Histology Uworld!

Wednesday, September 13, 2017 12:43 PM

Type 2 pneumocytes proliferate in injury to form type 1 pneumocytes. Type 2 produce surfactant.
Alveolar macrophages are self-maintaining population derived from fetal monocytes.
Principal clearing cells in terminal bronchioles.
PSGN symptoms: cola colored urine, periorbital edema, oliguric renal failure. High BP, red cell casts and mild proteinuria. Lab studies show decreased serum complement C3
level and elevated titers of streptococcal antibodies (e.g. anti-DNAse B, anti-hyaluronidase, antistreptolysin ASO which is detectable after skin infections. Most children
recover with supportive treatment without long term sequalae.
Classic light microscopy findings in PSGN are enlarged, diffusely hypercellular glomeruli due to leukocyte infiltration (N and Monos) and mesangial and endothelial cell
production. IF microscopy shows granular deposits o IgG,IgM, and C3 in the GBM and mesangium producing STARRY SKY appearance seen in the image. Electron micro show
SUBEPITHELIAL HUMPS, representing deposition of ag-ab complexes at the epithelial surface.
The proteins in PSGN do not deposit on GBM but are released in urine to disruption of the GBM.Results in dec plasma oncotic pressure leading to peripheral edema.
Complement activation in PSGN occurs via alternate and lectin pathways,resulting in glomerular C# deposition without significant C1/C4 deposits. Subepithelial C1q deposits
are characteristics of type 1 membranoproliferative GN.
Fibrin deposits are found inrapidly proliferative (cresecenteric) GN.
IgE deposists are sometimes seen in SLE and are indicator of poor prognosis and zare only in capillary walls.
Streptococcal pyogenic exotoxin B is granular deposition on GBM in PSGN and not M protein.
IMMUNOLOGY UWORLD CONTD
Most common system vasculitis in children (3-10years) is Henoch-Schonlein purpura HSP.Often occurs following infection. Caused by circulating IgA-antigen immune
complexes (type 3 HS). Deposition of these complexes in the walls of small vessels and mesangium leads to recruitment of neutrophils and lymphocytes as well as activation
of complement via alternate pathway and lectin pathways. Symptoms organ dysfunction and lower extremety,PALPABLE PURPURA,hematuria,arthralgias,abdominal pain.
Self-limited condition and resolves as circulating immune complexes clear. Treatment is supportive unless complicated (e.g. intussusception.
A palpable rash is also seen in disseminated Neisseria infections but it starts from trunk and spreads on entire body instead of lower extremities in HSP.Pts also have
tachycardia,fever,hypotension.
Chronic bronhcitis biopsy shows thickedned bronchial walls, neutro infiltrates(lymphocytic infiltration), mucus gland enlargement, SQUAMOUS METSAPLASIA of bronchial
mucosa.
There is no genetic predisposition to chronic brnchitis.
Most common causw of chronic bronchitis is smokingggggggg. Can't be more stressed.
Neoplasia can not lead to chronic bronchitis
2: polyarteritis nodosa is a necrotizing inflammation
3:carnitine def impairs transport of FA from cytoplasm to mitochondria, preventing beta oxidation of FA into acetyl coA, which leads to crdiac and
@: hypersensitivity pneumonitis pts have serum igGs that precipitate bacterial or fungal ags found in inhaled *organic dust particles causing interstitial alveolitis and
bronchiolitis via immune complex and complement deposition in vessel walls (type 3 H/S).
# pathogenesis of PSGN involves granular deposition of immune complexes containing group A streptococcal ags, IgG and C3 in GBM and mesangium. Type 3, immune
complex mediated H/S response.
@; goodpasture autoabs are agains GBM collagen (molecular thing)

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