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CIF > Kidney > Flashcards

Kidney Flashcards

1
Q

Describe the overall anatomy of a kidney

A

Half-circle like structure: Renal capsule surrounding the renal cortex for antimicrobial purpose. Renal pyrimids (/renal medullas) in the cortex around the major calyx. A renal lobe is a renal pyrimid and the surrounding cortex, ending in a papillary duct –> renal papilla. The renal papilla connects to the minor calyx –> major calyx –> ureter through the renal hilus. The renal artery and -vein also goes through the renal hilus.

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2
Q

Describe a renal corpusculum.

A

The renal corpusculum is a round structure in the kidney lobes. A RC is build up by a membrane called Bowmans capsule, surrounding the glomerulus of the RC. The glomeruslus of the RC is a capillary network, where certain types of plasma components is filtered out of the blood, and delivered to the nephron via Bowmans capsule. The afferent arteriole delivers the blood that needs to be filtrated to the glomerulus, whereas the efferent arteriole is draining the glomerulus of the filtered blood.

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3
Q

Which kind of cells are special for the renal corpusculum?

A

JG-cells in the affterent arteriole: baroreceptor cells
Podocysts covering the afferent capillaries (visceral layer)
In the distal convoluted tubule: macula densa cells: chemoreceptor cells

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4
Q

Which structures comprise a nephron?

A

Bowmans capsule, proximal convoluted tubule, loop of Henle, and distal convoluted tubule

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5
Q

Which kind of molecules is filtered by the nephrons?

A

Elctrolytes (Na+, K+, Cl-, Mg2+, Ca2+), HCO3-, H2O, small proteins, glucose, amino acids, lipids, urea

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6
Q

What happens in the proximal convoluted tubule?

A

Reabsorption: 65 % of Na+, 65 % of H2O, 50-60 % of Cl-, 60 % of K+, 60 % of Ca2+, 90 % of HCO3-, 100 % glucose and AAs (cotransport with Na+), 50 % of urea, lipids and small proteins (Mg2+ unknown)

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7
Q

What happens in the loop of Henle?

A

15 % of H2O is reabsorped

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8
Q

What happens in the distal convoluted tubule?

A

Reabsorption: 25 % of Na+, 30 % of K+, 30 % of Cl-. K+ absorption driving the reabsorption of Ca2+ and Mg2+

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9
Q

Describe the general osmolarity through a renal pyramid.

A

The osmolarity increases through the pyramid down to the papillary duct, starting at 300 mosm (same as plasma) –> 500 –> 700 –> 900 –> 1200

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10
Q

What is the difference between hypertonic, isotonic, and hypotonic?

A

Hypertonic: more solute, less H2O, isotonic: equal amounts, hypotonic: less solute, more H2O

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11
Q

Where in the nephron is hypertonic, and where is hypotonic?

A

Hypertonic: loop of Henle
Hypotonic: distal convoluted tubule

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12
Q

What channels is the Na+ and Cl- reabsorption driven by in the distal convoulted tubule?

A

Na+/K+ ATPase on the interstitial membrane: 3 Na+ in, 2 K+ out (K+ pump on same side ensuring the K+ gradient)

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13
Q

What does the nephron do?

A

Forms and ultrafiltrates the blood plasma, and selectively reabsorbs tubular fluid and secretes solutes into it

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14
Q

What does the glomerulus do?

A

Filtration unit: forms ultrafiltrate of plasma by bulk pressure driven transport

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15
Q

What is the function of the nephron?

A

Absorption and secretion: converts ultrafiltrate to urine by selective transepithelial transport

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16
Q

What drives the filtration in the glomeruli?

A

Hydrostatic and osmotic pressures

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17
Q

What solutes are absorbed in the kidney?

A

Glucose, amino acids, major body electrolytes

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18
Q

Which solutes are secreted by the kidney?

A

PAH (paraimmunohippurate)

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19
Q

Which solutes are filtered by the kidney?

A

Creatinine

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20
Q

Which solutes are both secreted and absorbed by the kidney?

A

K+, uric acid, urea

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21
Q

How is the glomeruli filtration rate found?

A

GFR = (U x V)/P

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22
Q

What is the GFR of a healthy person?

A

125 ml/min

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23
Q

How much H2O, Na+ and Cl- is excreted from a healthy person a day?

A

1-3 L H2O, 100-300 mmol Na+ and 100-500 mmol Cl-

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24
Q

Barter syndrome is caused by mutations in transporter I-V (one of them). What are the symptoms?

A

Salt-loss, polyurea (more urine), normal-low blood pressure, hypokalemia (K+ loss), hypertrophy of JGA (trying to increase renin secretion), and metabolic alkolosis (Na+ loss will affect the Na+/H+ exchanger –> more acidic urine, more alkaline blood plasma)

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25
Q

Liddle disease is caused by hyperactive Na+ channels (ENaC). What are the symptoms?

A

Increased Na+ reabsorbtion, increased K+ loss, hypertention (high blood pressure), hypekalemia (loss of K+), metabolic alkalosis, low renin and aldosterone.

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26
Q

Describe the driving force of Cl- and H2O.

A

Cl- and H2O transport is driven by Na+ reabsorbtion. Cl- can be transported paracellularly or transcellularly. H2O transport is passive, and follows NaCl/NaGlu transport.

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27
Q

What does aldosterone regulate?

A

Na+ and Cl- transport, by increasing transcription of Na/K ATPases (K+ channels?) and ENaC (Cl- follows)

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28
Q

What receptor does aldosterone bind to?

A

MR receptors

29
Q

Describe the molecular mechanisms of a liqorice shock.

A

Glycyrrhizin acid (liqorice) inhibits the conversion of cortisol to cortisone –> continously active MR receptor –> increased Na+ and H2O reabsorbtion –> increeased plasma volume –> increased blood pressure

30
Q

Which transporter in the kidney could a drug against high blood pressure target?

A

Na+ transporter (blocked Na+ transporter –> decreased Na+ reabsorbtion –> decreased H2O reabsorbtion –> decreased plasma volume –> decreased blood pressure). Also leads to diuresis (more urine)

31
Q

How much K+ and Ca2+ are secreted by a healthy person a day?

A

50-450 mmol K+, and 0.5-20 mmol Ca2+

32
Q

How much HCO3- and phosphates are secreted by a healthy person a day?

A

1 mmol HCO3-, and 5-20 mmol phosphates

33
Q

How much D-glucose and H+ are secreted by a healthy person a day?

A

0-1 mmol D-glucose, and 30 mmol H+

34
Q

What is the function of renin, and where is it secreted from?

A

Regulates blood pressure, and is secreted from JG cells in the afferent arteriole

35
Q

Where is all of the glucose reabsorbed?

A

In the proximal convoluted tubule

36
Q

What transporters is responsible for the luminal reabsorbtion of glucose?

A

SGLT2 in the early proximal convoluted tubule, and SGLT1 in the late proximal convoluted tubule

37
Q

What is the differences between the SGLT1 and -2 transporters?

A

1: high affinity, low capacity - reabsorbs app. 10 % of the filtrated glucose
2: low affinity, high capacity - reabsorbs over 90 % of the filtrated glucose

38
Q

Which transporters are responsible for the basolateral reabsorbtion of glucose?

A

GLUT2 in the early proximal convoluted tubule, and GLUT1 in the late proximal convoluted tubule

39
Q

What symptoms does familial rena glucosuria (mutation in SGLT2) exhibit?

A

Glucose in urine

40
Q

What symptoms does Fanconi-Bickel syndrome (mutation in GLUT2) exhibit?

A

No glucose reabsorbtion (very bad)

41
Q

Drugs targeting SGLT2 has been used for treatment of T2D. What is the pros and cons of this?

A

Pros: glycemic effects, modest weigth loss, lowers blood pressure, protective effects on cardiovascular system and the kidney
Cons: diuresis, thirst, urogenital infections

42
Q

Drugs targeting SGLT2 has been used for treatment of T2D. How does it work?

A

Pee out more glucose, increased fluid secretion, potential effects on blood pressure (lowers)

43
Q

What is the klotho gene?

A

It’s everywhere, and is very important
Membrane form: protein found in renal tubules
Secreted form: humoral factor that regulates activity of several glycoproteins on the cell surface
It regulates phosphate reabsorbtion in the kidney –> An “aging supressor”

44
Q

What transporters is responsible for Ca2+ transport on the luminal side of the nephrons, and what are they regulated by?

A

TRPV5 and -6
Regulated by PTH (para thyroid hormone)

45
Q

What transporters is responsible for Ca2+ transport on the basolateral side of the nephrons?

A

Ca2+/H+ exchanger (ATPase), and NCX1 (Na+/Ca2+ exchanger, also regulated by PTH)

46
Q

What transporters is responsible for K+ transport on the luminal side of the nephrons?

A

ROMK

47
Q

What transporters is responsible for K+ transport on the basolateral side of the nephrons, and what are they regulated by?

A

Na/K ATPase, driven by the K+ pump

48
Q

What is K+ secretion and uptake stimulated by?

A

Secretion: aldosterone
Uptake: K+ depletion or acid loading (increase in H+/K+ pump expression and K+ reabsorbtion)

49
Q

What is the Henderson-Hasselbach equation?

A

pH=pKa + log (conjugate base)/(weak acid)
pOH=pKb + log (conjugate acid)/(weak base)

50
Q

Describe the acid/base balance of the kidney.

A

Secrete H+, absorbs HCO3- + produces HCO3-

51
Q

What three pathways of H+ secretion are there?

A

1) CO2 dependent, 2) phosphate binding, 3) ammonium binding

52
Q

What transporters in the luminal side of the proximal tubules transports H+?

A

NHE3 - Na+/H+ exchanger activated by PKC, inhibited by PKA
Vascular H+ pump

53
Q

What transporters in the basolateral side of the proximal tubules transports HCO3-?

A

Boron transporter/eNBC: electrogenic NA+/HCO3- cotransporter
AE: Cl-/HCO3- exchanger

54
Q

What transporters in the luminal side of the collecting ducts transports H+?

A

Gastric- and non-gastric type H+/K+ pumps, vascular H+ pumps, anion exchanger (AE)

55
Q

What is the normal urine volume a day for a healthy person, and what is the osmolarity?

A

App. 1,5 L, app. 400 mOsm/l

56
Q

How does the transport of H2O differ between the loop of Henle and the distal tubules?

A

Loop of Henle: passive transport, follows NaCl
Distal tubules: active transport through aquaporrins

57
Q

What hormone regulates H2O permeability in nephrons, and how?

A

Arginine Vasopressin (AVP) aka anti-diuretic hormone (ADH) –> increases H2O reabsorbtion by facillitating the translocation of AQP2 in the luminal medullary collecting duct

58
Q

Briefly describe the signaling pathway of AVP.

A

AVP binds to V2 receptor (GPCR) –> G-alpha + ATP activates AC –> cAMP increase –> PKA activation –> protein phosphorylation –> transcription of AQP2 + translocation of AQP2 vesicles to luminal plasma membrane

59
Q

How is diabetes related to AVP?

A

Diabetics lack AVP, can either be
1) central: lesion in hypothalamus or pituitary
2) nephrogenic: e.g., mutation in AQP2
–> results in polyuria and hyperdipsia (thrist)
–> can lead to hyper-natremia , hypotension and shock if untreated

60
Q

What is Syndrome of Inappropiate Antidiuretic Hormone secretion (SIADH), and what can it be caused by?

A

Result of too much AVP –> high urine osmolality, hype-osmolar plasma, hyponatremia
Can be caused by tumours, cranial disorders, pulmonary disorders, and drugs

61
Q

What does the ECF volume control system modulate?

A

Urinary excretion of Na+ (or it is actually the effective circulating volume that modulates this)

62
Q

What does the extracellular osmolality modulate?

A

Urinary excretion of H2O

63
Q

What is renal autoregulation?

A

The kidneys regulation of blood flow

64
Q

What is the myogenic mechanism?

A

Intrinsic renal autoregulation:
High BP –> high GHP (glomeruli hydrostatic pressure) (–> high GFR) –> capilaries stretch –> stretch sensitive Na+ channels on smooth muscle cells are gated (influx of Na+) –> Ca2+ channels on SR are gated –> contraction –> vasoconstriction –> decreased GBF (glomeruli blood flow) –> lower GFR
Low BP –> low GHP –> capilaries don’t stretch –> stretch sensitive Na+ channels on smooth muscle cells are not gated –> Ca2+ channels on SR are not gated –> less contraction –> vasodilation –> increased GBF –> higher GFR

65
Q

What is the tubulo glomerular feedback mechanism?

A

Intrinsic renal autoregulation:
High BP –> high GFR –> high concentration of NaCl in ultrafiltrate –> macula densa cells in the distal convouluted tubule sense high conc of NaCl –> secretion of adenosine –> vasoconstriction of aferent arteriole –> lower GBF –> lower GFR –> lower NaCl conc
Adenosine –> inhibits JG cells secretion of renin
Low BP –> low GFR –> low concentration of NaCl in ultrafiltrate –> macula densa cells in the distal convouluted tubule sense low conc of NaCl –> secretion of PGI2 and NO –> vasodilation of aferent arteriole –> higher GBF –> higher GFR –> higher NaCl conc
PGI2 –> stimulates JG cells secretion of renin

66
Q

In which two ways can the autoregulation happen extrinsicly?

A

Sympathetic system
Renin-Angiotensin-Aldosteron system (RAAS)

67
Q

Describe the mechanisms behind sympathetic regulation of low BP

A

Only very low BP!
Baroreceptors in carotid cells in heart sense low BP –> signal to CNS –> release NA and adrenalin –> binds to beta-1 cells in heart –> higher HR and contractility –> higher CO –> higher BP
Adrenalin and NA binds to alfa-1 receptors on afferent artriole –> vasoconstriction (other organs needs the blood more) –> lower GFR
Adrenalin and NA also binds to alfa-1 receptors on systemic vessels –> vasoconstriction –> higher resistance –> higher BP
A and NA binds to beta-1 Rs on JG cells –> release of renin –> release of angio tension 2
High BP –> vice versa

68
Q

Describe the mechanisms of the RAAS for low BP.

A

Baroreceptors in JG cells sense low BP –> release of renin –> renin cleaves angiotensinogen into angiotensin 1 –> ACE from lungs cleaves AT1 into AT2 –> AT2 stimulates hypothalamus –> anterior pituitary release of ADH –> ADH stimulates transcription and translocation of AQPs in the collecting duct (+ thirst) –> increase of H2O reabsorbtion –> increase of BV –> increase of BP
ADH also acts on the adrenalin gland –> release of aldosterone –> increase Na+ and H2O reabsorbtion in distal convoluted tubule –> increase of BV –> increase of BP
AT2 binds to receptors on efferent arteriole –> vasoconstriction –> longer transit time
AT2 binds to receptors on proximal convoluted tubule –> increase of reabsorbtion of Na+ and H2O –> increase BV –> increase BP
AT2 also works on systemic vessels –> vasoconstriction –> increased resistance –> increased BP
=> higher GFR

69
Q

Describe the mechanisms of the RAAS for high BP.

A

All the processes of low BP does not happen
ANP is released –> blocks all affects of AT2

CIF (11 decks)

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