6/8 UWorld Flashcards

1
Q

Where are immune complex depositions in Post-strep glomerulonephritis

A

Type 3 HSR
Immune complex deposition sub-epithelially

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2
Q

Where are immune complex depositions in IgA nephropathy

A

Aka Berger disease (Henoch Schonlein purpura)

IgA immune complex deposits in mesangium

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3
Q

What is the cause of Alport syndrome

A
  • Due to defect in Type IV collagen (basement membrane)
    • Leads to splitting of the basement membrane longitudinally
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4
Q

Presentation of Alport syndrome

A

Presents as isolated hematuria, sensory hearing loss, and ocular disturbances

“Can’t see, can’t pee, can’t hear high C”

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5
Q

Where are immune complex depositions seen in diffuse proliferative glomerulonephritis

A

DPGN seen in Lupus

Immune complexes seen subendothelially and within the mesangium

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6
Q

Describe light microscopy of lupus nephritis (DPGN)

A
  • Light microscopy – deposits make basement membrane look thick – “wire looping” of capillaries
    • THINK: wire lupus
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7
Q

Describe the mechanism behind the following in nephrotic syndrome:

  • Edema
  • Increased risk of infection
  • Increased risk of thrombosis
  • Hyperlipidemia
A
  • Proteinuria > 3.5 g/day
  • Hypoalbuminemia – protein lost in urine
  • Edema – decreased oncotic pressure due to hypoalbuminemia
  • Increased risk of infection – loss of immunoglobulin in urine
  • Increased risk of thrombosis – loss of antithrombin III
  • Hyperlipidemia – liver tries to make more lipoproteins in order to make up for decreased oncotic pressure
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8
Q

What are the types of nephritic syndrome

A

Post-strep glomerulonephritis

Alport Syndrome

IgA Nephropathy

Diffuse proliferative glomerulonephritis

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9
Q

What are the types of nephrotic syndrome

A

Foot process effacement: Minimal change disease, focal segmental glomerulosclerosis

Immune deposition: Membranous nephropathy, Membranoproliferative glomerulonephritis

Other: Diabetes, Amyloidosis

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10
Q

What is a trigger for minimal change disease

A
  • Triggered by infections or immunizations
  • Most common cause of nephrotic syndrome in children
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11
Q

Where are the immune complex deposits in membranous nephropathy

A

subepithelial

  • H&E – thickening of basement membrane
  • EM – “spike and dome” appearance with subepithelial deposits (IgG and C3)
  • IF – granular
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12
Q
A
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13
Q

Describe biopsy of Diabetic nephropathy

A
  • Will show sclerosing of the mesangium with Kimmelstie-Wilson nodules (round acellular nodules)
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14
Q

Where in the glomerulus will you find amyloid depositis in Amyloid nephropathy

A

In the mesangium

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15
Q

What type of stone is a struvite stone?

A

Ammonium magnesium phosphate stone

  • Major risk factor = Urease + bacteria
  • Recall:
    • Urea is broken down by urease into NH3 and CO2
    • NH3 converted to NH4+ which can combine with magnesium and phosphate
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16
Q

What is the other symptom associated with Henoch Schonlein purpura other than palpable purpura and IgA nephropathy

A

Arthralgias

17
Q

What are the radioopaque (seen in XR) vs. radiolucent kidney stones

A

Radiopaque = calcium and struvite

Radiolucent = uric acid and cystine

18
Q

Describe histology of renal cell carcinoma

A
  • Will see polygonal clear cells filled with accumulated lipids and carbohydrates
19
Q

Horomones secreted by RCC

A
  • Hormones secreted by renal cell carcinoma:
    • Erythropoietin - polycythemia
    • ACTH - Cushing
    • PTH-related peptide - Hypercalcemia
    • Prolactin - hypogonadism, decreased libido, galactorrhea
20
Q

What is WAGR complex

A
  • Wilms tumor, Aniridia (absence of iris), Genitourinary malformation, mental/motor Retardation
21
Q

What disease is associated with thyroidization of the kidney

A
  • Chronic pyelonephritis
  • Eosinophilic casts dilate the tubules, causing the tubules to have a colloid/thyroid-like appearance
22
Q

What disease is associated with eosinophils in urine

A
  • Acute interstitial nephritis
    • Acute interstitial renal inflammation that results in acute renal failure
    • Presentation:
      • Fever, rash, eosinophilia, azotemia
23
Q

Describe BUN/Cr and FENa in pre-renal, intrinsic, and post-renal azotemia

A
  • (1) Pre-renal azotemia:
    • BUN/Creatinine > 20
      • BUN is reabsorbed, creatinine is not
    • FENa (fractional excretion of sodium) < 1%
      • Tubular function intact so Na+ can still be reabsorbed
  • (2) Intrinsic renal failure:
    • BUN/Creatinine < 15
      • Tubular dysfunction = decreased reabsorption of BUN
    • FENa > 2%
      • Tubular dysfunction = decreased reabsorption of Na+
  • (3) Post-renal azotemia:
    • Early stage
      • BUN/Cr > 20
      • FENa < 1%
    • Late stage - tubular damage occurs
      • BUN/Cr < 15
      • FENa > 2%
24
Q

Consequences of chronic renal failure

A
  • Inability to produce urine = water retention:
    • Peripheral edema, heart failure, pulmonary edema, HTN
  • Hyperkalemia (due to decreased renal excretion)
  • Metabolic acidosis
  • Uremia
  • Anemia (decreased erythropoietin production)
  • Hypocalcemia (due to decreased Vitamin D active form)
  • Renal osteodystrophy (due to decreased Vitamin D active form)
25
Q

Describe the pathogenesis of renal osteodystrophy

A
  • Recall:
    • Kidneys promote conversion of calcidiol to calcitriol (active form of Vitamin D)
  • Chronic renal disease = Vitamin D deficiency = hypocalcemia + hyperphosphatemia = secondary hyperparathyroidism = increased degradation of bone
26
Q

Disorders associated with ADPKD

A
  • Associated with cysts in the liver, berry aneurysms, mitral valve prolapse
27
Q

Common causes of acute interstitial nephritis

A
  • NSAIDs, Penicillin, Cephalosporin, Sulfonamides, Ciprofloxacin, Cimetidine, Allopurinol, PPIs, Indinavir, Mesalamine
  • REMEMBER the P’s:
    • Pee (diuretics), Pain-free (NSAIDs), Penicillin and Cephalosporins, PPIs, rifamPin
28
Q

Describe medullary cystic disease

A
  • Can lead to fibrosis and progressive renal insufficiency
  • Will present as cysts in the collecting ducts and shrunken kidney due to fibrosis
    • Vs. most other cystic diseases which will present with cystic dilation of kidney
29
Q

Describe the organ systems associated with each of the muscarinic receptors (M1, M2, M3)

A

M1 - enteric and CNS

M2 - heart

M3 - bladder, smooth muscles of eye

30
Q

Describe the sequence of events in the Gq pathway

A

Gq = activation of phospholipase C = cleavage of PIP2 into IP3 and DAG = IP3 increases intracellular calcium and DAG activates protein kinase C = leads to smooth muscle contraction

31
Q

What hormones use the Gq pathway?

A

GOAT HAG

GnRH, oxytocin, V1 (ADH), TRH, H1, Angiotensin II, Gastrin

32
Q

Describe the sequence of events in Gs/Gi pathways

A

Activation of Gs = activation of adenylate cyclase = adenylate cyclase cleaves ATP to form cAMP = cAMP activates protein kinase A

33
Q

What hormones use the Gs/Gi pathway

A

FLAT ChAMP

FSH, LH, ADH (V2), TSH, CRH, hCG, ACTH, MSH, PTH

34
Q
A
35
Q
  • Initial lesion (“herald patch”) followed by scaly erythematous plaques in a “Christmas tree” distribution on trunk
  • Self-resolving in 6-8 week
A

Pityriasis rosea

36
Q

What disorder gives you “notching” of the ribs on X-ray

A

Adult form of aortic coarctation

  • Collateral arteries form and engorged intercostal erode ribs
37
Q

Which is pre-central gyrus vs. post-central gyrus - motor or sensory cortex

A

Motor = pre-central

Sensory = post-central

38
Q

Name of non-selective beta-blocker

A

Propranolol

Causes decrease CO and increased peripheral resistance (B2 blocking causes vasoconstriction)