Week 3 - Chronic Kidney Disease Flashcards
what cuases chronic kidney disease
- gradual irreversible destruction of nephrons & loss of renal function
what does the destruction of nephrons & loss of renal function result in (3)
- increased workload on the remaining nephrons
- increased glomerular filtration pressure
- hyperfiltration ( of the remaining nephrons to attempt to maintain a normal GFR)
what does hyperfiltration predispose an individual to? (2)
- glomerulosclerosis which causes increased rate of nephron destruction
what is glomerulosclerosis
- fibrosis & scaring of the glomerulus
what are the top 3 causes of CKD
- diabetic nephropathy
- HTN
- glomerulosclerosis
end-stage renal failure presents as…
- complex of symptoms called uremia
list 5 causes of uremia
retained:
- fluid
- electrolytes
- waste products
- hormones
and loss of renal endocrine function (renin & erythropoitein)
how does end-stage renal failure effect our BMR
- causes reduced BMR = hypothermia
how does end-stage renal failure effect our blood lipoproteins? what causes this?
- causes increased blood lipoproteins
- due to decreased Na/K ATPase activity & lipoprotein lipase activity
uremia (CKD) produces clinical abnormalities in… ?? (8)
- fluid & electrolyte balance
- bone metabolism
- CNS
- cardiovascular
- pulmonary
- skin
- GI
- hematologic
- metabolic control (metabolic acidosis)
how many pathological stages of CKD are there?
3
describe pathological stage 1 of CKD (what is it, what % nephron lost, what happens if cause not detected)
- reduced renal reserve
- up to 50% of nephrons lost without causing S&S
- if cause is not detected, damage will continue
describe pathological stage 2 of CKD (what is it, what % nephron lost)
- renal insufficiency
- when more than 20% of nephrons remain
what does renal insufficiency result in? (4)
- decrease in GFR, reabsorption & secretion capacity
- results in moderate azotemia (elevated BUN)
describe pathological stage 3 of CKD (what is it, what % nephron lost)
- end-stage renal failure (uremia)
- occurs when less than 20% of nephrons remain
what does end-stage renal failure (pathological stage 3) result in (4)
GFR & tubular function greatly reduced =
- oliguria/anuria
- marked azotemia
- failure to conc. urine
how many clinical stages of CKD are there
5
describe stage 1 of CKD
- slightly diminished function
- kidney damage w normal or relatively high GFR (>90(
describe stage 2 of CKD
- mild reduction in GFR (60-89) with kidney damage
describe stage 3 of CKD
- moderate reduction in GFR (30-59)
describe stage 4 of CKD
- severe reduction in GFR (15-29)
- preparation for renal replacement theraoy
describe stage 5 of CKD
- established kidney failure (GFR < 15)
- permanent renal replacement therapy or end-stage kidney disease
what is normal GFR
125
describe CKD’s effect on sodium & fluid
- get sodium & fluid overload bc we are consuming faster than the kidney’s can clear (exceed the GFR since it is so low)
excess water & sodium can cause.. (5)
- circulatory congestion
- HTN
- ascites
- edema
- weight gain
what occurs with our water & sodium levels during times of loss (vomitting, diarrhea, etc.)
- we have a diminished reserve to converse Na and water
= hypovolemia & hyponatremia
= can lead to circulatory shock
how do we treat/prevent sodium & volume overload during CKD (3)
- restrict Na and water so we are not consuming it in excess
- measure ins & outs
- take multiple weight measuremenst throughout the day
describe CKD’s effect on potassium
- for the most part it can be maintained thru diet if GFR is in stage 2/3
- if GFR falls below 5, it can become a major problem
what 3 things increase the risk of hyperkalemia
- hemolysis
- acidosis
- infection
how does hemolysis increase the risk of hyperkalemia
- the rupture of RBC causes K to be leaked out
how does acidosis increase the risk of hyperkalemia
- during acidosis, we have exchange of H+ into the cell, and K+ out of the cell
what clinical abnormality does uremia cause to our metabolic control
- cause metabolic acidosis
at what point does metabolic acidosis occur during CKD? is it compensated
- occur moderately when GFR is greater than 20 & is compensated by increased respiration
- decompensated if GFR falls below 20 or if exposed to other acid loads
list 3 examples of other acid loads
- lactic acidosis
- infection
- pneumonia
describe the role of the kidney’s regarding vitamin D; why is this important?
- skin makes inactive vitamin D
- the kidneys are response for activating it
- imp so we can absorb Ca
describe the activation of vitamin D during CKD
- the kidneys get a reduced ability to activate vit D
describe the relation between vit D and calcium & how this is effected during CKD
- vitamin D allows Ca to be absorbed
- without activated vit D, consumed calcium cannot be absorbed in the gut and is lost in the feces = decreased Ca serum levels
what does a fall in serum Ca levels cause
- stimulates PTH secretion
what is the function of parathyroid hormone
- parathyroid hormone is released from the parathyroid gland when we have low Ca
- PTH activated osteoclasts which cause bone breakdown in an attempt to raise serum calcium
what 2 things does the bone contain that gets released when it is broken down?
- collagen
- hydroxyapatite (Ca++ and phosphate)
what else contributes to bone breakdown
- chronic acidosis
what does increased Ca and phosphate cause?
- calcifications in arteries, tendons, soft tissues, skin
kidney failure causes decreased GFR. How does this contribute to the formation of calcification in vascularture & soft tissues
decreased GFR = decreased PO4 excretion (can’t clear it out) = increased serum PO4 = calcifications
kidney failure causes decreased activation of vit D. Explain how this contributes to the formation of calcifications
decreased vit D activation = impaired Ca absorption from gut = decreased serum Ca = release of PTH = bone dimineralization (activation of osteoclasts) = increased Ca and PO4 = calcification
what is a consequence of increased parathyroid hormone
- osteitis fibrosa
what is osteitis fibrosa? what does this cause?
- patches of dimineralization in bones
- causes weak & easily fractured bones
what is a consequence of bone dimineralization due to the release of PTH
- ostesomalacia
what is osteomalacia
- softening/dimineralization of the bones due to vit D deficiency and increased PTH
what is the difference between osteomalacia and osteoporosis
- osteomalacia = decreased BD due vit D deficiency & increased PTH
- osteoporosis = decreased BD in absence ofvit D deficiency or PTH response (both PTH and vit D in range)
what cardiovascular & pulmonary symptoms does CKD cause r/t sodium & volume overload (3)
- circulatory congestion
- HTN
- edema & pulmonary edema
hypereninemia????
come back to this
what can irritation of uremic toxins cause in the CVS system?
- pericarditis
what is pericarditis
-inflammation of the pericardium (sac around the heart)
describe the effect of uremia on atherosclerosis?
- causes accelerated atherosclerosis
what causes accelerated atherosclerosis r/t CKD (2)
- elevation in bp (due to Na & water overload & hyperreninemia)
- hyperlipidemia caused by inhibition of lipoprotein lipase
what effect does CKD have on the hematological system (3)
- causes decreased production of erythropoietin
- abnormal hemostasis
- abnormal white cell function
what does decreased production of erythropoietin cause? how is this corrected?
- anemia with hematocrits of 20-25%
- NOT corrected by dialysis, and requires erythropoietin treatment
what does abnormal hemostasis & white cell function cause (2)
- bleeding
- immunosuppression
what effect does CKD have on the neurological system? (8)
- sleep disorders
- poor concentration
- memory loss
- seizures
- hiccups
- twitching
- coma
- sensory peripheral neuropathy
what causes the neurological effects of CKD (3)
- due to urea
- elevated organic acids or phenols
what causes elevated organic acids & phenols
- protein catabolism
what is a way we can prevent neurological symptoms of CKD
- protein restricted diet
what corresponds well with the degree of CNS disturbance?
- BUN
what are the effects of CKD on the GI (4)
- anorexia
- nausea
- vommiting
- uremic fetor (bad breath)
what causes uremic fetor
- when salivia enzymes breakdown urea into ammonium
what are the effects of CKD on the skin
- uremic frost & colour
what are 2 ways we can manage CKD
- drug therapy
2. nutritional therapy
what drugs can we give to treat hyperkalemia (4)
- Kayexalate
- insulin/glucose
- albuterol
- furosemide (lasix)
what is kayexalate
potassium binding agent
describe the use of insulin/glucose for hyperkalemia
- very quick response
- but does not last super long
why do we give glucose with insulin for hyperkalemia
- to prevent hypoglycemia
what is albuterol? how does it help with hyperkalemia
- short-acting beta adrenergic receptor agonist
- increases insulin
what is lasix
- a K+ losing diuretic (loop diruetic)
what med can we give to treat HTN and fluid overload associated with CKD
- furosemide (lasix)
what drug can we give to treat hyperphosphatemia r/t CKD
- sevelamer (renagel)
what is sevelamer
- phosphate binding agent
what can be given o treat anemia r/t CKD
- erythropoietin
what type of meds can be given to treat dyslipidemia r/t CKD
- statins
what is a potential complication of drug therapy
- many meds are 1st metabolized by the liver to produce water-soluble metabolites = then they need to be cleared by the kidneys
- if GFR is rlly low, the med metabolites will accumulate and can become toxic
list 4 types of nutritional therapy for management of CKD
- protein restriction (for neuro symptoms)
- na and fluid restriction
- potassium restriction
- phosphate restriction
