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Renal

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0% found this document useful (0 votes)
6 views

Renal

Uploaded by

haadovas4406qc
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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Fluids & Electrolytes

2 compartments
ICF = 40%
ECF = 20%
 Intravascular fluid = plasma = 3L = high conc of
proteins (albumin – oncotic pressure)
 Interstitial = 11 – 12L
 Transcellular = 1L
Homeostasis – maintaining balance internal
environment (ECF)
Fluid = Solution
a. Solvent – water
b. Solutes
Blood – (Liquid ) Plasma vs Serum
With CF without CF
Solutes
1. Electrolytes – ions (+)/(-)
ICF ECF
K+ Na+ 135 – 145 meq/L
PO4- Cl- 96 – 106 meq/L
Mg+ Ca+ 8.5 – 10.5 mg/dl
HCO3- 22 – 26 meq/L
K+ 3.5 – 5.5 meq/L
PO4- 2.5 – 4.5 mg/dl
Mg+ 1.3 – 2.5 mg/dl
2. Blood cells = RBC
Hematocrit 35 – 45%
3. Glucose = 70 – 110mg/dl
4. Creatinine = 0.6 – 1.2 mg/dl
5. Blood urea nitrogen (BUN) = 10 – 20mg/dl
6. Uric acid < 7mg/dl
7. Cholesterol
8. Fatty acids
9. Hormones
10. Enzymes
11. Drugs
12. Proteins
Concentration of ALL solutes/kg = Osmolality 280 – 300
mosm/kg

Fluid balance
Intake = Output
Drinking Urine
Food Lungs
Metabolism Skin
GIT
Regulate Fluid
1. Thirst mechanism (Thirst center)
Osmoreceptors detect changes in osmolality 
stimulate thirst center -> thirst -> drink!
Altered thirst mechanisms
a. Elderly
b. Altered level of consciousness
c. Psychiatric patients
2. Kidneys
3. Skin
4. Lungs
5. GIT
6. ADH – water retention
7. R-A-A-S
8. Atrial natriuretic peptide
Transport mechanisms
1. Simple diffusion – movt of solutes from higher
to lower concentration thru a semi permeable
membrane
ECF ICF
High Na
2. Facilitated diffusion – movt of solutes from
higher to lower conc with the help of a carrier
ECF ICF
I-R
Gluc -------

3. Active transport – movt of solutes from lower


to higher conc with help of a carrier and energy

ECF ICF
Na+ Na/K pump
Energy = ATP
K+

4. Osmosis – movt of solvent from lower to higher


concentration

Isotonic – similar conc with the cells = no osmosis


Hypertonic – higher conc than cells
1.5% NaCl Cells (0.9% NaCl) RBC shrink
(crenation)
Water
Hypotonic – lower conc than cells
0.3%NaCl 0.9% NaCl
Water - enter the cells  SWELL -> burst (hemolysis)
5. Filtration – movt of solutes & solvent from
higher pressure to lower pressure (kidneys)
Fluid Volume Excess
Fluid Volume Deficit

FVE
1. Inc water intake (water intoxication)/ IV fluid
overload
2. Dec water excretion – renal failure, inc ADH
(SIADH), inc aldosterone

Inc fluid ECF

 Inc intravascular fluid –> hypervolemia ->


hypertension -> bounding pulses
 Inc interstitial fluid -> bipedal edema -> weight
gain, pulmonary edema -> DOB
 Inc transcellular fluid
o Ascites
o Pleural effusion
o Pericardial effusion
Dtic tests
1. Osmolality
2. Hematocrit
3. Serum electrolytes
4. Central venous pressure (CVP)
Mgt:
1. Restrict fluid
2. Restrict Na
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Diuretics as ordered
7. Dialysis
8. Manage the cause
Fluid volume deficit
Etio:
1. Dec fluid intake – altered thirst mech, altered
loc
2. Inc fluid loss - diarrhea, diuresis, diaphoresis,
vomiting, DI, dec aldosterone
 Dec fluid in the ECF
o Dec intravascular fluid -> hypovolemia ->
hypotension// weak pulses -> SNS compensate
-> tachycardia
o Dec interstitial fluid -> poor skin turgor, sunken
eyes, slow capillary refill
o Dec transcelluar -> absent of tears
Mgt:
1. Inc OFI
2. IVF as ordered
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Manage the cause
Electrolyte imbalances
Functions of electrolytes
1. Maintaining osmolality
2. Maintain fluid in the body
3. Impulse transmission
4. Muscle contraction
5. Clot formation
6. Bone and teeth formation
7. Maintain acid/base balance
Na = 135 to 145meq/L
Hypernatremia/Hyponatremia

Hypernatremia
1. Hypervolemic hypernatremia water out of
 s/sx FVE brain cells
2. Hypovolemic hypernatremia shrink –
altered LOC
 s/sx FVD
Hyponatremia
1. Hypervolemic hyponatremia (dilutional)
s/sx of FVE
2. Hypovolemic hyponatremia
S/sx of FVD
Brain cells -> swell -> cerebral edema = inc ICP ->
altered LOC

Mgt:
1. Restrict fluid (FVE)
2. Administer fluid (FVD)
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Monitor serum Na
7. Manage the cause

Hyperkalemia/Hypokalemia

Hyperkalemia inc serum K > 5.5 meq/L


Etio:
a. Inc K intake/retention
b. Dec K excretion – renal failure, dec aldosterone,
K sparing diuretics
c. K shifting from ICF to ECF ex. Burns, prolonged
surgery, metabolic acidosis
 Muscle cells
o Cardiac ms -> dysrhythmias -> cardiac arrest
ECG peak or tall T wave
O Skeletal muscles -> muscle weakness and
paralysis
O Smooth ms (GIT) -> diarrhea, abd cramps
Mgt:
1. Restrict K rich food
2. Kayexalate
3. Glucose IV, Insulin IV -> push K into the cells
4. Dialysis
5. Ca gluconate – antagonize the effect of K on
cardiac muscles
6. Manage metabolic acidosis – sodium
bicarbonate

Hypokalemia dec K < 3.5 meq/L


Etio:
1. Dec K intake
2. Inc K loss – diarrhea, diuresis
3. K shifting (metabolic alkalosis)
 Muscle cells
- Skeletal ms -> ms weakness and paralysis
- Cardiac ms -> dysrhythmias (ECG – presence of
U wave)
- Smooth ms GIT -> constipation, ileus
Mgt:
1. Inc K rich food
2. K supplements – Kalium durule
3. KCl IV
 DO NOT GIVE IV BOLUS!
 Monitor urine output prior to administration
 Incorporate to IVF, turn the bag upside down
several times
 Infuse as ordered
4. Provide safety
5. Prevent aspiration
6. Support respiratory function
7. Manage metabolic alkalosis
8. Manage the cause
Calcium
- Bone/teeth
- Muscles
- Nerves
- Blood
o Unionized Ca binds w/ other substances
o Ionized Ca (free Ca++) = 8.5 to 10.5 mg/dl
Calcium
1. PTH -> inc Ca
a. Inc Ca resorption (bone)
b. Inc Ca reabsorption (kidneys)
c. Inc Ca absorption (GIT) – active Vit D (kidneys)
2. Calcitonin -> dec Ca
Hypocalcemia
Etio:
1. Pancreatitis
2. Kidney failure
3. Massive blood transfusion (citrated blood) 
citrate bind with calcium = dec ionized Ca
4. Respiratory alkalosis – dec pCO2 -> Ca binds
with proteins -> hypocalcemia
 Hypocalcemia increases irritability of nerves
o Paresthesia
o Tetany (carpopedal spasm)
o Chvostek’s sign
o Seizures
Mgt:
1. Inc calcium rich food
2. Provide safety
3. Calcium supplements with Vit D
4. Manage the cause

Hypercalcemia
Etio: inc PTH (hyperparathyroidism) – tumor
s/sx
 Formation of calcium stones
 Polyuria
 Inc osteoporosis -> bone weakness
Mgt:
1. Restrict Ca rich food
2. Avoid ca supplement
3. Diuretics as ordered
4. Increase oral fluid intake up to 3 L/day
5. Manage the cause
PO4 –
 Production of ATP
 Hypercalcemia = hypophosphatemia
 Hypocalcemia = hyperphosphatemia

Cl – major anion outside the cells


HCO3 –
 Measured anions
 Cl 96 92 110
 HCO3 22 inc = 26 8
Total 118 118 118

Dec Cl -> inc HCO3 = metabolic alkalosis


Inc Cl -> dec HCO3 = metabolic acidosis

Mg
- Impulse transmission -> heart -> dysrhythmias,
- NMJ
- Control the release of Ach receptors at NMJ
- Inc Mg -> inc control => ms weakness
- Dec Mg -> dec control => ms tetany
- Renal failure hyper Mg
- Alcoholism hypo Mg
Acid – solution with an excess H+ ( give off H+)
Base – solution with OH- ( accept H+)
Acid / Base balance
1 : 20
pH – 7.35 to 7.45
inc H+ => low pH
dec H+ => high pH
Regulation of A/B balance
1. Blood – buffer system ( weak acid and weak
base) – prevent sudden changes in the pH
H2CO3 – weak acid
HCO3 – weak base
HCl + HCO3 = H2CO3 + Cl-
(strong) ---------- weak acid
NaOH + H2CO3 = NaHCO3 + H2O
(strong) ----------- weak base

2. Kidneys remove HCO3/ retain HCO3


Respiratory acidosis = retain HCO3
Respiratory alkalosis = remove HCO3
3. Lung remove pCO2/retain pCO2
Metabolic acidosis = remove CO2
Metabolic alkalosis = retain pCO2
Disorders:
1. Metabolic acidosis – causes: diarrhea, diuresis,
renal failure, hyperkalemia, accumulation of
lactic acid, ketone bodies
2. Metabolic alkalosis – vomiting, Gastric
suctioning, Overdose of antacids
3. Respiratory acidosis – COPD, Lung diseases,
GBS, MG,ALS,SCI C3 = pCO2 retention
4. Respiratory alkalosis = hyperventilation, panic
attack = loss of pCO2

Interpretation:

1. pH 7.31 pCO2 48 HCO 26


respiratory acidosis, uncompensated
2. pH 7.33 pCO2 34 HCO3 19
metabolic acidosis, in partial compensation
3. pH 7. 35 pCO2 47 HCO3 27
respiratory acidosis compensated

pH 7.43 pCO2 46 HCO3 30


metabolic alkalosis compensated
Urinary tract
Lower UT
Urethra – passageway of urine from the UB to the
outside
Male – longer – genitourinary tract
Female – shorter and in close proximity with anus

Urethral sphincter

Urinary bladder – storage of urine


Urge – 150 ml

ANS
PNS – bladder emptying = erection
SNS – urinary retention = ejaculation = orgasm

Honeymoon cystitis = void prior to sexual intercourse

Urinary retention – most impt RF for UTI


Urinary incontinence
Urge incontinence – elderly ( dec bladder capacity )
- bladder training (scheduled urination)
Stress incontinence – obesity , several children – inc
intra abdominal pressure
Upper UT
Ureter – collapsible tube, passageway of urine from
the kidneys to the UB
- most painful site of stone
Kidneys – bean shaped in the posterior abdomen
12 cm long, 6 cm wide, 2.5 cm thick
Functional unit nephron
CVA costovertebral angle
Kidney functions
1. urine formation
2. excretion of waste products (BUN/Creatinine)
3. regulate water balance
4. regulate BP
5. regulate electrolytes – K,Mg,P
6. activate vit D
7. produce erythropoietin
8. produce of prostaglandin – inc renal blood flow
9. regulate acid/base balance

UT disorders
1. Inflammatory disorders
a. Infection
b. Trauma
c. Autoimmune disease
2. Obstructive disorders
a. Stones – urolithiasis
b. Tumor
c. Congenital lesions

Infection and stone formation -> impaired kidney


function

UTI
Lower UTI – urethritis/ cystitis = LOCAL inflammation
( uncomplicated UTI) – dysuria, low back pain,
hypogastric pain, burning sensation, urinary frequency
( irritative symptoms)
Etio: E. coli  urethrovesical reflux
RF:
Female
u. retention
immobilization
bed ridden
elderly
diaper
catheter
Dtic tests
1. Urine C/S
2. Urinalysis = pyuria (pus in the urine – WBC)
Female = 6/hpf and below = normal
Male = 0
Mgt:
1. Inc oral fluid intake up to 3L/day
2. Acidify the urine (cranberry juice)
3. Avoid urinary retention (bladder training)
4. Avoid RF (modifiable)
5. Drug therapy
a. Antibacterial drug as ordered
b. Analgesic = NSAIDs PRN
UPPER UTI
1. Pyelonephritis – inflammation of the renal
pelvis
2. Glomerulonephritis – inflammation of the
glomerulus

Acute PN
Etio: E. coli
RF lower UTI  ascending infection (renal pelvis) ->
systemic inflammation = fever and chills, pain in the
CVA and flank area, (+) kidney punch test = goldflam
test, leukocytosis
Dtic tests
1. C/S
2. UA
3. CBC
4. Kidney function test
Acute PN => Acute kidney injury ( Intra renal cause )
Mgt:
1. Inc OFI
2. Acidify the urine
3. Avoid all RF for lower UTI
4. Monitor kidney function test
5. TSB
6. Drug therapy
a. Antipyretic
b. Analgesic
c. Antibacterial drug as ordered
Repeated bouts of acute PN for more than 6 months->
chronic PN = Chronic Kidney disease

Glomerulonephritis (GN)
Acute GN
Chronic GN
Rapidly progressive GN
Nephrotic syndrome - proteinuria
Nephritic syndrome - hematuria
Acute GN
Etio: GABHS (throat infection), Staphylococcus (Skin
infection)  antigen /antibody complex  injury to
the glomerulus – inflammation of the glomerulus -> inc
capillary permeability -> proteinuria -> dec oncotic
pressure -> edema / -> hematuria -> tea colored urine
 Impairment of kidney function -> Acute KI
Nsg Dx: FVE

Mgt:
1. Restrict fluid
2. Restrict Na
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Inc protein in the diet
7. Monitor kidney function
8. Antibacterial drugs as ordered

Urolithiasis
Etio: supersaturation of urine
Nephrolithiasis  Ureterolithiasis
Cystolithiasis
Nephrolithiasis
 Hydronephrosis -> impaired kidney function
 Stone irritates the lining of the kidneys 
bleeding = Hematuria
Pain CVA and flan area
Ureterolithiasis
 Most painful site = severe, colicky in the flank
area radiating to the thigh and genitalia
 Hematuria
Cystolithiasis
 Pain – low back and hypogastric
 Hematuria
Dtic tests
1. UA – hematuria
2. Kidney function test
3. CT scan (CT stonography)
4. Intravenous pyelography (IVP)
5. KUB ultrasound
6. Stone analysis (strain all urine)
Mgt:
1. Inc OFI
2. If the stone is alkali – acidify the urine
3. If the stone is acid – alkalinize the urine
4. If the stone is uric acid – avoid purine rich food
5. If the stone is oxalate – avoid oxalate
containing food
6. If the stone is calcium – avoid calcium is NOT
recommended UNLESS there is true hypercalcemia
and true hypercalciuria
7. Avoid UTI
8. Removal of stones
a. Drug therapy – Rowatinex, Sambong
b. Percutaneous removal
c. Laparoscopic removal
d. ESWL – extra corporeal shockwave
lithotripsy
e. Open surgery

Acute Kidney Injury (AKI) – sudden impairment of


kidney function; reversible
Etio:
1. Pre renal causes – dec blood flow to the
kidneys
2. Intra renal causes – kidneys are damaged,
direct trauma, Acute PN, Acute GN, nephrotoxic
effects of drugs
3. Post renal – obstruction – stones/ tumor
Chronic kidney disease (CKD) – gradual and progressive
loss of kidney function
GN, PN, Urolithiasis
Diabetes Mellitus and Hypertension = nephropathy
- Irreversible
CKD = GFR normal 125ml/min
Stage I =/> 90ml/min – impaired kidney function
with normal or high GFR
Stage II 60 – 89ml/min - MILD
Stage III 30 – 59 ml/min - moderate
Stage IV 15 – 29 ml/min - severe
Stage V < 15 ml/min – ESRD/ESKD = Renal failure
(uremic syndrome = multiorgan affectation of severe
uremia)
 Skin – ashen gray color, uremic frost
 GIT – uremic fetor
 Lungs – pulmonary edema
 Heart – CHF
 Blood – anemia, thrombocytopenia
 Brain – altered LOC
 Musculoskeletal – renal osteodystrophy –
deformities
S/sx of kidney impairment
1. Oliguria
2. Azotemia (inc BUN & Crea)
3. Hypertension
4. Hyperkalemia – immediate indication for
dialysis
5. Hyperphosphatemia
6. Hypermagnasemia
7. Hypocalcemia
8. Anemia
9. Metabolic acidosis
10. Edema
Mgt = ESRD
1. Renal transplant
2. Dialysis – Peritoneal dialysis/Hemodialysis

Nsg Dx
Fluid volume excess
Fatigue
Imbalance nutrition
Risk for complications

Mgt:
1. Restrict fluid
2. Restrict Na
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Diet – restrict Na, K, P,Mg rich diet, inc Iron, Ca
rich diet, low fat, (AKI – inc protein; CKD – restrict
protein), inc carbohydrates
7. Provide safety
8. Provide rest
9. Monitor kidney function
10. Hypertension – ACE inhibitors, AIIR blockers
(ARBs)
11. Hyperkalemia – Kayexalate, Glucose IV, Insulin
IV, Calcium gluconate
12. Metabolic acidosis – sodium bicarbonate
13. Hyperphosphatemia – AlOH (Amphojel)
14. Hypocalcemia – Ca supplement
15. Anemia – iron supplements, Erythropoietin SQ

Peritoneal dialysis
Purposes:
1. To remove toxic wastes
2. To reestablish fluid and electrolyte balance
Principles
1. Simple diffusion
2. Osmosis
Complications
1. Peritonitis (primary)
2. Leakage
3. Bleeding

Hemodialysis
Purposes
1. To remove excess water
2. To remove nitrogenous waste
Principles
1. Simple diffusion
2. Osmosis
3. Ultrafiltration – artificial kidney – Dialyzer
Arterio-venous anastomosis
1. AV fistula
2. AV graft
 HOB/ front of the chart
NO BP monitoring
NO blood extraction
(site of AV fistula)
 Before hemodialysis
Assess:
Thrill - palpate
Bruit – auscultate

Complications:
1. Dysequilibrium syndrome – sudden changes in
fluids and electrolytes – headache, N & V,
lethargy, seizures ( slow down the rate of dialysis)
2. Hypotension
3. Atherosclerotic cvd (MI)
4. Gastric ulcers
5. Long term complications

Renal transplant
Donor – living/ cadaver
Living – nephrectomy = side lying (CVA), harvest kidney
Post op – monitor VS every 15 min, every 30 min,
every hour until stable
Ward – pain medication, monitor
Discharge teaching – live a healthy lifestyle, monior
kidney function tests regularly

Recipient (Patient)
Post op = Monitor UO hourly, monitor VS
1. Monitor s/sx of rejection
2. Monitor s/sx of infection -> inc WBC
a. Avoid exposure to people with infection – wear
masks
b. Handwashing
c.Avoid crowded places
3. Avoid rejection
a. Steroids for 3 – 4 months -> gradually
withdraw
b. Cyclosporine (immunosuppressant drug) –
for life

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