Unit 1 Renal Flashcards

1
Q

How does high salt intake contribute to greater excretion calcium in the kidneys

A

Since Ca2+ is coupled to Na+ reabsorption in the PCT, when there’s an increase in salt intake theres a decrease in salt reabsorption theres also a decreased Ca2+ reabsorption (inc. excretion).

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2
Q

What percent of Calcium is reabsorbed in the PCT?

A

65%

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3
Q

What is the MOA of calcium reabsorption in the PCT

A

Electrochemically- paracellularly

As the lumen have a net positive potential, calcium moves passively (REGULATED by Na+ reabsorption)

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4
Q

What is the MOA of calcium reabsorption in the TAL

A

Electrochemically- paracellularly

As the lumen develops a net positive potential due to the NKCC co transporter, calcium is reabsorbed paracellularly

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5
Q

What parts of the nephron reabsorbs calcium

A

PCT, TAL, DCT

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6
Q

What is the MOA of calcium reabsorption in the DCT

A

Actively-transcellular

PTH regulated process

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7
Q

What percent of calcium is reabsorbed in the TAL?

A

20%

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8
Q

What percent of calcium is reabsorbed in the DCT

A

7-10%

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9
Q

What can alkalemia do to calcium?

A

It can cause hypocalcemia. this is because theres less protons binding to proteins, which leads free calcium to bind to proteins. this causes less active calcium, thus hypocalcemia.

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10
Q

What is low when someone has diarrhea?

A

Bicarb—-> metabolic acidosis

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11
Q

What is low when someone is throwing up excessively?

A

HCl—-> metabolic alkalosis and hypochloremia

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12
Q

What kidney arterioles does angiotensin II affect?

A

Both afferent and efferent, BUT efferent more

Causes vasoconstriction

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13
Q

How does angiotensin II affect the filtration fraction?

A

A2 causes decreased RFF due to constriction of both renal arterioles.

GFR decreases overall as well but not as much as RPF due to increased constriction of efferent arteriole, which slightly increases GFR

Therefore, FF is increased

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14
Q

How does an increased FF change peritubular capillary oncotic pressure

A

Since more plasma is filtered into the glomerulus, this leaves more a higher protein concentration leaving the efferent arteriole, thus the oncotic pressure of the peritubular capillaries is higher.

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15
Q

What does the JGA regulate?

A

BP, GFR, renin secretion

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16
Q

Where is the JGA located?

A

Between the afferent arteriole and DCT

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17
Q

What components make up the JGA?

A

Mucula Densa

Juxtaglomerular cells

Mesangial cells

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18
Q

Function/location of macula densa

A

Regulate NaCl concentration
-if NaCl is high in DCT–> inhibits renin release (from JG cells)–> dec. aldosterone–> inc. Na excretion

-if NaCl is low in DCT–> stimulates renin release (from JG cells)–> inc. aldosterone–> inc. Na reabsorption

Located in the DCT where it meets afferent arterioles

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19
Q

Function/location of JG cells

A

Location: in the afferent arterioles near the macula densa

Regulates BP by secretion/inhibition of renin

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20
Q

Function/location of mesangial cells

A

between JG cells and macula densa

function = unknown

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21
Q

what can cause post-renal damage

A

Kidney stones, they can block ureters, cause back flow which can lead to AKI

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22
Q

Roadmap of how decreased renal artery resistance and lead to increased oxygen consumption.

A

Dec. resistance—> inc. flow–? increases hydrostaic pressure of arteriole–> Inc GFR –> Inc. sodium (normal) in tubule —> more transporters needed for reabsorption —> more Na-K ATPase —> increased O2 consumption

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23
Q

Calculate new plasma osmolarity of 80kg man who drank 2L of water

A

288 mOsm/L

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24
Q

What transporter is messed up in type 1 RTA

A

All in DCT and CD

-H+ ATPase –> decreased H+ secretion –> metabolic acidosis

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25
Q

What transporter is messed up in type 2 RTA

A

In PCT

-Na/H+ exchanger —> Decreased reabsorption of Bicarb–> Metabolic acidosis

-Na/Bicarb cotransporter –> decreased reabsorption of bicarb—> metabolic acidosis

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26
Q

What transporter is messed up in type 4 RTA

A

in DCT and CD

-Na transporters insensitive to aldosterone—> ENaC isnt working–> decreased Na+ reabsorption–> dec. proton pump activity–> dec. proton excretion–> metabolic acidosis

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27
Q

which RTA’s have hyperkalemia?

A

type 4 because aldosterone transporters arent working—> decreased K+ exchange—> dec. K+ excretion —> hyperkalemia

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28
Q

Which RTA’s have hypokalemia?

A

Type 1 and 2

this is due to decreased sodium reabsorption in proximal and distal convoluted tubules which leads to increased sodium reabsorption in the collecting duct, which leads to increased potassium excretion –> hypokalemia

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29
Q

Which RTA has kidney stones

A

RTA type 1, due to very alkaline urine.

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30
Q

What is the free water clearance equation?

A

V - Cosm
= V - (Uosm x V)/ Posm

answer can be negative

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31
Q

What does a negative Ch2o mean?

A

Body is conserving water

32
Q

What does a positive Ch2o mean?

A

Body is excreting excess water

33
Q

Why does the single effect have a greater effect of concentrating urine in the presence of ADH?

A

Because it further increases the medulla osmolarity in the TAL. This, along with ADH, further increases the drive of water out of the collecting duct and into the interstitium, which leads to the urine being more concentrated

34
Q

Which diuretic is the ONLY one that decreases calcium excretion

35
Q

What type of stone is present in RTA type 1

A

Calcium phosphate

36
Q

What conditions typically causes calcium phosphate stones

A

hyperparathyroidism

37
Q

What conditions typically causes calcium oxalate stones?

A

Hyperoxaluria.

Calciuria and oxaluria present

38
Q

What conditions are typically cause uric acid stones

39
Q

What conditions typically cause struvite stones

A

UTI’s with urease bacteria present

40
Q

What diuretic like response is present in barterr syndrome

A

Loop diuretics (TAL)

41
Q

What diuretic like response is present in gitelmann syndrome

A

Thiazide (DCT)

42
Q

What is Conn syndrome

A

Primary hyperaldosteronism- adrenal glands produce excess aldosterone

43
Q

What is the shape of cystine kidney stones

44
Q

ARPKD

A

small cysts in small people (kids)

45
Q

ADPCD

A

large cysts in large people (adults)

46
Q

Wilms tumor gene and inheritance

47
Q

Von Hippel Lindau disease gene and inheritance

48
Q

Tubular sclerosis gene and inheritance

A

TSC1/2, AD

49
Q

What do calcium phosphate stones look like under microscope

A

Wedge shaped prisms. They look like quart crystals

50
Q

What do calcium oxalate stones look like under the microscope?

A

Dumbell or envelope shape

51
Q

WHat do struvite stones look like under the microscope?

A

Coffin lid. Looks like a rectangle within a rectangle

52
Q

What do uric acid stones look like under the microscope?

A

Rhomboid, foot-ball shaped, yellowish and brown

53
Q

What do cystine stones look like under the microscope?

A

Hexagonal (6 sides), Benzene ring

54
Q

What parts of the nephron handles potassium

A

PCT, TAL, DCT/CD

55
Q

How is potassium handled in the PCT

A

Passive paracellular reabsorption via electrochemical gradient

56
Q

How is potassium handled in the TAL

A

Passive paracellular reabsorption via positive luminal potential created by NKCC co transporter

57
Q

How is potassium handled in the DCT/CD

A

Secreted via principal cells (Na+ exchanges for K+)

Reabsorbed via alpha intercalated cells by proton-potassium exchanger

58
Q

What percent of potassium is reabsorbed in the PCT

59
Q

What percent of potassium is reabsorbed in the TAL

60
Q

What percent of potassium is reabsorbed in the DCT/CD

A

depends on diet

61
Q

What parts of the nephron handles magnesium

A

PCT,TAL,DCT

62
Q

How is magnesium handled in the PCT

A

passive reabsorption parracellularly

63
Q

How is magnesium handled in the TAL

A

Passive paracellularly due to positive luminal potential via NKCC cotransporter

64
Q

How is magnesium handled in the DCT

A

Active transport via TPRM6 (Mag-Cal co transporter

65
Q

What percent of magnesium is reabsorbed in the PCT

66
Q

What percent of magnesium is reabsorbed in the TAL

67
Q

What percent of magnesium is reabsorbed in the DCT

68
Q

What affects potasium reabsorption

A

Diet, aldosterone, acid-base disturbances

69
Q

What part of the nephron handles phosphate

A

Mostly the PCT, barely the DCT or CD

70
Q

How does the PCT handle phosphate?

A

Actively via the Na+/phosphate cotransporter

71
Q

What effects PCT reabsorption of phosphate

A

High Phosphate= dec. reabsorption
inc PTH = dec. reabsorption

72
Q

What percentage of phosphate is reabsorbed in the PCT?

73
Q

Why is glutamine so important in the kidneys (PCT/CD)

A

It is broken down into ammonia and bicarb via glutaminase.

Therefore creating ammonia to buffer H+ in the urine and also bicarb for reabsorption and to buffer H+ in the blood

74
Q

What role does ammonia play in the TAL

A

It is moved into the interstitium to increase medullary osmolarity, and decrease osmolarity in the tubular lumen

75
Q

What role does ammonia play in the CD

A

It moves into tubular lumen as ammonia to buffer H+ (turns into ammonium). This is called diffusion trap.

76
Q

How does potassium levels affect ammonia production

A

Hypokalemia–> increases production
Hyperkalemia–> decreases production