CKD Flashcards
Primary Kidney Functions (3)
- Filtration (removing waste bropducts from Bloodstream)
- Regulation of fluid and electrolyte balance
- Excretion of metabolic waste products
Secondary Kidney functions
Help regulate BP (RAAS system)
Regulation of Bone density (MBD) Regulation of RBC cell production (Erythrepiosis) -
Chronic Kidney Disiese
Presence of kidney damage or GFR
- progressive or irreversible damage
<60 mL/minute/1.73m2 for 3 months or longer
Classified as 1 of 5 stages, depending on disease severity (measured by GFR)
Normal GFR is
125mL/min
Up to ____ of GFR may be lost without changes being seen in symptoms manifestations
80%
End result of CKD is
systemic disease involving every organ.
Leading cause of End stage Renal disease
DM 38%
Renal vascular dx 15%
ESRD treatment options
Renal replacement therapy (RRT)
- Hemodialysis (HD)
Peritoneal Dialysis (PD)
Transplant
The body is maximally compensated at stage 5, it needs help, or death will occur
Clinical manifestation of CKD (retained substances)
Urea
Creatinine
Phenols
Hormones
Electrolytes
Water
Other substances
Uremia
Syndrome that incorporates all signs and symptoms seen in various systems throughout the body due to the build-up of waste products and excess fluid associated with kidney failure.
When GFR is >10mL/min (ESRD)
Urinary system Clinical manifestations of CKD
Polyuria (Early stage)
- Resulting from inability of kidneys to conc urine
- Often Nocturia
SPecific gravity fixd around 1.1011
Oliguria (occuring as CKD worsens)
(>20mL/hr)
Anuria
(<40Ml per 24hour)
Improtant question to ask those on dialysis?
Do they make urine?
Metabolic distrurbances of CKDq
Waste product accumulation
- As GFR decreases;
BUN and Creatinine increases
Alterred carb metabolisms
- Caused.by impaired glucose use
- To cellular insensititvty of normal insulin
Defective carb metabolism
- DM pts who become uremic may need less insulin than before CKD
- Insulin depends on kidney excretion
Elevated triglycerides
- Hyperinsulinemiam stims hep production of triglycerides
- Altered lipid metabolism (decreased enzyme)
Why does BUN increase
Because of decreased excretion, but also because of protein intake, corticosteroids, and catabolism
Can result in N/V, lethargy, fatigure, impaaired thought porocess, and headache
Important to remember for CKD pts with DM on insulin
As CKD progresses, less insulin will be required
CKD effects on Electrolytes
Acid-base imbalances
Hyperkalemia
- Decreased potassium excretion by kidneys
Sodium
- Normal or low
Calcium and phosphate alteration
Magnesium alterations
Clincial manifestations of hypermagnesia
Absenece of reflex
Cardiac dysrythmias
Cardiac failure
Metabolic acidosis results from
Inability of kidneys to excrete acid load (primary ammonia)
Defective reabsorption/regeneration of bicarbonate
`
What is metabolic acidosis
Primarily related to amonia
Adults produce 80-90mmol of acid per day
- Normally this acid is buffered by Bicarbonate
- Since CKD causes Plasma Bicarbe to fall from a normal at 22-26mmol/L to 16-20mmol/L, Hydrogen ion conc increases (serum acidity)
The body tries to create an alternative buffer out of Phosphate, introducing other problems
Sometimes resp system tries to compensate through kusmos breathing (Only short time solution)
Hematological manifestations of CKD
Anemia - very common
nutritional def
Elevated PTH levels
Iron defs
Folic acid defs (Late stages during dialysis)
Why does anemia occur in CKD
Due to decreased production of erythropoietin, a hormone that stimulates RBC production in the bone marrow
Other factors: nutritional deficiencies, increased hemolysis of RBC’s, frequent blood sampling, and GI bleeding
Bleeding tendencies in CKD
Defect platlet funciton
Uually corretable with regular renal repleacement therapy
Why are CKD pts more suspectible to infection?
Changes in leukocyte function
Altered immune response and function
Diminished inflammatory response
CV system CKD manifestations
HTN - most common in ESRD
- Many CV complications result from HTN and high Triglyc levels resulting in quick progressing atherosclerosis
- Know that HTN can precede CKD and is resposible for most of CV manifestations of the disease
DW abt knowing these specifically
HF
Left Ventricle Hypertorphy
Periph edema
Dysrythmias
Uremic pericarditis
morbiitiy and mortality due to CVD secondary to CKD is
High
WHy is management of HTN so helpful
It prevents CV complications from DM
It slows the progression of CKD
Clinial manifestations of Resp System
Generally to do with fluid overall
Kussmaul’s
Dyspnea
PE
etc.
Often solved through vigorous fluid removal (Diuretics or dialysis)
GI system effects of CKD
All parts of GI are affected to to inflammation of mucosa related to excessive urea
S/S: Stomatitis with exudates and ulcerations
Uremic fedor
GI Bleed
Constipation from limited fluid intake and supplements
Most s/s resulting from build up of waste product
Why do Neuro clinical manifestations of CKD occur?
Changes are expected and attributed to
Increased nitrogenous waste products
Electrolyte imbalance
Metabolic acidosis
Axonal atrophy
Demyelination of nerve fibres
Generally speaking, the CNS becomes depressed
Neuro Clinical manifestations of CKD
Tx of neurological problems is dialysis or transplantation
- May slow or halt progression of neuropathies
Restless leg synd
Muscle twitching
Periph. Neuropathy
Decreased ability to concentrate
Do the prep guide**
MBD
Involved with absorbing calcium from the gut with vitamin D
Calcium and phosphate have what kind of relatioship
Inverse
Erythrepiosis
The process of creating RBCs
Acute kidney injury vs CKD
It is sudden and often reversible in acute (abrupt drop in eGFR)
What is a signfincatn eGFR change
5-10 is significant
> 10 is VERY significant
Within days or a week
Drop of eGFR corrrelates with a rise in
BUN and creatinine
Iron and CKD
Pts usally on supplemental iron
Clinically significant Hemaglobin level
bw 70 and 80
Urenia
Occuring in stage 5 CKD
Most systems are symptomatic by this time
Pts with low hemoglobin occuring with CKD
Should only be occuring in stage 5, earlier stages of CKD should not cause low Hg, therefore, this needs to be investigated and fixed
arteriovenous fistula
Don’t do a BP check on that arm
Same with stroke and masectomy
Should sound like a swooshing sound
Why would Hg be low in People with end stage CKD have
Bleeding tendencies
Multi-system disease
But ALSO we can never assume erythepoiten is the only reason, because there could be multiple
Clinical manifestations of CKD on Musculo-skeletal
CKD-MVD
- Including bone abnormaliities
-Changes in mineral blances
Resulting in skeltal comolications
CKD Mineral And Bone Disorder
Kidneys are responsible for converting calcium into it’s active form using Vit D
CKD = decreased active Vit D levels and reduced Calcium absorption, reduce serum caclium
In response thyroid gland releases PTH, stimulating bone demineralizing which increases calcium serum levels
- Phosphate is released as well =
Hyperphosphatemia, decreased vit D levels, and hypocalcium = excess secretion of PTH
- Can result in bone disease
CKD-MDB is COMMON from. CKD
- Skeletal and extra skeletal complications
CV calcifications - likely cause of high morbidity and mortality in CKD pts
- Mineral supplements must be given to combat this
Integ system clinical manifestations of CKD
Puritis - VERY common (itchy)
- sometimes need meds to reduce this
Uremic frost
Repro system effect of CKD
Men and women
Infertility
- decreased libido
Low sperm counts
Sexual dysfunction
Psychological changes resulting from CKD
Personality and behaviour changes
Emotional lability
withdrawal
Depression
Diagnostics of CKD
Hx and physical exam
urinalysis distick evaluations
Albumin creatine ratio
Earliest marker of kidney damage
Protein urea
High risk pts for CKD
DM
HTN
Vascular dx
Autoimmune dx
Low GFR (Below 60)
Chronic Edema
Normal urinalysis
Appearance shoudl be clear
Specific gravity compares conc of urine compared to water
pH is normal 4.6-8
Normally NO protein
Normally NO glucose
Normally NO ketones (Unless fasting)
Glucocyte esterase should have NONE unelss UTI
Bilirubin: (Product of RBC breakdown) SHOULD be NEGATIVE, indicates liver damage
RBCs: Can be present in menstruation/kidneystones/kidney infection/ UTI (RBC not typically in urine)
Normally NO Nitrites (UTI will have leukocyte esterase and NItritses)
Casts: Negative (indicate condition of kidneys
BUN
Blood test, urea levels in blood
elevated if insufficient secretion
Internal bleeding can shift levels
Elevation is broad indicator of kidney problam
Creatinine
Nitrogenous waste product of muscle metabolism
Generated at constant rate, and all is excreted by kidneys in urine
When creatinine levels are up, it indicates kidneys cannot excrete it fast enough
Creatinine Clearance
Creatinine Clearance
-commonly used to assess Glomerular Filtration Rate (GFR)
-determines how efficiently kidneys clear creatinine from the blood
GFR: determines how fast blood is filtered through the glomerulus
CT KUB
CT Kidneys, ureters, bladder scan to detect kidney abnormalities
Renal biopsy
Most helpful for CKD
Goals for CKD pts
Focus on prevention and early detection
Goals:
Preserve current function of kidneys
Delay progression
Treat clinical manifestation
prevent complications
Educate pts and family with CKD
Prepare pts for RRT or transplant
Collaborative care for CKD
Correction of extracellular fluid volume overload or deficit
Nutritional therapy
Erythropoietin therapy
Calcium supplementation, phosphate binders
Antihypertensive therapy
Measures to lower potassium
Adjustment of drug dosages to degree of renal function
HyperKalemia
C-Calcium gluconate- stabilize myocardium
B- β2-adrenergic agonists such as salbutamol to shift potassium into the cells
I- IV insulin (shift K+ into cells), and
G- IV Glucose to manage hypoglycemia
K- Kayexalate - immediate measures (lowers K+ levels in stage 4)
D(rop)- diuretics or Dialysis
“See” C BIG K+ D(rop)
Anything 6 and over we need to be concerned, 6.5 and over they should be on cardiac monitor
therapy for HTN with CKD
Lifestyle changes:
Weight loss
Diet recommendations
Sodium and fluid restriction
b) Antihypertensive drugs
Thiazide or loop diuretics
Calcium channel blockers
ACE inhibitors
ARB agents
How is CKD-MBD managed with drugs
Phosphate intake restriction
Phosphate binders
- Ca carbonate
Sevelamer hydrochloride
Should be administered with each meal
- Can cause constipation
Supplementing Vit D
Controlling secondary Hyperparathyoridism
- reduce PTH
- Subtotal parathyroidectomy
Anemia drug therapy in CKD pts
Erythropoietin
- Erythropoiesis-stimulating agents (ESA)
Administered IV or subcutaneously
Increased hemoglobin and hematocrit in 2–3 weeks
Adverse effect: hypertension
Target Hg be 110 (100-120) for CKD pts
Iron supplements
Folic acid supplements
Avoid Blood transfusions
Why is folic acid suppplementation for dialysis
Folic acid supplements
Needed for RBC formation
Removed by dialysis
Why don’t we jump to blood transfusions if CKD pts Hg is low?
We need to find source of problem, since it could be a bleed, but it could also be another source
Dyslipidemia and CKD
Statins usually used in clients with stage 1-3 CKD because of high levels of triglycerides
Drug toxicity
Increased risk with drugs bc kdineys are needed for excretion, therefore, dialysis and kidney failure heavily effects doses of drugs that need to be given
Drugs of particular concern for toxicity
Digoxin
Oral glycemic agents
Antibiotics
Opioids (hydromorphone, morphine)
Also, avoid NSAIDs and use Acetaminophen instead
Nutriotoinal therapy and CKD
ALL pts with CKD should see a dietitian
- Protein restriction can be helpful, but it also can be dangerous in late stages
Water restriction for those on dialysis
Sodium restriction
Potassium Restriction
Phosphate restrictions
Nursing management of CKD pts
Complete history of any existing renal disease, family history
A complete medication history
Prescription
OTC
Long-term health problems
Dietary habits
Clinical manifestations of CKD
Patient’s goals of care
(dialysis or transplants)
Nursing diagnosis of CKD
Excess fluid volume
Risk for electrolyte imbalance
Imbalanced nutrition: less than body requirements
Nursing implentation for care?
Daily weight, BP
Identify signs and symptoms of fluid overload, hyperkalemia and electrolyte imbalances
Strict dietary adherence
Medication education
Motivate clients in management of their disease.
Nursing management evaluation
Maintenance of ideal body weight
Acceptance of chronic disease
No infection
No edema
Hematocrit, hemoglobin, and serum albumin levels in acceptable range
