Chronic Kidney Disease Part 2 Flashcards
one or both: abnormalities of ca, phos, PTH, vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth or strength, vascular or other soft tissue calcification
CKD-MBD
alteration of bone morphology in patients with CKD, one measure of skeletal component
renal osteodystrophy
most important regulator of intestinal absorption of Phos
high dietary Phos
major site of intestinal calcium absorption
duodenum
vitamin D independent nonsaturable pathway
paracellular pahtway
vitamin D dependent, saturable pathway
transcellular pathway
inactivation of CaSR: Calcium and PTH
decrease in Calcium, increase PTH secretion
most important determinant of minute to minute secretion of PTH From stored secretory granules
extracellular concentration of ionized calcium
major source of the circulating levels of calcitriol
kidney
circulating factors that regulate phos excretion
phosphatonins - FGF23 and MEPE
surrogate of bone turnover in patients with CKD
PTH
bone turnover, microarchitecture, microfractures and mineralization
bone quality
alignment of strands of collagen has an irregular woven pattern
osteitis fibrosa cystica
histologically by absence of cellular activity, osteoid formation and endosteal fibrosis
low turnover (adynamic bone disease)
excess of unmineralized osteoid, wide osteoid seams, decreased mineralization rates
osteomalacia
bone biopsies with secondary hyperparathyroidism with mineralization defect: extensive osteoclastic and osteoblastic activity and increased endosteal peritrabecular fibrosis
mixed uremic osteodystrophy
assess the presence or absence of vascular calcification
plain radiographs
Vit D deficiency
less than 10 ng/mL
vit D insufficiency
10-30 ng/mL
decreased stratum corneum hydration and abnormal eccrine gland function
xerosis
mainstay of treatment of xerosis
hydration of skin
skin develops patterned scale with hyperkeratosis and occasionally epidermal hypogranulosis
acquired ichthyosis
most common alteration in pigment of hd patients
yellowish tint
cause of hyperpigmentation
increased melanin production, inc B melanocyte stimulating hormone
perforating folliculitis, Kyrle’s disease, reactive perforating collagenosis
acquired perforating dermatosis
crateriform, umbilicated or centrally hyperkeratotic papules and nodules resolve with scarring after 6-8 weeks
acquired perforating dermatosis
mainstay of treatment of calciphylaxis
supportive and preventive measures
calcium deposits in the tissue
metastatic calcification
trauma may result to
dystrophic calcification
deficiency of uroporphyringogen decarboxylase
porphria cutanea tarda
noninflamed blisters, erosions and crusts in dorsal of hands and forearms, blisters may heal with scarring
porphyria cutanea tarda
subepidermal cleft with minimal inflammation; festooning of the papillary dermis at the base of the celft; thickened vessel walls
porphyria cutanea tarda
IF findings in porphyria cutanea tarda
granular to linear staining of immunoglobulin G and C3 at the dermoepidermal junction
noninflamed blisters on the extremities: hands and forearms and other sun exposed areas
pseudophrphyria
drugs associated with pseudoporphyria
tetracycline, furosemide, naproxen, amoidarone and nalidixic acid
yellowish orange smooth papules and plaques that rapidly appear on buttocks and proximal extremities
eruptive xanthomas
histopathologic findings in eruptive xanthomas
extracellular lipid and foamy macrophages
vascular proliferation near or over an AV shunt
pseudo-kaposi’s sarcoma
ESRD patients who receive intravenous contrast with translucent papulonodular or vegetative lesions
iododerma
marked epidermal hyperplasia with intraepidermal pustules of neutrophils and eosinophils
iododerma
bound down indurated skin, cobblestone apperance, edema and erythema early on; exposure to gadolinium
nephrogenic systemic fibrosis
Histopath: increased dermal and/or subcutaneous fibroblast-like cells
cells stain with procollagen I and CD34
nephrogenic systemic fibrosis