Module 12 - Renal Failure Flashcards
Renal Medulla
Inner part of the kidney made of renal pyramids and tubular structures
Renal Cortex
Outer layer of the kidney
Renal Artery
supplies blood to the kidney
Renal Pyramid
channels output to renal pelvis for excretion
this is where the collecting ducts come together
Renal Calyx
channels connecting the renal pyramids to the renal pelvis
Renal Vein
about 99% of filtered blood is circulated through this vein
1% contains waste products and undergoes further processing
Renal Pelvis
Blood containing waste products forms urine here and is channeled away
Ureter
tube that terminates in the urethra
A lot of blood exchange happening in the kidneys occurs at …
the distal and proximal tubules (they help maintain acid base, fluid and electrolyte balances)
Both the distal and proximal tubules are involved in ___
reabsorption
Along with reabsorption, the distal tubule is involved in ___
excretion
Filtrate
the filtering fluid in the kidneys until nothing else is removed in which is becomes urine and is excreted
Parenchymal Tissue of the Kidney
Nephron
___ flow goes to the nephron
Arteriole
Afferent Arteriole
carries arteriole blood toward the Bowman’s Capsule
hydrostatic pressure going into the glomerulus
Efferent Arteriole
Carries arteriole blood away from the Bowman’s Capsule
hydrostatic pressure coming out of the glomerulus
What controls arteriole flow
pressure
Bowman’s Capsule
capsule surrounding the filter of the kidney, the Glomerulus
contains the glomerulus and acts as a filter for the urine/filtrate
Glomerulus
the filter of the kidney
A network of twisted capillaries acting as a filter for the passage of protein free and RBC free filtrate
What is abnormal to see go through the Bowmans capsule and why?
Normally in health, proteins and RBCs are too large to get through the bowman’s capsule - if proteins or RBC are in urine than that is abnormal
What is the pathway to through the nephron
Afferent Arteriole –> Bowmans Capsule and Glomerulus –> Proximal Convoluted Tubule –> Loop of Henle –> Distal Convoluted Tubule –> Collecting duct –> renal pyramids –> ureters –> Bladder –> Urethra and exit
Medullary Nephrons
Nephrons that go deeper into the kidney
since they are deeper they have greater urine concentrating ability, but will be damaged sooner
Cortical Nephrons
more shallow nephrons with lower concentrating ability
Why are Medullary nephrons injured before cortical ones?
Because of impaired/compromised blood flow
The deeper the medullary nephron goes…
the greater the ability to concentrate urine - but also the first to be damaged
Concentrating gradients of the kidney..
increase as you go from the cortex to the inner most layer
Proximal Convoluted Tubule (PCT)
Site of reabsorption of glucose, AA, metabolites, and electrolytes from filtrate
Reabsorbed substances returned to circulation
Loop of Henle
A U Shaped section of the nephron tubule located in the medulla
Extends from the PCT to the DCT
site for further concentration of filtrate through reabsorption
Distal Convoluted Tubule (DCT)
site from which filtrate enters the collecting tubules
Collecting Tubules/Ducts
Releases urine to the ureter
What does glucose do in the kidney in health
it will be reabsorbed, it is a small molecule that can pass through, but the body wants and gets it back
What area of the nephron reabsorbs glucose and other small substances?
PCT
Glucose in the urine is ___
abnormal
The concentrating mechanism of the nephron is …
the loop of Henle
What happens if you lose the loop of Henle?
You cannot concentrate filtrate/urine - isosthenuria
Nocturia will also occur
Isosthenuria
urine with the same concentration as the blood
this is d/t damage to the loop of Henle which is unable to reabsorb anything and concentrate the urine
What is one of the first signs of kidney damage
Nocturia - getting up a lot at night since more urine is made and not concentrated
What area of the nephron has acid base balance occur due to bicarbonate?
DCT
What area of the kidney does not have concentration occur?
DCT
In the kidney, Vascular pressure means…
hydrostatic pressure (push)
Ureters
16-18” muscular tubes that contract rhythmically to transport urine from each kidney to the bladder
tubes
Urinary Bladder
sac with muscular walls that collects and holds urine that is expelled from the ureters every few seconds
storage
detrusor muscle wall
Urethra
narrow tube leading out of the body through which urine is expelled from the bladder
In the nephron the fluid is ___, but you excrete ___
filtrate; urine
The kidney makes urine in __
drops
3 Steps of Waste Collection and Elimination in the Kidney
- Glomerular Filtration
- Tubular Reabsorption
- Tubular Secretion
Glomerular Filtration
Filtering the blood that flows through the kidney’s blood vessels, or glomeruli
It is like spraying water through a T shirt with only small things getting through, nothing large - but what filters depends on intactness of membrane and pressure applied!
Tubular Reabsorption
reabsorbing filtered fluid through the minute canals (tubules) that make up the kidney
Products going back to the body from the filtrate to the blood
Tubular Secretion
Release of filtered substances by the tubules
How are secretion and excretion different?
Secretion is moving things from one place in the body to another place in the body - like K into Urine
Excretion is moving things from inside the body to outside the body - like urinating
Tubular Reabsorption and Secretion/Excretion occur where?
In the PCT and DCT (both of them)
What kind of processes are reabsorption, secretion, and excretion
they can be active processes needing energy or a co transporter, OR they can be a passive process with a concentration gradient
What are the basic functions of the kidneys?
- Water, electrolyte, and acid base HOMEOSTAWSIS
- Excretion of nitrogenous metabolic waste products: urea, uric acid, and creatinine
- Detoxifying drugs, toxins, and their metabolites
- Endocrine regulation of ECF volume and blood pressure: RAA and ADH
- Secretion of erythropoietin to simulate RBC production
- Endocrine control of calcium and phosphate metabolism: Activation of vitamin D and excretion of phosphates
- Catabolism of hormones like insulin, glucagon, parathyroid hormone, calcitonin, and GH
How can penicillin display the renal detoxification ability
Penicillin is actively secreted by the PCT so it is in an inactive form !
Aldosterone holds…
Sodium and water follows that
If you hold sodium…
you rid potassium
How is RAA activated
Low flow states activate sensors in the JGA near the glomerulus (so pressure or amounts of sodium) which causes RAA to get aldosterone to act on DCT (late part) and the collecting duct (where ADH works) as an osmoregulor
What is the end result of RAA/ADH
increased circulating volume in response to low pressure in the kidneys
Where does Aldosterone work
on the DCT (late part)
Where does ADH work
on the collecting duct
How is ADH activated
it is secreted in response to sensors in the hypothalamus
The posterior pituitary will release ADH to increase circulating water
ADH governs ___
water
When does the kidney release erythropoietin
release when there is low O2 to stimulate RBC production and maturation
Why does the kidney activate Vitamin D?
to have endocrine control of calcium and phosphate metabolism
it will control calcium maintenance and cause ridding of phosphates
Kidneys are __ organs
selfish organs
they can and will shut everything else down
Chronic Renal Failure Diagnostic Tests
- radiographs or ultrasound
- Serum abnormalities in BUN, creatinine, creatinine clearance, and GFR
- Low plasma pH
- Anemia
What can X Rays show us about the kidneys
can only show size, not much else
could show a small, atrophied kidney
What can ultrasounds tell us about the kidneys
they can show small, cystic lesions and also whether the kidneys are solid
can tell us about mass and fluids
BUN increases with what?
- Dehydration
- Renal Failure/Insufficiency
Is BUN a specific test that can diagnose renal failure?
No
What is a better indicator of renal failure diagnosis than BUN?
Creatinine
Elevated creatinine levels tell us…
about kidney dysfunction
What are the best 2 diagnostics for diagnosing renal failure
- Creatinine Clearance
- Glomerular Filtration Rate (GFR)
Why may low plasma pH tell us about kidney failure
It means the blood is acidic and there is a potential METABOLIC acidosis occurring
RR will be faster and deeper to blow off CO2 to compensate
How can Anemia tell us there is a renal issue
there is no erythropoietin secreted to make new RBC or mature RBC since the kidney is not working
Oxygenation can also be affected from free floating urea in the blood too
What is something else that can contribute to anemia regarding kidney failure other than Erythropoietin issues?
High concentrations of urea bathing the RBCs and making them not function as well or live as long
There is then less oxygenation
What may electrolyte levels look like on lab tests of diminished renal function?
- Na+ - normal or decreased
- Cl- - normal or decreased
- K+ - normal or increased
- CO2 (Bicarb) - Decrease
- Ca+2 - Decrease
- Phosphorus - Increase
Why may potassium levels be high or normal with renal issues? Why is this bad?
The kidney has problems ridding of potassium with insufficiencies
This is bad because K works on resting membrane potential and cardiac function and can cause issues there
Never give what without showing the kidneys are working first?
IV Potassium
Calcium and Phosphorus has a ___ relationship
inverse
Why is the relationship between calcium and phosphorus important in renal issues?
hyperphosphatemia and hypocalcemia can occur (which sets the threshold for heart cell firing usually)
this can cause rhythm disturbances or abnormalities
How can ABGs tell us about diminished renal function
There is metabolic acidosis with renal failure since bicarbonate is not reabsorbed to rid of acids
Also CO2 on a venous panel will be low representing bicarbonate and we may see RR rate changes to compensate
So, Bicarbonate levels would be low indicating renal issues
Why is BUN a poor indicator of renal function
It rises also in dehydration, GI bleeds, and renal failure
What is creatinine reabsorption usually like
It normally is not reabsorbed and is secreted by tubules
But this level will increase in renal failure
What other things are creatinine levels dependent on?
Renal Clearance
Muscle Mass (higher means higher creatinine)
Sex
Age (muscle masses)
Is creatinine a good indicator by itself?
While rising levels usually indicate RF, this is not a good indicator by itself
Normal BUN:Creatinine Ratio
1:10
What is a renal failure BUN:Creatinine Ratio
> 20:1
Azotemia
accumulation of nitrogenous waste in blood (urea, creatinine, others)
If you see azotemia, you know what?
There is likely renal failure from nitrogenous things gathering in blood
The best indicator of kidney function is …
Creatinine Clearance
Clearance
refers to the complete removal of a substance form the blood
it is the amount of blood that can be cleared in a specific amount of time — how long it takes for product to get out of the blood (time dependent)
Creatinine Clearance
volume of blood in mL that the kidneys can clear of creatinine in 1 minute
Why is Creatinine Clearance the most accurate measure of GFR
It acts as the most accurate measure of Glomerular filtration rate (GFR) since creatinine is filtered by the glomeruli but not reabsorbed by the tubules
Glomerular Filtration Rate (GFR)
the rate at which the glomeruli filter blood
its about 120 mL/minute (about half a can of soda every minute)
What is GFR a function of
- Permeability of the capillary walls
- vascular (hydrostatic) pressure
- Filtration Pressure
What is the relationship between GFR and creatinine clearance?
direct relationship
since the tubules neither reabsorb nor secrete creatinine, the creatinine clearance = GFR
If tubules did reabsorb creatinine, what would happen between creatinine clearance and GFR?
Clearance < GFR
If tubules did secrete creatinine, what would happen between creatinine clearance and GFR
Clearance > GFR
24 Hour Creatinine Clearance Test
You look at the level of creatinine in the urine and compare it to a venous blood draw of creatinine
Gold standard for renal function is?
Creatinine clearance (and GFR)
What kind of factors can impact creatinine clearance
age, weight, gender
How does creatinine clearance differ between sexes?
Male - 1-2 gm/24 hours
Female 0.8-1.5 gm/24 hours
GFR Male Estimate Formula
(140-Age)*(Weight in Kg) / (72 * serum creatinine in mg/dL)
GFR Female Estimate Formula
(0.85) * Male Estimate
Creatinine Clearance Formula
[GFR + (Quantity of urine) * (creatinine concentration in urine)] / serum creatinine
The most accurate GFR is …
creatinine clearance
How will a CBC look with renal failure
Decreased RBC and Hgb
Low Hct - 25-35% (Anephric 12-20%)
Microcytic Hypochromic Anemia
Micocytic Hypochromic Anemia probably indicates what anemia?
Iron Deficiency Anemia
Anephric
no kidney function
How will serum proteins (albumin and globulin) alter with renal failure?
These plasma proteins which maintain oncotic pressure will be gone and the oncotic pressure will be missing meaning a lot of fluid enters interstitial spaces and stays there
This reflects the adequacy of protein intake
What is the primary function of plasma proteins like albumin and globulin?
to hold fluid in the vascular space
Why do renal patients need a strict diet of high biologic value protein?
The kidney cannot rid of metabolic waste during failure, when albumin is not being synthesized and is breaking down faster, so we need to have a healthy level but not too much as it can cause metabolic waste build up leading to toxicity
Chronic Renal Failure
Progressive and irreversible destruction of the kidneys
What is interesting about renal function and s/s of renal failure?
Until renal function is <50%, clinical manifestations are minimal as surviving nephrons take over the work of those lost
What happens to the surviving nephrons when renal function is below 50%?
the surviving nephrons increase rate of filtration, reabsorption, and secretion –> Hypertrophy occurs with increased size and release of cellular contents -> more nephron progressively die and the rest have trouble handling demand –> Damage and eventual death of remaining nephrons
What happens after the progressive loss of nephrons begins in renal failure?
Progressive loss of nephrons –> scar tissue forms –> renal blood flow reduced –> renin releases from low flow states –> Fluid overload and HTN
Why does HTN as a result of the RAA system speed up renal failure?
HTN accelerates renal failure by increasing filtration and demand for reabsorption of plasma proteins (workload)
It also impacts the heart
Causes for Chronic Renal failure
Chronic Glomerular Disease
Chronic Infections like chronic Pyelonephritis and Tuberculosis
Congenital Abnormalities like Polycystic Kidney Disease
Vascular Diseases like HTN or Nephrosclerosis
Obstructions like kidney stones
Collagen diseases like systemic lupus erythematous
Nephrotoxic agents like long term aminoglycoside therapy or Chemotherapy
Endocrine disorders like diabetic nephropathy
Glomerulonephritis
Affects the capillaries in the glomeruli\
Occurs from inflammation from something like a strep infection
Nephrosclerosis
Tons of nephron scarring
Why can kidney stones cause renal failure?
The cause back pressure into the kidneys
Aminoglycosides
an antibiotic that can be deadly to the kidney
Stages of Chronic Renal Failure`
- Reduced Renal Reserve
- Renal Insufficiency
- Renal Failure (RF)
- End Stage Renal Disease (ESRD)
What determines the stage of chronic renal failure?
GFR (which equals amount of creatinine cleared)
Reduced Renal Deserve
first stage
GFR between 35-50% of the normal rate
Serum BUN and creatinine is normal
no symptoms of impaired renal function
this stage occurs because of the buffer from having 2 kidneys
Renal Insufficiency
second stage
GFFR between 20-35% of the normal rate
Azotemia (Nitrogenous waste), Anemia (low RBC) , and HTN Begin
Early symptoms begin - isosthenuria, polyuria isotonic with plasma
Renal failure
third stage
GFR less than 20-25% the normal rate
kidneys cannot regulate volume and solute composition –> decreased urine output –> edema, metabolic acidosis (no reabsorb bicarb), hypercalcemia
over uremia (urea and nitrogenous waste) –> neurologic, GI and CV complications
End Stage Renal Disease (ESRD)
GFR less than 5% the normal rate
Atrophy and fibrosis in glomeruli and tubules
Dialysis or transplant needed for survival
no filtration ability left
Why may renal patients be tired constantly
they get up constantly at night to pee
Why do renal patients end up with pericarditis later one
irritation from urea (uremia)
Uremic Syndrome
a complication of s/s of chronic renal failure includes:
lethargy, fits, coma
epistaxis
anemia
sallow pigmentation and pruritic excoriations
bruising
amenorrhea, impotence, infertility
myopathy
peripheral neuropathy
red eye
anorexia, N/V
HTN, pericarditis, heart failure
pleurisy
dyspnea on exercise
nail changes
bone pain
edema
red eye and frost
Frost
crystallization of urine/uric acid on the brow in sweat
Why is there epistaxis in uremic syndrome?
urea covers the RBCs and blood contents making platelet functioning less
this is the same reason renal patients get bruising
What does Acidosis trigger?
the nausea center in the brain
Why are renal patient’s skin so itchy
the uremia on the skin leaking through sweat
intense scratching episodes can cause taking of skin off and cause secondary infection
How does the body function of body fluids change with renal disease
compensatory changes occur in tubular functions
decreased ability to synthesize ammonia and conserve bicarbonate occurs
Potassium cannot be excreted
cannot regulate sodium excretion
impaired ability to excrete phosphate
hyperphosphatemia and inability to activate vitamin D
What are some of the manifestations of the body fluid changes in renal disease
fixed specific gravity of urine (isosthenuria)
metabolic acidosis
hyperkalemia
salt wasting or sodium retention
hyperphosphatemia
hypocalcemia and increased levels of PTH followed by hypercalcemia
How can renal disease lead to hypercalcemia?
Hypocalcemia leads to signaling release of PTH from the parathyroid gland in order to increase calcium levels via absorption in the gut, activation of vitamin D in the kidneys, and increase reabsorption in DCT, and increase osteoclast activity
Since some of these are regulated by a failing kidney, the PTH must do most of the work to raise calcium and it continues since phosphorus cannot be rid of
this causes hypertrophy and sensitivity of vitamin D receptors leading to less sensitivity to Vitamin D and calcium levels by the parathyroid gland and thus continued release and increased PTH causing hypercalcemia
How does the hematologic system get altered with renal failure?
impaired synthesis of erythropoietin and effects of uremia on blood (this means anemia occurs)
impaired platelet function (qualitative defect from uremia)
Manifestations of the Renal failure related hematologic changes
Anemia
Bleeding tendencies
What are the multi systemic effects of chronic renal failure via alterations in the hematologic system
Anemia - shortened lifespan of RBCs in toxic serum, decreased production of erythropoietin and inhibition of bone marrow, bleeding from coagulation defects (qualitative in PLTs), anticoagulation during dialysis may cause heavy menstrual and GI bleeding, and blood sampling during dialysis, loss of blood d/t machine, and dialyzer malfunction can occur
Immune responsiveness is also depressed making them susceptible to infection
Treatment for the Hematologic Changes from CRF
- Epogen
- Dialysis to remove uremic toxins
- Transfusions - conservative administration
- Risk of excess Fe and K occur so treatment with chelating agents
Epogen
synthetic erythropoietin
given SQ 3x a week (very expensive)
What occurs as a result of renal treatment
racking up a lot of expenses
so they have separate coverage under their insurance plans and also have state programs to help
Why are transfusions given to CRF patients?
It is given to them to make up for the bleeding that occurs d./t bad clotting
Why are blood transfusions a conservative treatment for CRF?
Depresses function of normal bone marrow
Doing so decreases hepatitis risk
Potential for iron overload since blood breakdown from uremia releases iron that is stored
Why are CRF patients given chelating agents?
Hyperkalemia from lysing of cells in the dialyzer and transfusions breaking cells
High iron from transfusions and RBC breakdown
What alterations occur from CRF in the cardiovascular system
Activation of RAA mechanisms causing increases in vascular volume
Fluid retention and hypoalbuminemia
Excess ECF and anemia
Increased metabolic wastes in blood
Manifestations of the Cardiovascular changes from CRF
HTN
Edema
CHF and Pulmonary Edema
Uremic Pericarditis
____ is a potent vasoconstrictor
Angiotensin II
Why do cellular and interstitial edema co occur in CRF?
there is fluid retention causing cellular edema and then there is interstitial edema from hypoalbuminemia
This hypoalbuminemia occurs relatively to fluid retention decreasing oncotic pressure, but there is also albumin loss in liver disease
How can CRF lead to CHF
Workload and Anemia!
fluid retention gives a higher preload with HTN giving a higher afterload –> increased heart workload
Heart tissue is bathed in urea –> depressed pumping ability and RBC are not delivering oxygen like they should
This all leads to pulmonary edema and CHF
Often CRF goes alongside ___ making dialysis tricky
CHF
What are the multi system effects alterations in the cardiovascular system from CRF cause
HTN
Pericarditis r/t uremic effects and clotting defects
Myocardium issues
Hyperkalemia
What is another potent vasoconstrictor beside angiotensin II
ADH
Why does HTN occur in CRF
fluid overload from RAA and ADH functioning autonomously and being uncontrolled
How does renal ischemia lead to CHF
renail ischemia –> RAA –> Vasoconstriction –> HTN –> LVH –> CHF
What causes Hypertensive encephalopathy and what does it cause as a result?
high BP and excess blood volume cause HTN Encephalopathy
Increases ICP
HA
Retinal Changes
Seizure
Coma
CVAs
What are the two leading causes of eye disease and retinal changes?
Increased ICP
Diabetes
What can pericarditis r/t uremic effects and clotting defects from CRF lead to?
Pericardial Effusion
Cardiac Tamponade
Cardiac Tamponade
heart failure from a right sided problem like pericardial effusion that does not let the heart fill and pump
Why can high phosphorus hurt the heart?
High phosphorus will come back down by combining with calcium but then the body will put it in valves and other areas around the heart leading to dysfunction
If Calcium is low, PTH will pull it from bone to combine it but they then need to be placed in soft tissue and not bone
What can cause the Hyperkalemia in CRF
Dietary Indiscretion (high K foods)
Increased Catabolism of cells
Decreased K secretion
Blood transfusions
Surgery
Acidosis from ion shifting (H in causes K out)
Why are dietary restrictions on potassium so important in CRF
K is functional in resting membrane potential and a high level causes a higher potential and vice versa
this can lead to arrhythmias like Ventricular fibrillation that can cause death
What are some EKG changes seen with hyperkalemia?
change sin conductivity and repolarization
prolonged PR
widened QRS
high peak T waves
What is a common way CRF patients end up comiting suicide
excessive potassium intake
What alterations in the GI system occur from CRF
increased metabolic wastes
decreased platelet function and increased gastric acid secretion from hyperparathyroidism
What are the manifestations in the GI changes from CRF
Anorexia & N/V from metabolic wastes
GI Bleeding from decreased platelet function and hyperparathyroidism
Other than calcium release, what else does PTH cause excess release of
Gastric Acids
What alterations in the neurologic system occur from CRF
fluid and electrolyte imbalances
increases in metabolic acids and other small, diffusible particles such as urea
What are the manifestations of the neurologic alterations from CHF
HA (F&E imbalances)
S/S of Uremic Encephalopathy (toxicity of brain tissue from urea)
S/S of neuropathy
What are the signs and symptoms of uremic encephalopathy
lethargy
decreased alertness
loss of recent memory
delirium
coma
seizures
asterixis
muscle twitching
tremulousness
Asterixis
twitching and tremors associated with liver disease
“Liver flapping”
S/S of Neuropathy
restless leg syndrome
paresthesia
muscle weakness
paralysis
Primarily all Neurologic effects from CRF are due to what?
Uremic Toxin buildup in CSF - fluid overload occurs
What sort of multi system effects occur from alterations in the neurologic system from CRF
Cognition and consciousness changes from memory issues to confusion, disorientation, coma, convulsion, and even death
decreased concentration and attention span
decreased libido and impotence
muscle cramping (from hypocalcemia)
abnormal EEGs
ANS issues
behavior changes
peripheral neuropathy
What is an abnormal EEG indicative of in CRF
metabolic encephalopathy
What occurs from ANS dysfunction in CRF
orthostatic hypotension because baroreceptors in the carotid and aorta are not responding due to the urea
What behavior changes occur in CRF
personality changes
increased irritability
labile emotions
agitated depression
delusions
psychosis
What are the manifestations of peripheral neuropathy in CRF
gait changes
burning feet
restless legs
foot drop
cranial nerve issues with vision, hearing and smell
intestinal tract issues
urinary bladder issues (UTI or no urine made)
How do the peripheral neuropathy issues occur in CRF
they are symmetric and begin distally and work their way inward
Osteodystrophy
the disruption of normal calcium and phosphorus feedback loop leading to abnormal bone growth and major long term complications beginning early in CRF like bone pain, deformities, and fractures
In healthy adults, if serum calcium drops what happens
Parathyroid gland releases PTH –> this stimulates kidney production of activated Vitamin D which is needed for calcium absorption in the small intestine–> this leads to increased calcium reabsorption and phosphorus excretion in the urine as well as stimulation of calcium release from bone
What is the Result of PTH as a compensatory mechanisms
Return to normal calcium, phosphorus, and PTH levels
Why does PTH not work in CRF
In CRF kidneys cannot produce activated vitamin D OR excrete phosphorus
So phosphorus levels will rise and serum calcium will fall leading to PTH production –> the parathyroid gland will maintain calcium for a little bit by drawing calcium and phosphorus from bone –> eventually as kidney disease progresses the compensation mechanism goes haywire and leads to secondary hyperparathyroidism
What happens after the secondary hyperparathyroidism begins in CRF
Parathyroid gland continues to make PTH and becomes hypertrophic –> number and sensitivity of Vitamin D decrease and parathyroid gland becomes less responsive to calcium and vitamin D –> over time the bones respond less and less to PTH so more is needed to maintain typical rate of bone turnover —> as a result body’s ability to replace old bone with healthy new bone is compromised
Consequences of Parathyroid activity in CRF
abnormally high levels of PTH
hypocalcemia (or hypercalcemia if there is chronic hyperparathyroidism)
hyperphosphatemia
renal osteodystrophy
People with secondary hyperparathyroidism can end up with..;.
- Osteitis Fibrosa
2.Osteomalacia
- Both!
Osteitis Fibrosa
high turnover bone disease
an osteodystrophy
Osteomalacia
low turnover bone disease
an osteodystrophy
Both osteitis fibrosa and osteomalacia lead to what
weakened bones and increases the risk of fractures
Osteitis Fibrosa occurs from
hyperphosphatemia
hypocalcemia
low levels of activated vitamin D
secondary hyperparathyroidism
Osteomalacia occurs from
Aluminum intoxication
This is because aluminum blocks CA uptake in bone causing demineralization
What manifestations occur in the body from Osteitis Fibrosa and Osteomalacia
muscle weakness
bone pain and tenderness
spontaneous fracture (even from something like a cough from croup)
Without ____ calcium cannot be absorbed
vitamin D
How does Uremia lead to no calcium absorption
it inhibits vitamin D production and synthesis
How does Uremia ultimately effect the musculoskeletal system in CRF
- Decreased Absorption of Ca from intestines
- Decreased serum Ca and high phosphate levels d/t catabolism
- Parathyroid glands release PTH
- Ca is pulled from bone causing demineralization (osteomalacia)
- Ca and PO4 precipitate in cardiovascular tissue, liver, and joint tissue
- Pathological fractures and bone changes occur followed by “Red Eyes”
What causes CRF Red Eyes
Calcium Phosphate deposits in the eye
Treatments for the Musculoskeletal problems in CRF
- Activated Vitamin D therapy
- Parathyroidectomy
- Calcium Acetate or Carbonate - Not aluminum hydroxide gels
Calcitrol and Dihydrotachysterol (DHT)
activated forms of Vitamin D
Why may a parathyroidectomy be done in CRG
if hyperplasia occurs and starts functioning autonomously regardless of Serum Ca and Phosphate levels it may need removal to prevent osteodystrophy
Why do we no longer give aluminum hydroxide gels to CRF patients
it can lead to Osteomalacia
What do we give now rather than aluminum hydroxide gels to treat musculoskeletal problems in CRF
calcium acetate or carbonate
ex: phoslo or TUMS
TUMS c an be used for what purposes?
- Dyspepsia
- Allowing calcium absorption to occur
How does the skin function change with CRF
- Calcium Phosphate concentration products greater than 60-70 occur
- Salt Wasting
- Anemia
- Hyperparathyroidism
- High concentration of metabolic end products end up in body fluids
What are the manifestations of skin alterations in CRF
extracellular calcifications (CaPhos Deposits)
dry skin and mucous membranes (Salt wasting)
pale and sallow complexion (anemia)
pruritis (urea)
uremic frost and odor of urine on skin and breath - embarrassing for people
What sort of things can you see on the skin in a person with CRF
itching, crawling skin from deposits of urea and phosphates – > scratching causes excoriations that heal poorly
pallor from anemia and also a yellow brown or gray color from retained urinary pigments
bruises from capillary fragility and clotting defects
dry scaly skin from decreased oil gland activity and loss of subcu tissue
uremic frost made of urate cryustals
brittle thin spoon shaped nails from anemia
dry scaly hair that falls out easily
petechiae
Calciphylaxis
Usually fatal syndrome of vascular calcification, thrombosis and skin necrosis
occurs in ESRD
What is manifested in calciphylaxis
ischemic skin lesions with areas of necrosis appearing as violaceous lesions or completely black lesions
extensive on the body
happens because of calcium deposits in the blood vessels stopping blood flow
What is needed to diagnose calciphylaxis
skin biopsy to confirm
Changes in GU system function from CRF
impaired general health
decreased testosterone and estrogen
Manifestations of Altered GU function in CRF
impotence
loss of libido
amenorrhea
What kind of diet is needed for CRF
low quantity high quality proteins to reduce end products of protein metabolism the kidneys cannot excrete
low sodium
low potassium
fluid restriction to maintain fluid balance (can lead to always feelings thirsty)
What amount and what kind of proteins should be given to a CRF patient
0.5-1 g/kg of body weight daily of low quantity high quality complete proteins
these proteins have all the essential acids to increase anabolism (RBC, plasma, muscle proteins) and decrease catabolism (uremic waste)
Why is the diet for CRF low sodium and potassium
low sodium to prevent further fluid overload
low potassium since the kidney cannot rid K (salt substitutes for K must be avoided too)
How is fluid balance monitored in CRF?
through weight gain between dialysis treatments
What sort of medications are given in conservative therapy of CRF
Diuretics
Antihypertensives
Alkalizing Agents
Cation Exchange Resin
Anti emetics, Anti diarrheals, laxatives
Dietary supplements
synthetic erythropoietin
anticonvulsants
supplements
antipruitics
other vitamin supplements
Why are CRF pts given diuretics
to treat fluid overload and HTN
Thiazides and aldosterone antagonists are given
Why must one be careful giving aldosterone antagonists like Aldactone to CRF patients?
its a diuretic but it is potassium sparing
Why are CRF pts given antihypertensives
to control BP and edema
ace inhibitors and beta blockers
What is better for CRF patients, ace inhibitors or beta blockers
beta blocks because ace inhibitors can slow aldosterone making it hard to rid of K
Why are CRF pts given alkalizing agents
to treat metabolic acidosis
its sodium bicarbonate or sodium citrate
Why are CRF pts given Cation exchange resins
Na for K resins to treat hyperkalemia
insulin to use the GIK mechanism to get K into cells
Kayexalate to excrete K
calcium gluconate to depress myocardial irritability by raising thresholds
sodium bicarb
What level of K is a medical emergency
higher than 7 mEq/L
Why are CRF pts given anti emetics, anti diarrheas’, and laxatives
to relieve vomiting, nausea, constipation or gastric irritation
What to be aware of when giving anti emetics, anti diarrheals or laxatives to CRF patients
cannot give something like Aluminum or Milk of Magnesia because you need to give them something WITHOUT MAGNESIUM since they cannot excrete Mg either
Why are CRF pts given dietary supplements like iron and folic acid
to treat anemia
oral or parenteral iron because low protein diets are low in iron
folic acid is water soluble and is loss in dialysis so it should be replaced
Why are CRF pts given synthetic erythropoietin
Epogen
in order to get the reticulocyte count up
Why are CRF pts given anticonvulsants
to treat neurologic symptoms
Why are CRF pts given supplements like vitamin D (calcitriol) and calcium acetate/carbonate
to treat osteodystrophy
vitamin D will be an active form to bind calcium for absorption
calcium acetate or carbonate will lower serum K levels
Why are CRF pts given antipruritics?
to relieve itching
ex: Benadryl
What are some other vitamin supplements given to CRF patients
vitamin C (water soluble)
multivitamins with B complex and vitamin D
1 in 10,000 with ESRD need what?
Dialysis treatment or a Kidney transplant
What are the top 2 reasons for ESRD
- Diabetic Glomerulosclerosis (Nephropathy)
- Hypertensive Nephroangiosclerosis
both kill the kidney
What are some other reasons for ESRD
chronic glomerulonephritis
chronic pyelonephritis (reflux)
Polycystic kidney disease (PKD)
What racial group has a higher risk for ESRD and why
African americans d/t higher risk for HTN
Nephrosclerosis accounts for how many cases in African Americans compared to Caucasians?
1/3 of AA CRF cases
only 8% of cauc. cases
