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1 USMLE - Renal System > Pathology > Flashcards

Pathology Flashcards

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USMLE® Step 1 flashcards
1
Q

Horseshoe Kidney

A

Conjoined kidneys connected at lower pole
-#1 congenital abnormality
Gets stuck on root of enteric mesentery artery, it will be located low in abdomen

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2
Q

Renal Agenesis

A

Absence of formation
Unilateral: hypertrophy of existing kidney
-Problems exist later in life (renal failure)
Bilateral: Oligohydraminios
-lung hypoplasia, flat face, low set ears, developmental defects of extremities (Potter Sequence)
-Incompatible with life

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3
Q

Dysplastic Kidney

A

NON-inherited, congenital malformation of renal parenchyma.

  • Cysts and abnormal tissue (CARTILAGE)
  • Usually Unilateral, when bilateral MUST BE distinguished from inherited PKD (polycystic kidney disease)
  • If a second child is born after a child who develops dysplastic kidney the chances of 2nd child developing is is LOW
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4
Q

PKD (polycystic kidney disease)

A 
Inherited defect, BILATERALLY enlarged kidneys with cysts in RENAL CORTEX and MEDULLA
Autosomal Recessive
-Usually infants
-Renal failure and HTN
-Potters sequence
-Associated with congenital hepatic bebrosis and hepatic cysts
-PORTAL HYPERTENSION in a baby
Autosomal dominant
-Young adults (ADult)
-HTN, hematuria, worening renal failure
-Increased plasma renin
-APKD1 or APKD2 gene
-Associated with BERRY ANEURYSM (brain hemorrhage), hepatic cysts, mitral valve prolapse
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5
Q

Medullary Cystic Kidney Disease

A

Inherited Autosomal dominant defect

  • Cysts in MEDULLARY collecting ducts
  • Parenchymal fibrosis results in SHRUNKEN kidneys
  • Presents as worsening renal failure
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6
Q

Acute Renal Failure

A

Severe decrease in renal function
-AZOTEMIA, often oliguria
Prerenal, postrenal, intrarenal

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7
Q

Azotemia

A

High levels of nitrogen products in blood (urea, creatinine)

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8
Q

Oliguria

A

Low output of urine

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9
Q

Prerenal Azotemia

A

Due to decreased blood flow to kidneys (common cause of ARF)
-Low GFR, Azotemia, Oliguria
-BUN and creatinine in blood rise
BUN:Creatinine > 20 (Creatinine cannot be resorbed, urea can and will be resorbed back into blood)
-Tubular function is intact so FENa is 500 so kidney can still concentrate urine

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10
Q

Postrenal Azotemia

A

Obstruction of the urinary tract downstream of kidney

  • Increased pressure and DECREASED GFR
  • Azotemia and Oliguria
  • Increased pressure forces BUN back into blood so BUN:Cr > 20
  • Tubular function intact so FENa < 1% and Urine osmolality is > 500
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11
Q

Post Renal Azotemia - LONG term

A

Tubule damage causes decreased resorption of BUN

  • Thus BUN:Cr < 20
  • Decreased resorption of Na (FENa > 2%)
  • Inability to concentrate urine (Uosm < 500)
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12
Q

Acute Tubular Necrosis

A

Intrarenal Azotemia
-Injury and necrosis of tubular epithelial cells, MOST COMMON cause of ARF
-Necrotic cells plug tubules, obstruction: DECREASED GFR
-Brown, granular CASTS seen in urine (sloughed off epithelial cells, casted in shape of tubule)
-Decreased ability to resorb BUN so BUN:Cr < 20
-Decresed resorption of Na and inability to concentrate urine
FENa > 2%, Uosm < 500

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13
Q

FENa

A

Fractional excretion rate of sodium
-Normal about 1%
High FENa - more Na EXCRETED
Low FENa - more Na RESORBED

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14
Q

Ischemic ATN

A

Decreased blood supply results in necrosis of tubules, often PRECEDED by PRErenal azotemia
-Proximal tubule and medullary segment of TAL susceptible

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15
Q

Nephrotoxic ATN

A

Toxic agent results in necrosis of epithelial cells
-Proximal tubule
Agents: Aminoglycosides, heavy metals (lead), myoglobinuria (crush injuries), Ethylene glycol (antifreeze) OXYLATE CRYSTALS in urine, Radiocontrast dye, Urate (Tumor lysis syndrome, chemotherapy)
-Oliguria with brown granuler casts
-Elevated BUN and Cr
-Hyperkalemia with metabolic acidosis (decreased excretion of K and also WOA)
-Increased ANION GAP
-Reversible, oliguria can persist for 2-3 weeks before recovery

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16
Q

Acute Interstitial Nephritis

A

Drug-induced hypersensitivity reaction of interstitial and tubules, results in ARF

  • Common drugs: NSAIDS, Diuretics, and Penicillin
  • Oliguria with fever and RASH that arises days to weeks after starting drugs
  • EOSINOPHILIA
  • Resolve after cessation of drug
  • May progress to Renal papillary necrosis
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17
Q

Renal Papillary Necrosis

A 
Necrosis of renal papillae
-Gross hematuria and flank pain
Causes: 
-Chronic analgesia abuse (Phenacetin or aspirin use)
-Diabetes Mellitus
-Sickle Cell trait or disease
-Sever acute pyelonephritis
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18
Q

Nephrotic Syndrome

A

Glomerular disorder with proteinuria (>3.5g/day)

  • Hypoalbuminemia (edema)
  • Hypogammaglobulinemia (inc risk of infection)
  • Hypercoagulable state (lose ATIII (anti-thrombin III))
  • Hyperlipidemia and hypercholesterolemia (reaction of liver to thicken blood from loss of protein)
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19
Q

MCD (minimal change disease)

A

Most common cause of nephrotic syndrome in children

  • Usually idiopathic, but can be associated with Hodgkin lymphoma (Loose foot processes in glomerulus, cytokine mediated, in Hodgkin lymphoma you get massive production of cytokines from Reed-Sternberg cells)
  • Normal glomeruli on H&E stain, but on EM will have Effacement of foot processes*
  • NO immune complex deposits, negative immunofluorescence
  • Selective proteinuria (ONLY albumin)
  • Excellence response to CorticoSTEROIDS***
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20
Q

Focal Segmental Glomerular Syndrome

A

Most common cause of nephrotic syndrome in Hispanics and Blacks

  • Usually idiopathic, maybe HIV, Heroin, Sickle Cell**
  • If there’s a patient on any of these and develop nephrotic syndrome it is FSGS
  • Focal and segmental (pink) sclerosis on H&E
  • Effacement of foot processes on EM
  • Negative IF (immunofluorescence) NOT immune complex mediated
  • DO NOT respond to steroids (may progress from MCD) progresses to CRF
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21
Q

Membranous Nephropathy

A

Most common cause of nephrotic syndrome in Caucasian adults

  • Idiopathic but may be associated with Hep B or C, solid tumors or SLE**, drugs (NSAIDs, penicillin’s)
  • A patient with SLE that develops nephrotic syndrome, it is membranous*
  • On H&E thick basement membranes
  • IS DUE to Immune Complex so it will be a Positive Immunofluorescence test (granular, grainy appearance)
  • Spike and Dome appearance on EM
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22
Q

Membranoproliferative Glomerulonephritis. Type I or Type II

A

Thick capillary membranes on H&E, often with ‘tram-track’ appearance (due to proliferation of mesangial cells)

  • Due to immune complex deposition so it is IF positive
  • Types based on location of deposits
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23
Q

Membranoproliferative Glomerulonephritis. Type I

A

Deposits underneath the ENDOTHELIAL cells

  • SUBendothelial
  • Associated with HBV or HCV
  • More often ‘tram track’ presentation
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24
Q

Membranoproliferative Glomerulonephritis. Type II

A

Deposition of immune complexes WITHIN the BASEMENT membrane

  • Antibody called C3 nephritic factor (auto-antibody) that stabilizes the C3 convertase (converts C3 to C3a and C3b, it is usually destroyed rapidly)
  • The stabilization of C3 convertase results in over activation of compliment resting in inflammation and damage to the basement membrane
25
Q

Diabetes Mellitus

A

Hyperglycemia results in non enzymatic glycosylation of vascular basement membranes resulting in hyalin arteriolosclerosis (leaks protein into tunica media)

  • Efferent arteriole is more effected than the afferent, thus increases pressure within the glomerulus
  • This creates hyperfiltration initially resulting in miecroalbuminuria that eventually results in nephrotic syndrome
  • Kimmelstiel-Wilson Nodules* (dense sclerosis)
  • ACE Inhibitors help this
26
Q

Systemic Amyloidosis

A

Kidney is MOST commonly involved organ

  • Amyloid deposits in mesangium resulting in nephrotic syndrome
  • Characterized by apple-green birefringence under polarized light
27
Q

Nephritic Syndrome

A

Glomerular inflammation and BLEEDING (hematuria)

  • Limited proteinuria
  • Oliguria and azotemia
  • Salt retention with periorbital edema and HTN
  • RBC casts and dysmorphic RBC’s in urine
  • Biopsly: Hypercellular inflamed glomeruli, immune complex deposition activates compliment (C5a)
28
Q

Post Strep Glomerular Nephritis

A

Nephritic syndrom post group A beta-hemolitic strep infection (M PROTEIN)

  • 2-3 weeks after infection (usually seen in children - hematuria (cola colored), oliguria, HTN, periorbital edema)
  • Hallmark - granular IF, SUB-EPITHELIEAL HUMP on EM**
  • TX is supportive
  • Adults can progress to RPGN
29
Q

RPGN - Rapidly progressive glomerular nephritis

A

Nephritic syndrome that progresses to renal failure in weeks to months

  • Biopsy - CRESCENTS in bowman space made up of FIBRIN* AND MACROPHAGES*
  • IF: linear = basement membrane attachment (Goodpasture syndrome), granular = PSGN, negative = pauci-immune = test for ANCA (Wegeners c-ANCA)
30
Q

Goodpasture Syndrome

A

Antibody against glomerular and alveolar basement* membranes - hematuria and hemoptysis
-Young adult males

31
Q

Wegeners

A

c-ANCA

  • Lung, kidney, and ENT involvement
  • Hemoptysis, hematuria, and nasopharyngeal symptoms (sinusitis) - must differentiate from Goodpasture
32
Q

Churg-Straus

A

p-ANCA

-Eosinophilia, granulomatous inflammation, ASTHMA

33
Q

IgA Nephropathy

A

Most common cause world wide

  • IgA deposits in MESANGIUM of glomeruli
  • Gross or microscopic hematuria, RBC casts, following mucosal infections
  • May progress to RF
34
Q

Alport Syndrome

A

Inherited defect of type IV collagen, X-linked

  • Thinning and splitting of glomerular basement membrane
  • Isolated Hematuria**
  • Hearing loss and ocular disturbances, FAMILY history
35
Q

UTI

A

Usually ascending
-Risk- sexual intercourse, urinary stasis, gender, catheters
Cystitis
Pyonephritis

36
Q

Cystitis

A

Bladder infection
-Urinary pain (dysuria), urgensy/frequency, suprapubic pain
-NO systemic signs (fever, night sweats, etc)
Urinalysis - cloudy urin with < 10 abc/hpf
Dipstick- positive leukocyte esterase and nitrites
Goldstandard: CULTURE (over 100,000 CFU)
-E coli #1
-Staphylococcus Saprophyticus (young sexually active women)
-Klebsiella pneumoniae
-Proteus Mirabilis (alkaline urine)
-Enterococcus faecalis

37
Q

Sterile Pyuria

A

Pyuria with NEGATIVE culture

-suggests URETHRITIS due to Chlamydia Trachomatis or Neisseria gonorrhoeae

38
Q

Pyelonephritis

A

Kidney infection
- Usually caused by ascending infection, increaseased risk with vesicoureteral reflux
-Liver failure, flank pain, WBC casts, Leukocytosis, in addition of sx of cystitis
E Coli #1
Klebsiella
Enterococcus

39
Q

Chronic Pyelonephritis

A

Interstitial fibrosis and atrophy of tubules
- CHILDREN, due to vesicoureteral reflux (VUR) or obstruction (adults)
Leads to cortical scarring and blunted calyces, scarring at upper and lower poles indicate VUR
-Thyroidization of kidney

40
Q

Nephrolithiasis

A

Precipitation of urinary solute as a STONE

  • Risk: high concentration of solute or low urine volume
  • COLICKY pain with hematuria and UNILATERAL flank tenderness
41
Q

Calcium Oxylate or Phosphate stone

A

Most common type of stone*
-Check for hypercalcemia (think about Crohn disease) also form idiopathic hypercalciuria**
TX: Hydrochlorothiazide

42
Q

Ammonium magnesium Phosphate stone

A

Second most common type - due to alkalization of urine (stag horn calliculi)
Usually from UTI Proteus or Klebsiella

43
Q

Uric Acid Stone

A

Radiolucent (cannot see on X-ray)
Risk: Hot arid climates, low urine volume, acidic pH
GOUT patients*, hyperuricemia, leukemia, myeloproliferative disorders
Tx: hydration and alkalization of urine (potassium bicarbonate) or ALLOPURINOL

44
Q

Cystine Stone

A

Rare but most common in CHILDREN
-Staghorn calliculi
TX: hydration or alkalization of urine

45
Q

End-stage Kidney Failure

A

Results from glomerular, tubular, inflammatory or vascular insults
Most common cause: DM, HTN, Glomerular disease

46
Q

Tx of ESRF

A

Dialysis or renal transplant or renal transplant (cysts develop within SHRUNKEN kidneys)
-Increased risk for renal cell carcinoma*

47
Q

Symptoms of ESRF

A

UREMIA - increased nitrogenous waste in blood, nausea, anorexia, pericarditis, encephalopathy, urea crystals in skin

  • Salt and water retention (HTN), hyperkalemia, metabolic acidosis (anion gap)
  • Anemia (EPO from renal peritubular interstitial cells)
  • Hypocalcemia (decreased 1 alpha hydroxylation of vitamin D in kidney or due to hyperphosphatemia)
  • Renal osteodystrophy (damage to bone due to renal failure) osteitis fibrous cystic, osteomalacia, osteoporosis)
48
Q

Angiomyolipoma

A

Hamartoma comprised of blood vessels, smooth muscle, and adipose tissue
-Pts with TUBEROUS SCLEROSIS

49
Q

Renal Cell Carcinoma

A

Malignant epithelial tumor of the renal tubules

  • TRIAD - hematuria, palpable mass, and flank pain
  • Feber, weight loss, paraneoplastic syndrome** (could release EPO, renin, PRHrP, or ACTH)
  • May present with left sided varicocele (rare)
  • Yellow Mass* - clear cytoplasm (clear cell carcinoma)
  • involves LOSS of VHL which is a tumor suppressor gene
50
Q

Paraneopastic Syndrome

A

wer

51
Q

Sporatic pathway of Renal Cell Carcinoma

Hereditary pathway

A

Adult smoker** in upper pole of kidney

Multiple and bilateral tumors

52
Q

Von Hippel-Lindau Disease

A

Autosomal dominant disorder associated with loss of VHL gene

  • Predisposes patients for RCC***
  • also increased risk for hemangioblastoma of cerebellum and renal cell carcinoma
53
Q

Staging of RCC

A

T - based on tumor size and involvement of renal vein

N - based on spread to retroperitoneal lymph nodes

54
Q

Wilms Tumor

A

Most common renal tumor in CHILDREN**

  • Comprised of blastema**, primitive glomeruli, and tubules, and stromal cells
  • Present with large unilateral flank mass, HTN, and hematuria
  • WT1 mutation
55
Q

WAGR Syndrome

A

Wilms Tumor
Aniridia
Genetal abnormalities
Mental and motor Retardation

56
Q

Beckwith-Widemann Syndrome

A

Wilms Tumor
Neonatal hypoglycemia
Muscular Hemihypertrophy
Organomegaly (tongue)

57
Q

Urothelial Carcinoma

Risk. Papillary vs Flat pathway.

A

Malignant tumor arising from urothelial lining of renal pelvis, ureter, bladder, or urethra
-MOST COMMON type flower urinary tract cancer (bladder)
-Smoking*
-Napthylamine (in cigarette smoke)
-Azo dyes (hair dressers)
-Long term cyclophosphamide or phenacetin
Usually seen with PAINLESS HEMATURIA in elderly
Papillary pathway** (tumor starts low grade, progresses to high grade and invades)
Flat (starts as high grade and invades) associated with early p-53 mutations**
Field defect - MULTIFOCAL tumors that reoccur

58
Q

Renal Squamous Cell Carcinoma

A

Malignant proliferation of squamous cells; usually in the bladder**
-Arises in a background of squamous metaplasia
Risk: Chronic cystitis, Schistosoma Hematobium** (middle eastern male), Long-standing nephrolithiasis

59
Q

Renal Adenocarcinoma

A

Malignant proliferation of glands usually in the bladder*

-Arises from URACHAL REMNANT** (then tumor would be present at dome of bladder), cystitis glandularis, bladder exstrophy

1 USMLE - Renal System (5 decks)

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