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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
Type I Diabetes Mellitus
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
Type II Diabetes Mellitus
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
Adult polycystic kidney disease
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
Childhood polycystic kidney disease
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
Medullary sponge kidney
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
Familial juvenile nephronopthisis
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
Multicystic renal dysplasia
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
Morphology of benign nephrosclerosis
-Kidney of benign HTN, aging, DM - Hyaline arteriolar sclerosis (pink and smudgy) - kidney shrinks - finely granular cortical surface
33
Unilateral renal artery stenosis
-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
Diffuse cortical necrosis
-associated w/ shock & obstetrical accidents
35
Renal Stone types
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
Hyaline granular casts → Renal tubular epithelial casts → Waxy cast → Leukocyte cast → RBC cast → Oval fat bodies/ fatty cast → Broad waxy cast →
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
Benign renal neoplasms
- Renal "adenoma" - oncocytoma → intercalated cells of collecting ducts - angiomyolipoma → perivascular epithelioid cel - -tuberous sclerois
38
Malignant renal neoplasms
- 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
Bladder cancer risk factors
1) cigarettes 2) aromatic amines or aniline dyes 3) schistosoma haematobium (squamous carcinoma) present w/ painless hematuria and maybe obstruction
40
Cause of diabetic vascular disease
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
Cause of diabetic nerve & lens damage
↑ intracellular glucose in nerve/lens → sorbitol → fructose - -via aldose reductase - -uses up NADPH → ↓ antioxidant GSH - ↑ susceptibility to oxidative stress
42
conditions w/ elevated PSA
- prostate carcinoma - BPH - Prostatitis - infarct - instrumentation
43
Cadmium
-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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