Nyresygdomme, salt og vandbalance Flashcards by Nadia Sleiman

Three Components of Urine Formation

Filtration (Glomerulus)
Reabsorption (Inner medulla, the loop of Henle)
Secretion

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Antidiuretisk hormon

Gør nyrernes samlerør mere permeable overfor vand -> mere vand kan reabsorberes fra urin til blod -> blodets osmolaritet falder

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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

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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

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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

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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.

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Hyponatriæmi

Ubalance mellem vandindholdet og natriumindholdet i ekstracellulærvæsken

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Hyponatriæmi - Årsager

Sygdomme hvor niveauet af AHD er forhøjet

Sygdomme hvor niveauet af ADH er passende undertrykt

Hyponatriæmi med normal eller forhøjet plasmaosmolaritet

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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.

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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.

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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.)

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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.

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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.

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Blood K+ Levels Control Resting Potential (cont.) - Hypokalemia

lowers resting potential away from threshold

Cells fire less easily

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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

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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

+ 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 + Increased blood pressure + 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