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:
- increased intake of fluids as in psychogenic causes, stress, and anxiety
- increased GFR as in hyperthyroidism, fever, hypermetabolic states
- increased output of solutes as occurs in DM, hyperthyroidism, use of diuretics (present more solute at the DCT)
- inability of kidney to reabsorb water in DCT as in CDI, NDI, drugs, and chronic renal failure
2
Q
Oliguria
A
Output below the minimum volume (300-500 mL/day) Causes: -dehydration - blood loss - diarrhea - cardiogenic shock - kidney disease - enlarged prostate
3
Q
Anuria
A
virtual absence of urine production (< 50 mL/day)
Causes:
- kidney failure
-obstruction: such as kidney stone or tumor
- enlarged prostate
4
Q
Water diuresis
A
increased water excretion without corresponding increase in salt excretion
-primary cause: increased water intake, polydipsia, diabetes insipidus
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)
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
- 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
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
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
9
Q
Lactated Ringer’s (Hartmanns)
A
Isotonic Uses - dehydration - burns - Lower GI fluid loss - Acute fluid loss - hypovolemia due to third spacing
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
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
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
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
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
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
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
