Renal CN Flashcards

1
Q

Polyuria

A
>2.5 L urine/day
Causes:
- diabetes mellitus
- diabetes insipidus
- excess caffeine or alcohol
- kidney disease
- certain drugs such as diuretics
- sickle cell anemia 
-excessive water intake

usually associated with polydipsia (increased thirst)

four mechanisms of cause:

  1. increased intake of fluids as in psychogenic causes, stress, and anxiety
  2. increased GFR as in hyperthyroidism, fever, hypermetabolic states
  3. increased output of solutes as occurs in DM, hyperthyroidism, use of diuretics (present more solute at the DCT)
  4. inability of kidney to reabsorb water in DCT as in CDI, NDI, drugs, and chronic renal failure
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2
Q

Oliguria

A
Output below the minimum volume (300-500 mL/day)
Causes:
-dehydration
- blood loss
- diarrhea
- cardiogenic shock
- kidney disease
- enlarged prostate
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3
Q

Anuria

A

virtual absence of urine production (< 50 mL/day)
Causes:
- kidney failure
-obstruction: such as kidney stone or tumor
- enlarged prostate

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4
Q

Water diuresis

A

increased water excretion without corresponding increase in salt excretion
-primary cause: increased water intake, polydipsia, diabetes insipidus

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5
Q

Solute (osmotic) diuresis

A

increased water excretion with a concurrent increase in salt excretion

  • Primary cause: significant increase in the salt present in the tubular fluid
  • -> i.v. NaCl
  • -> hyperglycemia
  • -> high protein intake
  • -> recovery from Acute Kidney Injury (AKI)
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6
Q

Edema

A

Causes
1. Alteration in capillary hemodynamics (altered Staling Forces with increased net filtration pressure)- fluid moves from vascular space into interstitium
- edema not palpable until ISV increased by 2.5-3.0 L. Normal plasma volume is 3L
- edema fluid is not derived only from plasma
- compensatory renal retention of Na+ and H2O to maintain plasma volume in response to under filling of vasculature must occur in this situation to cause edema
Ex: congestive heart failure

  1. Renal retention of dietary Na+ and H2O expansion of ECF volume
    - inappropriate renal fluid retention
    - usually results in elevated blood pressure, expanded plasma and ISV
    - E.g. primary renal disease ( glomerulonephritis, nephrotic syndrome)
    —non-pitting edema- swollen cells due to increased ICF volume
    — pitting-edema - increased ISV
    — edema often treated with diuretics
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7
Q

Dextrose 5% in water (D5W)

A
-Isotonic
Uses: 
- fluid loss
- dehydration
-hypernatraemia

Gets into the intracellular space mostly then interstitial and lymphatic and least into the plasma volume

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8
Q

0.9% Sodium Chloride

A
Isotonic 
Uses
- Shock 
- Hyponatraemia
- blood transfusion
- resuscitation
- fluid challenges 
-DKA

Gets into the interstitial and laymphatic spaces mostly and plasma minorly

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9
Q

Lactated Ringer’s (Hartmanns)

A
Isotonic
Uses 
- dehydration
- burns
- Lower GI fluid loss
- Acute fluid loss
- hypovolemia due to third spacing
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10
Q

Dehydration

A
  • occurs due to decreased water intake, increased fluid loss, or both
  • elderly people: impaired thirst sensation, chronic illness, fever and sickness are common reasons for decreased water intake
  • increased fluid loss: from vomiting, diarrhea, diuresis and sweating
  • working in hot water without replacement
  • can either be hypernatremic or hyponatremic
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11
Q

Hyponatremic (hypotonic) Dehydration

A
  • loss of sodium is greater than the loss of water in ECF
  • serum sodium conc. In the ICF is greater than that of the ECF
  • Water shifts from ECF to ICF to establish osmotic equilibrium causing cells to swell and hypovolemia
  • Serum sodium and osmolality will be les than the normal range (130-135 mEq/L)
  • increased ICF causes edema, brain cell swelling, irritability, depression, confusion, weakness, muscle crams, anorexia, nausea, and diarrhea
  • pure sodium deficits cause hypotension, tachycardia, and decreased urine output
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12
Q

Hypernatremic (Hypertonic) Dehydration

A
  • loss of water is greater than the loss of sodium in ECF
  • serum sodium concentration in the ECF is greater than the ICF, water shifts from the ICF to the ECF
  • serum osmolarity will exceed 300 mOsm/kg
  • serum sodium will be more than 150 mEq/L
  • causing intracellular dehydration including shrinkage of brain cells
  • excess extracellular fluid causes edema and increased BP
  • high Sodium level causes muscular weakness and hyperactive reflexes
  • decreased ICF causes thirst, decreased urine output, confusion, and ultimately coma
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13
Q

Isosmotic volume contraction

A
  • Acute fluid loss conditions like hemorrhage, diarrhea and vomiting
  • diarrhea causes loss of isosmotic fluid from the GI tract
  • decrease in ECF volume and no change in body osmolality and ICF volume
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14
Q

Hyperosmotic Volume Contraction

A
  • Hypotonic fluid loss conditions like dehydration, diabetes insipidus, and alcoholism
  • insensible water loss from ECF, solute is left behind and becomes concentrated
  • decrease in ECF volume and ICF volume, but an increase in body osmolarity
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15
Q

Hyposmotic volume contraction

A
  • ICF volume increases, ECF volume decreases, osmolarity decreases
  • adrenal insufficiency due to loss of aldosterone leading to excessive loss of NaCl in urine
  • transient response: ECF osmolarity decreases and fluid shifts to ICF until osmolarity equilibrates
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16
Q

Isotonic Volume expansion

A
  • infusion of 0.9% NaCl
  • ECF increases
  • ICF remains constant
  • Osmolarity remains constant
17
Q

Hypertonic Volume Expansion

A
  • causes by High NaCl intake or 3-5% Ns concentration IV
  • ECF volume increases
  • ICF volume decreases
  • osmolarity increases
  • transiently ECF osmolarity increases so volume shift from ICF to ECF until osmolarity equilibrates
18
Q

Hyposmotic Volume Expansion

A
  • Gain of Hypotonic Fluid
  • conditions like excess water-drinking and SIADH (syndrome of inappropriate ADH)
  • increase in ECF and ICF but decrease in osmolality
19
Q

Hartnup Disease

A

Defective transport of neutral (nonpolar) amino acids

  • cause malabsorption from the intestinal lumen and decreased reabsorption from the filtrate
  • Alanine, serine, threonine, valine, leucine, isoleucine, phenylalanine, tyrosine, tryptophan, glutamine, asparagine, and histidine secreted in urine 5-10xs normal
  • TRP is precursor for 5HT and melatonin: the reason for the pellagra- like dermatosis (photosensitivity) triggered by sunlight, fever, drugs, or emotional or physical stress
  • TRP also precursor for Niacin (NAD/NADH): which produces the neurological symptoms seen (nystagmus, intermittent ataxia, tremors)
  • TREATMENT: niacin repletion (high protein diet and daily nicotinamide supplementation)
  • Trp reactions require B6
20
Q

Cystinuria

A
  • defective transport of dibasic amino acids- particularly COAL –> cystine, ornithine, arginine, lysine
  • proximal convoluted tubule can not reabsorb AAs
  • results in cystine crystals forming in the kidneys
  • pt. present with abdominal pain that comes in waves linked to kidney stones
  • dissolution of stones in alkaline urine (dietary changes)
21
Q

Phenylketonuria

A
  • defect in PAH (Phenylalanine Hydroxylase) which converts Phe to Tyr
  • most common IEU
  • must be diagnoses before 2 weeks of age
  • musty urine odor
  • Phe –> phenylpyruvate (neurotoxic) –> phenylacetate (neurotoxic)
  • Treatment: dietary limit of PHE, supplement TYR
22
Q

Secondary PKU

A
  • defect in BH4 (tetrahydrobiopterin or THB), an essential cofactor for PAH
  • essential in the production of NO from Arg
  • regenerated by NADH
  • production of monamine NTs from Tyr and Trp are also deficient leading to neurological dysfunction
  • Treatment; synthetic THB (BH4)
23
Q

Tyrosinemias

A

Elevated Blood levels or Tyr

  • transient in newborns b/c they don’t have enzyme for the conversion of Tyr
  • Type 1: defect in fumarylacetoacetate converts Tyr to Fumarate, accumulation of fumarylacetoacetate
    - cabbage-like smell in infants
    - excrete succinylacetone: toxic to liver and kidneys
    - interferes w/ TCA cycle
    - causes renal tubule dysfunction
    - inhibits biosynthesis of heme
    - inhibits porphobilinogen synthetase
    - develope severe liver failure if not treated
    - Nitisinone is the treatment
    - most common form
24
Q

Alkaptonuria

A
  • defect in homogentisate oxidase: an enzyme in Tyr degradation pathway
  • “black urine disease” or “black bone disease”
  • Characteristic Triad: homogentisic aciduria, ochronosis (accumulation in CT), and arthritis
25
Q

Ammonia Toxicity

A
  • excessive ammonia due to disorders of the urea cycle or liver failure
  • NH3 toxic because it can permeate membranes and NH4 can’t
  • causes pH imbalance, swelling of astrocytes in the brain which causes cerebral edema and intracranial hypertension
  • no a-ketoglutarate so TCA cycle halts
  • depletion of glutamate results in CNS depression
  • ammonia causes mitochondrial dysfunction
26
Q

Gout

A
  • high levels of uric acid in the blood (hyperuricemia)
    - 1* overproduction of uric acid
    - 2* underexcretion of uric acid- most cases
  • results in painful deposits of sodium urate in extremities
    - things crystallize at lower temps seen in extremities
  • sodium urate deposits in kidneys cause damage
  • diets rich in purines (beans, spinach, lentils), alcohol, meat, and seafood, simple carbs can make it worse
  • allopurinol: inhibits the production of uric acid
  • altered excretion can be caused by decreased glomerular filtration, decreased tubular secretion, or enhanced tubular reabsorption
    dec. tubular secretion occurs in: DKA, ethanol intoxication, starvation ketosis
27
Q

Hyperammonemia

A
  • defects in 3 transporters or any of 6 enzymes in the urea cycle
  • defects in mitochondria transporters result in more severe hyperammonemia
  • defect in ornithine transcarbamoylase results in excess carbamoyl phosphate and you then get orotic aciduria –> hyperammonemia and decreased BUN
  • treatment: limiting protein consumption and agents that promote excretion
28
Q

Carbamoyl Phosphate synthetase I

A
  • in the urea cycle
  • in the mitochondria
  • NAG-activated
29
Q

Carbamoyl Phosphate Synthetase II

A
  • 1st step in de novo pyrimidine synthesis
  • not NAG- dependent but it is PRPP-activated
  • in the cytosol
  • orotic acid is still an intermediate of UMP c aused by deficiency in UMP synthase
  • not accompanied by hyperammonemia or reduced BUN levels