Hypermagnesemia Marami depressant (Down symptoms) Altered LOC (Stupor, Obtunded, Lethargy, Coma) Deep tendon reflexes: Decreased, hyporeflexia Muscle weakness
Renal Fabs
Sodium:
- Purpose: Most important electrolyte of the brain.
- Stimulant of the brain
- Hangovers are most likely related to hyponatremia.
- Related to water balance because sodium attracts your
water.
Potassium
- Most important electrolyte of the heart
- Promotes your neuromuscular contractility
- Hyperkalemia: Overworking of the heart
- It could lead to the possibility of cardiac arrest
Chloride
- Has the same function as sodium
- Not really a priority. Calcium
- For the bones and teeth
- Significantly for the: neuromuscular contractility
- Muscles are related to the calcium
- Hypocalcemia: muscles will not contract
- Indirectly related to phosphate Magnesium
- Depressant
- OD: Pre-eclampsia
- Preeclampsia has a risk for seizures so we can use
magnesium to prevent it. - Magnesium sulfate toxicity must be monitored.
- Symptoms:
- Antidote:
- Calcium gluconate: Antagonist - Calcium decreases your magnesium
levels
Hypomagnesemia Konti depressant (Up
Symptoms)
Altered LOC (Confusion, Irritability)
Deep tendon reflexes:
Increased, hyperreflexia Seizures, Muscles cramps, Tremors
Insomnia, Increased RR HR Drowsiness, Decreased HR
RR BP Cause: Magnesium sulfate toxicity, renal failure (down glomerular filtration rate): increased waste and fluids
Cause: Alcoholism, decreased intake in the diet Magnesium in diet: Fiber, grains, legumes, spinach, nuts. MGT: Least to most invasive
- Oral magnesium rich
- Decreased tendon reflexes - Heart rate RRBP: Decreased - Urine output: Decreased
foods - Oral magnesium
supplements
MGT: Magnesium is eliminated via saline diuresis (urination), we can give diuretics and replace lost fluid via IV fluid
If magnesium is critically low: Intravenous
Observe magnesium sulfate toxicity
Hyperkalemia:
- Most important electrolyte in the heart.
- Cause metabolic acidosis
- “The body CARED too much about K+” - Hyperkalemia, Hypernatremia,
Hypocalcemia, Hyperphosphatemia,
Hypermagnesemia
- Excessive potassium intake
- Increased fluid or supplement
- Drugs:
- Potassium sparing drugs
- Spironolactone - ACE inhibitors
- Lisinopril - Captopril
- NSAIDs
- Take with food because
they are gastric irritants
Renal failure: decreased functional nephrons: diuretics are no longer effective (Dialysis)
Antidote to hypermagnesemia: Calcium gluconate, will be given via IV
- Cellular movement of K+ from intracellular to extracellular (burns, tissue damage, etc)
- Signs and symptoms of Hyperkalemia “MURDER”
- The potassium goes out of the cell to the
blood. The sodium goes in to the cells - Burns: HYPERkalemia
- Muscle weakness
- Too much contraction weakens the
muscle.
- Sodium: HYPOnatremia
- Urine output little or none (renal failure) - Respiratory failure  (due to muscle weakness)
- Adrenal insufficiency with Addison’s disease - Addison’s disease: Decreased
- Strongest respiratory muscle:
Diaphragm - It may cause cardiac arrest
aldosterone levels (Aldosterone: promotes water and sodium retention)
- Decreased aldosterone: decreased
- Decreased cardiac contractility
sodium leading to HYPOnatremia, leading to HYPERkalemia
- Weak pulse or Low HR
- Early: muscle twitches and cramps
- Renal failure: Decreased filtration rate
- Early signs and symptoms causes
cramps but if late, it gets tired and leads
to muscle weakness
- Increased electrolytes because blood
cannot be filtered
- Rhythm changes
- Tall peaked T waves, prolonged PR
interval
- Management of critical hyperkalemia
- Low potassium in the diet
- Initial management:
- Potassium wasting diuretics - Loop diuretics
- 10% Calcium gluconate: protects
myocardium - Not related to potassium
- Thiazide diuretics (Microcide)
- Fastest way to decrease your potassium
HYPOKALEMIA
- Causes
- Glucose insulin: stimulate uptake of
glucose with potassium
“Your body is trying to DITCH K+”
- Drugs:
- Insulin (Through IV)
- Given for the
hyperkalemia
- Correct metabolic acidosis to lower
plasma K+
- Renal failure: Metabolic acidosis - Usually VIA IV drips
- Via Enema or oral - Sodium rich - Sodium potassium exchange
- Loop diuretics : Wasting
- Furosemide
- Laxatives: Wasting
- Inadequate consumption of K+ - Too much water intake - Cushing’s syndrome
- Endocrine problem - Increased aldosterone
- Heavy fluid loss
- Nasogastric tube suction - Vomiting - Diarrhea - Wound drainage
- Asymptomatic: Late nadedetect - 7Ls (7 Lows)
- Failure in muscle
- Side effect of insulin:
HYPOGLYCEMIA - Therefore giving glucose to the
patient to counteract the side
effect of the insulin - For DM Type I: Insulin with
Potassium because side effect of
insulin in patients with DM is
hypokalemia.
- Increased sodium - HYPERnatremia causing
HYPOkalemia
- Sodium bicarbonate (Alkaline in nature)
- Metabolic acidosis: Increased
potassium
- Signs and symptoms
- Kayexelate
- Lethargic - Low shallow respirations…failure
- Potassium restriction
- Lethal Cardiac dysrhythmias
- ST depression - Shallow T wave - Projecting U wave
- Has a stimulant effect - Signs and Symptoms of Hypernatremia
- Earliest symptom of
Hypokalemia - But cannot be seen by
the naked eye - Needs ECG
- Usually caused by dehydration - FRIED SALT
- Lots of urine (Frequent and large
amount)
- Flushed skin and fever (low grade) - Restless, irritable, anxious and confused
(Up symptoms) - Increased blood pressure and fluid
retention - Edema, peripheral and pitting
- Problems with fluid loss
- Third spacing (Fluid entered
interstitial space)
- Leg cramps - Limp muscles - Low blood pressure (Severe)
- Decreased urine output
- Management
- Decreased contractility of heart
- Can be related to dehydration,
decreased urine output because
it is conserving fluid
concentration in the blood
- IV potassium replacement
- Not more than 10-20 mEq/hr - Critically low - Incorporated: mix with IV fluid - But if doctor’s order is more than 20, it is
required to have Cardiac monitor and
infusion pump
- Skin flushed - Agitation - Low grade fever - Thirst
- Management:
- High potassium diet - Oral potassium replacement
- I/O : Watch out for fluid volume deficit - Urine specific gravity:
- For stable patients - It should be given with juice to increase
palatability
concentration of the urine (NV: 1.010-1.030)
- Dehydrated: Concentrated:
- Monitor cardiac rhythm
Higher SG (>1.025) “Mabigat” - Neck veins: Flat - Weak and thready pulses - Increased HR and RR
SODIUM
- Sodium is the most important electrolyte of the brain
- Altered LOC (Up symptoms)
- Anxious
- Seizures/Headache
- Weight
- Most sensitive indicator of fluid
volume - In case of hypernatremia, there
will be weight loss
- Dry Mouth/Mucosa
- Poor skin turgor
- Via diuresis with replacement of fluid - Low sodium diet
- Canned food - Condiments - Instant foods, processed food
- Nausea and vomiting - Decreased stimulant
- Related to severe sodium losses
- Abdominal discomfort related to nausea
and vomiting
- Related to overhydration - Diluted sodium - I/O: Monitor for overhydration - Specific gravity: <1.010 urine is diluted
“Magaan” - Bounding pulses - Distended neck veins - BP: Increased BP, HRRR: Increased
(Vascular resistance) - Altered LOC: Down symptoms
- Weight gain because of overhydrated status
- Sodium tablet - 0.9 NaCl PNSS - Electrolyte drinks
- Stomach cramping
- Management of Hyponatremia
- How do we remove sodium?
- HYPONATREMIA
- Down symptoms - “SALTLOSS” - Stupor - Anorexia
- Lethargy - Tendon Reflexes - Limp Muscles - Orthostatic Hypotension
CALCIUM
- Drop in DP - With respect with rapid change in
position - There will be dizziness and risk for falls - Management:
HYPERCALCEMIA “BACKME”
- Bone pain
- Arrhythmias
- Cardiac arrest
- Kidney stones
- Muscle weakness
- Change position slowly, sit at the
bed side
- Late symptom of late hypercalcemia
because of the increased contractility
- Excessive urination
- Hydration to 3000 to 4000 mL to
flush calcium and to decreased
renal calculi formation
- Osmotic diuresis - With the effort to remove the calcium
- Parathormone (Katabi ng thyroid)
- Synthetic calcitonin can be given to
lower calcium levels
- Promote calcium balance - Promotes bone decalcification or bone
resorption (Sisirain ang buto para lumabas ang
calcium from the bone to the blood) - Calcitonin: from thyroid
- Monitor I and O, vital signs,
muscle weakness and heart rate
and rhythm
- Calcitonin:
HYPOCALCEMIA
- Signs and symptoms: “CATS”
- Promotes calcium uptake of the bone (Pinapapasok si calcium sa boto)
- Calcitonin and Parathormone has opposite
effect
- Increased parathormone
- That may lead to kidney stones - Increased contractility of the
heart, causing overworking of the
heart that will cause
ARRHYTHMIAS that would lead
to Cardiac Heart
- Weak brittle bones - Prone to pathologic fracture
- Promote calcium excretion via the urine - Loop diuretic
- Furosemide - Ethacrynic acid
- To promote calcium from the
blood to the bone
- Convulsions
- Can lead to cerebral edema - Decreased contractility - Increased ICP
- Arrhythmias
- Decreased calcium leads to decreased
contractility of the heart
- Tetany
- Numbness and stiffness of the muscles
due to loss of ability to contract
- Stridor and Spams
- Weakness of diaphragm
- Related to accidental removal of parathyroid
(Post thyroidectomy) - Unexpected - Hypocalcemia is lifetime - Malpractice of the doctor
- Hyperparathryoidism (Tumor)
- Increased bone decalcification - Increased calcium in the blood - Hypercalcemia
- Hypoparathyroidism
- Nursing Management for Hypercalcemia
- Calcium is for contractility
- Trousseau’s sign : Severe
- Possible mapagod si
heart if dumami si
calcium bigla
- Induction of carpopedal spasms by inflation of a
sphygmomanometer above SBP for 3 minutes - Response:
- Other Management
- Carpopedal spasms characterized by
- IV: Main - High calcium diet of the
filipinos (Sardines) - High calcium diet of the
world (Anchovies) - Vitamin D Supplements
- Chvotek’s sign
- Adduction of thumb - Flexion of metacarpophalangeal
joints - Extension of interphalangeal
joints - Flexion of the wrist
- Promotes calcium
absorption
- Contraction of the ipsilateral facial muscle
elicited by tapping the facial nerve just anterior
to the ear - Response:
KIDNEYS Mnemonic for functions “WET BREAD”
Management
- Twitching of the lip to spasm of all facial
muscles
- Vesicant solution
- Irritating to the vein causing
extravasation (Nasunog ang
ugat) - Can lead to Phlebitis - Management: Use bigger veins
Function of the kidney
Renal Failure
Water Balance
Hypervolemia : it can cause cerebral edema, congestive heart failure, portal hypertension, pulmonary hypertension
- Nursing management for Hypocalcemia
- IV: Calcium gluconate
Fluid restriction (1 to 1.5 L/day)
Diet: Low sodium diet
Diuretics : for acute renal failure, reversible, high percentage of functioning nephrons Chronic renal failure:
- More blood, better
dilution
- Bleeding gums and mucosa
- Calcium is related to your
clotting factors
- Watch out for: Cardiac Monitor
Electrolyte balance
Hypernatremia
Irreversible, decreased functioning of nephrons, diuretics are no long effective
Blood pressure control
Altered LOC: Different focusing, seizures, coma
Uremic Frosts (Acid): Itchy skin
Renal Encephalopathy: Safety is priority
Calamine lotions, antihistamines, oatmeal bath, cocoa butter lotions, cut fingernails short, sodium bicarbonate
Dialysis Calcium channel blockers Betablockers
Toxin Removal Urea (Ntirogen - byproduct of protein)
Hyperkalemia
Restrict Na in the diet
Insulin with glucose Sodium bicarbonate can be given
Phosphate binders to decrease phosphate (Ex. Alum hydroxide, Antacids)
Calcium gluconate: Severe cases Low protein source from high biologic source : Low nitrogen byproduct, white meat, Poultry, Dairy, Tofu
RAAS system: Renin and angiotensin aldosterone system
Aldosterone: sodium and water retention
Hypertension because of fluid volume excess
ACE inhibitors- causes hyperkalemia ARBS: Angiotensin receptor blockers (Sartans): Prevents aldosterone formation: Decreased Sodium and water retention
Hypocalcemia, Hyperphosphatem ia
Increased aldosterone: hypernatremia and hypervolemia
Hypermagnesemi a
Urea build up (Uremia) Nitrogen build up (Azotemia)
Urea build up: can cause renal encephalopathy:
Erythropoietin :
Decreased
Synthetic
Stimulates RBC production
erythropoietin: Decreased RBC production (Decrease oxygenation, easy fatigability, activity intolerance)
Hyperkalemia causes metabolic acidosis : Cardiac arrest
Hypocalcemia : Hyperphosphatem ia
erythropoietin : stimulates RBC production
Intrarenal failure: Inside the kidneys Nephron, glomerular, tubular damage : Decreased filtration rate, decreased urine production
Hypertension DM: decreased blood flow because viscous
Glomerulonephritis, nephrotoxic drugs, dye/contrast medium: Tubular necrosis (Tissue death) Tubular sclerosis (Tissue scarring)
> Renal calculi > Benign prostatic hyperplasia > Bladder cancer > Bladder failure
Acid balance
Sodium bicarbonate drip
D- Vitamin D : promotes absorption of calcium
Vitamin D supplements
Post renal failure (After the kidneys), with urine production but OBSTRUCTED
Causes:
- Acute renal failure
- High reversible in nature - Goal: to preserve kidney functioning
- Acute renal failure would cause chronic renal failure
- Chronic renal failure: Irreversible
Examples Decreased cardiac output or
related to heart future Hemorrhage Sepsis
Stages of Chronic Kidney Disease
- Stage 1: Kidney damage with normal or increased
EGFR
- Normal EGFR: 90 to 125mL/min
- Stage 2: Mild
- Weakness - Nausea and vomitin
- Stage 3: Moderate - Stage 4: Severe - Stage 5: Kidney failure
Renal transplant: High risk for rejection
- By the immune system
Causes of Renal Failure Prerenal failure (before the kidneys), decreased perfusion status - decreased filtration status - little to none urine production
Uses dialyzer to filter blood and remove waste (More efficient)
Access points: AV fistula (takes 3 months to be prepared), if not yet available, intrajugular catheter
For severe cases with decreased renal functioning
AV fistula care: Keep it clean and dry, avoid BP taking, phlebotomy, at the affected site
Check patency: Present bruit > (Aucultate: Whooshing sound) and thrill (palpate : machine like vibrations)
Prio complication: Disequilibrium syndrome
WHAT: It offers you cerebral edema - increased ICP - Altered LOC, BP decreased, HRRR increased, possible for coma and seizures WHY:Rapid removal of nitrogen waste related to
Dialysate: high in glucose that would cause hyperglycemic, hyperosmolar ultrafiltration Access point: Peritoneum (Between umbilicus and suprapubic area)
(More accessible) For young, milder cases, ambulatory with high renal functioning Dialysate: rich in glucose, watch out for hyperglycemia
Prio complication: Peritonitis
Clinical symptoms: Rigid boardlike abdomen, fever, increased HR RR Why? Dialysate -Rich in glucose - attracts infection
Management: Report, medical emergency, it may
- Management: immunosuppressants
- Ex. Azathioprine, steroids, cyclosporine - High risk for infection
- Symptom of kidney rejection
- Oliguria - Flank pain - Renal encephalopathy
DIALYSIS
- Hemodialysis
- Dialyzer serves as the kidney
- Peritoneal
- Dialysate : high in glucose - Osmosis: from lower to higher concentration
-
Hemodialysis Vs. Peritoneal dialysis
Hemodialysis
Peritoneal dialysis
rapid rate of HD Management: Stop, report
lead to septic shock Patient home based Teach sterile technique Peritoneum: risk of bowel perforation
- Decreased albumin, down oncotic pressure,
third spacing (Edema, Ascites, Anasarca) - Cause:
- Infections
AV Fistula: Large blood vessels, high chance of bleeding WOF: Muscle cramps. That is caused by rapid removal of fluid and sodium
Management: administer fluid and sodium (PNSS)
- Post GABS (Group A Beta
hemolytic Strep) : history of strep
throat infection or rarely impetigo - Bacterial endocarditis - Viral:HIV hepa B, Hepa C
- Autoimmune disorders
- SLE: Systemic lupus
erythematosus
- Systemic inflammation
- Good pasture’s syndrome
GLOMERULONEPHRITIS
- Inflammation of glomerulus inside the nephron
- Usually caused by Staphylococcus spp.
- Decreased EGFR: will cause increased fluid and waste
- Mimics pneumonia,
causes bleeding in the
lungs or glomerulus - With secretions
- IgA nephropathy
- Acute renal failure (Irreversible) - Long term, it will lead to chronic renal failure
- D/T recurrent episodes of
blood in the urine, can be
asymptomatic for years - Beurger’s disease:
cola-colored urine :
hematuria
- Headache and lethargy: renal encephalopathy
(increased urea)
- Urea: highly toxic to your brain
- Hypertension and Edema
- Other conditions
- Related to fluid retention
- High BP - Diabetic nephropathy - Focal segmental
glomerulosclerosis: scattered
scarring of glomeruli either
pathologic or idiopathic
- Fever
- Related to inflammatory responses
- Proteinuria
- Intraproblem
- Diagnostics:
- Urine: presence of RBCs, red cell casts,
WBCs, elevated creatinine and urea - Blood tests: Elevated BUN and
Creatinine - Kidney UTz, Xray, CT scan - Kidney biopsy
- Treatment
- General goal is to treat underlying cause
and preserve kidney function - To prevent the progression to chronic
renal failure - For GABS
- Collection of symptoms - Nephritic syndrome:
- Might improve without treatment, antibiotics can also be used
- Inflammation of the glomerulus - HIHO
- For autoimmune DO
- Corticosteroid or
immunosuppressants
- HTN - Inflammation of glomerulus - Hematuria - Oliguria
- For DM
- Blood sugar control via insulin or
OHA
- Nephrotic syndrome
- For hypertension
- Hypoalbuminemia: oncotic pressure problem >
Third spacing,
- Sodium restriction and loop
diuretics
- Ascites
- Dietary protein and potassium restriction
for BUN elevation, carbohydrates given
liberally - Fluid balance is utmost priority
- Hyperlipidemia
- Cholesterol - Oh my god! Ang taas ng cholesterol! - Oil or Olesterol
- Proteinuria
NEPHROTIC VS NEPHRITIC SYNDROME
- Foamy urine
- OEdema
- Weight gain - Periorbital
- Blood tests for albumin, cholesterol and
trigly - Kidney biopsy
- Causes of nephrotic syndrome
- DM - Chronic GN - SLE - Multiple myeloma
- Cancer of the plasma - Causes an abnormal globulins
- Amyloidosis of the kidneys
- Accumulation of amyloid proteins
in the kidney
- Renal vein thrombosis
- Emboli formation
- Infections (HIV, Hepa B and C, Malaria)
- Blood clots: due to poor filtration that
leads to loss of protein needed to
prevent clotting
- Aspirin or anticoagulants
- High BP and triglycerides: loss of
albumin stimulates liver to produce
albumin and produce cholesterol and
trigly consequently - Poor nutrition - Acute kidney injury - Chronic kidney disease - Higher risk of infection
- Urine test for albumin levels: Low,
hypoalbuminemia
- Management
Nephritic Syndrome
- Inflammation of glomerulus
- Down GFR
- Acute
- Major cause of Beurger’s disease
- Diagnostics
- Kidney biopsy
- Treatment
- Bed rest
- Complications
- Objective is to preserve renal function
and prevent complications
- Diuretics , ACE inhibitors, ARBS : To
decrease BP
- Antineoplastics : Multiple myeloma
- Immunosuppressants : Autoimmune
disorders
- Corticosteroid: Autoimmune disorders - Blood thinners: Prevents risk of clots - Low sodium diet
- Dietary restrictions of protein and
cholesterol
- Urine tests for hematuria, dark colored urine - Blood tests for uremia or azotemia
- Uremia: increased urea in the blood - Azotemia: increased nitrogen in the
blood
- Diagnostics
- A diet that is restricted in salt, potassium and
fluid - Medication to control BP - Medication to reduce inflammation - Medication to remove fluids from the body - Dialysis to replace kidney function in severe
cases
- Manageable
- Management
- Alpha blockers: relax bladder neck
muscles and muscle fibers of prostate,
making urination easier
Benign Prostatic Hyperplasia
- FUN-WISE
- Irritative symptoms
- Examples: alfuzosin, doxazosin,
tamsulosin, and silodosin - Side effects: dizziness and
harmless condition in which
semen goes back into the
bladder instead out of the tip of
the penis (Retrograde
ejaculation)
- Frequency - Urgency - Nocturia
- Priority is safety
- Obstructive symptoms
- 5-alpha reductase inhibitors
- Weak stream - Intermittency - Straining - Emptying incomplete
- Postrenal failure - Increased frequency and urgency to void
- Digital Rectal Exam
- PSA
- Shrink your prostate by
preventing hormonal changes
that cause prostate growth - Examples: Finasteride and
dutasteride - Side effect: Retrograde
ejaculation
- Tadalafil
- Studies suggest this medication - Often used to treat erectile
dysfunction - Can also treat prostate
enlargement - Sildenafil: Purpose: Vasodilator
- To decrease BP - SE: Penis erection - WOF: Hypotension
- Prostate gland: produces glucose and fluid for the
sperm to survive - Aging men: decreased sexual practice - BPH: causes obstruction of urine
- Diagnostics
- 1 finger, gloved with lubricant - Poc: left side lying, with knees
flexed/Sim lateral position, straighten the
colon
- Surgical procedures: Prostatectomy - Flush out clots and electrolytes
- TURP: Transurethral resection of
prostate gland (No incision)
- Normal within 24 hours
- Faster recovery - Risk for bladder clots and
bleeding
- Pinkish red because there is still
bleeding  (Increased flow rate)
- Normal after 24 to 48 hrs
- Clear na dapat (Decreased flow rate)
- Perform cystoclysis/
continuous bladder
irrigation
- Radical prostatectomy
- With incision - Via the rectum - Slower recovery
Cystoclysis
- Three way foley catheter
- Inflow port - Outflow port - Anchor
- Urobag:
- Below the bladder because it works via gravity
- Solution
- Ideally PNSS (with sodium)
- Equal concentration with bladder as
bladder has sodium - Prevents water toxicity - No osmosis (no movement of water)
- If distilled water, without sodium (Lower conc)
- There will be osmosis - Promotes water toxicity
- Priority
- Patent system
