UG II - Glomerular Diseases Flashcards

1
Q

ESKD Cx

  • Electrolytes
  • CPB
  • Hematologic
A

Electrolytes

  • Hyperkalemia
  • Oedema from RAAS - hypertension
  • Metab Acidosis
    • less bicarb reabsorbed, and poor NH4+ excretion

CPB

  • Kidney 1 alpha hydroxylase to make active Vit D
  • Hypocalcaemia
  • Hyperphosphataemia
    • Secondary hyper PTH - but response is shit due to Vit D deficiency;
  • – Osteodystrophy

GFR drops, PO4 increases, Osteocytes releases FGF23 to block vit D activation;

Blood
- Anaemia due to low EPO from kidneys

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2
Q

ESKD Histology [3]

- impt!

A

Chronic

  • interstitial fibrosis
  • glomerulosclerosis - scarring and fibrosis!!!
  • tubular atrophy
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3
Q

Nephrotic Vs Nephritic Syndrome

Plus 3 unique presentations each
- think systemic also lmao

A

Nephrotic - leaky filter - proteinuria
Nephritic - damaged filter - 0 GFR + some leaky - oliguria + proteinuria
– INFLAMMATION - RBC, WBC

Nephrotic - hypoalbuminemia - generalized edema; hyperlipidemia lol 2 only
Nephritic - HYPERTENSION, Azotaemia, hematuria
– azotaemia - more nitrogen in blood
– can be due to decreased GFR leading to increased creatinine;

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4
Q

Whats the function of

  • Macula Densa
  • JGA
A
  • DCT NaCl concentration - to stimulate renin from JGA + Vasodilate Afferent to increase GFR
  • Sense BP of Afferent - to secrete renin
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5
Q

Whats the anatomy @ glomerular capsule

A

Lumen
Endothelial - Fenestrated (holes)
Basement Membrane
Podocytes Epithelial Layer - Slit Diaphragm - w foot processes;

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6
Q

Glomerulonephritis definition

A

Increased cellularity + Inflammation cells

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7
Q

3 AB-mediated Glomerular Injury

Examples and Staining properties

A

Antibody-Antigen complex deposition - Type III HS

  • eg Lupus Nephritis; accumulation of IgA Nephropathy “glomerulonephritis”
  • Post Strep GNP!!!!
  • “granular staining”

Antibody- target self antigen - Type II HS

  • forms in-situ complexes
  • eg Anti-GBM disease - Goodpasture’s IgG staining - note systemic hence lung problems too; also GlomeruloNEPHRITIS
  • “linear staining”

Anti-Neutrophil Cytoplasmic AB ANAC

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8
Q

Nephrotic Syndrome common causes

A

Without inflammation - hence glomerulopathy
- Podocyte diseases common

  • Membranous Glomerulopathy - common in adults
    • Basement membrane w immune complex; then MAC formation after Complement activation;
    • narrowing of blood vessels, then leakage
  • Focal Segmental Glomerulosclerosis - glomerular sclerosis and podocyte damage
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9
Q

Systemic Stuff that damages kidneys, seen w stain;

Which kidney syndrome

A

Amyloidosis

  • accumulated fibrillary proteins forming Beta Pleated Sheets - oligomers of misfolded proteins which cannot be destroyed
  • deposit in kidneys
  • Congo Red stain, amorphous appearance

Present w Nephrotic Syndrome

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10
Q

Systemic Stuff thats hypertension lol

A

Hypertensive Nephrosclerosis

Benign
Renal arterioles - hyalinosis + muscular thickening
Malignant
- Fibrinoid Necrosis + Onion skinning lamination

Present w Nephrotic Syndrome

  • wo blood, FSGS, then Glomeruli will collapse
  • Glomerulosclerosis is hardening of the glomeruli in the kidney. It is a general term to describe scarring of the kidneys’ tiny blood vessels, the glomeruli, the functional units in the kidney that filter urea from the blood.
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11
Q

Whats top cause of nephrotic syndrome

A

Focal Segmental Glomerulosclerosis

  • fibrosis at glomeruli
  • leading cause of Nephrotic Syndrome
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12
Q

Systemic Stuff thats sweet

Pathophysiology and Presentation of all compartments
Histology [2]
Name 1 Cx

A

Diabetic Nephropathy

Hyperglycemia - Glycosylated Proteins and G. Collagen
and glycosylate glomerular proteins

  • membranes now glycosylated - leakier, porous
  • vascular atherosclerosis, hyalinosis; hypertension
  • mesangial widening (increase in matrix and cells) - forming nodules - damage then hyaline materials then nodule

Histology: Nodular deposits, increased mesangial matrix
Nephrotic Syndrome; ESKD

Thickening of both Glomerular BM and Tubular BM
Hyalinosis (protein leakage)
Glomerular Sclerosis as end stage

Tubular BM also thicken
Tubular Atropy

Interstitial Fibrosis - note inflammation + RAAS both present

Cx: Pyelonephritis

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