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year 2 > Path-kidney & diabetes exam > Flashcards

Path-kidney & diabetes exam Flashcards

1
Q

Nephritic syndrome

A
  • -visible hematuria (red cell casts)
  • azotemia (↑ BUN & creatinine)
  • mild to moderate proteinuria
  • edema
  • -hypertension
  • oliguria
  • Acute proliferative glomerulonephritis
  • Poststreptococcal GN
  • SLE
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2
Q

Nephrotic syndrome

A
  • Heavy proteinuria ( > 3.5 gm/day)
  • hypoalbuminemia ( <3 gm/day)
  • hyperlipidemia
  • LIPIDURIA
  • generalize edema (severe)

NO → azotemia, blood, HTN, and more protein than nephritic

  • membranous glomerulonephropathy
  • minimal change disease
  • focal segmental glomerulosclerosis
  • MPGN I
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3
Q

Rapidly progressive (crescentic) glomerulonephritis

A
  • Acute nephritis (signs of nephritic syndrome)
  • proteinuria
  • acute renal failure
  • Crescents in most of glomeruli
  • →parietal epithelial cells (line bowman’s) + monocytes & macrophages
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4
Q

Chronic renal failure

A

Progresses through 4 stages
–both kidneys become symmetrically smaller and granular

1) Diminished renal reserve– GFR 50% normal
- asymptomatic

2) Renal insufficiency– GFR 20-50% normal
- azotemia w/ anemia & HTN, polyuria, nocturia

3) Renal failure – GFR < 20-25% normal
- edema, acidosis, hypocalcemia, uremia may occur

4) End-stage renal disease– GFR <5% normal
- termal stage of Uremia

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5
Q

Uremia

A

Azotemia (↑ BUN & creatinine) + systemic manifestations
-waxy casts → not accute

  • Dehydration
  • Edema
  • Metabolic acidosis → hyperkalemia
  • Hypocalcemia → 2ry hyperparathyroidism
  • Hyperphosphatemia
  • renal osteodystrophy
  • anemia → **burr cells/echinocytes (normo-cytic/-chromic)
  • bleeding diatheses → nonthryombocyopenic purpura
  • HTN or CHF
  • fibrinous pericarditis
  • Retinopathy
  • hilar pneumonitis
  • urine smell to breath
  • pleural effusions
  • GI (nausea, vomiting, bleeding,ulcers, bad taste, coated tongue)
  • Neuromuscular (myopathy, neuropathy, encephalopathy
  • Dermatologic (sallow color, pruritits, dermatitis)
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6
Q

Acute proliferative GN

–Poststreptococcal glomerulonephritis

A

Clinical presentation → **Nephritic syndrome (+ rash)

Pathogenesis → Immune complex mediated
-circulated or planted Ag

Morphology → enlarged, hyper cellular glomeruli, red cell casts in urine

Light Microscopy:

  • diffuse ENDOcapillary proliferation
  • → endothelial & mesangial cells
  • leukocytic infiltration (PMN and monocytes)

Fluorescence Microscopy:
-Granular IgG and C3 → GBM and mesangium

Election microscopy → sub EPIthelial humps

Prognosis → excellent (better for child than adult)
-very low chance of → chronic GN

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7
Q 
Rapidly progressive (crescentic) GN
--Goodpasture syndrome
A

Clinical presentation: **Rapidly progressive GN (type I)

Pathogenesis: Anti-GBM COL4-A3 antigen

Light Microscopy:

  • EXTRAcapillary proliferation w/ crescents & necrosis
  • → proliferation of parietal cell
  • → migration of monocytes macrophages

Fluorescence Microscopy:
-LINEAR IgG and C3; fibrin b/w cell layers crescents

Prognosis → poor
-Very strong chance → chronic GN

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8
Q

Chronic glomeruplonephritis

A

Clinical presentation: **Chronic renal failure

Pathogenesis: variable

Light Microscopy → Hyalinized glomeruli

Fluorescence Microscopy: granular or negative

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9
Q

Membranous glomerulonephritis

-Drugs, disease (HBV, HCV)

A

Clinical presentation: **Nephrotic syndrome

Pathogenesis → in-situ immune complex formation

  • Ag mostly unknown
  • 85% idiopathic

Light Microscopy

  • early → normal
  • late → diffuse, uniform thickening of capillary wall/BM
  • silver stain → spikes of BM b/w deposits

Fluorescence Micro. → granular IgG & C3; diffuse

Election microscopy:

  • irregular dense sub epithelial deposits
  • **epithelial cell foot processes lost

Prognosis → good

  • -poor response to steroids
  • small/moderate chance → chronic GN
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10
Q

Minimal change disease (lipoid nephrosis)

A

Clinical presentation: **Nephrotic syndrome
-most frequent cause of NS in children

Pathogenesis → probably immune dysfunction

Light Micro. → normal; lipid in tubules

Fluorescence Micro. → negative

Election micro. → loss of foot processes
-NO deposits (vs. membranous w/ deposits)

Prognosis → Excellent
–good response to steroids

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11
Q

Focal segmental glomerulosclerosis

A

Clinical presentation: Nephrotic syndrome
-Non-nephrotic proteinuria

Pathogenesis

Light Micro. → focal and segmental sclerosis & hyaliniosis

  • collapsed BM,
  • ↑ mesangial matrix
  • hyaline masses

Fluorescence micro → IgM and C3 in sclerotic region

Prognosis → poor
-responds poorly to steroids

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12
Q

–MPGN type I

A

Clinical presentation: Nephrotic/nephrotic syndrome

Pathogenesis → immune complex

Electron Microscopy → subendothelial deposits

Prognosis: good
–small/moderate chance → chronic GN

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13
Q

–Dense deposit disease (MPGN type II)

A

Clinical presentation: Hematuria chronic renal failure

Pathogenesis

Light Microscopy:

  • mesangial & endocapillary proliferation
  • GBM thickening
  • splitting

Electron Microscopy → dense deposits

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14
Q

IgA nephropathy

A

Clinical presentation: Reccurent hematuria or proteinuria
-older children & young adults

Pathogenesis:

  • IgA1 polymeric complexes trapped in mesangium →activate alt C’ → injury
  • -genetic/acquired abnormality of immune regulation
  • → ↑ IgA synthesis in response to respiratory or GI exposure to environmental agents (recurrent hematuria)

Light Microscopy:

  • focal mesangial proliferative glomerulonephrtitis
  • mesangial widening

Fluorescence Microscopy:

  • prominant IgA in mesangium
  • +/- IgG, IgM and C3 in mesangium

Electron Microscopy:
-mesangial & paramesangial dense deposits

Prognosis → Good

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15
Q

Alport

A

Hereditary GN

Clinical presentation: Hematuria

Pathogenesis → nerve deafness, eye disorders

Prognosis → poor

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16
Q

Thin basement membrane

A

Hereditary GN

Clinical presentation: Hematuria

Pathogenesis: Benign familial hematuira

Electron Microscopy → thin BM

Prognosis → excellent

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17
Q

Acute Tubular/Kidney Injury

A
  • oliguria → uremia → recovery
  • most common cause of acute renal failure
  • Ischemic type → period of inadequate blood flow to peripheral organs, marked hypoTN, shock
  • Nephrotoxic type → drugs, contrast agents, poisons

Morphology → skip lesions + casts

  • Eosinophilic hyaline & Pigmented granular casts
  • -distal tubules & collecting ducts
  • -consist of Tamm-Horsfall protein → GP from cells of ascending think limb & distal tubules
  • Epithelial regeneration
  • -flattened epi cells w/ hyper chromatic nuclei & mitotic figures
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18
Q

Acute Pyelonephritis

A

-Acute suppurative inflammation of kidney due to bacterial infection (E. Coli, Proteus, Klebsiella)

  • Sudden onset pain at CVA, fever
  • dysuria, frequency, urgency
  • urine → pyruia
  • white cell casts → renal involvement

Morphology:

  • patchy interstitial suppurative inflammation
  • INTRAtubular aggregates of PMN
  • tubular necrosis

Predisposing conditions:

  • urinary / urinary tract obstruction
  • pregnancy
  • preexisting renal lesions
  • vesicoureteral reflux
  • diabetes
  • immunosuppression & immunodeficiency
19
Q

Chronic pyelonephritis morphology

A

due to **reflux nephropathy or chronic obstructive pyelonephritis

Gross:

  • irregularly scarred (mountain & valleys)
  • Hallmark → coarse, discrete, coritcomedullay scar overlying blunted, dilated calyx
  • if B/L → involvement is asymmetric (vs chronic GN)

Micro:

  • tubules → atrophy & hypertrophy
  • dilated tubule may contain colloid casts (thyroidization)
  • chronic interstitial inflammation & fibrosis → cortex & medulla
20
Q

Acute drug-induced interstitial nephritis

A

-drug is happen → binds tubular cells → immunogenic → injury due to IgE and CMI

  • Onset about **15 days after exposure to drug
  • Fever, EOSINOPHILIA, rash, renal abnormalities
  • -hematuria, mild proteinuria, leukocyturia (eosinophils)

Morphology:

  • interstitial edema
  • infiltration by lymphocytes & macrophages
  • EOSINOPHILS and PMN
  • may see granuloma
  • varying tubular necrosis & regeneration
21
Q

Analgesic Abuse Nephropathy

A
  • Papillary necrosis first → cortical tubulointerstitial nephritis
  • drug withdrawal → may stabilize or improve
  • -otherwise → chronic renal failure
  • transitional papillary carcinoma possible
  • Acetaminophen → phenacetin → damages cell
  • Aspirin → inhibits vasodilatory effects of PG

Gross:

  • cortical atrophy overlying necrotic papillae
  • -papillae at various stages of necrosis, calcification, fragmentation and sloughing

Micro → patchy/complete necrosis of papillae
-calcification

22
Q

Causes of papillary necrosis

A
  • Diabetes mellitus → several; all same stage of necrosis
  • Analgesic nephropathy → all; different stages of necrosis
  • Sickle-cell disease → few
  • obstruction
23
Q

Diabetes Criteria

A

1) HbA1c >= 6.5%
or
2) FPG >= 126 mg/dl after 8hrs fast (normal 70-100)
or
3) 2hr plasma glucose >= 200 mg/dl
(confirm all 3 by repeat test, esp. if acutely ill)

-Classic symptoms of hyperglycemia or hyperglycemic crisis, random plasma glucose >=200mg/L

24
Q

Prediabetes criteria

A
  • HbA1c 5.7-6.4%
  • FPG= 100-125 mg/dL (normal 70-100)
  • 2hr plasma glucose 140-199 mg/l
25
Q

Type I Diabetes Mellitus

A

CLINICAL:

  • Onset → childhood and adolescence
  • normal weight/ weight loss preceding diagnosis
  • progressive ↓ insulin levels
  • circulating islet autoAb:
  • -*anti-insulin
  • -*anti-GAD (glutamic acid decarboxylase)
  • -*anti-ICA512
  • DKA in absence of insulin therapy

GENETICS:

  • MHC II genes: HLA DR3/DR4
  • CTLA4
  • PTPN22
  • insulin gene VNTR (variable number tandem repeats)

PATHOGENESIS:
-Dysfunction in T cell selection & regulation → loss self-tolerance to islet autoAg

PATHOLOGY:

  • Insulitis → inflammatory infiltrate of T-cells & macrophages)
  • β-cell depletion, islet atrophy
26
Q

Type II Diabetes Mellitus

A

CLINICAL:

  • Onset → usually adult
  • vast majority obese
  • ↑ insulin early → normal to ↓ insulin late
  • no islet Ab
  • Nonketotic hyperosmolar coma more common

GENETICS → diabetogenic & obesity-related genes

  • TCF7L2
  • PPARG
  • FTO

PATHOGENESIS:

  • Insulin resistance in peripheral tissues
  • Failure of compensation by β cells

PATHOLOGY:

  • No insulinitis; amyloid deposition in islets
  • mild β-cell depletion
27
Q

Adult polycystic kidney disease

A

Inheritance → autosomal dominant (always B/L kidney)

Pathologic features:

  • asymptomatic until renal insufficiency at ~50
  • large multicystic kidneys (B/L abdominal masses)
  • liver cysts (40% polycystic liver disease)
  • **berry aneurysms → stroke
  • mitral valve prolapse → defect in BM
  • PKD1 on chr 16 → polycystin 1
  • PKD2 → disease at older age; later onset renal failure

Clinical features / complications

  • *hematuria, proteinuria (<2gm/day), polyuria
  • flank pain → hemorrhage, dilation
  • renal colic from passage of clots
  • *UTI, *renal stone
  • *HTN

Typical outcome → chronic renal failure at 40-60ys

28
Q

Childhood polycystic kidney disease

A

Inheritance → autosomal recessive (always B/L kidney)

Pathologic features:
-enlarged, cystic kidneys at birth

-PKHD1 on chr 6 → fibrocystin (cilium of tubular cells)

Perinatal & Neonatal:

  • most common
  • **Potter sequence at birth or rapid renal failure

Infantile & Juvenile:

  • Assoc w. congenital hepatic fibrosis → portal HTN
  • -↑ risk for cholangiocarcinoma
  • liver disease predominates w/ ↑ age

Typical outcome → variable, death in infancy or childhood

Morphology → parallel cylindrical slit like cysts in cortex
-at right angles to cortical surface (whole tubule dilates)

29
Q

Medullary sponge kidney

A

Inheritance → none

Pathologic features:

  • multiple cystic dilations of **collecting ducts → medulla of adults
  • discovered radiographically
  • -incidental or related to complications →

Clinical features / complications:

  • hematuria
  • UTI
  • recurrent renal stone (*calcifications in dilated ducts)

Typical outcome → benign

Morphology → dilated small cysts in medulla
- **cuboidal/ transitional cell lining

30
Q

Familial juvenile nephronopthisis

A

Inheritance → autosomal recessive
-manifest in childhood or adolescence (most common)

Pathologic features: (medullary problem not nephron)

  • corticomedullary cysts
  • shrunken kidneys
  • NPHP → nephrocystin (ciliary protein)

Clinical features / complications

  • salt wasting, polyuria, nocturia (start wetting bed again)
  • tubular acidosis
  • UREMIA
  • -azotemia
  • -↓ Ca → hyperparathyroidism → demineralized bone
  • -↑ phosohorus & K

Typical outcome → progressive renal failure beginning in childhood (most common genetic cause)

Morphology:

  • cysts in the medulla at corticomedullary junction
  • cortical tubular atrophy
  • interstitial fibrosis
31
Q

Multicystic renal dysplasia

A

Inheritance → sporadic (may be unilateral)

Pathologic features

  • irregular kidneys w/ cysts of variable sizes
  • enlarged, cystic kidney or flanks mass → at birth

Clinical features / complications
-assoc. w/ other renal abnormalities of lower UT

Morphology

  • cartilage, undifferentiated mesenchyme
  • immature collecting ductules
  • abnormal lobular organization

Typical outcome:

  • B/L → renal failure
  • U/L → surgical cure
32
Q

Morphology of benign nephrosclerosis

A

-Kidney of benign HTN, aging, DM

  • Hyaline arteriolar sclerosis (pink and smudgy)
  • kidney shrinks
  • finely granular cortical surface
33
Q

Unilateral renal artery stenosis

A

-Atherosclerosis causes most

  • Fibromuscular dysplasia also causes
  • -younger women
  • -fibrous, elastic tissue or muscular thickening of vessel wall
  • -→ beaded appearance on X-ray

→ causes renal vascular hypertension in C/L kidney
–hyaline arteriolar sclerosis

Ischemic Kidney:

  • small, shrunken
  • tubular atrophy
  • interstitial fibrosis w/ inflammatory cells
  • ↓ urine output
  • ↑ renin in renal bein

Normal Kidney:
arteriolar sclerosis

34
Q

Diffuse cortical necrosis

A

-associated w/ shock & obstetrical accidents

35
Q

Renal Stone types

A

Calcium Oxalate & Phosphate (70% of stones)

  • small cube/diamond shape
  • acidic urine
  • hypercalciuria w/o hypercalcemia (idiopathic)
  • ↑ GI calcium absorption or impaired reabsorption
  • radio-opaque
  • Oxalate crystals → ethelyene glycol

Magnesium Ammonium Phosphate (5-10%)

  • alkaline urine
  • assoc. w/ infection Proteus
  • Staghorn calculi → take shape of calyces & pelvis
  • look like bars of gold
  • radio-opaque

Uric Acid (5-10%)

  • rectangular, longer (parallelogram)
  • football/star shap
  • acidic urine
  • gout
  • leukemia, lymphoma- tumor lysis syndrome
  • radiolucent

Cystine (1-2%)

  • only hexagon shaped
  • hereditary causes
  • acidic urine
36
Q

Hyaline granular casts →
Renal tubular epithelial casts →
Waxy cast →
Leukocyte cast →

RBC cast →
Oval fat bodies/ fatty cast →
Broad waxy cast →

A

Hyaline granular casts → acute tubular injury
Renal tubular epithelial casts → acute tubular injury
Waxy cast → tubules atrophic (not acute)
Leukocyte cast → pyelonephritis

RBC cast → bleeding from glomerulus
Oval fat bodies/ fatty cast → always nephrotic
Broad waxy cast → caput end stage kidney

37
Q

Benign renal neoplasms

A
  • Renal “adenoma”
  • oncocytoma → intercalated cells of collecting ducts
  • angiomyolipoma → perivascular epithelioid cel
  • -tuberous sclerois
38
Q

Malignant renal neoplasms

A
  • conventional renal cell carcinoma (clear cell)
  • -→ renal tubular or collecting duct epithelial cell
  • -papillary
  • -chromophobe
  • -translocation
  • -collecting duct
  • Urothelial (transitional) cell carcinoma of calyces/pelvis
  • Wilms tumor (nephroblastoma) → stem cells
39
Q

Bladder cancer risk factors

A

1) cigarettes
2) aromatic amines or aniline dyes
3) schistosoma haematobium (squamous carcinoma)

present w/ painless hematuria and maybe obstruction

40
Q

Cause of diabetic vascular disease

A

Chronic hyperglycemia →

1) AGE → RAGE (T cell, macrophage, endo, vascular SM)
- Large vessels:
- -crosslink type I collagen → ↓ elasticity
- -crosslink & traps plasma & matrix proteins
- -traps LDL in atheroma

  • Small vessels
  • -binds type IV collagen of BM → crosslinks w/ albumin
  • → microangiopathy

2) Activated PKC
- ↑ VEGF → diabetic retinopathy
- ↑ TGFβ
- ↑ PAI-1 → procoagulation

41
Q

Cause of diabetic nerve & lens damage

A

↑ intracellular glucose in nerve/lens → sorbitol → fructose

  • -via aldose reductase
  • -uses up NADPH → ↓ antioxidant GSH
  • ↑ susceptibility to oxidative stress
42
Q

conditions w/ elevated PSA

A
  • prostate carcinoma
  • BPH
  • Prostatitis
  • infarct
  • instrumentation
43
Q

Cadmium

A

-pulmonary toxicity → obstructive lung disease

Nephrotoxicity

  • concentrates in proximal convoluted tubules
  • acute toxicity → proteinuria
  • chronic toxicity → hypercalciuria, osteopenia, gractures
  • -prostate & renal cancer risk

year 2 (15 decks)

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