CKD 2 Flashcards
causes for complications of CKD
pro-inflammatory state (uremia)
multiple electrolyte abnormalities
vascular stress
tissue dysfunction due to build up of waste products
CV effects of uremic syndrome
3.5x CVD mortality
CAD contributes to cause of death
CAD causes death in CKD why
- severe CAD develops (pro inflammatory state, hypertriclygeridemia, vascular stress)
- multiple co-morbidities makes disease more severe
- our reluctance to investigate and fully treat
heart disease and uremia
- high rate of accelerated and recurrent stenosis of coronary arteries
- metastatic calcification of valves and pericardium due to secondary hyperparathyroidism
- chronic anemia increases workload
- additional cardiovascular stress of HD
pericardial effusion and pericarditis
buildup of metabolic toxins
s/s: evidence of fluid overload chest pain fever friction rub
why does heart failure occur so easily in CKD?
uremic state
accelerated CAD
LVH/dilation
fluid overload
anemia
AV shunt
general rules for HF and uremia tx
managed by ACE/ARB and diuretics
- monitor K, Cr
- higher diuretic doses
- watch for toxicities
GI effects of uremic syndrome
occur early and frequently
- metallic taste, N/v anorexia
- weight loss (Decreased intake and catabolism)
- gastritis
- GI bleeding
CNS early effects in CKD
progressive cognitive dysfunction
memory problems
sleep disturbances
decreased DTR and vibratory sensation
late effects in CKD
lethargy, irritability, asterisks
frank encephalopathy
seizures
peripheral neuropathy
autonomic neuropathy
3 types of anemia seen in CKD
- anemia of chronic dz (decreased erythropoietin)
- iron def. anemia
- anemia of chronic disease
microcytic
treatment of anemia in CKD
Fe supplement and recombinant erythropoietin
HgB goal of 10 (too much = pro clotting)
bleeding diathesis
coagulopathy due to platelet dysfunction
- mild to mod decrease in platelet count
- abnormally poor platelet adhesiveness and aggregation
endocrine effects of uremia
women
decreased estrogen and progesterone levels
cycles are anovulatory
low libido and vaginal bleeding
pregnancy is rarely possible and fetal death occurs
endocrine effects of uremia
men
low levels of testosterone
result in impotence and low libido
immune effects of uremia
humoral and cellular immunologic dysfunction
late CKD considered relatively immunosuppressed
more likely to get rare/fungal infection
metabolic derangement in CKD
diabetic patients may require more or less insulin due to increased tissue resistance and decreased renal clearance respectively
lipid abnormalities (high trigs, accelerated arteriosclerosis)
skin derangement in CKD
yellowish skin
pruritus
nails: brown discoloration of distal nail bed, splinter hemorrhages, pale
NSF
caused by allergy to gadolinium contrast
symmetrical, bilateral fibrotic indurated papules, plaques, or subcutaneous nodules +/- erythema
first develops on ankles, lower legs, then move proximally
preceded by edema
NSF management
pathophys unknown
diagnosis of skin biopsy
chronic and unremitting
avoid gadolinium w/ GFR <30-44
secondary PTH
excretion of Ca++ in place of phosphorus
causing increased levels of PO4, decreased serum levels, stimulates PTH secretion
mobilizes calcium form bones to maintain normal levels
low bone turnover rates and decreased/absent bone formation
Parathyroid glands are hyperplasia
failing kidney can’t make vitamin D so absorption decreases
renal osteodystrophy
demineralized bones due to CKD
characterized by
bone pain, osteomalacia
spontaneous fracture
muscle weakness
metastatic calcifications
nonskeletal secondary hyperparathyroidism (6)
cardiovascular calcification soft tissue calcification endocrine disturbances compromised immune system neuro-behaviroal changes altered eryhtopoiesis
another cause of secondary hyperparathyroidism
vitamin D deficiency
unable to absorb calcium from diet resulting in overstimulation of parathyroid
its with CKD have both etiologies due to poor renal activation of vitamin D
labs of secondary hyperparathyroidism
LOW serum Ca
HIGH serum PTH
HIGH serum phosphate
treatment of secondary hyperparathyroidism
- reduce intake of phosphates
- place on phosphate binders
- normalization of vitamin D levels
- sensitivity change of PT receptors
phosphate binders
taken with meals, bind to injected phosphates and pass them thru GI without absorption
phosphate binders used (brand + generic)
- calcium acetate (phoslo)
- selevamer (renvela, renegel)
- fosrenol (lanthanum)
- sucroferric oxyhydroxide (velphoro)
medication given to normalize vitamin D levels
- Calcitriol (Rocaltrol) - ACTIVE vitamin D metabolite
- Doxercalciferol (Hectorol) - must be metabolized
- Paricalcitol (Zemplar) - binds to vitamin D receptor
Cinacalcet
Sensipar
calcimimetic, enhances sensitivity of parathyroid calcium receptor
tricks receptor into thinking lower level is acceptable
surgical treatment of secondary hyperparathyroid
partial removal (3.5 glands)
total parathyroidectomy
tertiary hyperparathyroidism
occurs in patients with longstanding CKD following renal transplant
tertiary hyperparathyroidism pathophys
parathyroid glands have been excessively active for several years by CKD
fail to recognize normalization of serum calcium levels after renal transplant and parathyroid is autonomously producing PTH
treatment of tertiary hyperparathyroidism
resistant to calcimimetics
calcifications occur in body tissue
total or subtotal parathyroidectomy
hungry bones
severe hyperparathyroidism pt has parathyroidectomy
post-op bone resorption remains same, and bones are hungry
its suffer repeated episodes to hypocalcemia despite supplementation
symptoms of hungry bones
symptoms of hypocalcemia
parasthesia in finger and mouth
seizures
hyperkalemia (levels and tx of MILD)
significant >5.5
need to r/o hemolysis
oral or rectal K binder (Kayexalate)
severe hyperkalemia treatment
IV calcium gluconate
hemodialysis
