Renal Flashcards
What do the kidney contain?
Cortex ➡️ outer layer of kidney
Contains glomeruli and tubular system of the nephron
Medulla ➡️ inner portion
Contains collecting ducts
Pelvis ➡️ upper end of ureter
Divides to form funnel shaped callyses that direct urine from kidneys to ureter
Contains filtered blood that was process into urine
Where are most nephrons found?
The outer area of cortex
Where are the juxtamedullary nephrons found?
Deeper in the cortex, closer to Medulla
What is the function of nephrons and what are the two major portions?
Nephrons are the functioning unit of the kidney
2 major portion:
- Renal corpuscle ➡️ glomerulus: located in Bowman’s capsule
- Renal tubules
- proximal convoluted tubule
- nephron loop
- distal convoluted tubule
The glomerulus originates from
Afferent arteriole ➡️ arriving to glomerulus
How does the kidney flow?
Bowman’s capsule ➡️ proximal convoluted tubule ➡️ descending limb ➡️ loop of Henle ➡️ ascending limb ➡️ distal convoluted tubule
Where is most of the filtered water and sodium reabsorbed?
Proximal Convoluted Tubule
Controls volume and sodium concentration within the vascular system
Activated when kidneys receive signal of low BP, low renal blood flow, low serum Na
Renin – angiotensin – aldosterone system
Renin – angiotensin – aldosterone system
Juxtaglomerular apparatus secretes renin
Renin converts angiotensinogen into angiotensin I ➡️ inc peripheral ctx, secretes aldosterone
Angiotensin I is converted to angiotensin II
What are the two main functions of angiotensin II
Strong vasoconstriction
Stimulates release of length from the adrenal glands which results in sodium reabsorption by kidney
What is synthesized by the nephrons to control renal perfusion by acting as a potent renal vasodilator?
Prostaglandins
What does the kidney do in terms of acid-base balance?
Alters absorption and secretion of hydrogen and bicarb ions
if a substance has the ability to except a free H+ ions, it’s a ?
Base
The ability to gain or lose an H+ ion determines whether a substance is an acid or a base
What are the two electrolyte imbalances increase H+ concentration?
Hypokalemia and hypochloremia
What is renal compensation?
Kidneys control pH and HCO3 the blood
Increase bicarb occurs in the proximal tubule when it senses increase H+ ions
What is the kidneys role in red blood cell production?
Decreased hematocrit or O2 tension
Produces erythropoietin
Increases red blood cell
What is the active form of vitamin D called?
Calciferol
Creatinine normal value
0.5-1.1 mg/dL
End product of muscle and protein metabolism
BUN and normal value
10-30 mg/dL
Concentration of urea in the blood
Estimation of filtrate that is cleared in the glomerulus
Glomerular filtration rate
Refers to kidneys concentrating ability
Urine osmolality
What is the difference in kids kidneys?
Proportionately larger
Renal blood flow and GFR are low at birth and gradually increase as the child develops
Limited ability of the newborn to conserve sodium and excrete excess sodium
Less able to concentrate urine
renal function mature by 1-2 years of age
Renal system purpose
F and E balance Acid-base balance Detoxification of blood and waste elimination Regulates blood pressure Erythropoietin production Vit D activation
Two types of fluid compartments
Intracellular fluid
Extracellular fluid
Three types of extra cellular fluid
Interstitial fluid
Plasma – intravascular
Transcellular water
‼️Normal sodium‼️
‼️ 135-145 mEq/L ‼️
The role of sodium
Main electrolyte in ECF Regulates fluid balance Osmolality Acid-base balance Nerve impulse Muscle contraction Filtered freely at glomerulus
Causes:
Diarrhea, vomiting/NG suctioning, SIADH, burns, fever
Manifestations:
Seizures, lethargy, cerebral edema, decreased LOC, dyspnea, respiratory failure
Hyponatremia
Low sodium levels that are corrected to quickly can result in
Osmotic demyelinization syndrome
High sodium levels that are corrected to quickly can result in
Cerebral edema
Causes:
increased sodium intake, insensible water loss, heat exposure, exercise, DI, diuresis
Manifestations:
Irritability, lethargic, coma, seizures, high pitched cry, flushed skin, muscle weakness, thirst
Hypernatremia
‼️athletes/sport in summer prone to ⬆️Na ‼️
Treatments of hypernatremia
Hypotonic saline
Dialysis
‼️ Normal potassium ‼️
3.5-5.5 mEq/L
The roles of potassium
➡️Mostly intracellular
➡️Responsible for neuromuscular activity and skeletal and cardiac muscles
➡️Renal function is essential
80-90% of intake is excreted by kidneys
The rest is eliminated through bowel and sweat
Relationship between serum pH and potassium
INVERSE
⬇️ pH = ⬆️ K ‼️ Acidosis = hyperkalemia
⬆️ pH = ⬇️ K ‼️ Alkalosis = hypokalemia
Causes for hypokalemia
Not usually related to diet
G.I. fluid loss
Severe diaphoresis
Metabolic alkalosis ➡️ K moves into cell as H+ moves out
Diuretics, corticosteroids, beta adrenergic agonist, Alpha adrenergic antagonist, insulin
Manifestations of hypokalemia
Lethargy Muscle weakness Hypo reflexia Paresthesia PVCs and flattened T waves ➡️ u waves Depressed ST Prolonged PR interval Wake irregular pulse Decreased bowel sounds and constipation
Hypokalemia can potentiate the action of
Digoxin and lead to dig toxicity
Causes for hyperkalemia
Acidosis ➡️ moves K+ out of cell while H+ moves in
Crushing and burn injuries
Medicines: beta adrenergic blockers, potassium sparing diuretics, chemo, ACE inhibitors, NSAID’s
Sickle cell disease
Insulin deficiency
Manifestations of hyperkalemia
Ventricular arrhythmias Peaked T waves Widening QRS Flatten P waves with a prolonged PRI AV conduction delays Muscle weakness Hyperactive reflexes Cramping and diarrhea Paresthesia
Managing MILD hyperkalemia
Loop diuretic
Correct underlying problems ➡️ manage acidosis
Treatment of moderate to severe hyperkalemia
‼️ 1. Calcium chloride or gluconate to manage cardiac effects
‼️ 2. 1-2 ml/kg 25% glucose and 0.1 units/kg regular insulin
‼️ 3. Sodium bicarb to move K+ into cells
‼️ 4. Sodium Ploystyrene sulfonate ➡️ kayexalate
Dialysis
Albuterol moves K+ into the cell and stimulates insulin release
Why are phosphorus levels higher in younger children?
Because of increased rate of skeletal growth
‼️ Normal phosphate level ‼️
2.5 - 4.5 mEq/L
The role of phosphate
3.5-6.5 for children under 5
Body controls phosphate through renal excretion
Vitamin D helps the reabsorption of phosphate and calcium from bone to ECF
Neuromuscular activity
Affect the production of red blood cell and teeth
Hypophosphatemia causes and manifestations
Causes:
Malabsorption
Excessive antacid ingestion
Manifestations: Irritability seizures ⬇️ myocardial function hemolytic anemia premature ectopic beats
Hyperphosphatemia Causes and Manifestations
Causes:
Renal failure
chemo
tumor lysis syndrome
Manifestations: Tachycardia hyperreflexia muscle cramps Tetany Diarrhea
Treatment for hyperphosphatemia
Calcium
Dialysis
Ionized calcium is
Free and not bound to albumin
‼️Normal total calcium and ionized calcium level‼️
Total calcium= 9-11 mg/dL
ICa= 1.2-1.8 or 4.8-5.2 mg/dL
The role of calcium
Neuromuscular excitability
CV function
Contributes to coagulation and thrombin formation
Reacts with phosphite to form bone salts
Causes for hypocalcemia
Vitamin D deficiency Renal disease Diuresis Hypoparathyroidism pancreatitis alkalosis
Manifestations of hypocalcemia
Depressed cardiac function neuromuscular irritability seizures Tetany Tingling Prolonged QT interval
Causes for hypercalcemia
Acidosis
hyperparathyroidism
prolonged immobilization
malignancies
Manifestations of hypercalcemia
Muscle weakness Lethargy Coma seizures anorexia nausea, vomiting and constipation bradycardia shortened QT
‼️Normal magnesium level‼️
1.8-2.3 mEq/L
Causes for Hypomagnesemia
Diarrhea malabsorption diuresis laxative ingestion burns
Manifestations of Hypomagnesemia
Neuromuscular excitability seizures headaches coma respiratory distress tachycardia PVCs
Causes for Hypermagnesemia
Renal disease
magnesium administration
Manifestations of hypermagnesemia
‼️Decreased ability to swallow‼️ Lethargy Muscle weakness seizures decreased gag reflex hypotension prolonged PRI Prolonged QRS and QT
What is acute renal failure (ARF) or Acute Kidney Injury (AKI)?
Sudden decrease or loss of kidney function due to loss of filtration and tubular reabsorption
What happens to the kidney on acute renal failure?
The kidney can no longer regulate: water and electrolytes
acid-base balance
nitrogenous waste products
hormone release
Three types of causes of ARF
Prerenal
intrinsic
post renal
Prerenal Failure
Decreased perfusion
Low urine sodium and high urine osmolality
Ex. Children, dehydration
Intrinsic Failure
Damage to filtering structures
affects glomerulus or tubules
Post renal Failure
Usually due to an obstruction
Obstruction causes the GFR to fall due to an increase in pressure
Since prerenal failure is due to have a perfusion what gets activated?
Renin angiotensin aldosterone system
Therefore, the child’s urine sodium level would be low
Pathophysiology to ARF
Decreased perfusion
Ischemic cell damage
Damage to nephrons
Findings on ARF
BUN > 80
Cr > 1.5
Oliguria is often present
What type of electrolyte imbalances on ARF patient?
Increased ‼️P U M P‼️ ⬆️Potassium ⬆️Urea ⬆️Magnesium ⬆️Phosphorus
Decreased ⬇️Calcium ⬇️Sodium ⬇️Glucose ⬇️Bicarb
What preventative measure increases the fluid flow and helps the renal tubules avoid obstruction?
Diuretics
- mannitol reduces swelling of the cells
- furosemide reverses the GFR
What type of medications has the highest potential to lead to intrinsic renal failure?
Antibiotics and contrast media
Obstructed renal tubules from inflamed cells in cellular debris
Can be due to extreme have a perfusion, anoxia, toxins, or obstructions
Acute Tubular Necrosis
What happens to the glomerular permeability on acute tubular necrosis?
⬆️ for protein
⬇️ for potassium
Increased glomerular permeability to plasma proteins due to a disturbance in the basement membrane
Nephrotic syndrome
Three types of nephrotic syndrome
Primary
secondary
congenital
‼️4 signs of nephrotic syndrome‼️
Massive proteinuria
Hypoalbuminemia
Hyperlipidemia
Edema
‼️Massive edema in nephrotic syndrome is followed by‼️
Massive proteinurea
Hypovolemia - Renin, ADH, aldosterone release
Manifestations of nephrotic syndrome
Wt gain Edema Ascites Dark frothy urine - d/t protein Diarrhea ‼️Muehrcke lines‼️
️Muehrcke lines
Lines in nail parallel with nail bed
Inflammation of glomeruli d/t autoimmune process against strep that causes antigen-antibody complex to become entrapped in the glomerular capillary membrane
Acute glomerulonephritis
What does the inflammatory damage and occlusion to the glomeruli result in?
⬇️ GFR and selective permeability
Manifestations of acute glomerulonephritis
Hematuria - rusty urine Mild proteinurea - low serum albumin Edema - systemic and periorbital HTN Hypervolemia Oliguria
Management of acute glomerulonephritis
‼️monitor and manage complications: CHF and encepalopathy‼️
Manage symptoms
Manifestations of ARF
Edema CHF Plum congestion Enlarged liver Tachycardia from shock or dehydration Cardiac arrhythmias Electrolyte imbalances - ⬆️ PUMP CNS signs - sz, lethargy ⬇️ or absent UO
Goals of treatment: ARF
Reduce sx Supportive care until renal function returns Meds - diuretics, low dose dopamine Dietary restrictions Dialysis if indicated
Inability of kidneys to filter and excrete waste
Chronic Renal Failure
Characteristics of chronic renal failure
Azotemia - BUN > 28, Cr > 1.5
Uremia - ⬆️ nitrogenous waste products
Why do children with chronic renal failure often experience growth retardation?
Calcium depletion affect bone growth
Water moves from an area of low particle concentration to high particle concentration
Osmosis
Particles move from high to low concentration
Diffusion
Differences in hydrostatic pressure cause water and particles to move
Filtration
A pressure causes water and particles to move through a membrane
Convection
Peritoneal dialysis
Catheter placed in anterior wall of abdomen
Peritoneal cavity acts as a semi-permeable membrane for water and solute diffusion
What is the role of glucose in peritoneal dialysis?
Osmotic pressure of glucose draws fluid from vascular space into peritoneum
⬆️ Glucose = ⬆️ Vascularity = ⬆️ fluid off
Who is not a candidate of PD?
Anyone who has:
- Draining abdominal wounds
- Respiratory distress
- Bowel perforation
Complications of PD
Peritonitis
Leak around cath
Hemodialysis
Rapidly removes fluid and wastes
Access:
- temporary vascular access: subclavian, IJ
- Femoral
Who is not a candidate for hemodialysis?
Patients with hemodynamic instability:
- Hypovolemia
- coagulation disorder
- vascular access problems
‼️ What is seen in disequilibrium syndrome d/t osmotic shift in the brain? ‼️
Headache N/V Muscle Twitching Blurred vision Restlessness
Proximal Tubular Diuretic Osmotic agent ⬆️ GF volume Slow the re absorption of Na and water at the proximal tubule Can temporarily ⬆️ intravascular volume
Mannitol
Carbonic anhydride inhibitor - limits the formation of carbonic acid from CO2 in the proximal cells
Less urinary bicarb is returned to the blood
Acetazolamide
Block reabsoption of Na and Cl is the distal tubule
Nephron is still able to concentrate urine
Potassium and calcium is lost in urine
Thiazides
Potassium sparing diuretic
Stop Na reabsoption and potassium secretion in the distal tubule
Can be used in combination with other drugs
‼️ Spironolactone ‼️
Loop of Henle diuretic
Inhibit NaCl transport in the ascending limb
Increased loss of K, H, Ca
Furosemide
