM - Spike and Dome

Poor response to steroids; progresses to CRF (treat underlying disease!)

19
Q

Type I Membranoproliferative Glomerulonephritis

A

Subendothelial depsoits; associated w/ HCV and HBV

Microscopy: Thick GBM on H&E w/ tram-track appearance
IF: granular
EM: Thick GBM on H&E w/ tram-track

Poor response to steroids; progresses to CRF

20
Q

Type II Membranoproliferative Glomerulonephritis

A

“Dense Deposit Disease” - intramembranous; associated w/ C3 nephritic factor (autoantibody that stabilizes c3 convertase, leading to overactivation of complement, inflammation, and low circulating levels)

Microscopy: Thick GBM on H&E w/ tram-track appearance
IF: granular
EM: Thick GBM on H&E w/ tram-track

Poor response to steroids; progresses to CRF

21
Q

DM Glomerulosclerosis

A

High serum glucose leads to nonenzymatic glycosylation of the vascular BM resulting in hyaline arteriolosclerosis.

Glomerular efferent arteriole is more affected than the afferent arteriole, leading to high glomerular filtration pressure. (Treat w/ ACEIs and ARBs) –> this leads to microalbuminuria (= first sign of DM glomerulopathy)

Eventually progresses to nephrotic syndrome –> characterized by sclerosis of the mesangium w/ formation of Kimmelstiel-Wilson Nodules

22
Q

Systemic Amyloidosis

A

Kidney is the most commonly involved organ in systemic amyloidosis.

Amyloid deposits in the mesangium, resulting in nephrotic syndrome

Characterized by apple-green biregringence under polarized light after staining w/ congo red.

23
Q

Nephritic Syndrome

A

Glomerular disorders characterized by glomerular inflammation and bleeding.

  • Limited proteinuria ( periorbital puffiness, occassionally pitting edema)
  • Oliguria and azotemia
  • Salt retention (periorbital puffiness and HTN)
  • RBC casts and dysmorphic RBCs in urine

Biopsy reveals hypercellular, inflammed glomeruli

Immune-complex deposition activates complement; C5a attracts neutrophils which mediate damage.

24
Q

Poststreptococcal Glomerulonephritis

A

Nephritic syndrome that arises after group A B-hemolytic strep infx of skin (impetigo) or pharynx (occurs w/ nephritogenic strains; may occur w/ nonstrep organisms as well)

Presents 2-3 weeks after infx as hematuria (cola-colored urine), oliguria, HTN, periorbital edema

Usually seen in children

Microscopic - hypercellular, inflamed glomeruli on H&E
IF- Granular
EM - Subepithelial humps

Rx - supportive –> children rarely (1%) progress to renal failure; adults 25% –>RPGN

25
Q

Rapidly Progressive Glomerulonephritis

A

Nephritic syndrome that progresses to renal failure in weeks/months.

Characterized by crescents in Bowman’s space (composed of fibrin and mphages)

Clinical picture and IF help resolve etiology

26
Q

IgA nephropathy

A

Most common nephropathy worldwide

IgA immune comples deposition in mesangium

Presents during childhood as episodic gross or microscopic hematuria w/ RBC casts, usually following mucosal infx (i.e. URI / gastroenteritis)

IgA immune comples deposition in the mesangium is seen on IF

May slowly progress to renal failure.

27
Q

Alport Syndrome

A

Inherited defect in type IV collagen; most commonly X-linked

Results in thinning and splitting of the GBM

PResents as isolated hematuria, sensory hearing loss, and occular disturbances.

28
Q

Cystitis

A

AKA bladder infection

Presents w/ dysuria, urinary frequency, urgency, and suprpubic pain; systemic signs (i.e. fever/chills) are usually absent.

Laboratory findings:

  1. )UA - cloudy urine with >10 WBCs/high power field
  2. ) Diptick - Positive leukocyte esterase (due to pyuria) and nitrates (bacteria convert nitrates to nitrites)
  3. ) Culture - greater than 10^5 cfu’s (gold standard = specific. 10^2 = sensitive)

Etiology:

  1. ) E.coli (80%)
  2. ) Staph saphrophyticus (esp. young sexually active women)
  3. ) Kleibsiella pneumoniae
  4. ) Proteus mirabilis - alkaline urine w/ ammonia scent (leading cause of ammonium magnesium phosphate crystals/struvite stone)
  5. ) Enterococcus faecalis

Sterile pyuria w/ negative culture –> think urethritis due to Chlymidia trachomatis or Neisseria gonorrhoae. (dominant presenting sign is dysuria)

29
Q

Pyelonephritis

A

Usually due to ascending infection; increased risk w/ vesicoureteral reflux.

Presents w/ FEVER, FLANK PAIN, WBC casts, and LEUKOCYTOSIS plus signs of cystitis.

Most common causes:

  1. ) E. coli (90%)
  2. ) Enterococcus faecalis
  3. ) Klebsiella species.
30
Q

Chronic Pyelonephrits

A

Interstitial fibrosis and atrophy of tubules due to multiple bouts of acute pyelo.

Due to vesicuoureteral reflux (children) or obstruction (BPH, cervical carcinoma)

Leads to cortical scarring w/ blunted calyces; scarring at upper and lower poles is characteristic vesicureteral reflux

Atrophic tubules containing eosinophilic proteinaceous material resemble thyroid follicles (thyroidization of the kidney); waxy casts may be seen in the urine

31
Q

Nephrolithiasis

A

Precipitation of a urinary solute as a stone.

Risk factors include high concentration of solute in urinary filtrate and low urine volume

Presents as a colicky pain w/ hematuria and unilateral flank tenderness. Stone is usually passed within hours (increase fluid intake) ; if not, surgical intervention may be required (if >5cm).

Types of stones:
Calcium oxalate/calcium phophate (most common)
Ammonium magnesium phosphate (second most common - secondary to urease + infx –> struvite)
Uric acid (third most common - arid climates - radiolucent - allopurinol = rx if gout)
Cystine (rare/children; cystinuria = genetic defect; staghorn)

32
Q

Calcium oxalate and/or calcium phosphate nepthrolithiasis

A

Frequency - most common type; usually adults

Causes - Idiopathic hypercalciuria; hypercalcemia and its related causes must excluded. Also seen in Crohn’s disease.

Rx - HCTZ (calcium sparing diuretic). Hydration. Surgery if >5cm.

33
Q

Ammonium magnesium phoshpate Nephrolithiasis

A

Frequency - second most common type

Causes - most common cause is infection w/ urease + organism (Proteus vulgaris or Klebsiella); alkaline urine leads to formation of stone.

Rx - classically results in a staghorn calculi in renal calyces which act as a nidus for uti. rx is surgical removal and eradication of pathogen.

34
Q

Uric Acid Nephrolithiasis

A

Frequency - third most comon (5%); radiolucent.

Causes - Risk factors include hot, arid climates, low urine volume, and acidic pH. Most common stone in patients with gout; hyperuricemia (i.e. leukemia or myeleoproliferative disorders = tumor lysis syndrome) increases risk.

Rx - hydration and alkalinization of urine (potassium bicarb); allopurinol is also administered in patients w/ gout.

35
Q

Cystine Nephrolithiasis

A

Frequency - rare cause of nephrothiasis; most commonly seen in children

Causes - cystinuria (a genetic defect of tubules that results in decreased reabsorption of cysteine)

rx- may form staghorn calculi. hydration and alkalinization of urine

36
Q

Chronic Renal Failure

A

End-stage kidney failure may result from glomerular, tubular, inflammatory, or vascular insults.

Most common causes: 1.) DM (45%) 2.) HTN (30%) and 3.) glomerulosclerosis (9%)

Clinical features:

  1. ) Uremia - azotemia w/ sx (nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy w/ asterixis (hand tremor), and deposit of urea crystals in skin
  2. ) Salt and water retention w/ resulting HTN
  3. ) Hyperkalemia w/ metabolic acidosis
  4. ) Anemia due to decreased EPO production in renal peritubular interstitial cells
  5. ) Hypocalcemia due to decreased 1-alpha-hydroxylation of vitamin D by proximal renal tubular cells and hyperphosphatemia
  6. ) Renal osteodystrophy - due to secondary hyperparathyrodisim. Osteomalacia and osteoporosis.

Rx: ACEIs and ARBs early; dialysis or renal transplant late.
-cysts often develope within shrunken end-stage kidneys during dialysis increasing risk of RCC.

37
Q

Angiomyolipoma

A

Hamartoma comprised of blood vessels, smooth muscle, and adipose tissue.

Increased frequency w/ tuberous sclerosis

38
Q

Renal Cell Carcinoma

A

Malignant epithelial tumor arising from kidney

  1. )Presents w/ triad of hematuria, palpable mass, and flank pain. (rarely together; hematuria is most common)
  2. )Fever, weight loss, or paraneoplastic syndrome (epo, renin, PTHrP, or ACTH) may also be present.
  3. ) Rarely can present with left varicocele

Gross exam reveals a yellow mass; microscopically , the most common variant exhibits CLEAR CYTOPLASM.

Pathogenesis involves loss of VHL (3p) tumor suppressor gene, which leads to increased IGF-1 (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF).

Tumors may be hereditary or sporadic.

  • sporadic –> males > 60. Single tumor at the upper pole of the kidney. Major risk factor is smoking.
  • genetic –> younger adults and bilateral. Von Hippel Lindau disease associated w/ inactivation of the VHL gene leading to increased risk for hemangioblastoma of the cerebellum and RCC

Stagin - T - based on size and involvement of renal vein (occurs commonly and increases risk of hematogenous spread to lungs and bone)
N - spread to retroperitoneal lymph nodes.

39
Q

Wilms Tumor

A

Malignant kidney tumor comprised of blastema (immature kidney mesenchyme), primative glomeruli and tubules, and stromal cells.

Most common malignant tumor in children - average age is 3 years old.

Presents as large, unilateral flank mass w/ hematuria and hypertension (due to renin secretion)

Most cases (90%) are sporadic; syndromic tumors may be seen w/:

  1. ) WAGR syndrome - Wilms tumor, Aniridia, Genital abnormalities, and mental and motor Retardation; associated w/ a deletion of WT1 tumor suppressor gene (located at 11p13)
  2. ) Denys-Drash syndrome- Wilms tumor, progresseive renal (glomerular) disease, and male pseudohermaphroditism; associated with mutations of WT1
  3. ) Beckwith - Widermann syndrome - Wilms tumor, neonatal hypoglycemia, myscular hemihypertrophy, and organomegaly (including tongue); associated w/ mutations in WT2 gene cluster (imprinted genes at 11p15.5 particularaly IGF-2
40
Q

Urothelial (Transisitional Cell) Carcinoma

A

Malignant tumor arising from the urothelial lining of the renal pelvis, ureter, bladder, or urethra.

Most common type of lower urinary tract cancer; usually arises in the bladder.

Major risk factor is smoking; additional risk factors are naphthylamine, azodyes (hair dressers), and long-term cyclophosphamide (add mesna!) or phenecatin use

Generally seen in older adults; classically presents w/ painless hematuria.

Arises via two distinct pathways

  1. ) Flat - develops as a high-grade flat tumor and then invades; associated w/ early p53 mutation
  2. ) papillary - develops as a low-grade papillary tumor that progresses to a high grade papillary tumor and then invades; not associated w/ early p53 mutation.

Tumors are often multifocal and recur “field defect” (entire urothelium is mutated)

41
Q

Squamous cell carcinoma of the bladder

A

Malignant proliferation of squamous cells, usually involving the bladder.

Arises in a background of squamous metaplasia (normal bladder surgace is not lined w/ squamous epithelium.)

Risk factors include: chronic cystitis (older woman), Schistoma haematobium infection (Egyptian male), and long standing nephrolithiasis.

42
Q

Adenocarcinoma of the bladder

A

Malignant proliferation of glands, usually involving the bladder.

Arises from a URACHAL REMNANT (develops at dome of bladder), cytstitis glandularis, or extrophy

USMLE Step I Pathology (14 decks)

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