Lífeðlisfræði nýrna Flashcards
Skilgreining á lactic acidosis:
Lactic acidosis is defined as a pH <7.35 and a lactate >5 mmol/L. It is a common finding in critically ill patients and is often associated with other serious underlying pathologies.
Mortality tengt lactic acidosis:
The mortality associated with lactic acidosis despite full supportive treatment remains at 60-90%.
Hvernig er lactic acidosis flokkuð?
Acquired lactic acidosis is classified into two subtypes:
- Type A is due to tissue hypoxia
- Type B is due to non-hypoxic processes affecting the production and elimination of lactate
Hvernig lactic acidosu fær maður almennt eftir left ventricular failure?
Left ventricular failure typically results in tissue hypoperfusion and a type A lactic acidosis.
Hvað er ergocalciferol?
Vítamín D2
Hvað er cholecalciferol?
Vítamín D3
Hvað er calcitriol og hvað gerir það?
1,25-dihydroxycholecalciferol (also known as calcitriol) is the hormonally active metabolite of vitamin D. Its actions increase the plasma concentration of calcium and phosphate.
5 aðal fúnksjónir 1,25-dihydroxycholecalciferol (calcitriols):
- Increases calcium and phosphate absorption in the small intestine
- Increases renal calcium reabsorption
- Increases renal phosphate reabsorption
- Increases osteoclastic activity (increasing calcium and phosphate resorption from bone)
- Inhibits 1-alpha-hydroxylase activity in the kidneys (negative feedback)
Hvers konar sýrubasatruflun er líklegast að sé til staðar hjá einstaklingi sem hefur innbyrt ethylene glycol (frostlög)?
Raised anion gap metabolic acidosis
Dæmi um 6 atriði sem valda respiratoriskri alkalosu:
- Hyperventilation (e.g. anxiety)
- Pulmonary embolism
- CNS disorders (e.g. CVA, SAH, encephalitis)
- Altitude
- Pregnancy
- Early stages of aspirin overdose
Dæmi um 6 atriði sem valda respiratoriskri acidosu:
- COPD
- Life-threatening asthma
- Pulmonary oedema
- Sedative drug overdose (e.g. opiates, benzodiazepines)
- Neuromuscular disease
- Obesity
Dæmi um 4 atriði sem valda metaboliskri alkalosu:
- Vomiting
- Potassium depletion (e.g. diuretic usage)
- Cushing’s syndrome
- Conn’s syndrome
Dæmi um 4 atriði sem valda metaboliskri acidosu með hækkuðu anjónabili:
- Lactic acidosis (e.g. hypoxaemia, shock, sepsis, infarction)
- Ketoacidosis (e.g. diabetes, starvation, alcohol excess)
- Renal failure
- Poisoning (e.g. late stages of aspirin overdose, methanol, ethylene glycol)
Dæmi um 4 atriði sem valda metaboliskri acidosu með normal anjónabili:
Renal tubular acidosis
Diarrhoea
Ammonium chloride ingestion
Adrenal insufficiency
Hvernig og hvar verður 25-hydroxycholecalciferol að 1,25-dihydroxycholecalciferol?
25-hydroxycholecalciferol is hydroxylated in the kidney by 1-alpha-hydroxylase to become 1,25-dihydroxycholecalciferol.
Dæmi um 2 atriði sem örva 1-alpha-hydroxylasa:
1-alpha-hydroxylase is stimulated by parathyroid hormone or hypophosphataemia and serves as the major control point in the production of 1,25-dihydroxycholecalciferol.
Hvaða elektrolytatruflun er oft tengd magnesiumskorti?
Magnesium deficiency is frequently associated with hypokalaemia. Concomitant magnesium deficiency also aggravates hypokalaemia and renders it refractory to treatment by potassium.
Hvað heita frumurnar sem hjálpa við sýrubasa-jafnvægi í distal convoluting tubule og collecting duct? Hvernig fara þær að því?
The intercalated cells in distal convoluted tubule and collecting duct assist with acid-base balance by controlling the levels of H+ and HCO3– ions.
HCO3– ions cross the basolateral membrane into the extracellular fluid in exchange for chloride via the anion exchanger channel. The H+ ions are secreted into the lumen via the potassium-hydrogen ATPase antiporter (H+/K+ATPase).
Once within the lumen of the tubule, the H+ ions react with either phosphate (HPO42-) or ammonia (NH3), producing new charged compounds (NH4+ and H2PO4–).
Because of their charge, they cannot re-enter the cell and are, therefore, excreted.
To prevent an accumulation of chloride ions and potassium ions within the cell, a potassium-chloride symporter on the basolateral membrane allows leakage of these ions back into the extracellular fluid.
Hvernig komast HCO3- jónir yfir basolateral himnuna í distal convoluting tubule og collecting duct?
HCO3– ions cross the basolateral membrane into the extracellular fluid in exchange for chloride via the anion exchanger channel.
Hvernig komast vetnisjónir yfir basolateral himnuna í distal convoluting tubule og collecting duct?
The H+ ions are secreted into the lumen via the potassium-hydrogen ATPase antiporter (H+/K+ATPase).
Hvað verður um H+ og HCO3- jónir sem eru komnar inn í lumenið í distal convoluting tubule og collecting duct?
Once within the lumen of the tubule, the H+ ions react with either phosphate (HPO42-) or ammonia (NH3), producing new charged compounds (NH4+ and H2PO4–).
Because of their charge, they cannot re-enter the cell and are, therefore, excreted.
Hvernig kemur líkaminn í veg fyrir það að klóríð og kalíum jónir safnist upp inni í frumum í distal convoluting tubules og collecting ducts?
To prevent an accumulation of chloride ions and potassium ions within the cell, a potassium-chloride symporter on the basolateral membrane allows leakage of these ions back into the extracellular fluid.
Hvað er erythropoietin og hvað gerir það? Hvar er það framleitt?
Erythropoietin is a glycoprotein hormone that is responsible for the control of erythropoiesis (red cell production).
It is mainly produced by interstitial fibroblasts in the kidney that lie in close proximity to the PCT. It is also produced in the perisinusoidal cells in the liver, but this mainly occurs in the fetal and perinatal periods.
Hvað örvar EPO framleiðslu og seyti í nýrum?
Hypoxia stimulates the production and secretion of erythropoietin in the kidney.
2 aðaláhrif EPO á rauð blóðkorn:
Erythropoietin has two main effects on red blood cells:
- It stimulates stem cells in the bone marrow to increase the production of red blood cells
- It targets red blood cell progenitors and precursors in the bone marrow and protects them from apoptosis
The resultant increase in red cell mass results in increased oxygen-carrying capacity and increased oxygen delivery.
Hvernig eru frumurnar í proximal convoluted tubule og hvers vegna?
The proximal convoluted tubule is where the majority of solute resorption occurs, and this resorption is driven by ATP-dependant transporters.
Cells are cuboidal with abundant mitochondria to provide energy and multiple microvilli (a brush border) to increase surface area.
Hvernig eru frumurnar í descending loop of Henle og hvers vegna?
The descending Loop of Henle has flat cells with few microvilli and few mitochondria, reflecting that in this segment, there is the movement of water by osmosis and no solute transport.
Hvernig eru frumurnar í ascending thick Loop of Henle og af hverju?
The ascending thick Loop of Henle has cuboidal cells which are impermeable to water and contain plentiful mitochondria providing energy to Na.K.2Cl transporters.
These measures contribute to the formation of the medullary concentration gradient and countercurrent multiplication.
Hvernig eru frumurnar í distal convoluted tubule og hvers vegna?
The distal convoluted tubule allows variable resorption and secretion to fine-control urine composition.
Mitochondria provide energy for membrane transporters. There are few microvilli.
Hvernig eru frumurnar í collecting duct og hvers vegna?
The collecting duct allows the final adjustments in urine concentration. Aquaporin channels are present in the cell membranes to allow the transcellular movement of water. The number of aquaporin channels is controlled by ADH.
Uþb hversu mikið af kalíum er endurupptekið í proximal convoluted tubule?
Ca 67%!
Hvernig er kalíum magni í utanfrumuvökva stýrt?
The extracellular fluid K+ concentration is primarily controlled through the secretion and reabsorption of potassium in the kidney. Potassium is freely filtered at the glomerulus and passes through to the proximal convoluted tubule (PCT) and loop of Henle where most of it is reabsorbed.
Hvernig fer endurupptaka kalíums í proximal convoluted tubule fram?
Approximately 67% of the filtered K+ is reabsorbed in the PCT.
K+ reabsorption in the PCT is primarily passive, occurring via a paracellular mechanism. Na.K.ATP-ase pumps move Na+ ions out of the proximal tubule cells and drive K+ into the cell. This net movement of Na+ ions creates an osmotic and an electrochemical gradient. Water moves out of the PCT down the osmotic gradient created by sodium and Cl– moves down the electrochemical gradient. K+ is reabsorbed and follows Cl– into the bloodstream.
Hversu mikið af kalíumi er endurupptekið í thick ascending limb í loop of Henle og hvernig?
Approximately 20% of the filtered K+ is reabsorbed in the thick ascending limb of the loop of Henle. This It occurs by two separate mechanisms; a transcellular and a paracellular pathway.
Hvernig virkar transcellular mekanisminn sem er önnur leið af tveimur til að endurtaka upp kalíum í thick ascending loop of Henle?
The transcellular mechanism is dependent upon the Na.K.ATP-ase pumps, which move Na+ ions into the bloodstream and K+ into the thick ascending limb. This keeps the intracellular concentration of Na+ ions low, creating a gradient for Na.K.Cl cotransporter on the apical membrane to pump Na+, K+ and Cl- ions into the cell from the lumen. K+ then enters the bloodstream via the Cl.K symporter or the K uniporter.
Hvernig virkar paracellular mekanisminn sem er önnur leið af tveimur til að endurtaka upp kalíum í thick ascending loop of Henle?
The paracellular mechanism is dependent upon the renal outer medullary potassium channel (ROMK). Movement of K+ through these ROMK channels leads to a positive voltage in the lumen, which provides a driving force for the passive reabsorption of K+ ions.
Hvað er mikið af filteruðu kalíum endurupptekið í distal convoluted tubule og collecting duct og í hvaða aðstæðum?
A further 10-12% of filtered potassium is reabsorbed in the distal convoluted tubule (DCT) and collecting duct (CD) when the body is attempting to preserve K+. It occurs via the transcellular pathway and is mediated by potassium-hydrogen ATPase antiporters (H.K.ATPases) in the intercalated cells. The apical H.K.ATPase mediates the movement of H+ out into the lumen, driving K+ into the intercalated cell. Then, the basolateral K+ channel allows the K+ building up in the intercalated cell to leak out into the bloodstream.
Hvar fer kalíum seyti í nýrunum fram og hversu mikið/hratt?
The secretion of K+ secretion mainly occurs in the late DCT and CD. K+ secretion enables long-term control of the serum K+.
The rate of secretion is variable and can be increased or decreased depending upon the amount of K+ present in the diet etc.
Hvernig fer kalíum seyti í distal convoluting tubule og collecting duct fram og hvaða frumur eru það?
K+ secretion in the late DCT and CD is mediated by the principal cells. Principal cells are the main Na+reabsorbing cells, and these make up the majority of the tubular cells in this region.
The exchange is once again driven by the function of the Na.K.ATP-ase pumps on the basolateral membrane. An electrochemical gradient is established that favours the movement of Na+ ions into the cell from the apical side. In the late DCT, the movement of Na+ ions occurs via an epithelial sodium channel (ENaC). K+ ions accumulate within the cell due to the action of Na.K.ATP-ase pumps. This promotes the secretion of potassium ions into the lumen of the tubule through a potassium uniporter.
Hvað er filtration fraction og hvað er það ca mikið hjá heilbrigðum einstaklingum?
The filtration fraction (FF) is the percentage of the plasma (not blood) delivered to the glomerulus that is filtered through the glomerulus to become ultrafiltrate.
In health 15-20% of plasma is filtered to become ultrafiltrate (i.e. FF = 15-20%).
Hvernig er hægt að reikna filtration fraction?
FF = GFR / RPF
Where:
- GFR is the glomerular filtration rate (ml/min), i.e. the amount of ultrafiltrate produced per minute.
- RPF is the renal plasma flow (ml/min), i.e. the volume of plasma passing through the glomerulus per minute
Hvernig er hægt að reikna renal plasma flow?
Renal plasma flow (RPF) is subtly different to renal blood flow (RBF), which is the volume of blood flowing through the glomerulus per minute.
RPF = RBF x (1-Haematocrit).
Hvaða áhrif hefur minnkun á plasma prótínum (t.d. hypoalbuminemia) á filtration fraction?
Decreased plasma protein (e.g. hypoalbuminaemia) has no impact on RPF but decreases the oncotic pressure in glomerular vessels, so GFR increases. As RPF remains steady but GFR increases, FF increases.
Hvaða áhrif hefur afferent arteriole constriction á filtration fraction?
Afferent arteriole constriction decreases RBF and RPF and thus decreases the pressure across the glomerulus and GFR. However, as both RPF and GFR decrease equally, FF remains constant.
Hvernig verður 1,25-dihydroxycholecalciferol til?
The synthesis of 1,25-dihydroxycholecalciferol starts in the epidermal layer of the skin, where 7-dehydrocholesterol is converted to cholecalciferol in the presence of UVB radiation.
Cholecalciferol is then hydroxylated in the endoplasmic reticulum of liver hepatocytes by 25-hydroxylase to become 25-hydroxycholecalciferol (calcifediol).
Finally 25-hydroxycholecalciferol is hydroxylated in the kidney by 1-alpha-hydroxylase to become1,25-dihydroxycholecalciferol. 1-alpha-hydroxylase is stimulated by parathyroid hormone or hypophosphataemia and serves as the major control point in the production of 1,25-dihydroxycholecalciferol.
