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Renal Flashcards

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1
Q

Effective solutes

A

Solutes which cannot passively diffuse across cell membranes.

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2
Q

Tonicity

A

Relative concentration that determines the direction and extent of H2O diffusion. Na+ sets tonicity.

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3
Q

Effective circulating volume

A

Blood volume that is required for adequate perfusion of the vital signs.

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4
Q

Total blood osmolality equation

A

2(Na+)+(blood glucose/18)+(BUN/2.8)

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5
Q

Effective osmolality equation

A

2(Na+)+(Blood glucose/18)

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6
Q

Renal circulation receives….of cardiac output.

A

20%

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7
Q

Renal function is mediated by 3 things:

A

1) internal mechanisms 2) extra and intrarenal endocrine systems 3) ANS (specifically SNS since kidneys are not innervated by PSNS)

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8
Q

Filtration

A

Movement of plasma constituents from glomerulus into Bowman’s capsule.

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9
Q

Reabsorption

A

The movement of constituents from the tubule luminal fluid (forming urine) into the renal interstitium; and/or recycling of these substances back into circulation.

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10
Q

Secretion

A

Movement of constituents from the renal circulation, interstitium, and/or tubule epithelium into the forming urine.

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11
Q

Renal Clearance

A

Volume of blood that can be 100% cleared of a solute per unit time.

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12
Q

GFR

A

Rate at which filtrate from the glomerulus into Bowman’s capsule.

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13
Q

Do cationic or anionic substances cross the glomerular filtration barrier easier?

A

Since glomerular filtration barrier carries a net negative charge, then cationic substances tend to cross the barrier with less resistance than anionic substances.

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14
Q

Normal GFR values: Young men Young women

A

Young men: 130 Young women: 120

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15
Q

GFR

A

High risk for the development of cardiovascular disease

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16
Q

GFR

A

Indicates renal failure and would require replacement via dialysis or kidney transplant.

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17
Q

Basal Scr

A

0.4-1.5

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18
Q

Factors increasing Scr

A

Black race Kidney Disease Large muscle mass Crushing injury Ingestion of meat Ketoacidosis

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19
Q

Factors decreasing Scr

A

Hispanic and Asian race Low muscle mass Vegetarian diet Malnutrition

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20
Q

Filtered Load

A

Amount of solute filtered into Bowman’s capsule per unit time.

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21
Q

Fractional excretion

A

Ratio of solute excreted:filtered load Cx/GFR

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22
Q

Tubular glomerular feedback (TGF) system

A

Regulated by concentration of Na+ in the forming urine as it reaches thick ascending limb in the region of macula Densa. Macula Densa is in close approximation with JG apparatus from afferent arteriole.

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23
Q

Macula Densa

A

Population of specialized cells in the region of the TAL that can sense levels of NaCl.

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24
Q

Juxtaglomerular apparatus

A

Region of modified smooth muscle cells of the afferent arteriole next to the Densa macula that secretes renin.

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25
TGF system mechanism
As GFR is increased to limit, lots of H2O and NaCl end up in the forming urine. Elevated NaCl delivery stimulates macula Densa depolarization. Macular cells secrete factors including ATP, adenosine, and thromboxane. Factors target afferent arteriole and causes vasoconstriction. This lowers Glomerular P and down modulates GFR.
26
Pressure natriuresis
In the event of an exaggerated volume expansion, sensitivity of TGF mechanism is decreased. Thus, high glomerular P and increased GFR are maintained to restore euvolemia.
27
Where are angiotensinogen and ACE found in the kidney?
Angiotensinogen is expressed within proximal tubule cells and ACE is present within the proximal tubule brush border.
28
In extra renal RAS, where are renin, angiotensinogen, and ACE found?
Renin is still produced by the JG cells in the kidney. Angiotensinogen is produced and secreted by hepatocytes.
29
ACE2
Enzyme expressed in renal and cardiac tissues that converts AII into angiotensin (1-7)
30
Angiotensin 1-7
They bind to Mas, g coupled receptor, and stimulates vasodilation, blocks proliferation, and promotes bradykinin production.
31
Renin
Protein hormone secreted by JG cells and catalyzes the conversion of angiotensinogen into Angiotensin I. It is regulated by SNS tone (JG cells express B1 receptors), distension of the afferent arteriolar epithelium (elevated BP), signals from macula Densa, ANP, and negative feedback by AII.
32
Plasma renin activity (PRA)
Indicator of RAS activity. Example: volume depletion leads to lowered BP which causes the secretion of renin leading to increase in PRA.
33
ACE promotes vasoconstriction by two ways:
1) production of AII 2) degradation of bradykinin
34
Iso-, hypo-, and hyperosmolality define the osmotic state of the...
Extracellular fluid
35
Renal AII response to Low BP
SNS tone increases AII production increases AII binds to AT1 receptors within efferent arteriolar vascular smooth muscle and induce vasoconstriction AT1 receptors are couples to activation of NHE3, NKCC2, NCC, and ENaC channels increasing sodium reabsorption. AII stimulates aldosterone production and secretion
36
Pharmaceutical manipulation on renal function
ACE inhibitors (-prils) inhibit the conversion of angiotensin I into angiotensin II. ARBs (-sartans) AT1 receptor blockers. Renin Inhibitors (Aliskiren) block the action of renin and thus prevent the conversion of angiotensinogen into angiotensin I.
37
ARB advantage over ACEI?
There is an ACE-indepedent pathway utilizing Chymases that converts AI into AII thus the patient might not respond to ACEI as well as ARBs.
38
ACE escape
The body's ability to use alterantive pathway such as the ACE independent Chymases to maintain AII levels in the body during the use of ACEi.
39
Effect of Norepi on renal function
Norepi binds to the alpha1 receptors in both arterioles causing vasoconstriction and a collective reduction of GFR and renal perfusion to maintain plasma volume. NE stimulates renin secretion from JG cells via B1 receptors. NE to some degree stimulates Na+ and H2O reabsorption from the tubules.
40
Effect of AVP on renal function
AVP binds to V1a receptors on peripheral arterioles to induce vasoconstriction. Within nephron, AVP binds to the V2 receptors to induce epression and activation of AQP2. AVP increases the rate of Na+ reabsorption from the TAL and DCT via NKCC (TAL), NCC (DCT), and ENaC (DCT). AVP also binds to V1b receptors in corticotropes of anterior pituitary to secrete ACTH.
41
Proximal tubule Sodium channels
Movement of sodium across the apical membrane s mediated by Na+-glucose cotransporters (SGLT1 and 2) and Na+-H+ exchangers (NHE-3). Movement across basal membrane is through Na+/K+ ATPases, Na+-HCO3- symptorters, and GLUT1 & 2.
42
Na+ transport in loop of Henle
Active transport in thin ascending limb NKCC2 in TAL pumps Na+, Cl-, and K+ into tubular cell. ROMK2 pumps K+ back into urine to drive NKCC2. NHE-3 exchanges Na+ in for H+ out. Na+/K+ ATPases and Cl-/HCO3- exchangers on basal membrane.
43
Channels in the DCT
NCC on the apical side to transfer Na+ and Cl- out of urine and into tubular cell. ENaC on apical side pumps Na+ out of urine and into tubular cell. On the basal side, Na+/K+ ATPases pumps sodium out and into the interstitium.
44
Part of the CCT that is targeted by aldosterone
Aldosterone-sensitive distal nephron (ASDN)
45
Effects of AVP, aldosterone, and AII on principle cells of CCT
AVP recruits Na+/K+ ATPases into basal membrane and activates apical Na+ channel protein (ENaC). AII also activates apical Na+ channel (ENaC) Aldosterone activates the ENaC channels. All three activate Na+/K+ ATPases on the basal side.
46
Acetazolamide
Weak diuretic, carbonic anhydrase inhibitor that blocks the H+ formation and HCO3- reabsorption in the proximal tubule.
47
Furosemide
Potent loop diuretic, fast acting, short lived and blocks NKCC2 in the TAL. K+ and Ca2+ wasting.
48
Thiazides
Weak diuretics blocks Na+ and Cl- reabsorption. Stimulates K+ secretion and Ca2+ reabsorption. Works on the DCT.
49
Amiloride
Blocks ENaC channels in the CCT. K+ sparing.
50
Sprionolactone and Eplerenone
Aldosterone anatagonists working on the CCT. K+ sparing diuretics.
51
What stimulates aldosterone secretion?
Adrenal glomerulosa cells express AT1 so aldosterone secretion is based on AII levels and hyperkalemia.
52
Salt-sensitive effect on the renal function curve
Salt sensitive is due to increases in dietary sodium induce elevation in BP. The curve will shift to the right with lower slope
53
Euvolemic Hyponatermia
Na+ contenet has not changed but something caused inordinate retention of H2O. Glucocorticoid deficiency, hypothyroidism or SIADH can cause this. Urine [Na+] is elevated since water is not excreted.
54
Hypovolemic Hyponatremia
Loss of TBW and Na+ with more Na+ lost than H2O. GI fluid loss, hemorrhage, sweating, diuretics, mineralocorticoid deficiency. Clinical signs of tachycardia, glattened neck veins, orthostatic hypotension. Urine [Na+] is decresed while BUN is elevated due to decreased renal perfusion. Treat by isotonic saline.
55
Pseudohypoaldosteronism
Type I hypoaldsoteronism. Fatal syndrome causes salt wasting Due to mutations in the SCNN1 gene encoding ENaC protein. Na+ reabsorption will be impaired.
56
What is the difference between neurogenic and nephrogenic?
Neurogenic is a loss in hormone production. Nephrogenic is a mutation disrupting the expression of the hormone receptor.
57
Diabetes Insipidus
Disruption in the AVP system in which body H2O and Na+ balances are often disrupted. This could be due to loss of production of AVP or disrupted expression of V2R or AQP2. Causes Polyruia of DILUTE urine, and polydipsia.
58
Syndrome of inappropriate ADH secretion
Congenital: gain of function mutation in which V2R is activated in absense of AVP. Induced: excessive secretion of AVP. Symptoms: Evolemic hypnatremia, highly concentrated urine (\>100 osmolality), hyposmolality. Treatment: Loop diuretics, fluid restrictions, Demeclocycline and lithium to block V2R mediated activation of AQP2.
59
Type 1 RTA
Could be autoimmune or induced by certain drugs and toxins. Net reduction in H+ secretion within collecting tubules. H+ ATPase and Cl-/HCO3- function impaired. hyper or hypokalemia Urine pH higher than 5.3
60
Type 2 RTA
Urinary loss of HCO3-, glucose, amino acids, and phosphate from proximal RTA. Defects in Na+/H+ ATPase, Na+/K+ ATPase, and carbonic anhydrase. Vitamin D deficiency Hyperaldosteronism can exacerbate the hypokalemia.
61
Type 4 RTA
Hyperkalemic RTA due to Aldosterone deficiency or resistance in the collecting tubule. H+ ATPase impaired. NH4+ recycling, NH3 secretion impaired.
62
Where are glucagon, insulin and somatostatin secreted from?
a cells: glucagon b cells: insulin gamma cells: somatostatin
63
Function of insulin
Promote lipogenesis, glycogenesis, muscle anabolism, and cellular uptake of K+ and free fatty acids.
64
Insulin bioactivity timeline
At very low levels of insulin, Cellular K+ uptake occurs, Next, FFA uptake in adipocytes occurs to promote lipogenesis. As insulin levels rise, impaired hepatic gluconeogenesis occurs. Followed by peripheral glucose uptake in the liver to promote glycogenesis.
65
Type 1 Diabetes Mellitus
Juvenile onset, hereditary autoimmune destruction of B cells. Hypoinsulinemia, hyperglycemia Polydipsia, polyuria, polyphagia
66
Type 2 Diabetes Mellitus
Syndrome of metabolic obesity Late onset with some genetic predisposition. Hyperinsulinemia with insulin resistance. Impaired glucose tolerance.
67
Metformin
Biguanide Impaires hepatic gluconeogenesis, intestinal glucose absorption and enhances peripheral glucose uptake.
68
Thiazolidenediones (piglitazone)
Insulin receptor sensitizer
69
Sulfonylureas
Insulin secretagogues, promotes insulin production
70
SGLT inhibitors
Impedes glucose reabsorption from forming urine
71
DPP-4 Inhibitor
Impedes degradation of glucagon-like peptide; GLP-1 promotes insulin secretion, inhibits glucagon secretion
72
What do the kidneys utilize for gluconeogenesis?
Lactate, glutamine, and glycerol
73
Nephrin
Transmembrane protein present within the slit diaphragm of glomerular podocytes. It helps in restricting protein filtration across the glomerulus. Upregulated RAS activity impairs the activity of nephrin.

Renal/Endo/repro (5 decks)

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