SOLUTES

Sodium —Major cation; ECF 135 - 145 meq/L

Potassium — Major cation; ICF 3.5 - 5.5 meq/L
Calcium — (ECF) 8.5 - 10.5 mg/dl
Chloride — major anion ECF 96 - 106 meq/mL
Phosphate — major anion ICF 2.5 - 4.5
Magnesium — ICF 1.3 - 2.5 mg/dl
Bicarbonate — ECF 22 - 26 meq/ml

Blood Cells
• Hct — concentration of RBC
• Normal: 35-45%
• Kapag bumaba ang RBC, baba din ang Hct
• But during dehydration, baba ang Hct

Glucose — 70 - 110 mg/dl

Creatinine — 0.6 - 1.2 mg/dl

• Kidney Function Test
• Creatinine is a byproduct of muscle
metabolism
• Non fasting
• For BUN and Crea: Advice client to drink a
lot of water before fasting

BUN — 10 - 20 mg/dl
• Byproduct of protein breakdown
• Non fasting

Enzymes
• CKMB, LDH (MI), AST (liver problem)
• Lipid profile: 10 hour fasting
• FBS: 8-10 hours

Hormones
• Hypersecretion — most common cause:
tumor
• Hyposecretion

Nutrients
Gasses
• Oxygen, carbon dioxide
• ABG
> pO2: 80-100 mmHg
> pCO2: 35-45 mmHG

Osmolality
• Concentration of all solutes per kg unit of blood
Note: 4. OSMOSIS
• Sodium affects the osmolality outside the • Movement of WATER (solvent) from lower to
cell higher concentration
• Potassium affects the osmolality inside the
cell ECF ICF (RBC)
• Serum osmolality: about the blood 0.9% NaCl 0.9% NaCl
• Urine osmolality: concentration of the Isotonic
urine, kapag mababa ang tubig, mababa - no movement
ang concentration
• High osmolality, decrease concentration Example:
• Osmolality is a good parameter for fluid ECF ICF
status 3% NaCl 0.9% NaCl
Hypotonic
- water will enter the cell —> Swell
TRANSPORT MECHANISMS
ECF
1. SIMPLE OR PASSIVE DIFFUSION 1.5% NaCl
• Movement of SOLUTES from higher to Hypertonic
lower concentration to a semi-permeable <—— Water Shrink
membrane (semi-permeable: not all
substances can pass through) If RBC swell —> burst = Hemolysis
If RBC shrink —> Crenation
ECF ICF
Na ——> Na
5. FILTRATION
2. FACILITATED DIFFUSION • Movement of SOLUTES and SOLVENT from
• Movement of SOLUTES from higher to higher to lower pressure
lower concentration to a semi-permeable
membrane with the help of a carrier pressure pressure
—————>
ECF ICF
Glucose —-> glucose • Organ: Kidneys
| • What do you call the artificial kidney in
| hemodialysis: Dialyzer
Carrier (Insulin binds to the receptor)

3. ACTIVE TRANSPORT HEMODYNAMICS

• Movement of SOLUTES from lower to Movement of —- in and out of the cell to maintain
higher concentration (against homeostasis
concentration gradient) requiring a carrier
and energy in the form of ATP Two forces acting in the blood vessel:
1. Hydrostatics pressure: push the fluid out of the BV
ECF | ICF > BP
Na <——- Na 2. Oncotic pressure: stops the homeostasis
| Albumin — major protein inside the BV; osmol
Na/ K| pump (attracts)
| > Very little amount of fluid —> lymphatics —>
drains fluid —> return to the blood vessel
K ——-> K
| Oncotic and Osmotic: same in physiology
Note:
A. Normal HP is slightly higher than OP
FLUID REGULATION
B. If there is too high hydrostatic
pressure (HPN) and OP is normal :
• More fluid will get out —>
accumulation of fluid in interstitial
space —> edema (feet: bipedal
edema)

C. Normal HP and OP is low:

• production of albumin -
LIVER
• excretion of protein -
proteinuria
FLUID DISTURBANCES
D. Too high HP and OP is low
(proteinuria) FLUID REGULATION
• Preeclampsia = systemic edema
1. Thirst mechanism (Thirst Center)
E. If Hydrostatic is normal and OP is • Osmoreceptors: cells that detect changes in
normal but Lymphatics is abnormal = osmolality —> thirsty
local edema • Altered thirst mechanism
• E.g. Elephantiasis > Elderly (one early sign: constipation)
> Altered LOC
capillary permeability — inc tendency of
the fluid to get out in BV due to inflammation 2. Kidneys
= local edema 3. Skin
• E.g. Burns 4. GIT
5. Lungs
Third spacing: (edema) fluid is not being used 6. Hormones
by the body in physiology process • ADH —> water retention —> Blood volume
—> BP
F. Normal HP but High OP
• Aldosterone — Na and water reabsorption (K
• Hyperosmotic state
> Hypervolemia secretion)
• Inc blood volume —> inc BP • Atrial Natriuretic Peptide (ANP) relaxes by atria
— Na and water reabsorption (K reabsorption)
Lahat ng inflammation, there is edema
7. RAAS (Renin Angiotensin Aldoesterone System)
• Blood volume —> BP

FLUID VOLUME EXCESS

FLUID VOLUME DEFICIT
 ⬆

FLUID VOLUME EXCESS Early sign of fluid overload:

difficulty breathing
ETIOLOGY
1. Increase fluid intake oral/IV (fluid overload)
2. Decrease fluid losses SIADH
> Renal failure • FVE — walang peripheral
> Increase ADH — (SIADH) edema but has cerebral edema
> Increase aldosterone - (Cushing’s disease)
3. Fluid shifting —> altered hemodynamics
> CHF
> Liver cirrhosis
> Proteinuria
(Glomerulonephritis)

Increase fluid in ECF — fluid in interstitial space —> weight gain (1kg=1L), edema (bipedal edema)
| pulmonary edema
|
| — fluid in the transcellular space —> Ascites, Pleural effusion
|
fluid in blood vessel
|
Increase blood volume — distended neck veins, bounding pulses
|
Increase BP
|
Increase CVP

DIAGNOSTIC TESTS
1. Osmolarity
2. Hematocrit
3. CVP
4. USG
> Weight of urine compared to water
> Normal: 1.010 - 1.030
> Water: 1.000

MANAGEMENT
1. Manage the cause
2. Restrict fluid
3. Restrict Na
4. Monitor I and O
5. Monitor VS
6. Weight patient daily
> (same patient, same clothes, same time)
7. Drug therapy
> Diuretics
8. Dialysis
 ⬇

FLUID VOLUME DEFICIT

ETIOLOGY
1. Decrease fluid intake
> Altered LOC
> Elderly
> Mental disorders
2. Increase fluid losses
> Diarrhea
> Diuresis
> Diaphoresis
> Vomiting
3. Fluid shifting
> Burn — capillary permeability —> BURN EDEMA

Decrease fluid in the ECF — fluid in the interstitial space —> dry mucosa and skin, sunken eyeball,
| Weight loss
| — fluid in the transcellular fluid —> lack of tears
|
Dec intravascular fluid
|
Dec blood volume —- capillary refill — flat neck veins
|
Dec BP — CVP — weak pulses
|
Hypovolemic Shock

MANAGEMENT
1. Manage the cause
2. Increase fluid intake (oral/IV)
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
 ⬆ ⬆

ELECTROLYTE IMBALANCES
MAGNESIUM
Mg — control release of Ach in the 2. Hypernatremic Hypovolemia — s/sx FVD
neuromuscular junction • Na, water
Mg needed for PTH to be released > Dehydration (water loss)

If: 3. Hypernatremic Euvolemia

Mg —> no control of Ach —> lalabas ng > Na, Normal water
lalabas —> muscle irritability —> tetany
The most sensitive cell to sodium changes:
Mg —> PTH —> decrease calcium —> Brain cells
tetany • If there is Na outside the cell —> water
will go outside the cell —> cell shrinks —>
PHOSPHATE brain cells = Altered LOC
• PO4 — has relationship with calcium
• CaPo4 — bone, teeth
• If in blood: inversely proportional MANAGEMENT
1. Restrict Na rich food
> PO4 Ca 2. Most common cause — administer water
> PO4 Ca 3. Provide safety — for LOC
• PO4 4. Manage the cause
> ATP (adenosine triphosphate) — 5. Monitor I and O
nagbibigay ng energy 6. Monitor VS
• E.g. soda 7. Weigh patient daily

CHLORIDE HYPONATREMIA
• Major anion in the body
• NaCl — salt • Serum Na less than 135 meq/L

Major anion outside the cell: ETIOLOGY

• Cl 1. Hyponatremic Hypervolemia — most
• HCO3 common — s/sx FVE
Measured anions — constant • Na, water
Kapag tataas yung isa, baba yung isa • Dilutional hyponatremia
• SIADH
• E.g. CHF, Renal failure — dumadami ang
SODIUM IMBALANCES water sa body

2. Hyponatremic Hypovolemia — FVD

HYPERNATREMIA • Na, water
• Increase serum Na >145 meq/ml • Severe burns
• Low aldosterone
ETIOLOGY
1. Hypernatremic hypervolemia — FVE 3. Hyponatremic Euvolemia
> Na, water
> Sea drowning
> Increase aldosterone
 ⬆ ⬆

If there is Na outside the cell —> water will

go inside the cell —> cerebral edema —> Altered Due to serum K:
LOC 1. Affect cardiac muscles —> dysrhythmias —>
cardiac arrest— ECG changes (Peak or tall T
wave)
MANAGEMENT 2. Affect the skeletal muscles —> muscle
1. Manage the cause weakness
2. Na rich food 3. Affect the smooth muscles (GIT) —
3. Most common cause: Restrict fluid motility —> diarrhea
4. Provide safety
5. Monitor I and O
6. Monitor VS MANAGEMENT
7. Weigh patient daily 1. Manage the cause
2. Restrict potassium rich foods (citrus fruits,
apple, raises, grapes, banana)
3. Monitor ECG
POTASSIUM IMBALANCES 4. Provide safety
5. Diarrhea = low residue, high protein diet —
HYPERKALEMIA replace fluids (if not renal cause; depends on
the cause)
> Increase serum K >5.5 meq/L
6. Administer Kayexalate
7. Calcium Gluconate — antagonize the effect of
ETIOLOGY
K on cardiac cells
1. Increase K intake
8. Glucose IV
> KCl IV overload Push K into the cells
9. Insulin IV
2. Decrease K loss
10. Dialysis
> Renal failure
11. K wasting diuretics (Furosemide) — no renal
> K sparring diuretic (Spironolactone)
failure
3. K shifting from ICF to ECF massive tissue
injury
> Severe burns
> Prolonged surgery HYPOKALEMIA
> Metabolic acidosis • Decrease serum K <3.5 meq/L

H+ outside the cell —> papasok sa cell —> ETIOLOGY

K+ will go out in the cell —> K+ outside 1. Decrease K intake
the cell > Undernourished
2. Increase K loss
> Dirrhea
The most sensitive cells to potassium
> Diuresis
changes: Muscle cells
> Increase aldosterone
3. K shifting from ECF to ICF
Metabolic Alkalosis

The most sensitive cells to potassium

changes: Muscle cells
 PTH
Due to serum K: 1. Increases Ca resorption
1. Affect skeletal muscles — muscle 2. Increase absorption of Ca from the GI tract
weakness and paralysis > PTH helps activate Vit D in the kidneys =
2. Affect cardiac muscles — dysrhythmias, active Vit D increases Ca absorption
ECG changes (prominent U wave) 3. Increase Ca reabsorption
hypUkalemia
3. Affect smooth muscle (GIT) —
abdominal distention —> constipation HYPERCALCEMIA
• Increase serum Ca more than 10.5 mg/dL
MANAGEMENT
ETIOLOGY
1. Manage the cause
1. Hyperparathyroidism
2. Increase K rich foods
2. Increase calcium intake
3. Provide safety
3. Increase bone resorption — kumukuha ng Ca sa
4. Replace potassium
bone nilalagay sa blood
a. Kalium Durule
> Resorption: Bone to blood
b. KCl IV
> Reabsorption:
Prior to administration:
> Monitor urine output
> Incorporate to IVF fluid Due to Ca:
> Invert the bag several times 1. Decrease excitability of nerves (CNS) —> CNS
> Start accurate infusions depression and altered LOC
> Monitor for Earliest adverse effect 2. Decrease excitability of nerves (CNS)
of KCl = phlebitis |
> Monitor ECG Dec impulses transmission from the nerves to the
> DO NOT GIVE IV PUSH muscles —> muscle weakness
3. Excess Ca precipitate to form stones in the urinary
tract
CALCIUM IMBALANCES
MANAGEMENT
CALCIUM 1. Manage the cause
1. Bone and teeth formation 2. Monitor ECG — shortened QT interval
2. Clot formation 3. Provide safety
3. Muscle contraction 4. Diuretics (Furosemide)
4. Impulse transmission 5. Restrict Ca rich food
5. Enzyme activation

2 FORMS OF CA
A. Unionized Ca HYPOCALCEMIA
• Ca blinded with other substances
• Decrease serum Ca <8.5 mg/dL
B. Ionized Ca
• Most common
• free/ unbound
ETIOLOGY
Normal: 8.5 - 10.5 mg/dL
1. Vit D deficiency
2. Pancreatitis
PTH — increase Ca
3. Hypoparathyroidism
Calcitonin — decrease Ca
4. Massive blood transfusion — citrated blood (citrate
is used to prevent blood clotting
 • Citrate bind with Ca —>
Decrease ionized Ca 2. Kidneys — regulate A/B balance by:
A. Remove HCO3
5. Alkalosis — hyperventilate —> B. Retain HCO3
respiratory alkalosis
> In response to Repirstory acidosis =
> pH — Ca binds with proteins
retain HCO3
—> decrease ionized Ca
> In response to Repsiratory Alkalosis =
Due to serum Ca: Remove HCO3
1. Increase irritability of the nerves —>
increase impulse transmission 3. Lungs — regulate A/B balance by
> Paresthesia A. Remove pCO2
> Tetany (Chvostek’s, Trousseau’s B. Retain pCO2
sign
> Seizures > In response to metabolic acidosis =
2. Affects cardiac muscles —> prolonged remove pCO2
QT interval
> In response to metabolic alkalosis =
retain pCO2
MANAGEMENT
1. Inc Ca rich food CO2 - acid
2. Inc Vit D rich food CO2 + H2O —> H2CO3
3. Vit D and Ca supplements
4. Provide safety
5. Manage the cause Note:
6. Seizure precautions HCO3 - base
7. Monitor ECG Metabolic
HCO3 — alkalosis
HCO3 — acidosis
ACID-BASE REGULATION
ACID — solution with an extra H+ (has the PCO2
ability to give off H+) Respiratory
BASE — solution with OH+ (accept H+)
CO2 — acidosis
In every 1 acid : 20 base CO2 — alkalosis

pH: 7.35 — 7.45

Regulation of A/B balance

1. Blood (buffer system) prevent sudden
changes in pH
A. Weak acid — H2CO3
B. Weak base — HCO3

HCL acid + HCO3 = H2 CO3 + Cl

weak acid
NaOH + H2CO3 = NaHCO3 + H2O
weak base
 ⬇

METABOLIC ACIDOSIS
Normal anion gap
High anion gap
Anion gap — unmeasured anions
> Lactate
> Sulfates
> Phosphate
> Ketones

Cl
HCO3
** measured anions — constant
Signs and symptoms of metabolic acidosis
HCO3 — metabolic acidosis with normal headache, confusion, drowsiness, increased
anion gap respiratory
rate and depth, nausea, vomiting.
Anaerobic metabolism Peripheral vasodilation and decreased
• Produce energy without O2 cardiac output occur when the pH drops to less
• Increase lactic acid than 7.
——- Additional physical assessment findings
include decreased blood pressure,
cold and clammy skin, dysrhythmias, and
shock.

ETIOLOGY

HCO3 —-> H+ —> pH —> lung compensate —> to normalize pH

Acid | |
H+ —> enter the cell remove CO2 (hyperventilate)
| (Kussmaul’s breathing)
|
K shifting to ECF ==> Hyperkalemia
 ⬇ ⬆

METABOLIC ALKALOSIS
ETIOLOGY

1. Increase HCO3 —> Dec H+ —> pH ——— lungs compensate

1. Decrease acids | | |
| | Retain CO2 (hypoventilate)
| Ca binds with proteins
| |
ionized ca (Hypocalcemia)
CAUSES :
1. Vomiting
2. Nasogastric suctioning
3. K wasting diuretics
4. Excessive alkali ingestion

MANAGEMENT
1. Metabolic acidosis — sodium bicarbonate and manage the cause
2. Metabolic — manage the cause

RESPIRATORY ACIDOSIS
• Alkalosis is primarily manifested by symptoms related to decreased calcium ionization,
> Tingling of the fingers and toes, dizziness, and hypertonic muscles.
• The ionized fraction of serum calcium decreases in alkalosis as more calcium combines with serum
proteins.
• Because it is the ionized fraction of calcium that influences neuromuscular activity, symptoms of
hypocalcemia are often the predominant symptoms of alkalosis.

ETIOLOGY
1. COPD
2. Respiratory center depression
3. Neuromuscular disease
4. Decrease respiratory rate

PCO2 —-> inc H+ —> pH —-> kidneys retain HCO3 —> to normalize pH
|
inc K
RESPIRATORY ALKALOSIS
Hyperventilation
• Anxiety
• Shouting
• Crying Give brown bag
• Panic attack

Hyperventilation —> loss of CO2 —> Dec H+ —> pH —> kidney remove HCO3
| |
Ca binds with proteins To normalize pH
|
Hypocalcemia

ABG ANALYSIS
pH: 7.35 — 7.45
PCO2: 35 — 45
HCO3: 22 — 26
O2: 80 — 100
O2 SAT: 95% — 100%
Base excess: -3 to +3

pH 7.31 pCO2 49 HCO3 24 — Respiratory acidosis, uncompensated

pH 7.35 pCO2 34 HCO3 18

Metabolic acidosis, compensated

pH 7.48 alkalosis
pCO2 46
HCO3 28 metabolic alkalosis, partially compensated

Kung sino yung malayo sa normal value, yun piliin mo

pH 7.32 pCO2 49 HCO3 27

Acid Respiratory

Answer: Respiratory acidosis in partial compensation

Ph ang magsasabi kung alkalosis o acidosis

URINARY TRACT TYPES
1. Urge incontinence — bladder training
> Scheduled time of urination
2. Stress incontinence
> Caused by inc intraabdominal
pressure
3. Urinary retention
> Most important risk factor for UTI
- bedridden
> bladder training

ANS
SNS — urinary retention
PNS — bladder emptying

LOWER URINARY TRACT Sexual response (Males)

SNS — ejaculation
Urethra PNS — erection
• Passageway of urine from the bladder to the
outside Females
• Female SNS — orgasm
> Shorter and close to the anus
• Male
> Longer urethra (genitourinary tract) Honeymoon Cystitis
• Inflammation of the urinary bladder
Ureter due to sexual intercourse
• Passageway of urine from the kidneys to the • Void first before sexual intercourse
urinary bladder; line by smooth muscles
• Uterolithiasis — most painful site of bone Kidneys
• Bean shaped organ located in the
Micturition/ urination — reflex posterior abdomen
• Costovertebral angle and flank area
Urinary bladder • 12 cm long
• Storage of urine • 6 cm wide
• 150 ml of urine — feel the urge to urinate — • 2.5 cm thick
be able to control urination

Elderly —-> bladder capacity

65-74 young old
75-84 middle old
85-99 old old
100 and above - elite old
UPPER URINARY TRACT EFP = HP (OP + TP)

Kidney Functions: A. FILTRATION

1. Urine formation • Water, NA, K, uric acid, urea, creatinine,
2. Excretion of waste products glucose
3. Regulate water balance • GFR (Glomerular Filtration Rate)
4. Regulate blood pressure 125 ml/min x 60 min/hr = 7500 ml/ hr x
5. Regulate acid/base 24/d = 180,000 ml/day = 180 L/day!
6. Regulate electrolyte — K, Mg, P
7. Activate Vit D B. REABSORPTION
8. Produce erythropoietin • Water, Electrolytes, uric acid, urea,
9. Production of prostaglandin — increases glucose
renal blood flow
C. SECRETION
Nephron • Creatinine, urea, uric acid, water,
• Functional unit electrolytes
• Urine formation
1. Filtration
2. Reabsorption
3. Secretion
RENAL DISORDERS
A. Inflammatory Disorders
1. Infection
2. Trauma
3. Autoimmune

B. Obstructive
1. Stones
2. Tumor
3. Congenital lesions

Stones and Infection

• Impaired Kinpdney Function
• Acute Kidney Injruy
• Cherinc kidney disease (
LOWER URINARY TRACT
INFECTION
8. Cotton underwear
9. Proper use of sanitary pads, liner,
CYSTITIS tampons
ETIOLOGY 10. Manage all risk factors
• E. Coli
PHARMACOLOGICAL TREATMENT
RISK FACTORS 1. Antibacterial drugs
1. Women > Co-trimoxazole
2. Stones > Ciprofloxacin
3. Catheter 2. Analgesic — NSAIDS
4. Pregnancy
5. Poor perineal hygiene
6. Improper use of sanitary napkins, Tampons, panty
URETHRITIS
liners Inflammation of the urethra
7. Bath tub
8. Urinary retention
9. Wearing nylon underwear UPPER URINARY
10. Immunocompromised
11. Sexual intercourse
12. Lack of water intake
TRACT INFECTION
SIGNS AND SYMPTOMS
1. Pain: Low back pain, hypogastric pain, dysuria,
PYELONEPHRITIS
burning sensation, urinary frequency (irritative • Inflammation of the renal pelvis
symptoms) • Ascending infection
• Acute PN ; Chronic PN
NURSING DIAGNOSIS
1. Acute pain
2. Disturbed elimination pattern: Urination
3. Risk for infection

DIAGNOSTIC TESTS
1. Culture/ Sensitivity
2. Urinalysis — Pyuria (WBC) bacteriuria

Empiric treatment — according to the professional

judgment

MANAGEMENT ETIOLOGY
1. Increase oral fluid intake up to 3 L / day • E. Coli
2. Acidify the urine (cranberry juice)
3. Avoid urinary retention HISTORY
4. Change catheter 1. Incomplete treatment
5. Proper perineal hygiene 2. Dec immune system
6. Shower instead of bath tub 3. Lower UTI
7. Bladder training
SIGNS AND SYMPTOMS GLOMERULONEPHRITIS
PN — systemic inflammation • Inflammation of the glomerulus
1. Fever and chills • No pain
2. Weakness • Acute GN, Chronic GN
3. Malaise
4. Fatigue ETIOLOGY
5. (+) kidney punch test (tenderness) • Bacterial infection: GABHS, Staphylococci
6. Impaired kidney function —> AKI |
7. Repeated bouts of acute PN —> antibody production
Chronic PN |
injury to the glomerulus — Ag-Ab complex
NURSING DIAGNOSIS causes injury to
1. Acute pain glomerulus
2. Hyperthermia |
3. Fatigue inflammation of the glomerulus
4. Risk for injruy |
5. Risk for infection Inc capillary permeability —> hematuria
| (tea colored urine)
DIAGNOSTIC TESTS
Proteinuria —> oncotic pressure —> edema
1. Culture/ Sensitivity
2 Urinalysis
3. Kidney function test
4. Kidney, Ureter, Bladder ultrasound
5. CBC

MANAGEMENT
1. Increase oral fluid intake up to 3 L /
day
2. Acidify the urine (cranberry juice)
3. TSB
4. Provide rest DIAGNOSTIC TEST
5. Promote safety 1. Urinalysis
6. Manage all risk factors 2. C/S (blood)
7. Avoid lower UTO 3. Kidney function test
4. Elevated ESR
PHARMACOLOGICAL TREATMENT 5. KUB ultrasound
1. Antibacterial 6. 24 hour urine collection
2. Antipyretic/ Analgesic drugs
NURSING DIAGNOSIS
1. FVE
2. Risk for infection
3. Risk for complications

MANAGEMENT
1. Restrict fluid
2. Restrict sodium
3. Monitor I and O
4. Monitor VS
5. Weigh patient daily
6. Prevent throat infection, skin infection
8. Avoid repeated bouts of GN
9. Monitor kidney function
10. Antibacterial drugs

1. Ureter — Uterolithiasis
2. Kidney — Nephrolithiasis
• Hydronephrosis —
edema of the kidneys
3. Bladder — Cystolithiasis

NEPHROLITHIASIS NURSING DIAGNOSIS

1. Increase oral fluid intake
• Pain in the costovertebral angle and flank area
• Hematuria 2. If stone is acidic, alkalinize urine;
3. If stone is alkali, acidify urine
4. If stone is uric acid — restrict purine rich
UTEROLITHIASIS food
• Severe pain in the flank are radiating to the 5. If stone is oxalate — restrict oxalate
thighs and genitalia containing food (nuts, strawberries)
• Hematuria 6. If stone is calcium — restrict calcium is
NOT recommended UNLESS the patient
CYSTOLITHIASIS has true hypercalcemia and hypercalceuria
7. Manage all risk factors
• Pain in the hypogastric and low back area
8. Removal of stones
• Hematuria

Pain + hematuria = stone

PHARMACOLOGICAL
Painless + hematuria = tumor
1. Pain reliever — NSAIDS
2. Drug therapy
> Sambong 500 mg
DIAGNOSTIC TESTS
> Rowatinex
1. CT stenographer
2. IVP — intravenous Pyelography
SURGICAL
3. Urinalysis
1. Cystoscopic removal
4. kidney function
2. ESWL (Extracorporeal Shockwave
5. KUB ultrasound / X-ray
Lithotripsy)
6. Stone dialysis
3. Laparoscopic removal
4. Open surgery
RENAL IMPAIRMENT

ACUTE KIDNEY INJURY (AKI)

• Sudden impairment of kidney function
(reversible, non progressive)

ETIOLOGY
1. Prerenal causes — blood flow (shock)
2. Intrarenal causes — kidneys are diseases (PN,
GN, Nephrotoxic drug effects)
3. Postrenal causes — obstruction (stones,
tumor, congenital lesions)

PHASES OF AKI
1. Initial phase — from injury to oliguria
2. Oliguria phase — renal impairment
3. Diuretic phase — kidneys removing excess
water
4. Recovery phase — 6 months to 12 months

CHRONIC KIDNEY DISEASE

• Gradual and progressive impairment of kidney
function (irreversible)

CAUSES
1. Hypertension
2. Diabetes Mellitus
> Nephrosclerosis
3. Chronic PN
4. Chronic GN
5. Stones

STAGES
GFR normal: 125 ml/min
1. Stage 1: =/> 90 ml/min (impaired kidney
function with normal or high GFR
2. Stage 2: 60-89 ml/min (mild)
3. Stage 3: 30-59 ml/min (moderate)
4. Stage 4: 15-29 ml/min (severe)
5. Stage 5: <15 ml/min (renal failure = ESRD)
ESRD PHARMACOLOGIC
Uremic syndrome — uremia = multi organ 1. Anti hypertensive
affectation 2. Sodium bicarbonate
• Skin: uremic frost 3. Drugs for Hyperkalemia
• GIT: Uremic fetor 4. Phosphate binding agent
• Blood: anemia, thrombocytopenia 5. Calcium and Vit D supplements
• Lungs: pulmonary edema 6. Iron supplements
• Heart: CHF 7. Erythropoietin injection
• CNS: altered LOC, uremic psychosis
• Musculoskeletal: Renal osteodystrophy MEDICAL MANAGEMENT
1. Dialysis
DIAGNOSTIC TEST 2. Renal Transplant
1. Kidney function test
2. Blood tests (CBC, Electrolytes)
3. CT scan
4. Ultrasound
5. Estimated GFR

AKI/ CKD DIALYSIS

Impaired kidney functions
1. Oliguria — Anura
2. In BUN and Crea (Azotemia) PERITONEAL DIALYSIS
3. HTN
4. Edema Purposes:
5. Met acidosis 1. Remove toxic waste
6. Hyperkalemia 2. Re establish fluid and electrolyte balance
7. Hyperphosphatemia
8. Hypermagnesemia Principles:
9. Anemia 1. Simple diffusion
10. Hypocalcemia 2. Osmosis

MANAGEMENT
1. Restrict fluid
HEMODIALYSIS
2. Restrict sodium
Purposes:
3. Monitor I and O
1. To remove nitrogenous waste
4. Monitor VS
2. To remove excess water
5. Weigh pt daily
6. DIET:
Principles:
> AKI: Low fat, low cholesterol, low K, P,
1. Simple diffusion
Mg rich food, High Ca and iron rich food,
2. Osmosis
high protein
3. Ultrafiltration (dialyzer)
> CKD: Restrict sodium, low fat, low
cholesterol, low K, P < Mg rich foods high
Ca and iron rich food, restrict proteins
7. AKI: Diuretics
CKD: Diuretics/ Dialysis
• Acute intermittent PD
• Warm before infusion Hemodialysis lasts for: 4-6 hours
• Dialysis solution: Normal ECF with high
glucose COMPLICATIONS
• Dwelling time: let the fluid stay there 1. Disequilibrium syndrome (lethargy,
headache, seizure, nausea and vomiting —
COMPLICATIONS slow down the rate of dialysis
1. Peritonitis 2. Hypotension
2. Bleeding 3. Atherosclerosis — MI
3. Leakage 4. Gastric ulcer

When is the feeding of ——-

Saan nilalagay ang new kidney?

Nilalagay sa Iliac region

RENAL TRANSPLANT
Donor: Cadaver, living donor (healthy) tissue
compatible
AV FISTULA
1. No BP monitoring Living donor: Nephrectomy
2. No blood extraction
3. Palpate fro thrill Post Op:
4. Auscultate for bruit • Monitor VS every 15, 30 hour until stable

Transfer Ward:
• Analgesic
• Upon discharge:
> Live a healthy lifestyle
> Monitor kidney function test regularly

Patient: Recipient

During Surgery:
Patient: Supine position
Post Op:
• Monitor VS
• Monitor urine output
• Monitor for acute rejection
> Monitor for s/sx of renal failure
> Monitor for s/sx if infection —> WBC —> destroy foreign tissue
• Prevent Rejection
a. Steroids — suppress WBC function
> Gradual withdrawal in 3-4 months
b. Immunosuppressant drugs:
> Cyclosporine
— for lifetime