Lífeðlisfræði nýrna Flashcards
1
Q
Skilgreining á lactic acidosis:
A
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.
2
Q
Mortality tengt lactic acidosis:
A
The mortality associated with lactic acidosis despite full supportive treatment remains at 60-90%.
3
Q
Hvernig er lactic acidosis flokkuð?
A
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
4
Q
Hvernig lactic acidosu fær maður almennt eftir left ventricular failure?
A
Left ventricular failure typically results in tissue hypoperfusion and a type A lactic acidosis.
5
Q
Hvað er ergocalciferol?
A
Vítamín D2
6
Q
Hvað er cholecalciferol?
A
Vítamín D3
7
Q
Hvað er calcitriol og hvað gerir það?
A
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.
8
Q
5 aðal fúnksjónir 1,25-dihydroxycholecalciferol (calcitriols):
A
- 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)
9
Q
Hvers konar sýrubasatruflun er líklegast að sé til staðar hjá einstaklingi sem hefur innbyrt ethylene glycol (frostlög)?
A
Raised anion gap metabolic acidosis
10
Q
Dæmi um 6 atriði sem valda respiratoriskri alkalosu:
A
- Hyperventilation (e.g. anxiety)
- Pulmonary embolism
- CNS disorders (e.g. CVA, SAH, encephalitis)
- Altitude
- Pregnancy
- Early stages of aspirin overdose
11
Q
Dæmi um 6 atriði sem valda respiratoriskri acidosu:
A
- COPD
- Life-threatening asthma
- Pulmonary oedema
- Sedative drug overdose (e.g. opiates, benzodiazepines)
- Neuromuscular disease
- Obesity
12
Q
Dæmi um 4 atriði sem valda metaboliskri alkalosu:
A
- Vomiting
- Potassium depletion (e.g. diuretic usage)
- Cushing’s syndrome
- Conn’s syndrome
13
Q
Dæmi um 4 atriði sem valda metaboliskri acidosu með hækkuðu anjónabili:
A
- 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)
14
Q
Dæmi um 4 atriði sem valda metaboliskri acidosu með normal anjónabili:
A
Renal tubular acidosis
Diarrhoea
Ammonium chloride ingestion
Adrenal insufficiency
15
Q
Hvernig og hvar verður 25-hydroxycholecalciferol að 1,25-dihydroxycholecalciferol?
A
25-hydroxycholecalciferol is hydroxylated in the kidney by 1-alpha-hydroxylase to become 1,25-dihydroxycholecalciferol.
16
Q
Dæmi um 2 atriði sem örva 1-alpha-hydroxylasa:
A
1-alpha-hydroxylase is stimulated by parathyroid hormone or hypophosphataemia and serves as the major control point in the production of 1,25-dihydroxycholecalciferol.
17
Q
Hvaða elektrolytatruflun er oft tengd magnesiumskorti?
A
Magnesium deficiency is frequently associated with hypokalaemia. Concomitant magnesium deficiency also aggravates hypokalaemia and renders it refractory to treatment by potassium.
18
Q
Hvað heita frumurnar sem hjálpa við sýrubasa-jafnvægi í distal convoluting tubule og collecting duct? Hvernig fara þær að því?
A
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.
19
Q
Hvernig komast HCO3- jónir yfir basolateral himnuna í distal convoluting tubule og collecting duct?
A
HCO3– ions cross the basolateral membrane into the extracellular fluid in exchange for chloride via the anion exchanger channel.
20
Q
Hvernig komast vetnisjónir yfir basolateral himnuna í distal convoluting tubule og collecting duct?
A
The H+ ions are secreted into the lumen via the potassium-hydrogen ATPase antiporter (H+/K+ATPase).
21
Q
Hvað verður um H+ og HCO3- jónir sem eru komnar inn í lumenið í distal convoluting tubule og collecting duct?
A
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.
22
Q
Hvernig kemur líkaminn í veg fyrir það að klóríð og kalíum jónir safnist upp inni í frumum í distal convoluting tubules og collecting ducts?
A
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.
23
Q
Hvað er erythropoietin og hvað gerir það? Hvar er það framleitt?
A
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.
24
Q
Hvað örvar EPO framleiðslu og seyti í nýrum?
A
Hypoxia stimulates the production and secretion of erythropoietin in the kidney.
25
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.
26
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.
27
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.
28
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.
29
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.
30
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.
31
Uþb hversu mikið af kalíum er endurupptekið í proximal convoluted tubule?
Ca 67%!
32
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.
33
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.
34
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.
35
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.
36
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.
37
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.
38
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.
39
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.
40
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%).
41
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
42
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).
43
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.
44
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.
45
Hvaða áhrif hefur efferent arteriole constriction á filtration fraction?
Efferent arteriole constriction doesn't affect RBF or RPF but increases the pressure across the glomerulus to increase GFR. As RPF remains steady but GFR increases, FF increases.
46
Hvers konar flutningur fer fram í proximal convoluting tubule sem gerir seyti ýmissa toxína og metabolic úrgangsefna mögulegt?
The PCT is also responsible for secreting several of organic compounds, such as toxins and metabolic waste products, from the blood in the peritubular capillary into the renal tubule. This occurs by secondary active transport.
Transporters that facilitate secretion are located on the basal surface of the PCT epithelial cells. An example of this process is the secretion of organic cations such as dopamine or morphine via the H+/OC+ exchanger.
47
Hvers vegna er kreatínín notað sem estimate fyrir GFR?
Creatinine is used to estimate GFR because it is an organic base naturally produced by muscle breakdown, it is freely filtered at the glomerulus, it is not resorbed from the nephron, it is not produced by the kidney, it is not toxic, and it doesn't alter GFR. In reality, a small volume (10-15%) is secreted into the tubule, which affects the accuracy of the calculation.
48
Hvort er glomerular filtration passivur eða aktívur prócess? Hvaða kraftar eru þar að verki?
Glomerular filtration is a passive process which depends upon the net hydrostatic pressure acting across the glomerular capillaries, countered by the oncotic pressure, and also influenced by the intrinsic permeability of the glomerulus.
49
Hver er meðal GFR fyrir heilbrigða unga kk vs. kvk og hversu hratt minnkar hann þegar við eldumst?
The mean values for glomerular filtration rate (GFR) in healthy young adults are 130ml/min/1.73m2 (men) and 120ml/min/1.73m2 (women). The GFR declines with age after the age of 40 at a rate of approximately 1 ml/min/year.
50
Hvernig reiknum við GFR?
The Cockcroft and Gault formula is as follows:
GFR (ml/min) = (140 – age in years) x weight (kg) x 1.23 (men) or 1.04 (women) / Plasma creatinine (mmol/l)
51
Hvaða annmarkar eru á Cockcroft and Gault formúlunni fyrir GFR?
The Cockcroft and Gault formula overestimates creatinine in obese patients as their endogenous creatinine production will be less than that predicted by overall body weight.
52
9 atriði sem valda type A lactic acidosis:
- Shock (including septic shock)
- Left ventricular failure
- Severe anaemia
- Asphyxia
- Cardiac arrest
- CO poisoning
- Respiratory failure
- Severe asthma and COPD
- Regional hypoperfusion
53
9 atriði sem valda type B lactic acidosis:
- Renal failure
- Liver failure
- Sepsis (non-hypoxic sepsis)
- Thiamine deficiency
- Alcoholic ketoacidosis
- Diabetic ketoacidosis
- Cyanide poisoning
- Methanol poisoning
- Biguanide poisoning
54
Hversu mikið af glúkósa er endurupptekið í proximal convoluted tubules?
100%
55
Hversu mikið af amínósýrum er endurupptekið í proximal convoluted tubules?
100%
56
Hversu mikið af Na er endurupptekið í proximal convoluted tubules?
67%
57
Hversu mikið af vatni er endurupptekið í proximal convoluted tubules?
65%
58
Hversu mikið af kalíum og klórjónum er endurupptekið í proximal convoluted tubules?
65%
59
Hvernig er glomerular filtration himnan uppbyggð?
The glomerular filtration membrane is composed of the fenestrated capillary endothelium, the basement membrane and the filtration slits formed by foot processes of podocytes (the epithelial cells of the renal corpuscle). The passage of substances across this membrane depends on molecular size and electrical charge.
60
Hvaða mólekúl fara frítt í gegnum glomerular filtration himnuna og hver ekki?
Molecules <7,000 Daltons in size are freely filtered (dissolved electrolytes and solutes such as urea, glucose, amino acids and creatinine).
Molecules >70,000 Daltons in size are not filtered at all (most plasma proteins, platelets and blood cells).
The filtration of molecules between 7,000 and 70,000 Daltons varies according to their size and charge. The basement membrane contains negatively charged glycoproteins which repel negative molecules; hence negatively charged molecules (most plasma proteins) are less readily filtered than positively charged molecules. Most negative molecules >50,000 Daltons are not filtered. This includes albumin, which is negatively charged and 60-65,000 Daltons in size.
61
Fer bilirubin gegnum glomerular filtration himnuna?
Unconjugated bilirubin is not filtered as it is insoluble so strongly bound to albumin in plasma. Conjugated bilirubin is soluble and passes freely through the filtration membrane.
62
Skilgreiningin á krónískri nýrnabilun:
CKD is defined as the presence of kidney damage (i.e. albuminuria) and/or decreased kidney function (i.e. glomerular filtration rate (GFR) <60 ml/minute per 1.73 m²) for three months or more, irrespective of clinical diagnosis.
63
Skilgreiningin á hraðaðri nýrnabilun:
Accelerated progression of CKD is defined as a sustained decrease in GFR of 25% or more and a change in GFR category within 12 months, or a sustained decrease in GFR of 15 ml/minute/1.73 m2 per year.
64
Skilgreiningin á lokastigs nýrnabilun:
End-stage renal disease (ESRD) is defined as severe irreversible kidney damage with a GFR of <15 ml/minute per 1.73 m².
65
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.
66
Hvernig verður 7-dehydrocholesterol að cholecalciferol?
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.
67
Hvernig verður cholecalciferol að 25-hydroxycholecalciferol?
Cholecalciferol is then hydroxylated in the endoplasmic reticulum of liver hepatocytes by 25-hydroxylase to become 25-hydroxycholecalciferol (calcifediol).
68
Hvað er anjónabil? Hvernig er það reiknað?
The anion gap represents the concentration of all the unmeasured anions in the plasma. It is the difference between the primary measured cations and the primary measured anions in the serum. It can be calculated using the following formula:
Anion gap = [Na+] – [Cl-] – [HCO3-]
69
Hvað er normal anjónabil?
The reference range varies depending upon which methodology is used to make the measurement but is usually 8 to 16 mmol/L.
70
Formúla fyrir anjónabil hjá nýrnasjúklingum:
Generally speaking, the value of K+ is low relative to the other three ions and has little effect on the equation. An alternative formula, which includes K+, is sometimes used, particularly by Nephrologists. In Renal units, the K+ covers a wider range and, therefore, has a more significant effect on the measured anion gap. In these circumstances, an alternative formula is used:
Anion gap = [Na+] + [K+] – [Cl-] – [HCO3-]
71
Hvers vegna fá einstaklingar high anion gap metabolic acidosis?
A high anion gap metabolic acidosis usually occurs as a consequence of the accumulation of organic acid or the impaired excretion of H+ ions.
72
Fyrir hvað stendur minnisreglan CAT MUDPILES?
Stendur fyrir orsakir high anion gap metabolic acidosis?
```
Carbon monoxide
Alcoholic ketoacidosis
Toluene
Metformin, Methanol
Uraemia
Diabetic ketoacidosis
Propylene glycol
Iron, Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
```
73
Hvers vegna fá einstaklingar normal anion gap acidosis?
A normal anion gap metabolic acidosis usually results from the loss of HCO3- ions from the extracellular fluid.
74
Fyrir hvað stendur minnisreglan CAGE?
Stendur fyrir normal anion gap metabolic acidosis.
Chloride excess
Acetazolamide, Addison’s disease
Gastrointestinal causes (diarrhoea, vomiting, fistulae)
Extra (Renal tubular acidosis)
75
Hvað getur valdið low anion gap metabolic acidosis?
A low anion gap is very rare indeed and, if present, is usually due to some sort of analytical error. When genuinely present, it can be caused by a decrease in unmeasured anions (e.g. low albumin) or by an increase in unmeasured cations (e.g. IgG paraprotein in multiple myeloma or hypercalcaemia).
76
Hvað er diabetes insipidus og í hvaða 2 flokka skiptist það?
Diabetes insipidus is the inability to produce concentrated urine. It is characterised by the presence of excessive thirst, polyuria and polydipsia. There are two distinct types of diabetes insipidus:
- Cranial (central) diabetes insipidus and;
- Nephrogenic diabetes insipidus
77
Hvað orsakar cranial diabetes insipidus?
Cranial diabetes insipidus is caused by a deficiency of vasopressin (anti-diuretic hormone). Patients with cranial diabetes insipidus can have a urine output as high as 10-15 litres per 24 hours, but adequate fluid intake allows most patients to maintain normonatraemia. 30% of cases are idiopathic, and a further 30% are secondary to head injuries. Other causes include neurosurgery, brain tumours, meningitis, granulomatous disease (e.g. sarcoidosis) and drugs, such as naloxone and phenytoin. A very rare inherited form also exists that is associated with diabetes mellitus, optic atrophy, nerve deafness and bladder atonia.
78
Hvað orsakar nephrogenic diabetes insipidus?
Nephrogenic diabetes insipidus is caused by renal resistance to the action of vasopressin. As with cranial diabetes insipidus, urine output is markedly elevated. Serum sodium levels can be maintained by secondary polydipsia or can be elevated. Causes of nephrogenic diabetes insipidus include chronic renal disease, metabolic disorders (e.g. hypercalcaemia and hypokalaemia) and drugs, including long-term lithium usage and demeclocycline.
79
Hvar og hvernig er angiotensin I breytt í angiotensin II?
Angiotensin I is converted to angiotensin II by the removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE). This primarily occurs in the lungs, although it does also occur to a lesser degree in endothelial cells and renal epithelial cells.
80
6 hlutverk angiotensin II:
- Vasoconstriction of vascular smooth muscle (resulting in increased blood pressure)
- Vasoconstriction of the efferent arteriole of the glomerulus (resulting in an increased filtration fraction and preserved glomerular filtration rate)
- Stimulation of aldosterone release from the zona glomerulosa of the adrenal cortex
- Stimulation of anti-diuretic hormone (vasopressin) release from the posterior pituitary
- Stimulation of thirst via the hypothalamus
- Acts on the Na+/H+ exchanger in the proximal tubule of the kidney to stimulate Na+ reabsorption and H+ excretion
81
4 atriði sem auka magn angiotensinogens í plasma:
- Increased corticosteroid levels
- Increased thyroid hormone levels
- Increased oestrogen levels
- Increased angiotensin II levels (EKKI angiotensin I)
82
Hversu mikið af filteruðu vatni hefur ÞEGAR verið endurupptekið þegar kemur að distal convoluted tubule? Hversu mikið er síðan endurupptekið í DCT?
The distal convoluted tubule (DCT) and collecting duct (CD) are the final two segments of the kidney nephron. Approximately 80% of filtered water has been recovered by the time the dilute forming urine enters the DCT. The DCT will recover another 10-15% before the forming urine enters the collecting ducts.
83
Hvað heitir ADH öðru nafni og hvað gerir það?
Antidiuretic hormone (ADH), which is also known as vasopressin, is a peptide hormone that regulates the body’s retention of water.
84
Hvaðan kemur ADH (vasopressin), hvar er það framleitt og hvar er það geymt?
It is derived from a prohormone precursor in the hypothalamus and is produced in the magnocellular and parvocellular neurosecretory cells of the paraventricular nucleus and supraoptic nucleus there. It is then transported via axons to the posterior pituitary, where it is stored in vesicles.
85
Hvað er normal pH í arterial astrup?
7,35-7,45
86
Hvað er normal PaO2 í arteríal astrup í kPa?
10 – 14 kPa
87
Hvað er normal PaCO2 í arteríal astrup í kPa?
4.5 – 6 kPa
88
Hvað er normal HCO3- í arteríal astrup í mmól per L?
22 – 26 mmol/l
89
Hvað er normal base excess í arteríal astrup?
-2 – 2 mmol/l
90
Hvað kemur á eftir Bowman´s capsule? Hvað heitir fyrsti parturinn af því fyrirbæri og hvar liggur hann anatomiskt í nýranu?
The renal tubule is the part of the nephron into which the glomerular filtrate passes after it has reached Bowman’s capsule. The first part of the renal tubule is the proximal convoluted tubule (PCT). The PCT lies in the renal cortex and is where the majority of solute reabsorption occurs.
91
Hvar gerist meirihluti solute reabsorption nýrans?
The majority of solute reabsorption occurs in the proximal convoluted tubule (PCT). Reabsorption is the process by which water and solutes are removed from the PCT and moved back into the bloodstream.
92
Með hvaða hætti gerist endurupptaka efna í proximal convoluted tubule?
Reabsorption in the PCT mainly occurs via the process of bulk transport, which is also referred to as ‘solvent drag’. In bulk transport, solutes in the ultrafiltrate are transported by the flow of water rather than specifically by ion pumps or other membrane transport proteins.
93
Hversu mikið af glúkósa, amínósýrum, Na, vatni, K og klór er endurupptekið í proximal convoluted tubule?
The solutes and water move from the PCT to the interstitium and then into peri-tubular capillaries via ion channels on the basolateral and apical membranes. The following percentages of these are reabsorbed at the PCT:
- 100% of glucose
- 100% of amino acids
- 67% of sodium
- 65% of water
- 65% of potassium
- 65% of chloride
94
Hvaða áhrif hefur samdráttur efferent arteriole á renal plasma flow, filtration fraction og GFR?
Vasoconstriction of the efferent arteriole of the glomerulus will decrease renal plasma flow, increase the filtration fraction and increase the glomerular filtration rate.
95
Hvaða áhrif hefur Vasoconstriction of afferent arteriole á renal plasma flow, filtration fraction og GFR?
Plasma flow: Minnkar
Filtration fraction: engin áhrif
GFR: Minnkar
96
Hvaða áhrif hefur Vasodilatation of afferent arteriole á renal plasma flow, filtration fraction og GFR?
Plasma flow: Eykst
Filtration fraction: engin áhrif
GFR: Eykst
97
Hvaða áhrif hefur Vasodilatation of efferent arteriole á renal plasma flow, filtration fraction og GFR?
Plasma flow: Eykst
Filtration fraction: Minnkar
GFR: Minnkar
98
Hver er formúlan til að reikna út anjónabil?
Anion gap = [Na+] – [Cl-] – [HCO3-]
Generally speaking, the value of K+ is low relative to the other three ions and has little effect on the equation. An alternative formula, which includes K+, is sometimes used, particularly by Nephrologists. In Renal units, the K+ covers a wider range and, therefore, has a more significant effect on the measured anion gap. In these circumstances, an alternative formula is used:
Anion gap = [Na+] + [K+] – [Cl-] – [HCO3-]
99
Fyrir hvað stendur anjónabilið?
The anion gap represents the concentration of all the unmeasured anions in the plasma. It is the difference between the primary measured cations and the primary measured anions in the serum. It can be calculated using the following formula:
100
Hvað er eðlilegt anjónabil?
The reference range varies depending upon which methodology is used to make the measurement but is usually 8 to 16 mmol/L.
101
Hvað orsakar hátt anjónabil? Minnisregla fyrir það?
A high anion gap metabolic acidosis usually occurs as a consequence of the accumulation of organic acid or the impaired excretion of H+ ions. The mnemonic CAT MUDPILES is a useful way of remembering the causes of a high anion gap metabolic acidosis:
- Carbon monoxide
- Alcoholic ketoacidosis
- Toluene
- Metformin, Methanol
- Uraemia
- Diabetic ketoacidosis
- Propylene glycol
- Iron, Isoniazid
- Lactic acidosis
- Ethylene glycol
- Salicylates
102
Hvað orsakar eðlilegt anjónabil? Minnisregla?
A normal anion gap metabolic acidosis usually results from the loss of HCO3- ions from the extracellular fluid. The mnemonic CAGE is a useful way of remembering the causes of a low anion gap metabolic acidosis:
- Chloride excess
- Acetazolamide, Addison’s disease
- Gastrointestinal causes (diarrhoea, vomiting, fistulae)
- Extra (Renal tubular acidosis)
103
Hvað orsakar lágt anjónabil?
A low anion gap is very rare indeed and, if present, is usually due to some sort of analytical error. When genuinely present, it can be caused by a decrease in unmeasured anions (e.g. low albumin) or by an increase in unmeasured cations (e.g. IgG paraprotein in multiple myeloma or hypercalcaemia).
104
Hvaða breytingar á EKG tengjast hyperkalemiu?
- K+ >5.5 mmol/l – peaked T waves (usually earliest sign of hyperkalaemia), repolarisation abnormalities
- K+ >6.5 mmol/l – P waves widen and flatten, PR segment lengthens, P waves eventually disappear
- K+ >7.0 mmol/l – Prolonged QRS interval and bizarre QRS morphology, conduction blocks (bundle branch blocks, fascicular blocks), sinus bradycardia or slow AF, development of a sine wave appearance (a pre-terminal rhythm)
- K+ >9.0 mmol/l – Cardiac arrest due to asystole, VF or PEA with a bizarre, wide complex rhythm.
105
Hvaða EKG breytingar eru fyrstar til að birtast í hyperkalemiu?
K+ >5.5 mmol/l – peaked T waves (usually earliest sign of hyperkalaemia), repolarisation abnormalities
106
Dæmi um 7 atriði sem geta valdið respiratoriskri alkalosu?
- Hyperventilation (e.g. anxiety, pain, fever)
- Pulmonary embolism
- Pneumothorax
- CNS disorders (e.g. CVA, SAH, encephalitis)
- High altitude
- Pregnancy
- Early stages of aspirin overdose
107
Dæmi um 7 atriði sem geta valdið respiratoriskri acidosu?
- COPD
- Life-threatening asthma
- Pulmonary oedema
- Respiratory depression (e.g. opiates, benzodiazepines)
- Neuromuscular disease (e.g. Guillain-Barré syndrome, muscular dystrophy
- Incorrect ventilator settings (hypoventilation)
- Obesity
108
Dæmi um 7 atriði sem geta valdið metaboliskri alkalosu:
- Vomiting
- Cardiac arrest
- Multi-organ failure
- Cystic fibrosis
- Potassium depletion (e.g. diuretic usage)
- Cushing’s syndrome
- Conn’s syndrome
109
Dæmi um 4 atriði sem geta valdið 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)
110
Dæmi um 4 atriði sem geta valdið metaboliskri acidosu með eðlilegu anjónabili:
- Renal tubular acidosis
- Diarrhoea
- Ammonium chloride ingestion
- Adrenal insufficiency
111
Í hvaða 3 lög skiptist glomerular filtration membrane?
1. Fenestrated capillary endothelium with relatively large pores which allow free movement of plasma proteins and solutes but restrict the movement of blood cells
2. Basement membrane, which is more selective and contains negatively charged glycoproteins but still allows free passage of water, nutrients and ions
3. Filtration slits formed by the foot processes of podocytes (specialised cells of the visceral epithelium layer of the capsule) which are the finest filter and restrict the movement of plasma proteins but still allow free movement of ions and nutrients
112
Hvað gera principal frumur í distal convoluted tubule og collecting duct?
Principal cells are the main Na+ reabsorbing cells in the late distal convoluted tubule and collecting duct, and these make up the majority of the tubular cells. The exchange is once again driven by the function of the Na.K.ATP-ase pumps on the basolateral membrane. As in the early DCT, 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). Also, 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.
