Chronic Kidney Disease Part 2 Flashcards by kristine galan

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

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alteration of bone morphology in patients with CKD, one measure of skeletal component

renal osteodystrophy

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most important regulator of intestinal absorption of Phos

high dietary Phos

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major site of intestinal calcium absorption

duodenum

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vitamin D independent nonsaturable pathway

paracellular pahtway

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vitamin D dependent, saturable pathway

transcellular pathway

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inactivation of CaSR: Calcium and PTH

decrease in Calcium, increase PTH secretion

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most important determinant of minute to minute secretion of PTH From stored secretory granules

extracellular concentration of ionized calcium

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major source of the circulating levels of calcitriol

kidney

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circulating factors that regulate phos excretion

phosphatonins - FGF23 and MEPE

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surrogate of bone turnover in patients with CKD

PTH

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bone turnover, microarchitecture, microfractures and mineralization

bone quality

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alignment of strands of collagen has an irregular woven pattern

osteitis fibrosa cystica

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histologically by absence of cellular activity, osteoid formation and endosteal fibrosis

low turnover (adynamic bone disease)

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excess of unmineralized osteoid, wide osteoid seams, decreased mineralization rates

osteomalacia

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bone biopsies with secondary hyperparathyroidism with mineralization defect: extensive osteoclastic and osteoblastic activity and increased endosteal peritrabecular fibrosis

mixed uremic osteodystrophy

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assess the presence or absence of vascular calcification

plain radiographs

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Vit D deficiency

less than 10 ng/mL

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vit D insufficiency

10-30 ng/mL

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decreased stratum corneum hydration and abnormal eccrine gland function

xerosis

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mainstay of treatment of xerosis

hydration of skin

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skin develops patterned scale with hyperkeratosis and occasionally epidermal hypogranulosis

acquired ichthyosis

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most common alteration in pigment of hd patients

yellowish tint

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cause of hyperpigmentation

increased melanin production, inc B melanocyte stimulating hormone

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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

rare complication of fistula construction leading to decreased distal perfusion involving brachial area

dialysis associated steal syndrome

pallor or a reticulated pink to blue discoloration of the skin with necrosis, ulceration or gangrene

dialysis associated steal syndrome

effective treatment of dialysis associated steal syndrome

fistula ligation and/or binding

B2 microglobulin deposition, carpal tunnel syndrome and destructive arthropathy

dialysis related amyloidosis

melanin deposition in the nail bed and plate, proximal white to normal half and a red brown distal half

lindsay's half and half nail

leukocytoclasia, fibrin thrombi, nonblanching papules and plaques in lower extremities

leukocytoclastic vasculitis

numerous flesh-colored to slightly tan, smooth papules on the face that histopathologically are fibrofolliculomas or trichodiscomas

Birt Hogg Dube syndrome

Birt Hogg Dubb syndrome is associated with what renal findings

renal cell carcinoma

adenoma sebaceum associated with angiomyolipoma

tuberous sclerosis

port wine stain, cysts, clear cell renal cell Ca

VHL syndrome

sebaceous neoplasia, genitourinary carcinoma

muir-torre syndrome

diagnosis of DKD

urine ACR 30 mg/g or higher, eGFR < 60 ml/min

most important risk factor in DM

duration

screening of DKD in type 2 DM is recommended at

time of diagnosis

screening of DKD in type 1 DM is recommended after

5 years of type 1 DM

important predictor of progression of advanced kidney disease, clinical hallmark of diabetes

hyperglycemia

abnormalities in heart rate and vascular dynamics: resting tachycardia and orthostatic hypotension

cardiac autonomic neuropathy

best currently available risk marker for DKD

albuminuria

hallmark of DKD

accumulation of extracellular matrix

early finding in DKD

tubular basement/GB membrane thickening

first lesion detected by light microscopy

mesangial expansion

first lesion identified by electron microscopy

GBM thickening

prominent round expansion of hypocellular mesangial matrix with palisading mesangial cells in the periphery of the nodule surrounded by glomerular capillaries

nodular glomerulosclerosis, kimmelstiel wilson nodules

where can nodular glomerulosclerosis be seen

DKD, light chain deposition disease, immune complex processes, idiopathic nodular glomerulosclerosis

fraying of the mesangial matrix, precursor of nodular lesions

mesangiolysis

subendothelial accumulations of hyaline in the glomerular capillary

fibrin caps

accumulation of hyaline under the parietal epithelial cell lining of Bowman's capsule

capsular drops

Kidney biopsy in DM patients

sudden onset proteinuria, onset of proteinuria less than 5 years from type 1 DM, proteinuria in absence of retinopathy, AKI, active urinary sediment, hematuria

Class 3 DKD Glomerular lesions

nodular lesions (KWL_ at least one

RAAS blocker of choice: Type 1 DM, Htn, Albuminuria

ACEi

Type 2 DM. htn, microalb RAAS blocker

ARB

Overt DKD

ARB

target Hba1c for prevention of DKD

treatment goal of dyslipidemia

LDL < 70-100

protein intake for DKD

0.8 g/kg/day

DM patients on dialysis with spontaneous resolultion of hyperglycemia with Hba1c less than 6%

Burnt-out DM

screening for anemia should begin at CKD stage

stage 3

EPO is produced in what cells within renal cortex

peritubular interstitial cells, fibroblasts

low hepcidin

iron mobilization

high hepcidin

iron overload

gold standard to monitor patients with iron overload disorders

liver magnetic resonance imaging

decrease ferritin

vitamin C deficiency, hypothyroidism

threshold tsat value below which iron therapy is indicated

20%

dual markers of iron status as well as of nutritional and protein balance

transferrin and TIBC

most sensitive indicator of functional iron deficiency

Retic Hegmoglobin content

reversal agent for LMW and UFH

protamine sulfate

thrombocytopenia 5-10 days after the start of heparin therapy, persistence of any acute thrombotic event, normal platelet count before heparin, trhombocytopenia with no other causes; resolution after heparin cesation; HIT antibody seroconversion

heparin induced thrombocytopenia

first 2 days after exposire to heparin and platelet count normalizes with continued heparin therapy

Type 1 HIT

immune mediated disorder that typically occurs 4-10 days after exposure to heparin and has life and limb threatening thrombotic complications

Type 2 HIT

acute confusional state characterized by recent onset of fluctuating awareness, disorganized thinking, impairment of memory and attention

delirium disorders

syndrome of delirium seen in inadequately treated ESKD - lethargy, confusion and seizures or coma

uremic encephalopathy

headache, visual disturbance, nausea, agitation,

dialysis dysequlibrium

syndrome of progressive dementia related to aluminum intoxication

dialysis dementia

management of chronic cognitive impairment mild to moderate dementia

cholinesterase inhibitors

treatment of moderate to severe Alzheimer's dementia

Memantine

distal symmetric, mixed sensorimotor polyneuropathy, symmetric muscle weakness, areflexia and loss of vibratory sense

uremic polyneuropathy

compression or ischemia of the ulnar or median nerves and often dialysis related, amyloidosis or AVF

mononeuropathy

repetitive cessation of respiration during sleep

sleep apnea

apnea associated with continued respiratory effort

obstructive

apnea associated with absence of respiratory effort

central

treatment of sleep apnea

CPAP

urge to move the legs associated with feelings of discomfort or paresthesias

restless leg syndrome

first line therapy for more severe symptoms

levodopa

second line for restless leg syndrome

gabapentin

sudden and repetitive movements of the lower extremities during sleep

periodic limb movements of sleep