Nyresygdomme, salt og vandbalance Flashcards
Three Components of Urine Formation
Filtration (Glomerulus)
Reabsorption (Inner medulla, the loop of Henle)
Secretion
Antidiuretisk hormon
Gør nyrernes samlerør mere permeable overfor vand -> mere vand kan reabsorberes fra urin til blod -> blodets osmolaritet falder
Renal Calculi (nyresten) - Ætiologi
- Saturation theory: urine is supersaturated with stone components
- Matrix theory: organic materials act as a nidus for stone formation
- Inhibitor theory: a deficiency of substances that inhibit stone formation
Four types of kidney stones:
Calcium stones (i.e., oxalate or phosphate)
Magnesium ammonium phosphate stones
Uric acid stones
Cystine stones
Urinary Tract Infections - Patologi
Bacteria usually enter through the urethra
Host defenses include: Washout phenomenon Protective mucus Local immune responses and IgA Normal bacterial flora
Beer Drinkers Potomania
Beer drinkers eller fejlernærede
- beer contains little or no sodium, potassium, or protein, and the carbohydrate load will suppress endogenous protein breakdown and therefore urea excretion
Potomania
Normal subjects excrete 600 to 900 mosmol/kg of solute per day (primarily sodium and potassium salts and urea) (s-osmolaritet 280-300 mOsm/kg).
thus, if the minimum urine osmolality is 60 mosmol/kg, the maximum urine output will be 10 to 15 L/day (for example, 900 mosmol/day ÷ 60 mosmol/kg = 15 L).
Beer drinkers, daily solute excretion may fall below 250 mosmol/kg, leading to a reduction in the maximum urine output to below 4 L/day even though the urine is appropriately dilute. Hyponatremia will ensue if more than this amount of fluid is taken in.
Hyponatriæmi
Ubalance mellem vandindholdet og natriumindholdet i ekstracellulærvæsken
Hyponatriæmi - Årsager
Sygdomme hvor niveauet af AHD er forhøjet
Sygdomme hvor niveauet af ADH er passende undertrykt
Hyponatriæmi med normal eller forhøjet plasmaosmolaritet
ED evaluation hyponatraemia
2 goals: to determine the chronicity of the hyponatremic state and to determine the cause.
Acute hyponatremia is less common than chronic hyponatremia and typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 days, patients given hypotonic fluids in the postoperative period).
The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.
The therapeutic goal is to increase serum sodium rapidly by 4-6 mEq/L over the first 1-2 hours.
First, the source of free water must be identified and eliminated.
ED evaluation hyponatraemia 2
In patients with healthy renal function and mild to moderately severe symptoms, serum sodium may correct spontaneously without further intervention.
Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium toward normal, but only enough to arrest the progression of symptoms.
An increase in serum sodium of 4-6 mEq/L is generally sufficient.
ED evaluation hyponatraemia 3
Chronic hyponatremia is more common than acute hyponatremia.
These patients lack any history of sudden free water loading.
The risk of CPM appears to be minimal in patients whose chronic hyponatremia is corrected at a rate of less than 0.5 mEq/L/hour or 12 mEq/L/day.
(Anecdotal reports suggest that therapeutic relowering of the serum sodium with hypotonic fluids and desmopressin (DDAVP) may help avert neurologic sequelae in patients whose chronic hyponatremia is inadvertently corrected too quickly.)
ED evaluation hyponatraemia 4
cause of the hyponatremic state
Hypovolemic hyponatremia: Patients have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that serum sodium increases no faster than 0.5 mEq/L/hour or 12 mEq/L/day.
Hypervolemic hyponatremia: Patients have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause.
Euvolemic hyponatremia: This implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition.
ED evaluation hyponatraemia 5
Complications related to hyponatremia include rhabdomyolysis, seizures, permanent neurologic sequelae related to ongoing seizures or cerebral edema, respiratory arrest, and death.
Complications related to therapy of hyponatremia include fluid overload and CPM.
Blood K+ Levels Control Resting Potential (cont.) - Hypokalemia
lowers resting potential away from threshold
Cells fire less easily
Blood K+ Levels Control Resting Potential - Hyperkalemia
raises resting potential toward threshold
Cells fire more easily
When resting potential reaches threshold, Na+ gates open and won’t close
Hyperkaliæmi - Behandling
Antagonisme af kaliums membranvirkninger
- Calcium
Tvang af ekstracellulært kalium ind i cellerne
- Insulin og glukose
- Natriumbikarbonat, primært ved metabolisk acidose
- Beta2-adrenerge agonister
Fjernelse af kalium fra kroppen
- Loop eller thiazid diuretica
- Cation exchange resin
- Dialyse (helst hæmodialyse, hvis alvorligt)
Extracellular Calcium Controls Nerve Firing
Hypercalcemia - Blocks more Na+ gates - Nerves are less able to fire Hypocalcemia - Blocks fewer Na+ gates - Nerves fire more easily
Respiratory Acidosis and Alkalosis
Respiratory acidosis Increased PCO2 Increased carbonic acid Increased H+ = low pH (<7.35) Increased bicarbonate
Respiratory alkalosis Decreased PCO2
Decreased carbonic acid
Decreased H+ = high pH (>7.45)
Decreased bicarbonate
Metabolic Acid Imbalances
Metabolic acidosis
- Increased levels of ketoacids, lactic acid, etc.
- Decreased bicarbonate levels
Metabolic alkalosis
- Decreased H+ levels
- Increased bicarbonate levels
Renin-angiotensin-aldosteron-systemet (RAAS)
Et blodtryks- og væskeregulerende system i menneskekroppen.
Renin-angiotensin-aldosteron-systemet (RAAS)
Et blodtryks- og væskeregulerende system i menneskekroppen
Renin-angiotensin-aldosteron-systemet (RAAS) - Beskrivelse
Blodtryksfald, fald i blodplasma- eller ekstracellulærvæsken, lavt indhold af natrium i blodet eller højt indhold af kalium i blodet
=> frigivelse af renin fra nyrerne
=> renin binder sig til angiotensinogen
=> derved omdannelse til det inaktive enzym angiotensin I
-> føres rundt i kredsløbet til lungernes kapillærer
=> omdannelse til det aktive hormon angiotensin II (vha. ACE (Angiotensin Konverterende Enzym) i karvæggen)
-> fortsætter rundt i hele kroppen (via blodbanen)
-> virker på arteriolernes glatte muskelceller
=> sammentrækning af
blodkarrene
=> stigning i blodtrykket
+ angiotensin II (via blodbanen) -> til binyrebarken
=> stimulerer frigivelse af hormonet aldosteron
-> nyrernes urinsamlerør (via blod)
=>øger tilbagesugningen af vand og natrium fra urinsamlerørene tilbage til blodbanen
=> øget væskemængde i blodbanen
=> stigning i blodtrykket
+ aldosteron udskiller kalium fra blodbanen ud i urinsamlerørene
Renin-angiotensin-aldosteron-systemet (RAAS) - Beskrivelse
Blodtryksfald, fald i blodplasma- eller ekstracellulærvæsken, lavt indhold af natrium i blodet eller højt indhold af kalium i blodet
=> frigivelse af renin fra nyrerne
=> renin binder sig til angiotensinogen
=> derved omdannelse til det inaktive enzym angiotensin I
-> føres rundt i kredsløbet til lungernes kapillærer
=> omdannelse til det aktive hormon angiotensin II (vha. ACE (Angiotensin Konverterende Enzym) i karvæggen)
-> fortsætter rundt i hele kroppen (via blodbanen)
-> virker på arteriolernes glatte muskelceller
=> sammentrækning af
blodkarrene
=> stigning i blodtrykket
+ angiotensin II (via blodbanen) -> til binyrebarken
=> stimulerer frigivelse af hormonet aldosteron
-> nyrernes urinsamlerør (via blod)
=>øger tilbagesugningen af vand og natrium fra urinsamlerørene tilbage til blodbanen
=> øget væskemængde i blodbanen
=> stigning i blodtrykket
+ aldosteron udskiller kalium fra blodbanen ud i urinsamlerørene
Renin-angiotensin-aldosteron-systemet (RAAS) - Beskrivelse (kort)
Renin Starts the RAA Pathway
- Which turns on the Na+/K+ ATPase in the distal tubule
- Na+ and water are reabsorbed
- Raises blood volume
- Does not change blood osmolarity
- K+ is secreted
- Lowers blood K+
Secretion
- Urate, hippurate, ketoacid anions
- penicillins, cephalosporins, salicylates, diuretics, radiocontrast media
- Creatinine, trimetoprim, quinidine
Cystic and Obstructive Disorders
Cystic disease of the kidney - Simple and acquired renal cysts - Medullary cystic disease - Autosomal dominant polycystic kidney disease Obstructive disorders - Hydronephrosis - Renal calculi
Consequences of Dilatation of Renal Tubules or Tract
Expansion of the kidney with urine (hydronephrosis)
- Increased pressure inside the renal capsule
- Compartment syndrome compresses blood vessels inside kidney
- Renal ischemia
Stasis of urine
- Risk of infection
- Stones
Glomerular Damage
Proliferative: number of cells increase
Sclerotic: amount of extracellular matrix increases
Membranous: thickness of glomerular capillary wall increases
All can decrease the efficiency of filtration
Allow blood cells, lipids, or proteins to pass into the urine
Disorders of Glomerular Function
Nephritic syndromes - Proliferative inflammatory response Nephrotic syndrome - Increased permeability of glomerulus Mixed nephritic and nephrotic responses Chronic glomerulonephritis Glomerular lesions associated with systemic disease
Nephritic Syndromes
Proliferative inflammatory response
- RAA pathway activated; hypertension
Inflammatory process damages the capillary wall
- Red blood cells escape into the urine
– Hematuria with red cell casts
- Hemodynamic changes decrease the GFR
– Azotemia (presence of nitrogenous wastes in the blood), oliguria
Tubulointerstitial Disorders
Acute tubular necrosis (ATIN or ATN) Pyelonephritis - Acute pyelonephritis - Acute hypersensitivity to drugs - Chronic pyelonephritis Drug-related nephropathies
When Kidneys Fail
Less waste is removed
More waste remains in the blood
Nitrogenous compounds build up in the blood
- BUN: Blood urea nitrogen
- Creatinine
– Renal function approximated by: initial creatinine level/current creatinine level
Acute Renal Failure
Prerenal - Decreased blood supply -- Shock, dehydration, vasoconstriction Postrenal - Urine flow is blocked -- Stones, tumors, enlarged prostate Intrinsic - Kidney tubule function is decreased -- Ischemia, toxins, intratubular obstruction
Chronic Renal Failure
Fewer nephrons are functioning
Remaining nephrons must filter more
- Hyperperfusion
- Hypertrophy
Chronic Renal Failure (CRF) - Development
Diminished renal reserve
- Nephrons are working as hard as they can
Renal insufficiency
- Nephrons can no longer regulate urine density
Renal failure
- Nephrons can no longer keep blood composition normal
End-stage renal disease
Uremia = “Urine in the Blood”
Renal filtering function decreases - Altered fluid and electrolyte balance -- Acidosis, hyperkalemia, salt wasting, hypertension Wastes build up in blood - Increased creatinine and BUN -- Toxic to CNS, RBCs, platelets Kidney metabolic functions decrease - Decreased erythropoietin - Decreased Vitamin D activation
Cardiovascular Consequences of CRF
Decreased blood viscosity
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Increased blood pressure
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Decreased oxygen supply
Less erythropoietin => anemia => lower blood viscosity => blood flows through vessels more swiftly => hear rate increases
Incrased workload on left heart => left ventricle dilation and hypertrophy => not enough oxygen to support LV contraction => angina ischemia LHF
