Renal Flashcards

1
Q

What do the kidney contain?

A

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

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2
Q

Where are most nephrons found?

A

The outer area of cortex

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3
Q

Where are the juxtamedullary nephrons found?

A

Deeper in the cortex, closer to Medulla

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4
Q

What is the function of nephrons and what are the two major portions?

A

Nephrons are the functioning unit of the kidney

2 major portion:

  1. Renal corpuscle ➡️ glomerulus: located in Bowman’s capsule
  2. Renal tubules
    - proximal convoluted tubule
    - nephron loop
    - distal convoluted tubule
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5
Q

The glomerulus originates from

A

Afferent arteriole ➡️ arriving to glomerulus

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6
Q

How does the kidney flow?

A

Bowman’s capsule ➡️ proximal convoluted tubule ➡️ descending limb ➡️ loop of Henle ➡️ ascending limb ➡️ distal convoluted tubule

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7
Q

Where is most of the filtered water and sodium reabsorbed?

A

Proximal Convoluted Tubule

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8
Q

Controls volume and sodium concentration within the vascular system

Activated when kidneys receive signal of low BP, low renal blood flow, low serum Na

A

Renin – angiotensin – aldosterone system

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9
Q

Renin – angiotensin – aldosterone system

A

Juxtaglomerular apparatus secretes renin

Renin converts angiotensinogen into angiotensin I ➡️ inc peripheral ctx, secretes aldosterone

Angiotensin I is converted to angiotensin II

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10
Q

What are the two main functions of angiotensin II

A

Strong vasoconstriction

Stimulates release of length from the adrenal glands which results in sodium reabsorption by kidney

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11
Q

What is synthesized by the nephrons to control renal perfusion by acting as a potent renal vasodilator?

A

Prostaglandins

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12
Q

What does the kidney do in terms of acid-base balance?

A

Alters absorption and secretion of hydrogen and bicarb ions

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13
Q

if a substance has the ability to except a free H+ ions, it’s a ?

A

Base

The ability to gain or lose an H+ ion determines whether a substance is an acid or a base

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14
Q

What are the two electrolyte imbalances increase H+ concentration?

A

Hypokalemia and hypochloremia

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15
Q

What is renal compensation?

A

Kidneys control pH and HCO3 the blood

Increase bicarb occurs in the proximal tubule when it senses increase H+ ions

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16
Q

What is the kidneys role in red blood cell production?

A

Decreased hematocrit or O2 tension
Produces erythropoietin
Increases red blood cell

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17
Q

What is the active form of vitamin D called?

A

Calciferol

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18
Q

Creatinine normal value

A

0.5-1.1 mg/dL

End product of muscle and protein metabolism

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19
Q

BUN and normal value

A

10-30 mg/dL

Concentration of urea in the blood

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20
Q

Estimation of filtrate that is cleared in the glomerulus

A

Glomerular filtration rate

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21
Q

Refers to kidneys concentrating ability

A

Urine osmolality

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22
Q

What is the difference in kids kidneys?

A

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

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23
Q

Renal system purpose

A
F and E balance
Acid-base balance
Detoxification of blood and waste elimination
Regulates blood pressure
Erythropoietin production
Vit D activation
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24
Q

Two types of fluid compartments

A

Intracellular fluid

Extracellular fluid

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25
Q

Three types of extra cellular fluid

A

Interstitial fluid
Plasma – intravascular
Transcellular water

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26
Q

‼️Normal sodium‼️

A

‼️ 135-145 mEq/L ‼️

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27
Q

The role of sodium

A
Main electrolyte in ECF
Regulates fluid balance
Osmolality
Acid-base balance
Nerve impulse
Muscle contraction
Filtered freely at glomerulus
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28
Q

Causes:
Diarrhea, vomiting/NG suctioning, SIADH, burns, fever

Manifestations:
Seizures, lethargy, cerebral edema, decreased LOC, dyspnea, respiratory failure

A

Hyponatremia

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29
Q

Low sodium levels that are corrected to quickly can result in

A

Osmotic demyelinization syndrome

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30
Q

High sodium levels that are corrected to quickly can result in

A

Cerebral edema

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31
Q

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

A

Hypernatremia

‼️athletes/sport in summer prone to ⬆️Na ‼️

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32
Q

Treatments of hypernatremia

A

Hypotonic saline

Dialysis

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33
Q

‼️ Normal potassium ‼️

A

3.5-5.5 mEq/L

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34
Q

The roles of potassium

A

➡️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

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35
Q

Relationship between serum pH and potassium

A

INVERSE

⬇️ pH = ⬆️ K ‼️ Acidosis = hyperkalemia

⬆️ pH = ⬇️ K ‼️ Alkalosis = hypokalemia

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36
Q

Causes for hypokalemia

A

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

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37
Q

Manifestations of hypokalemia

A
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
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38
Q

Hypokalemia can potentiate the action of

A

Digoxin and lead to dig toxicity

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39
Q

Causes for hyperkalemia

A

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

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40
Q

Manifestations of hyperkalemia

A
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
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41
Q

Managing MILD hyperkalemia

A

Loop diuretic

Correct underlying problems ➡️ manage acidosis

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42
Q

Treatment of moderate to severe hyperkalemia

A

‼️ 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

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43
Q

Why are phosphorus levels higher in younger children?

A

Because of increased rate of skeletal growth

44
Q

‼️ Normal phosphate level ‼️

A

2.5 - 4.5 mEq/L

45
Q

The role of phosphate

A

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

46
Q

Hypophosphatemia causes and manifestations

A

Causes:
Malabsorption
Excessive antacid ingestion

Manifestations:
Irritability
seizures
⬇️ myocardial function 
hemolytic anemia 
premature ectopic beats
47
Q

Hyperphosphatemia Causes and Manifestations

A

Causes:
Renal failure
chemo
tumor lysis syndrome

Manifestations:
Tachycardia 
hyperreflexia 
muscle cramps 
Tetany 
Diarrhea
48
Q

Treatment for hyperphosphatemia

A

Calcium

Dialysis

49
Q

Ionized calcium is

A

Free and not bound to albumin

50
Q

‼️Normal total calcium and ionized calcium level‼️

A

Total calcium= 9-11 mg/dL

ICa= 1.2-1.8 or 4.8-5.2 mg/dL

51
Q

The role of calcium

A

Neuromuscular excitability
CV function
Contributes to coagulation and thrombin formation
Reacts with phosphite to form bone salts

52
Q

Causes for hypocalcemia

A
Vitamin D deficiency 
Renal disease
Diuresis 
Hypoparathyroidism 
pancreatitis 
alkalosis
53
Q

Manifestations of hypocalcemia

A
Depressed cardiac function neuromuscular irritability 
seizures
Tetany
Tingling
Prolonged QT interval
54
Q

Causes for hypercalcemia

A

Acidosis
hyperparathyroidism
prolonged immobilization
malignancies

55
Q

Manifestations of hypercalcemia

A
Muscle weakness 
Lethargy
Coma 
seizures 
anorexia 
nausea, vomiting and constipation
bradycardia 
shortened QT
56
Q

‼️Normal magnesium level‼️

A

1.8-2.3 mEq/L

57
Q

Causes for Hypomagnesemia

A
Diarrhea 
malabsorption 
diuresis 
laxative ingestion 
burns
58
Q

Manifestations of Hypomagnesemia

A
Neuromuscular excitability 
seizures headaches
coma 
respiratory distress 
tachycardia 
PVCs
59
Q

Causes for Hypermagnesemia

A

Renal disease

magnesium administration

60
Q

Manifestations of hypermagnesemia

A
‼️Decreased ability to swallow‼️
Lethargy 
Muscle weakness 
seizures 
decreased gag reflex 
hypotension 
prolonged PRI
Prolonged QRS and QT
61
Q

What is acute renal failure (ARF) or Acute Kidney Injury (AKI)?

A

Sudden decrease or loss of kidney function due to loss of filtration and tubular reabsorption

62
Q

What happens to the kidney on acute renal failure?

A

The kidney can no longer regulate: water and electrolytes
acid-base balance
nitrogenous waste products
hormone release

63
Q

Three types of causes of ARF

A

Prerenal
intrinsic
post renal

64
Q

Prerenal Failure

A

Decreased perfusion
Low urine sodium and high urine osmolality
Ex. Children, dehydration

65
Q

Intrinsic Failure

A

Damage to filtering structures

affects glomerulus or tubules

66
Q

Post renal Failure

A

Usually due to an obstruction

Obstruction causes the GFR to fall due to an increase in pressure

67
Q

Since prerenal failure is due to have a perfusion what gets activated?

A

Renin angiotensin aldosterone system

Therefore, the child’s urine sodium level would be low

68
Q

Pathophysiology to ARF

A

Decreased perfusion
Ischemic cell damage
Damage to nephrons

69
Q

Findings on ARF

A

BUN > 80
Cr > 1.5
Oliguria is often present

70
Q

What type of electrolyte imbalances on ARF patient?

A
Increased ‼️P U M P‼️
⬆️Potassium
⬆️Urea
⬆️Magnesium 
⬆️Phosphorus
Decreased
⬇️Calcium
⬇️Sodium 
⬇️Glucose 
⬇️Bicarb
71
Q

What preventative measure increases the fluid flow and helps the renal tubules avoid obstruction?

A

Diuretics

  • mannitol reduces swelling of the cells
  • furosemide reverses the GFR
72
Q

What type of medications has the highest potential to lead to intrinsic renal failure?

A

Antibiotics and contrast media

73
Q

Obstructed renal tubules from inflamed cells in cellular debris

Can be due to extreme have a perfusion, anoxia, toxins, or obstructions

A

Acute Tubular Necrosis

74
Q

What happens to the glomerular permeability on acute tubular necrosis?

A

⬆️ for protein

⬇️ for potassium

75
Q

Increased glomerular permeability to plasma proteins due to a disturbance in the basement membrane

A

Nephrotic syndrome

76
Q

Three types of nephrotic syndrome

A

Primary
secondary
congenital

77
Q

‼️4 signs of nephrotic syndrome‼️

A

Massive proteinuria
Hypoalbuminemia
Hyperlipidemia
Edema

78
Q

‼️Massive edema in nephrotic syndrome is followed by‼️

A

Massive proteinurea

Hypovolemia - Renin, ADH, aldosterone release

79
Q

Manifestations of nephrotic syndrome

A
Wt gain
Edema
Ascites 
Dark frothy urine - d/t protein
Diarrhea
‼️Muehrcke lines‼️
80
Q

️Muehrcke lines

A

Lines in nail parallel with nail bed

81
Q

Inflammation of glomeruli d/t autoimmune process against strep that causes antigen-antibody complex to become entrapped in the glomerular capillary membrane

A

Acute glomerulonephritis

82
Q

What does the inflammatory damage and occlusion to the glomeruli result in?

A

⬇️ GFR and selective permeability

83
Q

Manifestations of acute glomerulonephritis

A
Hematuria - rusty urine 
Mild proteinurea - low serum albumin
Edema - systemic and periorbital 
HTN
Hypervolemia
Oliguria
84
Q

Management of acute glomerulonephritis

A

‼️monitor and manage complications: CHF and encepalopathy‼️

Manage symptoms

85
Q

Manifestations of ARF

A
Edema
CHF
Plum congestion 
Enlarged liver
Tachycardia from shock or dehydration 
Cardiac arrhythmias
Electrolyte imbalances - ⬆️ PUMP
CNS signs - sz, lethargy
⬇️ or absent UO
86
Q

Goals of treatment: ARF

A
Reduce sx 
Supportive care until renal function returns
Meds - diuretics, low dose dopamine 
Dietary restrictions 
Dialysis if indicated
87
Q

Inability of kidneys to filter and excrete waste

A

Chronic Renal Failure

88
Q

Characteristics of chronic renal failure

A

Azotemia - BUN > 28, Cr > 1.5

Uremia - ⬆️ nitrogenous waste products

89
Q

Why do children with chronic renal failure often experience growth retardation?

A

Calcium depletion affect bone growth

90
Q

Water moves from an area of low particle concentration to high particle concentration

A

Osmosis

91
Q

Particles move from high to low concentration

A

Diffusion

92
Q

Differences in hydrostatic pressure cause water and particles to move

A

Filtration

93
Q

A pressure causes water and particles to move through a membrane

A

Convection

94
Q

Peritoneal dialysis

A

Catheter placed in anterior wall of abdomen

Peritoneal cavity acts as a semi-permeable membrane for water and solute diffusion

95
Q

What is the role of glucose in peritoneal dialysis?

A

Osmotic pressure of glucose draws fluid from vascular space into peritoneum

⬆️ Glucose = ⬆️ Vascularity = ⬆️ fluid off

96
Q

Who is not a candidate of PD?

A

Anyone who has:

  1. Draining abdominal wounds
  2. Respiratory distress
  3. Bowel perforation
97
Q

Complications of PD

A

Peritonitis

Leak around cath

98
Q

Hemodialysis

A

Rapidly removes fluid and wastes

Access:

  1. temporary vascular access: subclavian, IJ
  2. Femoral
99
Q

Who is not a candidate for hemodialysis?

A

Patients with hemodynamic instability:

  • Hypovolemia
  • coagulation disorder
  • vascular access problems
100
Q

‼️ What is seen in disequilibrium syndrome d/t osmotic shift in the brain? ‼️

A
Headache
N/V
Muscle Twitching 
Blurred vision 
Restlessness
101
Q
Proximal Tubular Diuretic 
Osmotic agent
⬆️ GF volume
Slow the re absorption of Na and water at the proximal tubule
Can temporarily ⬆️ intravascular volume
A

Mannitol

102
Q

Carbonic anhydride inhibitor - limits the formation of carbonic acid from CO2 in the proximal cells

Less urinary bicarb is returned to the blood

A

Acetazolamide

103
Q

Block reabsoption of Na and Cl is the distal tubule

Nephron is still able to concentrate urine

Potassium and calcium is lost in urine

A

Thiazides

104
Q

Potassium sparing diuretic

Stop Na reabsoption and potassium secretion in the distal tubule

Can be used in combination with other drugs

A

‼️ Spironolactone ‼️

105
Q

Loop of Henle diuretic
Inhibit NaCl transport in the ascending limb
Increased loss of K, H, Ca

A

Furosemide