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CKD Flashcards

1
Q

Primary Kidney Functions (3)

A
  1. Filtration (removing waste bropducts from Bloodstream)
  2. Regulation of fluid and electrolyte balance
  3. Excretion of metabolic waste products
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2
Q

Secondary Kidney functions

A

Help regulate BP (RAAS system)
Regulation of Bone density (MBD)
Regulation of RBC cell production (Erythrepiosis) -

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3
Q

Chronic Kidney Disiese

A

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)

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4
Q

Normal GFR is

A

125mL/min

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5
Q

Up to ____ of GFR may be lost without changes being seen in symptoms manifestations

A

80%

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6
Q

End result of CKD is

A

systemic disease involving every organ.

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7
Q

Leading cause of End stage Renal disease

A

DM 38%
Renal vascular dx 15%

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8
Q

ESRD treatment options

A

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

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9
Q

retained substances in CKD

A

Urea
Creatinine
Phenols
Hormones
Electrolytes
Water
Other substances

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10
Q

Uremia

A

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)

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11
Q

Urinary system Clinical manifestations of CKD

A

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)

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12
Q

Improtant question to ask those on dialysis?

A

Do they make urine?

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13
Q

Metabolic distrurbances of CKDq

A

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)

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14
Q

Why does BUN increase

A

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

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15
Q

Important to remember for CKD pts with DM on insulin

A

As CKD progresses, less insulin will be required

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16
Q

CKD effects on Electrolytes

A

Acid-base imbalances

Hyperkalemia
- Decreased potassium excretion by kidneys
Sodium
- Normal or low
Calcium and phosphate alteration
Magnesium alterations

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17
Q

Clincial manifestations of hypermagnesia

A

Absenece of reflex
Cardiac dysrythmias
Cardiac failure

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18
Q

Metabolic acidosis results from

A

Inability of kidneys to excrete acid load (primary ammonia)
Defective reabsorption/regeneration of bicarbonate
`

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19
Q

What is metabolic acidosis

A

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)

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20
Q

Hematological manifestations of CKD

A

Anemia - very common
nutritional def
Elevated PTH levels
Iron defs
Folic acid defs (Late stages during dialysis)

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21
Q

Why does anemia occur in CKD

A

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

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22
Q

Bleeding tendencies in CKD

A

Defect platlet funciton
Uually corretable with regular renal repleacement therapy

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23
Q

Why are CKD pts more suspectible to infection?

A

Changes in leukocyte function
Altered immune response and function
Diminished inflammatory response

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24
Q

CV system CKD manifestations

A

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

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25
morbiitiy and mortality due to CVD secondary to CKD is
High
26
WHy is management of HTN so helpful
It prevents CV complications from DM It slows the progression of CKD
27
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)
28
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
29
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
30
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
31
Do the prep guide**
32
MBD
Involved with absorbing calcium from the gut with vitamin D
33
Calcium and phosphate have what kind of relatioship
Inverse
34
Erythrepiosis
The process of creating RBCs
35
Acute kidney injury vs CKD
It is sudden and often reversible in acute (abrupt drop in eGFR)
36
What is a signfincatn eGFR change
5-10 is significant >10 is VERY significant Within days or a week
37
Drop of eGFR corrrelates with a rise in
BUN and creatinine
38
Iron and CKD
Pts usally on supplemental iron
39
Clinically significant Hemaglobin level
bw 70 and 80
40
Urenia
Occuring in stage 5 CKD Most systems are symptomatic by this time
41
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
42
arteriovenous fistula
Don't do a BP check on that arm Same with stroke and masectomy Should sound like a swooshing sound
43
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
44
Clinical manifestations of CKD on Musculo-skeletal
CKD-MVD - Including bone abnormaliities -Changes in mineral blances Resulting in skeltal comolications
45
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-MBD 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
46
Integ system clinical manifestations of CKD
Puritis - VERY common (itchy) - sometimes need meds to reduce this Uremic frost
47
Repro system effect of CKD
Men and women Infertility - decreased libido Low sperm counts Sexual dysfunction
48
Psychological changes resulting from CKD
Personality and behaviour changes Emotional lability withdrawal Depression
49
Diagnostics of CKD
Hx and physical exam urinalysis distick evaluations Albumin creatine ratio
50
Earliest marker of kidney damage
Protein urea
50
High risk pts for CKD
DM HTN Vascular dx Autoimmune dx Low GFR (Below 60) Chronic Edema
51
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
52
BUN
Blood test, urea levels in blood elevated if insufficient secretion Internal bleeding can shift levels Elevation is broad indicator of kidney problam
53
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
54
CT KUB
CT Kidneys, ureters, bladder scan to detect kidney abnormalities
55
Renal biopsy
Most helpful for CKD
56
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
57
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
58
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
59
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
59
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
60
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
61
Why is folic acid suppplementation for dialysis
Folic acid supplements Needed for RBC formation Removed by dialysis
62
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
63
Dyslipidemia and CKD
Statins usually used in clients with stage 1-3 CKD because of high levels of triglycerides
64
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
65
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
66
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)
67
Nursing diagnosis of CKD
Excess fluid volume Risk for electrolyte imbalance Imbalanced nutrition: less than body requirements
68
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.
69
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
70
What blood test, if elevated, is a broad indicator of kidney dysfunction
BUN
71

NURS232 (27 decks)

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