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Week 4 Flashcards

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1
Q

How does the countercurrent multiplier work to keep increased osmotic pressure in medulla?

A
  1. Na+ reabsorption in thick ascending limb, ↑ medullary osmolarity
  2. H2O is drawn out of thin descending limb via AQP-1, equilibrating w/ medullary osmolarity
  3. Concentrated fluid moves around bend of loop into thick ascending limb
  4. Process repeat, increasing interstitial osmolality each time (to maintain increased osmotic gradient in medulla)
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2
Q

How does the countercurrent exchange work to keep increased osmotic pressure in medulla? (only discuss movement of Na) (3)

A
  1. Na+ transported out of thick ascending limb diffuses into descending vasa recta (which has low Na concn)
  2. Na+ is carried deeper into medulla
  3. diffuses out of vasc. → medulla to maintain high concentration of medulla
  4. Blood rising up through ascending vasa recta encounter less concn medulla and causes Na+ to diffuse out of ascending vasa recta and into descending limb
  5. Na+ in descending loop of Henle is taken back into deeper medulla
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3
Q

How does the countercurrent exchange work to keep increased osmotic pressure in medulla? (only discuss movement of Water) (3)

A
  • Water is drawn out of the descending vasa recta as it encounters a progressively large concentrated interstitium.
  • Then water enters the vasa recta and is removed from the medulla to maintain concentration in medulla
  • More water is drawn out of the upper descending limb, less is available to be drawn out from lower descending limb
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4
Q
  1. in the outer medulla (Blank A) is the primary solute making a high concn interstitium
  2. In the inner medulla (Blank B) is the primary solute making a high concn interstitium
A

Blank a- NaCl

Blank b- urea

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5
Q

How is urea recycled in the nephron? (3)

A
  • Urea is freely allowed to go into the glomerulus
    • Then 50% is reabsorbed in the proximal tubule
    • The remaining 50% eventually moves into ascending limb and the other 50% is secreted from the interstitium and put into the ascending limb = urea is back to 100% of filtered load
    • Then 50% is reabsorbed in the collecting duct where it enters medulla and other 50% is excreted
    • Only 50% of filtered load is excreted due to this recycling
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6
Q

ADH

  1. What brain structure first signals its release?
  2. Where is it released from?
  3. Purpose of ADH?
  4. What does it cause in the nephron (2)
A
  1. Hypothalamus instructs posterior pituitary to make ADH
  2. ADH is released from posterior pituitary
  3. causes the kidneys to release less water, decreasing the amount of urine produced
  4. increases presence of APQ-2 channels on principal cells to increase H2O reabsorption (inhibiting H2O from being excreted in urine) ++++ PLUS it also decreases the vasa recta blood flow to reduce dilution of the medullary interstitium
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7
Q

What are the major functions of the kidney?

  1. maintains plasma pH, electrolyte balance, removes (Blank A)
  2. blood formation via formation of (Blank B)
  3. blood pressure regulation
  4. Vitamin (Blank C) activation
A
  1. Blank A - waste
  2. Blank B- EPO
  3. Blank C - D
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8
Q

Differentiate between renal lobe and renal lobule

A
  1. renal lobe -contains renal pyramid and associated cortex tissue
  2. comprised of central collecting duct and its associated nephrons
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9
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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10
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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11
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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12
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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13
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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14
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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15
Q

Fill in the blank in this chart showing blood flow through the kidney -

A
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16
Q

what is the difference between cortical and juxtamedullary nephron?

A
  1. Cortical Nephron: closer to exterior capsule, shorter loop of Henle
  2. Juxtamedullary Nephron: closer to interior medulla, longer loop of H
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17
Q

Describe the function of each

  1. Mesangial cells
  2. Podocytes
  3. Macula Densa
  4. Juxtaglomerular Cells
A
  1. Mesangial Cells: specialized connective tissue, secrete ECM + type IV collagen+laminin to support glomerulus
  2. Podocytes: specialized squamous epithelial, contains foot processes that surround glomerulus
  3. Macula Densa: tightly clustered cell of distal convoluted tubule (monitor Na + levels / fluid volume)
  4. Juxtaglomerular Cells: connected to macula densa via gap junctions, release renin
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18
Q

Bowman’s capsule

  1. What is in the visceral side?
  2. What is in the parietal side?
  3. What is between the two?
A
  • Visceral layer of bowman’s capsule is arrow
  • Parietal layer of bowman’s capsule is arrowhead
  • Urinary space is triangle (it is much smaller in vivo)
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19
Q

where is the filtration barrier located in the renal corpuscle?

A
  1. This is along the edge of the fenestrated capillaries (glomerulus)
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20
Q

Describe the histology of these parts of the nephron

  1. Proximal convoluted tubule (types of cell, lumen description, etc)
  2. Distal convoluted tubule?
A
  1. Arrow – Eosinophilic cells that are taller cuboidal cells. The lumen is small and rugged
  2. Arrowhead – less eosinophilic cells that are shorter cuboidal cells with more nuclei. Lumen is smooth
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21
Q

Describe the histology of these parts of the nephron

  1. Proximal straight tubule
  2. Distal straight tubule
    3.
A
  1. Arrow – Look the same as convoluted ones - have a fuzzy lumen
  2. Arrowhead – Look the same as convoluted ones - have smooth lumen and more nuclei
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22
Q

Describe the histology of these parts of the nephron

  1. Loop of Henle
  2. Collecting ducts
A
  1. Triangle - Have very thin wall of simple squamous epithelium
  2. Bracket - Have a smooth lumen formed from cuboidal cells
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23
Q
  1. Basement membrane is composed of type (Blank A) collagen, laminin, and heparin sulfate
  2. Basement membrane is secreted by (Blank B) cells and (Blank C)
A
  1. Blank A - IV
    Blank B - endothelial
  2. Blank C - podocytes
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24
Q
  1. What are the foot process of podocytes called?
  2. Is this on the visceral or parietal epithelium ?
  3. What is the filtration slit diaphragm?
A
  1. Pedicels
  2. Visceral epithelium
  3. located between pedicels (blocks small proteins / organ anions)
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25
Filtration slit diaphragm 1. purpose of nephrin 2. purpose of cadherins
1. Nephrin is a prevalent protein that forms a zipper shape across diaphragm (image) 2. Cadherins proteins - link actin cytoskeleton of adjacent podocytes
26
1. urothelium - lines majority of (BLANK A) organs 2. this is a transitional epithelium that has (BLANK B) cells 3. The appearance of epithelium/dome cells depends on (BLANK C) → urothelium is thin when bladder is (BLANK D)
1. urinary 2. dome cells 3. distention 4. full - dome cells look distended
27
Ureter 1. what does the lumen look like? 2. What are the three layers of the ureter?
1. star shaped 2. mucosa, muscularis (w/ inner longitudinal and outer circular smooth muscle), adventitia
28
Urinary bladder 1. Thick or thin walled? 2. what are the three layers of urinary bladder?
1. thick 2. mucosa (where dome cells are), muscularis (3 thick layers of smooth muscle) , and adventitia
29
How does the micturition reflex lead to emptying of bladder?
1. sensory nerves on adventitia activate micturition reflex which then cause contraction of detrusor muscle and this empties the bladder (push urine out)
30
Female Urethra 1. length 2. What are glands of littre?
1. short 2. secrete mucus
31
Male Urethra 1. length 2. What are the three segments 3. has less or more glands of littre than female?
1. longer 2. prostatic (transitional epithelium), membranous (voluntary sphincter found here), penile/spongy (stratified epithelium by exit) 3. more
32
What are the three different “kidneys" that appear through embryo development
1. Pronephros 2. Mesonephros 3. Metanephros
33
1. Pronephros - forms and degenerates within week (BLANK A) 2. Mesonephros - interim kidney for (BLANK B) trimester - contributes to male (BLANK C) 3. Metanephros - appears in week (BLANK D) and develops into adult kidney
1. Blank a - 4 2. Blank b - 1st 3. Blank c- vas deferens 4. Blank d - 5
34
1. Ureteric bud is an outgrowth of the (BLANK A) duct and forms what 4 structures? 2. The metanephric mesenchyme (a mesoderm tissue) interacts with ureteric bud to differentiate the (BLANK B)
1. BLANK A- mesonephric duct 2. ureter, pelvis, calyces, collecting ducts 3. BLANK B - nephron
35
1. What is the wilms tumor a cause of? 2. Where does it most often occur
1. proliferation of metanephric mesenchyme - associated with WT1 mutation 2. usually occurs in one kidney
36
1. what is the urachus? 2. what happens when there is incomplete obliteration of the urachus
1. a remnant of a channel between the bladder and the umbilicus (belly button) where urine initially drains in the fetus during the 1st trimester of pregnancy. 2. Urine leakage occurs — PLUS — Urachul remnants may present as adenocarcinoma at dome of bladder in adulthood
37
1. If both kidneys are missing infant will be born with what disorder?
1. oligohydramnios/potter sequence - a lack of amniotic fluid and kidney failure in an unborn infant. A baby rarely survives this. There can be various physical appearances due to lack of amniotic fluid
38
Multicystic Dysplastic kidney 1. what is it caused by? 2. What is it?
1. abnormal ureteric bud and mesenchyme interaction 2. kidney is replaced by cysts
39
ureteropelvic junction (upj) obstruction 1. What is it?
1. when part of the kidney is blocked. Most often it is blocked at the renal pelvis. This is where the kidney attaches to one of the ureters (the tubes that carry urine to the bladder). The blockage slows or stops the flow of urine out of the kidney. Urine can then build up and damage the kidney. Sometimes surgery is needed to improve the flow of urine and other times the problem will improve on its own.
40
Duplex Collecting System 1. What causes it 2. what is it?
1. formation of two ureteric buds-bifurcation of ureteric buds 2. Formation of upper / lower kidneys with separate drainage - looks like two ureters for one kidney
41
Posterior Urethral Valves 1. Typical patient 2. What is it?
1. males only 2. Posterior urethral valves (PUV) are obstructive membranes that develop in the urethra (tube that drains urine from the bladder), close to the bladder. The valve can obstruct or block the outflow of urine through the urethra.
42
Vesicoureteral Reflux 1. what is it
1. backward urine flow from bladder to kidneys - recurrent UTIs seen
43
1. What is horsehoe kidney? 2. What vessel traps the kidneys to create this formation? 3. What does this do to kidney functioning?
1. fusion of inferior poles of both kidneys, preventing ascension from pelvis 2. inferior mesenteric artery 3. normal kidney functioning
44
# Define these terms 1. Glomerular Filtration Rate (GFR) 2. Renal Plasma Flow (RPF) 3. Filtration Fraction (FF) 4. Renal Clearance (CX)
1. Glomerular Filtration Rate (GFR): rate of fluid flowing across glomerulus (inulin / creatinine) 2. Renal Plasma Flow (RPF): rate of total plasma passing through the kidneys (PAH) 3. Filtration Fraction (FF): fraction of total plasma that is actually filtered (GFR / RPF) 4. Renal Clearance (CX): amount of blood component that is removed from plasma (units is volume per unit time)
45
What is the equation for renal clearance CX?
image
46
GFR 1. What three things determine GFR?
1. permeability 2. surface area 3. net filtration pressure (NFP) - depends on oncotic and hydrostatic pressure between glomerulus and bowman's capsule
47
1. What molecules are used to measure GFR? 2. Which one is better and why
1. inulin and creatinine 2. inulin - it is ONLY filtered (not secreted or reabsorbed) - which will indicate GFR rate. Creatinine can slightly overestimate GFR due to moderate secretion of creatinine.
48
GFR is (inversely or directly) proportional to the plasma concentration of creatinine
1. GFR is inversely proportional to plasma concn of creatinine. So if creatinine in plasma is really high then this means GFR is low and this can be due to some glomerular issue bc it is not filtrating creatinine correctly (worsening renal function)
49
1. Capillary hydrostatic pressure (PGC) is controlled via what? 2. Capillary oncotic pressure (∏GC) is controlled via what? 3. Bowman space hydrostatic pressure (PBC) is controlled via what?
1. dilation/constriction of afferent and efferent arteriole 2. alteration of plasma protein concentration 3. dilation/constriction of ureter
50
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
51
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
52
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
53
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
54
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
55
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
56
Explain how the action changes hydrostatic/oncotic pressure, GFR, RPR, FF
57
1. Explain the myogenic mechanism of regulating renal blood flow
* Change in smooth muscle tone of the afferent arterioles in response to to renal arterial pressure changes * Contractions when renal artery pressure increases * Relaxes when renal artery pressure decreases * This is an intrinsic property so no involvement of nerves
58
1. Explain the tubuloglomerular feedback method of regulating renal blood flow
1. vasoconstriction of afferent arteriole with ↑ NaCl in distal tubule (mediated/recognized by macula densa)
59
Tubuloglomerular Feeback 1. when macula densa senses increased NaCl, what occurs? 2. when macula densa senses decreased NaCl, what occurs? 3.
1. Increased NaCl → release of ATP / adenosine from macula densa → afferent vessel vasoconstriction / ↓ renin at JG apparatus 2. Decreased NaCl → release of PGE2 from macula densa → ↑ renin at JG apparatus
60
1. What affect does prostaglandins have on vessels near the glomerulus? 2. What affect does angiotensin II have on the vessels near the glomerulus?
1. dilate afferent arteriole 2. constrict efferent arteriole
61
Vasoconstrictors (decreases renal blood flow) 1. angiotensin II (preferentially constricts efferent) 2. (parasympathetic/sympathetic) stimulation 3. (BLANK A) (hint: its a polypeptide) 4. (BLANK B) (hint: its a drug)
1. sympathetic 2. endothelin 3. NSAIDs (inhibit prostaglandins which have dilatory effects)
62
Vasodilators (increase renal blood flow) 1. (BLANK A) (hint: it is inhibited by NSAIDs) 2. (BLANK B) inhibitors 3. NO 4. ANP and BNP 5. (BLANK C) - it is a hormone/NT
1. prostaglandins 2. ACE inhibitors (blunt effects of angiotensin II - which are dilatory effects) 3. dopamine
63
1. What is filtered load? 2. What is the equation?
1. **The total amount of substance (S) filtered into Bowman's space per time unit** 2. **Px means concn of substance x in plasma**
64
PROXIMAL TUBULE - bulk reabsorption of filtered solutes 1. does it use transcellular or paracellular movement? 2. PCT has iso-osmotic reabsorption - what does this mean?
1. both 2. iso-osmotic meaning when solutes move so do water keeping same osmolarity in filtrate and nephron
65
PROXIMAL TUBULE 1. What substances are reabsorbed in PCT? (8)
1. 100 % of glucose 2. 100% Amino acids 3. urea 4. H2O 5. HCO3- 6. NaCl 7. K+ 8. PO43- *where most of #3-9get reabsorbed*
66
PROXIMAL TUBULE 1. How does Glucose get reabsorbed? 2. what is the function of the basolateral Na/K ATPase channel?
1. Via Na/glucose co-transport 2. maintains a low Na concn in the epithelial cells so there is a concn gradient driving the movement of Na from lumen to epithelial cells/interstitium
67
PROXIMAL TUBULE 1. Other than the Na/Glucose transporter … how else is Na reabsorbed? 2. This mechanism can reabsorb Na as well as what? 3. What can induce this?
1. Na+/H+ anti transporter + carbonic anhydrase 2. Bicarbonate 3. Angiotension II
68
PROXIMAL TUBULE 1. Draw the way that bicarbonate is reabsorbed (hint: it used Carbonic anhydrase and also it involves reabsorption of Na+)
1. image
69
1. What is Hartnup Disease? 2. The deficiency this disease leads to can cause what? 3. In what part of the nephron does this occur in?
1. When a person is unable to absorb certain amino acids from the diet (tryptophan especially) → bc of lack of tryptophan/Na+ transporter in proximal tubule so AAs are excreted in urine 2. Deficiency in tryptophan causes niacin deficiency → causes skin rash resembling pellagra 3. Proximal convoluted tubule
70
1. What is Type II Renal Tubular Acidosis
1. When at the PCT - a person is unable to absorb bicarbonate (HCO3-) → this causes metabolic acidosis
71
How can carbonic anhydrase inhibitors act as diuretics?
1. inhibition of carbonic anhydrase inhibits H2CO3 from becoming CO2 and H2O. → CO2 and H2O then get reabsorbed and it becomes a method of H2O reabsorption 2. If CA is inhibited then H2O cannot be absorbed but this is not a major form of H2O reabsorption so this is why these are weak diuretics
72
1. What is Fanconi Syndrome 2. What is the inherited cause of this? (1) 3. What is the acquired cause of this? (3)
1. loss of proximal tubule functions - impaired absorption of essential solutes 2. inability to break down cystine so it accumulates in PCT 3. lead poisoning, multiple myeloma, drug induced
73
THIN DESCENDING LOOP OF HENLE 1. what is reabsorbed in this section of the nephron?
1. reabsorbs H2O
74
THIN DESCENDING LOOP OF HENLE 1. How is H2O reabsorbed? 2. What is this section IMPERMEABLE to?
1. passively - this is due to medullary hypertonicity 2. Na+ → this concentrates the urine bc the fluid in nephron reaches equilibrium with osmolarity of nephron
75
THICK ASCENDING LOOP OF HENLE 1. What substances does this section reabsorb transcellularly? 2. What does this absorption do to the urine? 3. What is this section impermeable to?
1. Na+/K+/Cl- (via the NKCC cotransporter) 2. This dilutes the urine because you are taking solutes out 3. H2O
76
THICK ASCENDING LOOP OF HENLE 1. What substances does this section reabsorb paracellulaly? 2. What is necessary to continue this paracellular reabsorption?
1. Mg2+ and Ca2+ 2. There is a positive charge inside the epithelial cells that pushes K+ out into intersitium and lumen. This creates a positive charge in lumen → which “pushes” Mg/Ca to move paracellulary into interstitium
77
THICK ASCENDING LOOP OF HENLE 1. what inhibits the NKCC cotransporter?
loop diuretics
78
DISTAL CONVULTED TUBULE 1. What is reabsorbed in this section? 2. What is this section impermeable to? 3. what does this do the urine?
1. Na+/Cl- (via one cotransporter) and Calcium 2. H2O 3. Further dilutes the urine (hypotonic urine) because you are taking out more solutes
79
DISTAL CONVULTED TUBULE 1. Via what protein is Na reabsorbed? 2. What about Cl? 3. What about Ca2+
1. Na and Cl are reabsorbed via a Na/Cl cotransporter 2. Calcium is reabsorbed through a concn gradient channel
80
DISTAL CONVULTED TUBULE 1. what inhibits the reabsorption of NaCl (Na/Cl cotransporter) 2. What does the parathyroid hormone do in this section?
1. Thiazide diuretics 2. increases Ca2+ absorption (by activated Na/Ca cotransporter which takes Calcium out of epithelial cell and into interstitium → this creates a concn gradient where Ca2+ will want to leave lumen and come into epithelial cell)
81
COLLECTING TUBULE (made up of principal, alpha intercalated, beta intercalated cells) 1. What is reabsorbed? - which part of collecting tubule 2. What is secreted? - which part of collecting tubule 3. What is impermeable? -which part of collecting tubule
1. Na and H2O (principal cell) 2. K (principal cell), H+ (alpha intercalated), bicarb (beta interacalated) 3. Nothing
82
COLLECTING TUBULE 1. What does aldosterone do in collecting tubule? (4)
1. increases Na/K ATPases in the basolateral side of principal cells AND increase ENaCs on apical side of principal cell → this is all to **INCREASE WATER REABSORPTION/INCREASING BLOOD VOLUME** 2. **INCREASES K+ SECRETION** (principal cell) 3. **INCREASES H+ SECRETION** (alpha intercalated)
83
COLLECTING TUBULE 1. what stimulates the release of aldosterone? (3)
1. angiotensin II 2. high K+ 3. low levels of ACTH
84
COLLECTING TUBULE 1. what does ADH/vasopression do in this section? (one main thing + smaller thing) 2. which of the three types of cells in collecting tubule does this occur in?
1. promotes free water retention by activating V2 receptors → increase cAMP → inserts AQP-2 which increase free water reabsorption 2. also - increases urea reabsorption to maintain high osmolarity of medulla 3. principal cell
85
Renin-Angiotensin-Aldosterone System 1. What is its purpose? 2. How is this system first activated? (3) 3. What is the first substance secreted and from where
1. Raises Na/H2O retention to increase blood pressure 2. Juxtaglomerular apparatus (made of JG cells which are modified smooth muscle of afferent arteriole + macula densa) can sense low stretch of vessels and low Na volumes indicated low blood pressure — sympathetic stimulation can also activate 3. JG cells secrete renin
86
RAAS system 1. sympathetic activation that acts on beta 1 receptor causes? 2. sympathetic activation that acts on alpha receptor causes? 3.
1. renin release 2. arteriole constriction
87
1. Renin leads to production of (BLANK A) 2. What does (BLANK A) cause in nephron (2)
1. angiotensin II 2. efferent arteriole constriction (decreased GFR) and increases Na/H2O retention in PCT via Na/H+ exchanger - this is all in effort to bring up blood volume and BP
88
Parathyroid Hormone 1. What are its functions in nephron? (3)
1. Increases Ca2+ reabsorption in DCT via stimulation of basolateral Ca2+ / Na+ antitransporter 2. Decreases PO4 3- reabsorption in PCT via inhibition of apical PO4 3- / Na+ cotransporter 3. Increases (1,25)-OH2 D3 activation in PCT via stimulation of 1ɑ hydroxylase
89
1. What does dopamine do in the nephron?
1. dilates afferent/efferent arterioles when it is in low doses 2. promotes Na/H2O excretion
90
1. What is effective circulating volume? 2. low ECV activates what?
1. the volume of arterial blood effectively perfusing tissue. 2. sympathetic nervous system/RAAS system to increase ECV
91
1. what is normal plasma Na+? 2. What things must happen in order to maintain normal Na+ plasma levels (Hint: water and sodium)
1. around 140 mEq/L 2. water intake must equal water excretion and sodium intake must equal sodium excretion. 1. plasma sodium is controlled by water retention/excretion. 2. If you have too much water then → hyponatremia → decreases ADH → water is excreted and back to normal w/no change in ECV 3. If you have too much salt then → hypernatremia →increase ADH → water is reabsorbed → normal osmolarity but now ECV is elevated
92
1. How does excess sodium affect ECV?
1. excess sodium in plasma increases osmolality → this leads to water retention → this normalizes sodium osmolality → ends up with now a higher ECV
93
How can heart failure lead to hypervolemia with low ECV?
1. The heart cannot pump blood effectively so kidney things there is decreased blood volume and induces SNS/RAAS to increased volume uptake. This just worsens the issue bc of congestion (pulmonary edema, pitting edema, increased JVP)
94
Regulation of Potassium 1. Short term K balance involves what? 2. Long term K balance involves what?
1. shifts K+ between ICF and ECF (98% of K is intracellular) 2. involves matching dietary intake of K+ to excretion of K+
95
Short Term Potassium Balance (shifting K+ between ICF and ECF) 1. What things shift K+ into the cell (4) - and explain how they do this?
1. insulin, epinephrine, aldosterone - upregulates Na/K ATPase on basolateral side (which takes Na out of epithelial cell and brings K+ into epithelial cell) 2. Alkalosis - low extracellular H+ downregulates H/K+ ATPase in alpha intercalated cell (H/K ATPase NORMALLY excretes K into extracellular but by downregulating this channel then K is kept inside the epithelial cell)
96
Short Term Potassium Balance (shifting K+ between ICF and ECF) 1. What things shift K+ out of the cell (5) - and explain how they do this?
1. Beta Blockers/Digoxin - Inhibit Na/K ATPase (prevents the Na/K ATPase from bringing in K into the epithelial cell) 2. Acidosis - high extracellular H+ upregulates H/K ATPase (H comes into cell and K leaves cell) 3. Hyperosmolarity - draws H2O/K+ out of cells 4. Cell lysis - releases intracellular K+ (remember that 98% of K is inside cell)
97
1. Proximal tubule accounts for (BLANK A)% of K reabsorption - how is it absorbed in PCT (passive/active)? 2. Thick Ascending Limb accounts for (BLANK B)% of K reabsorption - how is it absorbed in PCT (passive/active)? 3. intercalated cells of collecting duct accounts for (BLANK C)% of K reabsorption - how is it absorbed in PCT (passive/active)?
1. 65% - K+ follows Na+ and H2O when they are reabsorbed (passive - paracellular) 2. 20% - NKCC cotransporter (active) PLUS paracellular reabsorption (depends on positive lumen potential) 3. 10% - active reabsorption - depends on activity of K/H ATPase activity on alpha intercalated cell
98
1. What part of the nephron is responsible for determining the K+ content in urine? 2. Explain why Na delivery to this part is responsible for K+ secretion
1. principal cells of collecting duct - this is where secretion of K+ (K+ secretion depends on Na+ delivery to principal cells - 2. **Increased distal delivery of Na+ stimulates distal Na+ absorption, which will make the luminal potential more negative and, thus, increase K+ secretion**
99
1. What is the purpose of ROMK/BK Channels?
1. These are apical K+ channels that increase apical K+ permeability (reabsorption) → ROMK and BK channels open and close with different concns of dietary K+
100
1. How does low dietary K+ channels affect ROMK and BK channels? 2. What about moderate dietary K+? 3. What about high dietary K+? 4. Where are ROMK and BK found?
1. ROMK closed (sequestered in vesicle) and BK closed 2. ROMK open but BK stays closed 3. Both ROMK and BK open 4. Principal cells
101
1. How does high distal tubular flow affect NaCl and K movement 2. How low high distal tubular flow affect NaCl and K movement
1. High distal tubular flow increases the distal NaCl delivery and this leads to increased K+ secretion 2. Low tubular flow decreases NaCl delivery and this decreases K+ secretion
102
1. when does high tubular flow occur (to increase NaCl delivery)? (2)
1. diuretics decrease Na and H2O reabsorption early on in the nephron → this leads to more Na being delivered in distal nephron and increased K+ secretion (this is NOT K SPARING DIURETICS) 2. Increased ECF volume also leads to increased tubular flow
103
1. How does acute acidosis affect K secretion? 2. How does acute alkalosis affect K secretion?
1. ↓ Na+ / K+ ATPase activity / ↓ apical K + permeability → ↓ K+ secretion 2. ↑ Na+ / K+ ATPase activity → ↑ K+ secretion
104
Aldosterone Paradox - the primary confusing thought is that aldosterone encourages Na reabsorption early on in the nephron but aldosterone can also lead to secretion of K (when Na is reabsorbed in the distal nephron) - HOW CAN THESE TWO THINGS HAPPEN?
1. Depends on what the goal is + depends on how much Na is delivered to distal nephrone 2. If goal is Na reabsorption (hypovolemic state) [[Aldosterone activates Ang II → increases Na reabsorption in early nephron which reduces distal nephron Na+ delivery. Thus you get necessary Na reabsorption without a lot of K+ secretion]] 3. If goal is K+ secretion (euvolemic state) [[No activation of Ang II → therefore no reabsorption in proximal nephron. More Na is delivered in distal nephron to stimulate K+ secretion]]
105
1. What are some clinical presentations of hyperkalemia? 2. What about hypokalemia?
1. wide QRS complex, peaked T waves, arrhythmias, muscle weakness 2. U waves, flattened T waves, arrhythmias, muscle weakness
106
What can lead to hyperkalemia? (3)
1. acute/chronic kidney disease 2. aldosterone deficiency (aldosterone is needed for K secretion) 3. increased K release from cells (look at causes of K shift out of cells)
107
1. Does hypomagnesemia lead to hypo or hyperkalemia? 2. Does Bartter syndrome lead to hypo or hyperkalemia? - what is this syndrome?
1. hypokalemia - must correct Mg2+ before K+ corrects 2. Hypokalemia - congenital defect in NKCC transporter in TAL which leads to increased Na delivery to distal nephron and increased K secretion (hypokalemia)
108
1. What is Gitelman syndrome?
1. congenital defect in NaCl reabsorption in distal convoluted tubule - this leads to increased Na delivery to distal nephron (principal cells) and increased K+ secretion
109
1. What is Liddle syndrome?
1. congenital increase in ENaC activity in collecting tubules - this leads to more Na reabsorption that leads to increased K secretion
110
1. What is syndrome of mineralcorticoid excess (SAME) 2. How is this related to licorice intake?
1. caused by deficiency of 11β-hydroxysteroid dehydrogenase, which results in a defect of the peripheral metabolism of cortisol to cortisone. 2. With elevated cortisol you get same effect as aldosterone (increased K secretion) 3. licorice's active ingredient, glycyrrhizic acid inhibits the renal enzyme 11 β-hydroxysteroid dehydrogenase → causing hypokalemia
111
1. sodium disorders (hypo and hypernatremia) is a disorder of (BLANK A) balance 2. What Na value is indicative of hyponatremia? 3. What Na value is indicative of hypernatremia?
1. WATER 2. \<135 mEq/ L (due to excess of water) 3. \>145 mEq/ L (due to deficit of water)
112
1. Clinical presentation of hyponatremia? 2. What about hypernatremia?
1. nausea, malaise, stupor (neaer-unconsciousness), coma, seizures, brain swelling 2. irritability, stupor, coma
113
1. What is the treatment of hyponatremia? (3) 2. What is the treatment of hypernatremia? (2)
1. Fluid restriction, 3% saline infusion, vaptain drugs (block ADH to stop fluid absorption) 2. Water (idea PO), IV fluids (D5W → isotonic w/out adding sodium)
114
Hyponatremia 1. What can cause hyppnatremia (4)
1. heart failure/cirrhosis - decreased ECV which chronically elevates ADH and leads to excess water retention 2. Ineffective kidneys w/inability to properly excrete H2O 3. elevated ADH levels 4. Dietary causes (excess water intake, insufficient sodium intake)
115
1. What is SIADH? 2. What causes normal volume status in SIADH? 3.
1. too much ADH released which leads to increased water retention → hyponatremia w/high urinary Na levels (ADH increases aquaporins and this is how water is retained but does not retain Na) 2. RAAS is decreased preventing volume overload
116
1. what are the causes for hypernatremia? (2)
1. simple dehydration - loss of water through skin, lungs, etc → presents with elevated ADH 2. diabetes insipidus - loss of ADH activity leads to inability to retain water and concentrates Na (excessive water excretion)
117
What are the reasons for extra-renal sodium loss vs renal sodium loss that lead to hyponatremia
118
What are examples of dietary cause vs kidney dysfunction of hyponatremia
119
What are causes of excess ADH vs abnormal dilution that lead to hyponatremia
120
Fill out what these situations are called
121
Fill out what these situations are called
122
Fill out what these situations are called
123
What is the equation to determine plasma osmolarity determined by Na
124
1. What is the equation to calculate infusion volume in hypernatremia (water deficit) 2. calculate water deficit - rate of correction should not exceed (BLANK A)
1. should not exceed 10 mEq/L/day
125
1. What is the equation to calculate infusion volume in hyponatremia (sodium deficit) 2. calculate Na deficit, rate of correction should lie between (BLANK A)
1. should lie between 6-8 mEq/L/day
126
What is the equation for total body water (TBW) - this value is then used to calculate water/sodium deficits
127
Ca2+ excretion is variable with types of diuretics used. 1. Which type causes increased excretion 2. Which type causes decreased excretion
1. loop diuretics 2. thiazide diuretics
128
Carbonic Anhydrase Inhibitors 1. drug name 2. MOA/what part of nephron is acted on 3. Clinical use (3) 4. Adverse Effects (3)
1. Acetazolamide 2. Inhibits CA → prevents reabsorption of HCO3-/Na+ → so H2O/HCO3- excretion is increased 3. w/severe metabolic alkalosis, glaucoma, altitude sickness 4. metabolic acidosis, sulfide allergy, kidney stone + more
129
Osmotic Diuretics 1. drug name 2. MOA/what part of nephron is acted on 3. Clinical use (3) 4. Adverse Effects (2)
1. Mannitol 2. Acts on PCT - Mannitol is filtered in glomerulus but cannot be reabsorbed. Mannitol binds to water and since it cannot be reabsorbed then it inhibits reabsorption of water 3. drug overdose, elevated intracranial pressure, glaucoma 4. pulmonary edema, dehydration + more
130
Loop Diuretics 1. drug names (3) 2. MOA/what part of nephron is acted on 3. Clinical use (3) 4. Adverse Effects (4)
1. Furosemide, Bumetanide, Torsemide 2. TAL - Inhibits NKCC cotransporter, increased Na excretion and less H2O reabsorption bc of this +++ ALSO decreases medullary gradients 3. Edematous states (like CHF, cirrhosis), HTN, hypercalcemia 4. Hypokalemia, Hypocalcemia, Hypomagnesemia, Ototoxicity +more
131
Thiazide Diuretics 1. drug names (3) 2. MOA/what part of nephron is acted on 3. Clinical use (4) 4. Adverse Effects (4)
1. Hydrochlorothiazide (HCTZ) , Chlorthalidone, Metolazone 2. DCT - inhibits the Na/Cl cotransporter which brings in NaCl into epithelial cell. This leads to increased Na excretion - as well as water. **[[Decreased intracellular Na leads to increased Na/Ca cotransporter activity which takes Ca out of epithelial (basolateral) and induces Ca reabsorption (apical)]]** 3. Hypertension, recurrent Ca2+ kidney stones, osteoporosis, diabetes insipidus 4. Hypotension, Hyponatremia, Hypokalemia, elevated blood levels of GLUC (glucose, lipids, uric acid, calcium)
132
K+ Sparing Diuretics 1. drug names (4) 2. MOA/what part of nephron is acted on 3. Clinical use (3) 4. Adverse Effects (1)
1. Spironolactone, Eplerenone, Amiloride, Triameterene 2. collecting duct - Inhibits Na reabsorption via ENaCs (which prevents K secretion)…. this is going against influence of aldosterone 3. Hyperaldosteronism, Hypokalemia, HF, etc 4. Hyperkalemia which can lead to arrhythmia
133
Potassium Sparing Diuretics 1. spironolactone/eplerenone - MOA 2. Triamterene/Amiloride - MOA
1. Spironolactone / Eplerenone: competitive inhibitor of aldosterone (prevent channel expression) 2. Triamterene / Amiloride: direct inhibition of Na+ channels
134
ACE Inhibitors 1. drug names 2. MOA 3. Clinical use (3) 4. Adverse Effects (3)
1. Lisinopril (end in -pril) 2. Inhibits ACE which inhibits AT 2 and prevents constriction of efferent arterioles to decrease GFR - THIS IS MEANT TO DECREASE BP 3. Hypertension, HF, Proteinuria, etc 4. Cough, angioedema, teratogenic, more
135
Angiotensin II Receptor Blockers 1. drug names 2. MOA 3. Clinical use (3) 4. Adverse Effects
1. ARBs, Losartan (those ending -sartan) 2. Inhibits AT II from binding to AT1 receptor → inhibits RAAS effects (w/out increased bradykinin which lead to cough) in order to lower BP 3. Hypertension, HF, etc 4. Hyperkalemia, decreased GFR, same as ACE inhibitors
136
Aliskiren: SIA 1. MOA 2. Clinical use (3)
1. direct renin inhibitor to block angiotensinogen conversion to angiotensin 1 2. Hypertension (and in pts who are already using ACE inhibitors, ARBs)
137
What substance increases GFR
ANP - secreted from heart

Block 5 (7 decks)

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